{"_id": "WikiPedia_Gastroenterology$$$corpus_1", "text": "Abdominal angina  is  abdominal pain  after eating caused by a reduction of blood flow to the  celiac trunk ,\u00a0 superior mesenteric arteries  (SMA),  inferior mesenteric artery  (IMA), or the surrounding organs. [ 1 ]  Symptoms include  abdominal pain ,  weight loss ,  diarrhea ,  nausea ,  vomiting , and an aversion or fear of eating caused by the pain associated with eating."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2", "text": "Abdominal angina is caused by obstruction or  stenosis  of the  inferior mesenteric artery ,  celiac trunk , or  superior mesenteric artery . Gender, age, smoking,  hypertension ,  diabetes , and  hyperlipidemia  are risk factors for abdominal angina. The  digestive tract  relies on the celiac, superior mesenteric, and inferior mesenteric arteries for blood flow. Abdominal pain occurs when these arteries fail to provide adequate blood flow."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3", "text": "Abdominal angina is diagnosed using imaging to identify  stenosis . Differential diagnoses include  GERD ,  dietary sensitivities ,  constipation ,  pancreatitis , abdominal abscess,  appendicitis ,  irritable bowel syndrome ,  gastroenteritis ,  hepatitis , and gastrointestinal system inflammation.  Chronic mesenteric ischemia  requires surgical  revascularization  and treatment like  stents , transaortic  endarterectomy , or bypassing the arteries."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4", "text": "Abdominal angina often has a one-year delay between symptoms and treatment, leading to complications like  malnutrition  or bowel infarction. Abdominal angina is more prevalent in females with a 3:1 ratio, and the average age of onset is 60 years. Abdominal angina was first described by Dr. Baccelli in 1918 as lower abdominal pain after eating."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5", "text": "Symptoms of abdominal angina include postprandial  abdominal pain ,  weight loss ,  diarrhea ,  nausea ,  vomiting , and an aversion or fear of eating caused by the pain associated with eating. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6", "text": "Abdominal angina usually starts 30 minutes after eating and persists for one to three hours. Individuals typically express the pain as a dull ache by clenching their\u00a0fists over the  epigastrium  ( Levine sign ). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7", "text": "Sometimes people may reduce their caloric intake in an attempt to decrease pain which can lead to weight loss. There may also be changes in bowel habits, most commonly diarrhea from  malabsorption  or rarely  constipation . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8", "text": "Abdominal angina is caused by obstruction or\u00a0 stenosis  of the  inferior mesenteric artery  (IMA),\u00a0 celiac trunk , or\u00a0 superior mesenteric artery  (SMA). [ 4 ]  More than 95% of abdominal angina is caused by stenosis of the splanchnic arteries due to local  atherosclerosis . [ 5 ] [ 6 ]  The occlusion mainly affects the ostia or the last few centimetres of the  mesenteric arteries . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9", "text": "In rare cases, compression of the celiac trunk by the diaphragm's arcuate ligament can result in isolated occlusive disease (also known as\u00a0\" median arcuate ligament syndrome \"). [ 5 ]  Other less common causes of vascular obstruction include  vasculitis ,\u00a0chronic mesenteric  venous thrombosis ,  fibromuscular dysplasia ,  radiation enteritis , and, in rare cases, extrinsic obstruction or vessel encasement by a tumour. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_10", "text": "Approximately 82% of those with abdominal angina have  diabetes .  Hyperlipidemia , which frequently causes  peripheral vascular disease , raises the risk of abdominal angina\u00a0by 70% and correlates with the  atherosclerotic  aspect of the disease process. Smoking plays a part in the development of abdominal angina. Smokers account for 75% to 80% of all abdominal angina\u00a0cases. Age also plays\u00a0a role. The average age of onset is more than 60. This data corresponds with the vascular damage that occurs with age. Gender appears to play a role in the\u00a0development of abdominal angina. Women are threefold more likely to develop abdominal angina\u00a0than men.\u00a0 Hypertension  is another known risk factor. Six out of ten of those with abdominal angina\u00a0will be hypertensive. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_11", "text": "The  celiac ,  superior mesenteric , and  inferior mesenteric  arteries are the three primary blood vessels that support the  digestive tract .  Abdominal pain  happens because\u00a0the digestive processes require increased blood flow to the stomach. The stenotic or occluded artery cannot give adequate blood flow. The pain is caused by  ischemia  of the affected tissues, which do not receive the essential perfusion to preform digestion. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_12", "text": "The gastrointestinal system has significant  collateral circulation , which may worsen in cases of vascular  stenosis . Along with the protection provided by collateral blood flow, the colon possesses various other mechanisms to prevent  ischemia , such as opening of all mesenteric capillaries, redistribution of intramural blood supply, and improved oxygen extraction. But if those are exceeded, these defensive mechanisms become overwhelmed and no longer provide protection. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_13", "text": "Some people with a single-vessel lesion experience symptoms, while others with up to three lesions are asymptomatic; hence, the number of arteries required to cause symptoms of ischemia is debatable. The occurrence of angina is determined by factors besides the number of arteries affected, such as the location of the lesion, the time of advancement of the lesions, and concurrent disorders that impact  angiogenesis . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_14", "text": "Abdominal angina is diagnosed by identifying  stenosis  with imaging. [ 10 ]  Since the symptoms of abdominal angina overlap with various other disorders, other causes of symptoms are ruled out as a part of the diagnostic process.  Gastric ulcers ,  abdominal aortic aneurysms , and  gastrointestinal cancers  can have similar symptoms and can be ruled out by  esophagogastroduodenoscopy ,  CT scans , or  MR angiogram . Other differential diagnoses include  GERD , dietary or  food sensitivities ,  constipation ,  pancreatitis , abdominal abscess,  appendicitis ,  irritable bowel syndrome ,  gastroenteritis ,  hepatitis , and inflammation of the gastrointestinal system. [ 11 ]   Duplex ultrasound ,  MR angiography ,  angiography , and  computed tomography angiography  can be used to help confirm the diagnosis of abdominal angina. [ 3 ]  Duplex ultrasound may be used to screen for abdominal angina but is not ideal for visualizing stenosis. Angiography, MR angiography, or CT angiography can be used to further visualize the celiac and mesenteric arteries. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_15", "text": "Abdominal angina is treated differently based on the severity and cause.  Antibiotics  are often used in the case of  colonic ischemia  as there is often cooccuring infections. When possible the underlying cause of abdominal angina may be treated. This includes medications to treat  heart failure ,  hypertension ,  dysrhythmia , or  hyperlipidemia . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_16", "text": "The most effective treatment for  chronic mesenteric ischemia  is surgical  revascularization  and percutaneous treatment such as  stents . [ 12 ]  Surgical treatment may include transaortic  endarterectomy  of the effected arteries or creating a retrograde or anterograde bypass in the arteries. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_17", "text": "Similarly to other  vascular disorders , abdominal angina can be slowly progressive. There is often a one-year delay between the onset of symptoms and treatment. Complications of abdominal angina such as  malnutrition  or  bowel infarction  can cause increased morbidity and mortality in this population. [ 4 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_18", "text": "The prevalence of abdominal angina is unknown. It is more prevalent in females than males with a ratio of 3:1. The mean age of those affected is 60 years old. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_19", "text": "The term \"abdominal angina\" was first used by Dr. Baccelli in 1918. He used the term to describe a group of patients who had developed lower abdominal pain after eating. In 1936 Dunphy made the connection between abdominal angina and gastrointestinal necrosis. 21 years later Mikkelson introduced a surgery which could help restore blood flow to the gastrointestinal system. Although there was early interest in research, there has been very little subsequent research in the years following. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_20", "text": "Abdominal epilepsy  is a  rare condition  consisting of  gastrointestinal  disturbances caused by  epileptiform seizure activity . [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ]  It is most frequently found in children, though a few cases of it have been reported in adults. [ 6 ]  It has been described as a type of  temporal lobe epilepsy . [ 7 ]  Responsiveness to  anticonvulsants  can aid in the diagnosis. [ 8 ]  Distinguishing features of abdominal epilepsy include (1) Abnormal laboratory, radiographic, and endoscopic findings revealing  paroxysmal  GI manifestations of unknown origin (2) CNS symptoms (3) Abnormal  EEG . [ 9 ]  Most published medical literature dealing with abdominal epilepsy is in the form of individual  case reports . A 2005 review article found a total of 36 cases described in the medical literature. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_21", "text": "Abdominal epilepsy is marked by GI symptoms such as  abdominal pain  followed by uncontrollable  vomiting , usually preceded by  lethargy . Lethargy and confusion is the most common neurological symptoms associated with abdominal epilepsy. Other symptoms include generalized  tonic-clonic seizures  followed by sleep, and unresponsiveness. [ 10 ] [ 11 ]   Abdominal aura characterized by abdominal sensations precedes the abdominal seizure. This is associated with pain, nausea, hunger, gassiness especially in temporal lobe epilepsy. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_22", "text": "It is unknown as to what causes abdominal epilepsy. While a causal relationship between seizure activity and the GI symptoms has not been proven, the GI symptoms cannot be explained by other pathophysiological mechanisms, and are seen to improve upon  anticonvulsant  treatment. Because the condition is so rare, no high-quality studies exist. There have been too few reported cases to identify risk factors, genetic factors, or other potential causes. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_23", "text": "Criteria for diagnosis of abdominal epilepsy includes frequent periodic abdominal symptoms, an abnormal  electroencephalogram  (EEG) and significant improvement of gastrointestinal symptoms after taking anti-seizure medication. Medical testing for diagnosis can be completed using  MRI scans  of the brain,  CT scans  and  ultrasounds  of the abdomen,  endoscopy  of the gastrointestinal tract, and  blood tests . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_24", "text": "Typically, the diagnostic process begins with gathering information regarding the presence of common symptoms like paroxysmal abdominal pain and other gastrointestinal issues. Symptoms that persist continuously or for prolonged periods are less likely to indicate abdominal epilepsy. It's important to consider convulsions, alterations in consciousness, and other neurological symptoms alongside gastrointestinal symptoms when diagnosing abdominal epilepsy. Though every episode of it may not be accompanied by a neurological symptom. This often makes these neurological symptoms unnoticeable for the patient. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_25", "text": "This is followed by the necessary evaluation that comprises neurological and physical examination, laboratory test, abdominal imaging using CT and ultrasound, endoscopy. Next if the above are normal but the history still suggests for this syndrome an EEG must be performed. EEG findings alone too cannot distinguish between the kinds of epilepsy. Moreover, often an EEG report could be normal if an event is not accompanied by neurological symptoms. If it is doubtable a neurologist should be consulted. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_26", "text": "Like other forms of epilepsy, abdominal epilepsy is treated with anticonvulsant drugs, such as  phenytoin . Based on the clinical response additional medication may be used for complementing it or it could be used instead of phenytoin. Since no controlled studies exist, however, other drugs may be equally effective. [ 10 ]  Anticonvulsants target non-epileptic causes of abdominal pain via  sedative  mechanisms. It may also act just as a  placebo . The prognosis is generally good and most patients are benefitted from medicines alone. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_27", "text": "The pathophysiology behind abdominal epilepsy remains speculative. Several studies indicate that  insula  and  sylvian  fissures also known as  lateral sulcus  could be related to inducing abdominal epilepsy. Their location is found to coincide with the locations of the abdomen on the  Sensory homunculus . [ 14 ]  Any pathophysiological changes in the M2 portion of  cerebral artery  which flows through  lateral sulcus  are associated with the epilepsies of the  temporal  and  parietal  regions. [ 15 ]  The abdominal symptoms are believed to be associated with the transmission of impulses from the temporal lobe to the  dorsal motor nucleus  of the  vagus  nerve via the dense direct projections. The  hypothalamus  is also believed to induce  sympathetic  pathways from the  amygdala  in the medial temporal lobe to the  GI  tract to trigger such symptoms. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_28", "text": "Cerebral tumors have been assessed to be a plausible cause of abdominal epilepsy. [ 17 ]  Right  parietal  and  occipital   encephalomalacia , biparietal  atrophy , and bilateral perisylvian  polymicrogyria  has been possibly associated with  ictal  abdominal pain associated with abdominal epilepsy. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_29", "text": "French physician and scientist  Armand Trousseau  is commonly credited as being the first to describe the condition in 1868 in a boy with  paroxysmal  GI symptoms culminating in  grand mal  epileptic seizure. [ 19 ]  The first account of abdominal epilepsy supported by EEG tracings came in 1944 in an article by M.T. Moore, followed by subsequent case reports from the same group. [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_30", "text": "Abdominal migraine   (AM)  is a  functional disorder  that usually manifests in childhood and adolescence, without a clear pathologic mechanism or  biochemical  irregularity. Children frequently experience sporadic episodes of excruciating central  abdominal pain  accompanied by  migrainous  symptoms like  nausea ,  vomiting , severe  headaches , and general  pallor . [ 1 ]  Abdominal migraine can be diagnosed based on clinical criteria and the exclusion of other disorders. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_31", "text": "The  US Food and Drug Administration  has not approved any drugs for the treatment of abdominal migraine. The goal of treatment is usually to prevent attacks, and this is often achieved through nonpharmacologic intervention. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_32", "text": "Research has indicated that the incidence of abdominal migraine in children falls within the range of 0.4% [ 4 ]  to 4%. [ 2 ]  The condition primarily affects children aged 3 to 10 years, with a higher prevalence in females. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_33", "text": "Midline  abdominal pain  with  paroxysmal , recurrent, acute onset attacks that last an average of 17 hours are the hallmarks of abdominal migraine. [ 6 ]  There have been reports that these attacks can last anywhere from two to seventy-two hours. [ 5 ]  Although it has also been reported to be diffuse and colicky, the pain is usually described as dull and periumbilical. 91% of patients have  anorexia , 73% to 91% have  nausea , 35% to 50%  vomit , and 93% to 100% of patients have associated  pallor . [ 7 ]  The attack usually comes to an abrupt end. [ 5 ]  The average annual frequency of abdominal migraine attacks in patients is 14. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_34", "text": "Although nonspecific prodromes can occur before attacks, abdominal migraine attacks are usually sporadic. This can include behavioral and  mood swings ,  anorexia ,  flushing ,  diarrhea , and  auras  that include  numbness ,  slurred speech ,  tingling  in the distal extremities, and flashing lights. [ 5 ]  Weeks to months may pass between episodes, and during this time patients usually experience no symptoms. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_35", "text": "Abdominal migraine has been linked to specific alterations in the  gut-brain axis , vascular dysregulation, modifications in the  central nervous system , and genetic factors. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_36", "text": "Abdominal migraine pathophysiology may involve psychological factors.  Abuse  and stressful events are two risk factors for recurrent abdominal pain, for instance. Furthermore, it has been demonstrated that kids with  functional gastrointestinal disorders  experience  mental health conditions  like  anxiety  and  depression  more frequently than kids without these conditions. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_37", "text": "There are several typical causes of attacks of abdominal migraines.  Stressors  related to work and family life, irregular sleep patterns, extended fasts and food deprivation,  dehydration , exercise, travel, high- amine  foods, foods containing flavoring, coloring, and  monosodium glutamate  (MSG), and flashing lights are a few common triggers. [ 5 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_38", "text": "A significant hereditary component may be involved in abdominal and other migraines due to their strong familial incidence, [ 11 ]  especially in the case of mutations affecting  cell membrane transport  ( channelopathies ). [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_39", "text": "While the  pathophysiology  of  functional gastrointestinal disorders  (FGIDs) has many potential contributors, the etiology of abdominal migraine is still unknown. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_40", "text": "It is thought that abnormal electrical discharge from the  hypothalamus  that travels to the cortex and  autonomic nervous system [ 15 ]  or variations in the  cerebral artery's  blood flow velocity cause attacks. [ 16 ]  In patients with FGIDs, there appears to be a disruption in the complex  brain-gut axis . [ 17 ]  Many episodic  functional gastrointestinal disorders  in childhood have been linked to  mitochondrial disease , [ 18 ]   hypothalamic-pituitary-axis  dysfunction, and  gene mutations ; these associations have not, however, been studied in patients diagnosed with abdominal migraine. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_41", "text": "It's critical to rule out organic diseases as the source of a child's symptoms while also taking the patient's functional state into account. When diagnosing abdominal migraine, a patient's complete medical history and physical examination are crucial. Additionally, any potential alarm signs and symptoms should be carefully examined. The presence of visible or occult  blood in the stool ,  dysphagia ,  hematemesis ,  bilious  vomiting,  fever , changes in growth pattern, and  weight loss   are a few examples of alarm symptoms. [ 20 ]  Further imaging and testing should be carried out if these alarm signs or symptoms are apparent. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_42", "text": "The  Rome IV criteria  state that paroxysmal bouts of intense, acute periumbilical, midline, or diffuse  abdominal pain  lasting at least an hour, exhibiting a recurrent pattern, being incapacitating, and interfering with regular activities can be used to diagnose abdominal migraine if at least two of these episodes take place over a six-month period. There should be weeks or months without any symptoms in between attacks. The following symptoms must be present in at least two instances:  pallor ,  photophobia ,  headache ,  nausea ,  vomiting , and  anorexia . Lastly, there is no other medical diagnosis that can account for the symptoms. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_43", "text": "Abdominal migraine is defined by the  International Classification of Headache Disorders  III criteria as five or more episodes of abdominal pain lasting two to seventy-two hours. A minimum of two out of three of the following criteria must also be met by the pain: dull or \"just sore\" quality; midline location, periumbilical, or poorly localized; and moderate to severe intensity.  Pallor ,  nausea ,  vomiting , and  anorexia  are associated symptoms that the patient should have at least two of. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_44", "text": "Abdominal migraine must be distinguished from other causes of chronic or recurrent abdominal pain. These include  irritable bowel syndrome ,  peptic ulcer disease , and  gastroesophageal reflux disease . [ 3 ]  It must also be distinguished from causes of acute abdominal pain, such as  appendicitis , as wrong diagnosis may lead to unnecessary  appendectomy . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_45", "text": "Because there are so few studies in the literature, there are no firm recommendations for the treatment of abdominal migraines. [ 24 ]  The majority of treatment options are predicated on anecdotal evidence, a small number of studies conducted on a relatively small number of children, and a close correlation between abdominal migraines and both  migraine headaches  and FGIDs. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_46", "text": "When treating patients with abdominal migraines, doctors may find the STRESS mnemonic useful. It stands for stress management, travel advice, rest, emergency symptoms, sparkling lights, and snacks to avoid. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_47", "text": "Certain triggers, like bright light, restless nights, travel, and extended fasting, should probably be minimized or avoided once they have been identified. [ 19 ]  Emotional stressors from family or school activities can be a trigger for certain kids, so it's best to minimize or stay away from them. [ 3 ]  Although there are no particular randomized trials evaluating the efficacy of biofeedback and counselling in treating abdominal migraines, it is believed that these interventions may be helpful if emotional stress is a trigger factor in the development of migraine in children. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_48", "text": "It's unclear what function  elimination diets  serve. Nonetheless, in patients experiencing both migraine and  IBS  symptoms, an  immunoglobulin G  (IgG)-based elimination diet shows promise in lowering migraine episodes. [ 28 ]  There isn't much more proof that a child's diet has a significant impact on when migraines begin. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_49", "text": "In one study, 14 children with abdominal migraine were administered  pizotifen  syrup, a  serotonin  and  histamine  antagonist. After four months, 70% of the patients said their symptoms had improved. Their symptoms were noticeably milder and less frequent. [ 30 ]   Propranolol  and  cyproheptadine  syrup were found to alleviate symptoms in a retrospective review. [ 25 ]   Flunarizine  use was found to reduce the frequency and duration of abdominal migraine attacks in another retrospective review. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_50", "text": "Analgesics ,  triptans , and  antiemetics  may be helpful for sudden attacks of abdominal migraines. It has been suggested that patients with  nausea ,  vomiting , or  anorexia  might benefit more from nasal sprays or suppositories. [ 5 ]  Acute attacks have been reported to be resolved by  acetaminophen  and  ibuprofen . [ 32 ]  Intranasal  sumatriptan  alleviated the symptoms of abdominal migraine in two children, according to a case report. [ 33 ]  In refractory cases, intravenous  sodium valproate  has been reported to resolve abdominal migraine episodes. [ 34 ]  According to a case series, intravenous  dihydroergotamine  treatment prevented abdominal migraine attacks in five out of six pediatric patients. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_51", "text": "Abdominal migraine can have a significant impact on day-to-day life. [ 36 ]  Children may  miss school  or other activities. [ 36 ]  It resolves in many patients. [ 23 ] [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_52", "text": "Abdominal migraine primarily affects  children , for whom it is a common cause of chronic  abdominal pain . It may be as high as 9% or as low as 1% among children. [ 23 ]  It is rare in  adults . [ 3 ]  However, children diagnosed with abdominal migraines may have migraine headaches as adults. [ 38 ]  The mean age of diagnosis is 7 years. [ 39 ] [ 40 ]  It appears to be slightly more common in  women . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_53", "text": "This condition was first described in 1921 by Buchanan. [ 41 ]  It was once considered a controversial diagnosis. [ 42 ]  However, it is now accepted as a common cause of chronic abdominal pain in children. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_54", "text": "Aerophagia  (or  aerophagy ) is a condition of excessive air swallowing, which goes to the  stomach  instead of the  lungs . Aerophagia may also refer to an unusual condition where the primary symptom is excessive  flatus (farting) ,  belching (burping)  is not present, and the actual mechanism by which air enters the gut is obscure or unknown. [ 1 ]  Aerophagia in psychiatry is sometimes attributed to nervousness or  anxiety . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_55", "text": "Aerophagia is associated with excessively  chewing gum ,  smoking , drinking  carbonated drinks , eating too quickly, as well as anxiety, high  continuous positive airway pressure  and wearing loose  dentures . Aerophagia is also carried out deliberately as a voluntary action to increase the length and volume of a  belch , as any air successfully swallowed serves to increase the  partial pressure  in the stomach and expand a burp. [ 13 ] [ 14 ]  In people with cervical spinal blockages, inhaling can cause some air to enter the esophagus and stomach involuntarily. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_56", "text": "Aerophagia is diagnosed in 8.8% of cognitively delayed patients [ 16 ]  where the coordination between swallowing and respiration is impaired and not well-defined. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_57", "text": "Aerophagia is a dangerous potential side effect of  non-invasive ventilation  (NIV), commonly used in treatments of respiratory problems and cardiovascular critical care or in surgery when a general  anaesthetic  is required. In the case of aerophagia during NIV, it is normally diagnosed by experienced medical specialists who check on patients intermittently during NIV use for any emergent problems. The diagnosis is based on the sound heard by listening through a  stethoscope  placed outside the abdominal cavity. Using this approach, the problem is sometimes detected later than when it develops, possibly also later than necessary. Belated detection or response to aerophagia may lead to gastric distension, which in turn could elevate the  diaphragm  or cause aspiration of the stomach contents into the lungs [ 18 ]  or pneumatic rupture of the  esophagus  due to extreme gastric insufflation. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_58", "text": "Afferent loop syndrome  is an uncommon side effect of gastric surgery. [ 1 ]  The afferent loop is made up of a segment of  duodenum  and/or proximal  jejunum  located upstream of a double-barrel  gastrojejunostomy   anastomosis .  Abdominal pain  and distension are signs of increased intraluminal pressure resulting from the accumulation of enteric secretions in the obstructed afferent loop. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_59", "text": "Afferent loop syndrome may result from  volvulus , recurring  cancer , stomal  stenosis , adhesions, kinking at the anastomotic site, internal  herniation , and gastrointestinal stones. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_60", "text": "Laboratory investigations can help diagnose afferent loop syndrome, but imaging scans are required for a confirmation diagnosis. [ 2 ]  When diagnosing afferent loop syndrome,  abdominal CT  is regarded as the preferred radiographic investigation. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_61", "text": "The treatment of afferent loop syndrome is determined by the underlying cause. [ 1 ]  Surgical therapy, such as adhesiolysis,  bypass , or limb reconstruction, can usually eliminate the source in patients with benign etiologies. [ 4 ]  Treatment for patients with afferent loop syndrome due to recurrent tumors shifts to palliation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_62", "text": "Nonbilious  vomiting ,  nausea , and abrupt onset  stomach pain  in the right upper quadrant are common symptoms in patients with acute afferent loop syndrome.  Abdominal distension  and postprandial epigastric discomfort lasting anywhere from a few minutes to an hour are common symptoms experienced by patients with chronic afferent loop syndrome. Bilious projectile  vomiting  is a typical symptom of chronic afferent loop syndrome that relieves symptoms quickly. In patients with persistent afferent loop syndrome,  steatorrhea  and  diarrhea  may exacerbate intestinal stasis.  Iron deficiency anemia  and/or  vitamin B12 deficiency  can arise from the deconjugation of bile salts by bacteria. In order to avoid postprandial pain, patients frequently quit eating, which can result in significant weight loss. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_63", "text": "Right upper quadrant abdominal and/or epigastric tenderness\u00a0is the most common physical finding in afferent loop syndrome patients. There is a palpable abdominal bulge in the right upper quadrant in about one-third of people suffering from acute afferent loop syndrome. Patients may exhibit symptoms of  pancreatitis , such as  obstructive jaundice  or abdominal discomfort radiating to the side or back. Patients may show up with guarding, which is symptomatic of  peritonitis , and a stiff abdomen if intestinal perforation has occurred. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_64", "text": "Afferent loop syndrome can have either a benign or  malignant  etiology, depending on the type of obstructive lesion. Depending on where the lesion is located, there are three primary pathways that lead to benign etiology. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_65", "text": "Anastomotic stricture, foreign body impaction,  bezoars , and  enteroliths  are all potential causes of intraluminal blockage. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_66", "text": "Radiation enteritis  and scarring from marginal gastrojejunostomy ulceration are the causes of mechanical blockage of the intramural area. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_67", "text": "Conditions that cause external compression include internal  hernia ,  volvulus , entrapment, compression, kinking of the afferent loop, postoperative adhesion, and intussusception of the afferent loop. [ 9 ] [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_68", "text": "An antecolic afferent loop's redundancy increases the danger of kinking,  volvulus , and adhesion-induced limb entrapment when the bowel length exceeds 30 to 40 cm. Conversely, the risk of an internal  herniation  developing in a retrocolic afferent loop is increased by incorrectly closed mesocolic abnormalities. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_69", "text": "Locoregional tumor recurrence impeding the afferent loop at the anastomotic site or gastric residual is frequently linked to malignant afferent loop syndrome. [ 13 ]  Additional factors contributing to blockage include peritoneal  carcinomatosis  and regional  lymphadenopathy . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_70", "text": "The preferred radiographic study for diagnosing afferent loop syndrome is thought to be  abdominal CT . [ 3 ]  An blocked intestinal segment can be directly visualized with  CT scanning . It is also possible to look at other organs that could be affected by the obstruction, like the  biliary tree  and  pancreas . [ 2 ]  When afferent loop syndrome first manifests, the abdominal midline is often crossed by a fluid-filled tubular formation that lies between the super mesenteric artery and the  aorta . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_71", "text": "Three parameters determine the treatment plan: the type of obstructive lesion, the blockage site (inframesocolic or supramesocolic), and the patency of the major  anastomoses  for the  hepaticojejunostomy  and  pancreaticojejunostomy . The standard of care for afferent loop syndrome patients is typically surgery. Adhesiolysis,  bypass surgery , and excision with repair of the obstructive malignant lesions are the surgical therapy options available. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_72", "text": "The prognosis is good for patients who receive an early diagnosis and have surgery, with the exception of cases of advanced or recurring  cancer . A delay\u00a0in diagnosis is associated with a mortality rate that varies from 30% to 60%. [ 16 ]  Patients who experience afferent limb perforation and subsequent  peritonitis  and shock have poor prognoses. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_73", "text": "According to reports, 0.2% of patients after distal  gastrectomy  with  Roux-en-Y reconstruction , 1% after laparoscopic distal  gastrectomy  with Billroth II reconstruction, and 0.3\u20131.0% of patients following total  gastrectomy  with Billroth II or  Roux-en-Y reconstruction  have afferent loop syndrome. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_74", "text": "In 1950, Roux, Pedoussaut, and Marchal initially reported afferent loop syndrome in patients who had undergone gastric surgery and were experiencing bilious  vomiting . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_75", "text": "An  ameboma , also known as an  amebic granuloma , is a rare complication of  Entamoeba histolytica  infection, where in response to the infecting  amoeba  there is formation of annular colonic granulation, which results in a large local lesion of the bowel. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_76", "text": "The  ameboma  may manifest as a right lower quadrant abdominal mass, which may be mistaken for carcinoma,  tuberculosis ,  Crohn's disease ,  actinomycosis , or  lymphoma ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_77", "text": "Biopsy is necessary for definitive diagnosis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_78", "text": "This  infectious disease  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_79", "text": "Anorectal abscess  (also known as an  anal/rectal abscess  or  perianal/perirectal abscess ) is an  abscess  adjacent to the  anus . [ 1 ]   Most cases of perianal abscesses are sporadic, though there are certain situations which elevate the risk for developing the disease, such as  diabetes mellitus ,  Crohn's disease , chronic  corticosteroid  treatment and others. It arises as a complication of  paraproctitis . Ischiorectal, inter- and intrasphincteric abscesses have been described. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_80", "text": "It typically presents with pain and swelling in the perianal area. [ 2 ]  The pain may be dull, aching, or throbbing. It is worst when the person sits down and right before a bowel movement. After the individual has a bowel movement, the pain usually lessens. Other signs and symptoms of anorectal abscess include  constipation , drainage from the rectum,  fever  and chills, or a palpable mass near the anus. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_81", "text": "The condition can become extremely painful, and usually worsens over the course of just a few days. The pain may be limited and sporadic at first, but may worsen to a constant pain which can become very severe when body position is changed (e.g., when standing up, rolling over, and so forth). Depending upon the exact location of the abscess, there can also be excruciating pain during bowel movements, though this is not always the case. This condition may occur in isolation, but is frequently indicative of another underlying disorder, such as  Crohn's disease . [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_82", "text": "If left untreated, an  anal fistula  will almost certainly form, connecting the rectum to the skin. [ 3 ]  This requires more intensive surgery. Furthermore, any untreated abscess may (and most likely will) continue to expand, eventually becoming a serious systemic infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_83", "text": "Abscesses are caused by a high-density infection of (usually) common bacteria which collect in one place or another for any variety of reasons.  Anal abscesses, without treatment, are likely to spread and affect other parts of the body, particularly the groin and rectal lumen. [ 3 ]   All abscesses can progress to serious generalized infections requiring lengthy hospitalizations if not treated."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_84", "text": "Historically, many rectal abscesses are caused by bacteria common in the digestive system, such as  E. coli . While this still continues often to be the case, there has recently been an increase in the causative organism being  staphylococcus , as well as the difficult to treat community-acquired  methicillin-resistant S. aureus . Because of the increasing appearance of more exotic bacteria in anal abscesses, microbiological examination will always be performed on the surgical exudate to determine the proper course of any antibiotic treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_85", "text": "Diagnosis of anorectal abscess begins with a medical history and physical exam. Imaging studies which can help determine the diagnosis in cases of a deep non-palpable perirectal abscess include pelvic CT scan,  MRI  or trans-rectal ultrasound. These studies are not necessary, though, in cases which the diagnosis can be made upon physical exam. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_86", "text": "Anorectal abscesses are classified according to their anatomic location and the following are the most common types: perianal abscess, ischiorectal abscess, intersphincteric abscess and supralevator abscess. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_87", "text": "This condition is often initially misdiagnosed as  hemorrhoids , since this is almost always the cause of any sudden anal discomfort. The presence of the abscess, however, is suspected when the pain quickly worsens over one or two days and usual hemorrhoid treatments are ineffective in bringing relief.  Furthermore, any serious abscess will eventually begin to cause signs and symptoms of general infection, including  fever  and nighttime chills."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_88", "text": "A physician can rule out a hemorrhoid with a simple visual inspection, and usually appreciate an abscess by touch."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_89", "text": "Anal abscesses are rarely treated with a simple course of antibiotics. In almost all cases surgery will need to take place to remove the abscess. Treatment is possible in an  emergency department  under  local anesthesia , but it is highly preferred to be formally admitted to a hospital and to have the surgery performed in an  operating room  under  general anesthesia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_90", "text": "Generally speaking, a fairly small but deep incision is performed close to the root of the abscess.  The surgeon will allow the abscess to drain its  exudate  and attempt to discover any other related lesions in the area. This is one of the most basic types of surgery, and is usually performed in less than thirty minutes by the anal surgical team. Generally, a portion of the exudate is sent for microbiological analysis to determine the type of infecting bacteria.  The incision is not closed (stitched), as the damaged tissues must heal from the inside toward the skin over a period of time."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_91", "text": "The affected individual is often sent home within twenty-four hours of the surgery, and may be instructed to perform several ' sitz baths ' per day. These involve a small basin which is filled with warm water, and possibly with salts; usually fits over a toilet;  and soaks the affected area for a period of time. Another method of recovery involves the use of surgical packing. The initial packing is inserted by the surgical team, with redressing generally performed by hospital staff or a district nurse. During the week following the surgery, many patients will have some form of antibiotic therapy, along with some form of pain management therapy, consistent with the nature of the abscess."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_92", "text": "It is unclear whether internal packing of the perianal abscess influences time taken for healing, wound pain, development of fistulae, or abscess recurrence. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_93", "text": "The patient usually experiences an almost complete relief of the severe pain associated to his/her abscess upon waking from anesthesia; the pain associated with the opening and draining incision during the post-operative period is often mild in comparison."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_94", "text": "Additional images of anorectal abscess"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_95", "text": "Anismus  or  dyssynergic defecation  is the failure of normal relaxation of  pelvic floor  muscles during attempted  defecation . It can occur in both children and adults, and in both men and women (although it is more common in women). It can be caused by physical defects or it can occur for other reasons or unknown reasons. Anismus that has a behavioral cause could be viewed as having similarities with  parcopresis , or psychogenic fecal retention. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_96", "text": "Symptoms include  tenesmus  (the sensation of incomplete emptying of the rectum after defecation has occurred) and  constipation . Retention of stool may result in fecal loading (retention of a mass of stool of any consistency) or  fecal impaction  (retention of a mass of hard stool). This mass may stretch the walls of the rectum and colon, causing  megarectum  and/or  megacolon , respectively. Liquid stool may leak around a fecal impaction, possibly causing degrees of liquid fecal incontinence. This is usually termed  encopresis  or soiling in children, and  fecal leakage , soiling or liquid  fecal incontinence  in adults."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_97", "text": "Anismus is usually treated with dietary adjustments, such as  dietary fiber  supplementation. It can also be treated with a type of  biofeedback  therapy, during which a sensor probe is inserted into the person's  anal canal  in order to record the pressures exerted by the pelvic floor muscles. These pressures are visually fed back to the patient via a monitor who can regain the normal coordinated movement of the muscles after a few sessions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_98", "text": "Some researchers have suggested that anismus is an over-diagnosed condition, since the standard investigations or  digital rectal examination  and  anorectal manometry  were shown to cause paradoxical sphincter contraction in healthy controls, who did not have constipation or incontinence. [ 1 ]  Due to the invasive and perhaps uncomfortable nature of these investigations, the pelvic floor musculature is thought to behave differently compared to normal circumstances. These researchers went on to conclude that paradoxical pelvic floor contraction is a common finding in healthy people as well as in people with chronic constipation and fecal incontinence, and it represents a non-specific finding or laboratory artifact related to untoward conditions during examination, and that true anismus is actually rare."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_99", "text": "Symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_100", "text": "To understand the cause of anismus, an understanding of normal colorectal anatomy and physiology, including the normal defecation mechanism, is helpful. The relevant anatomy includes: the  rectum , the  anal canal  and the muscles of the  pelvic floor , especially  puborectalis  and the  external anal sphincter . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_101", "text": "The  rectum  is a section of bowel situated just above the anal canal and distal to the  sigmoid colon  of the  large intestine . It is believed to act as a reservoir to store stool until it fills past a certain volume, at which time the defecation reflexes are stimulated. [ 4 ]  In healthy individuals, defecation can be temporarily delayed until it is socially acceptable to  defecate . In continent individuals, the rectum can expand to a degree to accommodate this function. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_102", "text": "The anal canal is the short straight section of bowel between the rectum and the  anus . It can be defined functionally as the distance between the anorectal ring and the end of the  internal anal sphincter . The internal anal sphincter forms the walls of the anal canal. The internal anal sphincter is not under voluntary control, and in normal persons it is contracted at all times except when there is a need to defecate. This means that the internal anal sphincter contributes more to the resting tone of the anal canal than the external anal sphincter. The internal sphincter is responsible for creating a watertight seal, and therefore provides continence of liquid stool elements. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_103", "text": "The  puborectalis  muscle is one of the pelvic floor muscles. It is  skeletal muscle  and is therefore under voluntary control. The puborectalis originates on the posterior aspect of the  pubic bone , and runs backwards, looping around the bowel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_104", "text": "The point at which the rectum joins the anal canal is known as the anorectal ring, which is at the level that the puborectalis muscle loops around the bowel from in front. This arrangement means that when puborectalis is contracted, it pulls the junction of the rectum and the anal canal forwards, creating an angle in the bowel called the anorectal angle. This angle prevents the movement of stool stored in the rectum moving into the anal canal. It is thought to be responsible for gross continence of solid stool. Some believe the anorectal angle is one of the most important contributors to continence. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_105", "text": "Conversely, relaxation of the puborectalis reduces the pull on the junction of the rectum and the anal canal, causing the anorectal angle to straighten out. A  squatting posture  is also known to straighten the anorectal angle, meaning that less effort is required to defecate when in this position. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_106", "text": "Distension of the rectum normally causes the internal anal sphincter to relax (rectoanal inhibitory response, RAIR) and the external anal sphincter initially to contract (rectoanal excitatory reflex, RAER). The relaxation of the internal anal sphincter is an involuntary response. The external anal sphincter, by contrast, is made up of skeletal (or striated muscle) and is therefore under voluntary control. It can contract vigorously for a short time. Contraction of the external sphincter can defer defecation for a time by pushing stool from the anal canal back into the rectum. Once the voluntary signal to defecate is sent back from the brain, the abdominal muscles contract (straining) causing the intra-abdominal pressure to increase. The pelvic floor is lowered causing the anorectal angle to straighten out from ~90 o  to <15 o  and the external anal sphincter relaxes. The rectum now contracts and shortens in  peristaltic waves , thus forcing fecal material out of the rectum, through the anal canal and out of the anus. The internal and external anal sphincters along with the puborectalis muscle allow the feces to be passed by pulling the anus up over the exiting feces in shortening and contracting actions. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_107", "text": "In patients with anismus, the puborectalis and the external anal sphincter muscles fail to relax, with resultant failure of the anorectal angle to straighten out and facilitate evacuation of feces from the rectum. These muscles may even contract when they should relax (paradoxical contraction), and this not only fails to straighten out the anorectal angle, but causes it to become more acute and offer greater obstruction to evacuation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_108", "text": "As these muscles are under voluntary control, the failure of muscular relaxation or paradoxical contraction that is characteristic of anismus can be thought of as either maladaptive behavior or a loss of voluntary control of these muscles. Others claim that puborectalis can become  hypertrophied  (enlarged) or  fibrosis  (replacement of muscle tissue with a more fibrous tissue), which reduces voluntary control over the muscle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_109", "text": "Anismus could be thought of as the patient \"forgetting\" how to push correctly, i.e. straining against a contracted pelvic floor, instead of increasing abdominal cavity pressures and lowering pelvic cavity pressures. It may be that this scenario develops due to stress. For example, one study reported that anismus was strongly associated with sexual abuse in women. [ 7 ]  One paper stated that events such as pregnancy, childbirth, gynaecological descent or neurogenic disturbances of the brain-bowel axis could lead to a \"functional  obstructed defecation syndrome \" (including anismus). [ 8 ]  Anismus may develop in persons with  extrapyramidal motor disturbance  due to  Parkinson's disease . [ 9 ]   This represents a type of  focal dystonia . [ 10 ]  Anismus may also occur with  anorectal malformation ,  rectocele , [ 11 ]   rectal prolapse [ 12 ]  and  rectal ulcer . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_110", "text": "In many cases however, the underlying pathophysiology in patients presenting with obstructed defecation cannot be determined. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_111", "text": "Some authors have commented that the \"puborectalis paradox\" and \"spastic pelvic floor\" concepts have no objective data to support their validity. They state that \"new evidence showing that defecation is an integrated process of colonic and rectal emptying suggests that anismus may be much more complex than a simple disorder of the pelvic floor muscles.\" [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_112", "text": "Persistent failure to fully evacuate stool may lead to retention of a mass of stool in the rectum (fecal loading), which can become hardened, forming a  fecal impaction  or even  fecaliths . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_113", "text": "Liquid stool elements may leak around the retained fecal mass, which may lead to paradoxical diarrhoea and/or fecal leakage (usually known as  encopresis  in children and  fecal leakage  in adults). [ 14 ] [ 15 ] [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_114", "text": "When anismus occurs in the context of intractable  encopresis  (as it often does), resolution of anismus may be insufficient to resolve encopresis. [ 18 ]  For this reason, and because biofeedback training is invasive, expensive, and labor-intensive, biofeedback training is not recommended for treatment of encopresis with anismus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_115", "text": "The walls of the rectum may become stretched, known as  megarectum . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_116", "text": "In the  Rome IV classification , diagnostic criteria for \"functional defecation disorders\" are as follows: [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_117", "text": "2 subcategories exist within the functional defecation disorders category:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_118", "text": "For all of these Rome-IV diagnoses, diagnostic criteria must have been fulfilled for the last 3 months with symptom onset at least 6 months prior to diagnosis. [ 20 ]  The subcategories F3a and F3b are defined by age- and gender-appropriate normal values for the technique. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_119", "text": "Previous Rome criteria recommended that anorectal testing is not usually indicated in patients with symptoms until patients have failed conservative treatment (e.g., increased dietary fiber and liquids; elimination of medications with constipating side effects\nwhenever possible). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_120", "text": "Several definitions have been offered:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_121", "text": "Physical examination can rule out anismus (by identifying another cause) but is not sufficient to diagnose anismus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_122", "text": "The measurement of  pressures  within the rectum and anus with a  manometer  (pressure-sensing probe)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_123", "text": "defecating proctogram , and  MRI defecography"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_124", "text": "Anismus can be subcategorized into 4 types based on the results of anorectal manometry testing: [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_125", "text": "Anismus is classified as a functional defecation disorder. It is also a type of rectal outlet obstruction (a functional outlet obstruction). Where anismus causes constipation, it is an example of  functional constipation . Many authors describe an \" obstructed defecation syndrome \", of which anismus is a cause. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_126", "text": "The  Rome II classification  functional defecation disorders were divided into 3 types, [ 25 ]  however the symptoms the patient experiences are identical. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_127", "text": "It can be seen from the above classification that many of the terms that have been used interchangeably with anismus are inappropriately specific and neglect the concept of impaired propulsion. Similarly, some of the definitions that have been offered are also too restrictive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_128", "text": "The rectal cooling test is suggested to differentiate between rectal inertia and impaired relaxation/paradoxical contraction  [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_129", "text": "Other techniques include  manometry ,  balloon expulsion test ,  evacuation proctography  (see  defecating proctogram ), and MRI defecography. [ 28 ]   Diagnostic criteria are:  fulfillment of criteria for  functional constipation , manometric and/or EMG and/or radiological evidence (2 out of 3), evidence of adequate expulsion force, and evidence of incomplete evacuation. [ 28 ]   Recent dynamic imaging studies have shown that in persons diagnosed with anismus the  anorectal angle  during attempted  defecation  is abnormal, and this is due to abnormal (paradoxical) movement of the  puborectalis muscle . [ 29 ] [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_130", "text": "Initial steps to alleviate anismus include dietary adjustments and simple adjustments when attempting to defecate. Supplementation with a  bulking agent  such as  psyllium  will make stool more bulky, which decreases the effort required to evacuate. [ 23 ]  Similarly, exercise and adequate hydration may help to optimise  stool form . The anorectal angle has been shown to flatten out when in a  squatting position , and is thus recommended for patients with functional outlet obstruction like anismus. [ 5 ]  If the patient is unable to assume a squatting postures due to mobility issues, a low stool can be used to raise the feet when sitting, which effectively achieves a similar position. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_131", "text": "Treatments for anismus include biofeedback retraining, botox injections, and surgical resection. Anismus sometimes occurs together with other conditions that limit (see  contraindication ) the choice of treatments.  Thus, thorough evaluation is recommended prior to treatment. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_132", "text": "Biofeedback  training for treatment of anismus is highly effective and considered the gold standard therapy by many. [ 18 ] [ 33 ] [ 34 ] \nOthers however, reported that biofeedback had a limited therapeutic effect. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_133", "text": "Injections of  botulin toxin type-A  into the  puborectalis muscle  are very effective in the short term, and somewhat effective in the long term. [ 36 ]  Injections may be helpful when used together with biofeedback training. [ 37 ] [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_134", "text": "Historically, the standard treatment was  surgical resection  of the puborectalis muscle, which sometimes resulted in fecal incontinence. Recently, partial resection (partial division) has been reported to be effective in some cases. [ 35 ] [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_135", "text": "Paradoxical anal contraction during attempted defecation in constipated patients was first described in a paper in 1985, when the term anismus was first used. [ 40 ]  The researchers drew analogies to a condition called  vaginismus , which involves paroxysmal (sudden and short lasting) contraction of  pubococcygeus  (another muscle of the pelvic floor).  These researchers felt that this condition was a spastic dysfunction of the anus, analogous to 'vaginismus'. However, the term anismus implies a psychogenic etiology, which is not true although psychological dysfunction has been described in these patients. Hence:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_136", "text": "Latin  ani  - \"of the anus\" \nLatin  spasmus  - \"spasm\""}
{"_id": "WikiPedia_Gastroenterology$$$corpus_137", "text": "(Derived by extrapolation with the term vaginismus, which in turn is from the Latin  vagina  - \"sheath\" +  spasmus  - \"spasm\")"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_138", "text": "Many terms have been used synonymously to refer to this condition, some inappropriately. The term \"anismus\" has been criticised as it implies a  psychogenic  cause. [ 41 ]  In the most widely accepted classification systems ( ICD-11  and  Rome-IV ), the term \"dyssynergic defecation\" is preferred. [ 21 ] [ 20 ]  As stated in the Rome II criteria, the term \"dyssynergic defecation\" is preferred to \"pelvic floor dyssynergia\" because many patients with dyssynergic defecation do not report sexual or urinary symptoms, [ 25 ]  meaning that only the defecation mechanism is affected."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_139", "text": "Other synonyms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_140", "text": "Anorectal disorders  include conditions involving the anorectal junction [ 1 ]  as seen in the image. They are painful but common conditions like  hemorrhoids , tears,  fistulas , or  abscesses  that affect the  anal  region. [ 2 ] [ 3 ]  Most people experience some form of anorectal disorder during their lifetime. [ 4 ]   Primary care physicians  can treat most of these disorders, [ 2 ]  however, high-risk individuals include those with  HIV , roughly half of whom need surgery to remedy the disorders. [ 4 ]  Likelihood of  malignancy  should also be considered in high risk individuals. [ 5 ]  This is why it is important to perform a full history and physical exam on each patient. [ 5 ]  Because these disorders affect the  rectum , people are often embarrassed or afraid to confer with a  medical professional . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_141", "text": "Surgical Therapy. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_142", "text": "Surgical Therapy (for chronic fissures or when non-surgical therapy fails)\u00a0: Anal Dilation, [ 8 ]   Lateral Internal Sphincterotomy ,  Advancement Flaps ,  Fissurectomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_143", "text": "Itchiness , a  burning  sensation,  pus  discharge,  blood , and  swelling  in around the  rectum  and  anus , [ 4 ]   diarrhea . [ 12 ]  Other common symptoms include anal spasm, Bleeding with defecation [ 8 ]  and painful defecation. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_144", "text": "Doctors uses a variety of tools and techniques to evaluate the type of anorectal disorder, including  digital  and  anoscopic  investigations,  palpations , and  palpitations . The initial examination can be painful because a  gastroenterologist  will need to spread the  buttocks  and probe the painful area, which may require a  local anesthetic . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_145", "text": "Treatments range from recommendations for  over-the-counter products  to more invasive  surgical procedures ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_146", "text": "Among the most common outpatient advice given to patients with less severe disorders include a high- fiber  diet, application of  ointment , and increased water intake. More serious procedures include the removal of affected tissue, injection of  botulinum  toxin, or surgically opening the  fistula  tract in the  sphincter  muscle. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_147", "text": "A  bezoar  ( / \u02c8 b i z \u0254\u02d0 r /   BEE -zor ) is a mass often found trapped in the  gastrointestinal system , [ 2 ]  though it can occur in other locations. [ 3 ] [ 4 ]  A  pseudobezoar  is an indigestible object introduced intentionally into the digestive system. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_148", "text": "There are several varieties of bezoar, some of which have  inorganic  constituents and others  organic . The term has both modern (medical, scientific) and traditional usage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_149", "text": "Esophageal bezoars discovered in nasogastrically fed patients on mechanical ventilation and sedation are reported to be due to the precipitation of certain food types rich in casein, which are precipitated with gastric acid reflux to form esophageal bezoars. Bezoars can also be caused by  gastroparesis  due to the slowing of gastric emptying, which allows food to form a bolus. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_150", "text": "The word  bezoar  is derived from the  Persian   p\u0101d-zahr  ( \u067e\u0627\u062f\u0632\u0647\u0631 ), literally  ' antidote ' . [ 13 ]  The myth of the bezoar as an antidote reached Europe from the Middle East in the 11th century and remained popular until it started to fall into disrepute by the 18th century. [ 14 ]  People believed that a bezoar had the power of a universal  antidote  and would work against any  poison  \u2013 a drinking glass that contained a bezoar could allegedly neutralize any poison poured into it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_151", "text": "Ox bezoars ( niu-huang  ( \u725b\u9ec3 ) or   calculi bovis ) are used in  Chinese herbology [ vague ]  to treat various diseases. They are  gallstones  or gallstone substitutes formed from ox or cattle  bile . Some products allegedly remove  toxins  from the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_152", "text": "The   Andalusian  physician  Ibn Zuhr  ( d.  1161), known in the West as Avenzoar, is thought [ by whom? ]  to have made the earliest description of bezoar stones as medicinal items. [ 15 ]  Extensive reference to bezoars also appears in the  Picatrix ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_153", "text": "In 1567, French surgeon  Ambroise Par\u00e9  did not believe that it was possible for the bezoar to cure the effects of any poison and described an experiment to test the properties of the stone. A cook in the King's court was sentenced to death and chose to be poisoned rather than hanged, under the condition that he would be given a bezoar after the poison. Par\u00e9 administered the bezoar stone to the cook, but it had no effect, and the cook died in agony seven hours after taking the poison, proving that \u2013 contrary to popular belief \u2013 the bezoar could not cure all poisons. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_154", "text": "Modern examinations of the properties of bezoars by Gustaf Arrhenius and Andrew A. Benson of the  Scripps Institution of Oceanography  show that when bezoars are immersed in an arsenic-laced solution, they can remove the poison. The toxic compounds in arsenic are  arsenate  and  arsenite ; each is acted upon differently by the bezoars: arsenate is removed by being exchanged for phosphate in  brushite  found in the stones, while arsenite is bound to sulfur compounds in the protein of degraded hair, which is a key component in bezoars. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_155", "text": "A famous case in the  common law  of England ( Chandelor v Lopus , 79 Eng Rep. 3, Cro. Jac. 4,  Eng. Ct. Exch.  1603) announced the rule of  caveat emptor  (\"let the buyer beware\") if the goods purchased are not in fact genuine and effective. The case concerned a purchaser who sued for the return of the purchase price of an allegedly fraudulent bezoar."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_156", "text": "Bezoars were important objects in  cabinets of curiosity  and in natural-history collections, mainly for their use in early-modern pharmacy and in the study of animal health. [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_157", "text": "The  Merck Manual of Diagnosis and Therapy  notes that consumption of unripened  persimmons  has been identified as the main cause of epidemics of intestinal bezoars and that up to 90 percent of bezoars that occur from excessive consumption require surgery for removal. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_158", "text": "A 2013 review of three databases identified 24 publications presenting 46 patients treated with Coca-Cola for phytobezoars. Clinicians administered the cola in doses of 500\u00a0ml (18\u00a0imp\u00a0fl\u00a0oz; 17\u00a0US\u00a0fl\u00a0oz) to up to 3,000\u00a0ml (110\u00a0imp\u00a0fl\u00a0oz; 100\u00a0US\u00a0fl\u00a0oz) over 24 hours, orally or by  gastric lavage . A total of 91.3% of patients had complete resolution after treatment with Coca-Cola: 50% after a single treatment, with others requiring cola plus  endoscopic  removal. Doctors resorted to surgical removal in four cases. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_159", "text": "Bile acid malabsorption  ( BAM ), known also as  bile acid diarrhea , is a cause of several gut-related problems, the main one being chronic  diarrhea . It has also been called bile acid-induced diarrhea, cholerheic or choleretic enteropathy, bile salt diarrhea or bile salt malabsorption. It can result from  malabsorption  secondary to  gastrointestinal disease , or be a primary disorder, associated with excessive  bile acid  production.  Treatment with  bile acid sequestrants  is often effective. Depending on the severity of symptoms, it may be recognised as a disability in the United Kingdom under the Equality Act 2010."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_160", "text": "A persistent (chronic) history of  diarrhea , with watery or mushy, unformed stools, (types 6 and 7 on the  Bristol stool scale ), sometimes with  steatorrhea , increased frequency and urgency of  defecation  are common manifestations, often with  fecal incontinence  and other gastrointestinal symptoms such as abdominal swelling,  bloating  and  abdominal pain . [ 2 ] [ 3 ] [ 1 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_161", "text": "People with this disorder often report impairments of  mental health  and  well-being , including  fatigue ,  dizziness ,  anxiety  about leaving home (primarily due to fear of fecal incontinence),  depression , one survey reports. [ 1 ]  It contributes in delays in diagnosis. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_162", "text": "Bile acids  (also called  bile salts ) are produced in the  liver , secreted into the  biliary system , stored in the  gallbladder  and are released after meals stimulated by  cholecystokinin . They are important for the  digestion  and  absorption  of fats (lipids) in the  small intestine . Usually over 95% of the bile acids are absorbed in the terminal  ileum  and are taken up by the liver and resecreted. This  enterohepatic circulation  of bile acids takes place four\u2013six times in 24 hours and usually less than 0.5\u00a0g of bile acids enter the  large intestine  per 24\u00a0h. When larger amounts of bile acids enter the  large intestine , they stimulate water secretion and  intestinal motility  in the  colon , which causes symptoms of chronic  diarrhea . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_163", "text": "The  ileum  is very efficient at absorbing the glyco- and  taurine -conjugated forms of the bile salts. The  apical sodium-dependent bile salt transporter  (ASBT, IBAT, gene symbol  SLC10A2 ) is the first step in absorption at the brush-border membrane.  The cytoplasmic  ileal bile acid binding protein  (IBABP, ILBP, gene symbol  FABP6 ) and the basolateral heterodimer of  OST\u03b1  and  OST\u03b2  transfer bile acids through and out of the cell where they eventually enter the  portal vein .  These bile acid transporters are all highly expressed in the ileum but not in the liver, jejunum or colon. [ 6 ]   When expression of these specialized transporters is reduced, the intestine is less efficient at bile acid reabsorption (Type 1 bile acid malabsorption). If  intestinal motility  is affected by gastro-intestinal surgery, or bile acids are deconjugated by  small intestinal bacterial overgrowth , absorption is less efficient (Type 3 bile acid malabsorption).  A very small proportion of the patients with no obvious disease (Type 2 bile acid malabsorption) may have mutations in ASBT, [ 7 ]  but this mutation is not more common in most patients and does not affect function. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_164", "text": "Primary bile acid diarrhea (Type 2 bile acid \"malabsorption\") may be caused by an overproduction of bile acids. [ 5 ] [ 9 ]  Several groups of workers have failed to show any defect in ileal bile acid absorption in these patients, and they have an enlarged bile acid pool, rather than the reduced pool expected with malabsorption. [ 10 ]  The synthesis of bile acids in the liver is negatively regulated by the ileal hormone fibroblast growth factor 19 ( FGF19 ), and lower levels of this hormone result in overproduction of bile acids, which are more than the ileum can absorb. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_165", "text": "A study found that patients suffering from bile acid diarrhea are characterized by a dysmetabolic and prediabetic-like profile, with higher postprandial concentrations of glucose, insulin and glucagon, compared with matched healthy controls. [ 11 ]  The underlying mechanisms are not fully understood. Furthermore, gut microbiome composition differs from that of people who do not suffer from bile acid diarrhea. [ 12 ] [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_166", "text": "Several methods have been developed to identify the disorder but there are difficulties with all of them. [ 15 ]  Diagnosis of bile acid malabsorption is easily and reliably made by the  SeHCAT  test.  This  nuclear medicine  test involves two scans a week apart and so measures multiple cycles of bile acid excretion and reabsorption.  There is limited radiation exposure (0.3\u00a0mSv).  Retention of SeHCAT at 7 days is normally above 15%; values less than 15%, 10% and 5% predict respectively mild, moderate and severe abnormal retention and an increasing likelihood of response to  bile acid sequestrants . [ 16 ]   This test is not licensed in the USA, and is underutilized even where it is available. [ 17 ] [ 18 ]   Older methods such as the  14 C-glycocholic breath test are no longer in routine clinical use. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_167", "text": "Measurement of  7\u03b1-Hydroxy-4-cholesten-3-one , (C4), a bile acid precursor, in serum, shows the increased bile acid synthesis found in bile acid malabsorption. [ 20 ]  This test is an alternative diagnostic means when available.  Fasting blood  FGF19  values may have value in the recognition of the disease and prediction of response. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_168", "text": "The various biomarkers give similar diagnostic yields of around 25% in patients with functional bowel disorders with diarrhea. [ 19 ]   In countries such as the US, where SeHCAT is not available, fecal bile acids and C4 are available to make the diagnosis. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_169", "text": "Bile acid malabsorption was first recognized in patients with  ileal disease . [ 22 ]  When other causes were recognized, and an idiopathic, primary form described, [ 23 ]  a classification into three types was proposed: [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_170", "text": "Bile acid sequestrants  are the main agents used to treat bile acid malabsorption. [ 25 ]   Cholestyramine  and  colestipol , both in powder form, have been used for many years. Unfortunately, many patients find them difficult to tolerate; although the diarrhea may improve, other symptoms such as abdominal pain and bloating may worsen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_171", "text": "Colesevelam  is a tablet which is well tolerated and has been shown in placebo-controlled, randomized clinical trials to be effective. [ 26 ] [ 27 ] [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_172", "text": "The  farnesoid X receptor  agonist  obeticholic acid  has shown clinical and biochemical benefits in a proof of concept study. [ 30 ]   Tropifexor  is another farnesoid X receptor agonist that has been studied, showing improvements in biochemistry and colonic transit. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_173", "text": "Liraglutide , a  GLP-1 receptor agonist  had unexpected effects in clinical cases with co-existing bile acid diarrhoea [ 32 ]  which led to a randomised, double-blind, active-comparator, non-inferiority clinical trial. [ 33 ]  This trial demonstrated superiority in favour of liraglutide compared with colesevelam in reducing stool frequency and improved pathophysiological markers, suggesting it may be a new, safe and more effective treatment compared with current established, cheaper treatment modalities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_174", "text": "Bile acid malabsorption is common in Crohn's disease but not always recognized.  Most people with previous ileal resection and chronic diarrhea will have abnormal SeHCAT tests and can benefit from bile acid sequestrants. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_175", "text": "People with primary bile acid diarrhea are frequently misdiagnosed as having  irritable bowel syndrome . [ 17 ]  When SeHCAT testing  is performed, the diagnosis of primary bile acid diarrhea is commonly made. In a review of 18 studies of the use of SeHCAT testing in diarrhea-predominant irritable bowel syndrome patients, 32% of 1223 people had a SeHCAT 7-day retention of less than 10%, and 80% of these reported a response to cholestyramine, a bile acid sequestrant. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_176", "text": "A study from 2023 investigating the epidemiology of bile acid diarrhea in Denmark, found that people suffering from bile acid diarrhea seemed to have more co-morbidities, lower levels of income and education and more health care contacts compared with matches not suffering from bile acid diarrhea. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_177", "text": "Estimates of the population prevalence suggest that 1% of the adult population could have primary bile acid diarrhea (Type 2 bile acid malabsorption). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_178", "text": "A nationwide cohort study indicates an association between bile acid diarrhea and  gastrointestinal cancers . [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_179", "text": "Blind loop syndrome , also known as  stagnant loop syndrome , [ 1 ]  is a state that occurs when the normal bacterial flora of the  small intestine  proliferates to numbers that cause significant derangement to the normal physiological processes of digestion and absorption. In some cases of blind loop syndrome, overgrowth of  pathogenic  non- commensal  bacteria has also been noted. It has long been understood that from birth, and throughout life, large amounts of bacteria reside symbiotically within animal gastrointestinal tracts such as the  human gastrointestinal tract . The understanding of this  gut flora  has even led to novel treatments for bowel irregularity that utilize  so called \" probiotics \" or good bacteria that aid in normal digestion.\nThe problem of blind loop syndrome arises when the bacterial colonies residing in the upper gastrointestinal tract begin to grow out of control or are altered in their makeup thereby creating a burden on the normal physiological processes occurring in the small intestine. This results in problems, among others, of:   vitamin B12 deficiency , fat malabsorption and  steatorrhea , fat-soluble vitamin deficiencies and intestinal wall injury. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_180", "text": "Most of the symptoms of blind loop syndrome are non specific but nevertheless warrant the utmost attention. These include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_181", "text": "As a result of the concomitant vitamin and mineral deficiencies that occur as a result of the malabsorption associated with blind loop syndrome patients with advanced cases should be investigated for: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_182", "text": "Blind loop syndrome is a complication of surgical operations of the abdomen, as well as  inflammatory bowel disease  or  scleroderma . Another cause is jejunoileal diverticula. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_183", "text": "The overgrowth of bacteria in the small intestine is prevented by various mechanical and chemical factors which include the constant peristaltic movement of contents along the length of the gastrointestinal tract and the antibacterial properties of gastric secretions, pancreatic secretions and  bile . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_184", "text": "It follows that a disruption of any of these factors could lead to bacterial overgrowth and indeed blind loop syndrome has been found to occur in persons with anatomical anomalies that result in stagnation. Blind loop syndrome has also been associated with  achlorhydria , dysmotility,  fistulae , and  strictures . Chronic or high dose  opioid  therapy may contribute to blind loop syndrome by reducing gastric motility. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_185", "text": "Due to the disruption of digestive processes by the overgrowth of intestinal bacteria; malabsorption of bile salts, fat and fat-soluble vitamins, protein and carbohydrates results in damage to the mucosal lining of the intestine by bacteria or via the production of toxic metabolites."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_186", "text": "A physical examination may reveal a mass or distention of the abdomen. Tests which may be useful for diagnosis include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_187", "text": "The treatment of blind loop syndrome follows two basic principles. When a patient presents with symptoms of blind loop syndrome, the treating physician basically has two recognized options for management:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_188", "text": "Although it would seem to be the better way to go in terms of management, there has been recent criticism on the need for such testing because of reliability issues. However, there are options such as the  glucose breath test  and jejunal  aspiration  the explanations of which are beyond the scope of this current article.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_189", "text": "The \"treat empirically\" route also has its difficulties, which have all come under wide debate and study. Recommendations are varied but seem to find some common ground around the notion that treatment should be individualized to the specific circumstances under which a patient has developed blind loop syndrome since these circumstances affect the complex microbial make up of the affected bowel.  Tetracyclines  have been the mainstay of treatment for blind loop syndrome, but recent studies have concluded  rifaximin  to be very effective in the treatment of blind loop syndrome. However, a study by Di Stefano et al. concluded  metronidazole  to be more effective than  rifaximin  in the treatment of blind loop syndrome. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_190", "text": "Surgical management is reserved for fixing anatomical causes of bowel obstruction that interfere with normal function once they are amenable to such intervention. These conditions include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_191", "text": "Bowel infarction  or  gangrenous bowel  represents an irreversible injury to the intestine resulting from insufficient blood flow. It is considered a  medical emergency  because it can quickly result in  life-threatening infection  and death. [ 1 ]  Any cause of bowel  ischemia , the earlier reversible form of injury, may ultimately lead to infarction if uncorrected. The causes of bowel ischemia or infarction include primary vascular causes (for example,  mesenteric ischemia ) and other causes of bowel obstruction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_192", "text": "Primary vascular causes of bowel infarction, also known as  mesenteric ischemia , are due to blockages in the arteries or veins that supply the bowel. Types of mesenteric ischemia are generally separated into acute and chronic processes, because this helps determine treatment and prognosis. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_193", "text": "Bowel obstruction is most often caused by intestinal  adhesions , which frequently form after abdominal surgeries, or by chronic infections such as  diverticulitis ,  hepatitis , and  inflammatory bowel disease . The condition may be difficult to diagnose, as the symptoms may resemble those of other bowel disorders. [ 4 ]   Bowel volvulus  describes a specific form of bowel obstruction, where the intestine and/or mesentery are twisted, resulting in ischemia. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_194", "text": "The only treatment for bowel infarction is immediate surgical repair and eventually  removal of the dead bowel segment . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_195", "text": "Patients who have undergone extensive resection of the small bowel may develop  malabsorption , indicating the need for dietary supplements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_196", "text": "Bowel obstruction , also known as  intestinal obstruction , is a mechanical or  functional obstruction  of the  intestines  which prevents the normal movement of the products of  digestion . [ 2 ] [ 5 ]  Either the  small bowel  or  large bowel  may be affected. [ 1 ]  Signs and symptoms include  abdominal pain ,  vomiting ,  bloating  and not passing  gas . [ 1 ]  Mechanical obstruction is the cause of about 5 to 15% of cases of  severe abdominal pain of sudden onset  requiring admission to hospital. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_197", "text": "Causes of bowel obstruction include  adhesions ,  hernias ,  volvulus ,  endometriosis ,  inflammatory bowel disease ,  appendicitis ,  tumors ,  diverticulitis ,  ischemic bowel ,  tuberculosis  and  intussusception . [ 1 ] [ 2 ]  Small bowel obstructions are most often due to adhesions and hernias while large bowel obstructions are most often due to tumors and volvulus. [ 1 ] [ 2 ]  The diagnosis may be made on plain  X-rays ; however,  CT scan  is more accurate. [ 1 ]   Ultrasound  or  MRI  may help in the diagnosis of children or  pregnant  women. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_198", "text": "The condition may be treated conservatively or with  surgery . [ 2 ]  Typically  intravenous fluids  are given, a  nasogastric (NG) tube is placed through the nose into the stomach  to decompress the intestines, and  pain medications  are given. [ 2 ]   Antibiotics  are often given. [ 2 ]  In small bowel obstruction about 25% require surgery. [ 6 ]  Complications may include  sepsis , bowel  ischemia  and  bowel perforation . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_199", "text": "About 3.2 million cases of bowel obstruction occurred in 2015 which resulted in 264,000 deaths. [ 3 ] [ 7 ]  Both sexes are equally affected and the condition can occur at any age. [ 6 ]  Bowel obstruction has been documented throughout history, with cases detailed in the  Ebers Papyrus  of 1550 BC and by  Hippocrates . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_200", "text": "Depending on the level of obstruction, bowel obstruction can present with  abdominal pain ,  abdominal distension , and  constipation . Bowel obstruction may be complicated by  dehydration  and  electrolyte abnormalities  due to vomiting; respiratory compromise from pressure on the  diaphragm  by a distended abdomen, or  aspiration  of vomitus; bowel  ischemia  or  perforation  from prolonged distension or pressure from a foreign body and subsequently  sepsis  due to  bowel flora . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_201", "text": "In small bowel obstruction, the  pain  tends to be colicky (cramping and intermittent) in nature, with spasms lasting a few minutes. The pain tends to be central and mid-abdominal. Vomiting may occur before constipation. [ 10 ]  Common physical exam findings may include signs of  dehydration , abdominal distension with tympany, nonspecific abdominal tenderness, and high pitched tinkly bowel sounds. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_202", "text": "In large bowel obstruction, the pain is felt lower in the abdomen and the spasms last longer. Common symptoms include abdominal pain, distension, and severe constipation. [ 12 ]  Constipation occurs earlier and vomiting may be less prominent. Proximal obstruction of the large bowel may present as small bowel obstruction. [ 13 ]  Patients may notice a history of bloating and narrowing of stools before the onset of more severe symptoms. Symptoms can present quickly in the cases of  volvulus  and can present over a longer period of time in the setting of cancer. Common physical exam findings may include a palpable  hernia , abdominal distension with tympany, nonspecific lower abdominal tenderness, and a rectal mass. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_203", "text": "The main diagnostic tools are  blood tests ,  X-rays  of the abdomen, CT scanning, and  ultrasound . If a mass is identified,  biopsy  may determine the nature of the mass. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_204", "text": "Radiological  signs of bowel obstruction include bowel distension (small bowel loops dilated >3 cm) and the presence of multiple (more than 2) air-fluid levels on supine and erect abdominal  radiographs . [ 16 ]  Ultrasounds may be as useful as CT scanning to make the diagnosis. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_205", "text": "Contrast enema  or small bowel series or CT scan can be used to define the level of obstruction, whether the obstruction is partial or complete, and to help define the cause of the obstruction. The appearance of water-soluble contrast in the cecum on an abdominal radiograph within 24 hours of it being given by mouth predicts resolution of an adhesive small bowel obstruction with  sensitivity  of 97% and  specificity  of 96%. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_206", "text": "Colonoscopy , small bowel investigation with ingested camera or push  endoscopy , and  laparoscopy  are other diagnostic options."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_207", "text": "Differential diagnoses  of bowel obstruction include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_208", "text": "Causes of  small bowel  obstruction include: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_209", "text": "After abdominal surgery, the incidence of small bowel obstruction from any cause is 9%. In those where the cause of the obstruction was clear, adhesions are the single most common cause (more than half). [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_210", "text": "Causes of large bowel obstruction include: [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_211", "text": "Outlet obstruction is a sub-type of large bowel obstruction and refers to conditions affecting the anorectal region that obstruct  defecation , specifically conditions of the pelvic floor and anal sphincters. Outlet obstruction can be classified into four groups. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_212", "text": "Treatment of small and large bowel obstructions are initially similar and non-operative management is usually the initial management strategy as the majority of small bowel obstruction resolve spontaneously with non-operative management. [ 25 ] [ 26 ]  Patients are monitored by the surgical team for signs of improvement and resolution of the obstruction on imaging; if the obstruction does not clear then surgical management for the treatment of the causative lesion is required. [ 27 ]  In malignant large bowel obstruction, endoscopically placed self-expanding metal  stents  may be used to temporarily relieve the obstruction as a bridge to surgery, [ 28 ]  or as  palliation . [ 29 ]  Diagnosis of the type of bowel obstruction is normally conducted through initial plain  radiograph  of the abdomen, luminal contrast studies,  computed tomography scan , or  ultrasonography  prior to determining the best type of treatment. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_213", "text": "Further research is needed to find out if parenteral nutrition is of benefit to people with an inoperable blockage of the bowel caused by advanced cancer. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_214", "text": "In the management of small bowel obstructions, a commonly quoted surgical aphorism is: \"never let the sun rise or set on small-bowel obstruction\" [ 32 ]  because about 5.5% [ 32 ]  of small bowel obstructions are ultimately fatal if treatment is delayed. Improvements in radiological imaging of small bowel obstructions allow for confident distinction between simple obstructions, that can be treated conservatively, and obstructions that are surgical emergencies ( volvulus , closed-loop obstructions,  ischemic bowel , incarcerated  hernias , etc.). [ 2 ]  Exam findings of bowel compromise requiring immediate surgery include: severe abdominal pain, signs of  peritonitis  such as rebound tenderness,  elevated heart rate , fever, and elevated inflammatory markers on lab work, such as  lactic acid . [ 33 ] [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_215", "text": "A small flexible tube ( nasogastric tube ) may be inserted through the nose into the stomach to help decompress the dilated bowel. This tube is uncomfortable but relieves the abdominal cramps, distention, and vomiting.  Intravenous therapy  is utilized and the urine output may be monitored with a  catheter  in the  bladder . [ 35 ] [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_216", "text": "Most people with SBO are initially managed conservatively because in many cases, the bowel will open up. Some adhesions loosen up and the obstruction resolves. The patient is examined several times a day, and  X-ray images  are made to ensure he or she is not getting clinically worse. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_217", "text": "Conservative treatment involves insertion of a  nasogastric tube , correction of dehydration and  electrolyte  abnormalities.  Opioid  pain relievers may be used for patients with severe pain but alternate pain relievers are preferred as opioids can decrease bowel motility. [ 38 ] Antiemetics  may be administered if the patient is vomiting. Adhesive obstructions often settle without surgery. If the obstruction is complete surgery is usually required."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_218", "text": "Most patients improve with conservative care in 2\u20135 days. When the obstruction is cancer, surgery is the only treatment. Those with  bowel resection  or  lysis  of adhesions usually stay in the hospital a few more days until they can eat and walk. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_219", "text": "Small bowel obstruction caused by  Crohn's disease , peritoneal  carcinomatosis , sclerosing  peritonitis ,  radiation enteritis , and postpartum bowel obstruction are typically treated conservatively, i.e. without surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_220", "text": "The prognosis for non-ischemic cases of SBO is good with mortality rates of 3\u20135%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_221", "text": "Cases of SBO related to cancer are more complicated and require additional intervention to address the  malignancy , recurrence, and  metastasis , and thus are associated with a more poor prognosis. [ 41 ]  Surgical options in patients with malignant bowel obstruction need to be considered carefully as while it may provide relief of symptoms in the short term, there is a high risk of mortality and re-obstruction. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_222", "text": "All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. [ 43 ]  More than 90% of patients also form adhesions after major abdominal surgery. [ 44 ] \nCommon consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_223", "text": "Callous ulcer  is a chronic nonhealing  ulcer  with hard indurated base and inelastic margins. [ 1 ]   It usually contains unhealthy pale  granulation tissue . It may last for months to years and does not show any tendency to heal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_224", "text": "This cutaneous condition article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_225", "text": "Campylobacteriosis  is among the most common  infections  caused by a  bacterium  in humans, often as a  foodborne illness . It is caused by the  Campylobacter   bacterium , [ 2 ]  most commonly  C. jejuni . It produces an inflammatory, sometimes bloody,  diarrhea  or  dysentery  syndrome, and usually cramps, fever and pain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_226", "text": "The  prodromal symptoms  are fever, headache, and  myalgia , which can be severe, lasting as long as 24 hours. After 1\u20135 days, typically, these are followed by  diarrhea  (as many as 10 watery, frequently bloody, bowel movements per day) or  dysentery ,  cramps ,  abdominal pain , and  fever  as high as 40\u00a0\u00b0C (104\u00a0\u00b0F). In most people, the illness lasts for 2\u201310 days. It is classified as invasive/inflammatory diarrhea, also described as bloody diarrhea or dysentery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_227", "text": "There are other diseases showing similar symptoms. For instance, abdominal pain and tenderness may be very localized, mimicking  acute appendicitis . Furthermore,  Helicobacter pylori  is closely related to  Campylobacter  and causes  peptic ulcer disease . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_228", "text": "Complications include  toxic megacolon ,  dehydration  and  sepsis . Such complications generally occur in young children (< 1 year of age) and immunocompromised people. A chronic course of the disease is possible; this disease process is likely to develop without a distinct acute phase. Chronic campylobacteriosis features a long period of sub- febrile  temperature and  asthenia ; eye damage,  arthritis ,  endocarditis  may develop if infection is untreated. Occasional deaths occur in young, previously healthy individuals because of blood volume depletion (due to dehydration), and in people who are elderly or immunocompromised. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_229", "text": "Some individuals (1\u20132 in 100,000 cases) develop  Guillain\u2013Barr\u00e9 syndrome , in which the nerves that join the spinal cord and brain to the rest of the body are damaged, sometimes permanently. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_230", "text": "In patients with  HIV , infections may be more frequent, may cause prolonged bouts of dirty brown diarrhea, and may be more commonly associated with  bacteremia  and  antibiotic resistance . In participants of unprotected anal intercourse, campylobacteriosis is more localized to the distal end of the  colon  and may be termed a  proctocolitis . The severity and persistence of infection in patients with AIDS and  hypogammaglobulinemia  indicates that both cell-mediated and humoral immunity are important in preventing and terminating infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_231", "text": "Campylobacteriosis is caused by  Campylobacter  bacteria (curved or spiral, motile, non\u2013spore-forming,  Gram-negative  rods). The disease is usually caused by  C. jejuni , a spiral and comma-shaped bacterium normally found in cattle, swine, and birds, where it is nonpathogenic, but the illness can also be caused by  C. coli  (also found in cattle, swine, and birds),  C. upsaliensis  (found in cats and dogs) and  C. lari  (present in seabirds in particular). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_232", "text": "One effect of campylobacteriosis is tissue injury in the  gut . The sites of tissue injury include the  jejunum , the  ileum , and the  colon .  C jejuni  appears to achieve this by invading and destroying epithelial cells. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_233", "text": "C. jejuni  can also cause a latent autoimmune effect on the nerves of the legs, which is usually seen several weeks after a surgical procedure of the abdomen. The effect is known as an acute idiopathic demyelinating polyneuropathy (AIDP), i.e. Guillain\u2013Barr\u00e9 syndrome, in which one sees symptoms of ascending paralysis, dysaesthesias usually below the waist, and, in the later stages, respiratory failure. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_234", "text": "Some strains of  C jejuni  produce a  cholera -like enterotoxin, which is important in watery diarrhea observed in infections. The organism produces diffuse, bloody, edematous, and exudative enteritis. In a small number of cases, the infection may be associated with  hemolytic uremic syndrome  and  thrombotic thrombocytopenic purpura  through a poorly understood mechanism. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_235", "text": "The common  routes of transmission  for the disease-causing bacteria are fecal-oral, person-to-person sexual contact, [ citation needed ]  ingestion of contaminated food (generally unpasteurized (raw)  milk  and undercooked or poorly handled  poultry ), and waterborne (i.e., through contaminated  drinking water ). Contact with contaminated poultry, livestock, or household pets, especially puppies, can also cause disease. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_236", "text": "Animals farmed for meat are the main source of campylobacteriosis. A study published in  PLoS Genetics  (26 September 2008) by researchers from Lancashire, England, and Chicago, Illinois, found that 97 percent of campylobacteriosis cases sampled in Lancashire were caused by bacteria typically found in chicken and livestock. In 57 percent of cases, the bacteria could be traced to chicken, and in 35 percent to cattle. Wild animal and environmental sources were accountable for just three percent of disease. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_237", "text": "The infectious dose is 1000\u201310,000 bacteria (although ten to five hundred bacteria can be enough to infect humans).  Campylobacter  species are sensitive to  hydrochloric acid  in the  stomach , and acid reduction treatment can reduce the amount of  inoculum  needed to cause disease. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_238", "text": "Exposure to bacteria is often more common during travelling, and therefore campylobacteriosis is a common form of  travelers' diarrhea . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_239", "text": "Campylobacter  organisms can be detected by performing a  Gram stain  of a stool sample with high  specificity  and a  sensitivity  of ~60%, but are most often diagnosed by stool culture. Fecal  leukocytes  should be present and indicate the diarrhea to be inflammatory in nature. Methods currently being developed to detect the presence of  Campylobacter  organisms include antigen testing via an  EIA  or  PCR . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_240", "text": "The World Health Organization recommends the following: [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_241", "text": "The infection is usually  self-limiting , and in most cases, symptomatic treatment by liquid and  electrolyte replacement  is enough in human infections. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_242", "text": "Antibiotic treatment only has a marginal effect on the duration of symptoms, and its use is not recommended except in high-risk patients with  clinical complications . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_243", "text": "Erythromycin  can be used in children, and  tetracycline  in adults. Some studies show, however, that  erythromycin  rapidly eliminates  Campylobacter  from the stool without affecting the duration of illness. Nevertheless, children with  dysentery  due to  C. jejuni  benefit from early treatment with erythromycin. Treatment with antibiotics, therefore, depends on the severity of symptoms.  Quinolones  are effective if the organism is sensitive, but high rates of quinolone use in livestock mean that quinolones are now largely ineffective. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_244", "text": "Antimotility agents, such as  loperamide , can lead to prolonged illness or intestinal perforation in any invasive diarrhea, and should be avoided.   Trimethoprim/sulfamethoxazole  and  ampicillin  are ineffective against  Campylobacter . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_245", "text": "In the past, poultry infections were often treated by mass administration of  enrofloxacin  and  sarafloxacin  for single instances of infection. The FDA banned this practice, as it promoted the development of  fluoroquinolone -resistant populations. [ 11 ] \nA major broad-spectrum  fluoroquinolone  used in humans is  ciprofloxacin . The increasing resistance of the  Campylobacter  to fluoroquinolones and  macrolides  is of a major concern. [ citation needed ] \nA different approach, propagated within the EU is that  Campylobacter  mitigating measures should be undertaken mainly at the primary production level. An update of potential control options was released by EFSA on 30 April 2020. Vaccination, feed, and water additives, discontinued thinning,  employing few and well-trained staff, drinkers that allow standing water, addition of disinfectants to drinking water, hygienic anterooms, designated tools per broiler house were listed as most effective in mitigating the risk of Campylobacter in chicken thus reducing the risk of human campylobacteriosis. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_246", "text": "Campylobacteriosis is usually self-limited without any mortality (assuming proper hydration is maintained). However, there are several possible complications. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_247", "text": "Campylobacter  is one of the most common causes of human bacterial  gastroenteritis . [ 13 ]  For instance, an estimated 2 million cases of  Campylobacter   enteritis  occur annually in the  U.S. , accounting for 5\u20137% of cases of gastroenteritis. Furthermore, in the  United Kingdom  during 2000,  Campylobacter jejuni  was involved in 77.3% in all cases of laboratory confirmed  foodborne illness . [ 14 ]  About 15 of every 100,000 people are diagnosed with campylobacteriosis every year, and with many cases going unreported, up to 0.5% of the general population may unknowingly harbor  Campylobacter  in their gut. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_248", "text": "Unfortunately, the true incidence of campylobacteriosis is unknown in most countries, especially developing countries. The reasons are among others underreporting, difficulties with diagnosis and differences in reporting systems in different countries. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_249", "text": "A large animal reservoir is present as well, with up to 100% of poultry, including  chickens ,  turkeys , and waterfowl, having asymptomatic infections in their intestinal tracts. Infected  chicken  feces may contain up to 10 9  bacteria per 25\u00a0grams, and due to the animals' close proximity, the bacteria are rapidly spread to other  chickens . This vastly exceeds the infectious dose of 1000\u201310,000 bacteria for humans. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_250", "text": "In January 2013, the  UK 's  Food Standards Agency  warned that two-thirds of all raw chicken bought from UK shops was contaminated with campylobacter, affecting an estimated half a million people annually and killing approximately 100. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_251", "text": "In August\u2013September 2016, 5,200 people fell ill with campylobacteriosis in  Hastings , New Zealand, after the local water supply in Havelock North tested positive for the pathogen  Campylobacter jejuni . [ 17 ] [ 18 ]  Four deaths were suspected to be due to the outbreak. [ 19 ]  It is suspected that after heavy rain fell on 5\u20136 August, water contamination from flooding caused the outbreak, although this is the subject of a government Inquiry. [ 20 ]  It is the largest outbreak of waterborne disease ever to occur in New Zealand. All schools in Havelock North closed for two weeks, with the Hastings District Council advising an urgent notice to boil water for at least one minute before consumption. This notice was lifted on 3 September, with the outbreak officially under control. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_252", "text": "According to  Centers for Disease Control and Prevention , a multistate outbreak of human  Campylobacter  infection has been reported since 11 September 2017. In all, 55 cases were reported from 12 states (Florida, Kansas, Maryland, Missouri, New Hampshire, New York, Ohio, Pennsylvania, Tennessee, Utah, Wisconsin and Wyoming). Epidemiological and laboratory evidence indicated that puppies sold through  Petland  stores were a likely source of this outbreak.  Out of 55 cases reported, 50 were either employees of Petland or had recently purchased a puppy at Petland, or visited there before illness began. Five people out of 55 cases reported were exposed to puppies from various sources. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_253", "text": "Campylobacter  can spread through contact with dog  feces . It usually does not spread from one person to another. However, activities such as changing an infected person's diapers or sexual contact with an infected person can lead to infection. Regardless of where they are from, any puppies and dogs may carry  Campylobacter  germs. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_254", "text": "Carbonated soda treatment of phytobezoars  is the use of  carbonated soda  to try to dissolve a  phytobezoar . Bezoars consist of a solid and formed mass trapped in the  gastrointestinal system , usually in the  stomach . [ 1 ] [ 2 ] [ 3 ]  These can also form in other locations. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_255", "text": "Carbonated soda has been proposed for the treatment of gastric phytobezoars. In about 50% of cases studied, carbonated soda alone was found to be effective in gastric phytobezoar  dissolution . Unfortunately, this treatment can result in the potential of developing  small bowel obstruction  in a minority of cases, necessitating surgical intervention. [ 1 ]  It is one of many other stomach disorders that can have similar symptoms. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_256", "text": "Gastric phytobezoars are a form of  intestinal  blockage and are seen in those with poor gastric motility. The preferred treatment of bezoars includes different therapies and/or fragmentation to avoid surgery. Phytobezoars are most common and consist of various undigested substances including  lignin ,  cellulose ,   tannins ,  celery ,  pumpkin  skin,  grape  skins,  prunes ,  raisins , vegetables and fruits. [ 1 ]  Phytobezoars can form after eating  persimmons  and  pineapples . These are more difficult to treat and are referred to as  diospyrobezoars . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_257", "text": "Carbonated soda may help to dissolve phytobezoars. [ 7 ]  It can be given by a  naso-gastric tube  in children. [ 8 ]  Carbonated soda can also be given by mouth and during  endoscopy . [ 9 ]  It is effective in about half of the cases. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_258", "text": "It promotes dissolution by endoscopic techniques in the majority of the patients left, leading to a final success rate up to 91.3%. [ 6 ]  In some cases, regular use of  Coca-Cola  resulted in no recurrence 3\u201315 months after the first episode. [ 6 ]  Treatment has varied widely. Coca-Cola has been administered either as drinking beverage or as lavage. Some are treated with various combinations of drink, injection and irrigation. The volume of Coca-Cola in treatment varies along with daily dose and time of treatment. Dosages varied from 500\u00a0mL up to 3000\u00a0mL and treatment period 24\u00a0hours to 6\u00a0weeks. When lavage is used, a double-lumen nasogastric tube or two separate tubes using 3000\u00a0mL of Coca-Cola is administered during a 12-hour period. [ 6 ]   Alternative treatments are the use of cellulase, acetylcysteine, papain, pancreatic enzymes, saline solution, 0.1\u00a0N HCl and sodium bicarbonate. The protocol for the treatment of phytobezoars with Coca-Cola, i.e., dosage and timing, has not been standardized; further investigation has been encouraged. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_259", "text": "Trichobezoars  do not respond to treatment with Coca-Cola but instead this type may have to be surgically removed. [ 9 ]  Persimmon diospyrobezoars sometimes are resistant to Coca-Cola and require a different treatment. This can include endoscopic fragmentation and/or surgical approaches especially in urgent cases where the patient exhibits gastrointestinal bleeding. [ 1 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_260", "text": "Adverse effects have been observed with the use of papain such as gastric ulcer, hyponatremia and oesophageal perforation. [ 6 ]  These effects have not been observed with the use of Coca-Cola. Glucose levels during the administration of Coca-Cola have not been addressed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_261", "text": "In addition to Coca-Cola,  meat tenderizer  has been used to dissolve bezoars of the stomach. [ 10 ] [ 11 ]  When treatment with Coca-Cola is combined with endoscopic methods, the success of treatment approaches 90%. [ 6 ]   The mechanism by which Coca-Cola dissolves the bezoar is based upon its low pH, CO 2  bubbles, and  sodium bicarbonate  content. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_262", "text": "Some clinicians have described the mode of interaction is based upon the acidification of the gastric contents and the release of CO 2  that causes disintegration. Three and a half liters given nasogastrically over 12 hours has been found to dissolve these bezoars. [ 12 ]   Coca-Cola has a pH of 2.6. This is due to  carbonic  and  phosphoric acid  which resemble gastric acid. Gastric acid is believed to facilitate the digestion of fibers. In Coca-Cola, NaHCO 3  has a mucolytic effect and CO 2  bubbles enhance dissolving the bezoar. Coca-Cola reduces the size and softens the make-up of the bezoar, and combined with other treatments, enhances the dissolution. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_263", "text": "A phytobezoar was first  successfully treated with Coca-Cola\u00a0lavage in 2002. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_264", "text": "Cholera  ( / \u02c8 k \u0252 l \u0259r \u0259 / ) is an  infection  of the  small intestine  by some  strains  of the  bacterium   Vibrio cholerae . [ 4 ] [ 3 ]  Symptoms may range from none, to mild, to severe. [ 3 ]  The classic symptom is large amounts of watery  diarrhea  lasting a few days. [ 2 ]   Vomiting  and  muscle cramps  may also occur. [ 3 ]  Diarrhea can be so severe that it leads within hours to severe  dehydration  and  electrolyte imbalance . [ 2 ]  This may result in  sunken eyes , cold skin, decreased skin elasticity, and wrinkling of the hands and feet. [ 5 ]  Dehydration can cause the skin to turn  bluish . [ 8 ]  Symptoms start two hours to five days after exposure. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_265", "text": "Cholera is caused by a number of  types  of  Vibrio cholerae , with some types producing more severe disease than others. [ 2 ]  It is spread mostly by  unsafe water  and  unsafe food  that has been contaminated with  human feces  containing the bacteria. [ 2 ]  Undercooked  shellfish  is a common source. [ 9 ]  Humans are the only known host for the  bacteria . [ 2 ]   Risk factors  for the disease include poor  sanitation , insufficient clean  drinking water , and  poverty . [ 2 ]  Cholera can be diagnosed by a  stool test , [ 2 ]  or a rapid  dipstick test , although the dipstick test is less accurate. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_266", "text": "Prevention methods against cholera include improved sanitation and access to  clean water . [ 5 ]   Cholera vaccines  that are given by mouth provide reasonable protection for about six months, and confer the added benefit of protecting against another type of diarrhea caused by  E.\u00a0coli . [ 2 ]  In 2017, the  US Food and Drug Administration  (FDA) approved a single-dose, live, oral cholera vaccine called  Vaxchora  for adults aged 18\u201364 who are travelling to an area of active cholera transmission. [ 11 ]  It offers limited protection to young children. People who survive an episode of cholera have long-lasting immunity for at least three years (the period tested). [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_267", "text": "The primary treatment for affected individuals is  oral rehydration salts  (ORS), the replacement of fluids and electrolytes by using slightly sweet and salty solutions. [ 2 ]  Rice-based solutions are preferred. [ 2 ]  In children,  zinc supplementation  has also been found to improve outcomes. [ 6 ]  In severe cases,  intravenous fluids , such as  Ringer's lactate , may be required, and  antibiotics  may be beneficial. [ 2 ]  The choice of antibiotic is aided by  antibiotic sensitivity testing . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_268", "text": "Cholera continues to affect an estimated 3\u20135\u00a0million people worldwide and causes 28,800\u2013130,000\u00a0deaths a year. [ 2 ] [ 7 ]  To date,  seven cholera pandemics  have occurred, with the most recent beginning in 1961, and continuing today. [ 13 ]  The illness is rare in  high-income countries , and affects children most severely. [ 2 ] [ 14 ]  Cholera occurs as both  outbreaks  and  chronically in certain areas . [ 2 ]  Areas with an ongoing risk of disease include  Africa  and  Southeast Asia . [ 2 ]  The risk of death among those affected is usually less than 5%, given improved treatment, but may be as high as 50% without such access to treatment. [ 2 ]  Descriptions of cholera are found as early as the 5th century BCE in  Sanskrit literature . [ 5 ]  In Europe, cholera was a term initially used to describe any kind of gastroenteritis, and was not used for this disease until the early 19th century. [ 15 ]  The study of cholera in England by  John Snow  between 1849 and 1854 led to significant advances in the field of  epidemiology  because of his insights about transmission via  contaminated water , and a map of the same was the first recorded incidence of epidemiological tracking. [ 5 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_269", "text": "The primary symptoms of cholera are profuse  diarrhea  and  vomiting  of clear fluid. [ 17 ]  These symptoms usually start suddenly, half a day to five days after ingestion of the bacteria. [ 18 ]  The diarrhea is frequently described as \"rice water\" in nature and may have a fishy odor. [ 17 ]  An untreated person with cholera may produce 10 to 20 litres (3 to 5\u00a0US\u00a0gal) of diarrhea a day. [ 17 ]  Severe cholera, without treatment, kills about half of affected individuals. [ 17 ]  If the severe diarrhea is not treated, it can result in life-threatening  dehydration  and  electrolyte  imbalances. [ 17 ]  Estimates of the ratio of  asymptomatic  to symptomatic infections have ranged from 3 to 100. [ 19 ]  Cholera has been nicknamed the \"blue death\" [ 20 ]  because a person's skin may turn  bluish-gray  from extreme loss of fluids. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_270", "text": "Fever is rare and should raise suspicion for secondary infection. Patients can be lethargic and might have sunken eyes, dry mouth, cold clammy skin, or wrinkled hands and feet.  Kussmaul breathing , a deep and labored breathing pattern, can occur because of  acidosis  from  stool   bicarbonate  losses and  lactic acidosis  associated with poor  perfusion .  Blood pressure  drops due to dehydration, peripheral pulse is rapid and thready, and urine output decreases with time. Muscle cramping and weakness, altered consciousness,  seizures , or even  coma  due to  electrolyte imbalances  are common, especially in children. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_271", "text": "Cholera bacteria have been found in  shellfish  and  plankton . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_272", "text": "Transmission  is usually through the  fecal-oral route  of contaminated food or water caused by poor  sanitation . [ 2 ]  Most cholera cases in  developed countries  are a result of transmission by food, while in  developing countries  it is more often water. [ 17 ]  Food transmission can occur when people harvest seafood such as  oysters  in waters infected with  sewage , as  Vibrio cholerae  accumulates in  planktonic   crustaceans  and the oysters eat the  zooplankton . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_273", "text": "People infected with cholera often have diarrhea, and disease transmission may occur if this highly liquid stool, colloquially referred to as \"rice-water\", contaminates water used by others. [ 23 ]  A single diarrheal event can cause a one-million fold increase in numbers of  V. cholerae  in the environment. [ 24 ]  The source of the contamination is typically other people with cholera when their untreated diarrheal discharge is allowed to get into waterways,  groundwater  or  drinking water  supplies. Drinking any contaminated water and eating any foods washed in the water, as well as  shellfish  living in the affected  waterway , can cause a person to contract an infection. Cholera is rarely  spread directly from person to person . [ 25 ] [ note 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_274", "text": "V. cholerae  also exists outside the human body in natural water sources, either by itself or through interacting with  phytoplankton ,  zooplankton , or  biotic  and  abiotic  detritus. [ 26 ]  Drinking such water can also result in the disease, even without prior contamination through fecal matter. Selective pressures exist however in the aquatic environment that may reduce the virulence of  V. cholerae . [ 26 ]  Specifically, animal models indicate that the transcriptional profile of the pathogen changes as it prepares to enter an aquatic environment. [ 26 ]  This transcriptional change results in a loss of ability of  V. cholerae  to be cultured on standard media, a phenotype referred to as ' viable but non-culturable ' (VBNC) or more conservatively ' active but non-culturable ' (ABNC). [ 26 ]  One study indicates that the culturability of  V. cholerae  drops 90% within 24 hours of entering the water, and furthermore that this loss in culturability is associated with a loss in virulence. [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_275", "text": "Both toxic and non-toxic strains exist. Non-toxic strains can acquire  toxicity  through a  temperate   bacteriophage . [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_276", "text": "About 100 \u00a0 million bacteria must typically be ingested to cause cholera in a normal healthy adult. [ 17 ]  This dose, however, is less in those with lowered  gastric acidity  (for instance those using  proton pump inhibitors ). [ 17 ]  Children are also more susceptible, with two- to four-year-olds having the highest rates of infection. [ 17 ]  Individuals' susceptibility to cholera is also affected by their  blood type , with those with  type O blood  being the most susceptible. [ 17 ]  Persons with  lowered immunity , such as persons with  AIDS  or  malnourished  children, are more likely to develop a severe case if they become infected. [ 29 ]  Any individual, even a healthy adult in middle age, can undergo a severe case, and each person's case should be measured by the loss of fluids, preferably in consultation with a professional  health care provider . [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_277", "text": "The  cystic fibrosis  genetic  mutation  known as  delta-F508  in humans has been said to maintain a selective  heterozygous advantage :  heterozygous  carriers of the mutation (who are not affected by cystic fibrosis) are more resistant to  V. cholerae  infections. [ 30 ]  In this model, the genetic deficiency in the  cystic fibrosis transmembrane conductance regulator  channel proteins interferes with bacteria binding to the  intestinal epithelium , thus reducing the effects of an infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_278", "text": "When consumed, most bacteria do not survive the  acidic  conditions of the  human stomach . [ 31 ]  The few surviving bacteria conserve their energy and stored  nutrients  during the passage through the stomach by shutting down  protein  production. When the surviving bacteria exit the stomach and reach the  small intestine , they must propel themselves through the thick  mucus  that lines the small intestine to reach the intestinal walls where they can attach and thrive. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_279", "text": "Once the cholera bacteria reach the intestinal wall, they no longer need the  flagella  to move. The bacteria stop producing the protein  flagellin  to conserve energy and nutrients by changing the mix of proteins that they express in response to the changed chemical surroundings. On reaching the intestinal wall,  V. cholerae  start producing the  toxic proteins  that give the infected person a watery diarrhea. This carries the multiplying new generations of  V. cholerae  bacteria out into the drinking water of the next host if proper sanitation measures are not in place. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_280", "text": "The  cholera toxin  (CTX or CT) is an  oligomeric  complex made up of six  protein subunits : a single copy of the A subunit (part A), and five copies of the B subunit (part B), connected by a  disulfide bond . The five B subunits form a five-membered ring that binds to  GM1   gangliosides  on the surface of the intestinal epithelium cells. The A1 portion of the A subunit is an enzyme that  ADP-ribosylates   G proteins , while the A2 chain fits into the central pore of the B subunit ring. Upon binding, the complex is taken into the cell via receptor-mediated  endocytosis . Once inside the cell, the disulfide bond is reduced, and the A1 subunit is freed to bind with a human partner protein called  ADP-ribosylation factor 6  (Arf6). [ 33 ]  Binding exposes its active site, allowing it to permanently ribosylate the  Gs alpha subunit  of the  heterotrimeric G protein . This results in constitutive  cAMP  production, which in turn leads to the secretion of water, sodium, potassium, and bicarbonate into the lumen of the small intestine and rapid dehydration. The gene encoding the cholera toxin was introduced into  V. cholerae  by  horizontal gene transfer . Virulent strains of  V. cholerae  carry a variant of a  temperate   bacteriophage  called  CTX\u03c6 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_281", "text": "Microbiologists have studied the  genetic mechanisms  by which the  V. cholerae  bacteria turn off the production of some proteins and turn on the production of other proteins as they respond to the series of chemical environments they encounter, passing through the stomach, through the mucous layer of the small intestine, and on to the intestinal wall. [ 34 ]  Of particular interest have been the genetic mechanisms by which cholera bacteria turn on the protein production of the toxins that interact with host cell mechanisms to pump  chloride  ions into the small intestine, creating an ionic pressure which prevents sodium ions from entering the cell. The chloride and sodium ions create a salt-water environment in the small intestines, which through osmosis can pull up to six liters of water per day through the intestinal cells, creating the massive amounts of diarrhea. The host can become rapidly dehydrated unless treated properly. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_282", "text": "By inserting separate, successive sections of  V. cholerae  DNA into the DNA of other bacteria, such as  E. coli  that would not naturally produce the protein toxins, researchers have investigated the mechanisms by which  V. cholerae  responds to the changing chemical environments of the stomach, mucous layers, and intestinal wall. Researchers have discovered a complex cascade of regulatory proteins controls expression of  V. cholerae   virulence  determinants. [ 36 ]  In responding to the chemical environment at the intestinal wall, the  V. cholerae  bacteria produce the TcpP/TcpH proteins, which, together with the ToxR/ToxS proteins, activate the expression of the ToxT regulatory protein. ToxT then directly activates expression of  virulence  genes that produce the toxins, causing diarrhea in the infected person and allowing the bacteria to colonize the intestine. [ 34 ]  Current [ when? ]  research aims at discovering \"the signal that makes the cholera bacteria stop swimming and start to colonize (that is, adhere to the cells of) the small intestine.\" [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_283", "text": "Amplified fragment length polymorphism   fingerprinting  of the pandemic  isolates  of  V. cholerae  has revealed variation in the genetic structure. Two  clusters  have been identified: Cluster I and Cluster II. For the most part, Cluster I consists of strains from the 1960s and 1970s, while Cluster II largely contains strains from the 1980s and 1990s, based on the change in the clone structure. This grouping of strains is best seen in the strains from the African continent. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_284", "text": "In many areas of the world,  antibiotic resistance  is increasing within cholera bacteria. In  Bangladesh , for example, most cases are resistant to  tetracycline ,  trimethoprim-sulfamethoxazole , and  erythromycin . [ 38 ]  Rapid diagnostic  assay  methods are available for the identification of  multi-drug resistant  cases. [ 39 ]  New generation antimicrobials have been discovered which are effective against cholera bacteria in  in vitro  studies. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_285", "text": "A rapid  dipstick  test is available to determine the presence of  V. cholerae . [ 38 ]  In those samples that test positive, further testing should be done to determine antibiotic resistance. [ 38 ]  In  epidemic  situations, a clinical diagnosis may be made by taking a  patient history  and doing a brief examination. Treatment via hydration and over-the-counter hydration solutions can be started without or before confirmation by laboratory analysis, especially where cholera is a common problem. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_286", "text": "Stool and swab samples collected in the acute stage of the disease, before antibiotics have been administered, are the most useful specimens for laboratory diagnosis. If an epidemic of cholera is suspected, the most common causative agent is  V. cholerae  O1. If  V. cholerae   serogroup  O1 is not isolated, the laboratory should test for  V. cholerae  O139. However, if neither of these organisms is isolated, it is necessary to send stool specimens to a reference laboratory. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_287", "text": "Infection with  V. cholerae  O139 should be reported and handled in the same manner as that caused by  V. cholerae  O1. The associated diarrheal illness should be referred to as cholera and must be reported in the United States. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_288", "text": "The  World Health Organization  (WHO) recommends focusing on prevention, preparedness, and response to combat the spread of cholera. [ 35 ]  They also stress the importance of an effective surveillance system. [ 35 ]  Governments can play a role in all of these areas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_289", "text": "Although cholera may be life-threatening, prevention of the disease is normally straightforward if proper  sanitation  practices are followed. In  developed countries , due to their nearly universal advanced  water treatment  and sanitation practices, cholera is rare. For example, the last major outbreak of cholera in the United States occurred in 1910\u20131911. [ 43 ] [ 44 ]  Cholera is mainly a risk in  developing countries  in those areas where access to  WASH (water, sanitation and hygiene)  infrastructure is still inadequate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_290", "text": "Effective sanitation practices, if instituted and adhered to in time, are usually sufficient to stop an epidemic. There are several points along the cholera transmission path at which its spread may be halted: [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_291", "text": "Handwashing  with soap or ash after using a  toilet  and before handling food or eating is also recommended for cholera prevention by WHO Africa. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_292", "text": "Surveillance and prompt reporting allow for containing cholera epidemics rapidly. Cholera exists as a seasonal disease in many endemic countries, occurring annually mostly during  rainy seasons . Surveillance systems can provide early alerts to outbreaks, therefore leading to coordinated response and assist in preparation of preparedness plans. Efficient surveillance systems can also improve the risk assessment for potential cholera outbreaks. Understanding the seasonality and location of outbreaks provides guidance for improving cholera control activities for the most vulnerable. [ 51 ]  For prevention to be effective, it is important that cases be reported to national health authorities. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_293", "text": "Spanish physician  Jaume Ferran i Clua  developed the first successful cholera inoculation in 1885, the first to immunize humans against a bacterial disease. [ 52 ]  His vaccine and inoculation was rather controversial and was rejected by his peers and several investigation commissions but it ended up demonstrating its effectiveness and being recognized for it: out of the 30 thousand people he vaccinated only 54 died. [ 53 ] [ 54 ] [ 55 ] [ 56 ]  Russian-Jewish bacteriologist  Waldemar Haffkine  also developed a human cholera vaccine in July 1892. [ 53 ] [ 54 ] [ 55 ] [ 57 ]  He conducted a massive inoculation program in  British India . [ 55 ] [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_294", "text": "Persons who survive an episode of cholera have long-lasting immunity for at least 3 years (the period tested.) [ 12 ]  A number of safe and effective oral vaccines for cholera are available. [ 59 ]  The World Health Organization (WHO) has three prequalified oral cholera vaccines (OCVs): Dukoral, Sanchol, and Euvichol.  Dukoral , an orally administered, inactivated  whole-cell vaccine , has an overall efficacy of about 52% during the first year after being given and 62% in the second year, with minimal side effects. [ 59 ]  It is available in over 60 countries. However, it is not currently [ when? ]  recommended by the  Centers for Disease Control and Prevention  (CDC) for most people traveling from the United States to endemic countries. [ 60 ]  The vaccine that the  US Food and Drug Administration  (FDA) recommends,  Vaxchora , is an  oral attenuated live vaccine , that is effective for adults aged 18\u201364 as a single dose. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_295", "text": "One injectable vaccine was found to be effective for two to three years. The protective efficacy was 28% lower in children less than five years old. [ 62 ]  However, as of 2010 [update] , it has limited availability. [ 2 ]  Work is under way to investigate the role of mass vaccination. [ 63 ]  The WHO recommends immunization of high-risk groups, such as children and people with  HIV , in countries where this disease is  endemic . [ 2 ]  If people are immunized broadly,  herd immunity  results, with a decrease in the amount of contamination in the environment. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_296", "text": "WHO recommends that oral cholera vaccination be considered in areas where the disease is endemic (with seasonal peaks), as part of the response to outbreaks, or in a humanitarian crisis during which the risk of cholera is high. [ 64 ]  Oral Cholera Vaccine (OCV) has been recognized as an adjunct tool for prevention and control of cholera. The World Health Organization (WHO) has prequalified three bivalent cholera vaccines\u2014Dukoral (SBL Vaccines), containing a non-toxic B-subunit of cholera toxin and providing protection against V. cholerae O1; and two vaccines developed using the same transfer of technology\u2014ShanChol (Shantha Biotec) and Euvichol (EuBiologics Co.), which have bivalent O1 and O139 oral killed cholera vaccines. [ 65 ]  Oral cholera vaccination could be deployed in a diverse range of situations from cholera-endemic areas and locations of humanitarian crises, but no clear consensus exists. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_297", "text": "Developed for use in  Bangladesh , the \"sari filter\" is a simple and cost-effective  appropriate technology  method for reducing the contamination of drinking water. Used  sari  cloth is preferable but other types of used cloth can be used with some effect, though the effectiveness will vary significantly. Used cloth is more effective than new cloth, as the repeated washing reduces the space between the fibers. Water collected in this way has a greatly reduced  pathogen  count\u2014though it will not necessarily be perfectly safe, it is an improvement for poor people with limited options. [ 67 ]  In Bangladesh this practice was found to decrease rates of cholera by nearly half. [ 68 ]  It involves folding a  sari  four to eight times. [ 67 ]  Between uses the cloth should be rinsed in clean water and dried in the sun to kill any bacteria on it. [ 69 ]  A  nylon  cloth appears to work as well but is not as affordable. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_298", "text": "Continued eating speeds the recovery of normal intestinal function. The WHO recommends this generally for cases of diarrhea no matter what the underlying cause. [ 70 ]  A CDC training manual specifically for cholera states: \"Continue to breastfeed your baby if the baby has watery diarrhea, even when traveling to get treatment. Adults and older children should continue to eat frequently.\" [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_299", "text": "The most common error in caring for patients with cholera is to underestimate the speed\nand volume of fluids required. [ 72 ]  In most cases, cholera can be successfully treated with  oral rehydration therapy  (ORT), which is highly effective, safe, and simple to administer. [ 38 ]  Rice-based solutions are preferred to glucose-based ones due to greater efficiency. [ 38 ]  In severe cases with significant dehydration,  intravenous  rehydration may be necessary.  Ringer's lactate  is the preferred solution, often with added potassium. [ 17 ] [ 70 ]  Large volumes and continued replacement until diarrhea has subsided may be needed. [ 17 ]  Ten percent of a person's body weight in fluid may need to be given in the first two to four hours. [ 17 ]  This method was first tried on a mass scale during the  Bangladesh Liberation War , and was found to have much success. [ 73 ]  Despite widespread beliefs, fruit juices and commercial fizzy drinks like cola are not ideal for rehydration of people with serious infections of the intestines, and their excessive sugar content may even harm water uptake. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_300", "text": "If commercially produced oral rehydration solutions are too expensive or difficult to obtain, solutions can be made. One such recipe calls for 1 liter of boiled water, 1/2 teaspoon of salt, 6 teaspoons of sugar, and added mashed banana for potassium and to improve taste. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_301", "text": "As there frequently is initially  acidosis , the  potassium  level may be normal, even though large losses have occurred. [ 17 ]  As the dehydration is corrected, potassium levels may decrease rapidly, and thus need to be replaced. [ 17 ]  This is best done by Oral Rehydration Solution (ORS). [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_302", "text": "Antibiotic  treatments for one to three days shorten the course of the disease and reduce the severity of the symptoms. [ 17 ]  Use of antibiotics also reduces fluid requirements. [ 77 ]  People will recover without them, however, if sufficient hydration is maintained. [ 38 ]  The WHO only recommends antibiotics in those with severe dehydration. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_303", "text": "Doxycycline  is typically used first line, although some  strains  of  V. cholerae  have shown  resistance . [ 17 ]  Testing for resistance during an outbreak can help determine appropriate future choices. [ 17 ]  Other antibiotics proven to be effective include  cotrimoxazole ,  erythromycin ,  tetracycline ,  chloramphenicol , and  furazolidone . [ 78 ]   Fluoroquinolones , such as  ciprofloxacin , also may be used, but resistance has been reported. [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_304", "text": "Antibiotics improve outcomes in those who are both severely and not severely dehydrated. [ 80 ]   Azithromycin  and  tetracycline  may work better than  doxycycline  or  ciprofloxacin . [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_305", "text": "In Bangladesh  zinc  supplementation reduced the duration and severity of diarrhea in children with cholera when given with antibiotics and rehydration therapy as needed. It reduced the length of disease by eight hours and the amount of diarrhea stool by 10%. [ 81 ]  Supplementation appears to be also effective in both treating and preventing infectious diarrhea due to other causes among children in the developing world. [ 81 ] [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_306", "text": "If people with cholera are treated quickly and properly, the mortality rate is less than 1%; however, with untreated cholera, the mortality rate rises to 50\u201360%. [ 17 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_307", "text": "For certain genetic strains of cholera, such as the one present during the  2010 epidemic in Haiti  and the 2004 outbreak in India, death can occur within two hours of becoming ill. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_308", "text": "Cholera affects an estimated 2.8\u00a0million people worldwide, and causes approximately 95,000\u00a0deaths a year (uncertainty range: 21,000\u2013143,000) as of 2015 [update] . [ 84 ] [ 85 ]  This occurs mainly in the developing world. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_309", "text": "In the early 1980s, death rates are believed to have still been higher than three million a year. [ 17 ]  It is difficult to calculate exact numbers of cases, as many go unreported due to concerns that an outbreak may have a negative impact on the tourism of a country. [ 38 ]  As of 2004, cholera remained both  epidemic  and endemic in many areas of the world. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_310", "text": "Recent major outbreaks are the  2010s Haiti cholera outbreak  and the  2016\u20132022 Yemen cholera outbreak . In October 2016, an  outbreak of cholera  began in war-ravaged  Yemen . [ 87 ]   WHO  called it \"the worst cholera outbreak in the world\". [ 88 ]  In 2019, 93% of the reported 923,037 cholera cases were from  Yemen  (with 1911 deaths reported). [ 89 ]  Between September 2019 and September 2020, a global total of over 450,000 cases and over 900 deaths was reported; however, the accuracy of these numbers suffer from over-reporting from countries that report suspected cases (and not laboratory confirmed cases), as well as under-reporting from countries that do not report official cases (such as Bangladesh, India and Philippines). [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_311", "text": "Although much is known about the mechanisms behind the spread of cholera, researchers still do not have a full understanding of what makes cholera outbreaks happen in some places and not others. Lack of treatment of human  feces  and lack of treatment of drinking water greatly facilitate its spread. Bodies of water have been found to serve as a  reservoir  of infection, and seafood shipped long distances can spread the disease."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_312", "text": "Cholera had disappeared from the  Americas  for most of the 20th century, but it reappeared toward the end of that century, beginning with a severe outbreak in Peru. [ 90 ]  This was followed by the  2010s Haiti cholera outbreak [ 91 ]  and another outbreak of cholera in Haiti amid the  2018\u20132023 Haitian crisis . [ 92 ]  As of August 2021 [update]  the disease is endemic in Africa and some areas of eastern and western Asia (Bangladesh, India and Yemen). [ 91 ]  Cholera is not endemic in Europe; all reported cases had a travel history to endemic areas. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_313", "text": "The word cholera is from  Greek :  \u03c7\u03bf\u03bb\u03ad\u03c1\u03b1   kholera  from \u03c7\u03bf\u03bb\u03ae  khol\u0113  \"bile\". Cholera likely has its origins in the  Indian subcontinent  as evidenced by its prevalence in the region for centuries. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_314", "text": "References to cholera appear in the European literature as early as 1642, from the Dutch physician  Jakob de Bondt's  description in his De Medicina Indorum. [ 93 ]  (The \"Indorum\" of the title refers to the East Indies. He also gave first European descriptions of other diseases.) But at the time, the word \"cholera\" was historically used by European physicians to refer to any gastrointestinal upset resulting in yellow diarrhea. De Bondt thus used a common word already in regular use to describe the new disease. This was a frequent practice of the time. It was not until the 1830s that the name for severe yellow diarrhea changed in English from \"cholera\" to \"cholera morbus\" to differentiate it from what was then known as \"Asiatic cholera\", or that associated with origins in India and the East."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_315", "text": "Early outbreaks in the Indian subcontinent are believed to have been the result of crowded, poor living conditions, as well as the presence of pools of  still water , both of which provide ideal conditions for cholera to thrive. [ 94 ]  The disease first spread by travelers along  trade routes  (land and sea) to  Russia  in 1817, later to the rest of  Europe , and from Europe to  North America  and the rest of the world, [ 17 ]  (hence the name \"Asiatic cholera\" [ 1 ] ). Seven  cholera pandemics  have occurred since the early 19th century; the first one did not reach the Americas. The seventh  pandemic  originated in  Indonesia  in 1961. [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_316", "text": "The  first cholera pandemic  occurred in the Bengal region of India, near Calcutta starting in 1817 through 1824. The disease dispersed from India to Southeast Asia, the Middle East, Europe, and Eastern Africa. [ 96 ]  The movement of British Army and Navy ships and personnel is believed to have contributed to the range of the pandemic, since the ships carried people with the disease to the shores of the Indian Ocean, from Africa to Indonesia, and north to China and Japan. [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_317", "text": "The  second pandemic  lasted from 1826 to 1837 and particularly affected North America and Europe. Advancements in transport and global trade, and increased human migration, including soldiers, meant that more people were carrying the disease more widely. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_318", "text": "The  third pandemic  erupted in 1846, persisted until 1860, extended to North Africa, and reached North and South America. It was introduced to North America at  Quebec, Canada , via Irish immigrants from the Great Famine. In this pandemic, Brazil was affected for the first time."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_319", "text": "The  fourth pandemic  lasted from 1863 to 1875, spreading from India to Naples and Spain, and reaching the United States at  New Orleans, Louisiana  in 1873. It spread throughout the Mississippi River system on the continent."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_320", "text": "The  fifth  pandemic was from 1881 to 1896. It started in India and spread to Europe, Asia, and South America. The  sixth pandemic  ran from 1899 to 1923. These epidemics had a lower number of fatalities because physicians and researchers had a greater understanding of the cholera bacteria. Egypt, the Arabian peninsula, Persia, India, and the Philippines were hit hardest during these epidemics. Other areas, such as Germany in 1892 (primarily the city of Hamburg, where more than 8.600 people died) [ 99 ]  and Naples from 1910 to 1911, also had severe outbreaks."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_321", "text": "The  seventh pandemic  originated in 1961 in Indonesia and is marked by the emergence of a new strain, nicknamed  El Tor , which still persists (as of 2018 [update] [ 100 ] ) in developing countries. [ 101 ]  This pandemic had initially subsided about 1975 and was thought to have ended, but, as noted, it has persisted. There were a rise in cases in the 1990s and since."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_322", "text": "Cholera became widespread in the 19th century. [ 102 ]  Since then it has killed tens of millions of people. [ 103 ]  In  Russia  alone, between 1847 and 1851, more than one million people died from the disease. [ 104 ]  It killed 150,000 Americans during the second pandemic. [ 105 ]  Between 1900 and 1920, perhaps eight million people died of cholera in India. [ 106 ]  Cholera officially became the first  reportable disease  in the United States due to the significant effects it had on health. [ 17 ]   John Snow , in  England , in 1854 was the first to identify the importance of contaminated water as its source of transmission. [ 17 ]  Cholera is now no longer considered a pressing health threat in Europe and North America due to  filtering  and  chlorination  of water supplies, but it still strongly affects populations in  developing countries ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_323", "text": "In the past, vessels flew a yellow  quarantine  flag if any crew members or passengers had cholera. No one aboard a vessel flying a yellow flag would be allowed ashore for an extended period, typically 30 to 40 days. [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_324", "text": "Historically many different claimed remedies have existed in folklore. Many of the older remedies were based on the  miasma theory , that the disease was transmitted by bad air. Some believed that abdominal chilling made one more susceptible, and flannel and  cholera belts  were included in army kits. [ 108 ]  In the 1854\u20131855 outbreak in Naples, homeopathic  camphor  was used according to  Hahnemann . [ 109 ]  Dr. Hahnemann laid down three main remedies that would be curative in that disease; in early and simple cases  camphor ; in later stages with excessive cramping,  cuprum  or with excessive evacuations and profuse cold sweat,  veratrum album . These are the Trio Cholera remedies used by homoeopaths around the world. [ 110 ] \nT. J. Ritter's  Mother's Remedies  book lists tomato syrup as a home remedy from northern America.  Elecampane  was recommended in the United Kingdom, according to William Thomas Fernie. [ 111 ]  The first effective human vaccine was developed in 1885, and the first effective antibiotic was developed in 1948."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_325", "text": "Cholera cases are much less frequent in developed countries where governments have helped to establish water sanitation practices and effective medical treatments. [ 112 ]  In the 19th century the United States, for example, had a severe cholera problem similar to those in some developing countries. It had three large cholera outbreaks in the 1800s, which can be attributed to  Vibrio cholerae 's  spread through interior waterways such as the  Erie Canal  and the extensive Mississippi River valley system, as well as the major ports along the  Eastern Seaboard  and their cities upriver. [ 113 ]  The island of Manhattan in New York City touches the Atlantic Ocean, where cholera collected from river waters and ship discharges just off the coast. At this time, New York City did not have as effective a sanitation system as it developed in the later 20th century, so cholera spread through the city's water supply. [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_326", "text": "Cholera morbus is a historical term that was used to refer to  gastroenteritis  rather than specifically to what is now defined as the disease of cholera. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_327", "text": "One of the major contributions to fighting cholera was made by the physician and pioneer medical scientist  John Snow  (1813\u20131858), who in 1854 found a link between cholera and contaminated drinking water. [ 94 ]  Dr. Snow proposed a microbial origin for epidemic cholera in 1849. In his major \"state of the art\" review of 1855, he proposed a substantially complete and correct model for the cause of the disease. In two pioneering epidemiological field studies, he was able to demonstrate human  sewage  contamination was the most probable disease vector in two  major epidemics in London in 1854 . [ 115 ]  His model was not immediately accepted, but it was increasingly seen as plausible as medical microbiology developed over the next 30 years or so. For his work on cholera, John Snow is often regarded as the \"Father of Epidemiology\". [ 116 ] [ 117 ] [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_328", "text": "The bacterium was isolated in 1854 by Italian anatomist  Filippo Pacini , [ 119 ]  but its exact nature and his results were not widely known. In the same year, the  Catalan   Joaquim Balcells i Pascual  discovered the bacterium. [ 120 ] [ 121 ]  In 1856  Ant\u00f3nio Augusto da Costa Sim\u00f5es  and  Jos\u00e9 Ferreira de Macedo Pinto , two Portuguese researchers, are believed to have done the same. [ 120 ] [ 122 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_329", "text": "Between the mid-1850s and the 1900s, cities in developed nations made massive investment in clean water supply and well-separated sewage treatment infrastructures. This eliminated the threat of cholera epidemics from the major developed cities in the world. In 1883,  Robert Koch  identified  V. cholerae  with a microscope as the bacillus causing the disease. [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_330", "text": "Hemendra Nath Chatterjee , a Bengali scientist, was the first to formulate and demonstrate the effectiveness of  oral rehydration salt  (ORS) to treat  diarrhea . In his 1953 paper, published in  The Lancet , he states that  promethazine  can stop  vomiting  during cholera and then oral rehydration is possible. The formulation of the fluid replacement solution was 4\u00a0g of  sodium chloride , 25\u00a0g of  glucose  and 1000\u00a0ml of  water . [ 124 ] [ 125 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_331", "text": "Indian  medical scientist  Sambhu Nath De  discovered the  cholera toxin , the  animal model  of cholera , and successfully demonstrated the method of transmission of cholera pathogen  Vibrio cholerae . [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_332", "text": "Robert Allan Phillips , working at US  Naval Medical Research Unit Two  in Southeast Asia, evaluated the pathophysiology of the disease using modern laboratory chemistry techniques. He developed a protocol for rehydration. His research led the  Lasker Foundation  to award him its prize in 1967. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_333", "text": "More recently, in 2002, Alam,  et al. , studied stool samples from patients at the  International Centre for Diarrhoeal Disease  in  Dhaka, Bangladesh . From the various experiments they conducted, the researchers found a correlation between the passage of  V. cholerae  through the human digestive system and an increased infectivity state. Furthermore, the researchers found the bacterium creates a hyperinfected state where  genes  that control biosynthesis of  amino acids ,  iron  uptake systems, and formation of periplasmic nitrate reductase complexes were induced just before defecation. These induced characteristics allow the cholera vibrios to survive in the \"rice water\" stools, an environment of limited oxygen and iron, of patients with a cholera infection. [ 128 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_334", "text": "In 2017, the WHO launched the \"Ending Cholera: a global roadmap to 2030\" strategy which aims to reduce cholera deaths by 90% by 2030. [ 129 ]  The strategy was developed by the Global Task Force on Cholera Control (GTFCC) which develops country-specific plans and monitors progress. [ 130 ]  The approach to achieve this goal combines surveillance, water sanitation, rehydration treatment and oral vaccines. [ 129 ]  Specifically, the control strategy focuses on three approaches: i) early detection and response to outbreaks to contain outbreaks, ii) stopping cholera transmission through improved sanitation and vaccines in hotspots, and iii) a global framework for cholera control through the GTFCC. [ 129 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_335", "text": "The WHO and the GTFCC do not consider global cholera  eradication  a viable goal. [ 131 ]  Even though humans are the only host of cholera, the bacterium can persist in the environment without a human host. [ 132 ]  While global eradication is not possible, elimination of human to human transmission may be possible. [ 132 ]  Local elimination is possible, which has been underway most recently during the  2010s Haiti cholera outbreak . Haiti aims to achieve certification of elimination by 2022. [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_336", "text": "The GTFCC targets 47 countries, 13 of which have established vaccination campaigns. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_337", "text": "In many developing countries, cholera still reaches its victims through contaminated water sources, and countries without proper sanitation techniques have greater incidence of the disease. [ 134 ]  Governments can play a role in this. In 2008, for example, the  Zimbabwean cholera outbreak  was due partly to the government's role, according to a report from the  James Baker Institute . [ 22 ]  The Haitian government's inability to provide safe drinking water after the 2010 earthquake led to an increase in cholera cases as well. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_338", "text": "Similarly, South Africa's cholera outbreak was exacerbated by the government's policy of privatizing water programs. The wealthy elite of the country were able to afford safe water while others had to use water from cholera-infected rivers. [ 136 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_339", "text": "According to  Rita R. Colwell  of the  James Baker Institute , if cholera does begin to spread, government preparedness is crucial. A government's ability to contain the disease before it extends to other areas can prevent a high death toll and the development of an epidemic or even pandemic. Effective disease surveillance can ensure that cholera outbreaks are recognized as soon as possible and dealt with appropriately. Oftentimes, this will allow public health programs to determine and control the cause of the cases, whether it is unsanitary water or seafood that have accumulated a lot of  Vibrio cholerae  specimens. [ 22 ]  Having an effective surveillance program contributes to a government's ability to prevent cholera from spreading. In the year 2000 in the state of Kerala in India, the Kottayam district was determined to be \"Cholera-affected\"; this pronouncement led to task forces that concentrated on educating citizens with 13,670 information sessions about human health. [ 137 ]  These task forces promoted the boiling of water to obtain safe water, and provided chlorine and oral rehydration salts. [ 137 ]  Ultimately, this helped to control the spread of the disease to other areas and minimize deaths. On the other hand, researchers have shown that most of the citizens infected during the 1991 cholera outbreak in Bangladesh lived in rural areas, and were not recognized by the government's surveillance program. This inhibited physicians' abilities to detect cholera cases early. [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_340", "text": "According to Colwell, the quality and inclusiveness of a country's health care system affects the control of cholera, as it did in the  Zimbabwean cholera outbreak . [ 22 ]  While sanitation practices are important, when governments respond quickly and have readily available vaccines, the country will have a lower cholera death toll. Affordability of vaccines can be a problem; if the governments do not provide vaccinations, only the wealthy may be able to afford them and there will be a greater toll on the country's poor. [ 139 ] [ 140 ]  The speed with which government leaders respond to cholera outbreaks is important. [ 141 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_341", "text": "Besides contributing to an effective or declining public health care system and water sanitation treatments, government can have indirect effects on cholera control and the effectiveness of a response to cholera. [ 142 ]  A country's government can impact its ability to prevent disease and control its spread. A speedy government response backed by a fully functioning health care system and financial resources can prevent cholera's spread. This limits cholera's ability to cause death, or at the very least a decline in education, as children are kept out of school to minimize the risk of infection. [ 142 ]  Inversely, poor government response can lead to civil unrest and  cholera riots . [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_342", "text": "Unlike  tuberculosis  (\"consumption\") which in literature and the arts was often romanticized as a disease of denizens of the  demimonde  or those with an artistic temperament, [ 154 ]  cholera is a disease which almost entirely affects the poor living in unsanitary conditions. This, and the unpleasant course of the disease \u2013 which includes voluminous \"rice-water\" diarrhea, the hemorrhaging of liquids from the mouth, and violent muscle contractions which continue even after death \u2013 has discouraged the disease from being romanticized, or even being factually presented in popular culture. [ 155 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_343", "text": "In  Zambia , widespread cholera outbreaks have occurred since 1977, most commonly in the capital city of  Lusaka . [ 157 ]  In 2017, an outbreak of cholera was declared in Zambia after laboratory confirmation of  Vibrio cholerae  O1, biotype El Tor, serotype Ogawa, from stool samples from two patients with acute watery diarrhea. There was a rapid increase in the number of cases from several hundred cases in early December 2017 to approximately 2,000 by early January 2018. [ 158 ]  With intensification of the rains, new cases increased on a daily basis reaching a peak on the first week of January 2018 with over 700 cases reported. [ 159 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_344", "text": "In collaboration with partners, the Zambia Ministry of Health (MoH) launched a multifaceted public health response that included increased chlorination of the Lusaka municipal water supply, provision of emergency water supplies, water quality monitoring and testing, enhanced surveillance, epidemiologic investigations, a cholera vaccination campaign, aggressive case management and health care worker training, and laboratory testing of clinical samples. [ 158 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_345", "text": "The Zambian Ministry of Health implemented a reactive one-dose Oral Cholera Vaccine (OCV) campaign in April 2016 in three Lusaka compounds, followed by a pre-emptive second-round in December. [ 160 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_346", "text": "Nigeria"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_347", "text": "In June 2024, the  Nigeria Centre for Disease Control and Prevention  (NCDC) announced a total of 1,141 suspected and 65 confirmed cases of cholera with 30 deaths from 96 Local Government Areas (LGAs) in 30 states of the country. [ 161 ]  NCDC, in its public health advisory, said Abia, Bayelsa, Bauchi, Cross River, Delta, Imo, Katsina, Lagos, Nasarawa and Zamfara states were the 10 states that contributed 90 percent of the burden of cholera in the country at the time. [ 162 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_348", "text": "The city of  Kolkata ,  India  in the state of  West Bengal  in the  Ganges delta  has been described as the \"homeland of cholera\", with regular outbreaks and pronounced seasonality. In India, where the disease is  endemic , cholera outbreaks occur every year between  dry seasons  and  rainy seasons . India is also characterized by high population density, unsafe drinking water, open drains, and poor sanitation which provide an optimal niche for survival, sustenance and transmission of  Vibrio cholerae . [ 163 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_349", "text": "In  Goma  in the  Democratic Republic of Congo , cholera has left an enduring mark on human and medical history. Cholera pandemics in the 19th and 20th centuries led to the growth of epidemiology as a science and in recent years it has continued to press advances in the concepts of  disease ecology , basic membrane biology, and transmembrane signaling and in the use of scientific information and treatment design. [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_350", "text": "Chronic enteropathy associated with SLCO2A1  gene  is a rare  autosomal   recessive   enteropathy  that was first described in 1968. [ 1 ]  This condition was previously named chronic nonspecific multiple  ulcers  of the  small intestine . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_351", "text": "This  disease  occurs most commonly in women.  Symptom  onset is usually in  adolescence . Symptoms include  fatigue ,  oedema  and  abdominal pain . The disease course is  chronic  and while  immunosuppressants  have been tried these have not been shown to be helpful. On small bowel endoscopy the ulcers may be visible. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_352", "text": "Sequencing  the DNA of several  patients  suggested a  mutation  in the  SLCO2A1  gene. [ 4 ]  The presence of this mutation was confirmed by sequencing this gene in additional patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_353", "text": "This gene encodes a  prostaglandin  transporter. As  non-steroidal anti-inflammatory drugs  inhibit prostaglandin synthesis this helps to explain the known similarity in the  histological  findings between these conditions. The identification of this mutation suggests that prostaglandin replacement may be helpful but this will need to be tested in a  clinical trial . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_354", "text": "Within the small intestine there are multiple small shallow ulcers which may be linear or concentric. [ 5 ]   Stenosis  of the small bowel may be present due to healing of these ulcers. The ulcers resemble those associated with non steroidal use but occur in the absence of the use of these drugs. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_355", "text": "Immunohistochemical staining  for SLCO2A1 in gastro-duodenal tissue biopsy, may be helpful in distinguishing chronic enteropathy from  Crohn's disease . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_356", "text": "Coeliac disease  ( British English ) or  celiac disease  ( American English ) is a long-term  autoimmune disorder , primarily affecting the  small intestine , where individuals develop  intolerance  to  gluten , present in foods such as  wheat ,  rye  and  barley . [ 10 ]  Classic symptoms include gastrointestinal problems such as chronic  diarrhoea ,  abdominal distention ,  malabsorption ,  loss of appetite , and among children  failure to grow normally . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_357", "text": "Non-classic symptoms are more common, especially in people older than two years. [ 8 ] [ 15 ] [ 16 ]  There may be mild or absent gastrointestinal symptoms, a wide number of  symptoms involving any part of the body , or no obvious symptoms. [ 1 ]  Coeliac disease was first described in childhood; [ 6 ] [ 8 ]  however, it may develop at any age. [ 1 ] [ 8 ]  It is associated with other  autoimmune diseases , such as  Type 1 diabetes mellitus  and  Hashimoto's thyroiditis , among others. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_358", "text": "Coeliac disease is caused by a reaction to gluten, a group of various proteins found in  wheat  and in other grains such as  barley  and  rye . [ 9 ] [ 17 ] [ 18 ]  Moderate quantities of  oats , free of contamination with other gluten-containing grains, are usually tolerated. [ 17 ] [ 19 ]  The occurrence of problems may depend on the  variety  of oat. [ 17 ] [ 20 ]  It occurs more often in people who are  genetically predisposed . [ 10 ]  Upon exposure to gluten, an abnormal  immune  response may lead to the production of several different  autoantibodies  that can affect a number of different  organs . [ 4 ] [ 21 ]  In the small bowel, this causes an  inflammatory reaction  and may produce shortening of the  villi  lining the small intestine ( villous atrophy ). [ 10 ] [ 11 ]  This affects the absorption of nutrients, frequently leading to  anaemia . [ 10 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_359", "text": "Diagnosis is typically made by a combination of blood antibody tests and intestinal  biopsies , helped by specific  genetic testing . [ 10 ]  Making the diagnosis is not always straightforward. [ 22 ]  About 10% of the time, the autoantibodies in the blood are negative, [ 23 ] [ 24 ]  and many people have only minor intestinal changes with normal villi. [ 25 ]  People may have severe symptoms and they may be investigated for years before a diagnosis is achieved. [ 26 ] [ 27 ]  As a result of  screening , the diagnosis is increasingly being made in people who have  no symptoms . [ 28 ]  Evidence regarding the effects of screening, however, is not sufficient to determine its usefulness. [ 29 ]  While the disease is caused by a  permanent intolerance  to gluten proteins, [ 10 ]  it is distinct from  wheat allergy , which is much more rare. [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_360", "text": "The only known effective treatment is a strict lifelong  gluten-free diet , which leads to recovery of the intestinal lining ( mucous membrane ), improves symptoms, and reduces the risk of developing complications in most people. [ 13 ]  If untreated, it may result in  cancers  such as intestinal  lymphoma , and a slightly increased risk of early death. [ 3 ]  Rates vary between different regions of the world, from as few as 1 in 300 to as many as 1 in 40, with an average of between 1 in 100 and 1 in 170 people. [ 14 ]  It is estimated that 80% of cases remain undiagnosed, usually because of minimal or absent gastrointestinal complaints and lack of knowledge of symptoms and diagnostic criteria. [ 5 ] [ 26 ] [ 32 ]  Coeliac disease is slightly more common in women than in men. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_361", "text": "The classic symptoms of untreated coeliac disease include  diarrhea ,  steatorrhoea ,  iron-deficiency anemia , and weight loss or failure to gain weight. Other common symptoms may be subtle or primarily occur in organs other than the bowel itself. [ 34 ]  It is also possible to have coeliac disease without any of the classic symptoms at all. [ 18 ]  This has been shown to comprise at least 43% of presentations in children. [ 35 ]  Further, many adults with subtle disease may only present with fatigue,  anaemia  or  low bone mass . [ 28 ]  Many undiagnosed individuals who consider themselves asymptomatic are in fact not, but rather have become accustomed to living in a state of chronically compromised health. Indeed, after starting a gluten-free diet and subsequent improvement becomes evident, such individuals are often able to retrospectively recall and recognise prior symptoms of their untreated disease that they had mistakenly ignored. [ 5 ] [ 27 ] [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_362", "text": "Diarrhoea  that is characteristic of coeliac disease is chronic, sometimes pale, of large volume, and abnormally foul in odor.  Abdominal pain , cramping, bloating with  abdominal distension  (thought to be the result of fermentative production of bowel gas), and  mouth ulcers [ 36 ]  may be present. As the bowel becomes more damaged, a degree of  lactose intolerance  may develop. [ 18 ]  Frequently, the symptoms are ascribed to  irritable bowel syndrome  (IBS), only later to be recognised as coeliac disease. In populations of people with symptoms of IBS, a diagnosis of coeliac disease can be made in about 3.3% of cases, or four times more likely than in general. [ 37 ]  Screening them for coeliac disease is recommended by the  National Institute for Health and Clinical Excellence  (NICE), the  British Society of Gastroenterology  and the  American College of Gastroenterology , but is of unclear benefit in North America. [ 37 ] [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_363", "text": "Coeliac disease leads to an increased risk of both  adenocarcinoma  and  lymphoma  of the small bowel ( enteropathy-associated T-cell lymphoma  (EATL) or other  non-Hodgkin lymphomas ). [ 39 ]  This risk is also higher in first-degree relatives such as siblings, parents and children. Whether a gluten-free diet brings this risk back to baseline is not clear. [ 40 ]  Long-standing and untreated disease may lead to other complications, such as  ulcerative jejunitis  (ulcer formation of the small bowel) and stricturing (narrowing as a result of scarring with obstruction of the bowel). [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_364", "text": "The changes in the bowel reduce its ability to  absorb  nutrients, minerals, and the  fat-soluble vitamins  A, D, E, and K. [ 18 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_365", "text": "Coeliac disease has been linked with many conditions. In many cases, it is unclear whether the gluten-induced bowel disease is a causative factor or whether these conditions share a common predisposition."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_366", "text": "Coeliac disease is associated with several other medical conditions, many of which are autoimmune disorders:  diabetes mellitus type 1 ,  hypothyroidism ,  primary biliary cholangitis ,  microscopic colitis ,  gluten ataxia ,  psoriasis ,  vitiligo ,  autoimmune hepatitis ,  primary sclerosing cholangitis , and more. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_367", "text": "Coeliac disease is caused by an inflammatory reaction to  gliadins  and  glutenins  ( gluten  proteins) [ 50 ]  found in wheat and to similar proteins found in the crops of the  tribe   Triticeae  (which includes other common grains such as  barley  and  rye ) [ 18 ]  and to the tribe  Aveneae  ( oats ). [ 51 ]  Wheat subspecies (such as  spelt ,  durum , and  Kamut ) and wheat hybrids (such as  triticale ) also cause symptoms of coeliac disease. [ 51 ] [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_368", "text": "A small number of people with coeliac disease react to oats. [ 18 ]  Oat toxicity in coeliac people depends on the oat  cultivar  consumed because the prolamin genes, protein amino acid sequences, and the  immunoreactivities  of toxic prolamins are different in different oat varieties. [ 20 ] [ 53 ]  Also, oats are frequently cross-contaminated with other grains containing gluten. [ 20 ] [ 53 ] [ 54 ]  The term \"pure oats\" refers to oats uncontaminated with other gluten-containing cereals. [ 20 ]  The long-term effects of pure oat consumption are still unclear, [ 55 ]  and further studies identifying the cultivars used are needed before making final recommendations on their inclusion in a  gluten-free diet . [ 54 ]  Coeliac people who choose to consume oats need a more rigorous lifelong follow-up, possibly including periodic  intestinal biopsies . [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_369", "text": "Other cereals such as  corn ,  millet ,  sorghum ,  teff ,  rice , and  wild rice  are safe for people with coeliac disease to consume, as well as non-cereals such as  amaranth ,  quinoa , and  buckwheat . [ 52 ] [ 56 ]  Noncereal carbohydrate-rich foods such as potatoes and bananas do not contain gluten and do not trigger symptoms. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_370", "text": "There are various theories as to what determines whether a genetically susceptible individual will go on to develop coeliac disease. Major theories include surgery, pregnancy, infection and emotional stress. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_371", "text": "The eating of gluten early in a baby's life does not appear to increase the risk of coeliac disease but later introduction after six months may increase it. [ 58 ] [ 59 ]  There is uncertainty whether being breastfed reduces risk. Prolonging  breastfeeding  until the introduction of gluten-containing grains into the diet appears to be associated with a 50% reduced risk of developing coeliac disease in infancy; whether this persists into adulthood is not clear. [ 60 ]  These factors may just influence the timing of onset. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_372", "text": "Coeliac disease appears to be multifactorial, both in that more than one genetic factor can cause the disease and in that more than one factor is necessary for the disease to manifest in a person. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_373", "text": "Almost all people (95%) with coeliac disease have either the variant  HLA-DQ2   allele  or (less commonly) the  HLA-DQ8   allele . [ 28 ] [ 63 ]  However, about 20\u201330% of people without coeliac disease have also inherited either of these alleles. [ 64 ]  This suggests that additional factors are needed for coeliac disease to develop; that is, the predisposing HLA risk allele is necessary but not sufficient to develop coeliac disease. Furthermore, around 5% of those people who do develop coeliac disease do not have typical HLA-DQ2 or HLA-DQ8 alleles (see below). [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_374", "text": "The vast majority of people with coeliac have one of two types (out of seven) of the  HLA-DQ  protein. [ 64 ]   HLA-DQ is part of the  MHC class II antigen-presenting receptor  (also called the  human leukocyte antigen ) system and distinguishes cells between self and non-self for the purposes of the  immune system . The two subunits of the HLA-DQ protein are encoded by the HLA-DQA1 and HLA-DQB1 genes, located on the short arm of  chromosome 6 . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_375", "text": "There are seven HLA-DQ variants (DQ2 and DQ4\u2013DQ9). Over 95% of people with coeliac have the isoform of DQ2 or DQ8, which is inherited in families. The reason these genes produce an increase in the risk of coeliac disease is that the receptors formed by these genes bind to gliadin peptides more tightly than other forms of the antigen-presenting receptor. Therefore, these forms of the receptor are more likely to activate  T lymphocytes  and initiate the autoimmune process. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_376", "text": "Most people with coeliac bear a two-gene HLA-DQ2  haplotype  referred to as  DQ2.5 haplotype . This haplotype is composed of two adjacent gene  alleles , DQA1*0501 and  DQB1*0201 , which encode the two subunits, DQ \u03b1 5  and DQ \u03b2 2 . In most individuals, this DQ2.5 isoform is encoded by one of two chromosomes 6 inherited from parents (DQ2.5cis). Most coeliacs inherit only one copy of this DQ2.5 haplotype, while some inherit it from  both  parents; the latter are especially at risk for coeliac disease as well as being more susceptible to severe complications. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_377", "text": "Some individuals inherit DQ2.5 from one parent and an additional portion of the haplotype (either DQB1*02 or DQA1*05) from the other parent, increasing risk. Less commonly, some individuals inherit the DQA1*05 allele from one parent and the DQB1*02 from the other parent (DQ2.5trans) (called a trans-haplotype association), and these individuals are at similar risk for coeliac disease as those with a single DQ2.5-bearing chromosome 6, but in this instance, the disease tends not to be familial. Among the 6% of European coeliacs that do not have DQ2.5 (cis or trans) or DQ8 (encoded by the haplotype DQA1*03:DQB1*0302), 4% have the  DQ2.2  isoform, and the remaining 2% lack DQ2 or DQ8. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_378", "text": "The frequency of these genes varies geographically. DQ2.5 has high frequency in peoples of North and Western Europe ( Basque Country  and Ireland [ 68 ]  with highest frequencies) and portions of Africa and is associated with disease in India, [ 69 ]  but it is not found along portions of the West Pacific rim. DQ8 has a wider global distribution than DQ2.5 and is particularly common in South and Central America; up to 90% of individuals in certain Amerindian populations carry DQ8 and thus may display the coeliac  phenotype . [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_379", "text": "Other genetic factors have been repeatedly reported in coeliac disease; however, involvement in disease has variable geographic recognition. Only the HLA-DQ loci show a consistent involvement over the global population. [ 71 ]  Many of the loci detected have been found in association with other autoimmune diseases. One locus, the  LPP  or lipoma-preferred partner gene, is involved in the adhesion of extracellular matrix to the cell surface, and a minor variant ( SNP =rs1464510) increases the risk of disease by approximately 30%. This gene strongly associates with coeliac disease ( p  < 10 \u221239 ) in samples taken from a broad area of Europe and the US. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_380", "text": "The prevalence of coeliac disease genotypes in the modern population is not completely understood. Given the characteristics of the disease and its apparent strong heritability, it would normally be expected that the genotypes would undergo negative selection and to be absent in societies where agriculture has been practised the longest (compare with a similar condition,  lactose intolerance , which has been negatively selected so strongly that its prevalence went from ~100% in ancestral populations to less than 5% in some European countries). This expectation was first proposed by Simoons (1981). [ 72 ]  By now, however, it is apparent that this is not the case; on the contrary, there is evidence of  positive  selection in coeliac disease genotypes. It is suspected that some of them may have been beneficial by providing protection against bacterial infections. [ 73 ] [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_381", "text": "The majority of the proteins in food responsible for the immune reaction in coeliac disease are the  prolamins . These are storage proteins rich in  proline  ( prol- ) and  glutamine  ( -amin ) that dissolve in alcohols and are resistant to  proteases  and  peptidases  of the gut. [ 28 ] [ 75 ]  Prolamins are found in cereal grains with different grains having different but related prolamins: wheat (gliadin), barley ( hordein ), rye ( secalin ) and  oats  ( avenin ). [ 51 ]  One region of  \u03b1-gliadin  stimulates membrane cells,  enterocytes , of the intestine to allow larger molecules around the sealant between cells. Disruption of  tight junctions  allow peptides larger than three  amino acids  to enter the intestinal lining. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_382", "text": "Membrane leaking permits peptides of gliadin that stimulate two levels of the immune response: the innate response, and the adaptive (T-helper cell-mediated) response. One protease-resistant peptide from \u03b1-gliadin contains a region that stimulates lymphocytes and results in the release of  interleukin-15 . This  innate response to gliadin  results in immune-system signalling that attracts inflammatory cells and increases the release of inflammatory chemicals. [ 28 ]  The strongest and most common adaptive response to gliadin is directed toward an  \u03b12-gliadin fragment  of 33\u00a0amino acids in length. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_383", "text": "The response to the 33mer occurs in most coeliacs who have  a DQ2   isoform . This peptide, when altered by intestinal transglutaminase, has a high density of overlapping T-cell epitopes. This increases the likelihood that the DQ2 isoform will bind, and stay bound to, peptide when recognised by T-cells. [ 77 ]  Gliadin in wheat is the best-understood member of this family, but other prolamins exist, and hordein (from barley), secalin (from rye), and avenin (from oats) may contribute to coeliac disease. [ 28 ] [ 51 ] [ 78 ]  Avenin's toxicity in people with coeliac disease depends on the oat  cultivar  consumed, as prolamin genes, protein amino acid sequences, and the immunoreactivities of toxic prolamins vary among oat varieties. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_384", "text": "Anti-transglutaminase antibodies  to the enzyme  tissue transglutaminase  (tTG) are found in the blood of the majority of people with classic symptoms and complete villous atrophy, but only in 70% of the cases with partial villous atrophy and 30% of the cases with minor mucosal lesions. [ 23 ]  Tissue transglutaminase modifies gluten  peptides  into a form that may stimulate the immune system more effectively. [ 28 ]  These peptides are modified by tTG in two ways,  deamidation  or  transamidation . [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_385", "text": "Deamidation is the reaction by which a glutamate residue is formed by cleavage of the epsilon-amino group of a glutamine side chain. Transamidation, which occurs three times more often than deamidation, is the cross-linking of a glutamine residue from the gliadin peptide to a lysine residue of tTg in a reaction that is catalysed by the transglutaminase. Crosslinking may occur either within or outside the active site of the enzyme. The latter case yields a permanently covalently linked complex between the gliadin and the tTg. [ 80 ]  This results in the formation of new epitopes believed to trigger the primary immune response by which the autoantibodies against tTg develop. [ 81 ] [ 82 ] [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_386", "text": "Stored biopsies from people with suspected coeliac disease have revealed that  autoantibody  deposits in the  subclinical  coeliacs are detected prior to clinical disease. These deposits are also found in people who present with other autoimmune diseases, anaemia, or malabsorption phenomena at a much increased rate over the normal population. [ 84 ]  Endomysial components of antibodies (EMA) to tTG are believed to be directed toward cell-surface transglutaminase, and these antibodies are still used in confirming a coeliac disease diagnosis. However, a 2006 study showed that EMA-negative people with coeliac tend to be older males with more severe abdominal symptoms and a lower frequency of \"atypical\" symptoms, including autoimmune disease. [ 85 ]  In this study, the anti-tTG antibody deposits did not correlate with the severity of villous destruction. These findings, coupled with work showing that gliadin has an innate response component, [ 86 ]  suggest that gliadin may be more responsible for the primary manifestations of coeliac disease, whereas tTG is a bigger factor in secondary effects such as allergic responses and secondary autoimmune diseases. In a large percentage of people with coeliac, the anti-tTG antibodies also recognise a  rotavirus  protein called VP7. These antibodies stimulate  monocyte  proliferation, and rotavirus infection might explain some early steps in the cascade of  immune cell  proliferation. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_387", "text": "Indeed, earlier studies of rotavirus damage in the gut showed this causes villous atrophy. [ 88 ]   This suggests that viral proteins may take part in the initial flattening and stimulate self-crossreactive anti-VP7 production. Antibodies to VP7 may also slow healing until the gliadin-mediated tTG presentation provides a second source of crossreactive antibodies. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_388", "text": "Other intestinal disorders may have  biopsy  that look like coeliac disease including lesions caused by Candida. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_389", "text": "The inflammatory process, mediated by  T cells , leads to disruption of the structure and function of the small bowel's mucosal lining and causes malabsorption as it impairs the body's ability to absorb  nutrients , minerals, and fat-soluble  vitamins  A, D, E, and K from food. Lactose intolerance may be present due to the decreased bowel surface and reduced production of  lactase  but typically resolves once the condition is treated. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_390", "text": "Alternative causes of this tissue damage have been proposed and involve the release of  interleukin 15  and activation of the innate immune system by a shorter gluten peptide (p31\u201343/49). This would trigger killing of  enterocytes  by lymphocytes in the  epithelium . [ 28 ]  The villous atrophy seen on biopsy may also be due to unrelated causes, such as  tropical sprue ,  giardiasis  and  radiation enteritis . While positive serology and typical biopsy are highly suggestive of coeliac disease, lack of response to the diet may require these alternative diagnoses to be considered. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_391", "text": "Diagnosis  is often difficult and as of 2019, there continues to be a lack of awareness among physicians about the variability of presentations of coeliac disease and the diagnostic criteria, such that most cases are diagnosed with great delay. [ 26 ] [ 22 ]  It can take up to 12 years to receive a diagnosis from the onset of symptoms and the majority of those affected in most countries never receive it. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_392", "text": "Several tests can be used. The level of  symptoms  may determine the order of the tests, but  all  tests lose their usefulness if the person is already eating a  gluten-free diet .  Intestinal  damage begins to heal within weeks of gluten being removed from the diet, and  antibody  levels decline over months. For those who have already started on a gluten-free diet, it may be necessary to perform a  rechallenge  with some gluten-containing food in one meal a day over six weeks before repeating the investigations. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_393", "text": "Serological  blood tests are the first-line investigation required to make a diagnosis of coeliac disease. Its sensitivity correlates with the degree of histological lesions. People who present with minor damage to the small intestine may have seronegative findings so many patients with coeliac disease often are missed. In patients with villous atrophy, anti- endomysial  (EMA) antibodies of the  immunoglobulin A  (IgA) type can detect coeliac disease with a  sensitivity and specificity  of 90% and 99%, respectively. [ 90 ]   Serology  for  anti-transglutaminase antibodies  (anti-tTG) was initially reported to have a higher  sensitivity  (99%) and  specificity  (>90%). However, it is now thought to have similar characteristics to anti-endomysial antibodies. [ 90 ]  Both anti-transglutaminase and anti-endomysial antibodies have high sensitivity to diagnose people with classic symptoms and complete villous atrophy, but they are only found in 30\u201389% of the cases with partial villous atrophy and in less than 50% of the people who have minor mucosal lesions ( duodenal lymphocytosis ) with normal villi. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_394", "text": "Tissue transglutaminase  (abbreviated as tTG or TG2) modifies gluten  peptides  into a form that may stimulate the immune system more effectively. [ 28 ]  These peptides are modified by tTG in two ways, deamidation or transamidation. [ 79 ]  Modern anti-tTG assays rely on a human  recombinant protein  as an  antigen . [ 91 ]  tTG testing should be done first as it is an easier test to perform. An equivocal result on tTG testing should be followed by anti-endomysial antibodies. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_395", "text": "Guidelines recommend that a total serum IgA level is checked in parallel, as people with coeliac with IgA deficiency may be unable to produce the antibodies on which these tests depend (\"false negative\"). In those people, IgG antibodies against transglutaminase (IgG-tTG) may be diagnostic. [ 21 ] [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_396", "text": "If all these antibodies are negative, then anti-DGP antibodies (antibodies against deamidated gliadin peptides) should be determined. IgG class anti-DGP antibodies may be useful in people with IgA deficiency. In children younger than two years, anti-DGP antibodies perform better than anti-endomysial and anti-transglutaminase antibodies tests. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_397", "text": "Because of the major implications of a diagnosis of coeliac disease, professional guidelines recommend that a positive  blood test  is still followed by an  endoscopy / gastroscopy  and  biopsy . A negative serology test may still be followed by a recommendation for endoscopy and  duodenal  biopsy if clinical suspicion remains high. [ 21 ] [ 41 ] [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_398", "text": "Historically three other antibodies were measured: anti- reticulin  (ARA), anti- gliadin  ( AGA ) and anti-endomysial (EMA) antibodies. [ 94 ]  ARA testing, however, is not accurate enough for routine diagnostic use. [ 95 ]  Serology may be unreliable in young children, with anti- gliadin  performing somewhat better than other tests in children under five. [ 94 ]  Serology tests are based on  indirect immunofluorescence  (reticulin, gliadin and endomysium) or  ELISA  (gliadin or tissue  transglutaminase , tTG). [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_399", "text": "Other antibodies such as  anti\u2013 Saccharomyces cerevisiae  antibodies  occur in some people with coeliac disease but also occur in other autoimmune disorders and about 5% of those who donate blood. [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_400", "text": "Antibody testing may be combined with  HLA  testing if the diagnosis is unclear. TGA and EMA testing are the most sensitive serum antibody tests, but as a negative HLA-DQ type excludes the diagnosis of coeliac disease, testing also for HLA-DQ2 or DQ8 maximises sensitivity and negative predictive values. [ 64 ]  In the United Kingdom, the  National Institute for Health and Clinical Excellence  (NICE) does not (as of 2015) recommend the use of HLA typing to rule out coeliac disease outside of a specialist setting, for example, in children who are not having a biopsy, or in patients who already have limited gluten ingestion and opt not to have a gluten challenge. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_401", "text": "An  upper endoscopy  with  biopsy  of the  duodenum  (beyond the  duodenal bulb ) or  jejunum  is performed to obtain multiple samples (four to eight) from the duodenum. Not all areas may be equally affected; if biopsies are taken from healthy bowel tissue, the result would be a false negative. [ 41 ]  Even in the same bioptic fragment, different degrees of\ndamage may be present. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_402", "text": "Most people with coeliac disease have a  small intestine  that appears to be normal on endoscopy before the biopsies are examined. However, five findings have been associated with high specificity for coeliac disease: scalloping of the small bowel folds ( pictured ), paucity in the folds, a  mosaic  pattern to the  mucosa  (described as a \"cracked-mud\" appearance), prominence of the  submucosa   blood vessels , and a nodular pattern to the mucosa. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_403", "text": "European guidelines suggest that in children and adolescents with symptoms compatible with coeliac disease, the diagnosis can be made without the need for intestinal biopsy if  anti-tTG antibodies  titres are very high (10 times the upper limit of normal). [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_404", "text": "Until the 1970s, biopsies were obtained using metal capsules attached to a suction device. The capsule was swallowed and allowed to pass into the small intestine. After  x-ray  verification of its position, suction was applied to collect part of the intestinal wall inside the capsule. Often-utilised capsule systems were the  Watson capsule  and the  Crosby\u2013Kugler capsule . This method has now been largely replaced by  fibre-optic  endoscopy, which carries a higher sensitivity and a lower frequency of errors. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_405", "text": "Capsule endoscopy  (CE) allows identification of typical mucosal changes observed in coeliac disease but has a lower sensitivity compared to regular endoscopy and histology. CE is therefore not the primary diagnostic tool for coeliac disease. However, CE can be used for diagnosing T-cell lymphoma, ulcerative jejunoileitis, and adenocarcinoma in refractory or complicated coeliac disease. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_406", "text": "The classic pathology changes of coeliac disease in the small bowel are categorised by the \" Marsh  classification\": [ 101 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_407", "text": "Marsh's classification, introduced in 1992, was subsequently modified in 1999 to six stages, where the previous stage 3 was split in three substages. [ 103 ]  Further studies demonstrated that this system was not always reliable and that the changes observed in coeliac disease could be described in one of three stages: [ 18 ] [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_408", "text": "The changes classically improve or reverse after  gluten  is removed from the diet. However, most guidelines do not recommend a repeat biopsy unless there is no improvement in the symptoms on diet. [ 41 ] [ 93 ]  In some cases, a deliberate gluten challenge, followed by a biopsy, may be conducted to confirm or refute the diagnosis. A normal biopsy and normal serology after challenge indicates the diagnosis may have been incorrect. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_409", "text": "In untreated coeliac disease, villous atrophy is more common in children younger than three years, but in older children and adults, it is common to find minor intestinal lesions ( duodenal lymphocytosis ) with normal  intestinal villi . [ 11 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_410", "text": "At the time of diagnosis, further investigations may be performed to identify complications, such as  iron deficiency  (by  full blood count  and iron studies),  folic acid  and  vitamin B 12  deficiency  and  hypocalcaemia  (low calcium levels, often due to decreased  vitamin D  levels).  Thyroid function tests  may be requested during blood tests to identify  hypothyroidism , which is more common in people with coeliac disease. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_411", "text": "Osteopenia  and  osteoporosis , mildly and severely reduced bone mineral density, are often present in people with coeliac disease, and investigations to measure bone density may be performed at diagnosis, such as  dual-energy X-ray absorptiometry  (DXA) scanning, to identify the risk of fracture and need for bone protection medication. [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_412", "text": "Although blood antibody tests, biopsies, and genetic tests usually provide a clear diagnosis, [ 24 ] [ 90 ]  occasionally the response to gluten withdrawal on a  gluten-free diet  is needed to support the diagnosis. Currently,  gluten challenge  is no longer required to confirm the diagnosis in patients with intestinal lesions compatible with coeliac disease and a positive response to a gluten-free diet. [ 24 ]  Nevertheless, in some cases, a gluten challenge with a subsequent biopsy may be useful to support the diagnosis, for example in people with a high suspicion for coeliac disease, without a biopsy confirmation, who have negative blood antibodies and are already on a gluten-free diet. [ 24 ]  Gluten challenge is discouraged before the age of 5 years and during  pubertal  growth. [ 105 ]  The alternative diagnosis of  non-coeliac gluten sensitivity  may be made where there is only symptomatic evidence of gluten sensitivity. [ 106 ]  Gastrointestinal and extraintestinal symptoms of people with non-coeliac gluten sensitivity can be similar to those of coeliac disease, [ 16 ]  and improve when gluten is removed from the diet, [ 107 ] [ 108 ]  after coeliac disease and  wheat allergy  are reasonably excluded. [ 109 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_413", "text": "Up to 30% of people often continue having or redeveloping symptoms after starting a gluten-free diet. [ 13 ]  A careful interpretation of the symptomatic response is needed, as a lack of response in a person with coeliac disease may be due to continued ingestion of small amounts of gluten, either voluntary or inadvertent, [ 11 ]  or be due to other commonly associated conditions such as  small intestinal bacterial overgrowth  (SIBO),  lactose intolerance ,  fructose , [ 110 ]   sucrose , [ 111 ]  and  sorbitol [ 112 ]  malabsorption,  exocrine pancreatic insufficiency , [ 113 ] [ 114 ]  and  microscopic colitis , [ 114 ]  among others. In untreated coeliac disease, these are often transient conditions derived from the intestinal damage. [ 111 ] [ 112 ] [ 115 ] [ 116 ] [ 117 ]  They normally revert or improve several months after starting a gluten-free diet, but may need temporary interventions such as supplementation with  pancreatic enzymes , [ 116 ] [ 117 ]  dietary restrictions of lactose, fructose, sucrose or sorbitol containing foods, [ 111 ] [ 115 ]  or treatment with oral antibiotics in the case of associated bacterial overgrowth. [ 117 ]  In addition to gluten withdrawal, some people need to follow a low- FODMAPs  diet or avoid consumption of commercial gluten-free products, which are usually rich in  preservatives  and  additives  (such as  sulfites ,  glutamates ,  nitrates  and  benzoates ) and might have a role in triggering functional gastrointestinal symptoms. [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_414", "text": "There is debate as to the benefits of screening. As of 2017, the  United States Preventive Services Task Force  found insufficient evidence to make a recommendation among those without symptoms. [ 29 ]  In the United Kingdom, the  National Institute for Health and Clinical Excellence  (NICE) recommend testing for coeliac disease in first-degree relatives of those with the disease already confirmed, in people with persistent fatigue, abdominal or gastrointestinal symptoms, faltering growth, unexplained weight loss or iron, vitamin B 12  or folate deficiency, severe mouth ulcers, and with diagnoses of type 1 diabetes,  autoimmune thyroid disease , [ 21 ]  and with newly diagnosed  chronic fatigue syndrome [ 119 ]  and  irritable bowel syndrome . [ 38 ]   Dermatitis herpetiformis  is included in other recommendations. [ 120 ]  The NICE also recommend offering serological testing for coeliac disease in people with  metabolic bone disease  (reduced bone mineral density or  osteomalacia ), unexplained neurological disorders (such as  peripheral neuropathy  and  ataxia ), fertility problems or recurrent  miscarriage , persistently raised liver enzymes with unknown cause, dental enamel defects and with diagnose of  Down syndrome  or  Turner syndrome . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_415", "text": "Some evidence has found that early detection may decrease the risk of developing health complications, such as osteoporosis, anaemia, and certain types of cancer, neurological disorders,  cardiovascular diseases , and reproductive problems. [ 7 ] [ 28 ] [ 47 ] [ 121 ] [ 122 ]  They thus recommend screening in people with certain health problems. [ 122 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_416", "text": "Serology  has been proposed as a  screening  measure, because the presence of antibodies would detect some previously undiagnosed cases of coeliac disease and prevent its complications in those people. However, serologic tests have high sensitivity only in people with total villous atrophy and have a very low ability to detect cases with partial villous atrophy or minor intestinal lesions. [ 24 ]  Testing for coeliac disease may be offered to those with commonly associated conditions. [ 18 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_417", "text": "At present, the only effective treatment is a lifelong  gluten-free diet . [ 52 ]  No medication exists that prevents damage or prevents the body from attacking the gut when gluten is present. Strict adherence to the diet helps the intestines heal, leading to resolution of all symptoms in most cases and, depending on how soon the diet is begun, can also eliminate the heightened risk of osteoporosis and intestinal cancer and in some cases sterility. [ 123 ]  Compliance to a strict gluten-free diet is difficult for the patient, but evidence has accumulated that a strict gluten-free diet can result in resolution of diarrhea, weight gain and normalization of nutrient malabsorption, with normalization of biopsies in 6 months to 2 years on a gluten-free diet. [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_418", "text": "Dietitian  input is generally requested to ensure the person is aware which foods contain gluten, which foods are safe, and how to have a balanced diet despite the limitations. In many countries, gluten-free products are available on  prescription  and may be reimbursed by  health insurance  plans. Gluten-free products are usually more expensive and harder to find than common gluten-containing foods. [ 125 ]  Since ready-made products often contain traces of gluten, some coeliacs may find it necessary to cook from scratch. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_419", "text": "The term \"gluten-free\" is generally used to indicate a supposed harmless level of gluten rather than a complete absence. [ 127 ]  The exact level at which gluten is harmless is uncertain and controversial. A recent  systematic review  tentatively concluded that consumption of less than 10\u00a0mg of gluten per day is unlikely to cause histological abnormalities, although it noted that few reliable studies had been done. [ 127 ]  Regulation of the label \"gluten-free\" varies. In the European Union, the  European Commission  issued regulations in 2009 limiting the use of \"gluten-free\" labels for food products to those with less than 20\u00a0mg/kg of gluten, and \"very low gluten\" labels for those with less than 100\u00a0mg/kg. [ 128 ]  In the United States, the  FDA  issued regulations in 2013 limiting the use of \"gluten-free\" labels for food products to those with less than 20\u00a0 ppm  of gluten. [ 129 ] [ 130 ] [ 131 ]  The current international  Codex Alimentarius  standard allows for 20\u00a0ppm of gluten in so-called \"gluten-free\" foods. [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_420", "text": "Gluten-free diet improves  healthcare-related quality of life , and strict adherence to the diet gives more benefit than incomplete adherence. Nevertheless, gluten-free diet does not completely normalise the quality of life. [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_421", "text": "Even though it is unclear if coeliac patients have a generally increased risk of infectious diseases, they should generally be encouraged to receive all common vaccines against  vaccine preventable diseases  (VPDs) as the general population. Moreover, some pathogens could be harmful to coeliac patients. According to the European Society for the Study of Celiac Disease (ESsCD), coeliac disease can be associated with hyposplenism or functional asplenia, which could result in impaired immunity to encapsulated bacteria, with an increased risk of such infections. For this reason, patients who are known to be hyposplenic should be offered at least the pneumococcal vaccine. [ 134 ]  However, the ESsCD states that it is not clear whether vaccination with the conjugated vaccine is preferable in this setting and whether additional vaccination against  Haemophilus ,  meningococcus , and  influenza  should be considered if not previously given. [ 134 ]  However, M\u00e5rild et al. suggested considering additional vaccination against influenza because of an observed increased risk of hospital admission for this infection in celiac patients. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_422", "text": "Between 0.3% and 10% of affected people have refractory disease, which means that they have persistent villous atrophy on a gluten-free diet despite the lack of gluten exposure for more than 12 months. [ 114 ]  Nevertheless, inadvertent exposure to gluten is the main cause of persistent villous atrophy, and must be ruled out before a diagnosis of refractory disease is made. [ 114 ]  People with poor basic education and understanding of gluten-free diet often believe that they are strictly following the diet, but are making regular errors. [ 13 ] [ 114 ] [ 136 ]  Also, a lack of symptoms is not a reliable indicator of intestinal recuperation. [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_423", "text": "If alternative causes of villous atrophy have been eliminated,  steroids  or  immunosuppressants  (such as  azathioprine ) may be considered in this scenario. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_424", "text": "Refractory coeliac disease should not be confused with the persistence of symptoms despite gluten withdrawal [ 114 ]  caused by transient conditions derived from the intestinal damage, [ 111 ] [ 112 ] [ 115 ]  which generally revert or improve several months after starting a gluten-free diet, [ 116 ] [ 117 ]  such as  small intestinal bacterial overgrowth ,  lactose intolerance ,  fructose , [ 110 ]   sucrose , [ 111 ]  and  sorbitol [ 112 ]  malabsorption,  exocrine pancreatic insufficiency , [ 113 ] [ 114 ]  and microscopic colitis [ 114 ]  among others."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_425", "text": "Refractory celiac disease can be divided in type I and II. A recent studied compared patients with type I and II. Refractory celiac disease type I more frequently exhibits diarrhea, anemia, hypoalbuminemia, parenteral nutrition need, ulcerative jejuno-ileitis, and extended small intestinal atrophy. Among patients with refractory celiac disease type II is more common to develope lymphoma. Among these patients, atrophy extension was the only parameter correlated with hypoalbuminemia and mortality.\n [ 137 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_426", "text": "Globally coeliac disease affects between 1 in 100 and 1 in 170 people. [ 14 ] [ 138 ]  Rates, however, vary between different regions of the world from as few as 1 in 300 to as many as 1 in 40. [ 14 ]  In the United States it is thought to affect between 1 in 1750 (defined as clinical disease including dermatitis herpetiformis with limited digestive tract symptoms) to 1 in 105 (defined by presence of IgA TG in blood donors). [ 139 ]  Due to variable signs and symptoms it is believed that about 85% of people affected are undiagnosed. [ 140 ]  The percentage of people with clinically diagnosed disease (symptoms prompting diagnostic testing) is 0.05\u20130.27% in various studies. However, population studies from parts of Europe, India, South America, Australasia and the USA (using serology and biopsy) indicate that the percentage of people with the disease may be between 0.33 and 1.06% in children (but 5.66% in one study of children of the predisposed  Sahrawi people [ 141 ] ) and 0.18\u20131.2% in adults. [ 28 ]  Among those in primary care populations who report gastrointestinal symptoms, the rate of coeliac disease is about 3%. [ 90 ]  In Australia, approximately 1 in 70 people have the disease. [ 142 ]  The rate amongst adult blood donors in Iran, Israel, Syria and Turkey is 0.60%, 0.64%, 1.61% and 1.15%, respectively. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_427", "text": "People of African, Japanese and Chinese descent are rarely diagnosed; [ 143 ]  this reflects a much lower prevalence of the genetic  risk factors , such as  HLA-B8 . [ 144 ]  People of Indian ancestry seem to have a similar risk to those of Western Caucasian ancestry. [ 40 ]  Population studies also indicate that a large proportion of coeliacs remain undiagnosed; this is due, in part, to many clinicians being unfamiliar with the condition and also due to the fact it can be asymptomatic. [ 145 ]  Coeliac disease is slightly more common in women than in men. [ 33 ]  A large multicentre study in the U.S. found a prevalence of 0.75% in not-at-risk groups, rising to 1.8% in symptomatic people, 2.6% in second-degree relatives (like grandparents, aunt or uncle, grandchildren, etc.) of a person with coeliac disease and 4.5% in first-degree relatives (siblings, parents or children). [ 40 ]  This profile is similar to the prevalence in Europe. [ 40 ]  Other populations at increased risk for coeliac disease, with prevalence rates ranging from 5% to 10%, include individuals with  Down  and  Turner syndromes ,  type 1 diabetes , and autoimmune thyroid disease, including both  hyperthyroidism  (overactive  thyroid ) and  hypothyroidism  (underactive thyroid). [ 146 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_428", "text": "Historically, coeliac disease was thought to be rare, with a prevalence of about 0.02%. [ 146 ]  The reason for the recent increases in the number of reported cases is unclear. [ 138 ]  It may be at least in part due to changes in diagnostic practice. [ 147 ]  There also appears to be an approximately 4.5 fold true increase that may be due to less exposure to bacteria and other pathogens in Western environments. [ 138 ]  In the United States, the median age at diagnosis is 38 years. [ 148 ]  Roughly 20 percent of individuals with coeliac disease are diagnosed after 60 years of age. [ 148 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_429", "text": "The term  coeliac  comes from Greek \u03ba\u03bf\u03b9\u03bb\u03b9\u03b1\u03ba\u03cc\u03c2 ( koiliak\u00f3s ) 'abdominal' and was introduced in the 19th century in a translation of what is generally regarded as an  Ancient Greek  description of the disease by  Aretaeus of Cappadocia . [ 149 ] [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_430", "text": "Humans first started to cultivate grains in the  Neolithic  period (beginning about 9500\u00a0BCE) in the  Fertile Crescent  in Western Asia, and, likely, coeliac disease did not occur before this time.  Aretaeus of Cappadocia , living in the second century in the same area, recorded a malabsorptive syndrome with chronic diarrhoea, causing a debilitation of the whole body. [ 149 ]  His \"C\u0153liac Affection\" gained the attention of Western medicine when  Francis Adams  presented a translation of Aretaeus's work at the Sydenham Society in 1856. The patient described in Aretaeus' work had stomach pain and was atrophied, pale, feeble, and incapable of work. The diarrhoea manifested as loose stools that were white, malodorous, and flatulent, and the disease was intractable and liable to periodic return. The problem, Aretaeus believed, was a lack of heat in the stomach necessary to digest the food and a reduced ability to distribute the digestive products throughout the body, this incomplete digestion resulting in diarrhoea. He regarded this as an affliction of the old and more commonly affecting women, explicitly excluding children. The cause, according to Aretaeus, was sometimes either another chronic disease or even consuming \"a copious draught of cold water.\" [ 149 ] [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_431", "text": "The  paediatrician   Samuel Gee  gave the first modern-day description of the condition in children in a lecture at  Hospital for Sick Children, Great Ormond Street , London, in 1887. Gee acknowledged earlier descriptions and terms for the disease and adopted the same term as Aretaeus (coeliac disease). He perceptively stated: \"If the patient can be cured at all, it must be by means of diet.\" Gee recognised that milk intolerance is a problem with coeliac children and that highly starched foods should be avoided. However, he forbade rice, sago, fruit, and vegetables, which all would have been safe to eat, and he recommended raw meat as well as thin slices of toasted bread. Gee highlighted particular success with a child \"who was fed upon a quart of the best Dutch  mussels  daily.\" However, the child could not bear this diet for more than one season. [ 150 ] [ 151 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_432", "text": "Christian Archibald Herter , an American physician, wrote a book in 1908 on children with coeliac disease, which he called \"intestinal  infantilism \". He noted their growth was retarded and that fat was better tolerated than carbohydrate. The  eponym   Gee-Herter disease  was sometimes used to acknowledge both contributions. [ 152 ] [ 153 ]   Sidney V. Haas , an American paediatrician, reported positive effects of  a diet of bananas  in 1924. [ 154 ]  This diet remained in vogue until the actual cause of coeliac disease was determined. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_433", "text": "While a role for carbohydrates had been suspected, the link with wheat was not made until the 1940s by the Dutch paediatrician Dr  Willem Karel Dicke . [ 155 ]  It is likely that clinical improvement of his patients during the  Dutch famine of 1944  (during which flour was scarce) may have contributed to his discovery. [ 156 ]  Dicke noticed that the shortage of bread led to a significant drop in the death rate among children affected by coeliac disease from greater than 35% to essentially zero. He also reported that once wheat was again available after the conflict, the mortality rate soared to previous levels. [ 157 ]  The link with the gluten component of wheat was made in 1952 by a team from  Birmingham , England. [ 158 ]  Villous atrophy was described by British physician John W. Paulley in 1954 on samples taken at surgery. [ 159 ]  This paved the way for biopsy samples taken by endoscopy. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_434", "text": "Throughout the 1960s, other features of coeliac disease were elucidated. Its hereditary character was recognised in 1965. [ 160 ]  In 1966, dermatitis herpetiformis was linked to  gluten sensitivity . [ 150 ] [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_435", "text": "May has been designated as \"Coeliac Awareness Month\" by several coeliac organisations. [ 161 ] [ 162 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_436", "text": "Speaking generally, the various denominations of Christians celebrate a  Eucharist  in which a wafer or small piece of  sacramental bread  from wheat bread is blessed and then eaten. A typical wafer weighs about half a gram. [ 163 ]   Wheat flour  contains around 10\u201313% gluten, so a single communion wafer may have more than 50\u00a0mg of gluten, an amount that harms many people with coeliac, especially if consumed every day (see  Diet  above). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_437", "text": "Many Christian churches offer their communicants gluten-free alternatives, usually in the form of a rice-based cracker or gluten-free bread. These include the  United Methodist ,  Christian Reformed ,  Episcopal , the Anglican Church (Church of England, UK) and  Lutheran .  Catholics  may receive from the Chalice alone, or ask for gluten-reduced hosts; gluten-free ones however are not considered to still be wheat bread and hence invalid matter. [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_438", "text": "Roman Catholic  doctrine  states that for a valid  Eucharist , the bread to be used at  Mass  must be made from wheat. Low-gluten  hosts  meet all of the Catholic Church's requirements, but they are not entirely gluten free. Requests to use rice wafers have been denied. [ 165 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_439", "text": "The issue is more complex for priests. As a celebrant, a priest is, for the fullness of the sacrifice of the Mass, absolutely required to receive under both species. On 24 July 2003, the Congregation for the Doctrine of the Faith stated, \"Given the centrality of the celebration of the Eucharist in the life of a priest, one must proceed with great caution before admitting to Holy Orders those candidates unable to ingest gluten or alcohol without serious harm.\" [ 166 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_440", "text": "By January 2004, extremely low-gluten Church-approved hosts had become available in the United States, Italy and Australia. [ 167 ]  As of July 2017, the Vatican still outlawed the use of gluten-free bread for Holy Communion. [ 168 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_441", "text": "[ citation needed ]  The Jewish festival of  Pesach  (Passover) may present problems with its obligation to eat  Matzah , which is unleavened bread made in a strictly controlled manner from wheat, barley, spelt, oats, or rye."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_442", "text": "In addition, many other grains that are normally used as substitutes for people with gluten sensitivity, including rice, are avoided altogether on Passover by  Ashkenazi Jews . Many kosher-for-Passover products avoid grains altogether and are therefore gluten-free.  Potato starch  is the primary starch used to replace the grains."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_443", "text": "Coeliac disease is the preferred spelling in  Commonwealth English , while celiac disease is typically used in  North American English . [ 169 ] [ 170 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_444", "text": "The search for environmental factors that could be responsible for genetically susceptible people becoming intolerant to gluten has resulted in increasing research activity looking at gastrointestinal infections. [ 171 ]  Research published in April 2017 suggests that an often-symptomless infection by a common strain of  reovirus  can increase sensitivity to foods such as gluten. [ 172 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_445", "text": "Various treatment approaches are being studied, including some that would reduce the need for dieting. All are still under development, and are not expected to be available to the general public for a while. [ 28 ] [ 173 ] [ 174 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_446", "text": "Three main approaches have been proposed as new therapeutic modalities for coeliac disease: gluten detoxification, modulation of the  intestinal permeability , and modulation of the immune response. [ 175 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_447", "text": "Using  genetically engineered  wheat species, or wheat species that have been  selectively bred  to be minimally immunogenic, may allow the consumption of wheat. This, however, could interfere with the effects that gliadin has on the quality of dough."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_448", "text": "Alternatively, gluten exposure can be minimised by the ingestion of a combination of  enzymes  ( prolyl endopeptidase  and a barley glutamine-specific  cysteine endopeptidase  ( EP-B2 )) that degrade the putative 33-mer peptide in the  duodenum . [ 28 ]  Latiglutenase (IMGX003) is a  biotheraputic  digestive enzyme therapy currently being trialled that aims to degrade gluten proteins and aid gluten digestion. It was shown to mitigate intestinal mucosal damage and reduce the severity and frequency of symptoms in phase 2 clinical trials [ 176 ]  and is scheduled for phase 3 clinical trials. [ 177 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_449", "text": "Alternative treatments under investigation include the inhibition of  zonulin , an endogenous signalling protein linked to increased permeability of the bowel wall and hence increased presentation of gliadin to the immune system. One inhibitor of this pathway is  larazotide acetate , which is currently scheduled for phase 3 clinical trials. [ 178 ] [ needs update ]  Other modifiers of other well-understood steps in the pathogenesis of coeliac disease, such as the action of HLA-DQ2 or tissue transglutaminase and the MICA/NKG2D interaction that may be involved in the killing of enterocytes. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_450", "text": "Attempts to modulate the immune response concerning coeliac disease are mostly still in phase I of clinical testing; one agent (CCX282-B) has been evaluated in a phase II clinical trial based on small-intestinal biopsies taken from people with coeliac disease before and after gluten exposure. [ 175 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_451", "text": "Although popularly used as an  alternative treatment  for people with autism, there is no good evidence that a  gluten-free diet  is of benefit in the treatment of autism. [ 179 ] [ 180 ] [ 181 ]  In the subset of autistic people who have  gluten sensitivity , there is limited evidence that suggests that a gluten free diet may improve hyperactivity and mental confusion in those with autism. [ 179 ] [ 182 ] [ 183 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_452", "text": "Cronkhite\u2013Canada syndrome  is a rare  syndrome  characterized by multiple  polyps  of the  digestive tract . It is sporadic (i.e. it does not seem to be a  hereditary disease ), [ 1 ]  and it is currently considered acquired [ 2 ]  and  idiopathic  (i.e. cause remains unknown)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_453", "text": "About two-thirds of patients are of Japanese descent and the male to female ratio is 3:2. [ 3 ]   It was characterized in 1955 [ 4 ] [ 5 ]  by internal medicine physician Leonard Wolsey Cronkhite Jr. and radiologist Wilma Jeanne Canada. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_454", "text": "Polyps  are found throughout the GI tract (most frequently in the  stomach  and  large intestine , followed by the  small intestine ) though typically avoid the  esophagus . [ 6 ]  A  biopsy  will reveal them to be  hamartomas ; the possibility that they progress to cancer is generally considered to be low, [ 7 ]  although it has been reported multiple times in the past. Chronic  diarrhea  and  protein-losing enteropathy  are often observed. Possible collateral features include variable anomalies of  ectodermal  tissues, such as  alopecia ,  atrophy  of the  nails , or skin  pigmentation [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_455", "text": "There is no specific test to diagnose Cronkhite\u2013Canada syndrome. Diagnosis is based on symptoms and features of the disease. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_456", "text": "Nutritional support is fundamental, and may include dietary guidance, supplements, tube feeding, or intravenous solutions. [ 9 ]  Treatments proposed include  cromolyn sodium  and  prednisone , [ 10 ]  as well as histamine (H2) receptor antagonists or proton pump inhibitors. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_457", "text": "In  histology ,  cryptitis  refers to  inflammation  of an  intestinal crypt ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_458", "text": "Cryptitis is a non-specific histopathologic finding that is seen in several conditions, e.g.  inflammatory bowel disease , [ 1 ]   diverticular disease , [ 2 ]  radiation colitis, [ 3 ]  infectious  colitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_459", "text": "This  gastroenterology  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_460", "text": "Cuffitis  is inflammation at the anal transition zone or \"cuff\" created as a result of  ileal pouch-anal anastomosis  (IPAA). [ 1 ]  It is considered a variant form of  ulcerative colitis  that occurs in the rectal cuff. [ 2 ]  Cuffitis is a common complication of IPAA, particularly when a stapled  anastomosis  without  mucosectomy  procedure has been used. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_461", "text": "Symptoms of cuffitis mimic those of  pouchitis . [ 2 ]  In addition, patients with cuffitis often present with small volume bloody bowel movements. [ 2 ]  Often, cuffitis can produce the appearance of bright red blood on tissue. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_462", "text": "Surgery-associated  ischemia  may contribute inflammation at the anal transitional zone. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_463", "text": "Patients whose cuffitis is refractory to mesalamine and/or corticosteroids should be evaluated for other disease in the cuff area, such as  fistula  or anastomotic leaks. [ 2 ]  Cuffitis that is refractory to medication can also be a sign of  Crohn's disease  of the pouch. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_464", "text": "Chronic cuffitis can also contribute to the development of anastomotic  stricture . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_465", "text": "Cuffitis that is refractory, Crohn's-related, or is associated with surgical complications can contribute to pouch failure. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_466", "text": "Definitive diagnose of cuffitis is obtained by  endoscopy . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_467", "text": "Cuffitis is treated with  mesalamine  suppositories or topical application of  lidocaine  or  corticosteroid  medications. [ 2 ]   Systemic medications  are rarely used. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_468", "text": "Dientamoebiasis  is a medical condition caused by infection with  Dientamoeba fragilis , a single-cell parasite that infects the lower gastrointestinal tract of humans. It is an important cause of traveler's diarrhea, chronic abdominal pain, chronic fatigue, [ citation needed ]  and  failure to thrive  in children."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_469", "text": "The most commonly reported symptoms in conjunction with infection with  D. fragilis  include abdominal pain (69%) and diarrhea (61%). [ 1 ]  Diarrhea may be intermittent and may not be present in all cases. It is often chronic, lasting over two weeks. The degree of symptoms may vary from asymptomatic to severe, [ 2 ]  and can include weight loss, vomiting, fever, and involvement of other digestive organs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_470", "text": "Symptoms may be more severe in children. Additional symptoms reported have included: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_471", "text": "As many individuals are asymptomatic carriers of  D. fragilis ,  pathogenic and nonpathogenic variants are proposed to exist. A study of  D. fragilis  isolates from 60 individuals with symptomatic infection in Sydney, Australia, found all were infected with the same genotype, [ 4 ]  which is the most common worldwide, but differed from the genotype first described from a North American isolate and later also detected in Europe. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_472", "text": "Organisms similar to  D. fragilis  are known to produce a cyst stage that is able to survive outside the host and facilitate infection of new hosts. However, the exact manner in which it is transmitted is not yet known, as the organism is unable to survive outside its human host for more than a few hours after excretion, and no cyst stage has been found. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_473", "text": "Early theories of transmission suggested   D. fragilis  was unable to produce a cyst stage in infected humans, but some animal existed that in which it did produce a cyst stage, and this animal was responsible for spreading it. However, no such animal has ever been discovered. [ 3 ]  A later theory suggested the organism was transmitted by pinworms, which provided protection for the parasite outside the host. DNA has been detected in surface-sterilized eggs of  Enterobius vermicularis  eggs, thus suggesting the latter may harbor the former. [ 7 ]  Experimental ingestion of  pinworm eggs established infection in two investigators. Numerous studies reported high rates of coinfection with helminthes. [ 8 ]  However, recent study has failed to show any association between  D. fragilis  infection and pinworm infection. Parasites similar to  D. fragilis  are transmitted by consuming water or food contaminated with feces. [ 6 ]  The high rate (40%) of concomitant infection with other protozoa reported by at St. Vincent's Hospital, Sydney, Australia, supports the oral-fecal route of transmission. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_474", "text": "Diagnosis is usually performed by submitting multiple stool samples for examination by a parasitologist in a procedure known as an  ova and parasite  examination. About 30% of children with  D. fragilis  infection exhibit  peripheral blood   eosinophilia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_475", "text": "A minimum of three stool specimens having been immediately fixed in polyvinyl alcohol fixative, sodium acetate-acetic acid-formalin fixative, or Schaudinn's fixative should be submitted, as the protozoan does not remain morphologically identifiable for long. All specimens, regardless of consistency, are permanently stained prior to microscopic examination with an oil immersion lens. The disease may remain cryptic due to the lack of a cyst stage if these recommendations are not followed. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_476", "text": "The  trophozoite  forms have been recovered from formed stool, thus the need to perform the ova and parasite examination on specimens other than liquid or soft stools. DNA fragment analysis provides excellent sensitivity and specificity when compared to microscopy for the detection of  D. fragilis  and both methods should be employed in laboratories with  PCR  capability. The most sensitive detection method is parasite culture, and the culture medium requires the addition of  rice starch . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_477", "text": "An  indirect fluorescent antibody  (IFA) for fixed stool specimens has been developed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_478", "text": "Concomitant  pinworm  infection should also be excluded, although the association has not been proven.  Successful treatment of the infection with  iodoquinol ,  doxycycline ,  metronidazole ,  paromomycin , and  secnidazole  has been reported. [ 3 ] [ 2 ]  Resistance requires the use of combination therapy to eradicate the organism. All persons living in the same residence should be screened for  D. fragilis , as asymptomatic carriers may provide a source of repeated infection.  Paromomycin  is an effective prophylactic for travellers who will encounter poor sanitation and unsafe drinking water. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_479", "text": "Rates of infection increase in conditions of crowding and poor sanitation, and are higher in military personnel and mental institutions.\nThe true extent of disease has yet to emerge, as most laboratories do not use techniques to adequately identify this organism. An Australian study identified a large number of patients, considered to have  irritable bowel syndrome , who were actually infected with  Dientamoeba fragilis . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_480", "text": "Although  D. fragilis  has been described as an infection \"emerging from obscurity\", [ 3 ]  it has become one of the most prevalent gastrointestinal infections in industrialized countries, especially among children and young adults. A Canadian study reported a prevalence of around 10% in boys and girls aged 11\u201315 years, [ 6 ]  a prevalence of 11.5% in individuals aged 16\u201320, and a lower incidence of 0.3\u20131.9% in individuals over age 20."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_481", "text": "Early microbiologists reported that the organism was not pathogenic,  though six of the seven individuals from whom they isolated it were experiencing symptoms of dysentery. Their report, published in 1918, concluded the organism was not pathogenic because it consumed bacteria in culture, but did not appear to engulf red blood cells, as was seen in the best-known disease-causing amoeba of the time,  Entamoeba histolytica .  This initial report may still be contributing to the reluctance of physicians to diagnose the infection. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_482", "text": "Distal intestinal obstruction syndrome  ( DIOS ) involves obstruction of the distal part of the small  intestines  by thickened  intestinal content   and occurs in about 20% of mainly adult individuals with  cystic fibrosis . [ 1 ]  DIOS was previously known as  meconium ileus  equivalent , a name which highlights its similarity to the intestinal obstruction seen in newborn infants with cystic fibrosis. [ 2 ]  DIOS tends to occur in older individuals with  pancreatic insufficiency . Individuals with DIOS may be predisposed to bowel obstruction, though it is a separate entity than true  constipation . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_483", "text": "Signs and symptoms of DIOS include a sudden onset of crampy  abdominal pain ,  vomiting , and a palpable mass (often in the right lower quadrant) in the abdomen. The characteristic abdominal pain is typically located in the center or right lower quadrant of the abdomen. [ 1 ]   X-rays  of the abdomen may reveal  stool  in the colon and air-fluid levels in the  small intestines . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_484", "text": "A complete history and physical examination can be suggestive, especially if a palpable mass in the right lower quadrant of the abdomen is present (though this can be present in the absence of DIOS).  Ultrasound  and  computed tomography  (CT) imaging of the abdomen can confirm the diagnosis by demonstrating dilated loops of intestine with material in the intestinal lumen with bubbles. [ 1 ]  Air-fluid levels may be seen in those affected by DIOS. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_485", "text": "DIOS is sometimes classified by the degree of obstruction as incomplete or complete DIOS. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_486", "text": "Additional diagnoses which may present with similar symptoms to DIOS include severe  constipation ,  appendicitis , and  intussusception . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_487", "text": "Differentiation of DIOS from constipation is generally performed by a unit specializing in the treatment of cystic fibrosis. Adequate hydration and an aggressive regimen of laxatives are essential for treatment and prevention of DIOS.  Osmotic laxatives  such as  polyethylene glycol  are preferred. [ 1 ]  Individuals prone to DIOS tend to be at risk for repeated episodes and often require maintenance therapy with pancreatic enzyme replacement, hydration and laxatives (if the symptoms are also mild). [ 4 ] [ 5 ]  Oral contrast instillation into the colon/ileum under radiological control has been found to reduce the need for surgical intervention. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_488", "text": "Diversion colitis  is an  inflammation  of the colon which can occur as a complication of  ileostomy  or  colostomy , where symptoms may occur between one month and three years following surgery. [ 1 ]  It also occurs frequently in a  neovagina  created by  colovaginoplasty , with varying delay after the original procedure. [ 2 ]  Despite the presence of a variable degree of inflammation the most suggestive histological feature remains the prominent lymphoid aggregates."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_489", "text": "People may be asymptomatic but common symptoms are abdominal discomfort, anorectal pain,  mucous discharge  and rectal bleeding that develops from the inflamed  mucosa  of the distal, unused colon. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_490", "text": "Diagnosis is aided by knowing the full clinical history. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_491", "text": "In many milder cases after  ileostomy  or colostomy, diversion colitis is left untreated and disappears naturally. Possible pharmacologic treatments include  short-chain fatty acid  irrigation,  steroid   enemas  and  mesalazine . [ 4 ]  For surgical candidates,  reanastomosis  is a reversal procedure carried out to restore bowel continuity that effectively halts the symptoms of diversion colitis. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_492", "text": "Duodenal atresia  is the congenital absence or complete closure of a portion of the  lumen  of the  duodenum .  It causes increased levels of amniotic fluid during pregnancy ( polyhydramnios ) and intestinal obstruction in newborn babies.  Newborns present with bilious or non-bilous vomiting (depending on where in the duodenum the obstruction is) within the first 24 to 48 hours after birth, typically after their first oral feeding. Radiography shows a distended stomach and distended duodenum, which are separated by the pyloric valve, a finding described as the  double-bubble sign ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_493", "text": "Treatment includes suctioning out any fluid that is trapped in the stomach, providing fluids intravenously, and surgical repair of the intestinal closure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_494", "text": "During pregnancy, duodenal atresia is associated with increased  amniotic fluid  in the uterus, which is called  polyhydramnios . [ 1 ]   This increase in amniotic fluid is caused by the inability of the fetus to swallow the amniotic fluid and absorb it in their digestive tract. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_495", "text": "After birth, duodenal atresia may cause abdominal distension, especially of the upper abdomen.   Bilious  or non-bilious vomiting, depending on the position of the atresia in relation to the Ampulla of Vater, commonly occurs within the first day of life. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_496", "text": "Approximately 20\u201340 percent of all infants with duodenal atresia have  Down syndrome  and 50% have a congenital cardiac anomaly. [ 2 ]  Approximately 8% of infants with Down syndrome have duodenal atresia. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_497", "text": "Antenatal ultrasonography  allows for earlier detection and diagnosis of duodenal atresia. The duodenum is not typically filled with fluid on imaging, however if fluid is visualized on ultrasound, this may suggest duodenal atresia as it causes obstruction and fluid may not pass distal to the atretic area. [ 3 ]  Early diagnosis of duodenal atresia provides time for clinicians to provide prenatal counseling and prepare for postnatal management. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_498", "text": "The diagnosis of duodenal atresia is usually confirmed by  radiography .  An  X-ray  of the abdomen is the first step in evaluation. The x-ray should be obtained after placement of a  nasogastric tube  (feeding tube), evacuating the stomach and filling 40-50 ml of air  [ 5 ]  to demonstrate two large air filled spaces, the so-called \"double bubble\" sign. [ 6 ] [ 7 ]  The air is trapped in the stomach and proximal duodenum, which are separated by the  pyloric sphincter , creating the appearance of two bubbles visible on x-ray. [ 8 ]   Since the closure of the duodenum is complete in duodenal atresia, no air is seen in the distal duodenum. Note that the double bubble sign is typically pathologic however it is not specific for duodenal atresia and may indicate other pathologies such as annular pancreas or midgut volvulus. [ 9 ]  A limited  upper gastrointestinal series  using barium contrast can be used to differentiate between duodenal atresia and midgut volvulus. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_499", "text": "The cause of duodenal atresia is not known. Dr.  Julius Tandler  hypothesized in 1900 that the etiology of duodenal atresia was due to occlusion of the duodenal lumen and failure to re-canalize during embryological development. Research surrounding duodenal atresia in recent years has switched focus to the fibroblast growth factor pathway in mouse models as Tandler's original hypothesis was unable to account for the different types of duodenal atresia. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_500", "text": "Duodenal atresia is classified into 3 types: [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_501", "text": "Early treatment includes  removing fluids from the stomach  via a  nasogastric tube , and providing fluids  intravenously . [ 13 ]  The definitive treatment for duodenal atresia is surgery (duodenoduodenostomy or duodenojejunostomy), which may be performed  openly  or  laparoscopically . [ 14 ]  The surgery is required but not immediately urgent - a 24 to 48-hour delay is permissible to facilitate transport, further evaluation and fluid resuscitation. [ 13 ]  The initial repair has a 5 percent morbidity and mortality rate. [ 15 ]  Nasogastric suction is typically continued post-operatively and patients can be transitioned to small oral feeds once nasogastric tube output decreases significantly or stops completely. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_502", "text": "Prognosis is usually very good, although complications are more likely to occur when there are serious congenital anomalies. [ 13 ]  Complications from surgical repair include  Peptic ulcer disease ,  Gastroesophageal reflux disease ,  Cholecystitis ,  Esophagitis ,  Megaduodenum ,  Blind loop syndrome , and anastomotic leak. [ 10 ]   Late complications may occur in about 12 percent of patients with duodenal atresia, and the mortality rate for these complications is 6 percent. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_503", "text": "Duodenal atresia occurs in 1 in every 10,000 live births and is the most common intestinal atresia, constituting up to 60% of intestinal atresias. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_504", "text": "Duodenal lymphocytosis , sometimes called  lymphocytic duodenitis ,  lymphocytic duodenosis , or  duodenal intraepithelial lymphocytosis , is a condition where an increased number of intra-epithelial  lymphocytes  is seen in biopsies of the  duodenal   mucosa  when these are examined microscopically. This form of  lymphocytosis  is often a feature of  coeliac disease  but may be found in other disorders."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_505", "text": "The condition is characterised by an increased proportion of lymphocytes in the  epithelium  of the duodenum, usually when this is greater than 20\u201325 per 100  enterocytes . [ 1 ]    Intra-epithelial lymphocyte (IEL) are normally present in intestine and numbers are normally greater in the  crypts  and in the  jejunum ; these are distinct from those found in the  lamina propria  of the intestinal mucosa.  IELs are mostly  T cells . [ 1 ]   Increased numbers of IELs are reported in around 3% of in duodenal biopsies, depending on case mix, but may be increasingly being found, in up to 7%. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_506", "text": "The list of possible causes is wide, including coeliac disease,  environmental enteropathy  ( tropical sprue ),  autoimmune enteropathy ,  small intestinal bacterial overgrowth ,  NSAID  damage,  Helicobacter pylori , other infections and  Crohn's disease . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_507", "text": "Diagnosis is made by accurate counting of intraepithelial lymphocytes during histological examination of the duodenum. [ 1 ]   The definition of the condition includes the requirement that the duodenal histological appearances are otherwise unremarkable, specifically with normal  villous  architecture. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_508", "text": "In  coeliac disease  (also known as  gluten-sensitive enteropathy ), duodenal lymphocytosis is found in untreated or partially treated cases. This is the least severe type of change, known as the Marsh I stage, in the classification of histological changes in coeliac disease. Additional features including villous atrophy and  crypt   hyperplasia  are the other findings in other Marsh stages of coeliac disease. [ 4 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_509", "text": "Antibodies associated with coeliac disease were reported in around 11% of cases. [ 1 ]  These IgA  endomysial antibodies  and  anti-transglutaminase antibodies  are very sensitive and specific for coeliac disease implying that this proportion of duodenal lymphocytosis cases has definite coeliac disease.  Around 33% of cases have the  HLA-DQ 2 allele, which is found in over 90% of people with coeliac disease.  Absence of HLA-DQ2 (and the rarer HLA-DQ8) makes coeliac disease most unlikely. [ 5 ]   As antibody-negative coeliac disease is recognised, HLA status, persistence or progression of the duodenal IEL numbers following a gluten challenge, followed by symptomatic improvement on a gluten-free diet, has been used to be more certain about the diagnosis, which was made in 22% of one series of over 200 adult cases.  [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_510", "text": "Helicobacter infection is a common finding at  endoscopy  and although duodenal IEL counts were found to be slightly higher with this infection, this was not considered to be a meaningful cause in children. [ 6 ]   Other infections, including  Cryptosporidiosis  and  Giardiasis  can also be associated with an increase in IELs. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_511", "text": "The management is that of any identified associated disorder such as a  gluten free diet  for cases with coeliac disease [ 5 ]  or treatment of associated infections. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_512", "text": "When duodenal lymphocytosis is associated with other features of coeliac disease, in particular positive antibodies, or HLA-DQ2/8 and a family history, treatment with a  gluten -free diet produces an improvement in IEL numbers. [ 5 ]   Diarrhoea, thyroiditis, weakness and folate deficiency were other predictors of the development of gluten sensitivity and coeliac disease, which developed in 23 of 85 patients over 2 years in one series. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_513", "text": "Dysphagia  is difficulty in swallowing. [ 1 ] [ 2 ]  Although classified under \" symptoms and signs \" in  ICD-10 , [ 3 ]  in some contexts it is classified as a  condition  in its own right. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_514", "text": "It may be a sensation that suggests difficulty in the passage of solids or liquids from the mouth to the stomach, [ 7 ]  a lack of  pharyngeal  sensation or various other inadequacies of the swallowing mechanism. Dysphagia is distinguished from other symptoms including  odynophagia , which is defined as painful swallowing, [ 8 ]  and  globus , which is the sensation of a lump in the throat. A person can have dysphagia without odynophagia (dysfunction without pain), odynophagia without dysphagia (pain without dysfunction) or both together. A  psychogenic  dysphagia is known as  phagophobia . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_515", "text": "Dysphagia is classified into the following major types: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_516", "text": "Some patients have limited awareness of their dysphagia, so lack of the symptom does not exclude an underlying disease. [ 11 ]  When dysphagia goes undiagnosed or untreated, patients are at a high risk of  pulmonary aspiration  and subsequent  aspiration pneumonia  secondary to food or liquids going the wrong way into the lungs. Some people present with \"silent aspiration\" and do not cough or show outward signs of aspiration. Undiagnosed dysphagia can also result in dehydration, malnutrition, and kidney failure. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_517", "text": "Some signs and symptoms of oropharyngeal dysphagia include difficulty controlling food in the mouth, inability to control food or saliva in the mouth, difficulty initiating a swallow, coughing, choking, frequent  pneumonia , unexplained weight loss, gurgly or wet voice after swallowing, nasal regurgitation, and patient complaint of swallowing difficulty. [ 11 ]  When asked where the food is getting stuck, patients will often point to the cervical ( neck ) region as the site of the obstruction. The actual site of obstruction is always at or below the level at which the level of obstruction is perceived. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_518", "text": "The most common symptom of esophageal dysphagia is the inability to swallow solid food, which the patient will describe as 'becoming stuck' or 'held up' before it either passes into the stomach or is regurgitated. Pain on swallowing or  odynophagia  is a distinctive symptom that can be highly indicative of  carcinoma , although it also has numerous other causes that are not related to cancer.  Achalasia  is a major exception to usual pattern of dysphagia in that swallowing of fluid tends to cause more difficulty than swallowing solids. In achalasia, there is idiopathic destruction of parasympathetic ganglia of the  Auerbach's (Myenteric) plexus  of the entire esophagus, which results in functional narrowing of the lower  esophagus , and peristaltic failure throughout its length. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_519", "text": "Complications of dysphagia may include  aspiration ,  pneumonia ,  dehydration , and weight loss. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_520", "text": "The following table enumerates possible causes of dysphagia:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_521", "text": "Difficulty with or inability to swallow may be caused or exacerbated by usage of opiate and/or opioid drugs. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_522", "text": "All causes of dysphagia are considered as differential diagnoses. Some common ones are: [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_523", "text": "Esophageal dysphagia is almost always caused by disease in or adjacent to the esophagus but occasionally the lesion is in the pharynx or stomach. In many of the pathological conditions causing dysphagia, the lumen becomes progressively narrowed and indistensible. Initially, only fibrous solids cause difficulty but later the problem can extend to all solids and later even to liquids. Patients with difficulty swallowing may benefit from  thickened fluids  if the person is more comfortable with those liquids, although, so far, there is no scientific study that proves that those thickened liquids are beneficial. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_524", "text": "Dysphagia may manifest as the result of  autonomic nervous system  pathologies including stroke [ 23 ]  and  ALS , [ 24 ]  or due to rapid iatrogenic correction of an electrolyte imbalance. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_525", "text": "In older adults,  presbyphagia  - the normal healthy changes in swallowing associated with age - should be considered as an alternative explanation for symptoms. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_526", "text": "There are many ways to treat dysphagia, such as swallowing therapy, dietary changes, feeding tubes, certain medications, and surgery. Treatment for dysphagia is managed by a group of specialists known as a multidisciplinary team. Members of the multidisciplinary team include: a speech language pathologist specializing in swallowing disorders (swallowing therapist), primary physician, gastroenterologist, nursing staff, respiratory therapist, dietitian, occupational therapist, physical therapist, pharmacist, and radiologist. [ 11 ]  The role of the members of the multidisciplinary team will differ depending on the type of swallowing disorder present. For example, the swallowing therapist will be directly involved in the treatment of a patient with  oropharyngeal dysphagia , while a gastroenterologist will be directly involved in the treatment of an esophageal disorder. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_527", "text": "The implementation of a treatment strategy should be based on a thorough evaluation by the multidisciplinary team. Treatment strategies will differ on a patient to patient basis and should be structured to meet the specific needs of each individual patient. Treatment strategies are chosen based on a number of different factors including diagnosis, prognosis, reaction to compensatory strategies, severity of dysphagia, cognitive status, respiratory function, caregiver support, and patient motivation and interest. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_528", "text": "Adequate nutrition and hydration must be preserved at all times during dysphagia treatment. The overall goal of dysphagia therapy is to maintain or return the patient to, oral feeding. However, this must be done while ensuring adequate nutrition and hydration and a safe swallow (no aspiration of food into the lungs). [ 11 ]  If oral feeding results in increased mealtimes and increased effort during the swallow, resulting in not enough food being ingested to maintain weight, a supplementary nonoral feeding method of nutrition may be needed. In addition, if the patient aspirates food or liquid into the lungs despite the use of compensatory strategies, and is therefore unsafe for oral feeding, nonoral feeding may be needed. Nonoral feeding includes receiving nutrition through a method that bypasses the oropharyngeal swallowing mechanism including a nasogastric tube, gastrostomy, or jejunostomy. [ 11 ]  Some people with dysphagia, especially those nearing the  end of life , may choose to continue eating and drinking orally even when it has been deemed unsafe. This is known as \"risk feeding\". [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_529", "text": "A 2018 Cochrane review found no certain evidence about the immediate and long-term effects of modifying the thickness of fluids for swallowing difficulties in people with dementia. [ 28 ]  While thickening fluids may have an immediate positive effect on swallowing and improving oral intake, the long-term impact on the health of the person with dementia should also be considered. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_530", "text": "Compensatory treatment procedures are designed to change the flow of the food/liquids and eliminate symptoms but do not directly change the physiology of the swallow. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_531", "text": "Therapeutic treatment procedures \u2013 designed to change and/or improve the physiology of the swallow. [ 11 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_532", "text": "Patients may need a combination of treatment procedures to maintain a safe and nutritionally adequate swallow. For example, postural strategies may be combined with swallowing maneuvers to allow the patient to swallow in a safe and efficient manner. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_533", "text": "The most common interventions used for those with oropharyngeal dysphagia by speech language pathologists are rehabilitation of the swallow through oral motor exercises, texture modification of foods, thickening fluids and positioning changes during swallowing. [ 30 ]  The effectiveness of modifying food and fluid in preventing aspiration pneumonia has been questioned and these can be associated with poorer nutrition, hydration and quality of life. [ 31 ]  Also, there has been considerable variability in national approaches to describing different degrees of thickened fluids and food textures.\u00a0 However, in 2015, the International Dysphagia Diet Standardisation Initiative (IDDSI) group produced an agreed IDDSI framework consisting of a continuum of 8 levels (0\u20137), where drinks are measured from Levels 0 \u2013 4, while foods are measured from Levels 3 \u2013 7. [ 32 ]   It is likely that this initiative, which has widespread support among dysphagia practitioners, will improve communication with carers and will lead to greater standardisation of modified diets [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_534", "text": "Swallowing disorders can occur in all age groups, resulting from congenital abnormalities, structural damage, and/or medical conditions. [ 11 ]  Swallowing problems are a common complaint among older individuals, and the  incidence  of dysphagia is higher in the elderly, [ 33 ] [ 34 ]  and in patients who have had strokes. [ 35 ] \nDysphagia affects about 3% of the population. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_535", "text": "The word \"dysphagia\" is derived from the  Greek   dys  meaning bad or disordered, and the root  phag-  meaning \"eat\". [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_536", "text": "Enteric neuropathy  is a  degenerative   neuromuscular  condition of the digestive system. [ 1 ]  In simple terms the  gut  stops functioning, due to degradation of the nerves and muscles. The condition affects all parts of the  digestive tract . There is no known cure or treatment for enteric neuropathy at this time; it is only possible to work on symptom management."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_537", "text": "The name enteric neuropathy only seems to be used for diagnosis within the UK. The most common name worldwide for this condition is  Intestinal pseudoobstruction ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_538", "text": "The main symptom of enteric neuropathy is severe and constant pain. Other symptoms include  nausea ,  vomiting ,  diarrhoea ,  constipation ,  bloating  and  abdominal  abnormalities. In addition  malabsorption  and  poor nutrition  are common, as the digestive system begins to fail. Symptom management is very important and the main priority is usually to get on top of the pain. However, as most people may have been waiting for years for a diagnosis they are often already addicted to  painkillers  (such as  tramadol  and  oramorph ) and these have adverse effects on the primary condition. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_539", "text": "The diagnosis of enteric neuropathy is rather difficult, in that many symptoms present in ways that are common to many other  bowel-  and  gut -related diseases. It is common that many people undergo many  surgeries , sometimes over several years, to attempt to combat other possible diseases. The diagnosis itself is conducted by a physician  based on multiple tests and is subjective rather than definitive, which for those who have enteric neuropathy will show signs of severe abnormalities in the movement of the gut. An operation to take a section of muscle for  biopsy  which, if it shows signs of nerve degradation, assists in the diagnosis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_540", "text": "An  enterolith  is a mineral  concretion  or  calculus  formed anywhere in the  gastrointestinal system .  Enteroliths are uncommon and usually incidental findings but, once found, they require at a minimum  watchful waiting .  If there is evidence of complications, they must be removed. An enterolith may form around a  nidus , a small  foreign object  such as a seed, pebble, or piece of twine that serves as an irritant. In this respect, an enterolith forms by a process similar to the  creation of a pearl . An enterolith is not to be confused with a  gastrolith , which helps digestion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_541", "text": "Equine  enteroliths are found by walking pastures or turning over manure compost piles to find small enteroliths, during  necroscopy , and increasingly, during surgery for  colic .  Therefore, the incidence of asymptomatic enteroliths is unknown."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_542", "text": "Equine enteroliths are typically smoothly spherical or tetrahedral, [ 1 ]  consist mostly of the mineral  struvite [ 1 ] [ 2 ]  ( ammonium   magnesium   phosphate ), and have concentric rings of mineral precipitated around a nidus. [ 1 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_543", "text": "Enteroliths in  horses  were reported widely in the 19th century, infrequently in the early 20th century, and now increasingly.  They have also been reported in  zebras : five in a  zoo  in  California [ 4 ]  and one in a zoo in  Wisconsin . [ 5 ]   Struvite enteroliths are associated with elevated  pH  and mineral concentrations in the  lumen . [ 6 ]   In  California , struvite enteroliths are associated also with a high proportion of  alfalfa  in the feed and less access to grass pasture.  This association has been attributed to the cultivation of alfalfa on  serpentine soils , resulting in high concentrations of  magnesium  in the alfalfa. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_544", "text": "In  humans , enteroliths are rare and may be difficult to distinguish from  gall stones . Their chemical composition is diverse, and rarely can a nidus be found.  A  differential diagnosis  of an enterolith requires the enterolith, a normal gallbladder, and a  diverticulum . [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_545", "text": "An enterolith typically forms within a  diverticulum .  An enterolith formed in a  Meckel's diverticulum  sometimes is known as a Meckel's enterolith.  Improper use of  magnesium oxide  as a  long-term   laxative  has been reported to cause enteroliths and/or  medication bezoars . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_546", "text": "Most enteroliths are not apparent and cause no complications.  However, any complications that do occur are likely to be severe.  Of these,  bowel obstruction  is most common, [ 10 ]  followed by  ileus [ 11 ]  and  perforation .  Bowel obstruction and ileus typically occur when a large enterolith is expelled from a diverticulum into the  lumen .  Perforation typically occurs within the diverticulum. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_547", "text": "On plain X-rays, the visibility of the enterolith depends on its calcium content. Calcium-rich stones usually demonstrate a radiodense rim and a relatively radioluscent core. Choleic acid stones are almost always radiolucent. They sometimes can be visualized on CT scans without contrast; presence of contrast in the lumen may reveal the enterolith as a void.  Most often, they are visualized using ultrasound. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_548", "text": "Although recent surveys of enterolith composition are lacking, one early review notes struvite (as in equines),  calcium phosphate , and  calcium carbonate  and reports  choleic acid . [ 12 ]   Deoxycholic acid  and  cholic acid  have also been reported. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_549", "text": "In simple cases of obstruction, where there are no complications, a variety of non-surgical and surgical techniques are used to remove the enterolith. [ 11 ]   These include crushing the enterolith and milking it back to the stomach or forward to the colon, surgical removal via an uninvolved segment of the gastrointestinal tract, and  resection  of the involved segment. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_550", "text": "Enteropathy  refers to any  pathology  of the  intestine . [ 1 ]  Although  enteritis  specifically refers to an  inflammation  of the intestine, and is thus a more specific term than \"enteropathy\", the two terms are sometimes used interchangeably."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_551", "text": "Specific types of enteropathy include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_552", "text": "If the condition also involves the  stomach , it is known as \"gastroenteropathy\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_553", "text": "In pigs,  porcine proliferative enteropathy  is a diarrheal disease. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_554", "text": "Enteropathy-associated T-cell lymphoma  ( EATL ), previously termed  enteropathy-associated T-cell lymphoma, type I  and at one time termed enteropathy-type T-cell lymphoma (ETTL), is a complication of  coeliac disease  in which a malignant  T-cell lymphoma  develops in areas of the  small intestine  affected by the disease's intense  inflammation . [ 1 ]  While a relatively rare disease, it is the most common type of primary gastrointestinal T-cell lymphoma. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_555", "text": "EATL had been defined as a single type of small intestine lymphoma, but in 2008, the  World Health Organization  (WHO) divided the disease into two subtypes:  1)  EATL type I, which occurs in individuals with coeliac disease, a chronic immune disorder causing inflammatory responses to dietary  gluten  primarily in the upper reaches (i.e.  jejunum  and  duodenum ) of the small intestine; and  2)  EATL type II, a disorder similar to EATL type I that occurs without coeliac disease. While type I and II EATL share many similar features, post-2008 studies found some significant differences between the two types. In 2016, the WHO redefined the two diseases as separate entities, keeping the term enteropathy-associated T-cell lymphoma for the coeliac disease-associated lymphoma and terming type 2 disease as  monomorphic epitheliotropic intestinal T cell lymphoma  (MEITL). [ 3 ]  EATL is five to ten times more common than is MEITL. [ 4 ]  The WHO also defined a third type of intestinal T-cell lymphoma that cannot not be classified as EATL or MEITL as  peripheral T-cell lymphoma not otherwise specified  (ITCL-NOS). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_556", "text": "EATL arises from the malignant transformation of small-intestinal  intraepithelial lymphocytes  (IEL). IEL are a heterogeneous group of principally  T-cell  lymphocytes residing in  epithelial  tissues that interface the environment, such as the  mucosa  of the  bronchi ,  reproductive tract  and  gastrointestinal tract . [ 6 ]  At these sites, IEL are exposed and regulate immune responses to non-dietary and dietary  antigens ,  pathogenic  and non-pathogenic organisms and injured self tissues. [ 7 ]  Gastrointestinal tract IEL appear in the  epithelium  of the small intestine, colon, stomach and esophagus, residing between the epithelial cells that line these organs'  lumens . [ 7 ]  These IEL often exhibit  natural killer  and  cytotoxic T-cell  cell activation markers, [ 6 ]  contain various toxic agents (e.g.  perforin ,  granzyme ) and therefore are capable, if activated, of causing severe tissue injuries. [ 4 ]  With coeliac disease, the IEL react to the  glutelins  in dietary gluten by increasing their numbers, becoming pathologically active, producing chronic inflammation that injures intestinal cells, interfering with nutrient absorption and creating an environment conducive to their  malignant transformation  into EATL. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_557", "text": "Optimal treatment of EATL has used regimens consisting of intensive  chemotherapy ,  hematopoietic stem cell transplantation  and, in cases with bulky, obstructive and/or perforated bowel disease, surgical intervention. [ 3 ]  The disease has a five-year overall survival rate of only ~20%. [ 8 ]  However, recent studies focusing on the malignant IEL in EATL have increased understanding of the disease and suggested newer chemotherapy-based strategies and novel molecular targets that might be attacked therapeutically to improve the disease's prognosis. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_558", "text": "EATL typically occurs in patients with a history of coeliac disease and who may have been previously diagnosed with Type I or II refractory disease, [ 9 ]  but in any case, affected individuals present with worsening coeliac disease symptoms of abdominal pain,  malabsorption ,  diarrhea , weight loss, fever or  night sweats . [ 10 ] [ 3 ]  EATL diagnosis is more likely if symptoms develop suddenly, [ 4 ]  or if the serious symptoms of  bowel obstruction  and/or  bowel perforation  caused by bulky EATL masses develop. [ 10 ]  Patients with ulcerative  jejunitis  usually present with more severe symptoms, including more frequent  bowel perforations  and obstructions. [ 10 ]  Some patients with no history of coeliac disease present with symptoms or signs of a small-intestinal lymphoma but on diagnostic workup are found to have coeliac disease. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_559", "text": "The cause of EATL, while not fully understood, is by definition related to celiac disease. Individuals are  genetically predisposed  to develop celiac disease because of the specific types of  HLA-DQ  proteins expressed by their  antigen-presenting cells  (APC). HLA-DQ proteins are on the surface of APC and function to present foreign or self  antigens  to the  T cell receptors  (TCR) expressed on the surface of T-cells and thereby to stimulate these cells either to initiate or suppress  immune responses  to the presented antigens. HLA-DQ proteins are composed of \u03b1 and \u03b2  polypeptide chains  encoded by the  HLA-DQA1  and  HLA-DQB1  genes, respectively. Since there are several different  alleles  (i.e. gene variants) at these two  genetic loci , individuals are usually  heterozygous , i.e. have inherited different  alleles  from each parent at each locus; uncommonly, however, individuals are  homozygous  at one or both loci because their parents have the same alleles at one or both loci. The HLA-DQ proteins that predispose individuals to coeliac disease bind and respond specifically to gluten-related antigens presented to them by APC. [ 11 ]  The genetic predisposition to develop coeliac disease is clinically determined by identifying the  serotypes  of an individual's APC's HLA-DQ proteins using serotype-specific  antibody  preparations and/or by identifying the alleles at an individual's HLA-DQA1 and HLA-DQB1 genetic loci. Studies show that:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_560", "text": "IEL are a diverse population of lymphocytes, which unlike most peripheral lymphocytes, do not recirculate through the  blood  and/or  lymphatic system  but rather reside permanently in the  epithelium  of various organs. [ 11 ]  In the GI tract, IEL localize between the epithelial cells lining the colon, small intestine, stomach, and esophagus where they serve to maintain the  mucosal  barrier, combat infection by  pathogens , and regulate immune responses to antigens originating from the diet,  pathogens , and damaged tissues. [ 6 ]  Human IEL are classified into those which express the TCR (i.e. TCL+IEL) and those which do not (i.e. TCR-IEL). TCL+IEL are further divided into 4 subtypes, TCR\u03b1\u03b2+CD4+ IEL, TCR\u03b1\u03b2+CD4+CD8\u03b1\u03b1+ IEL, TCR\u03b1\u03b2+CD8\u03b1\u03b2+ IEL, and TCR\u03bb\u03b4+CD8\u03b1\u03b1+. These subtypes are based on the expression of alpha (\u03b1) and beta (\u03b2) chain-containing TCR (i.e. \u03b1\u03b2TCR); gamma (\u03b3) and delta (\u03b4) chain-containing TCR (i.e. \u03b3\u03b4TCR);  CD4 ;  CD8 \u03b1\u03b2; and/or  CD8 \u03b1\u03b1 by individual IEL.. A fifth TCL+IEL subtype, TCR\u03b1\u03b2+CD8\u03b1\u03b1+, occurs in mice but its presence in the human intestine is disputed. [ 11 ]  Human TCR-IEL are also divided into 4 sub-types: their: ILC1-like IEL have  morphological  and functional similarities to normal intestinal epithelial cells and express  NKp46 ; ICL3-like IEL have morphological similarities to normal epithelial cells and, similar to  Th1 cells , make  Interleukin 17  (IL-17) and  Interleukin 22  (IL-22)  cytokines  and express the  ROR\u03b3t  transcription factor and  NKp44 ; iCD3-IEL express  iCD3 ; and iCD8\u03b1-IEL express iCD3 and CD8\u03b1. [ 7 ]   CD3  designates a protein complex that is attached to the  cell surface membrane  whereas iCD3 refers to a CD3 protein complex in which one or more of its proteins resides abnormally in the cell's  cytosol [ 11 ]  Studies suggest that iCD3+IEL are the principal cell type that becomes malignant in EATL cases that are not classified as  de novo  (see next section). [ 7 ]  These cells also express  CD103  and, frequently,  CD30 . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_561", "text": "Coeliac disease patients may be  asymptomatic , minimally symptomatic, and/or well-controlled on a  gluten-free diet  (i.e. a diet free of cereal, rye, wheat, and barley [ 16 ] ) but nonetheless develop EATL. About 46% of all AETL cases occur in this setting and have had their malignancy described as  de novo  EATL. The remaining ~54% of EATL cases develop in coeliac disease patients whose disease becomes refractory to dietary control, exhibits increasing symptoms, and  progress over ~4\u201310 years through Type I refractor coeliac disease (Type 1 RCD) and Type II refractory coeliac disease (Type II RCD) to become EATL. [ 3 ]  The rates at which non-refractory celiac disease, Type I RCD, and Type II RCD progress to  de novo  or EATL are <1%, 3-14%, and 33-52%, respectively. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_562", "text": "De novo EATL  can occur in individuals whose coeliac disease was undiagnosed until EATL was found or who have mild/well-controlled coeliac disease. The findings in these patients usually differ little from those found in mild/well-controlled cases that do not progress to EATL; their small intestinal mucosa is populated by increased number of IEL and exhibits tissue destruction (e.g. small  intestinal villus   atrophy ), Nonetheless, their IEL are normal-appearing, small cells that on examination are polyclonal (i.e. genetically diverse), express CD3 and  CD8 , and do not have genetic abnormalities. The mechanism behind the development of EATL in these individuals is not understood. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_563", "text": "Type I RCD patients, who constitute 15\u201323% of all patients with RCD, [ 17 ]  are refractory to the gluten diet as evidenced by their worsening symptoms, increased tissue destruction, [ 10 ]  and rising numbers of TCR\u03b1\u03b2+CD*\u03b1\u03b2+IEL in tissue lesions. [ 3 ]  Some Type I RCD  patients may have failed to respond to the diet from the onset of their disease. If either cases, these patients show no change in the normal appearance and polyclonal nature of their small intestinal IEL and these IEL show no genetic abnormalities. [ 10 ]  The cause for these coeliac disease patients progressing to Type I RCD, after excluding the very common problem of failure to fully exclude gluten from their diets, is either due to their genetic makeup (see above section on genetics) or is unknown. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_564", "text": "Type I RCD patients may progress to Type II RCD as evidenced by their more severe symptoms, increased intestinal tissue destruction, and expanding numbers of intestinal IEL, particularly iCD3+IEL. [ 3 ]  Their IEL typically consist of genetically different subpopulations of cells that have a  monoclonal  rearrangement of their TCR and therefore are descendant from a single ancestral cell. [ 10 ]  Subpopulations of these IEL also have one or more of the following genetic abnormalities:  trisomy  of chromosome 1's long (or \"q\") arm at position 22\u201344 (abbreviated 1-q22-24); genomic alterations around the  TP53   tumor suppressor  gene at position 13.1 on the short or \"p\" arm of chromosome 17; genomic alterations around the  CDKN2A  tumor suppressor and  CDKN2B  cell proliferation regulator at position p21.3 on chromosome 9 that result in  loss of heterozygosity  for both genes; and/or  activating mutations  in  JAK1  (75% of cases) and  STAT3  (25% of cases). In Type II RCD, the same types of abnormal ILE found in the small intestine may be detected in the colon, stomach, [ 9 ]   mesenteric lymph nodes , blood, bone marrow, and epithelium of the airways and skin. [ 9 ]  Finally, the small intestinal lesions in Type II RCD contain  IL-2  and  IL-21 [ 18 ]  as well as increased levels of  IL-15 . [ 3 ]  Laboratory studies indicate that these 3  cytokines  acting individually or in  synergy  are potent stimulators of the  JAK1/STAT3  signaling pathway in iCD3+IEL and thereby promote these cells survival (by blocking  apoptosis ) and proliferation. [ 18 ] [ 19 ]  The small intestinal lesions also contain  a tumor necrosis factor  which stimulates iCD3+IEL survival and proliferation but does so by activating  NF-\u03baB ,  MAPK , and/or  c-Jun N-terminal kinases  rather than JAK1/STAT3 signaling pathway. [ 18 ]  These data suggest that:  a)  Type II RCD is a low grade lymphoma; [ 9 ]   2)  the intense inflammation in Type II RCD, perhaps amplified by the cited cytokines, promotes the proliferation, survival,  genome instability , and consequential genetic abnormalities in IEL; and  3)  one or more of these factors cause the transformation of Type II RD to EATL. [ 3 ] [ 9 ] [ 19 ]  As currently understood, the release of IL-15 by mucosal epithelial cells, the binding of IL-15 to the  IL-15R\u03b2   cell surface receptor  on iCD3+IEL, and the stimulation thereby of these cells appears particularly important in driving Type II RCD to EATL in a significant number of cases. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_565", "text": "Ulcerative jejunitis [ 16 ]  (also termed chronic ulcerative jejunitis, multifocal ulcerated microlymphomas, [ 8 ]  ulcerative jejunoilitis, [ 10 ]  and chronic ulcerative jejunoilitis [ 3 ] ) is regarded as a rare complications or severe form of Type II RCD in which the  jejunum  or jejunum plus  ileum  portions of the small intestine contain multifocal ulcers. Patients with this disorder have a higher risk of developing EATL than other Type II RCD patients. [ 10 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_566", "text": "Besides the genetic gene abnormalities found in Type II RCD, the malignant IEL in EATL consist of one or more subpopulations that have mutations: in other JAK-STAT pathway genes viz.,  STAT5B ,  JAK3 , and  SOCS1  ( SOCS1  inhibits STAT signaling);  tumor suppressor  genes  BCL11B  and  SETD2  ( SETD2  is also involved in regulating lymphocyte development); another gene involved in lymphocyte development,  PRDM1 ; a gene promoting activation of the tumor suppressor  p53 ,  IRF1 ;  DNA repair  genes  BRIP1  and  TERT  ( TERT  is also involved in maintaining DNA  telomeres  and thereby  chromosome   stability ); the  NRAS  and  KRAS   oncogenes ; a gene involved in  progression of the cell cycle  and thereby cellular proliferation,  STK10 ; a gene involved in promoting cell death by  apoptosis ,  DAPK3 ; a gene involved in regulating  Interferon gamma  actions, inhibiting  toll-like receptor  signaling, and regulating activation of  innate  and  adaptive  immune systems,  IRF4 ; a gene involved in cell signaling through various cell receptors,  GNAS ; a gene involved in production of the immunoglobulin,  IgA ,  BBX ; and two  chromatin remodeling  genes,  TET2  and  YLPM1 .  These cells also overexpress or under express various genes that impact cell survival, growth, and malignancy. It is likely that one or more of these genetic and gene expression abnormalities contribute to the malignant behavior of EATL. [ 3 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_567", "text": "The diagnosis of EATL is based on  endoscopic  findings of:  1)  flattened duodenal folds and small intestinal fissures and ulcers;  2)  biopsy findings of small intestinal inflammation, increased IEL, villous atrophy, and  crypt hyperplasia ;  3)  HLA-DG serology typing and/or gene allele analyses showing results compatible with coeliac disease (see above section on genetics); and  4)  positive  serology  tests for  IgA antitissue translutamase antibodies ,  IgA antibodies to deamidated gliadin peptides ,  IgG antibodies to deamidated gliadin peptides , and/or  IgA antibodies to antitissue translutamase . [ 10 ]  About 35% of EATL cases will be found to have spread of the disease to extra-intestinal sites [ 3 ]  with lesions in the mesenteric lymph nodes (~35% of cases), bone marrow (<10% of cases), and, uncommonly, blood that contain IEL with the same genetic abnormalities and cell markers as those found in the IEL of their intestinal lesions. [ 4 ]  Intestinal biopsy specimens of EATL lesions also commonly show the presence of mucosal inflammatory cells (particularly  eosinophils  and  histiocytes ); a greatly  expanded population of medium- to large-sized or  anaplastic  IEL expressing iCD3 as well as cytotoxic and cell activation markers (e.g.  granzyme B  and usually  TIA1  and  perforin ); and, frequently  CD30 . [ 8 ]  In most cases these IEL also show genetic abnormalities, particularly activating mutations in JAK1 and/or STAT3 and to lesser extents those cited in the above section on EATL. The malignant IEL in EATL do not express  CD56 . [ 3 ] [ 20 ]   Rarely, patients present with EATL who have no gastrointestinal symptoms of celiac disease but rather with extra-intestinal manifestations that are associated with the disease such as  dermatitis herpetiformis , [ 3 ]   psoriasis , other chronic skin conditions,  dental enamel  defects,  gluten-induced cerebellar ataxia ,  arthritis , and   arthralgias . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_568", "text": "Other gastrointestinal T-cell lymphomas can resemble, and therefore need to be  differentiated  from, EATL. These include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_569", "text": "Strict adherence to a gluten-free diet has been shown in some but not all studies to prevent in a significant number of cases the progression of coeliac disease to Type I RCD, Type II RCD, and EATL. [ 9 ]  For example, an Italian study of 1757 patients found that the morbidity of EATL over 3 years fell from 6.42 to 0.22 in coeliac disease patients kept on a strict gluten-free diet. While two other studies found that the risk of malignancy in the diseases did not fall on this diet, current opinion strongly favors using it in all stages of coeliac disease. [ 4 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_570", "text": "Efforts have also been made to treat refractory coeliac disease in order to prevent EATL. Treatment with  corticosteroids , particularly  budesonide  gives temporary improvement in symptoms and histological responses in 30\u201340% of patients [ 9 ]  but few have attained a good overall response. [ 16 ]  The addition of  azathioprine ,  cyclosporin , or a  monoclonal antibody  directed against  tumor necrosis factor-\u03b1  to the corticosteroid regimen, the use, as single agents, of purine analogs (i.e.  pentostatin ,  cladribine ) or monoclonal antibody directed against CD52 as well as the use of intensive  chemotherapy  regimens have shown little therapeutic effects. Furthermore, azathioprine, anti-CD52 antibody, and cladribine have been reported to increase the disease's progression to EATL. [ 9 ]  In summary, the role these drugs, intensive chemotherapy regimens, and  hematopoietic stem cell transplantation  in the treatment of refractory coeliac disease is unclear and has not been shown to improve, and in some cases may worsen, the chances that Type I and Type II RCD, will progress to EATL. [ 3 ] [ 10 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_571", "text": "Patients with refractory coeliac disease, especially those with Type II RCD, should be examined at regular intervals for the development of EATL using  magnetic resonance imaging ,  capsule endoscopy ,  CT scan , and  Positron emission tomography ;. [ 9 ]  These examinations should also be used whenever patients with refractory disease experience worsening symptoms. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_572", "text": "In eligible patients, surgery where necessary (required in >80% of patients) to repair obstructed or perforated bowel or remove bulky disease followed by a conditioning regimen of high-dose chemotherapy (usually the  CHOP  regimen) and  autologous stem cell transplantion  has been the mainstay of treating EATL. [ 4 ] [ 32 ]  Previous chemotherapy treatment regimens that did not use autologous stem cell transplantation reported poor prognoses with  overall survival , progression free, and mortality rates over a 5-year period of 22%, 3%, and 81%. respectively whereas a regimen that included intensive chemotherapy, conditioning, and autologous stem cell transplantation had rates of 60%, 52%, and 39%, respectively. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_573", "text": "A phase 2 study sponsored by the Imagine Institute [ 33 ]  and being conducted in Paris, France is recruiting patients to examine the efficacy and side effects of a new treatment regimen on EATL. The regimen consists of treatment with  brentuximab vedotin  plus CHP (i.e.  cyclophosphamide ,  Adriamycin ,  prednisone ) followed by consolidation chemotherapy and autologous hematopoietic stem cell transplantation. Brentuximab vedotin is a  chimeric   monoclonal antibody  that is complexed to the  antimitotic agent ,  monomethyl auristatin E ; the drug binds to the cell-membrane protein  CD30  to deliver thereby the antimitotic aged into CD30-bearing target cells. This study is based on a phase 1 study finding that a regimen consisting of brentuximab vedotin plus CHP achieved objective responses in all 26 patients tested, with complete remissions obtained in the only patient with EATL, all 6 patients with ALCL, and 16 of 19 patients with other types of T-cell/NK-cell lymphomas. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_574", "text": "A phase 1 study sponsored by the  National Institutes of Health Clinical Center  is recruiting patients that have CD30-expressing lymphomas such as EATL to examine the effects of a conditioning drug regimen (i.e. cyclophosphamide and  fludarabine ) followed by infusions of the patients'  chimeric antigen receptor T cells  that have been modified to target and destroy cells bearing CD30. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_575", "text": "A phase 1 study sponsored by the  NIH  and  Mayo Clinic USA  is recruiting patients with peripheral T-cell lymphomas, including EATL, to study the efficacy and toxicity of  nivolumab . Nivolumab is  monoclonal antibody   checkpoint inhibitor  that binds to the  programmed cell death protein 1  (PD-1) thereby blocking this protein from being activated by  programmed death-ligand 1  (PD-L1). Many types of cancer cells increase their expression of PD-LI in order to inhibit immune cells that express PD-1 from killing them. Nivolumab blocks this inhibition and has been found effective in suppressing the growth of certain cancers. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_576", "text": "A recently completed  Phase 2 ,  randomized ,  double-blinded ,  placebo-controlled ,  parallel group  study evaluated the efficacy and safety of a monoclonal antibody (termed AMG 714) directed against IL-15 in adult patients with Type II RCD. [ 37 ]  The study found potential therapeutic effects of the treatment in that it halted the malignant progression of IEL in these patients. [ 17 ]   Expanded access  or compassionate use requests for AMG 714 may be considered for adult patients with biopsy-proven Type II RCD who have failed all available treatment options and do not have EATL. To request access, use Responsible Party contact information found by hitting the \"More info...\" linkage on the following clinical trials page. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_577", "text": "aggressive:   S\u00e9zary disease"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_578", "text": "Eosinophilic gastroenteritis  ( EG  or  EGE ), also known as  eosinophilic enteritis , [ 1 ]  is a rare and  heterogeneous condition  characterized by patchy or diffuse  eosinophilic  infiltration of  gastrointestinal  (GI) tissue, first described by Kaijser in 1937. [ 2 ] [ 3 ]  Presentation may vary depending on location as well as depth and extent of bowel wall involvement and usually runs a chronic relapsing course. It can be classified into mucosal, muscular and serosal types based on the depth of involvement. [ 4 ] [ 5 ]  Any part of the GI tract can be affected, and isolated biliary tract involvement has also been reported. [ 6 ] [ 7 ] \nThe  stomach  is the  organ  most commonly affected, followed by the  small intestine  and the  colon . [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_579", "text": "EG typically presents with a combination of chronic nonspecific GI symptoms which include  abdominal pain ,  diarrhea , occasional  nausea  and  vomiting ,  weight loss  and  abdominal distension . Approximately 80% have symptoms for several years; [ 7 ]  a high degree of clinical suspicion is often required to establish the diagnosis, as the disease is extremely rare. It does not come all of a sudden but takes about 3\u20134 years to develop depending upon the age of the patient. Occasionally, the disease may manifest itself as an  acute abdomen  or  bowel obstruction . [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_580", "text": "Peripheral blood  eosinophilia  and elevated  serum   IgE  are usual but not universal. The damage to the  gastrointestinal tract  wall is caused by eosinophilic  infiltration  and  degranulation . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_581", "text": "As a part of  host defense  mechanism,  eosinophils  are normally present in gastrointestinal  mucosa , though the finding in deeper  tissue  is almost always pathologic. [ 16 ]  What triggers such dense infiltration in EG is not clear. It is possible that different  pathogenetic  mechanisms of disease is involved in several subgroups of patients. Food  allergy  and variable  IgE  response to food substances has been observed in some patients which implies role of  hypersensitive  response in pathogenesis. Many patients indeed have history of other  atopic  conditions like  eczema ,  asthma , etc. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_582", "text": "Eosinophil recruitment into inflammatory tissue is a complex process, regulated by a number of  inflammatory   cytokines . In EG  cytokines   IL-3 ,  IL-5  and granulocyte macrophage colony stimulating factor ( GM-CSF ) may be behind the recruitment and activation. They have been observed  immunohistochemically  in diseased intestinal wall. [ 17 ] \nIn addition  eotaxin  has been shown to have an integral role in regulating the  homing  of eosinophils into the  lamina propria  of stomach and small intestine. [ 18 ] \nIn the allergic subtype of disease, it is thought that food  allergens  cross the intestinal mucosa and trigger an inflammatory response that includes  mast cell  degranulation and recruitment of eosinophils. [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_583", "text": "Talley et al. [ 20 ]  suggested three diagnostic criteria which are still widely used:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_584", "text": "Hypereosinophilia , the hallmark of allergic response, may be absent in up to 20% of patients, but  hypoalbuminaemia  and other abnormalities suggestive of malabsorption may be present.  CT scans  may show nodular and irregular thickening of the folds in the distal stomach and proximal small bowel, but these findings can also be present in other conditions like  Crohn's disease  and  lymphoma . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_585", "text": "The  endoscopic  appearance in eosinophilic gastroenteritis is nonspecific; it includes erythematous, friable, nodular, and occasional ulcerative changes. [ 21 ] \nSometimes diffuse inflammation results in complete loss of  villi , involvement of multiple layers,  submucosal   oedema  and  fibrosis . [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_586", "text": "Definitive diagnosis involves  histological  evidence of eosinophilic infiltration in biopsy slides.  Microscopy  reveals >20 eosinophils per  high power field . [ 12 ] [ 20 ]  Infiltration is often patchy, can be missed and  laparoscopic  full thickness biopsy may be required."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_587", "text": "Radio isotope  scan using  technetium ( 99m Tc) exametazime -labeled  leukocyte   SPECT  may be useful in assessing the extent of disease and response to treatment but has little value in diagnosis, as the scan does not help differentiating EG from other causes of inflammation. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_588", "text": "When eosinophilic gastroenteritis is observed in association with eosinophilic infiltration of other organ systems, the diagnosis of  idiopathic   hypereosinophilic syndrome  should be considered. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_589", "text": "Corticosteroids are the mainstay of therapy with a 90% response rate in some studies. Appropriate duration of steroid treatment is unknown and relapse often necessitates long term treatment. Various steroid sparing agents e.g.  sodium cromoglycate  (a stabilizer of mast cell  membranes ),  ketotifen  (an  antihistamine ), and  montelukast  (a selective, competitive  leukotriene receptor antagonist ) have been proposed, centering on an allergic hypothesis, with mixed results. [ 19 ] [ 27 ]   Oral  budesonide  (an oral steroid) can be useful in treatment, as well. [ 28 ]  An elimination diet may be successful if a limited number of food allergies are identified. [ 21 ] [ 29 ]  An elemental diet may also be successful in the treatment of children. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_590", "text": "In a  randomized clinical trial ,  lirentelimab  was found to improve  eosinophil  counts and symptoms in individuals with eosinophilic gastritis and duodenitis. [ 31 ] [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_591", "text": "Epidemiology may differ between studies, as number of cases are small, with approximately 300 EG cases reported in published literature."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_592", "text": "EG can present at any age and across all races, with a slightly higher incidence in males. [ 33 ]  Earlier studies showed higher incidence in the third to fifth decades of life. [ 2 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_593", "text": "Epiploic appendagitis  ( EA ) is an uncommon, benign, self-limiting  inflammatory process  of the  epiploic appendices . Other, older terms for the process include  appendicitis epiploica  and  appendagitis , but these terms are used less now in order to avoid confusion with  acute appendicitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_594", "text": "Epiploic appendices are small, fat-filled sacs or finger-like projections along the surface of the upper and lower  colon  and  rectum . They may become acutely inflamed as a result of torsion (twisting) or  venous thrombosis . The inflammation causes pain, often described as sharp or stabbing, located on the left, right, or central regions of the  abdomen . There is sometimes  nausea  and  vomiting . The symptoms may mimic those of acute appendicitis,  diverticulitis , or  cholecystitis . The pain is characteristically intense during/after defecation or  micturition  (espec. in the sigmoid type) due to the effect of traction on the pedicle of the lesion caused by straining and emptying of the bowel and bladder.  Initial lab studies are usually normal. EA is usually diagnosed incidentally on  CT scan  which is performed to exclude more serious conditions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_595", "text": "Although it is self-limiting, epiploic appendagitis can cause severe pain and discomfort. It is usually thought to be best treated with an anti-inflammatory and a moderate to severe pain medication (depending on the case) as needed. Surgery is not recommended in nearly all cases.  Sand and colleagues, [ 1 ]  however, recommend laparoscopic surgery to excise the inflamed appendage in most cases in order to prevent recurrence."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_596", "text": "The condition commonly occurs in patients in their 40s and 50s predominantly in men. Epiploic appendagitis is normally misdiagnosed in most patients. [ 2 ]  Epiploic appendagitis presents with an acute onset of pain, commonly in the left lower quadrant the symptoms often lead to a misdiagnosis for diverticulitis. Diverticulitis manifests with evenly distributed lower abdominal pain accompanied with nausea, fever, and  leukocytosis . Patients with acute epiploic appendagitis do not normally report a change in bowel habits, while a small number may have constipation or diarrhea. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_597", "text": "It is rare however possible for epiploic appendagitis to result in a peritoneal loose body. Peritoneal loose body is a free floating mass of dead fibrous tissue surrounded by several layers of calcification (deposit of calcium salts). The loose body is the result of torsed,  infarcted  or detached epiploic appendages that eventually become  fibrotic  (inflammation and scarring) masses. If the loose body becomes large enough it can cause urinary retention (inability to empty bladder) or bowel obstructions. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_598", "text": "Epiploic appendages are also called  appendices epiploicae . The appendages themselves are 50\u2013100 appendages that are oriented in two rows anterior and posterior. The appendages are parallel to the superficial section of the  taenia coli . Furthermore, the appendages are between 0.5 and 5\u00a0cm long, each appendage is attached with one or two arterioles and a venule within vascular stalks attached to the colon. Torsion (twisting or wrenching motion) of the appendages can cause  ischemia  which can cause painful symptoms that mimic other conditions such as diverticulitis, and appendicitis; however, it is rare. The pain associated with the inflamed appendages is located in the left and sometimes in the right lower abdominal quadrant. Diagnosis of epiploic appendagitis can be challenging due to its infrequency. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_599", "text": "Epiploic appendagitis is more common in patients older than 40 years of age; however, it can occur at any age. \"The reported ages range from 12 to 82 years. Men are slightly more affected than women.\" [ 2 ]   Patients with epiploic appendagitis describe having a localized, strong, non-migratory sharp pain after eating. Patients generally have tender abdomens as a symptom. Symptoms do not include fever, vomiting, or leukocytosis. The pain is typically located in the right or left lower abdominal quadrant. When there is pain in the right lower quadrant, it can mimic appendicitis; however, it more commonly mimics diverticulitis, with pain present on the left side. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_600", "text": "There are several conditions that mimic the symptoms of epiploic appendicitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_601", "text": "Omental infarction :  Omental infarction  is uncommon reason for acute abdomen. It is similar to acute appendicitis. The pain is of a few days duration centering in the right lower or upper quadrant. Imaging is required to obtain an accurate diagnosis due to the common misdiagnosis of omental infarction as  appendicitis  or  cholecystitis . Omental infarction occurs commonly in pediatric patients approximately 15 percent of cases. The most frequent cause of non- torsion related omental infarction is due to trauma as well as  thrombosis  or the omental veins. The predisposition for omental infarction includes obesity, strenuous activity,  congestive heart failure , digitalis administration, recent abdominal surgery and trauma. [ 2 ]  \"The typical CT findings are a solitary large non-enhancing omental mass with heterogeneous attenuation, which is most often located in the right lower quadrant, deep to the rectus abdominis muscle and either anterior to the transverse colon or anteromedial to the ascending colon\". [ 2 ]  Omental Infarction can be difficult to differentiate from diverticulitis however omental infarction is not normally attributed with bowel wall thickening. It is rare that the colonic wall will be thickened due to spread of the inflammation from the  omentum  (a fold of peritoneum connecting or supporting abdominal structures) to the  tenia omentalis  of the colon. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_602", "text": "Diverticulitis :  Diverticulitis  normally happens in older patients than in epiploic appendagitis. The two inflammatory conditions are quite indistinguishable based on physical manifestations. Patients with diverticulitis will present with nausea, vomiting, fever, elevated leukocyte count, rebound tenderness, and will have more extensive lower abdominal pain than patients with epiploic appendagitis. Additionally inflammation from diverticulitis may spread to the epiploic appendages making it difficult to diagnose, for inflammation of the appendices epiploicae may be resultant to other inflammatory conditions in the colonic wall and surrounding  mesocolon . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_603", "text": "Ultrasound  and  CT scans  are the normal means of positive diagnosis of epiploic appendagitis. Ultrasound scans show \"an oval, non-compressible hyperechoic mass with a subtle  hypoechoic  rim directly under the site of maximum tenderness\". [ 4 ]  Normally, epiploic appendages cannot be seen on  CT  scan. [ 4 ]  After cross-sectional imaging and the increased use of abdominal CT for evaluating lower abdominal pain, EA is increasingly diagnosed.  Pathognomonic  CT scan data represent EA as 2\u20134\u00a0cm, oval shaped, fat density lesions, surrounded by inflammation. Contrasting with diverticulitis findings, the colonic wall is mostly unchanged. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_604", "text": "Epiploic appendagitis is self-limiting and can be managed conservatively with NSAIDs. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_605", "text": "Acute epiploic appendagitis is usually associated with obesity, hernia and unaccustomed exercise. The inflammation of the epiploic appendages normally resolves on its own for most patients. It is possible however uncommon for acute epiploic appendagitis to result in adhesion, bowel obstruction,  intussusception , intraperitoneal loose body,  peritonitis , and/or abscess formation. [ 2 ]  Treatment consists of reassurance of the patient and analgesics. Under non invasive treatment, symptoms resolve in two weeks. Hospitalization is not necessary. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_606", "text": "Fecal incontinence  ( FI ), or in some forms,  encopresis , is a lack of control over  defecation , leading to involuntary loss of bowel contents \u2014 including  flatus  (gas), liquid stool elements and  mucus , or solid  feces . FI is a  sign  or a  symptom , not a  diagnosis . Incontinence can result from different causes and might occur with either  constipation  or  diarrhea . Continence is maintained by several interrelated factors, including the  anal sampling mechanism , and incontinence usually results from a deficiency of multiple mechanisms. The most common causes are thought to be immediate or delayed  damage from childbirth , complications from prior  anorectal surgery  (especially involving the anal  sphincters  or hemorrhoidal vascular cushions), altered bowel habits (e.g., caused by  irritable bowel syndrome ,  Crohn's disease ,  ulcerative colitis , food intolerance, or constipation with overflow incontinence). [ 1 ]  An estimated 2.2% of community-dwelling adults are affected. [ 2 ]  However, reported prevalence figures vary. A prevalence of 8.39% among non-institutionalized U.S adults between 2005 and 2010 has been reported, and among institutionalized elders figures come close to 50%. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_607", "text": "Fecal incontinence has three main consequences: local reactions of the perianal skin and urinary tract, including  maceration  (softening and whitening of the skin due to continuous moisture),  urinary tract infections , or  decubitus ulcers  (pressure sores); [ 1 ]  a financial expense for individuals (due to the cost of medication and incontinence products, and loss of productivity), employers (days off), and  medical insurers  and society generally ( health care costs ,  unemployment ); [ 1 ]  and an associated decrease in  quality of life . [ 5 ]  There is often reduced self-esteem, shame, humiliation,  depression , a need to organize life around easy access to a  toilet , and avoidance of enjoyable activities. [ 1 ]  FI is an example of a  stigmatized  medical condition, which creates barriers to successful management and makes the problem worse. [ 6 ]  People may be too embarrassed to seek medical help and attempt to self-manage the symptom in secrecy from others."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_608", "text": "FI is one of the most psychologically and socially debilitating conditions in an otherwise healthy individual and is generally treatable. [ 2 ]  More than 50% of hospitalized seriously ill patients rated bladder or fecal incontinence as \"worse than death\". [ 7 ]  Management may be achieved through an individualized mix of dietary, pharmacologic, and surgical measures. Health care professionals are often poorly informed about treatment options, [ 2 ]  and may fail to recognize the effect of FI. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_609", "text": "FI affects virtually all aspects of peoples' lives, greatly diminishing physical and mental health, and affecting personal, social, and professional life. Emotional effects may include stress, fearfulness, anxiety, exhaustion, fear of public humiliation, feeling dirty, poor body image, reduced desire for sex, anger, humiliation, depression, isolation, secrecy, frustration, and embarrassment. Some patients cope by controlling their emotions or behavior. Physical symptoms such as skin soreness, pain and odor may also affect quality of life. Physical activity such as shopping or exercise is often affected. Travel may be affected, requiring careful planning. Working is also affected for most. Relationships, social activities and self-image likewise often suffer. [ 8 ]  Symptoms may worsen over time. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_610", "text": "FI is a sign or a symptom, not a diagnosis, [ 8 ]  and represents an extensive list of causes. Usually, it is the result of a complex interplay of several coexisting factors, many of which may be simple to correct. [ 8 ]  Up to 80% of people may have more than one abnormality that is contributing. [ 9 ]  Deficits of individual functional components of the continence mechanism can be partially compensated for a certain period, until the compensating components themselves fail. For example,  obstetric  injury may precede onset by decades, but  postmenopausal  changes in the tissue strength reduce in turn the competence of the compensatory mechanisms. [ 1 ] [ 10 ]  The most common factors in the development are thought to be obstetric injury and after-effects of anorectal surgery, especially those involving the anal sphincters and hemorrhoidal vascular cushions. [ 1 ]  The majority of incontinent persons over the age of 18 fall into one of several groups: those with structural anorectal abnormalities (sphincter  trauma , sphincter degeneration,  perianal fistula , rectal prolapse),  neurological disorders  ( multiple sclerosis ,  spinal cord  injury,  spina bifida ,  stroke , etc.), constipation/ fecal loading  (presence of a large amount of feces in the rectum with stool of any consistency), cognitive and/or behavioral dysfunction ( dementia ,  learning disabilities ), diarrhea,  inflammatory bowel diseases  (e.g. ulcerative colitis, Crohn's disease), irritable bowel syndrome,  disability  related (people who are frail, acutely unwell, or have  chronic / acute  disabilities), and those cases which are  idiopathic  (of unknown cause). [ 8 ] [ 11 ]   Diabetes mellitus  is also known to be a cause, but the mechanism of this relationship is not well understood. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_611", "text": "Anorectal anomalies  and spinal cord defects may be a cause in children. These are usually picked up and operated upon during early life, but continence is often imperfect thereafter. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_612", "text": "The functioning of the  anal canal  can be damaged, traumatically or atraumatically. The resting tone of the anal canal is not the only important factor; both the length of the high-pressure zone and its radial translation of force are required for continence. This means that even with normal anal canal pressure, focal defects such as the  keyhole deformity  can be the cause of substantial symptoms.  External anal sphincter  (EAS) dysfunction is associated with impaired voluntary control, whereas  internal anal sphincter  (IAS) dysfunction is associated with impaired fine-tuning of fecal control. [ 1 ]   Lesions  which mechanically interfere with, or prevent the complete closure of the anal canal can cause a liquid stool or mucous  rectal discharge . Such lesions include  piles  (inflamed hemorrhoids),  anal fissures ,  anal cancer , or fistulae. Obstetric injury may tear the anal sphincters, and some of these injuries may be occult (undetected). The risk of injury is greatest when labor has been especially difficult or prolonged, when  forceps  are used, with higher  birth weights , or when a midline  episiotomy  is performed. Only when there is post-operative investigation of FI such as  endoanal ultrasound  is the injury discovered. [ 2 ]  FI is a much under-reported complication of surgery. The IAS is easily damaged with an anal  retractor  (especially the  Park's anal retractor ), leading to reduced resting pressure postoperatively. Since the hemorrhoidal vascular cushions contribute 15% of the resting anal tone, surgeries involving these structures may affect continence status. [ 2 ]  Partial internal  sphincterotomy ,  fistulotomy , anal stretch ( Lord's operation ),  hemorrhoidectomy  or transanal advancement flaps may all lead to FI postoperatively, with soiling being far more common than solid FI. The \"keyhole deformity\" refers to scarring within the anal canal and is another cause of mucus leakage and minor incontinence. This defect is also described as a groove in the anal canal wall and may occur after posterior midline  fissurectomy  or fistulotomy, or with lateral IAS defects. Rare causes of traumatic injury to the anal sphincters include military or traffic accidents complicated by  pelvic fractures , spine injuries or  perineal   lacerations , insertion of  foreign bodies  in the rectum, and  sexual abuse . [ 2 ]  Nontraumatic conditions causing anal sphincter weakness include  scleroderma , damage to the  pudendal nerves , and IAS degeneration of unknown cause. [ 5 ]  Radiation-induced FI may involve the anal canal as well as the rectum, when  proctitis , anal fistula formation, and diminished function of internal and external sphincter occur. [ 2 ]  Irradiation may occur during  radiotherapy , e.g. for  prostate cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_613", "text": "Many people with FI have a generalized weakness of the  pelvic floor , especially  puborectalis . [ 5 ]  A weakened puborectalis leads to widening of the anorectal angle and impaired barrier to the stool in the rectum entering the anal canal, and this is associated with incontinence to solids. Abnormal descent of the pelvic floor can also be a sign of pelvic floor weakness. Abnormal descent manifests as  descending perineum syndrome  (>4\u00a0cm perineal descent). [ 5 ]  This syndrome initially gives constipation, and later FI. The pelvic floor is innervated by the  pudendal nerve  and the  S3  and  S4  branches of the  pelvic plexus . With recurrent straining, e.g. during difficult labour or long-term constipation, then stretch injury can damage the nerves supplying  levator ani . The pudendal nerve is especially vulnerable to irreversible damage, (stretch-induced pudendal  neuropathy ) which can occur with a 12% stretch. [ 2 ]  If the pelvic floor muscles lose their innervation, they cease to contract and their muscle fibres are in time replaced by fibrous tissue, which is associated with pelvic floor weakness and incontinence. Increased pudendal nerve terminal motor latency may indicate pelvic floor weakness. Any damage to the pudendal nerve occurring during childbirth may not become fully apparent until years later, for example at the onset of  menopause . [ 13 ]  The various types of prolapse of the posterior compartment (e.g.  external rectal prolapse ,  mucosal prolapse  and  internal rectal intussusception  &  solitary rectal ulcer syndrome ) may also cause coexisting  obstructed defecation . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_614", "text": "The  rectum  needs to be of a sufficient volume to store stool until defecation. The rectal walls need to be \"compliant\" i.e. able to distend to an extent to accommodate stool. Rectal sensation is required to detect the presence, nature, and amount of rectal contents. The rectum must also be able to evacuate its contents fully. There must also be efficient coordination of rectal sensation and relaxation of the anal canal. [ 14 ]   Rectal storage capacity (i.e. rectal volume + rectal compliance) may be affected in the following ways. Surgery involving the rectum (e.g.  lower anterior resection , often performed for colorectal cancer), radiotherapy directed at the rectum, and inflammatory bowel disease can cause scarring, which may result in the walls of the rectum becoming stiff and inelastic, reducing compliance. Reduced rectal storage capacity may lead to urge incontinence, where there is an urgent need to defecate as soon as stool enters the rectum, where normally stool would be stored until there was enough to distend the rectal walls and initiate the defecation cycle. Tumors and  rectal strictures  also may impair reservoir function. Conversely, increased rectal volume ( megarectum ), may cause fecal loading and overflow FI (see  overflow incontinence ). Reduced rectal sensation may be a contributory factor. [ citation needed ]  If the sensory nerves are damaged, the detection of stool in the rectum is dulled or absent, and the person will not feel the need to defecate until too late. Rectal hyposensitivity may manifest as constipation, FI, or both. Rectal hyposensitivity was reported to be present in 10% of people with FI. [ 15 ]  Pudendal neuropathy is one cause of rectal hyposensitivity and may lead to fecal loading/impaction, megarectum and overflow FI. [ 16 ]  Normal evacuation of rectal contents is 90\u2013100%. [ 2 ]  If there is incomplete evacuation during defecation, residual stool will be left in the rectum and threaten continence once defecation is finished. This is a feature of people with soiling secondary to obstructed defecation. [ 17 ]  Obstructed defecation is often due to  anismus  (paradoxical contraction or relaxation failure of the puborectalis). [ 2 ] :\u200a38\u200a  Whilst anismus is largely a  functional disorder ,  organic  pathologic lesions may mechanically interfere with rectal evacuation. Other causes of incomplete evacuation include non-emptying defects like a  rectocele . Straining to defecate pushes stool into the rectocele, which acts like a  diverticulum  and causes stool sequestration. Once the voluntary attempt to defecate, albeit dysfunctional, is finished, the voluntary muscles relax, and residual rectal contents are then able to descend into the anal canal and cause leaking. [ 2 ] :\u200a37"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_615", "text": "Nitrates ,  calcium channel antagonists ,  beta-adrenoceptor antagonists  ( beta-blockers ),  sildenafil ,  selective serotonin reuptake inhibitors"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_616", "text": "Cephalosporins ,  penicillins ,  macrolides"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_617", "text": "Glyceryl trinitrate  ointment,  diltiazem  gel,  bethanechol  cream,  botulinum toxin  A injection"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_618", "text": "Laxatives ,  metformin ,  orlistat , selective serotonin reuptake inhibitors, magnesium-containing  antacids ,  digoxin"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_619", "text": "Loperamide ,  opioids ,  tricyclic antidepressants , aluminium-containing antacids,  codeine"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_620", "text": "Benzodiazepines , tricyclic antidepressants, selective serotonin reuptake inhibitors,  anti-psychotics"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_621", "text": "Continence requires conscious and subconscious networking of information from and to the anorectum. Defects/brain damage may affect the  central nervous system  focally (e.g. stroke, tumor, spinal cord lesions, trauma, multiple sclerosis) or diffusely (e.g. dementia, multiple sclerosis, infection,  Parkinson's disease  or drug-induced). [ 1 ] [ 19 ]  FI (and  urinary incontinence ) may also occur during  epileptic seizures . [ 20 ]   Dural ectasia  is an example of a spinal cord lesion that may affect continence. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_622", "text": "Liquid stool is more difficult to control than formed, solid stool. Hence, FI can be exacerbated by diarrhea. [ 8 ]  Some consider diarrhea to be the most common aggravating factor. [ 2 ]   [ citation needed ]  Where diarrhea is caused by temporary problems such as mild infections or food reactions, incontinence tends to be short-lived. Chronic conditions, such as irritable bowel syndrome or  Crohn's disease , can cause severe diarrhea lasting for weeks or months. Diseases, drugs, and indigestible dietary fats that interfere with the  intestineal  absorption may cause  steatorrhea  (oily rectal discharge & fatty diarrhea) and degrees of FI. Respective examples include  cystic fibrosis ,  orlistat , and  olestra .  Postcholecystectomy diarrhea  is diarrhea that occurs following gall bladder removal, due to excess  bile acid . [ 22 ]  Orlistat is an  anti-obesity  (weight loss) drug that blocks the absorption of fats. This may give side effects of FI, diarrhea, and steatorrhea. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_623", "text": "This may occur when there is a large mass of feces in the rectum (fecal loading), which may become hardened ( fecal impaction ). Liquid stool elements can pass around the obstruction, leading to incontinence. Megarectum (enlarged rectal volume) and rectal hyposensitivity are associated with overflow incontinence. Hospitalized patients and care home residents may develop FI via this mechanism, [ 8 ]  possibly a result of lack of mobility, reduced alertness, the constipating effect of medication, and/or dehydration. In overflow incontinence, the rectum is constantly distended because of the presence of retained feces in the rectum. [ 24 ]  Therefore, the recto-anal inhibitory reflex (RAIR) is persistently activated, meaning the internal anal sphincter relaxes, which is not under voluntary control. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_624", "text": "The mechanisms and factors contributing to normal continence are multiple and interrelated. The puborectalis sling, forming the anorectal angle (see diagram), is responsible for the gross continence of solid stool. [ 5 ]  The IAS is an involuntary muscle, contributing about 55% of the resting anal pressure. Together with the hemorrhoidal vascular cushions, the IAS maintains continence of flatus and liquid during rest. The EAS is a voluntary muscle, that doubles the pressure in the anal canal during contraction, which is possible for a short time. The  rectoanal inhibitory reflex (RAIR)  is an involuntary IAS relaxation in response to rectal distension, allowing some rectal contents to descend into the anal canal where it is brought into contact with specialized sensory mucosa to detect consistency. The rectoanal excitatory reflex (RAER) is an initial, semi-voluntary contraction of the EAS and puborectalis which in turn prevents incontinence following the RAIR. Other factors include the specialized anti-peristaltic function of the last part of the sigmoid colon, which keeps the rectum empty most of the time, sensation in the lining of the rectum and the anal canal to detect when there is stool present, its consistency and quantity, and the presence of normal rectoanal reflexes and defecation cycle which completely evacuates stool from the rectum and anal canal. Problems affecting any of these mechanisms and factors may be involved in the cause. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_625", "text": "Identification of the exact causes usually begins with a thorough  medical history , including detailed questioning about symptoms, bowel habits, diet, medication, and other medical problems.  Digital rectal examination  is performed to assess resting pressure and voluntary contraction (maximum squeeze) of the sphincter complex and puborectalis. Anal sphincter defects, rectal prolapse, and abnormal perineal descent may be detected. [ 5 ]  Anorectal physiology tests assess the functioning of the anorectal anatomy.  Anorectal manometry  records the pressure exerted by the anal sphincters and puborectalis during rest and contraction. The procedure is also able to assess the sensitivity of the anal canal and rectum.  Anal electromyography  tests for nerve damage, which is often associated with obstetric injury. Pudendal nerve terminal motor latency tests for damage to the pudendal motor nerves. Proctography, also known as  defecography , shows how much stool the rectum can hold, how well the rectum holds it, and how well the rectum can evacuate the stool. It will also highlight defects in the structure of the rectum such as  internal rectal intussusception . Dynamic pelvic  MRI , also called MRI defecography is an alternative that is better for some problems but not as good for other problems. [ 25 ]   Proctosigmoidoscopy  involves the insertion of an  endoscope  (a long, thin, flexible tube with a camera) into the anal canal, rectum and sigmoid colon. The procedure allows for visualization of the interior of the gut and may detect signs of disease or other problems that could be a cause, such as inflammation, tumors, or scar tissue. Endoanal ultrasound, which some consider the gold standard for detection of anal canal lesions, [ 26 ]  evaluates the structure of the anal sphincters and may detect occult sphincter tears that otherwise would go unseen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_626", "text": "Functional  FI is common. [ 27 ]  The  Rome process  published  diagnostic criteria  for functional FI, which they defined as \"recurrent uncontrolled passage of fecal material in an individual with a developmental age of at least four years\". The diagnostic criteria are, one or more of the following factors present for the last 3 months: abnormal functioning of normally innervated and structurally intact muscles, minor abnormalities of sphincter structure/innervation (nerve supply), normal or disordered bowel habits, (i.e., fecal retention or diarrhea), and psychological causes. Furthermore, exclusion criteria are given. These are factors that all must be excluded for a diagnosis of functional FI, and are abnormal innervation caused by lesion(s) within the brain (e.g., dementia), spinal cord (at or below  T12 ), or  sacral nerve  roots, or mixed lesions (e.g., multiple sclerosis), or as part of a generalized peripheral or autonomic neuropathy (e.g., due to diabetes), anal sphincter abnormalities associated with a multisystem disease (e.g., scleroderma), and structural or neurogenic abnormalities that are the major cause. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_627", "text": "There is no globally accepted definition, [ 1 ]  but fecal incontinence is generally defined as the recurrent inability to voluntarily control the passage of bowel contents through the anal canal and expel it at a socially acceptable location and time, occurring in individuals over the age of four. [ 1 ] [ 2 ] [ 5 ] [ 8 ] [ 10 ]  \"Social continence\" has been given various precise definitions for the purposes of research; however, generally it refers to symptoms being controlled to an extent that is acceptable to the individual in question, with no significant effect on their life. There is no consensus about the best way to classify FI, [ 8 ]  and several methods are used."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_628", "text": "Symptoms can be directly or indirectly related to the loss of bowel control. The direct (primary) symptom is a lack of control over bowel contents which tends to worsen without treatment. Indirect (secondary) symptoms, which are the result of leakage, include  pruritus ani  (an intense itching sensation from the anus), perianal  dermatitis  (irritation and inflammation of the skin around the anus), and urinary tract infections. [ 1 ]  Due to embarrassment, people may only mention secondary symptoms rather than acknowledge incontinence. Any major underlying cause will produce additional signs and symptoms, such as protrusion of mucosa in external  rectal prolapse . Symptoms of fecal leakage (FL) are similar and may occur after defecation. There may be loss of small amounts of brown fluid and staining of the underwear. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_629", "text": "FI can be divided into those people who experience a defecation urge before leakage (urge incontinence), and those who experience no sensation before leakage (passive incontinence or soiling). [ 8 ]  Urge incontinence is characterized by a sudden need to defecate, with little time to reach a  toilet . Urge and passive FI may be associated with weakness of the  external anal sphincter  (EAS) and  internal anal sphincter  (IAS) respectively. Urgency may also be associated with reduced rectal volume, reduced ability of the rectal walls to distend and accommodate stool, and increased rectal sensitivity. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_630", "text": "There is a continuous spectrum of different clinical presentations from incontinence of flatus (gas), through incontinence of mucus or liquid stool, to solids. The term  anal incontinence  often is used to describe  flatus incontinence [ 8 ]  (that is, involuntary loss of flatus). [ 29 ]  In other sources, the term  anal incontinence  is distinguished as involuntary loss of feces or flatus caused by loss of control of the anal sphincter; [ 29 ] [ 30 ]  whereas  fecal incontinence  may be given the definition of involuntary loss of solid or liquid feces which may also be caused by enlarged skin tags, poor hygiene, hemorrhoids, rectal prolapse, and fistula in ano. [ 29 ] [ 30 ] [ 31 ]  It may occur together with incontinence of liquids or solids, or it may present in isolation. Flatus incontinence may be the first sign of FI. [ 2 ]  Once continence to flatus is lost, it is rarely restored. [ 8 ]  Anal incontinence may be equally disabling as the other types. [ 32 ]  However, the term  anal incontinence  is also often used interchangeably as a synonym for FI generally, [ 33 ]  and use a wider definition for FI which includes \nuncontrolled passage of feces or gas. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_631", "text": "Fecal leakage, fecal soiling and fecal seepage are minor degrees of FI, and describe incontinence of liquid stool, mucus, or very small amounts of solid stool. They cover a spectrum of increasing symptom severity (staining, soiling, seepage, and accidents). [ 1 ]  Rarely, minor FI in adults may be described as  encopresis . Fecal leakage is a related topic to  rectal discharge , but this term does not necessarily imply any degree of incontinence. Discharge generally refers to conditions where there is  pus  or increased mucus production, or anatomical  lesions  that prevent the anal canal from closing fully, whereas fecal leakage generally concerns disorders of IAS function and functional evacuation disorders which cause a solid fecal mass to be retained in the  rectum . Solid stool incontinence may be called complete (or major) incontinence, and anything less as partial (or minor) incontinence (i.e. incontinence of flatus (gas), liquid stool and/or mucus). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_632", "text": "In children over the age of four who have been toilet trained, a similar condition is generally termed encopresis (or soiling), which refers to the voluntary or involuntary loss of (usually soft or semi-liquid) stool. [ 35 ]  The term pseudoincontinence is used when there is FI in children who have anatomical defects (e.g. enlarged  sigmoid colon  or anal  stenosis ). [ 2 ]  Encopresis is a term that is usually applied when there are no such anatomical defects present. The  ICD-10  classifies nonorganic encopresis under \"behavioural and emotional disorders with onset usually occurring in childhood and adolescence\" and organic causes of encopresis along with FI. [ 36 ]  FI can also be classified according to gender, since the cause in females may be different from males, for example it may develop following radical  prostatectomy  in males, [ 37 ]  whereas females may develop FI as an immediate or delayed consequence of damage whilst giving birth.  Pelvic anatomy  is also different according to gender, with a wider  pelvic outlet  in females. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_633", "text": "Several severity scales exist. The  Cleveland Clinic  (Wexner) fecal incontinence score takes into account five parameters that are scored on a scale from zero (absent) to four (daily) frequency of incontinence to gas, liquid, solid, of need to wear pad, and of lifestyle changes. [ 1 ]  The Park's incontinence score uses four categories:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_634", "text": "The fecal incontinence severity index is based on four types of leakage (gas, mucus, liquid stool, solid stool) and five frequencies (once to three times per month, once per week, twice per week, once per day, twice or more per day). Other severity scales include AMS, Pescatori, Williams score, Kirwan, Miller score, Saint Mark's score, and the Vaizey scale. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_635", "text": "FI may present with signs similar to rectal discharge (e.g. fistulae, proctitis, or rectal prolapse), pseudoincontinence, encopresis (with no organic cause), and irritable bowel syndrome. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_636", "text": "FI is generally treatable with conservative management, surgery, or both. [ 2 ]  The success of treatment depends upon the exact causes and how easily these are corrected. [ 8 ]  Treatment choice depends on the cause and severity of the disease, and the motivation and general health of the person affected. Commonly, conservative measures are used together, and if appropriate surgery is carried out. Treatments may be attempted until symptoms are satisfactorily controlled. A treatment algorithm based upon the cause has been proposed, including conservative, non-operative and surgical measures (neosphincter refers to either  dynamic graciloplasty  or artificial bowel sphincter, lavage refers to retrograde rectal irrigation). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_637", "text": "Conservative measures include dietary modification, drug treatment, retrograde anal irrigation, biofeedback retraining anal sphincter exercises. Incontinence products refer to devices such as  anal plugs  and  perineal pads  and garments such as  diapers/nappies . Perineal pads are efficient and acceptable for only minor incontinence. [ 2 ]  If all other measures are ineffective  removing the entire colon  may be an option. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_638", "text": "Dietary modification may be important for successful management. [ 5 ]  Both diarrhea and constipation can contribute to different cases, so dietary advice must be tailored to address the underlying cause or it may be ineffective or counterproductive. In persons with disease aggravated by diarrhea or those with rectal loading by soft stools, the following suggestions may be beneficial: increase  dietary fiber ; reduce  wholegrain   cereals / bread ; reduce fruit and vegetables which contain natural laxative compounds ( rhubarb ,  figs ,  prunes / plums ); limit  beans ,  pulses ,  cabbage  and  sprouts ; reduce  spices  (especially   chili ); reduce  artificial sweeteners  (e.g. sugar-free  chewing gum ); reduce  alcohol  (especially  stout ,  beer  and  ale ); reduce  lactose  if there is some degree of  lactase deficiency ; and reduce  caffeine . Caffeine lowers the resting tone of the anal canal and also causes diarrhea. Excessive doses of  vitamin C ,  magnesium ,  phosphorus  and/or  calcium  supplements may increase FI. Reducing the olestra fat substitute, which can cause diarrhea, may also help. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_639", "text": "Pharmacological management may include anti-diarrheal/constipating agents and laxatives/stool bulking agents. Stopping or substituting any previous medication that causes diarrhea may be helpful in some (see  table ). There is no good evidence for the use of any medications, however. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_640", "text": "In people who have undergone  gallbladder removal , the  bile acid sequestrant   cholestyramine  may help minor degrees of FI. [ 41 ]  Bulking agents also absorb water, so may be helpful for those with diarrhea. A common side effect is  bloating  and  flatulence .  Topical agents  to treat and prevent dermatitis may also be used, such as topical  antifungals  when there is evidence of perianal  candidiasis  or occasionally mild topical anti-inflammatory medication. Prevention of secondary lesions is carried out by perineal cleansing,  moisturization , and the use of a skin protectant. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_641", "text": "Evacuation aids ( suppositories  or  enemas ) e.g.  glycerine  or  bisacodyl  suppositories may be prescribed. People may have a poor resting tone of the anal canal, and consequently may not be able to retain an enema, in which case  transanal irrigation  (retrograde anal irrigation) may be a better option, as this equipment utilizes an inflatable catheter to prevent loss of the irrigation tip and to provide a water tight seal during irrigation. A volume of lukewarm water is gently pumped into the colon via the anus. People can be taught how to perform this treatment in their own homes, but it does require special equipment. If the irrigation is efficient, the stool will not reach the rectum again for up to 48 hours. [ 43 ]  By regularly emptying the bowel using transanal irrigation, controlled bowel function is often re-established to a high degree in patients with bowel incontinence and/or constipation. This enables control over the time and place of evacuation and the development of a consistent bowel routine. [ 43 ]  However, persistent leaking of residual irrigation fluid during the day may occur and make this option unhelpful, particularly in persons with obstructed defecation syndrome who may have an incomplete evacuation of any rectal contents. Consequently, the best time to carry out the irrigation is typically in the evening, allowing any residual liquid to be passed the next morning before leaving the home. Complications such as  electrolyte imbalance  and  perforation  are rare. The effect of transanal irrigation varies considerably. Some individuals experience complete control of incontinence, and others report little or no benefit. [ 43 ]  It has been suggested that if appropriate, people be offered home retrograde anal irrigation. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_642", "text": "Biofeedback  (the use of equipment to record or amplify and then feed back activities of the body) is a commonly used and researched treatment, but the benefits are uncertain. [ 44 ]  Biofeedback therapy varies in the way it is delivered, but it is unknown if one type has benefits over another. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_643", "text": "The role of  pelvic floor exercises  and anal sphincter exercises in FI is poorly determined. While there may be some benefits they appear less useful than implanted sacral nerve stimulators. These exercises aim to increase the strength of the pelvic floor muscles (mainly levator ani). The anal sphincters are not technically part of the pelvic floor muscle group, but the EAS is a voluntary, striated muscle that therefore can be strengthened in a similar manner. It has not been established whether pelvic floor exercises can be distinguished from anal sphincter exercises in practice by the people doing them. This kind of exercise is more commonly used to treat urinary incontinence, for which there is a sound evidence base for effectiveness. More rarely are they used in FI. The effect of anal sphincter exercises are variously stated as an increase in the strength, speed, or endurance of voluntary contraction (EAS). [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_644", "text": "Electrical stimulation can also be applied to the anal sphincters and pelvic floor muscles, inducing muscle contraction without traditional exercises (similar to  transcutaneous electrical nerve stimulation , TENS). The evidence supporting its use is limited, and any benefit is tentative. [ 45 ]  In light of the above, intra-anal electrical stimulation (using an anal probe as an electrode) appears to be more efficacious than intra-vaginal (using a vaginal probe as an electrode). [ 45 ]  Rarely, skin reactions may occur where the electrodes are placed, but these issues typically resolve when the stimulation is stopped. Surgically implanted  sacral nerve stimulation  may be more effective than exercises, and electrical stimulation and biofeedback may be more effective than exercises or electrical stimulation by themselves. [ 44 ]  TENS is also sometimes used to treat FI by  transcutaneous tibial nerve stimulation . [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_645", "text": "In a minority of people, anal plugs may be useful for either standalone therapy or in concert with other treatments. [ 47 ]  Anal plugs (sometimes termed tampons) aim to block the involuntary loss of fecal material, and they vary in design and composition. [ 8 ]   Polyurethane  plugs were reported to perform better than those made of polyvinyl-alcohol. [ 47 ]  Plugs are less likely to help those with frequent bowel movements, [ 2 ]  and many find them difficult to tolerate. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_646", "text": "In women, a device that functions as an inflatable balloon in the vagina has been approved for use in the United States. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_647", "text": "Surgery may be carried out if conservative measures alone are not sufficient to control incontinence. There are many surgical options, and their relative effectiveness is debated due to a lack of good-quality evidence. The optimal treatment regime may be both surgical and non-surgical treatments. [ 49 ]  The surgical options can be considered in four categories: restoration and improvement of residual sphincter function (sphincteroplasty, sacral nerve stimulation, tibial nerve stimulation, correction of anorectal deformity), replacement/imitation of the sphincter or its function (anal encirclement,  SECCA procedure , non-dynamic graciloplasty,  perianal injectable bulking agents  and  implantable bulking agents ), dynamic sphincter replacement (artificial bowel sphincter, dynamic graciloplasty), antegrade continence enema ( Malone procedure ), and finally fecal diversion (e.g. colostomy). [ 1 ]  A surgical treatment algorithm has been proposed. Isolated sphincter defects (IAS/EAS) may be initially treated with sphincteroplasty and if this fails, the person can be assessed for sacral nerve stimulation. Functional deficits of the EAS and/or IAS (i.e. where there is no structural defect, or only limited EAS structural defect, or with neurogenic incontinence) may be assessed for sacral nerve stimulation. If this fails, neosphincter with either dynamic graciloplasty or artificial anal sphincter may be indicated. Substantial muscular and/or neural defects may be treated with neosphincter initially. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_648", "text": "FI is thought to be very common, [ 1 ]  but much under-reported due to embarrassment. One study reported a prevalence of 2.2% in the general population. [ 2 ]  It affects people of all ages but is more common in older adults (but it should not be considered a normal part of aging). [ 50 ]  Females are more likely to develop it than males (63% of those with FI over 30 may be female). [ 1 ]  In 2014, the  National Center for Health Statistics  reported that one out of every six seniors in the U.S. who lived in their own homes or apartment had FI. Men and women were equally affected. [ 51 ]  45\u201350% of people with FI have severe physical and/or mental disabilities. [ 1 ]  People with dementia are four times more likely to have fecal incontinence compared to people of similar ages. [ 52 ] [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_649", "text": "Risk factors include age, female gender, urinary incontinence, history of vaginal delivery (non- Caesarean section  childbirth), obesity, [ 32 ]  prior anorectal surgery, poor general health, and physical limitations. Combined urinary and fecal incontinence is sometimes termed double incontinence, and it is more likely to be present in those with urinary incontinence. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_650", "text": "Traditionally, FI was thought to be an insignificant complication of surgery, but it is now known that a variety of different procedures are associated with this possible complication, and sometimes at high levels. Examples are midline internal sphincterotomy (8% risk), lateral internal sphincterotomy,  fistulectomy , fistulotomy (18\u201352%), hemorrhoidectomy (33%),  ileo-anal reservoir reconstruction , lower anterior resection, total abdominal colectomy,  ureterosigmoidostomy , [ 32 ]  and  anal dilation  (Lord's procedure, 0-50%). [ 55 ]  Some authors consider obstetric trauma to be the most common cause. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_651", "text": "While the first mention of urinary incontinence occurs in 1500 BC in the  Ebers Papyrus , the first mention of FI in a medical context is unknown. [ 57 ]  For many centuries, colonic irrigation was the only treatment available. Stoma creation was described in AD 1776, FI associated with rectal prolapse in AD 1873 and anterior sphincter repair in AD 1875. During the mid 20th century, several operations were developed for instances where the sphincters were intact but weakened. [ 58 ]  Muscle transpositions using the  gluteus maximus  or the gracilis were devised, but did not become used widely until later. End-to-end sphincteroplasty is shown to have a high failure rate in 1940. In AD 1971, Parks and McPartlin first describe an overlapping sphincteroplasty procedure. Biofeedback is first introduced in 1974. [ 59 ]  In 1975, Parks describes post anal repair, a technique to reinforce the pelvic floor and EAS to treat idiopathic cases. Endoanal ultrasound is invented in 1991, which starts to demonstrate the high number of occult sphincter tears following vaginal deliveries. In 1994, the use of an endoanal coil during pelvic MRI shows greater detail of the anal canal than previously. During the last 20 years, dynamic graciliplasty, sacral nerve stimulation, injectable perianal bulking agents and radiofrequency ablation have been devised, mainly due to the relatively poor success rates and high morbidity associated with the earlier procedures. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_652", "text": "Persons with this symptom are frequently ridiculed and ostracized in public. It has been described as one of the most psychologically and socially debilitating conditions in an otherwise healthy individual. In older people, it is one of the most common reasons for admission into a care home. Persons who develop FI earlier in life are less likely to marry and obtain employment. Often, people will go to great lengths to keep their condition secret. It has been termed \"the silent affliction\" since many do not discuss the problem with their close family, employers, or clinicians. They may be subject to gossip, hostility, and other forms of social exclusion. [ 60 ] [ 61 ] [ 62 ]  The economic cost has not received much attention."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_653", "text": "In the Netherlands, a 2004 study estimated that total costs of patients with fecal incontinence were \u20ac2169 per patient per year. Over half of this was productivity loss in work. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_654", "text": "In the US, the average lifetime cost (treatment and follow-up) was $17,166 per person in 1996. The average hospital charge for sphincteroplasty was $8555 per procedure. Overall, in the US, the total charges associated with surgery increased from $34 million in 1998 to $57.5 million in 2003.  Sacral nerve  stimulation, dynamic  graciloplasty , and  colostomy  were all shown to be cost-effective. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_655", "text": "Some insults in Japan relate to incontinence, such as  kusotare/kusottare  and  shikkotare  which mean  shit hanger/leaker/oozer  and  piss leaker/oozer  respectively, though these have not been in common use since the 1980s. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_656", "text": "The case  Hiltibran et al v. Levy et al  in the  United States District Court for the Western District of Missouri  resulted in that court issuing an order in 2011. That order requires  incontinence briefs  funded by  Medicaid  to be given by the State of Missouri to adults who would be institutionalized without them. [ 66 ] [ 67 ] [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_657", "text": "Engineered  anal sphincters grown from  stem cells  have been successfully implanted in mice. New blood vessels developed and the tissue displayed normal contraction and relaxation. In the future, these methods may become part of the management of FI, replacing the need for high-morbidity implanted devices such as the artificial bowel sphincter. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_658", "text": "Fibrosing colonopathy  is a disease that arises in people with  cystic fibrosis  treated with high doses of  pancreatic enzyme supplements . [ 1 ] [ 2 ]  Symptoms are non-specific with  abdominal pain ,  abdominal swelling ,  vomiting , and  constipation . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_659", "text": "Risk factors include being young, prior surgery of the intestines, and the use of certain medications including  corticosteroids  and  H2 blockers . [ 2 ]  It may appear similar to  distal intestinal obstruction syndrome  or  inflammatory colitis  such as  Crohn's disease . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_660", "text": "A maximum dose of 10,000 IU of  lipase  per kilogram per day is recommended for  pancreatic enzyme supplementation  to prevent this condition. [ 3 ]  More than 60 cases have been described as of 1999. [ 2 ]  The disease was suggested to be caused by  methacrylic acid copolymer  which is used as coating for delayed release of enzymes but there is no reliable evidence for that. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_661", "text": "Clinical symptoms of fibrosing colonopathy can be similar to those of  intestinal obstruction  and include  constipation  or  diarrhea ,  abdominal pain ,  hematochezia , [ 5 ]   vomiting ,  nausea , and poor weight gain. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_662", "text": "The precise etiopathogenesis is still unknown. Young age (2\u201313 years), gastrointestinal history (DIOS,  meconium ileus ), abdominal surgery in the past,  HDPE , and use of  histamine H2-receptor blockers ,  corticosteroids , or recombinant human  deoxyribonuclease  (DNase) are risk factors. [ 7 ]  Fibrosing colonopathy and  cystic fibrosis  have a strong correlation. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_663", "text": "The afflicted colon's histologic findings include thickening of the  muscularis propria , submucosal fibrosis, a cobblestone-like appearance, and persistent mucosal inflammation. [ 8 ]  With relative rectal sparing, imaging can demonstrate diffuse narrowing, shortening, and loss of haustration of the colonic lumen. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_664", "text": "One of the most common locations for a  foreign body  is the  alimentary tract . It is possible for foreign bodies to enter the tract either from the  mouth , [ 1 ]  or from the  rectum . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_665", "text": "The objects most commonly swallowed by children are  coins . [ 3 ]  Meat impaction, resulting in  esophageal food bolus obstruction  is more common in adults. [ 4 ]  Swallowed objects are more likely to lodge in the  esophagus  or  stomach  than in the  pharynx  or  duodenum . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_666", "text": "If the person who swallowed the foreign body is doing well, usually an  x-ray  image will be taken which will show any metal objects, and this will be repeated a few days later to confirm that the object has passed all the way through the digestive system. Also it needs to be confirmed that the object is not stuck in the airways, in the bronchial tree. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_667", "text": "Most objects that are swallowed will, if they have passed the  pharynx , pass all the way through the  gastrointestinal tract  unaided. [ 6 ]  However, sometimes an object becomes arrested (usually in the terminal  ileum  or the  rectum ) or a sharp object penetrates the  bowel  wall. If the foreign body causes problems like pain, vomiting or bleeding it must be removed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_668", "text": "Swallowed  batteries  can be associated with additional damage, [ 7 ] [ 8 ]  with  mercury poisoning  (from  mercury batteries ) and  lead poisoning  (from  lead batteries ) presenting important risks. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_669", "text": "While swallowed coins typically traverse the alimentary tract without further incident, care must be taken to monitor patients, as reaction of the metals in the coin with gastric acid and other digestive juices may produce various toxic compounds if the coin remains within the alimentary tract for a prolonged period of time. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_670", "text": "Endoscopic foreign body retrieval  is the first-line treatment for removal of a foreign body from the alimentary tract. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_671", "text": "Glucagon  has been used to treat esophageal foreign bodies, with the intent that it relaxes the smooth muscle of the lower esophageal spincter to allow the foreign body to pass into the stomach. [ 10 ]  However, evidence does not support a benefit of treatment with glucagon, and its use may result in side effects. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_672", "text": "In 2018, an international team of six  paediatric  health-care professionals undertook a self-administered test, by swallowing a  Lego  piece (specifically, a  Lego minifigure   head ) and checking when the pieces appeared. They developed a Stool Hardness and Transit (SHAT) score to normalise stool consistency over time, and resulted in a Found and Retrieved Time (FART) score.  The principal finding of this study, the FART score (n = 5), ranged from 1.14\u2009days (27\u2009h 20\u2009min) to 3.04\u2009days (72\u2009h 35\u2009min), with an average retrieval time of 1.71\u2009days. Their conclusion: \"This international, multicentre trial identified that small objects, such as those swallowed by children, are likely to pass in 1\u20133 days without complication. This should offer reassurance for parents.\" [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_673", "text": "Functional gastrointestinal disorders  ( FGID ), also known as  disorders of gut\u2013brain interaction , include a number of separate  idiopathic  disorders which affect different parts of the  gastrointestinal tract  and involve  visceral hypersensitivity  and  motility  disturbances. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_674", "text": "Using the Delphi method, the  Rome Foundation  and its board of directors, chairs and co-chairs of the  ROME IV  committees developed the current definition for disorders of gut-brain interaction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_675", "text": "A group of disorders classified by GI symptoms related to any combination of: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_676", "text": "Terms such as  functional colonic disease  (or  functional bowel disorder ) refer in medicine to a group of  bowel  disorders which are characterized by chronic abdominal complaints without a structural or biochemical cause that could explain symptoms. Other  functional  disorders relate to other aspects of the process of  digestion . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_677", "text": "The consensus review process of meetings and publications organised by the Rome Foundation, known as the  Rome process , has helped to define the functional gastrointestinal disorders. [ 3 ]  Successively, the Rome I, Rome II, Rome III and Rome IV proposed consensual classification system and terminology, as recommended by the Rome Coordinating Committee. These now include classifications appropriate for adults, children and neonates/toddlers. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_678", "text": "The current  ROME IV classification , published in 2016, is as follows: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_679", "text": "A. Esophageal disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_680", "text": "B. Gastroduodenal disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_681", "text": "C. Bowel disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_682", "text": "D. Centrally mediated disorders of gastrointestinal pain"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_683", "text": "E. Gallbladder and sphincter of Oddi disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_684", "text": "F. Anorectal disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_685", "text": "G. Childhood functional GI disorders: Neonate/Toddler"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_686", "text": "H. Childhood functional GI disorders: Child/Adolescent"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_687", "text": "FGIDs share in common any of several physiological features including increased motor reactivity, enhanced visceral hypersensitivity, altered mucosal immune and inflammatory function (associated with bacterial  dysbiosis ), and altered central nervous system and  enteric nervous system  (CNS-ENS) regulation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_688", "text": "The pathophysiology of FGID has been best conceptualized using  biopsychosocial model  help to explain the relationships between an individual factors in their early life that in turn can influence their psychosocial factor and physiological functioning. This model also shows the complex interactions between these factors through the  brain-gut axis . [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ]  These factors affect how FGID manifest in terms of symptoms but also affect the clinical outcome. These factors are interconnected and the influences on these factors are bidirectional and mutually interactive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_689", "text": "Early life factors include genetic factors, psychophysiological and sociocultural factors, and environmental exposures."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_690", "text": "There is a strong link between FGIDs and psychosocial factors. Psychosocial factors influence the functioning of the GI tract through the brain-gut axis, including the GI tract's motility, sensitivity, and barrier function. Psychosocial factors also affect experience and behavior, treatment selection, and clinical outcome."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_691", "text": "Psychological stress or one's emotional response to stress exacerbates gastrointestinal symptoms and may contribute to FGID development and maintenance. [ 2 ] [ 13 ]  Specifically in children and adolescents, anxiety and depression may present as FGID-associated somatic complaints, such as  nausea ,  vomiting , and  abdominal pain . [ 14 ]  Similarly,  anxiety  in individuals with FGIDs is linked to greater pain severity, frequency, duration, chronicity, and disabling effects. [ 15 ]  This is because psychological stress can impact the gut's mucosal barrier functions, allowing bacteria and bacterial products to migrate and cause pain, diarrhea, and other GI symptoms. Conversely, since the  brain-gut axis  is bidirectional, GI inflammation and injury can amplify pain signals to the brain and contribute to worsened mental status, including  anxiety  and  depression  symptoms. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_692", "text": "Individuals with FGIDs may also experience poor socialization. Due to the nature of the disease, individuals with an FGID may have difficulty with regular school or work attendance and participation in extracurricular activities, leading to isolation and a lack of peer support. This lack of peer support may lead to depression and loneliness, conditions which exacerbate FGIDs symptoms. [ 16 ]  In addition, children with FGIDs are more likely to experience bullying. As such, stressful situations which influence socialization (seen as either a lack thereof or negative experiences) may lead to an impaired functioning in patients with FGIDs. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_693", "text": "Family interactions may also play a role in the development of FGIDs through their effects on the physical and psychosocial functioning of an individual. Family factors which may influence the development of an FGID include child attachment style, maladaptive parenting behaviors (paternal rejection and hostility), and even the parents' health status, as children of chronically ill parents experience increased  somatization , insecure attachment, and worsened biopsychosocial functioning. [ 18 ]  Each of these factors leads to the accumulation of stressors, which can ultimately lead to the development of an FGID. In addition, family units which have a member with an FGIDs diagnosis are more likely to face family functioning difficulties, including challenges to familial roles, communication, affective involvement, organization, and cohesion. These challenges arise due to the nature of the disease, and ultimately worsen symptoms for the FGID patient. [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_694", "text": "The physiology of FGID is characterized by abnormal motility, visceral hypersensitivity as well as dysregulation of the  immune system  and barrier function of the GI tract as well as inflammatory changes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_695", "text": "The brain-gut axis is a bidirectional mechanism in which psychosocial factors influence the GI tract and vice versa. Specifically, the emotional and cognitive centers of the brain influence GI activity and immune cell function, and the microbes within the gut regulate mood, cognition, and mental health. [ 29 ]  These two systems interact through several mechanisms. There are direct, physical connections between the central nervous system and nerve plexuses to the visceral muscles. In addition, neurotransmitters send signals related to thoughts, feelings, and pain regulation from the brain to the GI tract. The brain-gut axis influences the entire body through a variety of pathways; it regulates sensory, motor, endocrine, autonomic, immune, and inflammatory reactions. Within the physical and psychological interactions of FGIDs specifically, psychiatric disorders such as anxiety, depression, and even autism are well-linked to GI dysfunction. Conversely, functional GI diseases are linked to several comorbid psychiatric diseases. [ 29 ]  Negative emotions such as fear, anxiety, anger, stress, and pain may delay gastric emptying, decrease intestinal and colonic transit time, and induce defecation and diarrhea. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_696", "text": "Because FGIDs are known to be multifactorial with external stressors and environmental factors playing a role in their development, current research demonstrates that psychological treatments may be effective in relieving some symptoms of the disease. Interventions such as cognitive behavioral therapy (CBT), hypnotherapy, and biofeedback-assisted relaxation training (BART) each show promise in symptom reduction. [ 30 ]  Each of these therapies aims to alter an individual's thought patterns and behaviors while improving self-efficacy, which all work together to improve health outcomes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_697", "text": "Cognitive behavioral therapy is a treatment based on the theory that thinking affects one's feelings and behaviors. As such, alterations in one's thought process can have a positive or negative effect on actions and perceptions. Through the lens of FGIDs, a negative thought pattern may be associated with a negative physical experience of abdominal pain, discomfort, and general sickness. In theory, retraining the patient's thought patterns can alleviate these symptoms and improve quality of life. In patients with FGIDs, CBT is an effective treatment option; one study found 87.5% of participants to be completely pain-free following treatment. [ 16 ]  Internet-based CBT (iCBT) is similarly effective, and may be a good treatment option for individuals who either cannot afford or otherwise lack access to traditional CBT. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_698", "text": "Hypnotherapy, another method for reducing symptoms of FGIDs, teaches users how to alter their perception of uncomfortable sensations in the body. Gut-directed hypnotherapy specifically gives greater improvements in symptoms than standard treatment of the disease. [ 18 ]  Research demonstrates directed hypnotherapy to be an effective mechanism of reducing visceral hypersensitivity (a low pain threshold of the internal organs) and sympathetic activity, due to the reduced activity of the anterior cingulated cortex and state of relaxation achieved during hypnosis. [ 32 ]  For patients with irritable bowel syndrome (IBS) and functional abdominal pain (FAP), hypnotherapy reduces pain intensity and frequency. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_699", "text": "BART therapies monitor the physiological changes occurring with thoughts, feelings, and emotions. These therapies aim to teach patients how to visualize the effects of the interventions they are undergoing. BART is used to improve mood and somatic responses to anxiety disorders, which may relieve some of the psychological and physiological symptoms of FGIDs. [ 33 ]  The visual, real-time feedback given through BART empowers the patient to see the difference that the therapy is making, thus giving the patient control over the physiological components of the disease. This allows the patient to maximize their mind-body connection and eventually optimize symptom management and quality of life. BART allows the patient to break the positive feedback loop of anxiety and pain, thus reducing disease exacerbations."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_700", "text": "Antidepressants have been thoroughly studied as a potential treatment for FGIDs. Tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and selective norepinephrine reuptake inhibitors (SNRIs) show the most promise in treating some of the symptoms of FGIDs. TCAs, specifically amitriptyline, show promising results when examining common FGIDs symptoms such as pain and poor quality of life. [ 34 ]  SNRIs also demonstrate pain-relieving qualities. [ 30 ]  SSRIs are less effective in pain management, but may reduce symptoms of anxiety and depression, which would, in turn, reduce some FGIDs symptoms. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_701", "text": "Functional gastrointestinal disorders are very common. Globally, irritable bowel syndrome and functional dyspepsia alone may affect 16\u201326% of the population. [ 1 ] [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_702", "text": "There is considerable research into the causes, diagnosis and treatments for FGIDs. Diet, microbiome, genetics, neuromuscular function and immunological response all interact. [ 1 ]  A role for mast cell activation has been proposed as one of the factors. [ 36 ] [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_703", "text": "A  fundic gland polyp  is a type of  polyp , found in the  fundus  of the  stomach . Fundic gland polyps are found in 0.8 to 1.9% of patients who undergo  esophagogastroduodenoscopy , and are more common in middle-aged women. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_704", "text": "The risk of malignancy is very low or none, when sporadic. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_705", "text": "Fundic gland polyposis  is a medical syndrome with multiple fundic gland polyps. The condition has been described both in patients with  familial adenomatous polyposis  (FAP) and attenuated variants (AFAP), and in patients in whom it occurs sporadically. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_706", "text": "Fundic gland polyposis  is a medical syndrome where the  fundus  and the  body  of the  stomach  develop many  fundic gland polyps . The condition has been described both in patients with  familial adenomatous polyposis  (FAP) and attenuated variants (AFAP), and in patients in whom it occurs sporadically. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_707", "text": "Most patients with fundic gland polyps (FGPs) do not have any symptoms, and the diagnosis is made on  gastroscopy  done for other reasons.  Retrospective analysis of patients with sporadic FGPs shows that a high percentage do have symptoms, but that this is more likely to be related to the underlying disease responsible for the polyposis. [ 2 ]   These symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_708", "text": "The polyps on endoscopy are usually tiny, numerous and  sessile , [ 3 ]  and usually scattered throughout the fundus of the stomach, where  parietal cells  are more numerous.  They have the same colour as the gastric mucosa, and never have a stalk. [ 4 ] \nWhen the polyps are  biopsied , the pathology typically shows shortened  gastric pits , and both superficial and deep cystic lesions in the fundic glands, lined by all three types of cells of acid-producing mucosa: mucous,  parietal and chief cells. As sometimes parietal cell hyperplasia may develop deep dilations of gland, [ 5 ]  one should be really strict in the diagnosis of FGPs (i.e. the presence of deep and superficial dilations). Infrequently, the two lesions may coexist. [ 3 ]   Foci of dysplasia can sometimes be seen. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_709", "text": "FGPs can be found in association with the following genetic conditions: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_710", "text": "Sporadic FGPs [ 1 ]  have been associated with:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_711", "text": "The development of polyps depends on the underlying disorder. [ 17 ]  In sporadic cases of FGPs, more than 90% of patients have activating mutations in the \u03b2-catenin gene, so that they may be considered \"neoplastic\" polyps. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_712", "text": "In familial adenomatous polyposis, the abnormality is a mutation in the APC gene, resulting in its inactivity.  Attenuated FAP can occur from other mutations in the APC gene, and causes a  phenotype  wherein  colonic  polyps may be few in number. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_713", "text": "Both the \u03b2-catenin gene and the APC gene are involved in the same cell growth signalling pathway, but the APC gene is known to have a significantly higher association with the development of colorectal tumors. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_714", "text": "The most important consideration in evaluating patients with FGPs is distinguishing between sporadic form (patients without any other gastrointestinal condition, usually in middle age with female prevalence) and syndromic form.  This is to ascertain the risk of development of  gastric cancer  and to ascertain the risk of concomitant  colon cancer . [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_715", "text": "There is a risk of development of cancer with fundic gland polyposis, [ 22 ]  but it varies based on the underlying cause of the polyposis. [ 4 ]   The risk is highest with congenital polyposis syndromes, and is lowest in acquired causes. [ 4 ] [ 23 ]   As a result, it is recommended that patients with multiple fundic polyps have a  colonoscopy  to evaluate the colon. [ 4 ]  If there are polyps seen on colonoscopy,  genetic testing  and testing of family members is recommended. [ 4 ] \nIn the gastric adenocarcinoma associated with proximal polyposis of the stomach (GAPPS), there is a high risk of early development of proximal gastric adenocarcinoma. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_716", "text": "It is still unclear which patients would benefit with surveillance  gastroscopy , but most physicians recommend endoscopy every one to three years to survey polyps for dysplasia or cancer. [ 4 ]   In the event of high grade dysplasia, polypectomy, which is done through the endoscopy, or partial  gastrectomy  may be recommended.  One study showed the benefit of  NSAID  therapy in regression of gastric polyps, but the efficacy of this strategy (given the side effects of NSAIDs) is still dubious. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_717", "text": "Gallstone ileus  is a rare form of  small bowel obstruction  caused by an impaction of a  gallstone  within the  lumen  of the  small intestine . Such a gallstone enters the bowel via a  cholecysto - enteric   fistula . The presence of large stones, >2.5\u00a0cm in diameter, within the gallbladder are thought to predispose to fistula formation by gradual erosion through the  gallbladder  fundus. [ 1 ]  Once a fistula has formed, a stone may travel from the gallbladder into the bowel and become lodged almost anywhere along the  gastrointestinal tract .  Obstruction occurs most commonly at the near the distal  ileum , within 60\u00a0cm proximally to the ileocecal valve. [ 2 ] [ 3 ]  Rarely, gallstone ileus may recur if the underlying fistula is not treated. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_718", "text": "First described by  Thomas Bartholin  in 1654, the name \"gallstone ileus\" is a misnomer because an  ileus  is, by definition, a  non-mechanical  bowel motility failure  (as opposed to a mechanical obstruction by a stone)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_719", "text": "Diagnosis of gallstone ileus requires radiographic studies.  Classic radiographic findings are known as  Rigler's triad : [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_720", "text": "Initial management involves fluid resuscitation and potentially nasogastric suctioning. [ 1 ]  Since gallstone ileus constitutes a form of mechanical small bowel obstruction, it can be a surgical emergency and requires open or laparoscopic surgery to remove an impacted stone. [ 1 ]  The different strategies for surgical management are either enterolithotomy alone, allowing a delayed  cholecystectomy  after an inflammation-free period of 4\u20136 weeks (and therefore two-stage surgery) or enterolithotomy in combination with a  cholecystectomy  and  fistula  division (one-stage surgery). The different strategies for surgical management are controversial, and depend on factors such as patient fitness for surgery and comorbidities. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_721", "text": "Bouveret's syndrome  refers to reverse gallstone ileus where the gallstone propagates proximally and causes gastric outlet obstruction by being impacted in first part of duodenum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_722", "text": "Gastrointestinal bleeding  ( GI bleed ), also called  gastrointestinal hemorrhage  ( GIB ), is all forms of  bleeding  in the  gastrointestinal tract , from the  mouth  to the  rectum . [ 9 ]  When there is significant  blood  loss over a short time, symptoms may include  vomiting red blood ,  vomiting black blood ,  bloody stool , or  black stool . [ 1 ]  Small amounts of bleeding over a long time may cause  iron-deficiency anemia  resulting in  feeling tired  or  heart-related chest pain . [ 1 ]  Other symptoms may include  abdominal pain ,  shortness of breath ,  pale skin , or  passing out . [ 1 ] [ 9 ]  Sometimes in those with small amounts of bleeding no symptoms may be present. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_723", "text": "Bleeding is typically divided into two main types:  upper gastrointestinal bleeding  and  lower gastrointestinal bleeding . [ 2 ]  Causes of upper GI bleeds include:  peptic ulcer  disease,  esophageal varices  due to liver  cirrhosis  and  cancer , among others. [ 3 ]   Causes of lower GI bleeds include:  hemorrhoids , cancer, and  inflammatory bowel disease  among others. [ 2 ] [ 1 ]  Small amounts of bleeding may be detected by  fecal occult blood  test. [ 1 ]   Endoscopy  of the lower and upper gastrointestinal tract may locate the area of bleeding. [ 1 ]   Medical imaging  may be useful in cases that are not clear. [ 1 ]  Bleeding may also be diagnosed and treated during  minimally invasive   angiography  procedures such as  hemorrhoidal artery embolization . [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_724", "text": "Initial treatment focuses on  resuscitation  which may include  intravenous fluids  and  blood transfusions . [ 4 ]  Often blood transfusions are not recommended unless the  hemoglobin  is less than 70 or 80\u00a0g/L. [ 7 ] [ 12 ]  Treatment with  proton pump inhibitors ,  octreotide , and  antibiotics  may be considered in certain cases. [ 5 ] [ 6 ] [ 13 ]  If other measures are not effective, an  esophageal balloon  may be attempted in those with presumed esophageal varices. [ 2 ]   Endoscopy of the esophagus, stomach, and duodenum  or  endoscopy of the large bowel  are generally recommended within 24\u00a0hours and may allow treatment as well as diagnosis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_725", "text": "An upper GI bleed is more common than lower GI bleed. [ 2 ]  An upper GI bleed occurs in 50 to 150 per 100,000 adults per year. [ 8 ]  A lower GI bleed is estimated to occur in 20 to 30 per 100,000 per year. [ 2 ]  It results in about 300,000 hospital admissions a year in the  United States . [ 1 ]  Risk of death from a GI bleed is between 5% and 30%. [ 1 ] [ 7 ]  Risk of bleeding is more common in males and increases with age. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_726", "text": "Gastrointestinal bleeding can be roughly divided into two clinical syndromes:  upper gastrointestinal bleeding  and  lower gastrointestinal bleeding . [ 2 ]  About 2/3 of all GI bleeds are from upper sources and 1/3 from lower sources. [ 14 ]  Common causes of gastrointestinal bleeding include  infections ,  cancers , vascular disorders, adverse effects of medications, and  blood clotting disorders . [ 2 ]  Obscure gastrointestinal bleeding (OGIB) is when a source is unclear following investigation. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_727", "text": "Upper gastrointestinal bleeding is from a source between the  pharynx  and the  ligament of Treitz . An upper source is characterised by  hematemesis  (vomiting up blood) and  melena  (tarry stool containing altered blood). About half of cases are due to  peptic ulcer disease  ( gastric  or  duodenal ulcers ). [ 3 ]   Esophageal inflammation  and erosive disease are the next most common causes. [ 3 ]  In those with  liver cirrhosis , 50\u201360% of bleeding is due to  esophageal varices . [ 3 ]  Approximately half of those with peptic ulcers have an  H. pylori  infection. [ 3 ]  Other causes include  Mallory-Weiss tears , cancer, and  angiodysplasia . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_728", "text": "A number of medications are found to cause upper GI bleeds. [ 16 ]   NSAIDs  or  COX-2 inhibitors  increase the risk about fourfold. [ 16 ]   SSRIs ,  corticosteroids , and  anticoagulants  may also increase the risk. [ 16 ]  The risk with  dabigatran  is 30% greater than that with  warfarin . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_729", "text": "Lower gastrointestinal bleeding is typically from the colon, rectum or anus. [ 2 ]  Common causes of lower gastrointestinal bleeding include  hemorrhoids , cancer, angiodysplasia,  ulcerative colitis ,  Crohn's disease , and  aortoenteric fistula . [ 2 ]  It may be indicated by the passage of  fresh red blood rectally , especially in the absence of  bloody vomiting . Lower gastrointestinal bleeding could also lead to melena if the bleeding occurs in the small intestine or proximal colon. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_730", "text": "Gastrointestinal bleeding can range from small non-visible amounts, which are only detected by laboratory testing, to massive bleeding where bright red blood is passed and  shock  develops. Rapid bleeding may cause  syncope . [ 18 ]  The presence of bright red blood in stool, known as  hematochezia , typically indicates lower gastrointestinal bleeding. Digested blood from the upper gastrointestinal tract may appear black rather than red, resulting in \"coffee ground\" vomit or melena. [ 2 ]  Other signs and symptoms include  feeling tired ,  dizziness , and pale skin color. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_731", "text": "A number of foods and medications can turn the stool either red or black in the absence of bleeding. [ 2 ]   Bismuth  found in many antacids may turn stools black as may  activated charcoal . [ 2 ]  Blood from the vagina or urinary tract may also be confused with blood in the stool. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_732", "text": "Diagnosis is often based on direct observation of blood in the stool or vomit.  Although  fecal occult blood  testing has been used in an emergency setting, this use is not recommended as the test has only been validated for colon cancer screening. [ 19 ]  Differentiating between upper and lower bleeding in some cases can be difficult. The severity of an upper GI bleed can be judged based on the  Blatchford score [ 4 ]  or  Rockall score . [ 16 ]  The Rockall score is the more accurate of the two. [ 16 ]  As of 2008 there is no scoring system useful for lower GI bleeds. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_733", "text": "Gastric aspiration and or lavage , where a tube is inserted into the stomach via the nose in an attempt to determine if there is blood in the stomach, if negative does not rule out an upper GI bleed [ 20 ]  but if positive is useful for ruling one in. [ 14 ]  Clots in the stool indicate a lower GI source while melana stools an upper one. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_734", "text": "Recommended laboratory blood testing includes: cross-matching blood, hemoglobin, hematocrit, platelets, coagulation time, and electrolytes. [ 4 ]  If the ratio of  blood urea nitrogen  to  creatinine  is greater than 30 the source is more likely from the upper GI tract. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_735", "text": "A  CT angiography  is useful for determining the exact location of the bleeding within the gastrointestinal tract. [ 21 ]  Nuclear scintigraphy is a sensitive test for detecting occult gastrointestinal bleeding when direct imaging with upper and lower endoscopies are negative. Direct angiography allows for embolization of a bleeding source, but requires a bleeding rate faster than 1mL/minute. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_736", "text": "In patients with significant varices or cirrhosis  nonselective \u03b2-blockers  reduce the risk of future bleeding. [ 13 ]  With a target heart rate of 55\u00a0beats per minute B-blockers reduce the absolute risk of bleeding by 10%. [ 13 ]   Endoscopic band ligation  (EBL) is also effective at improving outcomes. [ 13 ]  Either B-blockers or EBL is recommended as initial preventative measures. [ 13 ]  In patients who have had a previous variceal bleed both treatments are recommended. [ 13 ]  Some evidence supports the addition of  isosorbide mononitrate . [ 23 ]  Testing for and treating those who are positive for  H. pylori  is recommended. [ 16 ]   Transjugular intrahepatic portosystemic shunting  (TIPS) may be used to prevent bleeding in people who re-bleed despite other measures. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_737", "text": "Among patients admitted to the ICU with high risk of bleeding, a PPI or H2RA appears useful. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_738", "text": "The initial focus is on  resuscitation  beginning with airway management and fluid resuscitation using either intravenous fluids and or blood. [ 4 ]  A number of medications may improve outcomes depending on the source of the bleeding. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_739", "text": "Based on evidence from people with other health problems  crystalloid  and  colloids  are believed to be equivalent for peptic ulcer bleeding. [ 4 ]   Proton pump inhibitor  (PPI) treatment before endoscopy may decrease the need for endoscopic hemostatic treatment, however it is not clear if this treatment reduces mortality, the risk of re-bleeding, or the  [ clarification needed ]  and the need for surgery. [ 26 ]  Oral and intravenous formulations may be equivalent; however, the evidence to support this is suboptimal. [ 27 ]  In those with less severe disease and where endoscopy is rapidly available, they are of less immediate clinical importance. [ 26 ]  There is tentative evidence of benefit for  tranexamic acid  which inhibits clot breakdown. [ 28 ]   Somatostatin  and  octreotide , while recommended for varicial bleeding, have not been found to be of general use for non variceal bleeds. [ 4 ]  After treatment of a high risk bleeding ulcer endoscopically giving a PPI once or a day rather than as an infusion appears to work just as well and is less expensive (the method may be either by mouth or intravenously). [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_740", "text": "For initial fluid replacement, colloids or  albumin  is preferred in people with cirrhosis. [ 4 ]  Medications typically include  octreotide  or, if not available,  vasopressin  and  nitroglycerin  to reduce portal venous pressures. [ 13 ]   Terlipressin  appears to be more effective than octreotide, but it is not available in many areas of the world. [ 16 ] [ 30 ]  It is the only medication that has been shown to reduce mortality in acute variceal bleeding. [ 30 ]  This is in addition to  endoscopic banding  or  sclerotherapy  for the varices. [ 13 ]  If this is sufficient then  beta blockers  and  nitrates  may be used for the prevention of re-bleeding. [ 13 ]  If bleeding continues, balloon tamponade with a  Sengstaken-Blakemore tube  or  Minnesota tube  may be used in an attempt to mechanically compress the varices. [ 13 ]  This may then be followed by a  transjugular intrahepatic portosystemic shunt . [ 13 ]  In those with cirrhosis,  antibiotics  decrease the chance of bleeding again, shorten the length of time spent in hospital, and decrease mortality. [ 5 ]  Octreotide reduces the need for blood transfusions [ 31 ]  and may decrease mortality. [ 32 ]  No trials of  vitamin K  have been conducted. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_741", "text": "The evidence for benefit of blood transfusions in GI bleed is poor with some evidence finding harm. [ 8 ]  In those in  shock   O-negative packed red blood cells  are recommended. [ 2 ]  If large amounts of pack red blood cells are used additional  platelets  and  fresh frozen plasma  (FFP) should be administered to prevent  coagulopathies . [ 4 ]  In  alcoholics  FFP is suggested before confirmation of a coagulopathy due to presumed blood clotting problems. [ 2 ]  Evidence supports holding off on blood transfusions in those who have a  hemoglobin  greater than 7 to 8 g/dL and moderate bleeding, including in those with preexisting  coronary artery disease . [ 7 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_742", "text": "If the INR is greater than 1.5 to 1.8 correction with fresh frozen plasma or  prothrombin complex  may decrease mortality. [ 4 ]  Evidence of a harm or benefit of  recombinant activated factor VII  in those with liver diseases and gastrointestinal bleeding is not determined. [ 34 ]  A  massive transfusion protocol  may be used, but there is a lack of evidence for this indication. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_743", "text": "The benefits versus risks of placing a  nasogastric tube  in those with upper GI bleeding are not determined. [ 4 ]  Endoscopic evaluation within 24\u00a0hours is recommended, [ 4 ]  in addition to medical management. [ 35 ]  A number of endoscopic treatments may be used, including:  epinephrine  injection, band ligation, sclerotherapy, and fibrin glue depending on what is found. [ 2 ]  Prokinetic agents such as  erythromycin  before endoscopy can decrease the amount of blood in the stomach and thus improve the operators view. [ 4 ]  They also decrease the amount of blood transfusions required. [ 36 ]  Early endoscopy decreases hospital and the amount of blood transfusions needed. [ 4 ]  A second endoscopy within a day is routinely recommended by some [ 16 ]  but by others only in specific situations. [ 22 ]  Proton pump inhibitors, if they have not been started earlier, are recommended in those in whom high risk signs for bleeding are found. [ 4 ]  High and low dose PPIs appear equivalent at this point. [ 37 ]  It is also recommended that people with high risk signs are kept in hospital for at least 72\u00a0hours. [ 4 ]  Those at low risk of re-bleeding may begin eating typically 24 hours following endoscopy. [ 4 ]  If other measures fail or are not available,  esophageal balloon tamponade  may be attempted. [ 2 ]  While there is a success rate up to 90%, there are some potentially significant complications including  aspiration  and  esophageal perforation . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_744", "text": "Colonoscopy  is useful for the diagnosis and treatment of lower GI bleeding. [ 2 ]  A number of techniques may be employed including clipping, cauterizing, and sclerotherapy. [ 2 ]  Preparation for colonoscopy takes a minimum of six hours which in those bleeding briskly may limit its applicability. [ 38 ]  Surgery, while rarely used to treat upper GI bleeds, is still commonly used to manage lower GI bleeds by cutting out the part of the intestines that is causing the problem. [ 2 ]   Angiographic embolization  may be used for both upper and lower GI bleeds. [ 2 ]   Transjugular intrahepatic portosystemic shunting  (TIPS) may also be considered. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_745", "text": "Death in those with a GI bleed is more commonly due to other illnesses (some of which may have contributed to the bleed, such as cancer or cirrhosis) than the bleeding itself. [ 2 ]  Of those admitted to a hospital because of a GI bleed, death occurs in about 7%. [ 16 ]  Despite treatment, re-bleeding occurs in about 7\u201316% of those with upper GI bleeding. [ 3 ]  In those with esophageal varices, bleeding occurs in about 5\u201315% a year and if they have bled once, there is a higher risk of further bleeding within six weeks. [ 13 ]  Testing and treating  H. pylori  if found can prevent re-bleeding in those with peptic ulcers. [ 4 ]  The benefits versus risks of restarting blood thinners such as  aspirin  or  warfarin  and  anti-inflammatories  such as  NSAIDs  need to be carefully considered. [ 4 ]  If aspirin is needed for cardiovascular disease prevention, it is reasonable to restart it within seven days in combination with a PPI for those with nonvariceal upper GI bleeding. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_746", "text": "Gastrointestinal bleeding from the upper tract occurs in 50 to 150 per 100,000 adults per year. [ 8 ]  It is more common than lower gastrointestinal bleeding which is estimated to occur at the rate of 20 to 30 per 100,000 per year. [ 2 ]  Risk of bleeding is more common in males and increases with age. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_747", "text": "A  gastrojejunocolic fistula  is a disorder of the human  gastrointestinal tract . It may form between the transverse colon and the upper  jejunum  after a  Billroth II  surgical procedure.  (The Billroth procedure attaches the jejunum to the remainder of the stomach.) Fecal matter thereby passes improperly from the colon to the stomach, and causes  halitosis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_748", "text": "Patients may present with  diarrhea , [ 1 ]   weight loss  and  halitosis  as a result of fecal matter passing through the  fistula  from the colon into the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_749", "text": "Globus pharyngis ,  globus hystericus  or  globus sensation  is the persistent but painless sensation of having a pill, food  bolus , or some other sort of obstruction in the  throat  when there is none. Swallowing is typically performed normally, so it is not a true case of  dysphagia , but it can become quite irritating. It is common, with 22\u201345% of people experiencing it at least once in their lifetime. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_750", "text": "The \"lump in the throat\" sensation that characterizes globus pharyngis is often caused by  inflammation  of one or more parts of the throat, such as the  larynx  or  hypopharynx , due to  cricopharyngeal spasm ,  gastroesophageal reflux  (GERD), or  laryngopharyngeal reflux .\nIn some cases the cause is unknown and symptoms may be attributed to a  psychogenic  cause  i.e.  a  somatoform  or  anxiety disorder . It has been recognised as a symptom of depression, which responds to anti-depressive treatment. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_751", "text": "The results of recent studies have strongly suggested that  GERD  is a major cause of globus, though this remains under considerable debate. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_752", "text": "A less common cause, distinguished by a \"lump in the throat\" accompanied with clicking sensation and considerable pain when swallowing, may be due to thyroid-cartilage rubbing against anomalous asymmetrical laryngeal anatomy  e.g.  the superior cornu abrading against the  thyroid lamina , [ 6 ] [ 7 ]  surgically trimming the offending thyroid-cartilage provides immediate relief in all cases. [ 8 ]  However this cause is frequently misdiagnosed, despite requiring a simple clinical examination involving careful palpation of the neck side to side which elicits the same click sensation (laryngeal crepitus) and pain as when swallowing, most cases are due to prior trauma to the neck. [ 8 ]  High resolution  computed tomographic  (CT) or  MRI  scan of the larynx is usually required to fully understand the anomalous laryngeal anatomy. Anterior displacement of the thyroid ala on the affected side while swallowing can help resolve symptoms. [ citation needed ]  Other anomalous laryngeal anatomy with the potential to cause the globus sensation include thyroid nodules or parathyroid adenomas. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_753", "text": "As  globus sensation  is a symptom, a diagnosis of  globus pharyngis  is typically a  diagnosis of exclusion . If globus sensation is presenting with other symptoms such as pain, swallowing disorders such as aspiration or regurgitation (dysphagia), weight loss, or voice change, [ 10 ]  an organic cause needs to be investigated, typically with  endoscopy .  Barium swallows  are not recommended as a diagnostic tool as although they are less invasive than endoscopy and may be reassuring to the patient, they commonly miss sinister causes. It is very rare that globus sensation presenting with no other symptoms has a sinister cause and therefore endoscopy is not recommended in this case. [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_754", "text": "Differential diagnosis must be made from  Eagle syndrome  which uses the patient's description of \"something caught in my throat\" as a diagnostic tool. Eagle syndrome is an elongation of the styloid process causing irritation to nerves and muscles in the region resulting in a number of unusual symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_755", "text": "Reassurance of the patient is recommendable when no cause can be found.\nIf a cause is identified, treat the cause symptomatically or, if possible, systemically. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_756", "text": "Hematochezia  is a form of  blood in stool , in which fresh  blood  passes through the  anus  while  defecating . It differs from  melena , which commonly refers to blood in stool originating from  upper gastrointestinal bleeding  (UGIB). [ 1 ]  The term derives from Greek \u03b1\u1f37\u03bc\u03b1 (\"blood\") and \u03c7\u03ad\u03b6\u03b5\u03b9\u03bd (\"to defaecate\"). Hematochezia is commonly associated with  lower gastrointestinal bleeding , but may also occur from a brisk upper gastrointestinal bleed. The difference between hematochezia and  rectorrhagia  is that rectal bleeding is not associated with defecation; instead, it is associated with expulsion of fresh bright red blood without stools. [ 2 ]  The phrase  bright red blood per rectum  is associated with hematochezia and rectorrhagia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_757", "text": "In adults, most common causes are  hemorrhoids  and  diverticulosis , both of which are relatively benign; however, it can also be caused by  colorectal cancer , which is potentially fatal. In a newborn infant, haematochezia may be the result of swallowed maternal blood at the time of delivery, but can also be an initial symptom of  necrotizing enterocolitis , a serious condition affecting premature infants. In babies, hematochezia in conjunction with abdominal pain is associated with  intussusception . In  adolescents  and young adults,  inflammatory bowel disease , particularly  ulcerative colitis , is a serious cause of hematochezia that must be considered and excluded."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_758", "text": "Hematochezia can be due to  upper gastrointestinal bleeding .  However, as the blood from such a bleed is usually chemically modified by action of  acid  and  enzymes , it presents more commonly as black \"tarry\" feces known as  melena . Haematochezia from an upper gastrointestinal source is an ominous sign, as it suggests a very significant bleed which is more likely to be life-threatening. Eating  beetroot  can cause harmless red-colored feces ( beeturia ) because of insufficient metabolism of a red pigment, and is a differential sign that may be mistaken as hematochezia. Consumption of dragon fruit ( pitaya ) or blackberries may also cause red or black discoloration of the stool and sometimes the urine (pseudohematuria). This too, is a differential sign that is sometimes mistaken for hematochezia. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_759", "text": "In infants, the  Apt test  can be used to distinguish  fetal hemoglobin  from maternal blood."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_760", "text": "Other common causes of blood in the stool include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_761", "text": "A complete blood count as well as an hemoglobin test should be performed when a patient presents symptoms of hematochezia. A colonoscopy may be necessary if there is suspicion of bleed from colon particularly in the elderly to look for the site and many causes of bleed like carcinoma, ulcerative colitis, rectal varices or other lesions and in certain instances upper gastrointestinal endoscopy may be required as well to look for any rapid and massive fresh bleed from upper gastrointestinal tract when there may not be sufficient time for the change of colour of blood to occur. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_762", "text": "High-altitude flatus expulsion  ( HAFE ) is a  gastrointestinal  syndrome which involves the spontaneous passage of increased quantities of  rectal gases  at high altitudes. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_763", "text": "High-altitude flatus expulsion was first described by Joseph Hamel in c. 1820 [ 2 ]  and occasionally described afterward. [ 3 ]  A landmark study of this phenomenon was published in 1981 by  Paul Auerbach  and York Miller. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_764", "text": "The feeling of fullness or need to expel brought on by this differential in  atmospheric pressure  has been verified by studies involving  military pilots  subjected to pressure changes simulating flight. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_765", "text": "This  human digestive system  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_766", "text": "Hirschsprung's disease  ( HD  or  HSCR ) is a  birth defect  in which  nerves  are missing from parts of the  intestine . [ 1 ] [ 3 ]  The most prominent symptom is  constipation . [ 1 ]  Other symptoms may include  vomiting ,  abdominal pain ,  diarrhea  and  slow growth . [ 1 ]  Most children develop signs and symptoms shortly after birth. However, others may be diagnosed later in infancy or early childhood. [ 4 ] [ 5 ]  About half of all children with Hirschsprung's disease are diagnosed in the first year of life. [ 4 ]  Complications may include  enterocolitis ,  megacolon ,  bowel obstruction  and  intestinal perforation . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_767", "text": "The disorder may occur by itself or in association with other  genetic disorders  such as  Down syndrome  or  Waardenburg syndrome . [ 1 ] [ 2 ]  About half of isolated cases are linked to a specific genetic  mutation , and about 20% occur within families. [ 1 ]  Some of these occur in an  autosomal dominant  manner. [ 1 ]  The cause of the remaining cases is unclear. [ 1 ]  If otherwise normal parents have one child with the condition, the next child has a 4% risk of being affected. [ 2 ]  The condition is divided into two main types, short-segment and long-segment, depending on how much of the bowel is affected. [ 1 ]  Rarely, the  small bowel  may be affected, as well. [ 2 ]  Diagnosis is based on symptoms and confirmed by  biopsy . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_768", "text": "Treatment is generally by surgery to remove the affected section of bowel. [ 2 ]  The surgical procedure most often carried out is known as a \" pull through \". [ 3 ]  Occasionally, an  intestinal transplantation  may be recommended. [ 2 ]  Hirschsprung's disease occurs in about one in 5,000 of newborns. [ 1 ]  Males are more often affected than females. [ 1 ]  The condition is believed to have first been described in 1691 by Dutch anatomist  Frederik Ruysch [ 6 ]  and is named after Danish physician  Harald Hirschsprung  following his description in 1888. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_769", "text": "Typically, Hirschsprung disease is diagnosed shortly after birth, although it may develop well into adulthood,  because of the presence of  megacolon , or because the baby fails to pass the first stool ( meconium ) [ 9 ]  within 48 hours of delivery.  Normally, 90% of babies pass their first meconium within 24 hours, and 99% within 48 hours. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_770", "text": "Some other signs and symptoms in newborns include a swollen belly, vomiting (green or brown vomit), and flatulence. In older children, some other signs and symptoms include chronic constipation, flatulence, swollen belly, fatigue, and failure to thrive. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_771", "text": "Other symptoms include symptoms of bowel perforation such as vomiting, constipation, poor feeding, lethargy, and diarrhea. Symptoms of bowel obstruction would include vomiting of bile and abdominal distension. Those who do not pass stools after 36 to 48 hours after birth should raise suspicion of Hirschsprung disease. Such suspicion can also be risen if there is only passage of stools after suppository, rectal exam, or enema. Children who do not respond to constipation treatment for six months should also raise suspicion of such disease.  Enterocolitis , an acute complication of Hirschsprung disease, is characterised by sudden onset of fever, abdominal distension, vomiting, passage of bloody stools or release of explosive gas or stools after rectal examination. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_772", "text": "Some cases are diagnosed later, into childhood, but usually before age 10. [ 9 ]  The child may experience fecal retention, constipation, or abdominal distention. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_773", "text": "Hirschsprung's disease can also present as part of multi system disorders, such as: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_774", "text": "The disorder may occur by itself or in association with other  genetic disorders  such as  Down syndrome . [ 2 ]  About half of isolated cases are linked to a specific genetic  mutation  and about 20% occur within families. [ 1 ]  Some of these occur in an  autosomal dominant  manner. [ 1 ]  The cause of the remaining cases is unclear. [ 1 ]  If otherwise normal parents have one child with the condition, the next child has a 4% risk of being affected. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_775", "text": "Several  genes  and specific regions on chromosomes ( loci ) have been shown or suggested to be associated with Hirschsprung's disease [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_776", "text": "The  RET  proto-oncogene accounts for the highest proportion of both familial and sporadic cases, with a wide range of mutations scattered along its entire coding region. [ 20 ]  A  proto-oncogene   can cause cancer if it is mutated or overexpressed. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_777", "text": "RET  is a gene that codes for proteins that assist  cells of the neural crest  in their movement through the digestive tract during the development of the embryo.  Those neural crest cells eventually form bundles of nerve cells called ganglions.  EDNRB  codes for proteins that connect these nerve cells to the digestive tract. Thus, mutations in these two genes could directly lead to the absence of certain nerve fibers in the colon. Research suggests that several genes are associated with Hirschsprung's disease. [ 22 ]  Also, new research suggests that mutations in genomic sequences involved in regulating  EDNRB  have a bigger impact on Hirschsprung's disease than previously thought. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_778", "text": "RET  can mutate in many ways and is associated with Down syndrome.  Since Down syndrome is comorbid in 2% of Hirschsprung's cases, a likelihood exists that  RET  is involved heavily in both Hirschsprung's disease and Down syndrome.   RET  is also associated with  medullary thyroid cancer  and  neuroblastoma , which is a type of cancer common in children.  Both of these disorders are more common in Hirschsprung's patients than in the general population.  One function that  RE T controls is the travel of the  neural crest cells  through the intestines in the developing  fetus . The earlier the  RET  mutation occurs in Hirschsprung's disease, the more severe the disorder becomes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_779", "text": "Common and rare DNA variations in the neuregulin 1 ( NRG1 ) and NRG3 ( NRG3 ) were first shown to be associated with the disease in Chinese patients through a Genome Wide Association Study by the Hong Kong team in 2009  [ 23 ]  and 2012, respectively [ 24 ]  Subsequent studies in both Asian and Caucasian patients confirmed the initial findings by the University of Hong Kong. Both rare and common variants in these two genes have been identified in additional Chinese, [ 25 ]  Thai, Korean, Indonesian, and Spanish patients. These two genes are known to play a role in the formation of the enteric nervous system; thus, they are likely to be involved in the pathology of Hirschsprung's disease, at least in some cases. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_780", "text": "Another gene associated with this condition is NADPH oxidase, EF-hand calcium binding domain 5 ( NOX5 ). [ 26 ]  This gene is located on the long arm of  chromosome 15  (15q23). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_781", "text": "During normal  prenatal development ,  cells from the neural crest  migrate into the large intestine (colon) to form the networks of nerves called the  myenteric plexus  (Auerbach plexus) (between the  smooth muscle  layers of the gastrointestinal tract wall) and the  submucosal plexus  (Meissner plexus) (within the submucosa of the gastrointestinal tract wall). In Hirschsprung disease, the migration is not complete and part of the colon lacks these  nerve bodies  that regulate the activity of the colon. The affected segment of the  colon  cannot relax and pass  stool  through the colon, creating an obstruction. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_782", "text": "The most accepted theory of the cause of Hirschsprung is a defect in the craniocaudal migration of neuroblasts originating from the neural crest that occurs during the first 12 weeks of  gestation .  Defects in the differentiation of  neuroblasts  into ganglion cells and accelerated ganglion cell destruction within the intestine may also contribute to the disorder. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_783", "text": "This lack of ganglion cells in the myenteric and submucosal plexus is well documented in Hirschsprung's disease. [ 9 ]  With Hirschsprung's disease, the segment lacking neurons (aganglionic) becomes constricted, causing the normal, proximal section of bowel to become distended with feces. This narrowing of the distal colon and the failure of relaxation in the aganglionic segment are thought to be caused by the lack of neurons containing nitric oxide synthase. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_784", "text": "The most cited feature is absence of ganglion cells: notably in males, 75% have none in the end of the colon (rectosigmoid) and 8% lack ganglion cells in the entire colon. The enlarged section of the  bowel  is found proximally, while the narrowed, aganglionic section is found distally, closer to the end of the bowel. The absence of ganglion cells results in a persistent overstimulation of nerves in the affected region, resulting in contraction. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_785", "text": "The equivalent disease in horses is  lethal white syndrome . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_786", "text": "Definitive diagnosis is made by suction biopsy of the distally narrowed segment. [ 30 ]  A histologic examination of the tissue would show a lack of ganglionic nerve cells. Diagnostic techniques involve  anorectal manometry , [ 31 ]   barium enema , and rectal  biopsy . The suction rectal biopsy is considered the current international  gold standard  in the diagnosis of Hirschsprung's disease. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_787", "text": "Radiologic findings may also assist with diagnosis. [ 33 ]  An abdominal x-ray can reveal a lack of stool in the large intestine or a bulging caused by blocked stool. [ 34 ]  Cineanography ( fluoroscopy  of  contrast medium  passing anorectal region) assists in determining the level of the affected intestines. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_788", "text": "Treatment of Hirschsprung's disease consists of surgical removal (resection) of the abnormal section of the colon, followed by  reanastomosis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_789", "text": "The first stage of treatment used to be a reversible  colostomy .  In this approach, the healthy end of the large intestine is cut and attached to an opening created on the front of the abdomen. The contents of the bowel are discharged through the hole in the abdomen and into a bag.  Later, when the patient's weight, age, and condition are right, the \"new\" functional end of the bowel is connected with the anus. The first surgical treatment involving surgical resection followed by reanastomosis without a colostomy occurred as early as 1933 by Doctor Baird in  Birmingham  on a one-year-old boy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_790", "text": "The Swedish-American surgeon  Orvar Swenson  (1909\u20132012), who discovered the cause of Hirschsprung's, first performed its surgical treatment, the  pull-through surgery , in 1948. [ 36 ]  The pull-through procedure repairs the colon by connecting the functioning portion of the bowel to the anus. The pull-through procedure is the typical method for treating Hirschsprung's in younger patients. Swenson devised the original procedure, and the pull-through surgery has been modified many times. [ 37 ] '"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_791", "text": "Currently,  several different surgical approaches are used, which include the Swenson, Soave, Duhamel, and Boley procedures. [ 37 ]  The Swenson procedure leaves a small portion of the diseased bowel. The Soave procedure, named after the Italian pediatric surgeon,  Franco Soave \u00a0[ it ]  (1917\u20131984), leaves the outer wall of the colon unaltered. The Boley procedure, pioneered by the American surgeon,  Scott Boley  (born 1941), is a small modification of the Soave procedure, so the term \"Soave-Boley\" procedure is sometimes used. [ 38 ] [ 39 ]   The Duhamel procedure, named for the French pediatric surgeon  Bernard Duhamel  (1917\u20131996), uses a  surgical stapler  to connect the good and bad bowel. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_792", "text": "For the 15% of children who do not obtain full bowel control, other treatments are available. Constipation may be remedied by laxatives or a high-fiber diet. In those patients, serious dehydration can play a major factor in their lifestyles. A lack of bowel control may be addressed by an  ileostomy  \u2013 similar to a colostomy, but uses the end of the small intestine rather than the colon. The Malone antegrade colonic enema (ACE) is also an option. [ 40 ]  In a  Malone ACE , a tube goes through the abdominal wall to the appendix, or if available, to the colon. The bowel is then flushed daily. [ 41 ]  Children as young as 6 years of age may administer this daily flush on their own. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_793", "text": "If the affected portion of the lower intestine is restricted to the lower portion of the rectum, other surgical procedures may be performed, such as a posterior rectal myectomy. The prognosis is good in 70% of cases. Chronic postoperative constipation is present in 7 to 8% of the operated cases. Postoperative  enterocolitis , a severe manifestation, is present in the 10\u201320% of operated patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_794", "text": "According to a 1984 study conducted in  Maryland , Hirschsprung's disease appears in 18.6 per 100,000 live births. [ 42 ]   In Japan, it occurs at a similar rate of about one in 5,000 births (20 per 100,000). [ 43 ]  It is more common in male than female (4.32:1) and in white rather than nonwhite. [ 44 ]   Nine percent of the Hirschsprung cases were also diagnosed as having Down syndrome. [ 42 ]  Most cases are diagnosed before the patient is 10 years of age. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_795", "text": "The first report of Hirschsprung's disease dates to 1691, [ 45 ]  when it was described by  Dutch   anatomist   Frederik Ruysch . [ 46 ]  However, the disease is named after  Harald Hirschsprung , the  Danish  physician who first described two infants who died of this disorder in 1888. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_796", "text": "Hirschsprung's disease is a  congenital  disorder of the colon in which certain nerve cells, known as  ganglion cells , are absent, causing  chronic   constipation . [ 47 ]  In patients with Hirschsprung disease, both myenteric and submucosal plexuses are absent. [ 48 ]  A barium enema is the mainstay of diagnosis of Hirschsprung's, though a rectal biopsy showing the lack of ganglion cells is the only certain method of diagnosis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_797", "text": "The first publication on an important genetic discovery of the disease was from Martucciello Giuseppe  et al.  in 1992. The authors described a case of a patient with total colonic aganglionosis associated with a 46, XX, del 10 (q11.21 q21.2) karyotype. [ 49 ]  The major gene of Hirschsprung disease was identified in this chromosomal 10 region, it was the RET proto-oncogene. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_798", "text": "The usual treatment is \"pull-through\" surgery where the portion of the colon that does have nerve cells is pulled through and sewn over the part that lacks nerve cells. [ 51 ]  For a long time, Hirschsprung's was considered a multifactorial disorder, where a combination of nature and nurture was considered to be the cause. However, in August 1993, two articles by independent groups in  Nature Genetics  said that Hirschsprung's disease could be mapped to a stretch of  chromosome 10 . [ 52 ] [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_799", "text": "EDAR  ( EDAR hypohidrotic ectodermal dysplasia )"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_800", "text": "Hyperchlorhydria , sometimes called  chlorhydria ,  sour stomach  or  acid stomach , [ 1 ]   [ 2 ]  refers to the state in the  stomach  where  gastric acid  levels are higher than the  reference range . The  combining forms  of the name ( chlor-  +  hydr- ), referring to  chlorine  and  hydrogen , are the same as those in the name of  hydrochloric acid , which is the  active constituent  of gastric acid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_801", "text": "In humans, the normal  pH  is around 1 to 3, which varies throughout the day.  The highest basal secretion levels are in the late evening (around 12\u00a0A.M. to 3\u00a0A.M.).  Hyperchlorhydria is usually defined as having a pH less than 2."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_802", "text": "In  Zollinger\u2013Ellison syndrome   gastrin  levels are increased, leading to excess gastric acid production, which can cause  gastric ulcers . [ 3 ] \n Hypercalcemia  also increases gastrin and gastric acid and can cause ulcers. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_803", "text": "This article about a  disease , disorder, or medical condition is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_804", "text": "An  ileosigmoid knot  or  compound volvulus  is an uncommon cause of\u00a0 intestinal blockage . [ 1 ]  The condition arises when  ileum  loops wrap\u00a0around the bottom of a redundant  sigmoid  loop. [ 2 ]  In some countries in Africa, Asia, and the Middle East, the ileosigmoid knot is a well-known ailment; this condition is uncommon in the West. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_805", "text": "Ileosigmoid knotting typically manifests as sudden, severe  abdominal pain . It can quickly worsen into  sigmoid colon  and  ileum  gangrene, which can lead to potentially fatal side effects like  sepsis , generalized  peritonitis ,  electrolyte imbalance , and  dehydration . [ 4 ]   Abdominal pain  and tenderness (100%) and distension of the abdomen (94%\u2013100%),  vomiting  and  nausea  (87\u2013100%), rebound tenderness (69%), as well as  shock  (0\u201360%) are the main symptoms and presentation indicators. [ 3 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_806", "text": "The ileosigmoid knot is caused by three things: eating a high-bulk diet while the  small bowel  is empty; having a long,  sigmoid colon  on a tiny pedicle; and having a long, mesentery, and freely moving  small bowel . The intestines become more mobile when a semi-liquid, heavy meal moves into the proximal  jejunum , and the heavier sections of the  jejunum  fall to the left lower quadrant. Around the base of the narrow  sigmoid colon , the empty loops of the  ileum  and distal  jejunum  rotate in a clockwise direction. With two closed-loop\u00a0obstructions\u2014one in the small bowel and the other in the  sigmoid colon \u2014further  peristalsis  creates an ileosigmoid knot. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_807", "text": "Even though radiographic findings indicate colonic obstruction, which is uncommon in small bowel obstruction, clinical features like  vomiting  point to  small bowel obstruction . [ 7 ]  Ileosigmoid knotting is frequently confused radiographically with a straightforward  sigmoid volvulus . On the other hand, in contrast to  sigmoid volvulus , attempts to deflate the enlarged colon with a flatus tube or  sigmoidoscope  frequently fail and may even be hazardous in ileosigmoid knotting. This is because the ileum firmly encloses the sigmoid colon's base, thwarting any such attempt. [ 4 ]  These three characteristics\u2014the inability to insert a  sigmoidoscope , radiographic evidence of primarily  large bowel obstruction , and the clinical picture of small  bowel obstruction \u2014might make up a helpful diagnostic triad. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_808", "text": "Due to their unfamiliarity, the radiographic findings of ileosigmoid knotting\u2014which include multiple air-fluid levels in the small intestine and a double loop of dilated sigmoid shadow\u2014are only occasionally described. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_809", "text": "The descending colon, medial deviation of the cecum, and \"the whirl sign,\" which is produced by the twisted  intestinal tract  and sigmoid mesocolon in ileosigmoid knot, are findings in a  CT scan  that are suggestive of ileosigmoid knotting. Furthermore, some have observed the radial distribution of the mesenteric vasculature and the intestine and believe this to be useful diagnostic data. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_810", "text": "Ileosigmoid knotting has been classified into the three types listed below: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_811", "text": "Type 1:  The  ileum , which is the active component, encircles the  sigmoid colon , which is the passive component, either clockwise or counterclockwise (type A when clockwise and type B when counterclockwise). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_812", "text": "Type 2:  In either a clockwise or counterclockwise direction, the  sigmoid colon , the active component, encircles an  ileum  loop, the passive component. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_813", "text": "Type 3:  The  sigmoid colon  (passive component) is encircled by the  ileocecal  segment (active component). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_814", "text": "Aggressive resuscitation with fluid and  electrolytes , along with the correction of any  acid-base imbalance , are the initial management measures. The earliest possible surgical intervention should be performed following hemodynamic stabilization. After the procedure, appropriate  antibiotic  therapy is started as soon as possible and is continued for 5-7 days.  Metronidazole ,  aminoglycosides , and  cephalosporins  are the typical  antibiotic  combinations. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_815", "text": "Males account for 80.2% of cases of ileosigmoid knotting, with a mean age of 40 years (range: 4-90 years). The literature indicates the presence of additional secondary causative factors in addition to the aforementioned anatomic prerequisites, such as late pregnancy,\u00a0 Meckel's diverticulitis  with a band, trans mesenteric  herniation , floating  cecum , and\u00a0ileocecal  intussusceptions . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_816", "text": "Ileosigmoid knotting is uncommon in the white population, although it is primarily documented in some African, Asian, and Middle Eastern countries. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_817", "text": "E Parker is credited with describing the first case of ileosigmoid knotting in 1846. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_818", "text": "Impaction  is  bowel obstruction  that can occur in various kinds of  animals  when they consume something that they cannot  digest , typically  substrate . Once the substance is ingested it will block the  digestive tract  and, if untreated, cause death."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_819", "text": "Some symptoms include a lack of appetite or  lethargy . On many reptiles a large blue seemingly bruised spot will be visible in the  abdomen ; however, this only shows through if the skin on the species is clear enough to see the lower internal organs. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_820", "text": "Common treatments involve placing the reptile in a lukewarm bath and gently rubbing the area under the impaction to help the passing of the consumed substance. Place both thumbs on the back at the middle, put the first two fingers of the hand under the belly and rub gently in a circular way until the reptile defecates. If this fails, the animal must have an  enema . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_821", "text": "Indolent T cell lymphoproliferative disorder of the gastrointestinal tract  or  Indolent T cell lymphoproliferative disorder of the GI tract  (ITCLD-GT) is a rare and recently recognized disorder in which mature  T cell  lymphocytes accumulation abnormally in the gastrointestinal tract (GI tract). [ 1 ]  This accumulation causes various lesions (e.g.  polyps , thickened mucosal folds, small areas of redness, and superficial ulcerations) in the  mucosal  layer lining the GI tract. Individuals with ITCLD-GT commonly complain of chronic  GI tract symptoms  such as nausea, vomiting, diarrhea, abdominal pain, and  rectal bleeding . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_822", "text": "Carbonnell et al. [ 3 ]  first described a case of an indolent GI tract lymphoproliferation disorder in 1994 and defined the lymphocytes involved in it to be T cells expressing the  CD4   glycoprotein  on their  surface membranes . Subsequent studies reported on patients who had a similar indolent GI tract disorder that involved T cells which expressed either the CD4,  CD8 , or neither surface membrane glycoprotein. The disorder resembled certain aggressive GI tract lymphomas and was variably termed  indolent  lymphoma  or indolent T cell lymphoproliferative disorder of the gastrointestinal tract. [ 4 ]  However, the disease differed from the aggressive lymphomas which it mimicked in having a prolonged and usually non-progressive course. Furthermore, the disorder's lesions consisted of normal-appearing T cells that proliferated very slowly and usually caused little or no tissue destruction. [ 5 ]  In 2017, the  World Health Organization  provisionally classified ITCLD-GT as an extranodal (i.e. usually not involving  lymph nodes ), indolent disorder in which various subtypes of T cells proliferate in the GI tract. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_823", "text": "While usually acting like a benign disease, ITCLD-GT has malignant features:  1)  its normal-appearing T cells are  clonal  in nature, i.e. descended from a single cell; [ 6 ]   2)  these T cells may contain genetic abnormalities [ 7 ]  that are known to occur in and contribute to the development of very aggressive lymphomas; [ 8 ]  and  3)  ITCLD-GI, after many years of indolent behavior, may progress to an aggressive lymphoma. [ 2 ]  Thus, ITCLD-GT can act as a  premalignat disorder . Nonetheless, most cases of it run an indolent, non-malignant course and when mistakenly treated as an aggressive lymphoma, do not responded to standard  chemotherapy  treatments. [ 5 ]  The disorder has also been mistaken for, and found unresponsive to therapies that treat  inflammatory  or  autoimmune  bowel diseases. [ 1 ] [ 4 ]  Clinically, ITCLD-GT must be distinguished from the malignant, inflammatory, and autoimmune bowel diseases that it mimics in order to avoid useless and potentially harmful therapies. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_824", "text": "ITCLD-GT occurs more commonly in males of middle age (median age 48.4, range 15\u201377 years in one study). [ 2 ]  Individuals with the disease present with GI tract symptoms which often are serious and/or debilitating [ 9 ]  and may mimic those occurring in malignant lymphoproliferative, inflammatory, or autoimmune bowel diseases. [ 4 ]  These symptoms include chronic  epigastric  pain, abdominal pain, heartburn, nausea, diarrhea, vomiting, weight loss, relapsing oral ulcers, relapsing colorectal ulcers, rectal bleeding, and/or  night sweats . [ 4 ]  Several patients presenting with these symptoms have been diagnosed with and unsuccessfully treated for  peripheral T-cell lymphoma , [ 5 ]  an inflammatory bowel disease (either  Crohn disease  or  ulcerative colitis ), [ 1 ]  or the autoimmune GI tract disorder, celiac disease. [ 10 ]  It has been shown or appears very likely that these patients had ITCLD-GT rather than the cited diagnoses. [ 1 ] [ 5 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_825", "text": "Most patients with ITCLD-GT have chronic, relapsing and recurring GI tract symptoms that persist over many years. In one retrospective study, 19 of 23 patients with CD4+ ITCLD-GT had persistent disease over a follow-up period of 1\u201314 years (median 4.8 years), 2 of 23 patients had clinical and morphologic (i.e. negative GI tract evaluations) remissions enduring for at least 5\u20137 years, and 1 of 23 patients developed and died from a  large-cell lymphoma  of undetermined type. In the same study, 10 of 10 patients with CD8+ ITCLD-GT had persistent disease that had not progressed to a malignancy over an observation period of 1\u201318 years (median 2 years) although one patient had developed bone marrow involvement and therefore may have had disease which was in the process of transforming to a malignant state. [ 4 ]  Other reports have found that the disorder in one patient with CD4-, CD8- ITCLD-GT disease progressed to involve the liver [ 5 ]  and the disorder in two patients with CD4+ ITCLD-GT disease progressed to an undetermined type of  large T-cell lymphoma . [ 9 ]  In another retrospective analysis, 6 of 34 (17.6%) patients with ITCLD-GT progressed to a malignant state as evidenced by its spread to the blood or bone marrow: 2 (5.6%) patients died as a direct result of this spreading. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_826", "text": "The lesions in ITCLD-GT consists of slowly growing, mature, and benign-appearing T cells. The reasons for their accumulations in the GI tract are unclear. However, these cells often carry potentially  oncogenic  mutations. In a recent study, the T cells in 4 of 5 patients with CD4+ T-cell disease carried a  STAT3 - JAK2   fusion gene . [ 6 ]  This gene consists of a fusion between the  STAT3  gene at position 2.2 on the long (or \"g\") arm of  chromosome 17  (location abbreviated 17q21.2) and the  JAK2  gene at position 24.1 on the short (\"q\") of  chromosome 9  (9p24.1). The disorder in two of the patients with this t(9;17)(p24.1;q21/2) fusion gene progressed to malignant lymphomas. [ 9 ]  Abnormalities in the expression and/or activity of  STAT3  and  JAK2 [ 11 ]  as well as various  JAK2  fusion genes [ 9 ]  are associated with the development and progression of various  myeloproliferative  and lymphoproliferative malignancies. These findings suggest that the  STAT3-JAK2 -fusion gene may contribute to the malignant progression and perhaps development of CD4+ ITCLD-GT. [ 9 ]  Numerous other genetic abnormalities occur in the T-cells of ITCLD-GT but unlike the  STAT3-JAK  fusion gene have been limited to single cases. These abnormalities include  trisomy  of  chromosome 5 , a t(4;16)(q26;p13) fusion between  interleukin-2  and  B-cell maturation antigen  genes, loses in the 4p26 and 16p13 chromosomal areas involved in formation of the t(4;16)9q26;p13) fusion gene, and one or more  copy number variations  in diverse areas of different chromosomes. [ 4 ]  The role(s), if any, of these abnormalities in ITCLD-GT is unclear. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_827", "text": "The cells involved in all cases of ITCLD-GT are mature T cells [ 1 ]  that exhibit a clonal rearrangement of their  T-cell receptors  and, therefore, are derived from a common ancestry cell. [ 4 ]  They express the  \u03b1\u03b2  as opposed to the  \u03b3\u03b4  surface membrane T-cell receptor and therefore are \u03b1\u03b2 rather than  \u03b3\u03b4 T-cells . In all reported cases, these T cells express the  CD3   cluster of differentiation   protein complex  but vary in their expression of the CD4 cluster of differentiation glycoprotein as well as the  CD8  glycoprotein component of the T cell receptor. Individuals with ITCLD-GT, therefore, have pathological accumulations of either CD4+, CD8+, or, very rarely, CD4-, CD8- T cells. [ 4 ]  A single case of CD4+, CD8+ T cell disease has been reported recently. [ 9 ]  There may be differences in the presentation, course, and malignant potential of ITCLD-GT based or these different expressions of CD4 and CD8 but this requires further study. Unlike certain types of T cell lymphomas for which it has been mistaken, the T cells in ITCLD-GT do not express the neutral cell  adhesion molecule ,  CD56 , and are not infected with the  Epstein\u2013Barr virus  and therefore do not express this virus's  latency proteins  or  latency ncRNAs . [ 1 ]  The origin of these cells is unknown but it is thought that the CD4+ and CD8+ T-cells derive from mucosal  T helper  and  cytotoxic T  lymphocytes, respectively. The CD4-, CD8- T cells that may cause rare cases of the disorder exhibit  cytology  and  morphology  features of both of the latter two mucosal cell types. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_828", "text": "Histological  analysis of tissues biopsied from the GI tract generally reveals dense infiltrates of small, mature lymphocytes in the mucosa that may displace [ 2 ]  but usually do not invade [ 4 ]  the  epithelium ; these cells sometimes extend through the  muscularis mucosa  to invade the  submucosa . [ 4 ]  The lesions may contain reactive  plasma cells ,  eosinophils ,  granulomas  (in CD4+ disease), and  lymphoid follicles . [ 2 ]  There is little or no tissue destruction. [ 1 ]  Immunohistochemistry analyses indicate that the small lymphocytes are CD4+, [ 9 ]  CD8+, [ 9 ]  CD4-/CD8-, [ 4 ]  or CD4+/CD8+ T-cells [ 9 ]  that stain for CD3 [ 4 ]  but not CD56 or Epstein-Barr virus products. [ 1 ]  Notably, the affected T cells have an extremely low rate of proliferation as determined by examining their  KI-67 protein  using  immunofluorescence  analysis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_829", "text": "The diagnosis of indolent T cell lymphoproliferative disorder of the GI tract depends on identifying the presentation, clinical course, and laboratory and histological findings given in the previous four sections. [ 4 ]  (Future studies may find that the diagnosis is supported by demonstrating the presence of the  STAT3-JAK2  fusion gene in the CD4+ T cells of suspicious tissues. [ 6 ] )"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_830", "text": "Inspection of the entire GI tract by  endoscopy  and  colonoscopy  generally finds  mucosal   redness , erosions, small superficial ulcerations, occasional small  polyps , [ 2 ]   fissures ,  diverticula , and, rarely, tumor-like masses and deep ulcers. [ 4 ]  These lesions may be localized, occur in multiple sites, or extend throughout the GI tract; [ 4 ]  they are more common in the small intestine and colon [ 2 ]  but can also occur in the stomach,  esophagus , oral cavity (e.g.  palate ), and rectum. [ 4 ]  Whole body  computed tomography scans  (i.e. CT scans) frequently find enlarged  mesenteric lymph nodes  (i.e. lymph nodes attached to the intestinal  mesentery ) and may show evidence of liver, spleen, and/or other organ involvement in cases which are advancing or have advanced to a malignant lymphoma.  Positron emission tomography  scans (i.e. PET scans) and  positron emission tomography\u2013computed tomography  scans (i.e. PET-CT scans) likewise often show that the mesenteric lymph nodes in ITCLD-GT exhibit modestly increased  metabolic  or  biochemical  activity and, in cases of progressing or overt malignant disease, show increased activity in other organs. [ 4 ]  Inspection of patients'  peripheral blood smearss  and  bone marrow tissues  may identify excessive numbers of ITCLD-GT's T cells and thereby likewise indicate progressing or malignant disease. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_831", "text": "Because of the radical differences in their prognoses and treatments, ITCLD-GT should be distinguished from the malignant, inflammatory, autoimmune, and other diseases that it can mimic. [ citation needed ]  Key findings that distinguish ITCLD-GT from the following major diseases which ITCLD-GT may mimic are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_832", "text": "Studies indicate that patients with ITCLD-GT should be treated conservatively. Chemotherapy regimens directed at malignant lymphoma and treatment regimens used to treat celiac disease, Crohn's disease, or ulcerative colitis have had little or no beneficial effects on the course of the disease. [ 4 ]  Patients should be follow regularly with peripheral blood and bone marrow examinations, GI tract endoscopic examinations [ 4 ]  and PET scans [ 2 ]  in order to detect the progression of ITCLD-GT to a malignant phase."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_833", "text": "Studies to date [ when? ]  indicate that most patients experience a prolonged course of persistent or recovering-relapsing GI tract symptoms. A small percentage of patients have had spontaneous and sustained recoveries or progressed to a malignant lymphoma. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_834", "text": "Inflammatory bowel disease  ( IBD ) is a group of  inflammatory  conditions of the  colon  and  small intestine , with  Crohn's disease  and  ulcerative colitis  (UC) being the principal types. [ 3 ]  Crohn's disease affects the small intestine and large intestine, as well as the mouth, esophagus, stomach and the anus, whereas UC primarily affects the colon and the rectum. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_835", "text": "In spite of Crohn's and UC being very different diseases, both may present with any of the following symptoms: abdominal pain,  diarrhea ,  rectal bleeding , severe internal cramps/muscle spasms in the region of the pelvis and  weight loss .  Anemia  is the most prevalent extraintestinal complication of inflammatory bowel disease (IBD). [ 9 ] [ 10 ]  Associated complaints or diseases include  arthritis ,  pyoderma gangrenosum ,  primary sclerosing cholangitis , and  non-thyroidal illness syndrome  (NTIS). [ 11 ]  Associations with  deep vein thrombosis  (DVT) [ 12 ]  and  bronchiolitis obliterans organizing pneumonia  (BOOP) have also been reported. [ 13 ]  Diagnosis is generally by assessment of inflammatory markers in stool followed by  colonoscopy  with  biopsy  of pathological lesions. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_836", "text": "IBD is a complex disease which arises as a result of the interaction of environmental and genetic factors leading to immunological responses and inflammation in the intestine. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_837", "text": "People living with IBD are very interested in diet, but little is known about the impact of diet on these patients. Recent reviews underlined the important role of nutritional counselling in IBD patients. Patients should be encouraged to adopt diets that are best supported by evidence and involve monitoring for the objective resolution of inflammation. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_838", "text": "A 2022 study found that diets with increased intake of fruits and vegetables, reduction of processed meats and refined carbohydrates, and preference of water for hydration were associated with lower risk of active symptoms with IBD, although increased intake of fruits and vegetables alone did not reduce risk of symptoms with Crohn's disease. [ 24 ]  A 2022 scientific review also found generally positive outcomes for IBD patients who adhered to the Mediterranean diet (high fruit and vegetable intake). [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_839", "text": "Dietary patterns are associated with a risk for ulcerative colitis. In particular, subjects who were in the highest  tertile  of the  healthy dietary pattern  had a 79% lower risk of ulcerative colitis. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_840", "text": "Gluten sensitivity  is common in IBD and associated with having flareups. Gluten sensitivity was reported in 23.6% and 27.3% of Crohn's disease and ulcerative colitis patients, respectively. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_841", "text": "A  diet  high in  protein , particularly animal protein, and/or high in sugar may be associated with increased risk of IBD and relapses. [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_842", "text": "Emerging evidence indicates that  bile acids  are important etiological agents in IBD pathogenesis. [ 30 ]  IBD patients have a consistent pattern of an increased abundance of primary bile acids such as  cholic acid  and  chenodeoxycholic acid  (and their conjugated forms), and a decreased abundance of secondary bile acids such as  lithocholic acid  and  deoxycholic acid . [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_843", "text": "The  human microbiota  consists of 10\u2013100 trillion microorganisms. [ 31 ]  Several studies have confirmed that the microbiota composition is different in patients with IBD compared to healthy individuals. [ 32 ]  This difference is more pronounced in patients with Crohn's disease than in those with ulcerative colitis. [ 33 ]  In IBD patients, there is a decrease or absence of beneficial bacteria such as  Bifidobacterium longum ,  Eubacterium rectale ,  Faecalibacterium prausnitzii , and  Roseburia intestinalis , while harmful species like  Bacteroides fragilis ,  Ruminococcus torques , and  Ruminococcus  are more abundant. [ 34 ] \nThe activation of  reactive oxygen species  and  reactive nitrogen species  leads to  oxidative stress  for both host cells and the  gut microbiome . Consequently, in IBD, there is a microbial imbalance, known as  dysbiosis , characterized by an increase in functional pathways involved in the microbial response to oxidative stress. This oxidative stress can promote the growth of certain species such as  R. gnavus . [ 35 ]  Another opportunistic bacterium called  A. muciniphila  contributes to IBD development and is more prevalent in individuals lacking  NOD-like receptor 6  (NLRP6). [ 36 ]  Both  R. gnavus  and  A. muciniphila  are bacterial species that are more abundant in IBD.\nPatients with IBD often exhibit stronger  antibody  and  T-cell  responses to microbial  antigens . [ 37 ]  The gut microbiome employs various approaches to interact with the host immune system. For instance,  B. fragilis , which is  symbiotic  in humans, can transfer immune regulatory molecules to immune cells through the secretion of  outer membrane vesicles . This mechanism plays a protective role in IBD by activating the non-classical  autophagy  pathway, dependent on  Atg16L1  and  NOD2  genes. [ 38 ]   B. thetaiotaomicron  induces the differentiation of  T regulatory cells  (Tregs) to modulate gut immunity, thus increasing the expression of  Gata3  and  FoxP3  genes. [ 39 ] \nThe colonization of  Clostridium  spp. can enhance the aggregation of ROR\u03b3T+ FOXP3 Treg cells, which inhibit the development of  Th2  and Th17 cells. Ultimately, this colonization could decrease the response of colonic Th2 and Th17 cells. [ 40 ] \nAlso  F. prausnitzii  attracts  CD4  and  CD8a  (DP8\u03b1) regulatory T cells. [ 41 ] \n E. coli  Nissle 1917 has the capability to inhibit the growth of  Salmonella  and other harmful bacteria. It prevents these pathogens from adhering to and invading  intestinal epithelial  cells, which significantly reduces the likelihood of inflammation in the gut and may also prevent the onset of IBD. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_844", "text": "Loss of integrity of the  intestinal epithelium  plays a key  pathogenic  role in IBD. [ 43 ]  Dysfunction of the  innate immune system  as a result of abnormal signaling through immune receptors called  toll-like receptors  (TLRs)\u2014which activates an immune response to molecules that are broadly shared by multiple pathogens\u2014contributes to acute and chronic inflammatory processes in IBD colitis and associated cancer. [ 44 ]  Changes in the composition of the  intestinal microbiota  are an important environmental factor in the development of IBD. Detrimental changes in the intestinal microbiota induce an inappropriate (uncontrolled)  immune response  that results in damage to the intestinal epithelium. Breaches in this critical barrier (the intestinal epithelium) allow further infiltration of microbiota that, in turn, elicit further immune responses. IBD is a multifactorial disease that is nonetheless driven in part by an exaggerated immune response to gut microbiota that causes defects in epithelial barrier function. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_845", "text": "Oxidative stress  and  DNA damage  likely have a role in the pathophysiology of IBD. [ 46 ]  Oxidative DNA damage as measured by  8-OHdG  levels was found to be significantly increased in people with IBD compared to healthy controls, and in inflamed mucosa compared with noninflamed mucosa. [ 46 ]  Antioxidant capacity as measured by the total action of all antioxidants detected in blood plasma or body fluids was found to be significantly decreased in people with IBD compared to healthy controls, and in inflamed mucosa compared with noninflamed mucosa. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_846", "text": "A genetic component to IBD has been recognized for over a century. [ 47 ]  Research that has contributed to understanding of the genetics include studies of ethnic groups (e.g.,  Ashkenazi Jews ,  Irish ), familial clustering, epidemiological studies, and twin studies. With the advent of molecular genetics, understanding of the genetic basis has expanded considerably, particularly in the past decade. [ 48 ]  The first gene linked to IBD was  NOD2  in 2001."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_847", "text": "Genome-wide association studies have since added to understanding of the genomics and pathogenesis of the disease. More than 200  single nucleotide polymorphisms  (SNPs or \"snips\") are now known to be associated with susceptibility to IBD. [ 49 ]  One of the largest genetic studies of IBD was published in 2012. [ 50 ]  The analysis explained more of the variance in Crohn's disease and ulcerative colitis than previously reported. [ 48 ]  The results suggested that commensal microbiota are altered in such a way that they act as pathogens in inflammatory bowel diseases. Other studies show that mutations in IBD-associated genes might interfere with the cellular activity and interactions with the  microbiome  that promote normal immune responses. [ 51 ]  Many studies identified that  microRNAs  dysregulation involved in IBD and to promote  colorectal cancer . [ 52 ]  By 2020,  single-cell RNA sequencing  analysis was launched by a small consortium using IBD patient biopsy material in a search for therapeutic targets. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_848", "text": "According to an article published on Nature, ETS2 gene plays a vital role in the development of the disease. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_849", "text": "The diagnosis is usually confirmed by  biopsies  on  colonoscopy .  Fecal calprotectin  is useful as an initial investigation, which may suggest the possibility of IBD, as this test is sensitive but not specific for IBD. [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_850", "text": "Inflammatory bowel diseases are  autoimmune diseases , in which the body's own immune system attacks elements of the digestive system. [ 57 ]  The chief types of IBD are  Crohn's disease  (CD) and  ulcerative colitis  (UC). [ 58 ]  Several other conditions are variously referred to either as being inflammatory bowel diseases or as being similar to but distinct from inflammatory bowel diseases. These conditions include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_851", "text": "Crohn's disease and ulcerative colitis are both common differential diagnoses for the other, and confidently diagnosing a patient with one of the two diseases may sometimes not be possible. No disease specific markers are currently known in the blood that would enable the reliable separation of patients with Crohn's disease and ulcerative colitis. [ 63 ]  Physicians tell the difference between Crohn's disease and UC by the  location  and  nature  of the inflammatory changes. Crohn's can affect any part of the  gastrointestinal tract , from  mouth  to  anus  ( skip lesions ), although a majority of the cases start in the  terminal ileum . Ulcerative colitis, in contrast, is restricted to the  colon  and the rectum. [ 64 ]   Microscopically , ulcerative colitis is restricted to the  mucosa  ( epithelial lining  of the gut), while Crohn's disease affects the full thickness of the bowel wall (\"transmural lesions\"). Lastly, Crohn's disease and ulcerative colitis present with extra-intestinal manifestations (such as liver problems, arthritis, skin manifestations and eye problems) in different proportions. [ 65 ]  In 10\u201315% of cases, a definitive diagnosis neither of Crohn's disease nor of ulcerative colitis can be made because of idiosyncrasies in the presentation. In these cases, a diagnosis of  indeterminate colitis  may be made. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_852", "text": "Irritable bowel syndrome  can present with similar symptoms as either disease, as can  nonsteroidal anti-inflammatory drug  (NSAID)  enteritis  and  intestinal tuberculosis . Conditions that can be mistaken particularly for Crohn's disease include  Beh\u00e7et's disease  and  coeliac disease , while conditions that can be symptomatically similar to ulcerative colitis in particular include acute self-limiting  colitis ,  amebic colitis ,  schistosomiasis  and  colon cancer . [ 67 ]  Other diseases may cause an increased excretion of fecal calprotectin, such as  infectious diarrhea , untreated  celiac disease ,  necrotizing enterocolitis , intestinal  cystic fibrosis  and  neoplastic pediatric tumor cells . [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_853", "text": "Liver function tests  are often elevated in IBD, and are often mild and generally return spontaneously to normal levels. [ 69 ]  The most relevant mechanisms of elevated liver functions tests in IBD are drug-induced hepatotoxicity and fatty liver. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_854", "text": "CD and UC are chronic inflammatory diseases, and are not medically curable. [ 73 ]  However, Ulcerative Colitis can in most cases be cured by  proctocolectomy , although this may not eliminate extra-intestinal symptoms. An  ileostomy  will collect feces in a bag. Alternatively, a pouch can be created from the small intestine; this serves as the rectum and prevents the need for a permanent ileostomy. Between one-quarter and one-half of patients with  ileo-anal pouches  do have to manage occasional or chronic  pouchitis . [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_855", "text": "Surgery cannot cure Crohn's disease but may be needed to treat complications such as abscesses, strictures or fistulae. [ 75 ]  Severe cases may require  surgery , such as  bowel resection ,  strictureplasty  or a temporary or permanent  colostomy  or  ileostomy . In Crohn's disease, surgery involves removing the worst inflamed segments of the intestine and connecting the healthy regions, but unfortunately, it does not cure Crohn's or eliminate the disease. At some point after the first surgery, Crohn's disease can recur in the healthy parts of the intestine, usually at the resection site. [ 76 ]  (For example, if a patient with Crohn's disease has an ileocecal anastomosis, in which the caecum and terminal ileum are removed and the ileum is joined to the ascending colon, their Crohn's will nearly always flare-up near the anastomosis or in the rest of the ascending colon). [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_856", "text": "Medical treatment of IBD is individualised to each patient. [ 73 ]  The choice of which drugs to use and by which route to administer them (oral, rectal, injection, infusion) depends on factors including the type, distribution, and severity of the patient's disease, as well as other historical and biochemical prognostic factors, and patient preferences. For example,  mesalazine  is more useful in  ulcerative colitis  than in  Crohn's disease . [ 70 ]  Generally, depending on the level of severity, IBD may require  immunosuppression  to control the symptoms, with drugs such as  prednisone ,  tumor necrosis factor inhibitors  (TNF inhibitors), [ 78 ]   azathioprine ,  methotrexate , or  6-mercaptopurine . [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_857", "text": "Steroids , such as the glucocorticoid  prednisone , are frequently used to control disease flares and were once acceptable as a maintenance drug.  Biological therapy for inflammatory bowel disease , especially the TNF inhibitors, are used in people with more severe or resistant Crohn's disease and sometimes in ulcerative colitis. [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_858", "text": "Treatment is usually started by administering drugs with high anti-inflammatory effects, such as prednisone. Once the inflammation is successfully controlled, another drug to keep the disease in remission, such as  mesalazine  in UC, is the main treatment. If further treatment is required, a combination of an immunosuppressive drug (such as azathioprine) with mesalazine (which may also have an anti-inflammatory effect) may be needed, depending on the patient. Controlled release  budesonide  is used for mild ileal Crohn's disease. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_859", "text": "Exclusive enteral nutrition is a first-line therapy in pediatric Crohn's disease with weaker data in adults. [ 81 ] :\u200a331\u200a [ 82 ]  Evidence supporting exclusive enteral nutrition in ulcerative colitis is lacking. [ 81 ] :\u200a333"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_860", "text": "Nutritional deficiencies play a prominent role in IBD. Malabsorption, diarrhea, and GI blood loss are common features of IBD. Deficiencies of B vitamins, fat-soluble vitamins, essential fatty acids, and key minerals such as magnesium, zinc, and  selenium  are extremely common and benefit from replacement therapy. Dietary interventions, including certain exclusion diets like the  specific carbohydrate diet  (SCD) can be beneficial for symptom management. [ 83 ]  Dietary fiber interventions, such as psyillium supplementation (a mixture of soluble and insoluble fibers), may relieve symptoms as well as induce/maintain remission by altering the microbiome composition of the GI tract, thereby improving regulation of immune function, reducing inflammation, and helping to restore the intestinal mucosal lining. [ 84 ]  Low serum levels of  alanine transaminase  can be a marker of  sarcopenia  which is underdiagnosed in patients with IBD and associated with a higher disease activity. [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_861", "text": "Anemia  is commonly present in both ulcerative colitis and Crohn's disease. Due to raised levels of inflammatory  cytokines  which lead to the increased expression of  hepcidin ,  parenteral iron  is the preferred treatment option as it bypasses the gastrointestinal system, has lower incidence of adverse events and enables quicker treatment. Hepcidin itself is also an anti-inflammatory agent. In the murine model very low levels of iron restrict hepcidin synthesis, worsening the inflammation that is present. [ 86 ]  Enteral nutrition has been found to be efficient to improve hemoglobin level in patients with IBD, especially combined with erythropoietin. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_862", "text": "Gastrointestinal bleeding , occurring especially during ulcerative colitis relapse, can contribute to anemia when chronic, and may be life-threatening when acute. To limit the possible risk of dietary intake disturbing  hemostasis  in acute gastrointestinal bleeding, temporary  fasting  is often considered necessary in hospital settings. [ 88 ]  The effectiveness of this approach is unknown; a  Cochrane  review in 2016 found no published clinical trials including children. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_863", "text": "Low levels of vitamin D are associated with  crohn's disease  and  ulcerative colitis  and people with more severe cases of inflammatory bowel disease often have lower vitamin D levels. It is not clear if vitamin D deficiency causes inflammatory bowel disease or is a symptom of the disease. [ 90 ]   There is some evidence that vitamin D supplementation therapy may be associated with improvements in scores for clinical inflammatory bowel disease activity and biochemical markers. [ 90 ]  Vitamin D treatment may be associated with less inflammatory bowel disease reoccurrence of symptoms (relapse). It is not clear if this treatment improves the person's quality of life or what the clinical response to vitamin D treatment. The ideal treatment regime and dose of vitamin D therapy has not been well enough studied. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_864", "text": "There is preliminary evidence of an infectious contribution to IBD in some patients that may benefit from antibiotic therapy, such as with  rifaximin . [ 91 ]  The evidence for a benefit of rifaximin is mostly limited to Crohn's disease with less convincing evidence supporting use in ulcerative colitis. [ 92 ] [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_865", "text": "The use of oral  probiotic  supplements to modify the composition and behaviour of the microbiome has been considered as a possible therapy for both induction and maintenance of remission in people with Crohn's disease and ulcerative colitis. A Cochrane review in 2020 did not find clear evidence of improved remission likelihood, nor lower adverse events, in people with Crohn's disease, following probiotic treatment. [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_866", "text": "For ulcerative colitis, there is low-certainty evidence that probiotic supplements may increase the probability of clinical remission. [ 95 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects. [ 95 ]  Although there was no clear evidence of greater remission when probiotic supplements were compared with  5\u2010aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy. [ 95 ]  Whereas in people who are already in remission, it is unclear whether probiotics help to prevent future relapse, either as a monotherapy or  combination therapy . [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_867", "text": "Fecal microbiota transplant  is a relatively new treatment option for IBD which has attracted attention since 2010. [ 97 ] [ 98 ]  Some preliminary studies have suggested benefits similar to those in  Clostridioides difficile  infection  but a review of use in IBD shows that FMT is safe, but of variable efficacy. Systematic reviews showed that 33% of ulcerative colitis, and 50% of Crohn's disease patients reach clinical remission after  fecal microbiota transplant . [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_868", "text": "Complementary and alternative medicine approaches have been used in inflammatory bowel disorders. [ 100 ]  Evidence from controlled studies of these therapies has been reviewed; risk of bias was quite heterogeneous. The best supportive evidence was found for herbal therapy, with  Plantago ovata  and  curcumin  in UC maintenance therapy,  wormwood  in CD, mind/body therapy and self-intervention in UC, and  acupuncture  in UC and CD. [ 101 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_869", "text": "Stem cell therapy  is undergoing research as a possible treatment for IBD. A review of studies suggests a promising role, although there are substantial challenges, including cost and characterization of effects, which limit the current use in clinical practice. [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_870", "text": "Patients with IBD have a higher prevalence of depressive and anxiety disorders compared to the general population, women with IBD are more likely than men to develop affective disorders since up to 65% of them may have depression and anxiety disorder. [ 103 ] [ 104 ] \nCurrently, there is no evidence to recommend psychological treatment, such as  psychotherapy ,  stress management  and patient's education, to all adults with IBD in general. [ 105 ]  These treatments had no effect on  quality of life ,  emotional well-being  and disease activity. [ 105 ]  The need for these approaches should be individually assessed and further researched to identify subgroups and determine type of therapy that may benefit individuals with IBD. [ 105 ]  In adolescents population such treatments may be beneficial on  quality of life  and  depression , although only short-term effects have been found, which also imposes the need for further research. [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_871", "text": "A meta analysis of interventions to improve mood (including talking therapy, antidepressants, and exercise) in people with IBD found that they reduced inflammatory markers such as C-reactive protein and faecal calprotectin. Psychological therapies reduced inflammation more than antidepressants or exercise. [ 106 ] [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_872", "text": "Crohn's and Colitis Australia, the peak body for IBD in Australia, where prevalence is one of the highest in the world, reviewed the quality of care for patients admitted to Australian hospitals. They found that only one hospital met accepted standards for multidisciplinary care, but that care was improved with the availability of even minimal specialised services. [ 108 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_873", "text": "While IBD can limit quality of life because of pain, vomiting, and diarrhea, it is rarely fatal on its own. Fatalities due to complications such as  toxic megacolon ,  bowel perforation  and surgical complications are also rare. [ 112 ]  Fatigue is a common symptom of IBD and can be a burden. [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_874", "text": "Around one-third of individuals with IBD experience persistent gastrointestinal symptoms similar to  irritable bowel syndrome  (IBS) in the absence of objective evidence of disease activity. [ 114 ]  Despite enduring the side-effects of long-term therapies, this cohort has a quality of life that is not significantly different to that of individuals with uncontrolled, objectively active disease, and escalation of therapy to biological agents is typically ineffective in resolving their symptoms. [ 115 ]  The cause of these IBS-like symptoms is unclear, but it has been suggested that changes in the  gut-brain axis , epithelial barrier dysfunction, and the  gut flora  may be partially responsible. [ 116 ] [ needs update ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_875", "text": "While patients of IBD do have an increased risk of  colorectal cancer , this is usually caught much earlier than the general population in routine surveillance of the colon by colonoscopy, and therefore patients are much more likely to survive. [ 117 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_876", "text": "New evidence suggests that patients with IBD may have an elevated risk of  endothelial dysfunction  and  coronary artery disease . [ 118 ] [ 119 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_877", "text": "The goal of treatment is toward achieving remission, after which the patient is usually switched to a lighter drug with fewer potential side effects. Every so often, an acute resurgence of the original symptoms may appear; this is known as a \"flare-up\". Depending on the circumstances, it may go away on its own or require medication. The time between flare-ups may be anywhere from weeks to years, and varies wildly between patients \u2013 a few have never experienced a flare-up. [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_878", "text": "Life with IBD can be challenging; however, many with the condition lead relatively normal lives. IBD carries a psychological burden due to stigmatization of being diagnosed, leading to high levels of anxiety, depression, and a general reduction in the quality of life. [ 121 ] [ 122 ]  Although living with IBD can be difficult, there are numerous resources available to help families navigate the ins and out of IBD, such as the  Crohn's and Colitis Foundation of America  (CCFA)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_879", "text": "IBD resulted in a global total of 51,000 deaths in 2013 and 55,000 deaths in 1990. [ 123 ]  The increased incidence of IBD since  World War II  has been correlated to the increase in meat consumption worldwide, supporting the claim that animal protein intake is associated with IBD. [ 124 ]  However, there are many environmental risk factors that have been linked to the increased and decreased risk of IBD, such as smoking, air pollution and greenspace, urbanization and Westernization. [ 125 ]  Inflammatory bowel diseases are increasing in Europe. [ 126 ]  Incidence and prevalence of IBD has risen steadily for the last decades in Asia, which could be related changes in diet and other environmental factors. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_880", "text": "Around 0.8% of people in the UK have IBD. [ 128 ]  Similarly, around 270,000 (0.7%) of people in Canada have IBD, [ 129 ]  with that number expected to rise to 400,000 (1%) by 2030. [ 130 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_881", "text": "The following treatment strategies are not used routinely, but appear promising in some forms of IBD."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_882", "text": "Initial reports [ 131 ]  suggest that  helminthic therapy  may not only prevent but even control IBD: a drink with roughly 2,500 ova of the  Trichuris suis  helminth taken twice monthly decreased symptoms markedly in many patients. It is even speculated that an effective \"immunization\" procedure could be developed\u2014by ingesting the cocktail at an early age. [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_883", "text": "Prebiotics  and  probiotics  are focusing increasing interest as treatments for IBD. Currently, there is evidence to support the use of certain probiotics in addition to standard treatments in people with ulcerative colitis but there is no sufficient data to recommend probiotics in people with Crohn's disease. Both single strain and multi-strain probiotics have been researched for mild to moderate cases of ulcerative colitis.  The most clinically researched multi-strain probiotic with over 70 human trials is the  De Simone Formulation . [ 133 ]   Further research is required to identify specific probiotic strains or their combinations and prebiotic substances for therapies of intestinal inflammation. [ 134 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_884", "text": "Currently, the probiotic strain, frequency, dose and duration of the probiotic therapy are not established. [ 135 ]  In severely ill people with IBD there is a risk of the passage of viable bacteria from the gastrointestinal tract to the internal organs (bacterial translocation) and subsequent  bacteremia , which can cause serious adverse health consequences. [ 135 ]  Live bacteria might not be essential because of beneficial effects of probiotics seems to be mediated by their DNA and by secreted soluble factors, and their therapeutic effects may be obtained by systemic administration rather than oral administration. [ 135 ] [ 136 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_885", "text": "In 2005  New Scientist  published a joint study by  Bristol University  and the  University of Bath  on the apparent healing power of  cannabis  on IBD. Reports that cannabis eased IBD symptoms indicated the possible existence of  cannabinoid receptors  in the intestinal lining, which respond to molecules in the plant-derived chemicals.  CB1 cannabinoid receptors  \u2013 which are known to be present in the  brain  \u2013 exist in the  endothelial cells  which line the gut, it is thought that they are involved in repairing the lining of the gut when damaged. [ 137 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_886", "text": "The team deliberately damaged the cells to cause inflammation of the gut lining and then added synthetically produced  cannabinoids ; the result was that gut started to heal: the broken cells were repaired and brought back closer together to mend the tears. It is believed that in a healthy gut, natural endogenous cannabinoids are released from endothelial cells when they are injured, which then bind to the CB1 receptors. The process appears to set off a wound-healing reaction, and when people use cannabis, the cannabinoids bind to these receptors in the same way. [ 137 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_887", "text": "Previous studies have shown that CB1 receptors located on the nerve cells in the gut respond to cannabinoids by slowing gut  motility , therefore reducing the painful muscle contractions associated with diarrhea.  CB2 , another cannabinoid receptor predominantly expressed by  immune cells , was detected in the gut of people with IBD at a higher concentration. These receptors, which also respond to chemicals in cannabis, appear to be associated with  apoptosis  \u2013 programmed cell death \u2013 and may have a role in suppressing the overactive  immune system  and reducing  inflammation  by mopping up excess  cells . [ 137 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_888", "text": "Activation of the  endocannabinoid system  was found efficient in ameliorating  colitis  and increasing the survival rate of mice, and reducing remote  organ  changes induced by colitis, further suggest that modulation of this system is a potential  therapeutic  approach for IBDs and the associated remote organ lesions. [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_889", "text": "Alicaforsen is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human  ICAM-1  messenger  RNA  through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. [ 139 ]  ICAM-1 propagates an inflammatory response promoting the extravasation and activation of  leukocytes  (white blood cells) into inflamed tissue. [ 139 ]  Increased expression of ICAM-1 has been observed within the inflamed intestinal  mucosa  of people with ulcerative colitis, pouchitis and Crohn's, where ICAM-1 over production correlated with disease activity. [ 140 ]  This suggests that ICAM-1 is a potential therapeutic target in the treatment of these diseases. [ 141 ] [ 142 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_890", "text": "Cannabinoid CB2 receptor  agonists  are found to decrease the induction of ICAM-1 and  VCAM-1  surface expression in human  brain tissues  and primary human brain endothelial cells (BMVEC) exposed to various pro-inflammatory mediators. [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_891", "text": "In 2014, an alliance among the  Broad Institute ,  Amgen  and  Massachusetts General Hospital  formed with the intention to \"collect and analyze patient DNA samples to identify and further validate genetic targets.\" [ 144 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_892", "text": "In 2015, a meta-analysis on 938 IBD patients and 953 controls, IBD was significantly associated with having higher odds of  vitamin D  deficiency. [ 145 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_893", "text": "Gram-positive bacteria present in the lumen could be associated with extending the time of relapse for ulcerative colitis. [ 134 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_894", "text": "Bidirectional pathways between  depression  and IBD have been suggested  [ 146 ]  and psychological processes have been demonstrated to influence self-perceived physical and psychological health over time. [ 147 ]  IBD-disease activity may impact  quality of life  and over time may significantly affect individual's  mental well-being , which may be related to the increased risk to develop  anxiety  and/or depression. [ 146 ] [ 148 ] [ 149 ]  On the other hand, psychological distress may also influence IBD activity. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_895", "text": "Higher rates of  anxiety  and depression are observed among those with IBD compared to healthy individuals, which correlated with disease severity. [ 148 ] [ 150 ]  Part of this phenotypic correlation is due to a shared genetic overlap between IBD and psychiatric comorbidities. [ 151 ]  Moreover, anxiety and depression rates increase during active disease compared with inactive phases. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_896", "text": "Flu vaccines are recommended for people with IBD in the UK; however, research suggests that vaccine uptake is low. Researchers analysed data on 13,631 adults with IBD on immune-suppressing drugs during the 2018 \u2013 2019 flu season. Only half of this population received a vaccine during this period and few (32%) were vaccinated before the flu circulated in the community. This could be due to the belief that flu vaccines cause IBD flares; however, the same study did not find a link between vaccination and IBD flares. [ 152 ] [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_897", "text": "IBD also occurs in dogs and is thought to arise from a combination of host genetics, intestinal microenvironment, environmental components and the immune system. There is an ongoing discussion, however, that the term \"chronic enteropathy\" might be better to use than \"inflammatory bowel disease\" in dogs because it differs from IBD in humans in how the dogs respond to treatment. For example, many dogs respond to only dietary changes compared to humans with IBD, who often need  immunosuppressive  treatment. Some dogs may also need immunosuppressant or antibiotic treatment when dietary changes are not enough. After having excluded other diseases that can lead to vomiting, diarrhea, and abdominal pain in dogs, intestinal biopsies are often performed to investigate what kind of inflammation is occurring (lymphoplasmacytic,  eosinophilic , or  granulomatous ). In dogs, low levels of  cobalamin  in the blood have been shown to be a risk factor for negative outcome. [ 154 ] [ 155 ] [ 156 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_898", "text": "An  inflammatory fibroid polyp   (IFP)  is an uncommon  digestive system   tumor . [ 1 ]  J. Vanek initially identified it as a separate pathological entity in 1949 when he reported six case reports of eosinophilic infiltration in gastric submucosal  granulomas . [ 2 ]  It is a single, non-encapsulated polypoid lesion that is typically submucosal. It is characterized by a large number of small blood vessels, oedematous  connective tissue , and an inflammatory eosinophilic infiltrate. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_899", "text": "Inflammatory fibroid polyp has also been referred to as polypoid myo-endothelioma, [ 4 ]  fibroma with eosinophilic infiltration, [ 5 ]  inflammatory pseudotumour, [ 5 ]  myxoma, [ 6 ]  haemangiopericytoma, [ 7 ]  eosinophilic granuloma, [ 5 ]  Vanek's tumour, [ 8 ]  and gastric eosinophilic submucosal granuloma. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_900", "text": "When the lesions are symptomatic, they typically measure less than 3\u00a0cm in size and are linked to symptoms such as  iron deficiency anemia , bleeding,  weight loss , and dyspeptic symptoms. Significant complications like  obstruction ,  intussusception , and even  hypovolemic shock  can result from larger lesions. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_901", "text": "The tumor's size, location, and complications will affect how it presents itself. [ 1 ]  Common symptoms include  epigastric pain  and bleeding in the stomach and intestinal symptoms. [ 10 ]  When it is in the  esophagus , symptoms such as bleeding, [ 11 ]   gastroesophageal reflux , [ 12 ]  and  dysphagia  may occur. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_902", "text": "Although the inflammatory fibroid polyp's natural history is unknown, it has been known to grow quickly, within a few months, [ 1 ]  and to reach sizes of up to 20\u00a0cm. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_903", "text": "Inflammatory fibroid polyps emerge from the  submucosa  and pierce the  lamina propria , causing the mucosal layer to bulge. On rare occasions, they may develop ulcers through the  mucosa , resulting in bleeding and symptoms similar to  hypovolemic shock . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_904", "text": "The inflammatory fibroid polyp is a benign lesion whose cause is unknown; [ 13 ]  some reports attribute its genesis to  myofibroblasts , [ 16 ]  while others propose vascular or perivascular tissue. [ 17 ]  It is widely acknowledged that this is a reactive process to chemical, physical, or microbiological stimuli rather than a  neoplasm . [ 18 ]  In the past, it was believed that the etiology was caused by an inflammatory reaction to an underlying  granuloma . [ 15 ]  An irritating stimulus is frequently linked to the development of a submucosal granuloma (such as trauma,  tuberculosis ,  helicobacter pylori ,  Crohn's disease , or\u00a0 sarcoidosis ). [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_905", "text": "Parasites have also been implicated as a potential cause of inflammatory fibroid polyps. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_906", "text": "There have been suggestions that a factor that has not yet been identified [ 21 ]  may cause  hyperplasia  of vessels and  stromal cells , leading to localized vascular inflammation. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_907", "text": "The inflammatory fibroid polyp may be connected to neoplastic and neoplastic GI lesions occurring simultaneously or synchronously, but the literature does not support a causal relationship. [ 23 ] [ 24 ]  Isolated reports have been made of inflammatory fibroid polyps at different locations coexisting with  granular cell tumors [ 25 ]  and certain  immune system  conditions, such as  neurofibromatosis , [ 26 ]   Crohn's disease , [ 10 ] [ 27 ]   ankylosing spondylitis , [ 22 ]  and  human immunodeficiency virus infection , [ 28 ]  however, these results are inconsistent and most likely coincidental. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_908", "text": "Inflammatory fibroid polyps have demonstrated a higher incidence in individuals with a family history of gastrointestinal polyps. [ 29 ]  Activating mutations in the  platelet-derived growth factor receptor alpha  ( PDGFRA ) gene were found in 70% of cases in a genetic study involving inflammatory fibroid polyps. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_909", "text": "Over 90% of gastrointestinal polyps found during routine endoscopic examination are present in patients who are asymptomatic and do not appear to be cancerous. [ 31 ]  By using a gross examination alone, these polyps cannot be identified from those that need additional treatment. [ 15 ]  Consequently, to identify the type of polyp and whether underlying  dysplasia  is present, histological analysis is always recommended. [ 32 ]  To accurately determine the type of polyp, additional diagnostic techniques such as tandem  biopsies ,  immunohistochemistry  staining, and  endoscopic ultrasound  (EUS) may also be required. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_910", "text": "An inflammatory fibroid polyp presents histologically as an exuberant, [ 10 ]  non-encapsulated, localized proliferation of spindle-shaped  mononuclear cells , [ 4 ]  with an inflammatory infiltrate that is frequently dominated by  eosinophils . [ 33 ]  The fuzzy borders visible on  endoscopic ultrasound  correspond with the non-encapsulated proliferating spindle cells. [ 34 ]  Most inflammatory fibroid polyps are vascular, consisting of a network of varying diameter blood vessels. [ 35 ]  Occasionally, the spindle-shaped cells are arranged in a concentric pattern that resembles \"onion skin\". [ 36 ] [ 4 ]  Surface ulceration in focal areas can occasionally be observed. [ 6 ]  Though usually polypoidal, [ 7 ]  the lesion is thought to originate in the lower layer of the  lamina propria [ 23 ]  and may be sessile. [ 24 ] [ 7 ]  The layers of the muscle wall atrophy, fraying, and splitting are brought on by inflammatory fibroid polyps. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_911", "text": "When inflammatory fibroid polyps from different GI sites are stained with  immunohistochemistry , the spindle cell component exhibits nearly 100% positivity for  vimentin [ 5 ]  and  CD34 , [ 17 ]  but varying staining for smooth muscle actin,  HHF-35 , KP1, and Mac 387. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_912", "text": "The literature describes four histopathological groups into which inflammatory fibroid polyps can be divided: classical fibrovascular, nodular, sclerotic, and edematous. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_913", "text": "The only available treatment option is surgical excision of the lesion using either an open or endoscopic approach, depending on the location and size of the tumor. [ 1 ]  In certain instances, a formal  oesophagectomy  or lateral oesophagotomy was required for resection. [ 37 ]  Moreover, reports of using  Nd YAG laser  and thermocautery to treat tiny polyps exist. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_914", "text": "Individuals who have inflammatory fibroid polyps usually show up in their fifth or seventh decade of life. [ 38 ]  In children, it is uncommon. [ 39 ]  Even though the female-to-male ratio has varied from 2.8:1 [ 24 ]  to 0.7:1, [ 7 ]  both sexes seem to be equally affected. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_915", "text": "Intestinal metaplasia  is the transformation ( metaplasia ) of  epithelium  (usually of the  stomach  or the  esophagus ) into a type of epithelium resembling that found in the  intestine .  In the esophagus, this is called  Barrett's esophagus . Chronic inflammation caused by  H. pylori  infection in the stomach and  GERD  in the esophagus are seen as the primary instigators of metaplasia and subsequent  adenocarcinoma  formation. Initially, the transformed epithelium resembles the  small intestine  lining; in the later stages it resembles the lining of the  colon . It is characterized by the appearance of  goblet cells  and expression of intestinal cell markers such as the  transcription factor ,  CDX2 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_916", "text": "Although  H. pylori  infection can cause gastrointestinal metaplasia, its eradication does not reverse the process. [ 1 ]   Bile reflux  is an additional pathogenic factor in gastrointestinal metaplasia that can continuously irritate the  gastric mucosa .  Bile acids in refluxed fluid are widely reported to be associated with gastrointesinal metaplasia. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_917", "text": "Although it was originally reported that people of East Asian ethnicity with gastric intestinal metaplasia are at increased risk of  stomach cancer , [ 3 ]  it is now clear that gastric intestinal metaplasia is also a risk factor in low-incidence regions like Europe. [ 4 ]  Risk factors for progression of gastric intestinal metaplasia to full blown cancer are smoking and family history. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_918", "text": "Intestinal metaplasia lesions that have an active  DNA damage  response are likely to experience extended latency in the premalignant state until the incidence of damages overrides the DNA damage response leading to clonal expansion and progression to cancer. [ 6 ]  During the DNA damage response, proteins are expressed that detect DNA damages and activate downstream responses like  DNA repair ,  cell cycle checkpoints  or  apoptosis . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_919", "text": "Intestinal neuronal dysplasia  ( IND ) is an inherited disease of the intestine that affects one in 3000 children and adults. The intestine uses  peristalsis  to push its contents toward the  anus ; people with IND have a problem with the  motor neurons  that lead to the intestine, inhibiting this process and thus preventing digestion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_920", "text": "It can often be confused for  Hirschsprung's disease , as both have similar symptoms. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_921", "text": "IND can be grouped into NID A and NID B, with the \"A\" form affecting the  sympathetic  innervation, and the \"B\" version affecting the  parasympathetic  innervation. [ 2 ] [ 3 ] \nIn 2002 Martucciello and colleagues published the first analysis of associated anomalies in IND population is an important clinical approach to investigate possible pathogenetic correlations. Two recessive syndromes were identified (3 families). The first was characterized by NID B, intestinal malrotation, and congenital short bowel, the second by NID B, short stature, mental retardation, and facial dysmorphism. In this study, gastrointestinal anomalies accounted for 67.4% of all associated disorders. These data suggest a strong correlation between IND and intestinal development. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_922", "text": "Conservative treatment involves the long term use of  laxatives  and  enemas , and has limited success. Dietary changes in order to control the disease are ineffective and high fiber diets often worsen the symptoms in children. As a last resort, surgical treatment (internal sphincter myectomy or  colon resection ) is used. [ 5 ]   In extreme cases, the only effective cure is a complete transplant of the affected parts. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_923", "text": "A famous case of IND is that of Adele Chapman, who had a triple transplant of the small intestine, pancreas and liver, the first of its kind in the UK; therefore the official charity of IND is the Adele Chapman Foundation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_924", "text": "An  intestinal parasite infection  is a condition in which a  parasite  infects the  gastro-intestinal tract  of humans and other animals. Such parasites can live anywhere in the body, but most prefer the intestinal wall."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_925", "text": "Routes of exposure and infection include ingestion of undercooked meat, drinking infected water,  fecal\u2013oral transmission  and skin absorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_926", "text": "Some types of  helminths  and  protozoa  are classified as intestinal parasites that cause infection\u2014those that reside in the  intestines . These infections can damage or sicken the host (humans or other animals). If the intestinal parasite infection is caused by helminths, the infection is called  helminthiasis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_927", "text": "Signs and symptoms depend on the type of infection. Intestinal parasites produce a variety of symptoms in those affected, most of which manifest themselves in gastrointestinal complications and general weakness. [ 1 ]  Gastrointestinal conditions include  inflammation  of the  small  and/or  large intestine ,  diarrhea / dysentery ,  abdominal pains , and  nausea / vomiting . These symptoms negatively impact nutritional status, including decreased absorption of  micronutrients , loss of appetite, weight loss, and intestinal blood loss that can often result in  anemia . It may also cause physical and mental disabilities,  delayed growth  in children, and skin irritation around the anus and vulva. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_928", "text": "The prevalence of intestinal parasites is the  highest among children that are  living in the poorest communities in developing nations. [ 1 ]  The most common causes of intestinal parasites are through consumption of contaminated water, infected soil, inadequate sanitation and hygiene, and improper hygiene. [ 3 ]  Specifically, lack of access to facilities for safe disposal of human waste can result in intestinal parasites and disease. Poor hygiene habits or lacking available hygiene resources, such as  hand washing  facilities, also negatively impact rates of disease. [ 4 ]  Parasitic contamination can also occur from eating raw produce, [ 5 ]   soil-eating behaviour , [ 6 ]  and low availability of safe drinking water. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_929", "text": "Parasites can get into the intestines by going through the mouth from uncooked or unwashed food, contaminated  water  or hands, or by  skin  contact with  larva  infected  soil ; they can also be transferred by the sexual act of  anilingus  in some cases. When the organisms are swallowed, they move into the intestines, where they can reproduce and cause symptoms. Children are particularly susceptible if they are not thoroughly cleaned after coming into contact with infected soil that is present in environments that they may frequently visit such as sandboxes and school playgrounds. People in developing countries are also at particular risk due to drinking water from sources that may be contaminated with parasites that colonize the gastrointestinal tract. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_930", "text": "Due to the wide variety of intestinal parasites, a description of the symptoms rarely is sufficient for diagnosis. Instead, medical personnel use one of two common tests: they search stool samples for the parasites, or apply an adhesive to the  anus  to search for eggs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_931", "text": "Major groups of parasites include  protozoans  (organisms having only one cell) and  parasitic worms  (helminths). Of these, protozoans, including  cryptosporidium ,  microsporidia , and  isospora , are most common in  HIV -infected persons. Each of these parasites can infect the digestive tract, and sometimes two or more can cause infection at the same time."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_932", "text": "Good hygiene is necessary to avoid reinfection.  The Rockefeller Foundation 's hookworm campaign in Mexico in the 1920s was extremely effective at eliminating hookworm from humans with the use of  anthelmintics . However, preventative measures were not adequately introduced to the people that were treated. Therefore, the rate of reinfection was extremely high and the project evaluated through any sort of scientific method was a marked failure. More education was needed to inform the people of the importance of wearing shoes, using  latrines  (better access to  sanitation ), and good hygiene. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_933", "text": "Intestinal parasite prevention methods are not isolated to specific geographical areas; however, many of the research-based interventions have primarily taken place in underdeveloped countries and regions, where sanitation is a large concern for spreading disease. [ citation needed ] Current best practice behaviors that prevent intestinal parasites include: using proper hand washing practices, using correctly-built latrines with ample ventilation, having a piped water source, and wearing shoes. [ 8 ] [ 9 ]  Currently, in some parts of Ethiopia where disease prevalence is high, up to 80% of people in a population lack access to washing facilities. While this is high, 93% did have access to a latrine, but only 29.2% of those latrines had proper construction to decrease parasitic infections. [ 9 ]  Behavioral interventions have focused on promoting washing, sometimes with soap, in context of education at schools and child care facilities. [ 10 ]  In recent studies, the best interventions follow a multidisciplinary approach by:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_934", "text": "Specific evidence-based interventions that may lower disease prevalence include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_935", "text": "Drugs are frequently used to kill parasites in the host. In earlier times,  turpentine  was often used for this, but modern drugs do not poison intestinal worms directly. Rather, anthelmintic drugs now inhibit an enzyme that is necessary for the worm to make the substance that prevents the worm from being digested. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_936", "text": "For example,  tapeworms  are usually treated with a medicine taken by mouth. The most commonly used medicine for tapeworms is  praziquantel . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_937", "text": "Human intestinal spirochetosis , often called just  intestinal spirochetosis  when the human context is implicit, is an infection of the  colonic -type  mucosa  with certain species of  spirochetal  bacteria. Similar infections sometimes occur in pigs, dogs, and birds;  porcine intestinal spirochaetosis  is an economically important disease of livestock."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_938", "text": "No clear association exists with complaints. However, potential associations include  abdominal pain  and watery  diarrhea , which may be seen with  blood ; however, these findings are not specific and may be due to a number of other causes. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_939", "text": "Human intestinal spirochetosis is caused by  Brachyspira pilosicoli  and  Brachyspira aalborgi . [ 3 ]  Porcine and avian intestinal spirochetosis are caused by  Brachyspira hyodysenteriae  and  Brachyspira pilosicoli . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_940", "text": "It is diagnosed by examination of  tissue , i.e.,  biopsy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_941", "text": "Symptomatic individuals can be treated with oral metronidazole."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_942", "text": "Intestinal varices  are dilated submucosal  veins  in the  intestine . [ citation needed ] One treatment includes a  transjugular intrahepatic portosystemic shunt . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_943", "text": "This article about a medical condition affecting the circulatory system is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_944", "text": "An  intracolonic explosion  or  colonic gas explosion  is an explosion inside the  colon  of a person due to ignition of explosive gases such as  methane . This can happen during colonic exploration, as a result of the electrical nature of a  colonoscope ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_945", "text": "A colonic gas explosion is rare; [ 1 ]  however, the result can be acute colonic  perforation , which can be fatal. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_946", "text": "An explosion is triggered by a combination of combustible gases such as hydrogen or methane, combustive gas such as oxygen, and heat. An explosion can also be caused by Crohn's disease. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_947", "text": "Careful bowel preparation, such as cleansing the colon before a procedure, is key to preventing an intracolonic explosion. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_948", "text": "This  surgery  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_949", "text": "Ischemic colitis  (also spelled  ischaemic colitis ) is a medical condition in which inflammation and injury of the  large intestine  result from inadequate blood supply ( ischemia ). Although uncommon in the general population, ischemic colitis occurs with greater frequency in the elderly, and is the most common form of  bowel ischemia . [ 1 ] [ 2 ] [ 3 ]  Causes of the reduced blood flow can include changes in the  systemic circulation  (e.g.  low blood pressure ) or local factors such as  constriction of blood vessels  or a  blood clot . In most cases, no specific cause can be identified. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_950", "text": "Ischemic colitis is usually suspected on the basis of the clinical setting,  physical examination , and laboratory test results; the diagnosis can be confirmed by  endoscopy  or by using sigmoid or endoscopic placement of a visible light spectroscopic catheter (see  Diagnosis ). Ischemic colitis can span a wide spectrum of severity; most patients are treated supportively and recover fully, while a minority with very severe ischemia may develop  sepsis  and become critically, [ 5 ]  sometimes fatally, ill. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_951", "text": "Patients with mild to moderate ischemic colitis are usually treated with IV fluids,  analgesia , and  bowel rest  (that is, no food or water by mouth) until the symptoms resolve. Those with severe ischemia who develop complications such as sepsis, intestinal  gangrene , or  bowel perforation  may require more aggressive interventions such as  surgery  and  intensive care . Most patients make a full recovery; occasionally, after severe ischemia, patients may develop long-term complications such as a  stricture [ 7 ]  or chronic  colitis . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_952", "text": "Three progressive phases of ischemic colitis have been described: [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_953", "text": "Symptoms of ischemic colitis vary depending on the severity of the ischemia. The most common early signs of ischemic colitis include  abdominal pain  (often left-sided), with mild to moderate amounts of  rectal bleeding . [ 11 ]  The sensitivity of findings among 73 patients were: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_954", "text": "Physical examination [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_955", "text": "Ischemic colitis is often classified according to the underlying cause.  Non-occlusive  ischemia develops because of low blood pressure or constriction of the vessels feeding the colon;  occlusive  ischemia indicates that a  blood clot  or other blockage has cut off blood flow to the colon. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_956", "text": "In hemodynamically unstable patients (i.e. shock) the mesenteric perfusion may be compromised. This condition is commonly asymptomatic, and usually only apparent through a systemic inflammatory response. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_957", "text": "Mostly the result of a thromboembolism. Commonly the embolism is caused by  atrial fibrillation , valvular disease,  myocardial infarction , or  cardiomyopathy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_958", "text": "In addition, ischemic colitis is a well-recognized complication of abdominal aortic aneurysm repair, when the origin of the inferior mesenteric artery is covered by the aortic graft. [ 13 ] [ 14 ]   In a 1991 review concerning 2137 patients the accidental inferior mesenteric artery ligation was the most common cause (74%) of ischemic colitis. [ 15 ]  Thus, patients without adequate collateralization are at risk for ischemia of the descending and sigmoid colon.  Bloody diarrhea and leukocytosis in the postoperative period are essentially diagnostic of ischemic colitis. The complication can be prevented through careful selection of subjects that may require replanting inferior mesenteric artery (IMA) and completing the pre surgical procedure information with an instrumental evaluation during surgical treatment. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_959", "text": "The colon receives blood from both the  superior  and  inferior mesenteric arteries . The blood supply from these two major arteries overlaps, with abundant collateral circulation via the  marginal artery of the colon . However, there are weak points, or \"watershed\" areas, at the borders of the territory supplied by each of these arteries, such as the splenic flexure and the rectosigmoid junction. These watershed areas are most vulnerable to ischemia when blood flow decreases, as they have the fewest vascular collaterals. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_960", "text": "The  rectum  receives blood from both the inferior mesenteric artery and the  internal iliac artery ; the rectum is rarely involved by colonic ischemia due to this dual blood supply. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_961", "text": "Under ordinary conditions, the colon receives between 10% and 35% of the total cardiac output. [ 17 ] [ 18 ]  If blood flow to the colon drops by more than about 50%, ischemia will develop. The arteries feeding the colon are very sensitive to vasoconstrictors; presumably this is an evolutionary adaptation to shunt blood away from the bowel and to the  heart  and  brain  in times of stress. [ 19 ]  As a result, during periods of  low blood pressure , the arteries feeding the colon clamp down vigorously; a similar process can result from vasoconstricting drugs such as  ergotamine ,  cocaine , or  vasopressors . This vasoconstriction can result in non-occlusive ischemic colitis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_962", "text": "A range of pathologic findings are seen in ischemic colitis, corresponding to the spectrum of clinical severity. In its mildest form, mucosal and submucosal  hemorrhage  and  edema  are seen, possibly with mild  necrosis  or  ulceration . [ 4 ]  With more severe ischemia, a pathologic picture resembling  inflammatory bowel disease  (i.e. chronic ulcerations, crypt  abscesses  and pseudopolyps) may be seen. [ 20 ]  In the most severe cases, transmural infarction with resulting perforation may be seen; after recovery, the muscularis propria may be replaced by fibrous tissue, resulting in a stricture. [ 4 ]  Following restoration of normal blood flow,  reperfusion injury  may also contribute to the damage to the colon. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_963", "text": "Ischemic colitis must be differentiated from the many other causes of  abdominal pain  and  rectal bleeding  (for example,  infection ,  inflammatory bowel disease ,  diverticulosis , or  colon cancer ). It is also important to differentiate ischemic colitis, which often resolves on its own, from the more immediately life-threatening condition of acute  mesenteric ischemia  of the  small bowel . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_964", "text": "There are devices which test the sufficiency of oxygen delivery to the colon. The first device approved by the U.S. FDA in 2004 uses visible light spectroscopy to analyze capillary oxygen levels. Use during aortic aneurysm repair detected when colon oxygen levels fell below sustainable levels, allowing real-time repair. In several studies, Specificity has been 90% or higher for acute colonic ischemia, and 83% for chronic mesenteric ischemia, with a sensitivity of 71%-92%. This device must be placed using endoscopy, however. [ 22 ] [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_965", "text": "There is a recent optical test, but it requires endoscopy (see Diagnosis). There are no specific blood tests for ischemic colitis. The sensitivity of tests among 73 patients were: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_966", "text": "Plain  X-rays  are often normal or show non-specific findings. [ 25 ]  In a series of 73 patients, plain abdominal radiography (56%) showing colic distension in 53% or a pneumoperitoneum in 3%. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_967", "text": "CT scans  are often used in the evaluation of abdominal pain and rectal bleeding, and may suggest the diagnosis of ischemic colitis, pick up complications, or suggest an alternate diagnosis. [ 26 ] [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_968", "text": "Endoscopic  evaluation, via  colonoscopy  or flexible  sigmoidoscopy , is the procedure of choice if the diagnosis remains unclear. Ischemic colitis has a distinctive endoscopic appearance; endoscopy can also facilitate alternate diagnoses such as  infection  or  inflammatory bowel disease .  Biopsies  can be taken via endoscopy to provide more information. Visible light spectroscopy, performed using catheters placed through the 5\u00a0mm channel of the endoscope, is diagnostic (see Diagnosis). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_969", "text": "Except in the most severe cases, ischemic colitis is treated with supportive care.  IV fluids  are given to treat  dehydration , and the patient is placed on bowel rest (meaning nothing to eat or drink) until the symptoms resolve. If possible, cardiac function and oxygenation should be optimized to improve oxygen delivery to the ischemic bowel. A  nasogastric tube  may be inserted if an  ileus  is present. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_970", "text": "Antibiotics  are sometimes given in moderate to severe cases; the data supporting this practice date to the 1950s, [ 29 ]  although there is more recent animal data suggesting that antibiotics may increase survival and prevent  bacteria  from crossing the damaged lining of the colon into the bloodstream. [ 30 ] [ 31 ] [ 32 ]  The use of  prophylactic  antibiotics in ischemic colitis has not been prospectively evaluated in  humans , but many authorities recommend their use based on the animal data. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_971", "text": "Patients being treated supportively are carefully monitored. If they develop worsening symptoms and signs such as  high white blood cell count ,  fever , worsened abdominal pain, or increased bleeding, then they may require  surgical intervention ; this usually consists of  laparotomy  and  bowel resection . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_972", "text": "Most patients with ischemic colitis recover fully, although the prognosis depends on the severity of the ischemia. Patients with pre-existing  peripheral vascular disease  or ischemia of the ascending (right) colon may be at increased risk for complications or death. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_973", "text": "Non-gangrenous ischemic colitis, which comprises the vast majority of cases, is associated with a mortality rate of approximately 6%. [ 34 ]  However, the minority of patients who develop  gangrene  as a result of colonic ischemia have a mortality rate of 50\u201375% with surgical treatment; the mortality rate is almost 100% without surgical intervention. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_974", "text": "About 20% of patients with acute ischemic colitis may develop a long-term complication known as  chronic ischemic colitis . [ 8 ]  Symptoms can include recurrent infections, bloody diarrhea, weight loss, and chronic abdominal pain. Chronic ischemic colitis is often treated with surgical removal of the chronically diseased portion of the bowel. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_975", "text": "A  colonic stricture  is a band of scar tissue which forms as a result of the ischemic injury and narrows the  lumen  of the colon. Strictures are often treated observantly; they may heal spontaneously over 12\u201324 months. If a  bowel obstruction  develops as a result of the stricture, surgical resection is the usual treatment, [ 36 ]  although  endoscopic dilatation  and  stenting  have also been employed. [ 37 ] [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_976", "text": "The exact incidence of ischemic colitis is difficult to estimate, as many patients with mild ischemia may not seek medical attention. Ischemic colitis is responsible for about 1 in 2000 hospital admissions and is seen on about 1 in 100 endoscopies. [ 4 ]  Men and women are affected equally; ischemic colitis is a disease of the elderly, with more than 90% of cases occurring in people over the age of 60. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_977", "text": "Isolated superior mesenteric artery dissection (ISMAD)  is a rare but potentially life-threatening condition that causes acute abdominal pain. It refers to a dissection that occurs solely in the  superior mesenteric artery  (SMA), typically spontaneously, and does not involve the  aorta . [ 1 ] \nAlthough  aortic dissection  can frequently extend into its peripheral territories, it is rare for these branches to have dissection without main aortic trunk involvement. The SMA is the most common site of dissection among visceral arteries compared to other gastrointestinal arteries. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_978", "text": "ISMAD primarily manifests through a sudden onset of pain, which can vary in location and intensity. [ 2 ]   The nature of the pain and its location can provide clues to the diagnosis of ISMAD. [ 2 ]  The types of pain reported in ISMAD cases include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_979", "text": "ISMAD is more common in males, accounting for 80.6% of cases, and typically occurs in individuals in their fifth decade of life, with a mean age of 55.7 years. [ 2 ]  Other risk factors include smoking and hypertension. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_980", "text": "ISMAD can be associated with isolated arterial dissections and aneurysms, such as those in the celiac and renal arteries, suggesting a systemic component. [ 5 ]  It has been linked to certain vascular diseases like  fibromuscular dysplasia , medial degeneration, and  atherosclerosis . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_981", "text": "The structure of the SMA itself can contribute to ISMAD. Certain anatomical variants are more susceptible to shear stress, leading to dissection. This stress occurs when the SMA, lacking mechanical support from the pancreas, bends within the mesenteric root. The anterior wall, the most common site of ISMAD, faces increased stress due to the SMA's convexity after bending. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_982", "text": "Genetics also plays a role in ISMAD. It has been hypothesized that a genetic component exists, as most reported cases are from East Asia. This hypothesis is supported by a familial case of ISMAD from China linked to a chromosomal locus of 5q13\u201314. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_983", "text": "In terms of the diagnosis of ISMAD, the following is done: [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_984", "text": "The management of isolated superior mesenteric artery dissection (ISMAD) often involves conservative treatment, which includes blood pressure lowering therapy,  analgesics , and initial bowel rest. [ 4 ]  Periodic follow-ups with  CT angiography  are a part of the conservative treatment approach. Over time, many patients show improvement or no change in their condition as observed through these follow-ups. A small percentage of patients reported mild abdominal discomfort during the follow-up period, but no patient developed recurrent abdominal pain following conservative treatment. Importantly, there was no mortality related to SISMAD. These observations suggest that conservative treatment can be an effective approach for managing patients with SISMAD. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_985", "text": "In cases where conservative treatment is not sufficient, endovascular procedures may be considered. These include stenting/stent-grafting of the true lumen, (coil) embolization of the false lumen/aneurysm, catheter-directed local thrombolysis, percutaneous transluminal angioplasty, and catheter-directed local papaverine infusion at 30 mg/h. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_986", "text": "In related surgical procedures such as Minimally Invasive Pancreaticoduodenectomy (MIPD), various approaches for dissection around the SMA have been reported, including anterior, posterior, right, and left approaches. [ 7 ] While these methods are not specifically used for ISMAD, understanding these surgical techniques could potentially inform future treatment strategies for ISMAD. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_987", "text": "The prognosis for patients with ISMAD who undergo conservative treatment is generally positive. Follow-up studies show that the majority of patients either improve or do not show progression of the condition. This is evidenced by CT angiograms, which often show a decrease in the size of the false lumen, a decrease in the length of the dissection, or complete remodeling of the dissection. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_988", "text": "During the follow-up period, some patients reported mild, nonspecific abdominal discomfort. However, no patient developed recurrent abdominal pain following conservative treatment, and there was no mortality related to ISMAD. These findings further support the effectiveness of conservative treatment for managing patients with ISMAD. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_989", "text": "In cases where conservative treatment is not sufficient, endovascular procedures may be considered. These include stenting/ stent -grafting of the true lumen, (coil) embolization of the false lumen/aneurysm, catheter-directed local thrombolysis, percutaneous transluminal angioplasty, and catheter-directed local papaverine infusion at 30 mg/h. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_990", "text": "Keriorrhea  is the production of greasy, orange-colored stools which results from the consumption of indigestible  wax esters  found in  oilfish  and  escolar . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_991", "text": "This medical  symptom  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_992", "text": "Lower gastrointestinal bleeding  ( LGIB ) is any form of  gastrointestinal bleeding  in the  lower gastrointestinal tract . LGIB is a common reason for seeking medical attention at a hospital's emergency department. [ 1 ]  LGIB accounts for 30\u201340% of all gastrointestinal bleeding and is less common than  upper gastrointestinal bleeding  (UGIB). [ 2 ]  It is estimated that UGIB accounts for 100\u2013200 per 100,000 cases versus 20\u201327 per 100,000 cases for LGIB. [ 3 ]  Approximately 85% of lower gastrointestinal bleeding involves the  large intestine , 10% are from bleeds that are actually upper gastrointestinal bleeds, and 3\u20135% involve the  small intestine . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_993", "text": "A lower gastrointestinal bleed is defined as bleeding originating distal to the  ileocecal valve , which includes the  colon ,  rectum , and  anus . [ 2 ]  LGIB was previously defined as any bleed that occurs distal to the  ligament of Treitz , which included the aforementioned parts of the intestine and also included the last 1/4 of the  duodenum  and the entire area of the  jejunum  and  ileum . [ 1 ]  This has been divided into middle gastrointestinal bleeding (from the ligament of Treitz to the ileocecal valve) and lower gastrointestinal bleeding which involves a bleed anywhere from the ileocecal valve to the anus. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_994", "text": "The  stool  of a person with a lower gastrointestinal bleed is a good (but not infallible) indication of where the bleeding is occurring. Black tarry appearing stools medically referred to as  melena  usually indicates blood that has been in the GI tract for at least 8 hours. [ 1 ]  Melena is four-times more likely to come from an upper gastrointestinal bleed than from the lower GI tract; however, it can also occur in either the duodenum and jejunum, and occasionally the portions of the  small intestine  and  proximal colon . [ 5 ]  Bright red stool, called  hematochezia , is the sign of a fast moving active GI bleed. [ 1 ]  The bright red or maroon color is due to the short time taken from the site of the bleed and the exiting at the anus. The presence of hematochezia is six-times greater in a LGIB than with a UGIB. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_995", "text": "Occasionally, a person with a LGIB will not present with any signs of internal bleeding, especially if there is a chronic bleed with ongoing low levels of blood loss. In these cases, a diagnostic assessment or pre-assessment should watch for other signs and symptoms that the patient may present with. These include, but are not limited to,  hypotension ,  tachycardia ,  angina ,  syncope ,  weakness ,  confusion ,  stroke ,  myocardial infarction / heart attack , and  shock ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_996", "text": "The following are possible causes of a LGIB:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_997", "text": "Diagnostic evaluation must be performed after patients have been adequately resuscitated. If an upper GI source is suspected, an  upper endoscopy  should be performed first.  Lower gastrointestinal series  evaluation can be performed with  anoscopy , flexible  sigmoidoscopy ,  colonoscopy , rarely  barium enema , and various  radiologic  studies. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_998", "text": "The history in these patients should focus on factors that could be associated with potential causes: blood coating the stool suggests hemorrhoidal bleeding while blood mixed in the stool implies a more proximal source; bloody diarrhea and tenesmus is associated with  inflammatory bowel disease  while bloody diarrhea with fever and  abdominal pain  especially with recent travel history suggests infectious colitis; pain with defecation occurs with hemorrhoids and anal fissure; change in stool caliber and weight loss is concerning for  colon cancer ; abdominal pain can be associated with inflammatory bowel disease, infectious colitis, or ischemic colitis; painless bleeding is characteristic of diverticular bleeding,  arteriovenous malformation  (AVM), and radiation proctitis;  nonsteroidal anti-inflammatory drug  (NSAID) use is a risk factor for diverticular bleeding and NSAID-induced colonic ulcer; and recent colonoscopy with polypectomy suggests postpolypectomy bleeding. Patients should be asked about symptoms of hemodynamic compromise, including dyspnea, chest pain, lightheadedness, and fatigue. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_999", "text": "Orthostatic hypotension  implies at least a 15% loss of blood volume and suggests a more severe bleeding episode. Evaluate for abdominal tenderness, masses, and  enlargement of the liver  and  spleen . Additional key elements include a careful and thorough inspection of the anus, palpation for rectal masses, characterization of the stool color, and a stool guaiac card test to evaluate for the presence of blood. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1000", "text": "Among the blood tests that should be performed are a  complete blood count ,  prothrombin time ,  partial thromboplastin time ,  electrolytes , and typing and cross-matching for transfusion of blood products. [ 8 ] \nA  clotting abnormality  and  low platelet concentration in the blood  should be immediately corrected if possible. Platelets should be maintained above 50,000/mL and clotting abnormalities should be corrected with  vitamin K  or  fresh frozen plasma . Vitamin K should be taken orally unless the patient has  cirrhosis  or biliary obstruction, in which case it should be administered subcutaneously. The full effect of vitamin K is not obtained for 12\u201324 hours, unlike fresh frozen plasma which immediately reverses clotting abnormalities. The intravenous formulation of  vitamin K  reverses coagulopathy more quickly and may be used in cases of severe bleeding, however, patients should be monitored for anaphylaxis. The effects of fresh frozen plasma last about 3\u20135 hours and large volumes (> 2\u20133 L) may be required to completely reverse clotting abnormalities, depending on the initial prothrombin time. Recombinant activated factor VII has been approved for use in patients with  hemophilia  A and B with factor VIII and IX inhibitors. Evidence of possible benefit in patients with  cirrhosis  and GI bleeding has been demonstrated, although the optimal dose is unclear and recombinant activated factor VII is very expensive. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1001", "text": "Anoscopy is useful only for diagnosing bleeding sources from the anorectal junction and anal canal, including internal  hemorrhoids  and anal fissures. It is superior to flexible sigmoidoscopy for detecting hemorrhoids in an outpatient setting and can be performed quickly in the office or at the bedside as an adjunct to flexible sigmoidoscopy and colonoscopy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1002", "text": "Flexible sigmoidoscopy  uses a 65-cm long sigmoidoscope that visualizes the left  colon . It can be performed without sedation and only minimal preparation with enemas. However, the diagnostic yield of flexible sigmoidoscopy in acute lower GI bleeding is only 9%. The role of anoscopy and flexible sigmoidoscopy in inpatients with acute lower GI bleeding is limited, as most patients should undergo colonoscopy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1003", "text": "Colonoscopy is the test of choice in the majority of patients with acute Lower GI bleeding as it can be both diagnostic and therapeutic. The diagnostic accuracy of colonoscopy in lower GI bleeding ranges from 48% to 90%, and urgent colonoscopy appears to increase diagnostic yield. This wide range in yield is partially explained by different criteria for diagnosis, as often if no active bleeding, nonbleeding visible vessel, or adherent clot is found, bleeding is attributed to a lesion if blood is present in the area. The presence of fresh blood in the  terminal ileum  is presumed to indicate a non colonic source of bleeding.\nThe overall complication rate of colonoscopy in acute lower GI bleeding is 1.3%. Bowel preparation is safe and well tolerated in most patients. The complication rate of colonoscopy in an unprepped colon may be higher. About 2\u20136% of colonoscopy preparations in acute lower GI bleeding are poor. Between 4 and 8 L of G olytely  should be administered orally or via nasogastric tube until the effluence is clear. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1004", "text": "In most cases requiring emergency hospital admission, the bleeding will resolve spontaneously. [ 2 ] [ 10 ]  If a patient is suspected of having  severe blood loss  they will most likely be placed on a vital sign monitor and administered oxygen either by  nasal cannula  or  simple face mask . An  intravenous catheter  will be placed into an easily accessible area and IV fluids will be administered to replace lost blood volume. [ 1 ]  Endoscopic evaluation with a  colonoscopy  (and possibly an  esophagogastroduodenoscopy  to exclude an UGIB) should typically occur within 24 hours of hospital presentation. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1005", "text": "If the person with LGIB is on low-dose  aspirin  for prevention of a first heart attack (i.e., the person has never had a heart attack before), stopping the aspirin is recommended. [ 2 ]  In contrast, if the person has previously had a heart attack, the aspirin should be continued despite the active LGIB due to the benefits of preventing another heart attack and consequent death outweighing the risk of bleeding. [ 2 ]   Dual antiplatelet therapy  (e.g., use of both aspirin and  clopidogrel ) should continue if the person with a LGIB underwent  stenting  of the heart's  coronary arteries  within the last 30 days or a recent  acute coronary syndrome  episode (e.g.,  unstable angina  or a  myocardial infarction ) within 90 days of the LGIB event. [ 2 ]  Individuals at high risk of another heart attack but not meeting the above criteria should continue their aspirin during the LGIB event but stop the other antiplatelet medication for 1\u20137 days following cessation of the bleed. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1006", "text": "Predicting which patients will develop adverse outcomes, complications or severe bleeding can be difficult. One recent study identified poor kidney function (creatinine > 150 \u03bcm), age over 60 years, abnormal haemodynamic parameters on presentation (low blood pressure) and persistent bleeding within the first 24 hours as risk factors for worse outcome. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1007", "text": "Surgical intervention  is warranted in cases of LGIB that persist despite attempts to stop the bleeding with endoscopic or interventional radiology interventions. [ 2 ]   It is most likely that a  surgical consult  will be ordered if the patient is unable to be stabilized by non-invasive techniques, or if a perforation is found that requires surgery (e.g., subtotal  removal of the colon ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1008", "text": "Malabsorption  is a state arising from abnormality in  absorption  of  food nutrients  across the  gastrointestinal (GI) tract . Impairment can be of single or multiple nutrients depending on the abnormality. This may lead to  malnutrition  and a variety of  anaemias . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1009", "text": "Normally the human gastrointestinal tract digests and absorbs dietary nutrients with remarkable efficiency. A typical Western diet ingested by an adult in one day includes approximately 100 g of fat, 400 g of carbohydrate, 100 g of protein, 2 L of fluid, and the required  sodium ,  potassium ,  chloride ,  calcium ,  vitamins , and other elements.  [ citation needed ]   Salivary ,  gastric ,  intestinal ,  hepatic , and  pancreatic  secretions add an additional 7\u20138 L of protein-, lipid-, and electrolyte-containing fluid to intestinal contents. This massive load is reduced by the small and large intestines to less than 200 g of stool that contains less than 8 g of fat, 1\u20132 g of nitrogen, and less than 20\u00a0mmol each of  Na + ,  K + ,  Cl \u2212 ,  HCO \u2212 3 ,  Ca 2+ , or  Mg 2+ ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1010", "text": "If there is impairment of any of the many steps involved in the complex process of nutrient digestion and absorption, intestinal  malabsorption  may ensue. If the abnormality involves a single step in the absorptive process, as in primary  lactase deficiency , or if the disease process is limited to the very proximal small intestine, then selective malabsorption of only a single nutrient may occur. However, generalized  malabsorption  of multiple dietary nutrients develops when the disease process is extensive, thus disturbing several digestive and absorptive processes, as occurs in  coeliac disease  with extensive involvement of the  small intestine . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1011", "text": "Depending on the nature of the disease process causing malabsorption and its extent, gastrointestinal symptoms may range from severe to subtle or may even be totally absent.  Diarrhea ,  weight loss ,  flatulence , abdominal  bloating , abdominal  cramps , and pain may be present. Although diarrhea is a common complaint, the character and frequency of stools may vary considerably ranging from over 10 watery stools per day to less than one voluminous putty-like stool, the latter causing some patients to complain of constipation. On the other hand, stool mass is invariably increased in patients with  steatorrhea  and generalized malabsorption above the normal with 150\u2013200 g/day. Not only do unabsorbed nutrients contribute to stool mass but mucosal fluid and electrolyte secretion is also increased in diseases associated with mucosal inflammation such as  coeliac disease . In addition, unabsorbed fatty acids, converted to hydroxy-fatty acids by colonic flora, as well as unabsorbed  bile acids  both impair absorption and induce secretion of water and electrolytes by the colon adding to stool mass. Weight loss is common among patients with significant intestinal malabsorption but must be evaluated in the context of caloric intake. Some patients compensate for fecal wastage of unabsorbed nutrients by significantly increasing their oral intake. Eliciting a careful dietary history from patients with suspected malabsorption is therefore crucial. Excessive flatus and abdominal bloating may reflect excessive gas production due to fermentation of unabsorbed carbohydrate, especially among patients with a primary or secondary  disaccharidase  deficiency, such as  lactose intolerance  or  sucrose intolerance . Malabsorption of dietary nutrients and excessive fluid secretion by inflamed small intestine also contribute to abdominal distention and bloating. Prevalence, severity, and character of abdominal pain vary considerably among the various disease processes associated with intestinal malabsorption. For example, pain is common in patients with chronic pancreatitis or pancreatic cancer and  Crohn's disease , but it is absent in many patients with coeliac disease or postgastrectomy malabsorption. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1012", "text": "Substantial numbers of patients with intestinal malabsorption present initially with symptoms or laboratory abnormalities that point to other organ systems in the absence of or overshadowing symptoms referable to the gastrointestinal tract. For example, there is increasing epidemiologic evidence that more patients with coeliac disease present with  anemia  and  osteopenia  in the absence of significant classic gastrointestinal symptoms. Microcytic,  macrocytic , or dimorphic anemia may reflect impaired  iron , folate, or  vitamin B12  absorption.  Purpura ,  subconjunctival hemorrhage , or even frank bleeding may reflect hypoprothrombinemia secondary to vitamin K malabsorption. Osteopenia is common, especially in the presence of  steatorrhea . Impaired calcium and vitamin D absorption and chelation of calcium by unabsorbed fatty acids resulting in fecal loss of calcium may all contribute. If calcium deficiency is prolonged, secondary hyperparathyroidism may develop. Prolonged malnutrition may induce amenorrhea, infertility, and impotence. Edema and even ascites may reflect hypoproteinemia associated with protein losing enteropathy caused by  lymphatic obstruction  or extensive mucosal inflammation. Dermatitis and peripheral neuropathy may be caused by malabsorption of specific vitamins or micronutrients and essential fatty acids. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1013", "text": "Symptoms can manifest in a variety of ways and features might give a clue to the underlying condition. Symptoms can be  intestinal  or extra-intestinal - the former predominates in severe malabsorption. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1014", "text": "The main purpose of the  gastrointestinal tract  is to  digest  and  absorb  nutrients ( fat ,  carbohydrate ,  protein , micronutrients ( vitamins  and  trace minerals ), water, and  electrolytes .  Digestion  involves both mechanical and  enzymatic  breakdown of food.  Mechanical processes  include chewing, gastric churning, and the to-and-fro mixing in the  small intestine .  Enzymatic hydrolysis  is initiated by intraluminal processes requiring gastric, pancreatic, and biliary secretions. The final products of digestion are absorbed through the  intestinal epithelial  cells. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1015", "text": "Malabsorption constitutes the pathological interference with the normal physiological sequence of  digestion  (intraluminal process), absorption (mucosal process) and transport (postmucosal events) of nutrients. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1016", "text": "Intestinal  malabsorption can be due to: [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1017", "text": "There is no single, specific test for malabsorption. As for most medical conditions, investigation is guided by  symptoms  and signs. A range of different conditions can produce malabsorption and it is necessary to look for each of these specifically. Many tests have been advocated, and some, such as tests for pancreatic function are complex, vary between centers and have not been widely adopted. However, better tests have become available with greater ease of use, better sensitivity and specificity for the causative conditions. Tests are also needed to detect the systemic effects of deficiency of the malabsorbed nutrients (such as anaemia with vitamin B12 malabsorption). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1018", "text": "Some [ who? ]  prefer to classify malabsorption clinically into three basic categories: [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1019", "text": "Treatment is directed largely towards management of underlying cause: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1020", "text": "Megacolon  is an abnormal dilation of the  colon  (also called the large  intestine ). [ 1 ] [ 2 ]  This leads to  hypertrophy  of the colon. [ 2 ]  The dilation is often accompanied by a  paralysis  of the  peristaltic  movements of the bowel. In more extreme cases, the  feces  consolidate into hard masses inside the colon, called  fecalomas  (literally,  fecal tumor ), which can require  surgery  to be removed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1021", "text": "A human colon is considered abnormally enlarged if it has a  diameter  greater than 12\u00a0 cm [ 3 ]  in the  cecum  (it is usually less than 9\u00a0cm [ 4 ] ), greater than 6.5\u00a0cm [ 3 ]  in the  rectosigmoid  region and greater than 8\u00a0cm [ 3 ]  for the  ascending colon . The transverse colon is usually less than 6\u00a0cm in diameter. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1022", "text": "A megacolon can be either  acute  or  chronic . It can also be classified according to cause. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1023", "text": "External signs and symptoms are  constipation  of very long duration, [ 2 ]  abdominal  bloating , abdominal tenderness and  tympany ,  abdominal pain ,  palpation  of hard fecal masses and, in  toxic megacolon ,  fever , low blood  potassium ,  tachycardia  and may lead to  shock .  Stercoral ulcers  are sometimes observed in chronic megacolon, which may lead to perforation of the intestinal wall in approximately 3% of the cases, leading to  sepsis  and risk of death. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1024", "text": "Also called  Hirschsprung's disease , it is a  congenital  disorder of the colon in which  nerve cells  of the  myenteric plexus  in its walls, also known as ganglion cells, are absent.  It is a rare disorder (1:5000), with prevalence among males being four times that of females.  Hirschsprung's disease develops in the  fetus  during the early stages of  pregnancy .  A genetic predisposition to Hirschsprung's disease has been linked to  chromosome 13  where a  missense mutation  at an ultraconserved region impairs functionality of the W276C receptor.  Seven other genes seem to be implicated, however.  If untreated, the patient can develop  enterocolitis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1025", "text": "Toxic megacolon is mainly seen in  ulcerative colitis  and  pseudomembranous colitis , two chronic  inflammations  of the colon (and occasionally, in the other type of  inflammatory bowel disease ,  Crohn's disease ). Its mechanism is incompletely understood. It is probably due to excessive production of  nitric oxide , at least in ulcerative colitis. The prevalence is about the same for both sexes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1026", "text": "In patients with HIV/AIDS,  cytomegalovirus  (CMV) colitis is the leading cause of toxic megacolon and emergency laparotomy. CMV may also increase the risk of toxic megacolon in non-HIV/AIDS patients with IBD. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1027", "text": "Megacolon can be associated with  Chagas disease . [ 11 ]  Chagas disease is caused by  Trypanosoma cruzi , a flagellate  protozoan  transmitted by the  assassin bug . Chagas disease can also be acquired congenitally, through blood transfusion or organ transplant, and rarely through contaminated food (for example  garapa ). There are several theories on how megacolon (and also  megaesophagus ) develops in Chagas disease. The   Austrian - Brazilian   physician  and  pathologist   Fritz K\u00f6berle  was the first to propose the  neurogenic hypothesis  based on the documented destruction of the  myenteric plexus  in the walls of the intestinal tracts of Chagas patients. In this, the destruction of the  autonomic nervous system  innervation of the colon leads to a loss of the normal  smooth muscle  tone of the wall and subsequent gradual dilation. His research proved that, by extensively quantifying the number of neurons of the autonomic nervous system in the Auerbach's plexus, that: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1028", "text": "Why  T. cruzi  causes the destruction, however, remains to be determined. There is evidence for the presence of specific  neurotoxins  as well as a disorderly  immune system  reaction. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1029", "text": "Diagnosis  is achieved mainly by plain and contrasted  radiographical  and  ultrasound  imaging. Colonic marker transit studies are useful to distinguish colonic inertia from functional outlet obstruction causes. In this test, the patient swallows a water-soluble bolus of  radiocontrast agent  and films are obtained 1, 3, and 5 days later. Patients with colonic inertia show the marker spread throughout the large intestines, while patients with outlet obstruction exhibit slow accumulations of markers in some places. A  colonoscopy  can also be used to rule out mechanical obstructive causes.  Anorectal manometry  may help to differentiate acquired from congenital forms. Rectal biopsy is recommended to make a final diagnosis of Hirschsprung disease. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1030", "text": "Possible treatments include: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1031", "text": "There are several surgical approaches to treat megacolon, such as a  colectomy [ 2 ] [ 14 ]  (removal of the entire colon) with ileorectal  anastomosis  (ligation of the remaining ileum and rectum segments), or a total  proctocolectomy  (removal of colon, sigmoid and rectum) followed by  ileostomy  or followed by ileoanal anastomosis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1032", "text": "Megarectum  is a large  rectum  as a result of underlying  nerve  supply abnormalities or  muscle  dysfunction, which remains after disimpaction of the rectum.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1033", "text": "The Principles of Surgery textbook describes any rectum that can hold more than 1500cc of fluid as a megarectum. The term megarectum is also used for a large rectal mass on  rectal examination , a wide rectum on an  abdominal x-ray , the presence of impaired rectal sensation or the finding of large maximal rectal volumes on  anorectal manometry . In addition, can be the bloating of the colon due to infection, also called  megacolon .  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1034", "text": "On  defecography , megarectum is suggested by a rectal width of >9\u00a0cm at the level of the distal  sacrum . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1035", "text": "Melanosis coli , also  pseudomelanosis coli , is a disorder of pigmentation of the wall of the  colon , often identified at the time of  colonoscopy . It is benign and may have no significant correlation with disease. The brown pigment is  lipofuscin  in  macrophages , not  melanin . [ citation needed ]  It is most commonly associated with the use of certain laxatives."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1036", "text": "The most common cause of melanosis coli is the extended use of  laxatives , and commonly  anthraquinone  containing laxatives such as  senna ,  aloe vera , and other plant  glycosides . [ 1 ]  The anthranoid laxatives pass through the gastrointestinal tract unabsorbed until they reach the large intestine, where they are changed into their active forms. The resulting active compounds cause damage to the cells in the lining of the intestine and leads to apoptosis (a form of cell death). The damaged (apoptotic) cells appear as darkly pigmented bodies that may be taken up by scavenger cells known as macrophages. When enough cells have been damaged, the characteristic pigmentation of the bowel wall develops. The condition can develop after just a few months of laxative use. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1037", "text": "However, other causes are identified, including an increase in colonic epithelial  apoptosis . [ 3 ]   Endoscopically , the  mucosa  may show a brownish discoloration in a  moir\u00e9 pattern . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1038", "text": "On  biopsy , melanosis coli shows characteristic pigment-laden  macrophages  within the mucosa on  PAS  staining. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1039", "text": "The histologic  differential diagnosis  of mucosal pigmentation is:  lipofuscin  (melanosis coli),  hemosiderin-laden macrophages , and  melanin  (rare)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1040", "text": "No adverse effects or consequences of melanosis coli have been identified. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1041", "text": "The condition is unrelated to true melanoses, such as  Peutz\u2013Jeghers syndrome  and  smoker's melanosis . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1042", "text": "Peutz\u2013Jeghers syndrome causes pigmentation of the skin and mucous surfaces with  melanin , and polyps in the  digestive tract ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1043", "text": "Pseudomelanoses of other parts of the  gastrointestinal tract  have also been reported, and are of unclear relevance. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1044", "text": "Patients with  colostomies  can have melanosis involving the  stoma , which is also of no significance. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1045", "text": "Microsporidiosis  is an opportunistic intestinal infection that causes  diarrhea  and  wasting  in  immunocompromised  individuals ( HIV , for example). It results from different species of  microsporidia , a group of microbial (unicellular) fungi. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1046", "text": "In  HIV -infected individuals, microsporidiosis generally occurs when  CD4 +  T cell  counts fall below 150."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1047", "text": "Microsporidia  have emerged with significant mortality risk in  immunocompromised  individuals. These are small, single-celled, obligately  intracellular parasites  linked to water sources as well as wild, and domestic animals. [ 2 ]  They were once considered  protozoans  or  protists , but are now known to be  fungi , [ 3 ]  or a sister group to fungi. [ 4 ]   The most common causes of microsporidiosis is  Enterocytozoon bieneusi  and  Encephalitozoon intestinalis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1048", "text": "At least 15 microsporidian species have been recognized [ 5 ]  as human  pathogens , spread across nine genera:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1049", "text": "The primary causes are  Enterocytozoon bieneusi  and  Encephalitozoon intestinalis . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1050", "text": "(Coded to  image  at right)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1051", "text": "The best option for diagnosis is using PCR. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1052", "text": "Diagnosis with Microsporidia can be done through  gram - positive ,  acid-fast  spores in stool and biopsy material with morphologic demonstration of the organism. Initial detection through light microscopic examination of tissue sections, stools, duodenal aspirates, nasal discharges,  bronchoalveolar lavage  fluids, and conjunctival smears. [ 7 ]  Definitive diagnosis can also be achieved through fluorescein-tagged antibody  immunofluorescence  or electron microscopy, [ 7 ]  and species identification can be done through  PCR . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1053", "text": "Although it is classified as a  protozoal disease  in  ICD-10 , their phylogenetic placement has been resolved to be within the  Fungi , and some sources classify microsporidiosis as a  mycosis , [ 9 ]  however, they are highly divergent and rapidly evolving. [ 10 ] [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1054", "text": "Fumagillin  has been used in the treatment. [ 6 ] [ 13 ]  Another agent used is  albendazole . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1055", "text": "Because of its severe mortality risk in immunocompromised individuals, two main agents are used:  Albendazole , which inhibits  tubulin , and  Fumagillin , which inhibits methionine aminopeptidase type two. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1056", "text": "Microvillus inclusion disease , previously known as  Davidson's disease ,  congenital microvillus atrophy  and, less specifically,  microvillus atrophy  (note: microvillus is often misspelled as microvillous), is a rare  genetic disorder  of the  small intestine  that is inherited in an  autosomal recessive  pattern. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1057", "text": "It is characterized by chronic, intractable  diarrhea  in new-born infants, starting in the first few days of life. [ 3 ] \nThis results in  metabolic acidosis  and severe  dehydration . Pregnancy and birth are usually normal. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1058", "text": "It is caused by a congenital villus atrophy, atrophy of apical  microvilli  and intracellular accumulation of apical enzymes and transporters in the  epithelial cells  of the small intestine. [ 4 ]  MVID is in most cases caused by mutations in the MYO5B gene. Other genes are also responsible of the disease:  STXBP2  or Munc18-2 (also causing  Familial Hemophagocytic Lymphohistiocytosis (FHL) , STX3 and UNC45A. [ citation needed ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1059", "text": "Prenatal screening  in utero  is currently offered by several medical centers since the  gene (s) involved in the disease were recently discovered to be  MYO5B ; [ 6 ] [ 7 ]  Diagnosis is typically made by  biopsy  of the small intestine. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1060", "text": "The appearance of microvillous inclusion disease on  light microscopy  is similar to  celiac sprue ; however, it usually lacks the intraepithelial  lymphocytic  infiltration characteristic of celiac sprue and stains positive for  carcinoembryonic antigen  (CEA). [ 2 ]  The definitive diagnosis is dependent on  electron microscopy . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1061", "text": "The differential diagnosis of chronic and intractable diarrhea is: [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1062", "text": "It is nearly always fatal unless, like short bowel syndrome patients, treated with  parenteral nutrition  or an  intestinal transplant . [ 3 ]  The patient is often classified as being in \"intestinal failure\" and treated with the cohort of patients known as \"short bowel syndrome\" patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1063", "text": "One patient from the UK was documented as achieving nutritional independence at age 3. [ 10 ]  On 26 June 2009, a six-year-old girl with microvillus inclusion disease became the third person in the UK to die of swine flu. This was attributed to her weakened immune system. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1064", "text": "Microvillus inclusion disease is extremely rare, however, no prevalence data have been published. An estimate of a few hundred children with the disease in Europe has been made but no time frame to which this count applies is given. Countries with a higher degrees of  consanguinity  experience higher prevalence rates due to its autosomal recessive transmission. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1065", "text": "Microvillus inclusion disease was first described in 1978 by Davidson et al. [ 13 ]  It was originally described as  familial enteropathy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1066", "text": "Monomorphic epitheliotropic intestinal T cell lymphoma  (MEITL) (formerly termed enteropathy-associated T cell lymphoma, type II) is an extremely rare  peripheral T-cell lymphoma  that involves the malignant proliferation of a type of  lymphocyte , the  T cell , in the  gastrointestinal tract  (i.e. GI tract). [ 1 ]  Over time, these T cells commonly spread throughout the  mucosal  lining of a portion of the GI tract [ 2 ]  (particularly the jejunum and ileum of the small intestine [ 3 ] ), lead to GI tract nodules and ulcerations, and cause symptoms such as abdominal pain, weight loss, diarrhea,  obstruction ,  bleeding , and/or  perforation . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1067", "text": "In 2008, the  World Health Organization  defined a specific type of lymphoma,  enteropathy-associated T cell lymphoma  (EATL), as having two different types: EATL type I, a lymphoma occurring in patients with the chronic,  autoimmune  GI tract disorder,  celiac disease , and EATL type II, a similar bowel lymphoma that was not associated with celiac disease. However, subsequent studies found significant clinical, pathologic, and pathophysiological differences between these two types of lymphoma. Consequently, the World Health Organization (2016) redefined these lymphomas as separate entities, terming the celiac disease-associated lymphoma as enteropathy-associated T cell lymphoma (EATL) and the lymphoma not associated with celiac disease as monomorphic epitheliotropic intestinal T cell lymphoma (MEITL). [ 4 ]  MEITL is only 1/5 to 1/10 as common as EATL. [ 5 ]  The Organization (2016) also termed a third type of intestinal T cell lymphoma that could not be classified as ATL or MEITL as  intestinal T cell lymphoma, not otherwise specified . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1068", "text": "MEITL is a highly aggressive GI tract lymphoma [ 7 ]  which typically has had very short survival times following its diagnosis. [ 2 ]  The disease often occurs in elderly patients who are afflicted with other ailments and consequently have little tolerance for the standard  chemotherapy  regimens that are used to treat other types of lymphomas. Moreover, these therapeutic regimens have shown little effectiveness in treating MEITL. To date, the best but still only marginally effective therapeutic interventions for the disease have been treatments that incorporate  hematopoietic stem cell transplantation  into chemotherapy plus surgical (when needed to treat local bowel issues such as obstruction or perforation) regimens. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1069", "text": "MEITL has been seen more often in Asians and individuals of  Hispanic  descent, in males (male to female ratio of ~2 to 1), and in mature or elderly individuals (median age ~60 years). [ 2 ]  Patients may present with irregular bowel movements, abdominal pain,  hematochezia  (i.e. the anal passage of fresh blood), [ 2 ]   B symptoms  (i.e. fever,  night sweats , weight loss),  loss of appetite , [ 5 ]  and/or bowel  perforations  and/or  obstructions . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1070", "text": "The malignant T cells in MEITL can be identified by: their expression of  cluster of differentiation  (i.e. CD)  cell surface molecules   CD3 ,  CD8 , and  CD56 ; by their failure to express  CD4 ,  CD5 , or  CD30 ; and, in particular, by their overexpression of  megakaryocyte-associated tyrosine kinase . They are not infected with the  Epstein-Barr virus  and therefore do not express this virus's products (e.g.  EBER1 or EBER2 ). [ 3 ]  In most individuals with the disease, these T cells are  \u03b3\u03b4 rather than \u03b1\u03b2 T-cells  based on their expression of \u03b3\u03b4 rather than \u03b1\u03b2  T-cell receptors . They also commonly express  cytotoxic T cell  activation markers such as  TIA1 ,  granzyme B , and  perforin  and therefore may have derived from or be related to  cytotoxic T cell  lymphocytes. However, in up to 25% of cases the malignant cells in MEITL also express markers of  B cell  lymphocytes. Detection of these \" tumor marker \" molecules on or in the lymphocytes of diseased tissues is critical for diagnosing MEITL; however, it does not clearly establish the original type of lymphocytes which became MEITL's malignant cells. This issue requires further studies. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1071", "text": "MEITL is thought to arise from  intraepithelial lymphocytes  that normally reside in the  epithelial  lining of the GI tract and over time acquire abnormalities that promote their survival, proliferation,  avoidance of the  immune system , and thereby malignancy. These cells are not infected with the Epstein-Barr virus and therefore have not become malignant as a consequence of this  virus's malignancy-producing  effects on lymphocytes as it does in other types of GI tract lymphomas. Rather, the malignant T cells in MEITL bear various genetic abnormalities that may promote their malignancy.  Restriction fragment length polymorphism  studies indicate that these cells have abnormal gains in  minisatellites , i.e. repetitive small DNA sequences, in  chromosomes  1, 5, 7, 8, 9, 13, 16, and 18. These minisatellites disrupt the production of some genes but the potential relevancies of these disruptions have not been defined. [ 4 ]   Genetic abnormalities commonly found in MEITL that do have potentially pro-malignant effects include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1072", "text": "Further studies are required to determine which, if any, of these genetic abnormalities play a role in the development and/or progression of MEITL and therefore are therapeutic targets for treating the disease. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1073", "text": "The symptoms of MEITL are generally non-specific. The diagnosis depends on  endoscopic  findings in the GI tract, histological findings on biopsied specimens from involved areas of the GI tract, evidence of disease involvement outside of the GI tract, and the differentiation of MEITL from other GI tract lymphomas and benign lymphoproliferative diseases. Endoscopy typically shows multiple raised and/or ulcerated lesions involving the  jejunum  or  ileum , and less commonly, the  duodenum ,  stomach , or  colon . [ 3 ]  These lesions may occur at multiple sites or spread throughout large areas of the GI tract. Biopsied tissues show abnormally broad  intestinal villi  caused by the infiltration of sheets of uniformly-sized lymphocytes. These lymphocytes may also infiltrate and disrupt the architecture of nearby  intestinal crypts  and the  epithelial lining . Unlike celiac disease-associated EATL, the lesions usually have little evidence of inflammatory cells (particularly lymphoplasmacytoid cells, i.e. cells showing a mixture of  B cell  and  plasma cell   morphological  features) or of infiltration of the epithelium lining by the types of lymphocytes seen in celiac disease. [ 2 ]  The lymphocytes in these lesions are T cells expressing the marker molecules and genetic abnormalities given in the above Pathophysiology section. [ 3 ] [ 4 ] [ 8 ]   CT scans  commonly reveal involvement of  mesenteric lymph nodes . [ 2 ]  Advanced cases have involvement of the  bone marrow [ 5 ]  and/or dissemination into other organs. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1074", "text": "MEITL must be  differentiated  from the following GI tract disorders with which it shares some common features."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1075", "text": "There is no standard treatment for MEITL. Most individuals have been treated by surgical resections of involved areas with or without  anthracycline -based  chemotherapy . In these cases, responses have been short-lived and/or poor with 1 year overall survival rates, 1 year progression free survival rates, and median survival times of 36%, 21%, and 7 months, respectively. [ 5 ]  A retrospective study of patients treated with resection, chemotherapy and  autologous hematopoietic stem cell transplantation  had a higher 1-year and 5-year overall survival (100%, 33%) compared to one-year survival (73%) and five-year survival (14%) without transplantation; a second retrospective study supported the usefulness of transplantation in that high-dose lymphoma chemotherapy followed by transplantation and standard-dose lymphoma chemotherapy with or without surgical resection increased 5-year overall survival from 22 to 60% and 5-year disease progression-free survival from 22 to 52%. [ 13 ]  While further studies, particularly  randomized controlled trials , are needed to investigate the best treatments for MEITL, the use of lymphoma chemotherapy, hematopoietic stem cell transplantation, and, where needed, surgical resections are the currently recommended treatments for MEITL. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1076", "text": "Mucositis  is the painful  inflammation  and  ulceration  of the  mucous membranes  lining the  digestive tract , usually as an adverse effect of   chemotherapy  and  radiotherapy  treatment for cancer. [ 1 ]  Mucositis can occur anywhere along the gastrointestinal (GI) tract, but  oral mucositis  refers to the particular inflammation and ulceration that occurs in the mouth. [ 2 ]  Oral mucositis is a common and often debilitating complication of cancer treatment. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1077", "text": "Oral and gastrointestinal (GI) mucositis affects almost all patients undergoing high-dose chemotherapy and  hematopoietic stem cell transplantation  (HSCT), 80% of patients with  cancers of the head and neck  receiving radiotherapy, and a wide range of patients receiving chemotherapy. Alimentary tract mucositis increases mortality and morbidity and contributes to rising health care costs. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1078", "text": "For most cancer treatment, about 5\u201315% of patients get mucositis. However, with 5- fluorouracil  (5-FU), up to 40% get mucositis, and 10\u201315% get grade 3\u20134 oral mucositis. [ 4 ]   Irinotecan  is associated with severe GI mucositis in over 20% of patients. Seventy-five to eighty percent of bone marrow transplantation recipients experience mucositis, of which oral mucositis is the most common and most debilitating, especially when melphalan is used. In grade 3 oral mucositis, the patient is unable to eat solid food, and in grade 4, the patient is unable to consume liquids as well. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1079", "text": "Radiotherapy to the head and neck or to the pelvis or abdomen is associated with Grade 3 and Grade 4 oral or GI mucositis, respectively, often exceeding 50% of patients. Among patients undergoing head and neck radiotherapy, pain and decreased oral function may persist long after the conclusion of therapy. Fractionated radiation dosage increases the risk of mucositis to > 70% of patients in most trials. Oral mucositis is particularly profound and prolonged among  HSCT  recipients who receive total-body irradiation. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1080", "text": "Oral cancer  patients undergoing chemotherapy usually become symptomatic four to five days after beginning treatment, reaching a peak at around day 10, and then slowly improving over the course of a few weeks. Mucositis associated with radiotherapy usually appears at the end of the second week of treatment and may last for six to eight weeks. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1081", "text": "As a result of cell death in reaction to chemo- or radio-therapy, the mucosal lining of the mouth becomes thin, may slough off and then become red, inflamed and ulcerated. The ulcers may become covered by a yellowish-white fibrin clot called a pseudomembrane. Peripheral  erythema  is usually present. Ulcers may range from 0.5\u00a0cm to greater than 4\u00a0cm. Oral mucositis can be severely painful.  The degree of pain is usually related to the extent of the tissue damage.  Pain is often described as a burning sensation accompanied by reddening. Due to pain, the patient may experience trouble speaking, eating, or even opening the mouth. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1082", "text": "Dysgeusia , or an alteration in taste perception, is common, especially for those who are receiving concomitant radiation therapy to the neck and mouth area. \"Taste blindness\", or an altered sense of taste, is a temporary condition that occurs because of effects on taste buds that are mostly located in the tongue. Sometimes, only partial recovery of taste occurs. Common complaints are of food tasting too sweet or too bitter or of a continuous metallic taste. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1083", "text": "Sores or ulcerations can become infected by  virus ,  bacteria  or  fungus . Pain and loss of taste perception makes it more difficult to eat, which leads to weight loss. Ulcers may act as a site for local infection and a portal of entry for oral flora that, in some instances, may cause  septicaemia  (especially in immunosuppressed patients). Therefore, oral mucositis can be a dose-limiting condition, disrupting a patient\u2019s optimal cancer treatment plan and consequentially decreasing their chances of survival. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1084", "text": "The  pathophysiology  of mucositis is complex and multifactorial. Currently, Sonis' five phase model is the accepted explanation for the process. [ 5 ] [ 6 ]  The 5 stages are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1085", "text": "Diagnosis is based on the symptoms the patient is experiencing and the appearance of the tissues of the mouth following  chemotherapy ,  bone marrow  transplants or  radiotherapy . Red burn-like sores or ulcers throughout the mouth is enough to diagnose mucositis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1086", "text": "The severity of oral mucositis can be evaluated using several different assessment tools.\nTwo of the most commonly used are the World Health Organization (WHO) Oral Toxicity score [ 9 ]  and the National Cancer Institute Common Toxicity Criteria (NCI-CTC) for Oral Mucositis. [ 10 ]  While the NCI system has separate scores for appearance (erythema and ulceration) and function (pain and ability to eat solids, liquids, or nothing by mouth), the WHO score combines both elements into a single score that grades the severity of the condition from 0 (no oral mucositis) to 4 (swallowing not possible such that patient needs supplementary nutrition). Another scale developed in 1999, the Oral Mucositis Assessment Scale (OMAS) has been shown to be highly reproducible between observers, responsive over time, and accurate in recording symptoms associated with mucositis.   The OMAS provides an objective assessment of oral mucositis based on assessment of the appearance and extent of redness and ulceration in various areas of the mouth. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1087", "text": "A 2015 Cochrane systematic review assessing the prevention of chemotherapy-induced oral mucositis concluded that oral cryotherapy leads to large reductions in the incidence of oral mucositis of all severities in adults receiving  5-FU  treatment for solid cancers. The evidence also indicates a reduction of oral mucositis in adults receiving high-dose melphalan-based cancer treatment prior to haematopoietic stem cell transplantation, although there is uncertainty regarding the size of the reduction in this instance. No evidence was found for use of this preventive measure in children. Oral cryotherapy involves the placement of rounded ice chips in the mouth, which cools the oral tissues and causes  vasoconstriction . This decreases blood flow to the region and, hence, also restricts the amounts of the chemotherapy drugs delivered to the tissues. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1088", "text": "Treatment of mucositis is mainly supportive.  Oral hygiene  is the mainstay of treatment; patients are encouraged to clean their mouth every four hours and at bedtime, more often if the mucositis becomes worse. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1089", "text": "Water-soluble jellies can be used to lubricate the mouth. Salt mouthwash can soothe the pain and keep food particles clear so as to avoid infection. Patients are also encouraged to drink plenty of liquids, at least three liters a day, and avoid alcohol. Citrus fruits, alcohol, and foods that are hot are all known to aggravate mucositis lesions. Medicinal  mouthwashes  may be used such as  Chlorhexidine gluconate  and viscous  Lidocaine  for relief of pain. However, care should be taken as the high doses of viscous  lidocaine  my cause adverse effects. [ 12 ]  A study reported that  lidocaine  has a potential toxicity; when it was tested on patients with oral mucositis who underwent a  bone marrow transplant , lidocaine anesthetic  mouthwash  was found to be systemically absorbed. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1090", "text": "Palifermin  is a human KGF (keratinocyte growth factor) that has shown to enhance epithelial cell proliferation, differentiation, and migration. Experimental therapies have been reported, including the use of cytokines and other modifiers of  inflammation  (e.g., IL-1, IL-11, TGF-beta3),  amino acid  supplementation (e.g., glutamine),  vitamins , colony-stimulating factors,  cryotherapy , and laser therapy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1091", "text": "Symptomatic relief of the pain of oral mucositis may be provided by barrier protection agents such as concentrated oral gel products (e.g.  Gelclair ).  Caphosol  is a mouth rinse which has been shown to prevent and treat oral mucositis caused by radiation and high-dose chemotherapy.  MuGard  is a FDA-cleared mucoadhesive oral protectant, developed by  Access Pharmaceuticals, Inc. , that is designed to form a protective hydrogel coating over the oral mucosa while a patient is undergoing chemotherapy and/or radiotherapy cancer treatments to the head and neck. [ 14 ]  Additionally, the efficacy of MuGard for the prevention or treatment of mucositis has been tested by a prospective, randomized clinical trial in which 43% of head and neck cancer patients using MuGard prophylactically never got oral mucositis.\n NeutraSal  is an FDA-cleared calcium phosphate mouth rinse that has been shown in an open-label, observational registry trial to prevent and reduce the severity of oral mucositis caused by radiation and high-dose chemotherapy.  In the trial, 56% of the radiotherapy patients reported 0 (WHO score) or no mucositis, which is significantly lower than historical rates.  Another super saturated calcium phosphate rinse on the market and cleared by the FDA is the US based  SalivaMAX.  The Mayo Clinic has been testing the antidepressant doxepin in a mouthwash to help treat symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1092", "text": "In 2011, the FDA cleared  episil  oral liquid for the management and relief of pain of oral lesions with various etiologies, including oral mucositis/stomatitis which may be caused by chemotherapy or radiation therapy.  The transformative mechanism of action of episil creates a lipid membrane that mechanically bonds to the oral cavity mucosa to coat and soothe inflammation and ulcerations, and blanket painful lesions. [ 15 ]   In a multicenter, randomized, double-blind, single-dose study involving 38 head and neck cancer patients with oral mucositis (WHO grades 2-3) undergoing radiation therapy, episil clinically demonstrated fast-acting relief that lasted up to 8 hours. [ 16 ] [ 17 ]  Episil oral liquid is marketed in the US by  Cangene ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1093", "text": "In a 2012 randomized controlled pilot study involving pediatric patients, topical application of honey was found to reduce recovery time compared to benzocaine gel in grade 2 and 3 chemotherapy-induced oral mucositis to a degree that was statistically significant. In grade 3 oral mucositis, honey was as effective as a mixture of honey, olive oil and propolis, while both treatments were found to reduce recovery time compared to the benzocaine control. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1094", "text": "Clinical research is ongoing in oral mucositis. A recent phase 2 exploratory trial in oral mucositis reported that dusquetide, [ 19 ] [ 20 ] [ 21 ]  a unique innate immune modulator with a mechanism that potentially addresses each of the phases of OM pathophysiology, is able to reduce the duration of severe oral mucositis, as well as reducing the incidence of infection"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1095", "text": "Natural killer cell enteropathy , also termed  NK cell enteropathy (NKCE), and a closely related disorder,  lymphomatoid gastropathy  (LG), are non-malignant diseases in which one type of  lymphocyte , the  natural killer cell  (i.e. NK cell), proliferates excessively in  the  gastrointestinal tract  (GI tract). [ 1 ]  This proliferation causes red, sore-like spots, raised lesions, erosions, and ulcers in the  mucosal  layer surrounding the GI tract lumen. Both disorders cause either no or only vague  symptoms of GI tract disturbances  such as nausea, vomiting, and  bleeding . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1096", "text": "In 2006, a persistent but apparently benign disease that involved the proliferation of NK cells at multiple sites throughout the intestines was described. This disorder appeared similar to and easily mistaken for a highly malignant disease,  extranodal NK/T-cell lymphoma, nasal type . [ 3 ]  In 2010, a similarly non-malignant disorder that involved the proliferation of NK cells in the stomach was described. The disease mimicked gastrointestinal lymphomas. [ 4 ]  Since these first descriptions, several  case series  and  case reports  have been published on these  enteropathies . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1097", "text": "The two NK cell proliferation diseases have been termed NK cell enteropathy and lymphomatoid gastropathy with NKCE being seen mostly in the United States and Korea and LG being seen mostly in Japan. [ 6 ]  Besides this geographical difference, the only other critical difference between the two diseases is that the lesions in NKCE occur in the  small intestine ,  colon , stomach, and/or  esophagus  while those of LG are limited to the stomach. [ 7 ]  Since the pathophysiological features of the two diseases are virtually identical, NKCE and LG are now commonly viewed as manifestations of the same disease. [ 2 ] [ 5 ] [ 7 ] [ 6 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1098", "text": "Only 36 patients with NKCE or LG have been reported as of January 2019. [ 5 ]  Nonetheless, these diseases are emerging as important clinical entities because they  1)  are newly described and likely to be diagnosed more often as they become better known and  2)  have been mistaken for, and treated as, various types of pre-malignant and malignant  lymphomas  of the GI tract. Given the radical differences in the prognoses and treatments of NKCE and LG compared to the lymphomas that they can mimic, the evaluation of many lymphocyte-proliferating disorders of the GI tract must consider and rule out the possibility that they are NKCE or LG rather than a  pre-malignant disorder  or malignant  lymphoma . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1099", "text": "Most cases of NKCE [ 9 ]  and LG [ 5 ]  have been reported in middle-aged or older individuals. Patients diagnosed with NKCE (medium age 46 years) have presented with vague abdominal pain, indigestion, vomiting, diarrhea, [ 5 ]  constipation, [ 6 ]  weight loss, anemia, and/or GI bleeding. [ 5 ]  Two patients complained of  biliary colic  (i.e. gallbladder pain) and were found to have typical lesions of NKCE in their  cystic ducts . [ 5 ]  These two cases indicate that NKCE involvement is not totally limited to the  alimentary canal . Three of 15 individuals diagnosed with NKCE disease reported no symptoms, their disease being found on  endoscopy  conducted for screening purposes. Typically, patients diagnosed with LG (medium age 58 years) have been asymptomatic at presentation with their disease being detected during GI tract examinations done for other reasons. Three of twenty patients diagnosed with LG complained of pain or discomfort in the upper abdominal region. Symptomatic individuals with either disease generally have a long history of persistent or intermittent symptoms. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1100", "text": "NK cells normally occupy the GI tract where they contribute to  innate immunity [ 7 ]  by becoming active in killing  pathogen -infected and cancerous cells. [ 10 ]  The proliferating lymphocytes in NKCE and LG express  CD56  and  CD7  proteins on their  cell surface membrane ,  CD3\u03b3  protein in their  cytoplasm , and  granzyme B ,  perforin , and  T-cell intracellular antigen-1   cytotoxic  proteins within their  cytoplasmic granules . This pattern of protein expression identifies these cells as NK cells that, because of their expression of the cytotoxic granule-bound proteins, have been activated. [ 7 ]  However, the cause(s) for the activation of these cells as wells as for their rapid proliferation to produce NKCE [ 5 ]  and LG [ 8 ]  is unknown. To date, no evidence of NK cell  clonality  (i.e. cells developing from a single precursor) or for these cells to bear gene mutations or  chromosome abnormalities  have been reported in NKCE or LG. These findings help distinguish LB and NKCE from many lymphomas and support the conclusion that neither disease is malignant. [ 6 ]  The NK cells in LG and NKCE are not infected with the  Epstein-Barr virus  (EBV), as evidenced by their failure to express this virus's  latency proteins  and  latency ncRNAs . This finding indicates that EBV is not the cause for the NK cell activation and excessive proliferation seen in NKCE and LG and distinguishes these diseases from malignant diseases they can mimic such as extranodal NK/T-cell lymphoma, nasal type. [ 5 ]  In isolated reports, LG has occurred in individuals with  Helicobacter pylori  infection of the stomach or a history of  stomach cancer , [ 7 ]  while NKCE has been reported to occur in patients with  gluten sensitivity [ 10 ]  or circulating  anti-gliadin antibodies . Both of the latter conditions are associated with the development of GI tract lymphomas. [ 5 ]  However, the relationship of any of these findings to the  etiology  of LB and NKCE is unclear. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1101", "text": "Biopsies of NKCE tissues reveal atypical medium to large lymphocytes identified by  immunohistochemistry  to be NK cells that are multiplying at a moderately rapid rate [ 9 ]  and that lack evidence of being infected by the Epstein-Barr virus. [ 2 ]  These cells are located primarily in the  lamina propria , i.e.  loose connective tissue  lying just below the  epithelium  lining the GI tract. There is generally little invasion of these cells into the  epithelium ,  submucosa , or glands of the GI tract, and the lesions almost always show a complete absence of vascular injury due to invasion by these cells. [ 9 ]  The lesions in LG closely resemble those of NKCE. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1102", "text": "The diagnoses of NKCE and LG depends on clinical and pathological findings indicating that the two diseases:  a)  are indolent and non-malignant;  b)  usually manifested by mild, vague, or no symptoms;  c)  localize to the GI tract without involvement of the head, neck, or organs such as the liver and spleen;  d)  consist of one or more lesions localized primarily to the  lamina propria  of the esophagus, stomach, small intestine, and/or large intestine (for NKCE} or to the stomach (for LG); and  e)  involve lesions which contain medium-to large-sized, atypical, and non-clonal lymphocytes that are activated NK cells (see Pathophysiology section) which proliferate at moderately rapid rates (as gauged by, e.g. analysis of their  Ki-67 protein levels ), lack evidence of Epstein-Barr virus infection, gene mutations, or chromosome abnormalities, and show little evidence of centering around, and destroying, blood vessels. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1103", "text": "In early studies, aggressive  chemotherapy  with or without  bone marrow translanton  and  gastric resections  were used to treat NKCE and LG, respectively, based on the assumptions that these diseases were malignant. [ 5 ]  Since there was no evidence that these treatments influenced the underlying disease [ 5 ] [ 6 ]  and since NKCE and LG are essentially benign disorders, they must be distinguished from the malignant diseases which they mimic. [ 5 ]  Three malignant or potentially premalignant diseases which can closely resemble NKCE and LG along with some clinical and laboratory findings which differentiate them from NKCE and LT are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1104", "text": "Other diseases which NKCE and LG may superficially resemble and require consideration as being in their differential diagnoses include:  peripheral T-cell lymphoma not otherwise specified ,  T cell lymphomas  that consist of mature T cells and occur in the GI tact, [ 10 ]   MALT lymphoma  of the stomach, [ 13 ]  and other types of stomach lymphomas. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1105", "text": "Patients with NKCE or LG should be treated for symptom relief but, as currently recommended, not for the underlying NK cell proliferative disease. Regular follow-ups that include repeated endoscopic analyses of their GI tracts and tests for the spreading of the disease to other organs are recommended to insure the original diagnosis is correct. [ 2 ] [ 6 ] [ 9 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1106", "text": "NKCE and LG usually follow a persistent or regressing-relapsing coarse but uncommonly spontaneously relapses without a recurrence even in cases that have been mistreated with chemotherapy, bone marrow transplantation, or gastric resection. Patients with LG are less likely to have persistent or regressing-relapsing coarse. Symptoms of the disease usually remain vague and mild. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1107", "text": "Necrotizing enterocolitis  ( NEC ) is an intestinal disease that affects premature or very low birth weight infants. [ 4 ] [ 1 ]  Symptoms may include  poor feeding ,  bloating , decreased activity,  blood in the stool ,  vomiting  of  bile ,  multi-organ failure , and potentially  death . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1108", "text": "The exact cause is unclear. [ 1 ]  However, several risk factors have been identified. Consistently described risk factors include  formula feeding , intestinal  dysbiosis ,  low birth weight , and  prematurity . [ 5 ]  Maternal factors such as  chorioamnionitis ,  cocaine abuse ,  intrauterine growth restriction ,  intrahepatic cholestasis during pregnancy , increased  body mass index , lack of prenatal steroids, mode of delivery,  placental abruption ,  pre-eclampsia , and  smoking  have not been consistently implicated with the development of NEC. [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ]  Other risk factors potentially implicated include  congenital heart disease ,  birth asphyxia ,  exchange transfusion , and  prelabor rupture of membranes . [ 1 ]  The underlying mechanism is believed to involve a combination of  poor blood flow  and  infection  of the intestines. [ 2 ]  Diagnosis is based on symptoms and confirmed with  medical imaging . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1109", "text": "Prevention includes the use of  breast milk  and  probiotics . [ 2 ]  Treatment includes  bowel rest ,  orogastric tube ,  intravenous fluids , and intravenous  antibiotics . [ 2 ]  Surgery is required in those who have  free air in the abdomen . [ 2 ]  A number of other  supportive  measures may also be required. [ 2 ]  Complications may include  short-gut syndrome ,  intestinal strictures , or  developmental delay . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1110", "text": "About 7% of those who are born prematurely develop NEC; however the odds of an infant developing this illness is directly related to the  intensive care unit  they are placed in. [ 4 ] [ 2 ] [ 11 ] [ 12 ] [ 13 ]  Onset is typically in the first four weeks of life. [ 2 ]  Among those affected, about 25% die. [ 1 ]  The sexes are affected with equal frequency. [ 14 ]  The condition was first described between 1888 and 1891. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1111", "text": "The condition is typically seen in premature infants, and the timing of its onset is generally inversely proportional to the gestational age of the baby at birth (i.e., the earlier a baby is born, the later signs of NEC are typically seen). [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1112", "text": "Initial symptoms include feeding intolerance and  failure to thrive , increased gastric residuals,  abdominal distension , and  bloody stools . Symptoms may progress rapidly to abdominal discoloration with  intestinal perforation  and  peritonitis  and systemic  hypotension  requiring  intensive medical support . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1113", "text": "The exact cause is unclear. [ 1 ]  Several risk factors have been implicated: [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1114", "text": "Diagnosis is usually suspected clinically, but often requires the aid of diagnostic imaging, most commonly  radiography , which can show the intestines and may show areas with dead tissue or a bowel perforation. [ 18 ]  Specific radiographic signs of NEC are associated with specific Bell's stages of the disease: [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1115", "text": "Ultrasonography  has proven to be useful, as it may detect signs and complications of NEC before they are evident on radiographs, specifically in cases that involve a paucity of bowel gas, a gasless abdomen, or a sentinel loop. [ 21 ]  Diagnosis is ultimately made in 5\u201310% of very-low-birth-weight infants (<1,500g). [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1116", "text": "Diagnosis of NEC is more challenging in premature infants, due to inexplicit symptoms and radiographic signs. The most preterm infant is at highest risk of developing NEC. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1117", "text": "Prevention includes the use of breast milk and probiotics. [ 2 ]  A 2012 policy by the  American Academy of Pediatrics  recommended feeding preterm infants  human milk , finding \"significant short- and long-term beneficial effects,\" including reducing the rate of NEC by a factor of one-half to three-quarters. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1118", "text": "Small amounts of oral feeds of human milk starting as soon as possible, while the infant is being primarily fed intravenously, primes the immature gut to mature and become ready to receive greater intake by mouth. [ 25 ]  Human milk from a  milk bank  or donor can be used if mother's milk is unavailable. The gut mucosal cells do not get enough nourishment from arterial blood supply to stay healthy, especially in very premature infants, where the blood supply is limited due to immature development of the capillaries, so nutrients from the lumen of the gut are needed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1119", "text": "Towards understanding intervention with human milk, experts have noted cow's and human milk differ in their immunoglobular and glycan compositions. [ 26 ] [ 27 ]  Due to their relative ease of production, human milk oligosaccharides (HMO) are a subject of particular interest in supplementation and intervention. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1120", "text": "A  Cochrane  review in 2020 (updated in 2023) found low- to moderate-quality evidence that supplementation of probiotics enterally \"prevents severe NEC, as well as all-cause mortality in preterm infants\" but cautioned that the evidence was not sufficient to inform policy and practice and that further high-quality trials are needed. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1121", "text": "Advancing  enteral feed  volumes at lower rates does not appear to reduce the risk of NEC or death in very preterm infants and seems to increase the risk of invasive infection. [ 30 ]   Not beginning feeding an infant by mouth for more than 4 days does not appear to have protective benefits. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1122", "text": "If a baby is diagnosed with NEC, treatment should begin immediately. [ 18 ]  Treatment consists primarily of supportive care, including providing bowel rest by stopping enteral feeds, gastric decompression with intermittent suction, fluid repletion to correct electrolyte abnormalities and  third-space  losses, support for blood pressure,  parenteral nutrition , [ 32 ]  and prompt antibiotic therapy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1123", "text": "Monitoring is clinical, although serial supine and left lateral decubitus abdominal X-rays should be performed every six hours. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1124", "text": "As an infant recovers from NEC, feeds are gradually introduced. \"Trophic feeds\" or low-volume feeds (<20 ml/kg/day) are usually initiated first. How and what to feed are determined by the extent of  bowel  involved, the need for surgical intervention, and the infant's clinical appearance. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1125", "text": "Where the disease is not halted through medical treatment alone, or when the  bowel perforates , immediate emergency surgery to resect the dead bowel is generally required, although abdominal drains may be placed in very unstable infants as a temporizing measure. Surgery may require a  colostomy , which may be able to be reversed at a later time. Some children may develop  short bowel syndrome  if extensive portions of the bowel must be removed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1126", "text": "In the case of an infant whose bowel is left in discontinuity, the surgical creation of a mucous  fistula  or connection to the distal bowel may be helpful, as this allows for refeeding of  ostomy  output to the distal bowel. This refeeding process is believed to improve bowel adaptation and aid in advancement of feeds. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1127", "text": "Typical recovery from NEC if medical, nonsurgical treatment succeeds, includes 10\u201314 days or more without oral intake, and then demonstrated ability to resume feedings and gain weight. Recovery from NEC alone may be compromised by co-morbid conditions that frequently accompany  prematurity . Long-term complications of medical NEC include bowel obstruction and anemia. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1128", "text": "In the United States, NEC caused 355 deaths per 100,000 live births in 2013, down from 484 per 100,000 live births in 2009. Rates of death were almost three times higher for the black population than for the white population. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1129", "text": "When NEC is diagnosed and treated immediately, the prognosis for babies is generally very good. Most babies recover fully without any additional health problems. [ 18 ]  Overall, about 70-80% of infants who develop NEC survive. [ 36 ]   Medical management of NEC shows an increased chance of survival compared to surgical management. [ 36 ]   Despite a significant mortality risk, long-term prognosis for infants undergoing NEC surgery is improving, with survival rates of 70\u201380%. However, \"Surgical NEC\" survivors are still at risk for possible long-term complications, such as narrowing of the intestines [ 18 ]  or  Short bowel syndrome  and  neurodevelopmental disability ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1130", "text": "The  NEC Society  is a 501(c)(3), non-profit organization dedicated to building a world without necrotizing enterocolitis (NEC) through research, advocacy, and education. The NEC Society was launched in January 2014 by Jennifer Canvasser after her son, Micah, died from complications of NEC just before his first birthday. The NEC Society is a patient-led organization that collaborates with expert clinicians and researchers to better understand, prevent, and treat this devastating neonatal intestinal disease. Today, patient-families and experts from around the world work together to improve outcomes for the most vulnerable infants at risk of NEC. Their work and numerous initiatives combine the patient-family perspective with solutions based on the best available scientific evidence."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1131", "text": "The  NEC Society hosts an in-person, biennial Symposium where clinicians, scientists and patient-families come together to listen, learn and collaborate. It is held as an \u201c All-In Meeting \", where all stakeholders are fully integrated and empowered. Patient-families are central to the planning, preparation, and execution of the meeting. Each session is dedicated to a baby affected by NEC. Patient-families take part in each session as faculty and also present posters."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1132", "text": "Neurogenic bowel dysfunction  ( NBD ) is reduced ability or inability to control  defecation  due to deterioration of or injury to the  nervous system , resulting in  fecal incontinence  or  constipation . [ 1 ]  It is common in people with  spinal cord injury  (SCI),  multiple sclerosis  (MS) or  spina bifida . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1133", "text": "The  gastrointestinal tract  (GI tract) has a complex control mechanism that relies on coordinated interaction between muscular contractions and neuronal impulses (nerve signals). [ 3 ]  Fecal incontinence or constipation occurs when there is a problem with normal bowel functioning. This could be for a variety of reasons. The normal defecation pathway involves contractions of the colon which helps mix the contents, absorb water and propel the contents along. This results in feces moving along the colon to the  rectum . [ 4 ]  The presence of stool in the rectum causes reflexive relaxation of the  internal anal sphincter  ( rectoanal inhibitory reflex ), so the contents of the rectum can move into the  anal canal . This causes the conscious feeling of the need to defecate. At a suitable time the brain can send signals causing the  external anal sphincter  and  puborectalis muscle  to relax as these are under voluntary control and this allows defecation to take place. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1134", "text": "Spinal cord injury and other neurological problems mostly affect the  lower GI tract  (i.e.,  jejunum ,  ileum , and  colon ) leading to symptoms of incontinence or constipation. However, the  upper GI tract  (i.e.,  esophagus ,  stomach , and  duodenum ) may also be affected and patients with NBD often present with multiple symptoms. [ 6 ] [ 7 ]  Research shows there is a high prevalence of upper abdominal complaints, for example a study showed that approximately 22% of SCI patients reported feeling bloated, [ 6 ] [ 8 ]  and about 31% experienced abdominal distension. [ 6 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1135", "text": "In NBD there may be  fecal incontinence ,  constipation , or both combined. [ 10 ]  One type of constipation which may occur in people with NBD is  obstructed defecation . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1136", "text": "NBD may reduce quality of life as it often leads to difficulties with personal relationships and social life, and may also reduce self-esteem and independence. [ 5 ]  Fecal incontinence may increase the risk of  depression  and  anxiety . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1137", "text": "Different neurological disorders affect the GI tract in different ways:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1138", "text": "Bowel dysfunction caused by a spinal cord injury will vary greatly depending on the severity and level of the spinal cord lesion. In complete spinal cord injury both sensory and motor functions are completely lost below the level of the lesion so there is a loss of voluntary control and loss of sensation of the need to defecate. [ 12 ]  An incomplete spinal cord injury is one where there may still be partial sensation or motor function below the level of the lesion. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1139", "text": "Colorectal dysfunction due to spinal cord injury can be classified in to two types: an\u00a0 upper motor\u00a0neuron lesion  or  lower motor neuron lesion . Problems with the upper motor neuron in a neurogenic bowel results in a hypertonic and spastic bowel because the defecation reflex centre, which causes the involuntary contraction of muscles of the rectum and anus, remains intact. [ 5 ]  However, the nerve damage results in disruption to the nerve signals and therefore there is an inability to relax the anal sphincters and defecate, often leading to constipation. [ 5 ]  An upper motor neuron lesion is one that is above the  conus medullaris  of the spinal cord and therefore above vertebral level T12. [ 13 ]  On the other hand, a lower motor neuron lesion can cause  areflexia  and a flaccid external anal sphincter so most commonly leading to incontinence. Lower motor neuron lesions are damage to nerves that are at the level of or below the conus medullaris and below vertebral level T12. However, both upper and lower motor neuron disorders can lead to constipation and/ or incontinence. [ 14 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1140", "text": "Spinal cord injury above the  S2 ,  S3 ,  S4  level results in preserved reflexes in the rectum and anal canal. Hence the sphincter will remain contracted. [ 12 ]  Spinal cord injury below this level results in absent reflexes. In this situation, the rectum will be flaccid and the sphincter will be relaxed. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1141", "text": "Patients with  spina bifida  have a  neural tube  that has failed to completely form. This is most commonly in the lower back area in the region of the conus medullaris or  cauda equina . Therefore, spina bifida affects the bowel similarly to a lower motor neuron spinal cord injury, resulting in a flaccid, unreactive rectal wall. The anal sphincter does not contract and close, leading to stool leakage. [ 12 ]  Most patients with spina bifida also have  hydrocephalus  which may result in intellectual deficits, thereby potentially contributing to fecal incontinence. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1142", "text": "There are a variety of symptoms associated with multiple sclerosis that are all caused by a loss of  myelin , the insulating layer surrounding the neurons (nerve cells). This means the nerve signals are interrupted and are slower. This causes muscle contractions to be irregular and fewer, resulting in an increased colon transit time. [ 12 ]  The feces stay in the colon for a longer period of time, meaning that more water is absorbed. This leads to harder stools and therefore increases the symptoms of constipation. This neurological problem can also result in reduced sensation of rectal filling and weakness of the anal sphincter because of weak muscular contraction so can cause stool leakage. [ 12 ]  In patients with multiple sclerosis, constipation and fecal incontinence often coexist, and they can be acute, chronic or intermittent due to the fluctuating pattern of MS. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1143", "text": "Damage to the defecation centre within the  medulla oblongata  of the brain can lead to bowel dysfunction. A stroke or acquired brain injury may lead to damage to this centre in the brain. Damage to the defecation centre can lead to a loss of coordination between rectal and anal contractions and also a loss of awareness of the need to defecate. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1144", "text": "This condition differs as it affects both the extrinsic and enteric nervous systems due to the decreased  dopamine  levels in both. This results in less smooth muscle contraction of the colon, increasing the colon transit time. [ 12 ]  The reduced dopamine levels also causes dystonia of the striated muscles of the pelvic floor and external anal sphincter. This explains how Parkinson's disease can lead to constipation. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1145", "text": "Twenty percent of people with  diabetes mellitus  experience fecal incontinence due to irreversible autonomic  neuropathy . This is due to the high blood glucose levels over time damaging the nerves, which can lead to impaired rectal sensation. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1146", "text": "There are different types of neurons involved in innervating the lower GI tract these include: the  enteric nervous system ; located within the wall of the gut, and the extrinsic nervous system; comprising  sympathetic  and  parasympathetic  innervation. [ 3 ]  The enteric nervous system directly controls the gut motility, whereas the extrinsic nerve pathways influence gut contractility indirectly through modifying this enteric innervation. [ 3 ]  In almost all cases of neurogenic bowel dysfunction it is the extrinsic nervous supply affected and the enteric nervous supply remains intact. The only exception is Parkinson's disease, as this can affect both the enteric and extrinsic innervation. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1147", "text": "Defecation involves conscious and subconscious processes, when the extrinsic nervous system is damaged either of these can be affected. Conscious processes are controlled by the  somatic nervous system , these are voluntary movements for example the contraction of the striated muscle of the external anal sphincter is instructed to do so by the brain, which sends signals along the nerves innervating this muscle. [ 15 ] [ 16 ]  Subconscious processes are controlled by the  autonomic nervous system ; these are involuntary movements such as contraction of the smooth muscle of the internal anal sphincter or the colon. The autonomic nervous system also provides sensory information; this could be about the level of distension within the colon or rectum. [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1148", "text": "In order to correctly manage neurogenic bowel dysfunction it is important to accurately diagnose it. This can be done by a variety of methods, the most commonly used would be taking a clinical history and carrying out physical examinations which may include: abdominal, neurological and rectal examinations. [ 17 ]  Patients may use the  Bristol Stool Chart  to help them describe and characterise the morphological features of their stool, this is useful as it gives an indication of the transit time. [ 18 ]  An objective method used to evaluate the motility of the colon and help with diagnosis is the colon transit time. [ 19 ]  Another helpful test to diagnose this condition may be an abdominal X-ray as this can show the distribution of feces and show any abnormalities with the colon, for example a  megacolon . [ 14 ]  Methods used for diagnosis may vary depending on if the patient is ncontinent or constipated. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1149", "text": "Management and treatment for neurogenic bowel dysfunction depends on symptoms and biomedical diagnosis for cause of the condition. [ 14 ]  General practitioners will often refer patients to gastroenterologist to effectively manage the neurogenic bowel dysfunction. Research has been conducted on a variety of therapy and treatments for neurogenic bowel dysfunction including: diet modification, laxatives, magnetic and electrical stimulation, manual evacuation of feces and abdominal massage, enemas, and pulsed irrigation evacuation (PIE). [ 15 ] [ 20 ] [ 21 ]  Efficacy studies for pulsed irrigation evacuation with PIEMED demonstrated favorable results, removing stool of 98% of patients who used it for ineffective bowel routine, symptomatic impaction, or asymptomatic impaction. [ 20 ]  In the most severe of cases of neurogenic bowel dysfunction induced  fecal impaction , surgical interventions like colostomy are used to disrupt the dense mass of stool. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1150", "text": "Non-occlusive disease  (NOD) or  Non-occlusive mesenteric ischaemia  (NOMI) is a life-threatening condition including all types of  mesenteric ischemia  without mesenteric obstruction. It mainly affects patients above 50 years of age who suffer from cardiovascular disease ( myocardial infarction ,  congestive heart failure  or  aortic regurgitation ), hepatic,  chronic kidney disease  or  diabetes mellitus . It can be triggered also by a previous  cardiac surgery  with a consequent heart shock. [ 1 ] [ 2 ]  It represents around 20% of cases of acute mesenteric ischaemia. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1151", "text": "Non-occlusive mesenteric ischemia occurs due to severe  vasoconstriction  of  mesenteric vessels  supplying the intestine.  Acute abdominal pain  is the only early acute symptom in those patients, which makes early diagnosis difficult. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1152", "text": "CT angiography  would be helpful in differentiating occlusive from non-occlusive causes of mesenteric ischaemia. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1153", "text": "Non-occlusive disease has a poor prognosis with survival rate between 40-50%. [ 1 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1154", "text": "Pancolitis  or  universal colitis , in its most general sense, refers to  inflammation  of the entire  large intestine  comprising the cecum, ascending, transverse, descending, sigmoid colon and rectum. It can be caused by a variety of things such as  inflammatory bowel disease , more specifically a severe form of  ulcerative colitis . A diagnosis can be made using a number of techniques but the most accurate method is direct visualization via a  colonoscopy . [ 1 ]   Symptoms  are similar to those of ulcerative colitis but more severe and affect the entire large intestine. Patients generally exhibit symptoms including  rectal bleeding  as a result of  ulcers ,  pain in the abdominal region ,  inflammation  in varying degrees, and  diarrhea  (often  containing blood ),  fatigue ,  fever , and  night sweats . [ 2 ] [ 3 ]  Due to the loss of function in the large intestine patients may lose large amounts of weight from being unable to procure nutrients from food. [ 4 ]  In other cases the blood loss from ulcers can result in  anemia  which can be treated with  iron supplements . Additionally, due to the chronic nature of most cases of pancolitis, patients have a higher chance of developing  colorectal  cancer . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1155", "text": "The precise causes of pancolitis are unclear, although physicians currently believe that  autoimmune diseases  and  genetic predispositions  might play a role in its progress. Genes that are known to put individuals at risk for  Crohn's disease  have been shown to also increase risk of other IBD including pancolitis. [ 5 ]  Furthermore, an individual may also develop pancolitis if ulcerative colitis of only a small portion of the colon is left untreated or worsens. [ 3 ]  Current treatment of pancolitis is focused on forcing the disease into remission, a state where the majority of the symptoms subside. Ultimately, the goal is to reach an improved quality of life, reduction in need for medicine, and minimization of the risk of cancer. [ 3 ] [ 6 ]  Medication utilized in treatment includes  anti-inflammatory agents  and  corticosteroids  to alleviate inflammation and  immunomodulators  which act to suppress the  immune system . Immunomodulators are used in severe cases of ulcerative colitis and often utilized to treat patients with pancolitis who have shown little improvement with anti-inflammatories and corticosteroids. [ 2 ] [ 3 ] [ 5 ]  However, in this case it can further expose the patient to other diseases due to the compromised immune system. A final option of treatment is available in the form of  colorectal surgery . Generally, this option is reserved for only the cases in which cancer development is highly suspected or major  internal bleeding  from ulcers occurs. In this case the entire colon and rectum  are removed  which both cures the pancolitis and prevents any chance of colon cancer. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1156", "text": "Perianal hematoma  is a  hematoma  located in, or on the border of the  anus . [ 1 ] [ 2 ]  It is sometimes inappropriately referred to as an external  hemorrhoid . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1157", "text": "The symptoms of a perianal hematoma can present over a short period of time. Pain, varying from mild to severe, [ 3 ]  will occur as the skin surrounding the rupture expands due to pressure. This pain will usually last even after the blood has clotted, and may continue for two to four days. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1158", "text": "Perianal hematoma are caused by the rupture of a small  vein  that drains  blood  from the anus. [ 4 ]  This rupture may be the result of forceful or strained bowel movement,  anal sex  or caused by heavy lifting,  coughing  or straining. Once the rupture has formed, blood quickly pools within a few hours and, if left untreated, forms a  clot . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1159", "text": "It is diagnosed with a visual and physical examination by a general practitioner or proctologist."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1160", "text": "Management of thrombosed perianal hematoma has been poorly studied as of 2018. [ 5 ]  If diagnosed within the first few hours of presentation, the pooling blood may be evacuated using a  syringe . Once the blood has clotted, removal by this method is no longer possible and the clot can be removed via an incision over the lump under local anesthetic. The incision is not stitched but will heal. Care needs to be taken in regard to bleeding from the wound and possible infection with fecal bacteria. If left alone it will usually heal within a few days or weeks. [ 6 ]  The topical application of a cream containing a  heparinoid  is often advised to clear the clot. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1161", "text": "Peutz\u2013Jeghers syndrome  (often abbreviated  PJS ) is an  autosomal dominant   genetic disorder  characterized by the development of benign  hamartomatous   polyps  in the  gastrointestinal tract  and hyperpigmented  macules  on the  lips  and  oral mucosa  ( melanosis ). [ 2 ]  This  syndrome  can be classed as one of various  hereditary  intestinal polyposis syndromes [ 3 ]  and one of various hamartomatous polyposis syndromes. [ 4 ]  It has an incidence of approximately 1 in 25,000 to 300,000 births. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1162", "text": "The risks associated with this syndrome include a substantial risk of  cancer , especially of the breast  and gastrointestinal tracts. [ 6 ] [ 7 ]  Colorectal is the most common malignancy, with a lifetime risk of 39 percent, followed by breast cancer in females with a lifetime risk of 32 to 54 percent. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1163", "text": "Patients with the syndrome also have an increased risk of developing carcinomas of the liver, lungs, breast, ovaries, uterus, testes, and other organs. Specifically, it is associated with an increased risk of  sex-cord stromal tumor with annular tubules  in the ovaries. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1164", "text": "Due to the increased risk of malignancies, direct surveillance is recommended. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1165", "text": "The average age of first diagnosis is 23. The first presentation is often bowel obstruction or intussuseption from the hamartomatous gastrointestinal polyps. [ 8 ]  Dark blue, brown, and black pigmented mucocutaneous macules, are present in over 95 percent of individuals with Peutz\u2013Jeghers syndrome. [ 8 ]  Pigmented lesions are rarely present at birth, but often appear before 5 years of age. The macules may fade during puberty. The melanocytic macules are not associated with malignant transformation. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1166", "text": "Complications associated with Peutz\u2013Jeghers syndrome include obstruction and intussusception, which occur in up to 69 percent of patients, typically first between the ages of 6 and 18, though surveillance for them is controversial. [ 7 ] [ 8 ]  Anemia is also common due to gastrointestinal bleeding from the polyps. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1167", "text": "In 1998, a gene was found to be associated with the mutation. On  chromosome 19 , the gene known as  STK11  ( LKB1 ) [ 10 ]  is a possible  tumor suppressor gene . It is inherited in an  autosomal dominant  pattern, which means that anyone who has PJS has a 50% chance of passing the disease on to their offspring. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1168", "text": "Peutz\u2013Jeghers syndrome is rare and studies typically include only a small number of patients.  Even in those few studies that do contain a large number of patients, the quality of the evidence is limited due to pooling patients from many centers, selection bias (only patients with health problems coming from treatment are included), and historical bias (the patients reported are from a time before advances in the diagnosis and treatment of Peutz\u2013Jeghers syndrome were made). Probably due to this limited evidence base, cancer risk estimates for Peutz\u2013Jeghers syndrome vary from study to study. [ 11 ]  There is an estimated 18\u201321% risk of ovarian cancer, 9% risk of endometrial cancer, and 10% risk of cervical cancer, specifically  adenoma malignum . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1169", "text": "The main criteria for clinical diagnosis are: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1170", "text": "Having two of the three listed clinical criteria indicates a positive diagnosis.  The oral findings are consistent with other conditions, such as  Addison's disease  and  McCune\u2013Albright syndrome , and these should be included in the  differential diagnosis .  90\u2013100% of patients with a clinical diagnosis of PJS have a mutation in the  STK11 / LKB1  gene. Molecular  genetic testing  for this mutation is available clinically. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1171", "text": "Resection of the polyps is required only if serious bleeding or intussusception occurs. Enterotomy is performed for removing large, single nodules. Short lengths of heavily involved intestinal segments can be resected. Colonoscopy can be used to snare the polyps if they are within reach. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1172", "text": "Most patients will develop flat, brownish spots ( melanotic macules ) on the skin, especially on the lips and oral mucosa, during the first year of life, and a patient's first  bowel  obstruction due to  intussusception  usually occurs between the ages of six and 18 years. The cumulative lifetime cancer risk begins to rise in middle age. Cumulative risks by age 70 for all cancers, gastrointestinal (GI) cancers, and pancreatic cancer are 85%, 57%, and 11%, respectively. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1173", "text": "A 2011 Dutch study followed 133 patients for 14 years. The cumulative risk for cancer was 40% and 76% at ages 40 and 70, respectively. 42 (32%) of the patients died during the study, of which 28 (67%) were cancer related. They died at a median age of 45. Mortality was increased compared with the general population. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1174", "text": "A family with sinonasal polyposis were followed up for 28 years. Two cases of sinonasal type adenocarcinoma developed. This is a rare cancer. This report suggested that follow up of sinus polyps in this syndrome may be indicated. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1175", "text": "Some suggestions for surveillance for cancer include the following: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1176", "text": "Follow-up care should be supervised by a physician familiar with Peutz\u2013Jeghers syndrome. Genetic consultation and counseling as well as urological and gynecological consultations are often needed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1177", "text": "First described in a published case report in 1921 by  Jan Peutz  (1886\u20131957), a Dutch Internist, it was later formalized into the syndrome by American physicians at Boston City Hospital,  Harold Joseph Jeghers  (1904\u20131990) and Kermit Harry Katz (1914\u20132003), and Victor Almon McKusick (1921\u20132008) in 1949 and published in the  New England Journal of Medicine . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1178", "text": "Pharyngitis  is  inflammation  of the back of the  throat , known as the  pharynx . [ 2 ]  It typically results in a  sore throat  and  fever . [ 2 ]  Other symptoms may include a  runny nose ,  cough ,  headache , difficulty swallowing, swollen  lymph nodes , and a  hoarse voice . [ 1 ] [ 6 ]  Symptoms usually last 3\u20135 days, but can be longer depending on cause. [ 2 ] [ 3 ]  Complications can include  sinusitis  and  acute otitis media . [ 2 ]  Pharyngitis is a type of  upper respiratory tract infection . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1179", "text": "Most cases are caused by a  viral infection . [ 2 ]   Strep throat , a  bacterial infection , is the cause in about 25% of children and 10% of adults. [ 2 ]  Uncommon causes include other bacteria such as  gonococcus ,  fungi , irritants such as  smoke ,  allergies , and  gastroesophageal reflux disease . [ 2 ] [ 4 ]  Specific testing is not recommended in people who have clear symptoms of a viral infection, such as a  cold . [ 2 ]  Otherwise, a  rapid antigen detection test  or  throat swab  is recommended. [ 2 ]   PCR  testing has become common as it is as good as taking a throat swab but gives a faster result. [ 8 ]  Other conditions that can produce similar symptoms include  epiglottitis ,  thyroiditis ,  retropharyngeal abscess , and occasionally  heart disease . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1180", "text": "NSAIDs , such as  ibuprofen , can be used to help with the pain. [ 2 ]  Numbing medication, such as topical  lidocaine , may also help. [ 4 ]  Strep throat is typically treated with  antibiotics , such as either  penicillin  or  amoxicillin . [ 2 ]  It is unclear whether  steroids  are useful in acute pharyngitis, other than possibly in severe cases, but a recent (2020) review found that when used in combination with antibiotics they moderately reduced pain and the likelihood of resolution. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1181", "text": "About 7.5% of people have a sore throat in any 3-month period. [ 5 ]  Two or three episodes in a year are not uncommon. [ 1 ]  This resulted in 15 million physician visits in the United States in 2007. [ 4 ]  Pharyngitis is the most common cause of a sore throat. [ 11 ]  The word comes from the  Greek word   pharynx  meaning \"throat\" and the suffix  -itis  meaning \"inflammation\". [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1182", "text": "Pharyngitis is a type of inflammation caused by an  upper respiratory tract infection . It may be classified as acute or chronic. Acute pharyngitis may be  catarrhal ,  purulent , or  ulcerative , depending on the  causative agent  and the  immune capacity  of the affected individual. Chronic pharyngitis may be catarrhal,  hypertrophic , or  atrophic . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1183", "text": "Tonsillitis  is a subtype of pharyngitis. [ 14 ]  If the inflammation includes both the  tonsils  and other parts of the throat, it may be called  pharyngotonsillitis  or  tonsillopharyngitis . [ 15 ]  Another subclassification is  nasopharyngitis  (the common cold). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1184", "text": "Clergyman's sore throat  or  clergyman's throat  is an archaic term formerly used for chronic pharyngitis associated with overuse of the voice as in public speaking. It was sometimes called  dysphonia clericorum  or chronic  folliculitis  sore throat. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1185", "text": "Most cases are due to an  infectious organism  acquired from close contact with an infected individual. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1186", "text": "These comprise about 40\u201380% of all infectious cases and can be a feature of many different types of viral infections. [ 11 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1187", "text": "A number of different bacteria can infect the human throat. The most common is  group A streptococcus  ( Streptococcus pyogenes ), but others include  Streptococcus pneumoniae ,  Haemophilus influenzae ,  Bordetella pertussis ,  Bacillus anthracis ,  Corynebacterium diphtheriae ,  Neisseria gonorrhoeae ,  Chlamydophila pneumoniae ,  Mycoplasma pneumoniae ,  and  Fusobacterium necrophorum . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1188", "text": "Streptococcal pharyngitis or strep throat is caused by a  group A beta-hemolytic streptococcus  (GAS). [ 20 ]  It is the most common bacterial cause of cases of pharyngitis (15\u201330%). [ 19 ]  Common symptoms include  fever ,  sore throat , and large lymph nodes. It is a contagious infection, spread by close contact with an infected individual. A definitive diagnosis is made based on the results of a  throat culture .  Antibiotics  are useful to both prevent complications (such as  rheumatic fever ) and speed recovery. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1189", "text": "Fusobacterium necrophorum  is a normal inhabitant of the oropharyngeal  flora  and can occasionally create a  peritonsillar abscess . In one out of 400 untreated cases,  Lemierre's syndrome  occurs. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1190", "text": "Diphtheria  is a potentially life-threatening upper respiratory infection caused by  Corynebacterium diphtheriae , which has been largely eradicated in developed nations since the introduction of childhood  vaccination  programs, but is still reported in the  Third World  and increasingly in some areas in  Eastern Europe . Antibiotics are effective in the early stages, but recovery is generally slow. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1191", "text": "A few other causes are rare, but possibly fatal, and include  parapharyngeal space  infections:  peritonsillar abscess  (\"quinsy abscess\"),  submandibular space infection  (Ludwig's angina), and  epiglottitis . [ 23 ] [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1192", "text": "Some cases of pharyngitis are caused by  fungal infection , such as  Candida albicans , causing  oral thrush . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1193", "text": "Pharyngitis may also be caused by mechanical, chemical, or thermal irritation, for example cold air or  acid reflux . Some medications may produce pharyngitis, such as  pramipexole  and  antipsychotics . [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1194", "text": "Differentiating a viral and a bacterial cause of a sore throat based on symptoms alone is difficult. [ 29 ]  Thus, a throat swab often is done to rule out a bacterial cause. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1195", "text": "The modified  Centor criteria  may be used to determine the management of people with pharyngitis. Based on five clinical criteria, it indicates the probability of a streptococcal infection. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1196", "text": "One point is given for each of the criteria: [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1197", "text": "The  Infectious Disease Society of America  recommends against  empirical treatment  and considers antibiotics only appropriate following positive testing. [ 29 ]  Testing is not needed in children under three, as both group A strep and  rheumatic fever  are rare, except if they have a sibling with the disease. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1198", "text": "The majority of the time, treatment is symptomatic. Specific treatments are effective for bacterial, fungal, and  herpes simplex  infections."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1199", "text": "Gargling  salt water  is often suggested, but there is no evidence to support or discourage this practice. [ 4 ]   Alternative medicines  are promoted and used for the treatment of sore throats. [ 37 ]  However, they are poorly supported by evidence. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1200", "text": "Acute pharyngitis is the most common cause of a  sore throat  and, together with cough, it is diagnosed in more than 1.9 million people a year in the United States. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1201", "text": "Pneumatosis intestinalis  (also called  intestinal pneumatosis ,  pneumatosis cystoides intestinalis ,  pneumatosis coli , or  intramural bowel gas ) is  pneumatosis  of an  intestine , that is, gas  cysts  in the bowel wall. [ 1 ] [ 2 ]  As a  radiological sign  it is highly suggestive for  necrotizing enterocolitis . This is in contrast to gas in the  intestinal lumen  (which is relieved by  flatulence ). In  newborns , pneumatosis intestinalis is considered  diagnostic  for necrotizing enterocolitis, and the gas is produced by bacteria in the bowel wall. [ 3 ]  The pathogenesis of pneumatosis intestinalis is poorly understood and is likely multifactorial.  PI itself is not a disease, but rather a clinical sign.  In some cases, PI is an incidental finding, whereas in others, it portends a life-threatening intra-abdominal condition. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1202", "text": "This  medical sign  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1203", "text": "Pouchitis  is an umbrella term for inflammation of the  ileal pouch , an artificial rectum surgically created out of ileum (the last section of the small intestine) in patients who have undergone a  proctocolectomy  or total colectomy (removal of the colon and rectum). [ 1 ]  The ileal pouch-anal anastomosis is created in the management of patients with  ulcerative colitis ,  indeterminate colitis ,  familial adenomatous polyposis ,  cancer , or rarely, other  colitides . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1204", "text": "A variety of mechanisms can be the cause of pouchitis including inflammatory factors such as a dysbiosis sparked inflammation or Crohn's disease of the pouch, surgical causes including surgical join leaks and pelvic sepsis, or infectious from  Clostridioides difficile  (C Diff) or  Cytomegalovirus  (CMV).  It is possible to have more than one factor causing pouch inflammation at the same time. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1205", "text": "The incidence of a first episode of pouchitis at 1, 5 and 10 years post-operatively is 15%, 33%, and 45% respectively. [ 3 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1206", "text": "Patients with pouchitis typically present with bloody  diarrhea , urgency in passing stools, or discomfort while passing stools.  The loss of blood and/or dehydration resulting from the frequent stools will frequently result in nausea.  Extreme cramping and pain can occur with pouchitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1207", "text": "Endoscopic  evaluation of the pouch ( pouchoscopy ) in patients with pouchitis usually reveals erythematous pouch  mucosa , loss of pseudocolonic vasculature or other architecture, and friability of the mucosa.  Biopsies show evidence of inflammatory cells or  red blood cells  in the  lamina propria ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1208", "text": "Symptoms of pouchitis include increased stool frequency, urgency, incontinence, nocturnal seepage, abdominal cramping, pelvic discomfort, and  arthralgia . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1209", "text": "Symptom severity does not always correlate with severity of endoscopically or histologically evaluated pouch inflammation. [ 6 ]  Additionally, these symptoms are not necessarily specific for pouchitis, as they may arise from other inflammatory or functional pouch disorders such as  Crohn's disease  of the pouch,  cuffitis , pouch sinus, or irritable pouch syndrome. [ 6 ]  The most reliable tool for diagnosis is endoscopy combined with histologic features (derived from tissue  biopsies  obtained during endoscopy). [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1210", "text": "Once a diagnosis of pouchitis is made, the condition is further classified. The activity of pouchitis is stratified as: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1211", "text": "The duration of pouchitis is defined as acute (less than or equal to four weeks) or chronic (four weeks or more) and the pattern classified as infrequent (1\u20132 acute episodes), relapsing (three or fewer episodes) or continuous. Finally, the response to medical treatment as labelled as treatment responsive or treatment refractory, with the medication for either case being specified. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1212", "text": "First line treatment is usually with  antibiotics , specifically with  ciprofloxacin  and  metronidazole . [ 7 ]   Ampicillin  or  piperacillin  can also be considered as alternatives to empiric ciprofloxacin and metronidazole.  Administration of metronidazole at a high daily dose of 20\u00a0mg/kg can cause symptomatic peripheral  neuropathology  in up to 85% of patients. This can be a limiting factor in the use of maintenance metronidazole to suppress chronic pouchitis. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1213", "text": "Other therapies which have been shown to be effective include  probiotics  for pouchitis, [ 10 ]  the application of which usually begins as soon as any antibiotic course is completed so as to re-populate the pouch with beneficial bacteria."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1214", "text": "Biologics , such as anti-tumor necrosis factor antibodies, may also be useful but the evidence for their use is largely anecdotal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1215", "text": "A pilot study on the effect of reducing dietary  FODMAP  intake on bowel function in people without a colon indicates there might be a relation between pouchitis and FODMAP diets. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1216", "text": "Alicaforsen  (an  antisense  inhibitor which targets the  messenger RNA  for the production of human  ICAM-1  protein) was evaluated in a Phase 3 clinical trial, which did not meet the co-primary endpoints in the primary analysis (an adaptation of the Mayo Score of improvement in endoscopic remission and bowel frequency). [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1217", "text": "Proctocolitis  is a general term for  inflammation  of the  rectum  and  colon . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1218", "text": "Proctocolitis has many possible causes. Common infectious causes of proctocolitis include  Chlamydia trachomatis , LGV ( Lymphogranuloma venereum ),  Neisseria gonorrhoeae ,  HSV , and  Helicobacter  species. It can also be idiopathic (see  colitis ), vascular (as in  ischemic colitis ), or autoimmune (as in  inflammatory bowel disease ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1219", "text": "Anoscopy  can be used to diagnose the majority of cases of proctocolitis. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1220", "text": "Antibiotics, such as  ceftriaxone  and  doxycycline , if there is  infection [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1221", "text": "Protein losing enteropathy  ( PLE ) is a syndrome in which  blood proteins  are lost excessively via the  gastrointestinal (GI) tract . It may be caused by many different underlying diseases that damage the lining of the GI tract ( mucosa ) or cause blockage of its  lymphatic drainage . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1222", "text": "The signs and symptoms of protein losing  enteropathy  include diarrhea, fever, and general abdominal discomfort. [ 4 ]  Swelling of the legs due to  peripheral edema  can also occur; however, if the PLE is related to a systemic disease such as  congestive heart failure  or  constrictive pericarditis , then these symptoms could be due directly to the underlying illness. [ 2 ]   In severe cases,  anasarca , a generalized form of edema, may develop. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1223", "text": "The causes of protein-losing enteropathy can include GI conditions (among other causes), like the following: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1224", "text": "The pathophysiology of protein losing enteropathy is a result of plasma protein loss to the GI tract  lumen . [ 2 ]  PLE is a complication of a disorder, be it lymphatic obstruction or mucosal injury. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1225", "text": "Protein losing enteropathy is a syndrome, characterized by a collection of signs and symptoms that are due to an underlying primary medical condition. Thus, there are many different pathophysiologic mechanisms of intestinal protein loss. Erosive disease, is characterized by mucosal damage or erosions of the colon  intestinal epithelium  and  capillary  bed underlying the epithelium, leading to a leakage of proteins from the capillaries into the  interstitial  space and then into the intestinal lumen where they are lost from the body. [ 8 ]  This type of inflammation may be seen in  inflammatory bowel diseases ,  peptic ulcers  and infections. [ 8 ]  A second pathological mechanism, the non-erosive type, is characterized by increased intestinal permeability causing protein to be lost from the interstitium into the intestinal lumen. [ 8 ]  This increased intestinal permeability may be seen in  eosinophilic gastroenteritis  and other conditions causing increased inflammation in the gut, or certain genetic disorders affecting the cell adhesions between gut  enterocytes . [ 8 ]  And a third type is due to intestinal  lymphangiectasia  in which the lymphatic vessels that drain interstitial fluid from the gut are damaged, leading to a blockage of lymphatic drainage and a buildup of interstitial fluid near the gut, thus causing leakage of proteins into the gut. [ 8 ]  This may be due to primary or congenital disease states of the lymphatic system or secondary (acquired) damage to the lymphatic system. [ 8 ]  Possible secondary causes of lymphangiectasis include  congestive heart failure  or  constrictive pericarditis . These conditions cause an increase in the  central venous pressure . The lymphatic system drains into the central venous system following a negative pressure gradient to the  subclavian vein  via the  thoracic duct  or  right lymphatic duct . However, any pathological mechanism that leads to increased central venous pressure may also cause increased lymphatic pressure, thus impairing lymphatic drainage at the gut and lead to protein losing enteropathy. [ 8 ]  Certain infections such as  Whipple disease  can also lead to impaired lymphatic drainage by destroying the lymphatic  lacteals , which are lymphatic capillaries underlying  intestinal villi  and facilitating the drainage of lymph from the gut. [ 8 ]  Congenital disorders of the lymphatic system such as  Primary Intestinal Lymphangiectasia  are due to congenitally dilated or malformed lacteals that lead to lymph leakage into the small bowel, causing protein loss and protein losing enteropathy. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1226", "text": "The widespread hypoproteinemia seen in protein losing enteropathy may present with complications related to the specific proteins lost, especially in severe disease. A decrease in  antibodies  (also known as immune globulins) may lead to an increased susceptibility to infections. [ 8 ]  And the loss of inhibitory coagulation factors may lead to a  hypercoagulable state . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1227", "text": "In  pediatric protein losing enteropathy , changes in  epithelial  cells contribute to the pathogenesis of PLE by augmenting the rate of efflux of serum proteins. Congenital molecular mutations, poor lymphatic drainage and/or inflammation may cause epithelial  matrix  changes. [ 10 ]  The absence of  proteoglycans , which are  glycosaminoglycan  chains attached to protein, may contribute to PLE and augment inflammatory  cytokines . Children who have certain  congenital glycosylation defects  may have protein losing enteropathy. [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1228", "text": "The diagnosis of protein losing enteropathy is made by excluding other causes of protein loss.  Endoscopy  can be used to localize the cause of the protein loss in the bowel. Different methods of quantifying protein loss in the bowel include faecal excretion of  alpha 1-antitrypsin , a marker of protein losing enteropathy, as well as viral serologies, which may be useful to determine the cause of the PLE. [ 1 ]  Alpha 1-antitrypsin is a blood protein that is lost in the gut, however, it is not actively secreted or absorbed by the gut, and it resists proteolysis in the gut lumen, thus making it a preferred protein for quantification of gut protein loss in protein losing enteropathy. [ 8 ]  Fecal alpha 1-antitrypsin may be quantified in a random stool sample, or more accurately, in a 24-hour stool sampling to quantify the amount of protein loss in PLE. [ 8 ]  In suspected cases of local disease, or when PLE is suspected to be due to lymph drainage abnormalities,  lymphangiography  may be used to localize the areas of lymphatic leakage. [ 8 ]  Imaging of the  thoracic  or  abdominopelvic  cavities may also aid in the diagnosis, possibly by identifying masses impairing lymphatic and venous drainage from the intestines and thus contributing to PLE. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1229", "text": "Treatment for protein losing enteropathy depends upon the underlying condition; according to Rychik and Spray (2002) this could mean treatment of  hypoproteinemia  or of the  intestinal mucosa . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1230", "text": "For causes related to the heart, treatment for PLE after the  Fontan operation  treatment must be equal to the level of hypoproteinemia present. Therefore, it is useful to categorize patients based on their serum  albumin  levels, if less than normal (typically less than 3.5 g/dL) but greater than 2.5 g/dL, this can be seen as a mild form of protein losing enteropathy. Symptomatic management of edema with  furosemide  (and aldactone) can provide relief for the individual with mild hypoproteinemia. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1231", "text": "Dogs can also suffer from PLE. Because the proteins are lost from the intestine, these dogs have low levels of albumin in the blood. Chronic enteropathy is one of the possible reasons for PLE and it has been shown in a study that hypoalbuminaemia is a risk factor for negative outcome and the prognosis is guarded for these dogs. [ 15 ]  Gastrointestinal lymphoma and intestinal lymphangiectasia are other diseases that can cause protein losing enteropathy in dogs. [ 16 ]  The Breed Lundehunds seem to be predisposed for PLE. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1232", "text": "Pseudodiarrhea , also known as  hyperdefecation  or excess stool, is defined as increased stool frequency (more than three times daily) with a normal daily stool weight of less than 300 g. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1233", "text": "Pseudodiarrhea is often associated with rectal urgency and accompanies  irritable bowel syndrome ,  hyperthyroidism , and anorectal disorders such as  proctitis .  Patients with rectal obstruction (e.g., from fecal impaction, obstruction due to a vaginal  pessary ) may also present with pseudodiarrhea, since only liquid stool can make it through. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1234", "text": "Pseudodiarrhea may be more common than chronic diarrhea and should always be considered in patients complaining of chronic diarrhea. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1235", "text": "Radiation enteropathy  is a  syndrome  that may develop following abdominal or pelvic  radiation therapy  for  cancer . [ 1 ] [ 2 ]  Many affected people are  cancer survivors  who had treatment for  cervical cancer  or  prostate cancer .  It has also been termed  pelvic radiation disease  with  radiation proctitis  being one of its principal features [ 3 ]  and  radiation-induced lumbar plexopathy (RILP)  being a rare consequence. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1236", "text": "People who have been treated with  radiotherapy  for pelvic and other abdominal cancers frequently develop gastrointestinal symptoms. [ 3 ] [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1237", "text": "These include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1238", "text": "Gastrointestinal symptoms are often found together with those in other systems including  genitourinary disorders  and  sexual dysfunction . The burden of symptoms substantially impairs the patients'  quality of life . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1239", "text": "Nausea, vomiting, fatigue, and diarrhea may happen early during the course of radiotherapy.  Radiation enteropathy represents the longer-term, chronic effects that may be found after a latent period most commonly of 6 months to 3 years after the end of treatment.  In some cases, it does not become a problem for 20\u201330 years after successful curative therapy. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1240", "text": "A large number of people receive abdominal and or pelvic  radiotherapy  as part of their cancer treatment with 60\u201380% experiencing gastrointestinal symptoms. [ 1 ]   This is used in standard therapeutic regimens for  cervical cancer ,  prostate cancer ,  rectal cancer ,  anal cancer ,  lymphoma  and other abdominal malignancies.  Symptoms can be made worse by the effects of surgery, chemotherapy or other drugs given to treat the cancer. [ 5 ]   Improved methods of radiotherapy have reduced the exposure of non-involved tissues to radiation, concentrating the effects on the cancer.  However, as the parts of the intestine such as the  ileum  and the  rectum  are immediately adjacent to the cancers, it is impossible to avoid some radiation effects. [ 1 ]   Previous intestinal surgery, obesity, diabetes, tobacco smoking and vascular disorders increase the chances of developing enteropathy. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1241", "text": "Early radiation enteropathy is very common during or immediately after the course of radiotherapy.  This involves cell death, mucosal  inflammation  and epithelial barrier dysfunction. This injury is termed  mucositis  and results in symptoms of nausea, vomiting, fatigue, diarrhea and abdominal pain. [ 1 ] [ 6 ]   It recovers within a few weeks or months."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1242", "text": "The delayed effects, found 3 months or more after radiation therapy, produce pathology which includes  intestinal   epithelial  mucosal  atrophy , vascular  sclerosis , and progressive  fibrosis  of the  intestinal wall , among other changes in intestinal  neuroendocrine  and immune cells and in the  gut microbiota . [ 1 ] [ 6 ]  These changes may produce  dysmotility , strictures,  malabsorption  and bleeding.  Problems in the terminal ileum and rectum predominate. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1243", "text": "Multiple disorders are found in patients with radiation enteropathy, so guidance including an algorithmic approach to their investigation has been developed. [ 5 ] [ 7 ]   This includes a holistic assessment with investigations including  upper endoscopy ,  colonoscopy , breath tests and other nutritional and gastrointestinal tests.  Full investigation is important as many cancer survivors of radiation therapy develop other causes for their symptoms such as  colonic polyps ,  diverticular disease  or  hemorrhoids . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1244", "text": "Prevention of radiation injury to the small bowel is a key aim of techniques such as  brachytherapy , field size, multiple field arrangements, conformal radiotherapy techniques and intensity-modulated radiotherapy.  Medications including  ACE inhibitors ,  statins  and  probiotics  have also been studied and reviewed. [ 2 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1245", "text": "In people presenting with symptoms compatible with radiation enteropathy, the initial step is to identify what is responsible for causing the symptoms. Management is best with a multidisciplinary team including gastroenterologists, nurses, dietitians, surgeons and others. [ 1 ]  Medical treatments include the use of  hyperbaric oxygen  which has beneficial effects in  radiation proctitis  or anal damage. [ 10 ]  Nutritional therapies include treatments directed at specific malabsorptive disorders such as low fat diets and  vitamin B12  or  vitamin D  supplements, together with  bile acid sequestrants  for  bile acid diarrhea  and possibly antibiotics for  small intestinal bacterial overgrowth . [ 2 ]  Probiotics have all been suggested as another therapeutic avenue. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1246", "text": "Endoscopic therapies including  argon plasma coagulation  have been used for bleeding  telangiectasia  in radiation proctitis and at other intestinal sites, although there is a rick of perforation. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1247", "text": "Surgical treatment may be needed for  intestinal obstruction ,  fistulae , or perforation, which can happen in more severe cases. [ 12 ]   These can be fatal if patients present as an emergency, but with improved radiotherapy techniques are now less common. [ citation needed ] \nA systematic review has found there is some promising evidence for non-surgical interventions for late rectal damage, however due to low quality evidence no conclusions could be drawn. [ 13 ]  Optimal treatment usually produces significant improvements in quality of life. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1248", "text": "An increasing number of people are now surviving cancer, with improved treatments producing cure of the malignancy ( cancer survivors ).  There are now over 14 million such people in the US, and this figure is expected to increase to 18 million by 2022. [ 14 ]   More than half are survivors of abdominal or pelvic cancers, with about 300,000 people receiving abdominal and pelvic radiation each year.  It has been estimated there are 1.6 million people in the US with post-radiation intestinal dysfunction, a greater number than those with  inflammatory bowel disease  such as  Crohn's disease  or  ulcerative colitis . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1249", "text": "New agents have been identified in animal studies that may have effects on intestinal radiation injury. [ 1 ]   The research approach in humans has been reviewed. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1250", "text": "Radiation proctitis  or  radiation proctopathy  is a condition characterized by damage to the rectum after exposure to  x-rays  or other  ionizing radiation  as a part of  radiation therapy . [ 1 ]  Radiation proctopathy may occur as acute inflammation called  \"acute radiation proctitis\"  (and the related  radiation colitis ) or with chronic changes characterized by  radiation associated vascular ectasiae (RAVE) and chronic radiation proctopathy . [ 2 ] [ 1 ]   Radiation proctitis most commonly occurs after pelvic radiation treatment for  cancers  such as  cervical cancer ,  prostate cancer ,  bladder cancer , and  rectal cancer . RAVE and chronic radiation proctopathy involves the lower  intestine , primarily the  sigmoid colon  and the rectum, and was previously called chronic radiation proctitis,  pelvic radiation disease  and  radiation enteropathy . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1251", "text": "Acute radiation proctopathy often causes pelvic pain, diarrhea, urgency, and the urge to defecate despite having an empty colon (tenesmus). [ 4 ]  Hematochezia and fecal incontinence may occur, but are less common. [ 4 ]  Chronic radiation damage to the rectum (>3 months) may cause rectal bleeding, incontinence, or a change in bowel habits secondary. Severe cases may lead to with strictures or fistulae formation. [ 5 ] [ 4 ]  Chronic radiation proctopathy can present at a median time of 8-12 months following radiation therapy. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1252", "text": "Acute radiation proctopathy occurs due to direct damage of the lining ( epithelium ) of the colon. [ 1 ]  Rectal biopsies of acute radiation proctopathy show superficial depletion of epithelial cells and acute inflammatory cells located in the lamina propria. [ 4 ]  By contrast, rectal biopsies of RAVE and chronic radiation proctopathy demonstrates ischemic endarteritis of the submucosal arterioles, submucosal fibrosis, and neovascularization. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1253", "text": "Where chronic radiation proctopathy or RAVE is suspected, a thorough evaluation of symptoms is essential. Evaluation should include an assessment of risk factors for alternate causes of proctitis, such as  C. difficile colitis ,  NSAID use , and travel history. [ 6 ]  Symptoms such as diarrhea and painful defecation need to be systematically investigated and the underlying causes each carefully treated. [ 7 ]  Testing for parasitic infections ( amebiasis ,  giardiasis ) and sexually transmitted infections ( Neisseria gonorrhoeae  and  herpes simplex virus ) should be considered. [ 6 ]  The location of radiation treatment is important, as radiation directed at regions of the body other than the pelvis (eg brain, chest, etc) should  not  prompt consideration of radiation proctopathy. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1254", "text": "Endoscopy is the mainstay of diagnosis for radiation damage to the rectum, with either  colonoscopy  or  flexible sigmoidoscopy . RAVE is usually recognized by the macroscopic appearances on endoscopy characterized by vascular ectasias. [ 8 ]  Mucosal biopsy may aid in ruling out alternate causes of proctitis, but is not routinely necessary and may increase the risk of fistulae development. [ 6 ]   Telangiectasias  are characteristic and prone to bleeding. [ 3 ]  Additional endoscopic findings may include pallor (pale appearance), edema, and friability of the mucosa."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1255", "text": "Radiation proctitis can occur a few weeks after treatment, or after several months or years:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1256", "text": "Several methods have been studied in attempts to lessen the effects of radiation proctitis. Acute radiation proctitis usually resolves without treatment after several months. When treatment is necessary, symptoms often improve with hydration, anti-diarrheal agents, and discontinuation of radiation. [ 4 ]   Butyrate   enemas  may also be effective. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1257", "text": "In contrast, RAVE and chronic radiation proctopathy usually is not self-limited and often requires additional therapies. [ 4 ]  These include  sucralfate ,  hyperbaric oxygen therapy ,  corticosteroids ,  metronidazole ,  argon plasma coagulation ,  radiofrequency ablation  and  formalin  irrigation. [ 1 ] [ 3 ] [ 11 ]  The average number of treatment sessions with argon plasma coagulation to achieve control of bleeding ranges from 1 to 2.7 sessions. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1258", "text": "In rare cases that do not respond to medical therapy and endoscopic treatment, surgery may be required.  Overall, less than 10 percent of individuals with radiation proctopathy require surgery. [ 4 ]  In addition, complications such as obstruction and fistulae may require  surgery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1259", "text": "Up to 30 percent of individuals who receive pelvic radiation therapy for cancer may develop radiation proctopathy. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1260", "text": "Rectal bleeding  refers to  bleeding  in the  rectum , thus a form of  lower gastrointestinal bleeding . There are many causes of rectal hemorrhage, including inflamed  hemorrhoids  (which are dilated vessels in the perianal fat pads), rectal  varices ,  proctitis  (of various causes),  stercoral ulcers , and  infections .  Diagnosis is usually made by  proctoscopy , which is an  endoscopic  test. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1261", "text": "Those with rectal bleeding may notice bright red blood in their stool. Symptoms associated with rectal bleeding include having several bowel movements in a day, feelings of incomplete rectal evacuation, straining, hard or lumpy stools, feelings of urgency, loose or watery stools, and leakage of bowel movement. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1262", "text": "Bleeding from the rectal area could indicate premalignant  polyps  or  colorectal cancer . [ 3 ]  Compared to  colorectal cancer ,  anal lesions  or benign colorectal conditions are far more common causes of rectal bleeding. [ 4 ]  Other causes of rectal bleeding include  hemorrhoids , full-thickness  rectal prolapse ,  fissures , sentinel tags,  ulcers ,  rhagades , external  thromboses  with extravasation of blood clot, prolapsed  polyps  or tags, anal trauma or anal-receptive intercourse,  abscess ,  fistula  opening, dermatologic conditions of the perianal region, hypertrophied papilla, and distal  proctitis . An ulcer could be caused by  Crohn's disease ,  anal cancer ,  HIV , or another  STD .  Inflammatory bowel diseases  may also cause rectal bleeding. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1263", "text": "Certain medications, such as  calcium channel blockers  or  proton pump inhibitors , can exacerbate anorectal symptoms by causing  diarrhea  or  constipation , or they can exacerbate bleeding (e.g.,  Coumadin ,  nonsteroidal anti-inflammatory drugs ). A history of  hemorrhoidectomy , fissure surgery, fistula surgery,  polypectomy , or  colectomy  may be relevant. Gastrointestinal symptoms can also result from other procedures like  gastric bypass  or  cholecystectomy . Any prior assessment, such as a  colonoscopy  or flexible  sigmoidoscopy , may also be important, as well as any history of  polypectomy  carried out in connection with one of these operations. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1264", "text": "Any complaint of bleeding should be followed up with a  complete blood count  (CBC) in order to determine the extent of the bleeding and guide treatment. The  partial thromboplastin time  (PTT) and the  international normalized ratio  (INR), which can be used to detect bleeding tendencies, are additional crucial lab tests to obtain. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1265", "text": "Testing for  STIs , such as  gonorrhea  and  chlamydia , should be conducted on patients who engage in anal receptive sex. [ 6 ]  No matter if there are other clinical symptoms present or not,  endoscopies  are the gold standard for examining rectal bleeding and should be completed on patients over 40. To check for a distal source of bleeding, such as internal  hemorrhoids ,  proctitis ,  rectal ulcers ,  malignancies , or  varices , one can use an  anoscope  or rigid procto- sigmoidoscope . When proximal lower GI pathology is suspected, a colonoscopy needs to be performed. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1266", "text": "If there is a significant amount of bleeding or the patient is too unstable to be put under anesthesia for an endoscopic procedure,  CT angiography  may be pursued. It could be challenging to pinpoint the precise location of the blood if there is a lot of blood in the stomach. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1267", "text": "Tagged red blood cell  scintigraphies  are a precise way to locate the bleeding vessels and pinpoint the area where they are bleeding. It can be applied to chronic and recurrent rectal bleeding with no apparent cause. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1268", "text": "Rectitis  is an inflammation of the inner  rectum . It mainly affects the rectal  mucous membrane . [ 1 ]   The condition can be acute or it may be a chronic condition. Rectitis may be caused due to conditions such as  ulcerative colitis  or  Chron's disease . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1269", "text": "The Restroom Access Act , also known as  Ally's Law , is legislation passed by several U.S. states that requires retail establishments that have toilet facilities for their employees to also allow customers to use the facilities if the customer has a medical condition requiring immediate access to a toilet, such as  inflammatory bowel disease  or  Crohn\u2019s disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1270", "text": "The law is named for Ally Bain, a 14-year-old girl from Illinois who had a flare-up of her  Crohn's disease  while shopping at a large retail store and was subsequently denied use of the employee-only restroom, causing her to soil herself. Bain's mother vowed it would never happen to anyone else. The two met with Illinois State Representative  Kathy Ryg , helped her draft a bill, and testified before a committee at the state capital. The bill was signed into law in August 2005, making Illinois the first U.S. state to do so."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1271", "text": "As of January 2024, at least 20 U.S. states had passed versions of the law. They include Arkansas, California, [ 1 ]  Colorado, Connecticut, Delaware, [ 2 ] \nIllinois, Kentucky, Louisiana, [ 3 ]  Maryland, Massachusetts, Michigan, Minnesota, New Hampshire, [ 4 ]  New York, Ohio, Oregon, Tennessee, Texas, Wisconsin, and Washington. [ 5 ] [ 6 ]  A Virginia bill, which levies fines of $100 for non-compliance, was adopted in the 2024 General Assembly session and went in to effect on July 1, 2024. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1272", "text": "There is support for a federal version of the act, but some small-business people object to the public using their employee bathrooms. [ 8 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1273", "text": "In general, each state requires that the customer present a document signed by a medical professional attesting that the customer uses an  ostomy  device or has  Crohn's disease ,  ulcerative colitis , or other  inflammatory bowel disease  or medical condition requiring access to a toilet facility without delay. In at least two states, Oregon and Tennessee, the customer can present an identification card issued by a national organization advocating for the eligible medical condition. [ 9 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1274", "text": "Some states also include pregnancy as a covered medical condition. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1275", "text": "The Restroom Access Act of  Illinois  states:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1276", "text": "In Australia, the association Crohn's & Colitis Australia (CCA) encourages businesses to support people with such medical conditions by recognizing the Can't Wait Card issued by the CCA. [ 11 ]  The CCA states:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1277", "text": "Other countries including the UK have similar programs of voluntary participation by businesses, one such program in the UK is the Bladder & Bowel Community's Just Can't Wait Card. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1278", "text": "A card with no country specific indications is available explaining the possibility of legislation and the gravity of the card holders disability and need for restroom access. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1279", "text": "Retained antrum syndrome  or retained gastric antrum syndrome is one of the rare  postgastrectomy syndromes . It happens after  Billroth II  surgery and the mechanism involved is the inadequate removal of the distal  antrum  and  pylorus  during resection of the antrum and  gastrojejunostomy . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1280", "text": "Lack of the usual acid-secreting  gastric glands  makes the  antral segment  continually exposed to the alkaline environment of the duodenum, which causes it to secrete excessive acid and be prone to form  ulcers . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1281", "text": "Sandifer syndrome  (or  Sandifer's syndrome ) is an  eponymous   paediatric  medical disorder, characterised by  gastrointestinal  symptoms and associated  neurological  features. [ 1 ] [ 2 ] [ 3 ]  There is a significant correlation between the  syndrome  and  gastro-oesophageal reflux disease  (GORD); however, it is estimated to occur in less than 1% of children with reflux. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1282", "text": "Onset is usually confined to infancy and early childhood, [ 2 ]  with peak prevalence at 18\u201336 months. [ 4 ]   In rare cases, particularly where the child is severely mentally impaired, onset may extend to adolescence. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1283", "text": "The classical symptoms of the syndrome are  spasmodic torticollis  and  dystonia . [ 3 ] [ 4 ] [ 5 ]   Nodding and rotation of the head, neck extension, gurgling, writhing movements of the limbs, and severe  hypotonia  have also been noted. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1284", "text": "Spasms may last for 1\u20133 minutes and may occur up to 10 times a day.  Ingestion of food is often associated with occurrence of symptoms; this may result in reluctance to feed.  Associated symptoms, such as  epigastric  discomfort, vomiting (which may involve  blood ) and abnormal eye movements have been reported.  Clinical signs may also include anaemia. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1285", "text": "Diagnosis is made on the basis of the association of gastro-oesophageal reflux with the characteristic movement disorder. Neurological examination is usually normal. Misdiagnosis as benign infantile spasms or epileptic seizures is common, particularly where clear signs or symptoms of gastro-oesophageal reflux are not apparent. Early diagnosis is critical, as treatment is simple and leads to prompt resolution of the movement disorder. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1286", "text": "Successful treatment of the associated underlying disorder, such as GORD or hiatus hernia, may provide relief. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1287", "text": "Sandifer syndrome is not typically life-threatening [ 4 ]  and the prognosis is typically good. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1288", "text": "Sandifer syndrome was first described in 1964 by Austrian neurologist  Marcel Kinsbourne  in  The Lancet . [ 6 ] [ 7 ]  Kinsbourne named the syndrome after his mentor, British neurologist  Paul Sandifer , who had initially cared for the patients described in Kinsbourne's case reports. [ 8 ] [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1289", "text": "Redirect to:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1290", "text": "Small intestinal bacterial overgrowth  ( SIBO ), also termed  bacterial overgrowth , or  small bowel bacterial overgrowth syndrome  ( SBBOS ), is a disorder of excessive  bacterial  growth in the  small intestine . Unlike the  colon  (or large bowel), which is rich with bacteria, the small bowel usually has fewer than 100,000 organisms per millilitre. [ 1 ]  Patients with bacterial overgrowth typically develop symptoms which may include  nausea ,  bloating ,  vomiting ,  diarrhea ,  malnutrition ,  weight loss , and  malabsorption [ 2 ]  by various mechanisms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1291", "text": "The  diagnosis  of bacterial overgrowth is made by a number of techniques, with the  gold standard [ 3 ]  being an  aspirate  from the  jejunum  that grows in excess of 10 5   bacteria  per millilitre.  Risk factors  for the development of bacterial overgrowth include dys motility ;  anatomical  disturbances in the bowel, including  fistulae ,  diverticula  and  blind loops  created after surgery, and resection of the  ileo-cecal valve ;  gastroenteritis -induced alterations to the small intestine; and the use of certain medications, including  proton pump inhibitors ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1292", "text": "Small bowel bacterial overgrowth syndrome is treated with an  elemental diet  or  antibiotics , which may be given in a cyclic fashion to prevent tolerance to the antibiotics, sometimes followed by  prokinetic drugs  to prevent recurrence if dysmotility is a suspected cause."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1293", "text": "Symptoms traditionally linked to SIBO include  bloating ,  diarrhea ,  constipation , and abdominal pain/discomfort.  Steatorrhea  may be seen in more severe cases. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1294", "text": "Bacterial overgrowth can cause a variety of  symptoms , many of which are also found in other conditions, making the  diagnosis  challenging at times. [ 4 ]  Many of the symptoms are due to  malabsorption  of nutrients due to the effects of bacteria which either metabolize nutrients or cause inflammation of the small bowel, impairing absorption. The symptoms of bacterial overgrowth include  nausea ,  flatus , [ 5 ]   constipation , [ 6 ]  bloating, abdominal distension, abdominal pain or discomfort, diarrhea, [ 7 ]  fatigue, and weakness. SIBO also causes an increased  permeability of the small intestine . [ 8 ]  Some patients may lose weight. Children with bacterial overgrowth may develop  malnutrition  and have difficulty attaining  proper growth .  Steatorrhea , a sticky type of diarrhea where  fats  are not properly absorbed and spill into the stool, may also occur. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1295", "text": "Patients with bacterial overgrowth that is longstanding can develop complications of their illness as a result of malabsorption of nutrients. [ 9 ]  Laboratory test results may include elevated   folate  (vitamin B 9 ), and, less commonly,  vitamin B 12  deficiency or other nutritional deficiencies. [ 4 ]   Anemia  may occur from a variety of mechanisms, as many of the nutrients involved in production of  red blood cells  are absorbed in the affected small bowel.  Iron  is absorbed in the more proximal parts of the small bowel, the  duodenum  and  jejunum , and patients with malabsorption of iron can develop a  microcytic anemia , with small red blood cells. Vitamin B 12  is absorbed in the last part of the small bowel, the  ileum , and patients who malabsorb vitamin B 12  can develop a  megaloblastic anemia  with large red blood cells. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1296", "text": "In recent years, several proposed links between SIBO and other disorders have been made. However, the usual methodology of these studies involves the use of  breath testing  as an indirect investigation for SIBO. Breath testing has been criticized by some authors for being an imperfect test for SIBO, with multiple known false positives. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1297", "text": "Some studies reported up to 80% of patients with  irritable bowel syndrome  (IBS) have SIBO (using the  hydrogen breath test ). IBS-D is associated with elevated hydrogen numbers on breath tests while IBS-C is associated with elevated methane numbers on breath tests. [ 11 ]  Subsequent studies demonstrated statistically significant reduction in IBS symptoms following therapy for SIBO. [ 12 ] [ 11 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1298", "text": "Various mechanisms are involved in the development of diarrhea and IBS-D in bacterial overgrowth. First, the excessive bacterial concentrations can cause direct inflammation of the small bowel cells, leading to an  inflammatory diarrhea . The malabsorption of  lipids ,  proteins  and  carbohydrates  may cause poorly digestible products to enter into the  colon . This can cause an  osmotic diarrhea  or stimulate the colonic cells to cause a  secretory diarrhea . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1299", "text": "There is a lack of consensus however, regarding the suggested link between IBS and SIBO. Other authors concluded that the abnormal breath results so common in IBS patients do not suggest SIBO, and state that \"abnormal fermentation timing and dynamics of the breath test findings support a role for abnormal intestinal bacterial distribution in IBS.\" [ 13 ]  There is general consensus that breath tests are abnormal in IBS; however, the disagreement lies in whether this is representative of SIBO. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1300", "text": "Certain people are more predisposed to the development of bacterial overgrowth because of certain risk factors.  These factors can be grouped into four categories: (1)  motility  disorders, impaired movement of the small bowel, or anatomical changes that lead to stasis (a state in which the normal flow of a body liquid stops); (2) disorders of the  immune system ; (3) interference with the production of proteolytic enzymes, gastric acid, or bile; and (4) conditions that cause more bacteria from the  colon  to enter the  small bowel . [ 4 ] \nIn some people, methanogens may reside in the oral cavity, as evidenced by reductions in breath methane levels following mouthwash with chlorhexidine. [ 15 ]  This may affect results from hydrogen-methane breath testing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1301", "text": "Absence or impairment of the  migrating motor complex  (MMC), a cyclical motility pattern in the small intestine, and phase III of the MMC in particular, is associated with the development of SIBO. [ 16 ]  Problems with motility may either be diffuse, or localized to particular areas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1302", "text": "MMC impairment may be a result of post-infectious  irritable bowel syndrome , drug use, or  intestinal pseudo-obstruction  among other causes. [ 17 ]  There is an overlap in findings between  tropical sprue , post-infectious  irritable bowel syndrome  and small intestinal bacterial overgrowth in the pathophysiology of the three conditions and also SIBO can similarly sometimes be triggered by an acute gastrointestinal infection. [ 18 ] [ 19 ] [ 20 ]  As of 2020, there is still controversy about the role of SIBO in the pathogenesis of common functional symptoms such as those considered to be components of  irritable bowel syndrome . [ 4 ]  Diseases like  scleroderma [ 21 ]  cause diffuse slowing of the bowel, leading to increased bacterial concentrations. More commonly, the small bowel may have anatomical problems, such as out-pouchings known as  diverticula  that can cause bacteria to accumulate. [ 22 ]  After surgery involving the  stomach  and  duodenum  (most commonly with  Billroth II  antrectomy), a  blind loop  may be formed, leading to stasis of flow of intestinal contents. This can cause overgrowth, and is termed  blind loop syndrome . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1303", "text": "Systemic or metabolic disorders may lead to conditions allowing bacterial overgrowth as well. For example, diabetes can cause intestinal neuropathy,  pancreatitis  leading to  pancreatic insufficiency  can impair digestive enzyme production, and bile may be affected as part of  cirrhosis of the liver . [ 24 ]  The use of  proton pump inhibitors , a class of medication used to reduce stomach acid, is associated with an increased risk of developing SIBO. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1304", "text": "Finally, abnormal connections between the  bacteria -rich colon and the small bowel can increase the bacterial load in the small bowel. Patients with  Crohn's disease  or other diseases of the  ileum  may require surgery that removes the  ileocecal valve  connecting the small and large bowel; this leads to an increased reflux of bacteria into the small bowel. [ citation needed ]  After  bariatric surgery  for obesity, connections between the stomach and the  ileum  can be formed, which may increase bacterial load in the small bowel. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1305", "text": "The diagnosis of bacterial overgrowth can be made by physicians in various ways.  Malabsorption  can be detected by a test called the  D-xylose absorption test .  Xylose  is a sugar that does not require enzymes to be digested. The  D-xylose test  involves having a patient drink a certain quantity of D-xylose, and measuring levels in the  urine  and  blood ; if there is no evidence of D-xylose in the  urine  and  blood , it suggests that the small bowel is not absorbing properly (as opposed to problems with enzymes required for digestion). [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1306", "text": "The gold standard for detection of bacterial overgrowth is the aspiration of more than 10 5  bacteria per millilitre from the small bowel. The normal small bowel has less than 10 4  bacteria per millilitre. [ citation needed ]  Some experts however, consider aspiration of more than 10 3  positive if the flora is predominately colonic type bacteria as these types of bacteria are considered pathological in excessive numbers in the small intestine. The reliability of aspiration in the diagnosis of SIBO has been questioned as SIBO can be patchy and the reproducibility can be as low as 38 percent. Breath tests have their own reliability problems with a high rate of false positive. Some doctors factor in a patients' response to treatment as part of the diagnosis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1307", "text": "Breath tests have been developed to test for bacterial overgrowth. These tests are either based on bacterial metabolism of  carbohydrates  to  hydrogen ,  methane , or  hydrogen sulfide , or based on the detection of by-products of digestion of carbohydrates that are not usually metabolized. The  hydrogen breath test  involves having the patient fast for a minimum of 12 hours then having them drink a substrate usually glucose or  lactulose , then measuring expired hydrogen and methane concentrations typically over a period of several hours. It compares well to jejunal aspirates in making the diagnosis of bacterial overgrowth. [ citation needed ]   Carbon-13  ( 13 C) and  carbon-14  ( 14 C) based tests have also been developed based on the bacterial metabolism of D-xylose. Increased bacterial concentrations are also involved in the deconjugation of bile acids. The  glycocholic acid  breath test involves the administration of the bile acid  14 C glycocholic acid, and the detection of  14 CO 2 , which would be elevated in bacterial overgrowth. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1308", "text": "However, some physicians suggest that if the suspicion of bacterial overgrowth is high enough, the best diagnostic test is a trial of treatment.  If the symptoms improve, an empiric diagnosis of bacterial overgrowth can be made. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1309", "text": "There is insufficient evidence to support the use of inflammatory markers, such as  fecal calprotectin , to detect SIBO. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1310", "text": "SIBO may be defined as an increased number of bacteria measured via exhaled hydrogen and/or methane gas following the ingestion of  glucose , or via analysis of small bowel aspirate fluid. [ 3 ]  Nevertheless, as of 2020, the definition of SIBO as a clinical entity lacks precision and consistency; it is a term generally applied to a clinical disorder where symptoms, clinical signs, and/or laboratory abnormalities are attributed to changes in the numbers of bacteria or in the composition of the bacterial population in the small intestine. [ 4 ]  The main obstacle to accurately define SIBO is limited understanding of the normal intestinal microbial population. Future advances in sampling technology and techniques for counting bacterial populations and their metabolites should provide much-needed clarity. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1311", "text": "The  archaeon   Methanobrevibacter smithii , has been associated with symptoms of SIBO which result in a positive methane breath test. [ 29 ]  In addition to the  archaeon , a few bacteria can also produce methane, such as members of the  Clostridium  and  Bacteroides  genus. Production of methane therefore, may not be bacterial, nor limited to the small intestine, and it has been proposed that the condition should be classified as a separate 'intestinal  methanogen  overgrowth' (IMO). [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1312", "text": "Treatment strategies should focus on identifying and correcting the root causes, where possible, resolving nutritional deficiencies, and administering antibiotics. This is especially important for patients with indigestion and malabsorption. [ 4 ]  Although whether antibiotics should be a first line treatment is a matter of debate. Some experts recommend  probiotics  as first line therapy with antibiotics being reserved as a second line treatment for more severe cases of SIBO.  Prokinetic drugs  are other options but research in humans is limited. [ 30 ] [ 31 ] [ unreliable source? ]  A variety of antibiotics, including  tetracycline ,  amoxicillin-clavulanate ,  metronidazole ,  neomycin ,  cephalexin  and  trimethoprim-sulfamethoxazole  have been used; however, the best evidence is for the use of  rifaximin , a poorly-absorbed antibiotic. [ 2 ]  Although  irritable bowel syndrome  has been shown to respond to the treatment of poorly-absorbed antibiotics, there is limited evidence on the effectiveness of such treatment in cases of SIBO, and as of 2020, randomized controlled trials are still needed to further confirm the eradicating effect of such treatment in SIBO. [ 4 ] \nA course of one week of antibiotics is usually sufficient to treat the condition. However, if the condition recurs, antibiotics can be given in a cyclical fashion in order to prevent tolerance. For example, antibiotics may be given for a week, followed by three weeks off antibiotics, followed by another week of treatment. Alternatively, the choice of antibiotic used can be cycled. [ 28 ]  There is still limited data to guide the clinician in developing antibiotic strategies for SIBO. Therapy remains, for the most part, empiric. However, concerns exist about the potential risks of long-term broad-spectrum antibiotic therapy. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1313", "text": "Probiotics  are bacterial preparations that alter the bacterial flora in the bowel to cause a beneficial effect. Animal research has demonstrated that probiotics have barrier enhancing, antibacterial, immune modulating and anti-inflammatory effects which may have a positive effect in the management of SIBO in humans. [ 4 ]   Lactobacillus casei  has been found to be effective in improving breath hydrogen scores after six weeks of treatment presumably by suppressing levels of a small intestinal bacterial overgrowth of fermenting bacteria. [ citation needed ]   Lactobacillus plantarum ,  Lactobacillus acidophilus , and  Lactobacillus casei  have all demonstrated effectiveness in the treatment and management of SIBO. Conversely,  Lactobacillus fermentum  and  Saccharomyces boulardii  have been found to be ineffective. [ 4 ] [ failed verification ]  A combination of  Lactobacillus plantarum  and  Lactobacillus rhamnosus  has been found to be effective in suppressing bacterial overgrowth of abnormal gas producing organisms in the small intestine. [ 32 ] [ non-primary source needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1314", "text": "A combination of probiotic strains has been found to produce better results than therapy with the antibiotic drug  metronidazole . [ 33 ] [ non-primary source needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1315", "text": "An  elemental diet  has been shown to be highly effective for eliminating SIBO with a two-week diet demonstrating 80% efficacy and a three-week diet demonstrating 85% efficacy. [ 34 ] [ 35 ] [ non-primary source needed ]  An elemental diet works via providing nutrition for the individual while depriving the bacteria of a food source. [ 36 ]  Additional treatment options include the use of  prokinetic  drugs such as  5-HT 4  receptor  agonists or  motilin  agonists to extend the SIBO free period after treatment with an elemental diet or antibiotics. [ 37 ] [ non-primary source needed ]  A diet void of certain foods that feed the bacteria can help alleviate the symptoms. [ 38 ]  For example, if the symptoms are caused by bacterial overgrowth feeding on indigestible carbohydrate rich foods, following a  FODMAP  restriction diet may help. [ 38 ] [ non-primary source needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1316", "text": "The  specific carbohydrate diet  ( SCD ) is a restrictive diet originally created to manage  celiac disease ; it limits the use of complex carbohydrates ( disaccharides  and  polysaccharides ).  Monosaccharides  are allowed, and various foods including fish, aged cheese and  honey  are included. Prohibited foods include cereal grains, potatoes and lactose-containing dairy products. [ 1 ]  It is a  gluten-free diet  since no grains are permitted. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1317", "text": "In 1924,  Sidney V. Haas  (1870\u20131964) described the first SCD for the treatment of children with celiac disease; this was known as the  banana  diet. [ 2 ] [ 3 ]  Haas described a trial with 10 children; all 8 children treated with bananas went into remission, and the two control children died. [ 4 ]  The banana SCD was the cornerstone of celiac therapy for decades until bread shortages in the Netherlands caused by World War II caused children with celiac disease to improve, which led to the isolation of wheat proteins, not starches, as the cause of celiac disease. [ 4 ]  Before the banana SCD, one out of four children with celiac died. [ 3 ]  After more research, he described the SCD as a treatment for celiac disease and  inflammatory bowel disease  (IBD) in his 1951 medical textbook  The Management of Celiac Disease ; Haas never accepted the finding that wheat gluten was the damaging part of wheat; he insisted it was starch and called the discovery about a gluten a \"disservice.\" [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1318", "text": "The diet was later re-popularized by biochemist Elaine Gottschall, the mother of one of Haas's patients, in her 1996 book  Breaking the Vicious Cycle. [ 2 ] [ 6 ]  Gottschall's daughter was reported to been cured of ulcerative colitis in two years by SCD. [ 1 ]  Gottschall described the theory of how restricting diet might reduce gut inflammation associated with various medical conditions. [ 2 ]   Gottschall asserted that the diet could \"cure\" a number of medical conditions without providing data. [ 6 ]    Gottschall advocated using SCD to treat  Crohn's disease ,  ulcerative colitis ,  diverticulitis ,  cystic fibrosis ,  chronic diarrhea , and  autism . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1319", "text": "The claims that the SCD is beneficial for children with autism are based on the supposition they have too much harmful bacteria in their gut.   [ 7 ]  While limited evidence suggests the SCD can be beneficial, there is a concern the restrictive nature of the diet may cause  nutritional deficiencies . [ 8 ]  Parents adopting the SCD for their children are at risk of experiencing guilt when their expectations of improvement are dashed. [ 7 ] [ 9 ]  The SCD is one of many unevidenced treatments offered for children with  special needs  that have the characteristic signs of being  pseudoscientific . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1320", "text": "A 2013 review on SCD and other exclusion diets concluded: \"However, we lack large prospective controlled trials to provide the dietary recommendations patients\u2019 desire. Taken together, studies of exclusive enteral nutrition, exclusion diets, and semi-vegetarian diets suggest that minimizing exposure of the intestinal lumen to selected food items may prolong the remission state of patients with inflammatory bowel disease. Even less evidence exists for the efficacy of the SCD,  FODMAP , or  Paleo diet . \" [ 2 ]   It also said that the diet risks imposition of an undue financial burden and potentially causes malnutrition. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1321", "text": "As of 2017 [update]  there was preliminary evidence that the SCD may help relieve the symptoms of adults with inflammatory bowel disease. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1322", "text": "The Gut and Psychology Syndrome Diet (GAPS Diet) is an even more restrictive variant of the SCD, devised by a Russian neurologist. [ 11 ] [ 12 ]  The diet is promoted with claims it can treat a wide variety of conditions including autism, schizophrenia and epilepsy. [ 11 ] [ 12 ]  Like the SCD, claims of the diet's usefulness for children with autism are not supported by scientific studies. [ 11 ]   Harriet Hall  has described the GAPS diet as \"a mishmash of half-truths, pseudoscience, imagination, and untested claims\", [ 12 ]  and  Quackwatch  includes the GAPS Diet in its  Index of questionable treatments . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1323", "text": "Steatorrhea  (or  steatorrhoea ) is the presence of excess  fat  in  feces . Stools may be bulky and difficult to flush, have a pale and oily appearance, and can be especially foul-smelling. [ 1 ]  An oily anal leakage or some level of  fecal incontinence  may occur. There is increased fat excretion, which can be measured by determining the fecal fat level. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1324", "text": "Impaired digestion or absorption can result in fatty stools.\nPossible causes include  exocrine pancreatic insufficiency , with poor digestion from lack of  lipases , loss of  bile salts , which reduces  micelle  formation, and small intestinal disease-producing  malabsorption . Various other causes include certain medicines that block fat absorption or indigestible or excess oil/fat in diet. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1325", "text": "The absence of  bile  secretion can cause the feces to turn gray or pale. Bile is responsible for the brownish color of feces. In addition to this, bile also plays a role in fat absorption, where dietary lipids are combined so that pancreatic lipases can hydrolyze them before going towards the small intestine. Without bile acids, this pathway would have a hard time occurring, which would lead to fat malabsorption and make steatorrhea more probable to occur. [ 2 ]  Other features of fat malabsorption may also occur such as reduced bone density, difficulty with vision under low light levels, bleeding, bruising, and slow blood clotting times. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1326", "text": "Orlistat  (also known by trade names Xenical and Alli) is a diet pill that works by blocking  the enzymes that digest fat . As a result, some fat cannot be absorbed from the gut and is excreted in the feces instead of being metabolically digested and absorbed, sometimes causing oily anal leakage. [ 6 ] [ 7 ] [ 8 ]  Vytorin (ezetimibe/simvastatin) tablets can cause steatorrhea in some people. [ 6 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1327", "text": "Some studies have shown that stool lipids are increased when whole nuts are eaten, compared to nut butters, oils or flour [ 9 ]  and that lipids from whole nuts are significantly less well absorbed. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1328", "text": "Consuming  jojoba oil  has been documented to cause steatorrhea and anal leakage because it is indigestible. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1329", "text": "Consuming  escolar  and  oilfish  (sometimes mislabelled as  butterfish ) will often cause steatorrhea, also referred to as gempylotoxism or gempylid fish poisoning or  keriorrhea . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1330", "text": "The fat substitute  Olestra , used to reduce digestible fat in some foods, was reported to cause leakage in some consumers during the test-marketing phase. As a result, the product was reformulated before general release to a hydrogenated form that is not liquid at physiologic temperature. The U.S.  Food and Drug Administration  warning indicated excessive consumption of Olestra could result in \"loose stools\"; however, this warning has not been required since 2003. [ 7 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1331", "text": "Steatorrhea should be suspected when the stools are bulky, floating and foul-smelling. [ 1 ]    Specific tests are needed to confirm that these properties are in fact due to excessive levels of fat.  Fats in feces can be measured over a defined time (often five days). [ 14 ]  Other tests include the (13)C-mixed triglycerides test and fecal  elastase , to detect possible fat maldigestion due to  exocrine pancreatic insufficiency , [ 14 ]  or various specific tests to detect other causes of  malabsorption  such as  celiac disease . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1332", "text": "Treatments are mainly correction of the underlying cause, as well as digestive enzyme supplements. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1333", "text": "Stercoral perforation [ 1 ]  is the perforation or rupture of the  intestine 's walls by its internal contents, such as hardened  feces  or foreign objects. Hardened stools may form in prolonged  constipation  or other diseases which cause obstruction of transit, such as  Chagas disease ,  Hirschprung's disease , toxic  colitis ,  hypercalcemia , and  megacolon . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1334", "text": "Symptoms can include  abdominal distension , pain, and nausea. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1335", "text": "Stercoral perforation is a rare and very dangerous, life-threatening situation, as well as a  surgical emergency , because the spillage of contaminated intestinal contents into the  abdominal cavity  leads to  peritonitis , a rapid  bacteremia  ( bacterial infection  of the  blood ), with many  complications . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1336", "text": "This article related to  pathology  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1337", "text": "Stercoral ulcer  is an  ulcer  of the  colon  due to pressure and irritation resulting from severe, prolonged  constipation  due to a large bowel obstruction, damage to the  autonomic nervous system , or stercoral colitis. It is most commonly located in the  sigmoid colon  and  rectum . Prolonged constipation leads to production of fecaliths, leading to possible progression into a  fecaloma . These hard lumps irritate the rectum and lead to the formation of these ulcers. It results in fresh bleeding per rectum (i.e.  hematochezia ). These ulcers may be seen on imaging, such as a  CT scan  but are more commonly identified using  endoscopy , usually a  colonoscopy . [ 1 ]  Treatment modalities can include both surgical and non-surgical techniques."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1338", "text": "Typical patients will present with a history of constipation, likely chronic constipation. Patient populations vulnerable to chronic constipation include, but are not limited to, the elderly, persons with  dementia , those with damage to the autonomic nervous system, infectious diseases, or intestinal vascular compromise. Some patients, due to their condition, may have limitations in reporting their symptoms. Typical symptoms can include  abdominal pain ,  abdominal distention ,  abdominal cramping ,  nausea ,  vomiting ,  fever ,  rectal bleeding , and possible  bowel perforation . [ 2 ]  Patients that develop bowel perforation may present in an acute state with severe abdominal pain and signs of perforation, such as abdominal distention,  guarding  and  rigidity , and air in the abdominal cavity. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1339", "text": "Stercoral ulcers can lead to a complication known as stercoral colitis. Stercoral colitis is a relatively rare form of inflammatory  colitis  that can develop as a result of chronic  constipation  leading to the formation of hardened stool, known as fecaloma. Fecalomas can then lead to distention, possibly causing focal  necrosis  and possibly ulceration. Additional distention in the area can lead to compromise of the vascular supply, leading to intestinal  ischemia [ 2 ] \nThis form of colitis can be due to a wide range of etiologies, coinciding with most causes of constipation. Other etiologies range from a  stroke , intestinal vascular compromise, or any other damage to the  autonomic nervous system  to more rare diseases such as  Chagas disease  and  Hirschsprung's disease . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1340", "text": "Ensuring a proper diagnosis involves a variety of tools by the clinician. An efficient  abdominal exam , along with a  rectal exam  aids in diagnosis. Typically patients will have tenderness to palpation on exam. Rebound tenderness or guarding may present with perforation of the ulcer with air leaking into the abdomen. In these patients, their exam may be far more acute with abdominal rigidity and need for immediate surgical intervention. Additionally, a rectal exam may reveal stool present in the  rectal vault , pointing to the fact that constipation has been or is still present. These patients may even have blood on their rectal exam, due to passing small amounts of stool around the ulcer and adjacent  fecaloma . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1341", "text": "Patients may have unstable vital signs if they have been having rectal bleeding, have developed stercoral colitis, and/or have had a perforation of the ulcer. These vital sign changes may be an acute fever,  elevated heart rate , and/or  decreased blood pressure . Laboratory evaluation may not be as specific in pointing to a diagnosis. Patients may have non-specific  leukocytosis  with elevated  acute phase reactants . However, these are neither specific nor sensitive so the clinician must take into account all aspects of the patient's illness to reach the diagnosis. If a patient presents with severe symptoms it may be useful to order blood cultures and preoperative labs such as  type and screen  and  coagulation testing . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1342", "text": "Imaging studies have been shown to be a key aspect in diagnosing patients with stercoral ulcers and stercoral colitis. Patient status on presentation is important to take into consideration when deciding what imaging study to order. Patients who are acutely ill and showing signs of perforation will need an upright  Chest x-ray  to determine if there is free air in the peritoneum. The imaging study of choice is an  CT scan  of the abdomen with  IV contrast , considering the patient's  renal function  is adequate. Findings that can be seen are fecal impaction with dilation of the  rectosigmoid junction  commonly, but any part of the colon can be dilated. Additionally, fecalomas may be seen as masses in the colon. In the case of ulceration, the part of the colon adjacent to the fecaloma will be thickened. This thickening of the bowel will help differentiate from stercoral colitis and stercoral ulcer from fecal impaction as the colon is typically not thickened in cases of fecal impaction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1343", "text": "Treatment of these patients is typically dependent on a case-to-case basis as the overall patient presentation has to be considered. If the patient presents in an acutely ill state with possible  sepsis  or shock, they will need adequate IV fluid hydration with possible broad-spectrum  antibiotics . Additionally, these patients may need surgery if perforation has occurred. Patients without these symptoms should be managed conservatively with either manual or endoscopically guided fecal disimpaction. A bowel regimen should also be started to ensure that bowel movements become normal.  Opioid  pain medication should be avoided as these medications can slow  colonic motility  and possibly worsen constipation. The key to management and prognosis is identifying the cause or causes of the underlying constipation. Patients should be encouraged to increase  fiber ,  fluids , and  fruits  in their habits. Osmotic and stimulant  laxatives  can also be considered to aid patients if they have trouble making the necessary changes to their diet. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1344", "text": "A  stress ulcer  is a single or multiple  mucosal  defect usually caused by physiological (not psychological)  stress  which can become complicated by  upper gastrointestinal bleeding . These ulcers can be caused by  shock ,  sepsis , trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1345", "text": "It was previously thought that  peptic ulcers  (a different type of ulcer) could be caused by psychological stress but this was proven false with the discovery of  Helicobacter pylori  and its role in the formation of this ulcer. Stress ulcers are a different condition and are formed by different mechanisms. The term  stress ulcer  is a proper medical term and should not be misinterpreted as indicating that these ulcers are caused by emotional stress. Here the term  stress  refers to extreme physiological changes in the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1346", "text": "Another distinction between peptic and stress ulcers is their location in the upper  gastrointestinal tract . Whereas ordinary  peptic ulcers  are found commonly in the  gastric antrum  and the  duodenum , stress ulcers are usually found in the  fundic mucosa  and can be located anywhere within the  stomach  and proximal  duodenum . Stress ulcers tend to present with multiple lesions whereas in peptic ulcers this is much more uncommon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1347", "text": "Stress ulcers, as defined by overt bleeding and hemodynamic instability, decreased  hemoglobin , and/or need for transfusion, were seen in 1.5% of patients in the 2252 patients in the Canadian Critical Care Trials group study. [ 1 ]  People with stress ulcers have a longer ICU length of stay (up to eight days) and a higher mortality (up to four-fold) than patients who do not have stress ulceration and bleeding. [ 2 ]  While the bleeding and transfusions associated with the stress ulcerations contribute to the increased mortality, the contribution of factors like  low blood pressure ,  sepsis , and  respiratory failure  to the mortality independently of the stress ulceration cannot be ignored. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1348", "text": "Risk factors for stress ulcer formation that have been identified are numerous and varied.  However, two landmark studies and one position paper exist that addresses the topic of risk factors for stress ulcer formation:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1349", "text": "The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1350", "text": "The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive  gastroduodenitis . Occasionally, there may be a large acute ulcer in the duodenum (Curling's ulcer). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1351", "text": "Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1352", "text": "The pathogenic mechanisms are similar to those of erosive gastritis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1353", "text": "The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1354", "text": "Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1355", "text": "Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1356", "text": "The need for medications to prevent stress ulcer among those in the intensive care unit is unclear. As of 2014, the quality of the evidence is poor. [ 7 ]  It is unclear which agent is best or if prevention is needed at all. [ 8 ]  Benefit may only occur in those who are not being fed. [ 9 ]  Possible agents include  antacids ,  H2-receptor blockers ,  sucralfate , and  proton pump inhibitors  (PPIs). Tentative evidence supports that PPIs may be better than H2 blockers. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1357", "text": "Concerns with the use of stress ulcer prophylaxis agents include increased rates of  pneumonia  and   Clostridioides difficile  colitis . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1358", "text": "The principles of management are the same as for the chronic ulcer. [ 11 ]  The steps of management are similar as in erosive gastritis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1359", "text": "Endoscopic means of treating stress ulceration may be ineffective and operation required. [ 11 ]  It is believed that shunting blood away from the mucosa makes the mucous membrane ischaemic and more susceptible to injury. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1360", "text": "Treatment of stress ulceration usually begins with prevention. Careful attention to respiratory status, acid-base balance, and treatment of other illnesses help prevent the conditions under which stress ulcers occur. Patients who develop stress ulcers typically do not secrete large quantities of gastric acid; however, acid does appear to be involved in the pathogenesis of the lesions. Thus it is reasonable either to neutralize acid or to inhibit its secretion in patients at high risk. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1361", "text": "In case of severe hemorrhagic or erosive gastritis and stress ulcers, a combination of antacids and H2-blockers may stop active bleeding and prevent bleeding from happening again. In selected patients, either endoscopic therapy or selective infusion of vasopressin into the left gastric artery may help control the hemorrhage. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1362", "text": "Among those in the intensive care unit, ulceration resulting in bleeding is very rare. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1363", "text": "Superior mesenteric artery  ( SMA )  syndrome  is a  gastro - vascular  disorder in which the third and final portion of the  duodenum  is compressed between the  abdominal aorta  (AA) and the overlying  superior mesenteric artery .  This  rare , potentially life-threatening syndrome is typically caused by an angle of 6\u201325\u00b0 between the AA and the SMA, in comparison to the normal range of 38\u201356\u00b0, due to a lack of retroperitoneal and  visceral fat  ( mesenteric  fat). In addition, the aortomesenteric distance is 2\u20138 millimeters, as opposed to the typical 10\u201320. [ 1 ]  However, a narrow SMA angle alone is not enough to make a diagnosis, because patients with a low BMI, most notably children, have been known to have a narrow SMA angle with no symptoms of SMA syndrome. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1364", "text": "SMA syndrome is also known as Wilkie's syndrome, cast syndrome, mesenteric root syndrome, chronic duodenal ileus and intermittent arterio-mesenteric occlusion. [ 3 ]  It is distinct from  nutcracker syndrome , which is the entrapment of the left  renal vein  between the AA and the SMA, although it is possible to be diagnosed with both conditions. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1365", "text": "Signs and symptoms include early satiety,  nausea ,  vomiting , extreme \"stabbing\" postprandial  abdominal pain  (due to both the duodenal compression and the compensatory reversed  peristalsis ), abdominal distention/distortion,  burping , external hypersensitivity or tenderness of the abdominal area,  reflux , and  heartburn . [ 5 ]  In infants, feeding difficulties and poor weight gain are also frequent symptoms. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1366", "text": "In some cases of SMA syndrome, severe  malnutrition  accompanying spontaneous  wasting  may occur. [ 7 ]  This, in turn, increases the duodenal compression, which worsens the underlying cause, creating a cycle of worsening symptoms. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1367", "text": "Fear of eating is commonly seen among those with the chronic form of SMA syndrome. For many, symptoms are partially relieved when in the left lateral decubitus or knee-to-chest position, or in the prone (face down) position. A Hayes maneuver, which corresponds to applying pressure below the umbilicus in cephalad and dorsal direction, elevates the root of the SMA, also slightly easing the constriction. Symptoms can be aggravated when leaning to the right or taking a  face up  position. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1368", "text": "Retroperitoneal  fat and  lymphatic tissue  normally serve as a cushion for the duodenum, protecting it from compression by the SMA. SMA syndrome is thus triggered by any condition involving an insubstantial cushion and narrow  mesenteric  angle. SMA syndrome can present in two forms: chronic/congenital or acute/induced. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1369", "text": "Patients with the chronic, congenital form of SMA syndrome predominantly have a lengthy or even lifelong history of abdominal complaints with intermittent exacerbations depending on the degree of duodenal compression. Risk factors include anatomic characteristics such as: asthenic (very thin or \"lanky\") body build, an unusually high insertion of the duodenum at the  ligament of Treitz , a particularly low origin of the SMA, or  intestinal malrotation  around an axis formed by the SMA. [ 9 ]   Predisposition is easily aggravated by any of the following: poor motility of the digestive tract, [ 3 ]  retroperitional  tumors ,  loss of appetite ,  malabsorption ,  cachexia , exaggerated lumbar  lordosis ,  visceroptosis , abdominal wall laxity, peritoneal adhesions, abdominal trauma, [ 10 ]  rapid linear adolescent growth spurt,  weight loss ,  starvation ,  catabolic  states (as with  cancer  and  burns ), and history of neurological injury. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1370", "text": "The acute form of SMA syndrome develops rapidly after traumatic incidents that forcibly hyper-extend the SMA across the duodenum, inducing the obstruction, or sudden weight loss for any reason. Causes include prolonged supine bed rest, scoliosis surgery, left nephrectomy, ileo-anal pouch surgery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1371", "text": "SMA syndrome is usually difficult to differentiate with  anorexia nervosa . [ 12 ]  Patients with SMA syndrome can be hindered restoring weight in those with anorexia nervosa. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1372", "text": "Diagnosis is very difficult, and usually one of exclusion. SMA syndrome is thus considered only after patients have undergone an extensive evaluation of their  gastrointestinal tract  including  upper endoscopy , and evaluation for various malabsorptive, ulcerative and inflammatory intestinal conditions with a higher diagnostic frequency. Diagnosis may follow  X-ray  examination revealing duodenal dilation followed by abrupt constriction proximal to the overlying SMA, as well as a delay in transit of four to six hours through the gastroduodenal region.  Standard diagnostic exams include abdominal and pelvic  computed tomography  (CT) scan with oral and IV contrast,  upper gastrointestinal series  (UGI), and, for equivocal cases, hypotonic duodenography.  In addition, vascular imaging studies such as  ultrasound  and contrast  angiography  may be used to indicate increased bloodflow velocity through the SMA or a narrowed SMA angle. [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1373", "text": "Despite multiple case reports, there has been controversy surrounding the diagnosis and even the existence of SMA syndrome since symptoms do not always correlate well with radiologic findings, and may not always improve following surgical correction. [ 16 ]  However, the reason for the persistence of gastrointestinal symptoms even after surgical correction in some cases has been traced to the remaining prominence of reversed  peristalsis  in contrast to direct peristalsis. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1374", "text": "Since females between the ages of 10 and 30 are most frequently affected, it is not uncommon for physicians to initially and incorrectly assume that  emaciation  is a choice of the patient instead of a consequence of SMA syndrome.  Patients in the earlier stages of SMA syndrome often remain unaware that they are ill until substantial damage to their health is done, since they may attempt to adapt to the condition by gradually decreasing their food intake or naturally gravitating toward a lighter and more digestible diet. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1375", "text": "SMA syndrome can present in  acute , acquired form (e.g. abruptly emerging within an inpatient stay following scoliosis surgery) as well as  chronic  form (i.e. developing throughout the course of a lifetime and advancing due to environmental triggers, life changes, or other illnesses). According to a number of recent sources, at least 70% of cases can typically be treated with medical treatment, while the rest require surgical treatment. [ 5 ] [ 11 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1376", "text": "Medical treatment is attempted first in many cases. In some cases, emergency surgery is necessary upon presentation. [ 11 ]  A six-week trial of medical treatment is recommended in pediatric cases. [ 5 ]  The goal of medical treatment for SMA syndrome is resolution of underlying conditions and weight gain. Medical treatment may involve nasogastric tube placement for duodenal and gastric decompression, mobilization into the prone or left lateral decubitus position, [ 20 ]  the reversal or removal of the precipitating factor with proper  nutrition  and replacement of fluid and  electrolytes , either by surgically inserted jejunal  feeding tube ,  nasogastric intubation , or  peripherally inserted central catheter  (PICC line) administering  total parenteral nutrition  (TPN). Pro-motility agents such as  metoclopramide  may also be beneficial. [ 21 ]   Symptoms may improve after restoration of weight, except when reversed peristalsis persists, or if regained fat refuses to accumulate within the mesenteric angle. [ 17 ]  Most patients seem to benefit from nutritional support with  hyperalimentation  irrespective of disease history. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1377", "text": "If medical treatment fails, or is not feasible due to severe illness, surgical intervention is required. The most common operation for SMA syndrome,  duodenojejunostomy , was first proposed in 1907 by Bloodgood. [ 7 ]  Performed as either an   open surgery  or  laparoscopically , duodenojejunostomy involves the creation of an  anastomosis  between the  duodenum  and the  jejunum , [ 23 ]  bypassing the compression caused by the AA and the SMA. [ 1 ]   Less common surgical treatments for SMA syndrome include Roux-en-Y duodenojejunostomy, gastrojejunostomy, anterior transposition of the third portion of the duodenum, intestinal derotation, division of the  ligament of Treitz  (Strong's operation), and transposition of the SMA. [ 24 ]  Both transposition of the SMA and lysis of the duodenal suspensory muscle have the advantage that they do not involve the creation of an intestinal anastomosis. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1378", "text": "The possible persistence of symptoms after surgical bypass can be traced to the remaining prominence of reversed  peristalsis  in contrast to direct peristalsis, although the precipitating factor (the duodenal compression) has been bypassed or relieved. Reversed peristalsis has been shown to respond to duodenal circular drainage\u2014a complex and invasive open surgical procedure originally implemented and performed in China. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1379", "text": "In some cases, SMA syndrome may occur alongside a serious, life-threatening condition such as cancer or AIDS. Even in these cases, though, treatment of the SMA syndrome can lead to a reduction in symptoms and an increased quality of life. [ 25 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1380", "text": "Delay in the diagnosis of SMA syndrome can result in fatal  catabolysis  (advanced  malnutrition ),  dehydration ,  electrolyte  abnormalities,  hypokalemia , acute gastric rupture or  intestinal perforation  (from prolonged  mesenteric ischemia ), gastric distention, spontaneous  upper gastrointestinal bleeding ,  hypovolemic shock , and  aspiration pneumonia .\n [ 1 ] [ 14 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1381", "text": "A 1-in-3 mortality rate for Superior Mesenteric Artery syndrome has been quoted by a small number of sources. [ 28 ]  However, after extensive research, original data establishing this mortality rate has not been found, indicating that the number is likely to be unreliable. While research establishing an official mortality rate may not exist, two recent studies of SMA syndrome patients, one published in 2006 looking at 22 cases [ 11 ]  and one in 2012 looking at 80 cases, [ 19 ]  show mortality rates of 0% [ 11 ]  and 6.3%, [ 19 ]  respectively. According to the doctors in one of these studies, the expected outcome for SMA syndrome treatment is generally considered to be excellent. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1382", "text": "According to a 1956 study, only 0.3% of patients referred for an upper-gastrointestinal-tract barium studies fit this diagnosis, and is thus a  rare disease . [ 29 ]  Recognition of SMA syndrome as a distinct clinical entity is controversial, due in part to its possible confusion with a number of other conditions, [ 30 ]  though it is now widely acknowledged. [ 1 ]  However, unfamiliarity with this condition in the medical community coupled with its intermittent and nonspecific symptomatology probably results in its underdiagnosis. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1383", "text": "As the syndrome involves a lack of essential fat, more than half of those diagnosed are  underweight , sometimes to the point of sickliness and  emaciation .  Females are impacted more often than males, and while the syndrome can occur at any age, it is most frequently diagnosed in early adulthood.  The most common co-morbid conditions include mental and behavioral disorders including eating disorders and depression, infectious diseases including tuberculosis and acute gastroenteritis, and nervous system diseases including muscular dystrophy, Parkinson's disease, and cerebral palsy. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1384", "text": "SMA syndrome was first described in 1861 by  Carl Freiherr von Rokitansky  in victims at autopsy, but remained pathologically undefined until 1927 when Wilkie published the first comprehensive series of 75 patients. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1385", "text": "American actor, director, producer, and writer  Christopher Reeve  had the acute form of SMA syndrome as a result of  spinal cord injury . [ citation needed ]  Former model Lisa Brown died in 2017 due to her SMAS after her insurance denied the potentially life saving surgery she needed. Her initial surgery failed causing her to require an intestinal transplant that was expected to cost up to $1 million leading her insurance to deny it. She planned her own funeral.  [ 32 ]   [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1386", "text": "In 2017 the only US non-profit began distributing grants to those with SMAS. They are registered to the IRS under the name Superior Mesenteric Artery Syndrome Research, Awareness and Support, but also work under the DBA of SMAS Patient Assistance. They offer several resources on their website smasyndrome.com and their Facebook business page. SMAS Patient assistance works to disprove inaccurate information, educate on better diagnostic testing, and more successful surgeries such as Duodenal Deroation with LADDS.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1387", "text": "Tropical sprue  is a  malabsorption  disease commonly found in tropical regions, marked with abnormal flattening of the  villi  and  inflammation  of the lining of the  small intestine . [ 1 ] [ 2 ]  It differs significantly from  coeliac sprue . It appears to be a more severe form of  environmental enteropathy . [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1388", "text": "The illness usually starts with an attack of acute  diarrhoea ,  fever  and  malaise  following which, after a variable period, the patient settles into the chronic phase of diarrhoea,  steatorrhoea ,  weight loss ,  anorexia , malaise, and nutritional deficiencies. [ 1 ] [ 2 ] [ 3 ] \nThe symptoms of tropical sprue are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1389", "text": "Left untreated, nutrient and  vitamin deficiencies  may develop in patients with tropical sprue. [ 1 ] [ 2 ]   These deficiencies may have these symptoms:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1390", "text": "The cause of tropical sprue is not known. [ 2 ]   It may be caused by persistent bacterial, viral, amoebal, or  parasitic infections . [ 5 ]   Folic acid deficiency , effects of malabsorbed fat on  intestinal motility , and persistent  small intestinal bacterial overgrowth  may combine to cause the disorder. [ 6 ]  A link between  small intestinal bacterial overgrowth  and tropical sprue has been proposed to be involved in the etiology of post-infectious  irritable bowel syndrome  (IBS). [ 7 ]  Intestinal immunologic dysfunction, including deficiencies in secretory immunoglobulin A (IgA), may predispose people to malabsorption and bacterial colonization, so tropical sprue may be triggered in susceptible individuals following an acute enteric infection. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1391", "text": "Diagnosis of tropical sprue can be complicated because many diseases have similar symptoms.  The following investigation results are suggestive: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1392", "text": "Tropical sprue is largely limited to within about 30 degrees north and south of the  equator .  Recent travel to this region is a key factor in diagnosing this disease in residents of countries outside of that geographical region. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1393", "text": "Other conditions which can resemble tropical sprue need to be differentiated. [ 4 ]   Coeliac disease  (also known as  coeliac sprue  or gluten sensitive enteropathy ), has similar symptoms to tropical sprue, with the flattening of the  villi  and  small intestine inflammation  and is caused by an  autoimmune disorder  in genetically susceptible individuals triggered by ingested  gluten .  Malabsorption can also be caused by  protozoan infections ,  tuberculosis ,  HIV/AIDS ,  immunodeficiency ,  chronic pancreatitis  and  inflammatory bowel disease . [ 2 ]   Environmental enteropathy  is a less severe, subclinical condition similar to tropical sprue. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1394", "text": "Preventive measures for visitors to tropical areas where the condition exists include steps to reduce the likelihood of  gastroenteritis .  These may comprise using only  bottled water  for drinking, brushing teeth, and washing food, and avoiding fruits washed with tap water (or consuming only peeled fruits, such as  bananas  and  oranges ).  Basic sanitation is necessary to reduce fecal-oral contamination and the impact of environmental enteropathy in the developing world. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1395", "text": "Once diagnosed, tropical sprue can be treated by a course of the antibiotic  tetracycline  or  sulphamethoxazole/trimethoprim (co-trimoxazole)  for 3 to 6 months. [ 2 ] [ 8 ] \nSupplementation of vitamins B 12  and folic acid improves appetite and leads to a gain in weight. [ 4 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1396", "text": "The prognosis for tropical sprue may be excellent after treatment.  It usually does not recur in people who get it during travel to affected regions.  The recurrence rate for natives is about 20%, [ 2 ]  but another study showed changes can persist for several years. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1397", "text": "Tropical sprue is common in the  Caribbean , Central and  South America , and  India  and southeast  Asia .  In the Caribbean, it appeared to be more common in Puerto Rico and Haiti.  Epidemics in southern India have occurred. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1398", "text": "The disease was first described by  William Hillary [ 11 ]  in 1759 in  Barbados . [ 12 ]  Tropical sprue was responsible for one-sixth of all casualties sustained by the Allied forces in India and Southeast Asia during World War II. [ 2 ]  The use of folic acid and vitamin B 12  in the treatment of tropical sprue was promoted in the late 1940s by Dr.  Tom Spies  of the  University of Alabama , while conducting his research in Cuba and Puerto Rico. [ 13 ] [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1399", "text": "Upper gastrointestinal bleeding  ( UGIB ) is  gastrointestinal bleeding  in the  upper gastrointestinal tract , commonly defined as bleeding arising from the  esophagus ,  stomach , or  duodenum . Blood may be observed in  vomit  or in altered form as  black stool . Depending on the amount of the blood loss, symptoms may include  shock ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1400", "text": "Upper gastrointestinal bleeding can be caused by  peptic ulcers ,  gastric erosions ,  esophageal varices , and rarer causes such as  gastric cancer . The initial assessment includes measurement of the  blood pressure  and  heart rate , as well as  blood tests  to determine the  hemoglobin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1401", "text": "Significant upper gastrointestinal bleeding is considered a  medical emergency .  Fluid replacement , as well as  blood transfusion , may be required.  Endoscopy  is recommended within 24 hours and bleeding can be stopped by various techniques. [ 1 ]   Proton pump inhibitors  are often used. [ 2 ]   Tranexamic acid  may also be useful. [ 2 ]  Procedures (such as  TIPS  for variceal bleeding) may be used. Recurrent or refractory bleeding may lead to need for  surgery , although this has become uncommon as a result of improved endoscopic and medical treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1402", "text": "Upper gastrointestinal bleeding affects around 50 to 150 people per 100,000 a year. It represents over 50% of cases of gastrointestinal bleeding. [ 2 ]  A 1995 UK study found an estimated mortality risk of 11% in those admitted to hospital for gastrointestinal bleeding. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1403", "text": "Persons with upper gastrointestinal bleeding often present with  hematemesis ,  coffee ground vomiting ,  melena , or  hematochezia  (maroon-coloured stool) if the hemorrhage is severe.  The presentation of bleeding depends on the amount and location of hemorrhage. A person with upper gastrointestinal bleeding may also present with complications of  anemia , including  chest pain ,  syncope ,  fatigue  and  shortness of breath . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1404", "text": "The  physical examination  performed by the  physician  concentrates on the following things: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1405", "text": "Laboratory findings include  anemia ,  coagulopathy , and an elevated  BUN-to-creatinine ratio ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1406", "text": "A number of medications increase the risk of bleeding including  NSAIDs  and  SSRIs .  SSRIs  double the rate of upper gastrointestinal bleeding. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1407", "text": "There are many causes for upper gastrointestinal hemorrhage.  Causes are usually anatomically divided into their location in the upper gastrointestinal tract. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1408", "text": "People are usually stratified into having either  variceal  or non-variceal sources of upper gastrointestinal hemorrhage, as the two have different treatment algorithms and prognosis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1409", "text": "The causes for upper gastrointestinal hemorrhage include the following:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1410", "text": "The strongest predictors of an upper gastrointestinal bleed are black stool, age <50 years, and blood urea nitrogen/creatinine ratio 30 or more. [ 8 ] [ 9 ]  The diagnosis of upper gastrointestinal bleeding is assumed when  hematemesis  (vomiting of blood) is observed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1411", "text": "A  nasogastric aspirate  can help determine the location (source) of bleeding and help understand the best initial diagnostic and treatment plan. Nasogastric aspirate has a sensitivity of 42%, specificity 91%,  negative predictive value  64%, positive predictive value 92% and overall accuracy of 66% in differentiating upper gastrointestinal bleeding from bleeding distal to the  ligament of Treitz . [ 8 ]  A positive aspirate is more helpful than a negative aspirate (If the aspirate is positive, an upper gastrointestinal bleed is likely; if the aspirate is negative, the source of a gastrointestinal bleed is probably, but not certainly, lower). A smaller study found a sensitivity of 79% and specificity of 55%, somewhat opposite results from Witting. [ 10 ]  The accuracy of the aspirate is improved by using the Gastroccult test. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1412", "text": "Determining whether blood is in gastric contents, either vomited or aspirated specimens, may be a challenge when determining the source of the hemorrhage. Slide tests are based on  orthotolidine  (Hematest reagent tablets and Bili-Labstix) or guaiac (Hemoccult and Gastroccult). There is some evidence that orthotolidine-based tests more sensitive than specific, the Hemoccult test's sensitivity reduced by the acidic environment; and the Gastroccult test be the most accurate. [ 11 ]  The sensitivity, specificity, positive predictive value, and negative predictive value have been reported as follows: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1413", "text": "Holman used simulated gastric specimens and found the Hemoccult test to have significant problems with non-specificity and false-positive results, whereas the Gastroccult test was very accurate. [ 12 ] \nHolman found that by 120 seconds after the developer was applied, the Hemoccult test was positive on  all  control samples."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1414", "text": "A scoring system called the  Glasgow-Blatchford  bleeding score found 16% of people presenting with upper gastrointestinal bleed had Glasgow-Blatchford score of \"0\", considered low. Among these people there were no deaths or interventions needed and they were able to be effectively treated in an outpatient setting. [ 13 ] \n [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1415", "text": "Score is equal to \"0\" if the following are all present:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1416", "text": "The predictive values cited are based on the prevalences of upper gastrointestinal bleeding in the corresponding studies. A  clinical calculator can be used to generate predictive values for other prevalences. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1417", "text": "The initial focus is on  resuscitation  beginning with airway management and fluid resuscitation using either intravenous fluids and or blood. [ 15 ]  A number of medications may improve outcomes depending on the source of the bleeding. [ 15 ]   Proton pump inhibitor  medications are often given in the emergent setting before an endoscopy and may reduce the need for an endoscopic haemotstatic treatment. [ 16 ]  Proton pump inhibitors decrease gastric acid production. [ 16 ]  There is insufficient evidence to determine if proton pump inhibitors decrease death rates, re-bleeding events, or the need for surgical interventions. [ 16 ]  After the initial resuscitation has been completed, treatment is instigated to limit the likelihood of re-bleeds and correct any anemia that the bleeding may have caused. Those with a  Glasgow Blatchford score  less than 2 may not require admission to hospital. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1418", "text": "Based on evidence from people with other health problems  crystalloid  and  colloids  are believed to be equivalent for peptic ulcer bleeding. [ 15 ]  In people with a confirmed peptic ulcer, proton pump inhibitors do not reduce death rates, later bleeding events, or need for surgery. [ 18 ]  They may decrease signs of bleeding at endoscopy however. [ 18 ]  In those with less severe disease and where endoscopy is rapidly available, they are of less immediate clinical importance. [ 16 ]   Tranexamic acid  might be effective to reduce mortality, but the evidence for this is weak. [ 15 ] [ 19 ]  But the evidence is promising. [ 20 ]   Somatostatin  and  octreotide  while recommended for variceal bleeding have not been found to be of general use for non-variceal bleeds. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1419", "text": "For initial fluid replacement colloids or  albumin  is preferred in people with cirrhosis. [ 15 ]  Medications typically includes  octreotide  or if not available  vasopressin  and  nitroglycerin  to reduce portal pressures. [ 21 ]  This is typically in addition to  endoscopic banding  or  sclerotherapy  for the varices. [ 21 ]  If this is sufficient then  beta blockers  and  nitrates  may be used for the prevention of re-bleeding. [ 21 ]  If bleeding continues then balloon tamponade with a  Sengstaken-Blakemore tube  or  Minnesota tube  may be used in an attempt to mechanically compress the varices. [ 21 ]  This may then be followed by a  transjugular intrahepatic portosystemic shunt . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1420", "text": "If large amounts of pack red blood cells are used additional  platelets  and  fresh frozen plasma  should be administered to prevent  coagulopathies . [ 15 ]  Some evidence supports holding off on blood transfusions in those who have a  hemoglobin  greater than 7 to 8 g/dL and only moderate bleeding. [ 15 ] [ 22 ]  If the INR is greater than 1.5 to 1.8 correction with fresh frozen plasma,  prothrombin complex  may decrease mortality. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1421", "text": "Upper endoscopy within 24\u00a0hours is the recommended treatment. [ 15 ] [ 23 ]  The benefits versus risks of placing a  nasogastric tube  in those with upper gastrointestinal bleeding are not well known. [ 15 ]   Prokinetic agents  to empty the stomach such as  erythromycin  before endoscopy can decrease the amount of blood in the stomach and thus improve the operators view. [ 15 ]  This erythromycin treatment may lead to a small decrease in the need for a blood transfusion, but the overall balance of how effective erythromycin is compared to potential risks is not clear. [ 15 ] [ 23 ]  Proton pump inhibitors, if they have not been started earlier, are recommended in those in whom high risk signs for bleeding are found. [ 15 ]  It is also recommended that people with high risk signs are kept in hospital for at least 72\u00a0hours. [ 15 ] \nBlood transfusions are not generally recommended to correct anemia, but blood transfusions are recommended if the person is not stable (cardiovascular system instability). [ 22 ]  Oral iron can be used, but this can lead to problems with compliance, tolerance, darkening stools which may mask evidence of rebleeding and tends to be slow, especially if used in conjunction with proton pump inhibitors.  Parenteral  Iron is increasingly used in these cases to improve patient outcomes and void blood usage. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1422", "text": "Depending on its severity, upper gastrointestinal bleeding may carry an estimated mortality risk of 11%. [ 3 ]  However, survival has improved to about 2 percent, likely as a result of improvements in medical therapy and endoscopic control of bleeding. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1423", "text": "About 75% of people presenting to the  emergency department  with gastrointestinal bleeding have an upper source. [ 9 ]  The diagnosis is easier when the people have  hematemesis . In the absence of hematemesis, 40% to 50% of people in the emergency department with gastrointestinal bleeding have an upper source. [ 8 ] [ 10 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1424", "text": "Very early onset inflammatory bowel disease  ( VEOIBD ) is a type of  IBD  which starts in people younger than 6 years of age. According to age we can distinguish more specifically two categories within the VEOIBD diagnosis - neonatal  IBD  (patients younger than 1 month) and infantile  IBD  (patients younger than 2 years old). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1425", "text": "VEIOBD patients present with severe form of the disease that responds poorly to conventional therapies. The symptoms often include not only gastrointestinal tract, but also other tissues, such as  pituitary gland ,  spleen ,  liver ,  skin ,  respiratory tract  or  blood . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1426", "text": "On the other hand, other types of  primary immunodeficiency  can often manifest with IBD-like symptoms, too. These include the  IPEX syndrome ,  Wiskott-Aldrich syndrome ,  XIAP syndrome  or  chronic granulomatous disease . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1427", "text": "Inflammatory bowel diseases  (IBDs), such as  Crohn's disease  (CD) or  Ulcerative Colitis  (UC), are chronic inflammatory conditions of the  gastrointestinal tract . Up-to-date findings show that the pathogenesis is influenced by both environmental and genetic factors. A considerable number of  monogenic  disorders can be found especially among patients with VEOIBD. Causal mutations can be found in genes involved in epithelial barrier formation ( COL7A1 ,  FERMT1 ),  innate  ( CYBB ,  G6PC3 ), as well as the  specific immune response  and immune regulation ( IL10 ,  IL10RA ,  FOXP3 ). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1428", "text": "Vibriosis  or  vibrio infection  is an infection caused by  bacteria  of the genus  Vibrio . About a dozen species can cause vibriosis in humans, with the most common in multiple countries across the  Northern Hemisphere  being  Vibrio parahaemolyticus ,  Vibrio vulnificus , and  Vibrio alginolyticus . [ 1 ] [ 6 ]   Vibrio cholerae , can also commonly cause vibriosis, though only those strains that do not produce cholera-specific toxins: non-O 1 or non-O 139. [ 9 ]  Bacteria that produce these toxins are classified by the World Health Organization as causing  cholera , which is a more severe disease. [ 1 ]  Vibriosis is also an animal disease, and can cause harm to wild and farmed fish among others. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1429", "text": "The genus  Vibrio  includes various species that can cause illness in humans, including  Vibrio parahaemolyticus  and  Vibrio vulnificus . These bacteria thrive in warm, brackish water and are often found in  shellfish  such as  oysters ,  clams , and  mussels . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1430", "text": "Vibriosis can be contracted through:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1431", "text": "The symptoms of vibriosis can vary depending on the species involved:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1432", "text": "Vibriosis incidence is influenced by  environmental  factors such as  water temperature  and  salinity . Warmer temperatures, including in relation to  global warming , have been linked to increased prevalence of vibriosis as  Vibrio  bacteria thrive in warmer conditions. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1433", "text": "In some regions, vibriosis is referred to as \"bath-sore fever\" or \"bathing fever\" due to its association with warm water activities, especially during unusually warm summers. The term highlights the seasonal nature of the infections, which typically occur during the warmer months when people are more likely to engage in water-related activities. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1434", "text": "Diagnosis of vibriosis involves:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1435", "text": "Treatment of vibriosis depends on the severity and type of infection:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1436", "text": "Preventative measures to reduce the risk of vibriosis include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1437", "text": "Whipple's disease  is a  rare   systemic  infectious disease caused by the  bacterium   Tropheryma whipplei . First described by  George Hoyt Whipple  in 1907 and commonly considered as a gastrointestinal disorder, Whipple's disease primarily causes  malabsorption , but may affect any part of the human body, including the heart, brain, joints, skin, lungs and the eyes. [ 1 ]  Weight loss, diarrhea, joint pain, and arthritis are common presenting symptoms, but the presentation can be highly variable in certain individuals, and about 15% of patients do not have the standard signs and symptoms. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1438", "text": "Whipple's disease is significantly more common in men, with 87% of patients diagnosed being male. [ 3 ]  When recognized and treated, Whipple's disease can usually be cured with long-term antibiotic therapy, but if the disease is left undiagnosed or untreated, it can ultimately be fatal. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1439", "text": "The most common symptoms are  diarrhea ,  abdominal pain ,  weight loss , and  joint pains . The joint pains may be due to migratory nondeforming arthritis, which may occur many years before any digestive-tract symptoms develop; they tend to involve the large joints, but can occur in any pattern and tend not to damage the joint surface to the point that the joint becomes deformed. Fever and  chills  occur in a small proportion of people. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1440", "text": "In its more advanced form,  malabsorption  (insufficient absorption of nutrients from the diet) leads to  wasting  and the enlargement of  lymph nodes  in the abdomen. Neurological symptoms (discussed below) are more common in those with the severe form of the abdominal disease. Chronic malabsorptive diarrhea leads to the poor absorption of fat, causing  steatorrhea  (fatty, offensive-smelling stool), flatulence, and abdominal distension. Protein-losing enteropathy may also occur, causing depletion of  albumin , a blood protein, which may lead to  peripheral edema  caused by the lowered  oncotic pressures . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1441", "text": "Hyperpigmentation of the skin occurs in almost half; some also have skin nodules. Various eye problems, such as  uveitis , may occur; this is typically associated with deteriorating vision and pain in the affected eye.  Endocarditis  (infection of the  heart valve ) has been reported in a small number of cases, sometimes in people with no other symptoms of Whipple's disease; this is typically noticed as breathlessness and leg swelling due to fluid accumulation as the heart is unable to pump fluid through the body. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1442", "text": "Of those affected by Whipple's disease, 10\u201340% have problems related to the involvement of the  brain ; the symptoms relate to the part of the brain that is affected. The most common problems are  dementia ,  memory loss ,  confusion , and decreased  level of consciousness . Eye-movement disturbances and myorhythmia (rapidly repetitive movements of the muscles) of the face, together referred to as oculomasticatory myorhythmia, are highly characteristic for Whipple's disease. Weakness and poor coordination of part of the body,  headaches ,  seizures , and a number of more uncommon neurological features are present in some cases. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1443", "text": "T. whipplei  is one of the  Actinomycetes , and is a distant relative of the  Mycobacterium avium complex , explaining in part why Whipple's disease is similar to the diseases caused by MAC bacteria. [ 6 ]  The disease is common in  farmers  and those exposed to soil and animals, suggesting that the infection is acquired from these sources. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1444", "text": "Individuals who are most susceptible to the disease are those with decreased ability to perform intracellular degradation of ingested pathogens or particles, particularly within macrophages. Several studies indicate that defective  T-lymphocyte  (particularly TH1 population) function may be an important predisposing factor for the disease. [ 7 ]  In particular, circulating cells which are  CD11b  (also known as integrin alpha) expressive are reduced in susceptible individuals. CD11b has a vital role in activation of macrophages to destroy intracellularly ingested  T. whipplei  bacteria. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1445", "text": "Common clinical signs and symptoms of Whipple's disease include diarrhea, steatorrhea, abdominal pain, weight loss, migratory arthropathy, fever, and neurological symptoms. [ 8 ]  Weight loss and diarrhea are the most common symptoms that lead to identification of the process, but may be preceded by chronic, unexplained, relapsing episodes of nondestructive seronegative arthritis, often of large joints. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1446", "text": "Endoscopy  of the  duodenum  and  jejunum  can reveal pale yellow shaggy mucosa with erythematous eroded patches in patients with classic intestinal Whipple's disease, and small bowel  X-rays  may show some thickened folds. Other pathological findings may include enlarged  mesenteric lymph nodes , hypercellularity of  lamina propria  with \"foamy macrophages\", and a concurrent decreased number of  lymphocytes  and  plasma cells , per high power field view of the biopsy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1447", "text": "Diagnosis is made by  biopsy , usually by  duodenal   endoscopy , which reveals  PAS -positive  macrophages  in the lamina propria containing non acid-fast , Gram-positive bacilli. [ 5 ] [ a ]   Immunohistochemical  staining for antibodies against  T. whipplei  has been used to detect the organism in a variety of tissues, and a  polymerase chain reaction -based assay is also available, [ 5 ]   which can be confirmatory if performed on blood,  vitreous  fluid,  synovial  fluid, heart valves, or  cerebrospinal fluid . [ 11 ]  PCR of saliva, gastric or intestinal fluid, and stool specimens is highly sensitive, but not specific enough, indicating that healthy individuals can also harbor the causative bacterium without the manifestation of Whipple's disease, but that a negative PCR is most likely indicative of a healthy individual. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1448", "text": "Treatment is with  penicillin ,  ampicillin ,  tetracycline , or  co-trimoxazole  for one to two years. [ 2 ]  Any treatment lasting less than a year has a relapse rate around 40%. [ citation needed ]  Expert opinion as of 2007 is that Whipple's disease should be treated with  doxycycline  with  hydroxychloroquine  for 12 to 18 months. [ 3 ]  Hydroxychloroquine increases antibiotic and bactericides activity against the replication of the bacteria in acidic vacuoles of macrophages by increasing the macrophage intraphagosomal pH. [ 12 ]  Sulfonamides ( sulfadiazine  or  sulfamethoxazole ) may be added for treatment of neurological symptoms. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1449", "text": "The disease is regarded as extremely rare, with an  incidence  (new number of cases per year) of one case per million people. The patients are predominantly male, with various studies and sources typically reporting a ratio between 2:1 and 3:1 of male to female patients. [ 13 ]  In the United States and some other countries, it occurs predominantly in those of  Caucasian ethnicity , suggesting a possible  genetic predisposition  in that population. [ 5 ] [ 13 ]   T. whipplei  appears to be an environmental organism that is commonly present in the gastrointestinal tract, but remains asymptomatic. [ 5 ]  Several lines of evidence suggest that some defect\u2014inherited or acquired\u2014in immunity is required for it to become pathogenic. [ 14 ]  The possible immunological defect may be specific for  T. whipplei , since the disease is not associated with a substantially increased risk of other infections. [ 15 ]  The disease is usually diagnosed in  middle age  (median 49 years). Studies from  Germany  have shown that age at diagnosis has been rising since the 1960s. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1450", "text": "Whipple described the disease in 1907 in a paper in the now-defunct  Bulletin of Johns Hopkins Hospital . The patient was a 36-year-old medical missionary. Whipple referred to the disease as \"intestinal  lipodystrophy \". [ 1 ]  It was long presumed to be an infectious disease, but the causative organism was only fully identified in 1992. [ 16 ]  In 2003, doctors from  Johns Hopkins Hospital , together with the French microbiologist  Didier Raoult  applied novel diagnostic methods to stored tissue samples from Whipple's original patient, and demonstrated  T. whipplei  in these tissues. [ 3 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1451", "text": "Alcohol flush reaction  is a condition in which a person develops flushes or blotches associated with  erythema  on the face, neck, shoulders, ears, and in some cases, the entire body after consuming  alcoholic beverages . The reaction is the result of an accumulation of  acetaldehyde , a metabolic byproduct of the  catabolic  metabolism of  alcohol , and is caused by an  aldehyde dehydrogenase 2  deficiency. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1452", "text": "This syndrome has been associated with lower than average rates of alcoholism, possibly due to its association with adverse effects after drinking alcohol. [ 5 ]  However, it has also been associated with an increased risk of  esophageal cancer  in those who do drink. [ 4 ] [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1453", "text": "The reaction is informally termed  Asian flush  due to its frequent occurrence in  East Asians , with approximately 30 to 50% of Chinese, Japanese, and Koreans showing characteristic physiological responses to drinking alcohol that includes facial flushing,  nausea , headaches and a  fast heart rate . The condition may be also highly prevalent in some  Southeast Asian  and  Inuit  populations. [ 4 ] [ 2 ] [ 3 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1454", "text": "The most obvious symptom of alcohol flush reaction is flushing on a person's face and body after drinking alcohol. [ 4 ]  Other effects include \"nausea, headache and general physical discomfort\". [ 9 ]  People affected by this condition show greater reduction in  psychomotor functions  on alcohol consumption than those without. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1455", "text": "Many cases of  alcohol-induced respiratory reactions , which involve  rhinitis  and worsening of  asthma , develop within 1\u201360 minutes of drinking alcohol and are due to the same causes as flush reactions. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1456", "text": "Disulfiram , a drug sometimes given as treatment for alcoholism, induces effects similar to alcohol flush or hangover causing the  disulfiram-alcohol reaction . It inhibits  acetaldehyde dehydrogenase , causing a five-to ten-fold increase in the concentration of acetaldehyde in the body after drinking alcohol, as happens spontaneously in people subject to flush. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1457", "text": "Alcohol flush reaction is a condition that is experienced more frequently by people of East Asian descent, giving rise to names such as \"Asian flush\" or \"Asian glow\". [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1458", "text": "Around 20\u201330% of East Asians carry the rs671 (ALDH2*2) allele on chromosome 12, which results in a less functional  acetaldehyde dehydrogenase  enzyme, responsible for the breakdown of acetaldehyde, and accounts for most incidents of alcohol flush reaction worldwide. According to the analysis by  HapMap  project, 20% to 30% of people of Chinese, Japanese, and Korean ancestry have at least one  ALDH2*2  allele, while it is rare among Europeans and sub-Saharan Africans. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1459", "text": "The rs671 allele is native to  East Asia  and most common in southeastern China. Analysis correlates the rise and spread of rice cultivation in  South China  with the spread of the allele. [ 5 ]  The reasons for this positive selection are not known, but it has been hypothesized that elevated concentrations of acetaldehyde may have conferred protection against certain parasitic infections, such as  Entamoeba histolytica . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1460", "text": "Additionally, in around 80% of  East Asians , the rapid accumulation of acetaldehyde is worsened by another gene variant; in this case the allele  ADH1B*2 ,  which results in the  alcohol dehydrogenase   enzyme  converting alcohol to toxic  acetaldehyde  more quickly than other gene variants common outside East Asia. [ 5 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1461", "text": "Those with facial flushing due to ALDH2 deficiency may be  homozygotes , with two alleles of low activity, or  heterozygotes , with one low-activity and one normal allele. Homozygotes for the trait find consumption of large amounts of alcohol to be so unpleasant that they are generally protected from  esophageal cancer , but heterozygotes are able to continue drinking. However, an ALDH2-deficient drinker has four to eight times the risk of developing esophageal cancer as a drinker not deficient in the enzyme. [ 4 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1462", "text": "Because most East Asians have a  variant  in the  ADH gene , this risk is lowered somewhat because the  ADH  variant reduces the risk of esophageal cancer four-fold. However, ALDH2-deficient people who do not carry this ADH variant are at the highest risk of cancer as these risk factors act in a multiplicative manner through increasing exposure time to salivary acetaldehyde. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1463", "text": "The idea that acetaldehyde is the cause of the flush is also shown by the clinical use of  disulfiram  (Antabuse), which blocks the removal of acetaldehyde from the body via ALDH inhibition. The high acetaldehyde concentrations described share similarity to symptoms of the flush (flushing of the skin, accelerated heart rate, shortness of breath, throbbing headache, mental confusion and blurred vision). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1464", "text": "For measuring the level of flush reaction to alcohol, the most accurate method is to determine the level of acetaldehyde in the blood stream. This can be measured through a breathalyzer test or blood test. [ 17 ]  Additionally, measuring the amount of alcohol metabolizing enzymes  alcohol dehydrogenases  and  aldehyde dehydrogenase  through  genetic testing  can predict the amount of reaction that one would have. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1465", "text": "Anorectal varices  are  collateral  submucosal blood vessels  dilated  by backflow in the veins of the  rectum . [ 1 ]  Typically this occurs due to  portal hypertension  which shunts venous blood from the  portal system  through the  portosystemic anastomosis  present at this site into the  systemic venous system . [ 2 ] [ 3 ]  This can also occur in the  esophagus , causing  esophageal varices , and at the level of the  umbilicus , causing  caput medusae . [ 4 ]  Between 44% and 78% of patients with portal hypertension get anorectal varices. [ 3 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1466", "text": "Blood from the superior portion of the  rectum  normally drains into the  superior rectal vein  and via the  inferior mesenteric vein  to the  liver  as part of the  portal venous system . Blood from the middle and inferior portions of the  rectum  is drained via the  middle  and  inferior rectal veins . In  portal hypertension , venous resistance is increased within the  portal venous system ; when the pressure in the portal venous system increases above that of the  systemic , blood is shunted through the  portosystemic anastomoses . The shunting of blood and consequential increase of pressure through the collateral veins causes the  varicosities . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1467", "text": "The terms  rectal varices  and  haemorrhoids  are often used interchangeably, but this is not correct. [ 6 ]  Haemorrhoids are due to prolapse of the  rectal venous plexus  and are no more common in patients with portal hypertension than in those without. [ 7 ]  Rectal varices, however, are found only in patients with portal hypertension and are common in conditions such as  cirrhosis . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1468", "text": "Unlike esophageal varices, rectal varices are less prone to bleeding, are less serious when a bleed does occur, and are easier to treat because of the more accessible location. [ 9 ]  However, in some cases, rectal varices can result in severe bleeding.  [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1469", "text": "Typically, treatment consists of addressing the underlying portal hypertension. Some treatments include portosystemic shunting, ligation, and under-running suturing. [ 5 ]  Insertion of a  transjugular intrahepatic portosystemic shunt  (TIPS) has been shown to alleviate varices caused by portal hypertension. [ 1 ]  Successful treatment of portal hypertension that subsequently reduces anorectal varices provides a confirmation of the initial diagnosis, allowing for a distinction between varices and hemorrhoids, which would not have been alleviated by reduction of portal hypertension. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1470", "text": "Autoimmune gastrointestinal dysmotility  ( AGID ) is an  autoimmune disease   autonomic neuropathy  affecting the  gastrointestinal  organs and  digestive system  of the body. Dysmotility is when the strength or coordination of the  esophagus ,  stomach  or  intestines   muscles  do not work as they should. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1471", "text": "Often AGID is a symptom of other problems, including  colon cancer ,  lupus , lung, breast, or  ovarian   carcinoma  or  thymoma . or other diseases."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1472", "text": "AGID is diagnosed with a complete medical history, exam of patients motility and with special blood tests looking for autoantibodies consistent with neurologic autoimmunity. [ 2 ]  Blood tests included evaluations of immunofluorescence (neuronal nuclear and cytoplasmic antibodies), radioimmunoprecipitation assays (neuronal and muscle plasma membrane cation channel antibodies), and enzyme-linked immunosorbent assay (muscle striational antibodies). A finding, along with medical history, of ganglionic neuronal acetylcholine receptor and N-type voltage-gated calcium channel autoantibodies in the blood stream would result in a medically acceptable diagnosis of AGID. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1473", "text": "Medications to relieve nausea and vomiting or to enhance mobility may be helpful, as may  cholinesterase inhibitors .   Immunotherapy  and  plasma exchange  have also been reportedly effective. [ 4 ]   Pyridostigmine  is a pharmaceutical treatment option for patients with AGID. [ 3 ] \nIn severe cases patients with AGID are required to abandon eating foods, requiring them to get nourishment through a process called  parenteral nutrition , where the patient is fed via a permanent  IV  and the liquid  nourishment  is infused directly in the blood stream, as opposed to a feeding tube. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1474", "text": "Azotorrhea  is the excessive discharge of  nitrogenous  substances in the  feces  or  urine . As in when people eat a diet high in  protein  they may suffer from increased amount of  amino acid  byproduct (nitrogen) being broken and excreted through defecation or urination. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1475", "text": "Creatorrhea  is the abnormal  excretion  of  muscle fibre  in  feces . [ 1 ]  The term is made from the prefix  creat-  or  creato-  which comes from Greek  kreas  meaning \" flesh \". The suffix  -rrhea  (or  -rrhoea ) comes from Greek  -rrhoia  meaning \"flow,\" hence discharge. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1476", "text": "Digestion of food is achieved through a mixture of  mechanical  and  chemical processes . Failure to produce or secrete chemicals known as  digestive enzymes  can lead to failure digesting or breaking down specific components of ingested food. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1477", "text": "Where there is a failure to produce, release, or convert  trypsinogen \u2014an inactive enzyme precursor or  zymogen \u2014muscle fibres are not properly digested and are therefore released in the feces. Trypsinogen is produced in the pancreas and released into the  alimentary canal  where it is converted to the active enzyme  trypsin . [ 2 ] \nInflammation of the  pancreas , or  pancreatitis  can therefore precipitate this condition, [ 3 ]  as can  cystic fibrosis [ 4 ]  which also affects the production of digestive enzymes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1478", "text": "An  enterocutaneous fistula  ( ECF ) is an abnormal communication between the  small  or  large bowel  and the skin that allows the contents of the  stomach  or intestines to leak through an opening in the skin. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1479", "text": "The  mnemonic   HIS FRIENDS  can be used to memorize characteristics which impede the closure of  ECF. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1480", "text": "H: high output\nI: IBD\nS:short tract"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1481", "text": "Congenital types: tracheoesophageal, vitellointestinal duct, patent urachus, rectovaginal"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1482", "text": "Acquired: trauma (postoperative), radiation, malignancy, infection"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1483", "text": "Low-output fistula: < 500 mL/day"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1484", "text": "High-output fistula: > 500 mL/day"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1485", "text": "Low-output fistula: < 200 mL/day"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1486", "text": "Moderate-output fistula: 200\u2013500 mL/day"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1487", "text": "High-output fistula: > 500 mL/day [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1488", "text": "The majority will close spontaneously within approximately 6 weeks. If it has not closed by 12 weeks, it is unlikely to do so and definitive surgery should be planned. The median time to definitive repair from  fistula  onset was 6 months (range 1 day to 28 months). The 6-month time course is commonly utilized by groups with significant experience treating fistulas, owing to the trend in encountering a less hostile abdomen than in the early phases. [ 4 ]  Some evidence also suggests that  somatostatin  can be an effective treatment with respect to reducing closure time and improving the spontaneous closure rate of enterocutaneous fistulas. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1489", "text": "Functional abdominal pain syndrome  ( FAPS ),  chronic functional abdominal pain  ( CFAP ), or  centrally mediated abdominal pain syndrome  ( CMAP ) is\u00a0a  pain syndrome  of\u00a0the  abdomen , that\u00a0has been present for at least six months, is not well connected to gastrointestinal function, and is accompanied by some loss of everyday activities. The discomfort is persistent, near-constant, or regularly reoccurring. The absence of symptom association with food intake or  defecation  distinguishes functional abdominal pain syndrome from other  functional gastrointestinal illnesses , such as  irritable bowel syndrome  (IBS) and  functional dyspepsia . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1490", "text": "Functional abdominal pain syndrome is a  functional gastrointestinal disorder  meaning that it is not associated with any organic or structural pathology. Theories on the mechanisms behind functional abdominal pain syndrome include changes in descending modulation,  central sensitization  of the spinal  dorsal horn , peripheral enhancement of the  visceral pain  afferent signal, and, central amplification."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1491", "text": "The diagnosis of functional abdominal pain syndrome is made based on clinical features and diagnostic criteria. A thorough clinical history must be taken to accurately diagnose functional abdominal pain syndrome. Diagnostic testing to rule out organic disorders should only be done when alarm features are present. Differential diagnosis of functional abdominal pain syndrome includes a variety of other  functional gastrointestinal disorders ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1492", "text": "There is no well-established treatment for functional abdominal pain syndrome. General measures such as a positive  physician-patient relationship  are beneficial.  Antidepressants  are often used to treat other  functional gastrointestinal disorders  and may be helpful in treating functional abdominal pain syndrome. Psychological interventions including various forms of  therapy  can also be helpful. While the exact presence of functional abdominal pain syndrome is unknown studies show that it affects between 0.5% and 2% of  North Americans . Functional abdominal pain syndrome is more common in women than men and usually occurs in the fourth decade of life."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1493", "text": "Functional abdominal pain syndrome is characterized by frequent or chronic  stomach pain  and a reduction in everyday activity. [ 2 ]  The pain is persistent, near-constant, or regularly reoccurring. The pain is not related to food intake or  defecation . [ 1 ]  Functional abdominal pain is usually periumbilical and is not accompanied by  weight loss ,\u00a0 vomiting ,\u00a0 diarrhea , nocturnal symptoms, or slowed growth. [ 3 ]  Typically, the level of abdominal pain in functional abdominal pain syndrome seldom varies, with maximum pain being felt the majority of the\u00a0time. functional abdominal pain syndrome is frequently coupled with a proclivity to experience and report additional  somatic symptoms  of discomfort, such as  chronic pain  believed to be connected to the gynecological or  urinary systems . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1494", "text": "Functional abdominal pain syndrome is a  functional gastrointestinal disorder . [ 4 ]   Functional gastrointestinal disorders  (FGD) are common medical conditions characterized by recurrent and persistent gastrointestinal symptoms caused by improper functioning of the enteric system in the absence of any identifiable organic or structural  pathology ,\u00a0such as  ulcers ,\u00a0 inflammation ,\u00a0 tumors  or masses. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1495", "text": "The pain from functional abdominal pain syndrome is thought to be caused by changes in descending modulation,  central sensitization  of the spinal dorsal horn, peripheral enhancement of the  visceral pain  afferent signal, and, lastly, central amplification. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1496", "text": "Peripheral sensitization, also known as elevated ascending visceral afferent signalling, can happen following  GI tract   inflammation  or damage. [ 6 ]  For example, about one-third of individuals with  IBS  report that their symptoms started after an acute infection episode; this is a phenomenon known as postinfectious IBS (PI-IBS). [ 7 ]  PI-IBS\u00a0has consistently been linked to the existence of a low-grade inflammatory infiltrate. [ 8 ]  According to theory, this inflammatory infiltration results in increased sensitivity and field of peripheral receptors, the latter of which causes  hyperalgesia  by recruiting and activating  nociceptors  that were previously silent. [ 2 ]  Furthermore, it was discovered that the best indicators of who would develop PI-IBS were stress, as measured by traumatic life events, and a  neurotic personality  features. [ 8 ]  These convergent lines of data support the hypothesis that  inflammation  and/or injury in a psychologically predisposed person may cause visceral afferents to become peripherally sensitized, increasing the amount of nociceptive information that ascends to the spinal dorsal horn. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1497", "text": "Peripheral  nociceptors  become more sensitive, which increases the amount of impulses that reach the spinal dorsal horn.  Central sensitization  may result from an increase in the frequency and amplitude of peripheral signals that reach the spinal dorsal horn. An increase in presynaptic  glutamate  release causes  central sensitization  by removing the  magnesium  ion block of the  N-methyl-d-aspartate  (NMDA) receptor. The end result is an overall increase in dorsal horn neuron responsiveness, which frequently lasts longer than the initial shock when combined with the activation of other important enzymes. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1498", "text": "The anterior  cingulate cortex  is home to the majority of the central descending modulatory systems. These modulatory systems allow afferent signals from the periphery to be gated, which allows for the amplification or even restriction of the signal. They interface with the spinal dorsal horn. [ 2 ]  The pro-nociceptive condition that characterizes many chronic visceral pain syndromes is thought to be mostly caused by anomalies in the descending pain modulatory system. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1499", "text": "Since pain is the primary symptom of functional abdominal pain syndrome, obtaining a complete medical history and conducting a comprehensive physical examination continue to be essential components of the diagnosing process. [ 10 ]  The functional abdominal pain syndrome patient should be asked to provide a thorough history that thoroughly examines the timeline of pain occurrences, especially in connection with surgery, infection, or traumatic life events. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1500", "text": "In a patient with functional abdominal pain syndrome, the clinical examination should be normal by definition. Nonetheless, as a starting point, it is important to look closely for the existence of abdominal scars from prior operations or investigations. Similarly,  Carnett's sign , which involves palpating a sore spot both before and after the patient tenses their  abdominal wall , could be helpful. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1501", "text": "Diagnostic testing to rule out organic disease should not be done frequently in the absence of alarm signs, similar to other functional GI problems (ie, unexplained  weight loss ,\u00a0bloody bowel movements,  abdominal mass ,\u00a0 anorexia ). If the physical examination yields negative results, no more diagnostic testing is necessary. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1502", "text": "The  Rome IV  diagnostic criteria for functional abdominal pain syndrome is as follows: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1503", "text": "To fit the  Rome IV  diagnostic criteria for functional abdominal pain syndrome the patient must fit all of the above criteria and the criteria must be met over the past three months, with the onset of symptoms occurring at least six months before diagnosis. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1504", "text": "When diagnosing functional abdominal pain syndrome, a number of other  functional GI illnesses  should be taken into account initially.  IBS  may be taken into consideration if the pain is accompanied by changes in bowel motions (frequent, loose stools or harder, infrequent stools). Functional gall bladder disease or  sphincter of Oddi dysfunction  should be considered if the pain is significant, occurs at different intervals (not daily), and is located in the right upper quadrant or  epigastrium . Consider  functional dyspepsia  if the discomfort is in the  epigastrium  and does not meet the criteria for functional gallbladder disease. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1505", "text": "There is no definite agreement on how to best manage functional abdominal pain syndrome in adults. As a result, the majority of currently employed therapies are founded on data and firsthand knowledge from other  functional bowel diseases  and  chronic pain syndromes . It is helpful to categorize therapy modalities into three groups: psychological interventions, pharmaceutical therapies, and general measures. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1506", "text": "The  doctor-patient interaction  is essential to the management of a patient with functional abdominal pain syndrome and to a successful outcome. A crucial component of treatment is, in particular, validating a patient's symptoms in a caring, interdisciplinary setting. In the framework of routine outpatient reviews, the patient and the doctor should also decide on and establish realistic treatment goals. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1507", "text": "Antidepressants , especially low-dose  tricyclic antidepressants  (TCAs), have been shown to be beneficial in the treatment of  functional gastrointestinal disorders  and  chronic pain . [ 13 ]  They may also be helpful in the treatment of functional abdominal pain syndrome due to their dual effects of direct pain management and antidepressant properties. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1508", "text": "Trials utilizing  tricyclic antidepressants  have generally outperformed those using  selective serotonin-reuptake inhibitors  in other  chronic pain disorders . [ 14 ]   Venlafaxine  and  duloxetine  are two examples of more recent medications with combined  serotonin and norepinephrine reuptake inhibitors  (SNRIs), which have been shown to reduce pain in some somatic pain disorders and may be helpful in functional abdominal pain syndrome. [ 15 ]  Patients with co-occurring  anxiety  and  depression  may benefit from both  SNRIs  and  selective serotonin-reuptake inhibitors  (SSRIs). The majority of  analgesics , such as  aspirin  and  nonsteroidal anti-inflammatory medications , don't really help much, maybe because they mostly have peripheral effects. [ 1 ]  Because of the risk of addiction and narcotic bowel syndrome, narcotic  analgesics  should be avoided. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1509", "text": "There hasn't been a study explicitly looking at adult functional abdominal pain syndrome and psychological  therapy . Studies on non-gastrointestinal pain diseases and other painful  functional gastrointestinal illnesses , however, point to the potential benefit of psychological therapies. [ 1 ]  Stress management,  hypnosis , [ 17 ]  dynamic or  interpersonal psychotherapy , [ 18 ] [ 19 ]  and  cognitive behavioral therapy  are among the interventions that may prove advantageous. [ 20 ] [ 21 ]  The most effective way to manage impairment resulting from refractory  chronic pain  may be to refer patients to pain treatment clinics for multidisciplinary treatment programs. [ 22 ]  While the previously discussed psychological treatments have demonstrated improvements in mood, coping,  quality of life , and health care costs, their effect on specific visceral or  somatic symptoms  is less clear, indicating that their most effective application may be in conjunction with symptomatic treatment. [ 20 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1510", "text": "Due to a lack of data and methodological challenges in distinguishing functional abdominal pain syndrome from other more prevalent  functional gastrointestinal diseases  like  IBS  and  functional dyspepsia , the epidemiology of the disease is not fully understood. Nonetheless, compared to  functional dyspepsia  or  IBS , functional abdominal pain syndrome is generally thought to be a less frequent. [ 1 ]  The stated prevalence rates in  North America  are between 0.5% and 2%, and they are consistent with reports from other nations. [ 24 ] [ 25 ] [ 26 ]  The condition affects women more frequently than men (3:2), with a peak in prevalence occurring in the fourth decade of life. [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1511", "text": "Gastrointestinal diseases  (abbrev.  GI diseases  or  GI illnesses ) refer to diseases involving the  gastrointestinal tract , namely the  esophagus ,  stomach ,  small intestine ,  large intestine  and  rectum ; and the  accessory organs of digestion , the  liver ,  gallbladder , and  pancreas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1512", "text": "The oral cavity is part of the gastrointestinal system and as such the presence of alterations in this district can be the first sign of both systemic and gastrointestinal diseases. [ 1 ]  By far the most common oral conditions are  plaque -induced diseases (e.g.,  gingivitis ,  periodontitis ,  dental caries ). Oral symptoms can be similar to lesions occurring elsewhere in the digestive tract, with a pattern of swelling, inflammation, ulcers, and fissures. If these signs are present, then patients are more likely to also have anal and esophageal lesions and experience other extra-intestinal disease manifestations. [ 2 ]   Some diseases which involve other parts of the GI tract can manifest in the mouth, alone or in combination, including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1513", "text": "Oesophageal diseases include a spectrum of disorders affecting the  oesophagus . The most common condition of the oesophagus in Western countries is  gastroesophageal reflux disease , [ 4 ]  which in chronic forms is thought to result in changes to the  epithelium  of the oesophagus, known as  Barrett's oesophagus . [ 5 ] :\u200a863\u2013865"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1514", "text": "Acute  disease might include  infections  such as  oesophagitis , trauma caused by the ingestion of corrosive substances, or rupture of  veins  such as  oesophageal varices ,  Boerhaave syndrome  or  Mallory-Weiss tears . Chronic diseases might include  congenital  diseases such as  Zenker's diverticulum  and  esophageal webbing , and  oesophageal motility disorders  including the  nutcracker oesophagus ,  achalasia ,  diffuse oesophageal spasm , and  oesophageal stricture . [ 5 ] :\u200a853,\u200a863\u2013868"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1515", "text": "Oesophageal disease may result in a  sore throat ,  throwing up blood , difficulty  swallowing  or  vomiting . Chronic or congenital diseases might be investigated using  barium swallows ,  endoscopy  and  biopsy , whereas acute diseases such as reflux may be investigated and diagnosed based on  symptoms  and a  medical history  alone. [ 5 ] :\u200a863\u2013867"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1516", "text": "Gastric diseases refer to diseases affecting the  stomach . Inflammation of the stomach by infection from any cause is called  gastritis , and when including other parts of the gastrointestinal tract called  gastroenteritis . When gastritis persists in a chronic state, it is associated with several diseases, including  atrophic gastritis ,  pyloric stenosis , and  gastric cancer . Another common condition is  gastric ulceration ,  peptic ulcers . Ulceration erodes the  gastric mucosa , which protects the tissue of the stomach from the stomach acids. Peptic ulcers are most commonly caused by a bacterial  Helicobacter pylori   infection . [ 5 ]   Epstein\u2013Barr virus  infection is another factor to induce gastric cancer. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1517", "text": "As well as peptic ulcers,  vomiting blood  may result from abnormal arteries or veins that have ruptured, including  Dieulafoy's lesion  and  Gastric antral vascular ectasia . Congenital disorders of the stomach include  pernicious anaemia , in which a targeted  immune  response against  parietal cells  results in an inability to absorb  vitamin B12 . Other common symptoms that stomach disease might cause include  indigestion  or  dyspepsia ,  vomiting , and in chronic disease, digestive problems leading to forms of  malnutrition . [ 5 ]   :\u200a850\u2013853\u200a  In addition to routine tests, an  endoscopy  might be used to examine or take a  biopsy  from the stomach. [ 5 ]   :\u200a848"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1518", "text": "The  small  and  large intestines  may be affected by  infectious , autoimmune, and physiological states. Inflammation of the intestines is called  enterocolitis , which may lead to  diarrhea ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1519", "text": "Acute conditions affecting the bowels include  infectious diarrhea  and  mesenteric ischaemia . Causes of  constipation  may include  faecal impaction  and  bowel obstruction , which may in turn be caused by  ileus ,  intussusception ,  volvulus .  Inflammatory bowel disease  is a condition of unknown aetiology, classified as either  Crohn's disease  or  ulcerative colitis , that can affect the intestines and other parts of the gastrointestinal tract. Other causes of illness include  intestinal pseudoobstruction , and  necrotizing enterocolitis . [ 5 ] :\u200a850\u2013862,\u200a895\u2013903"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1520", "text": "Diseases of the intestine may cause  vomiting ,  diarrhoea  or  constipation , and altered  stool , such as with  blood in stool .  Colonoscopy  may be used to examine the large intestine, and a person's stool may be sent for  culture  and  microscopy . Infectious disease may be treated with targeted  antibiotics , and inflammatory bowel disease with  immunosuppression . Surgery may also be used to treat some causes of bowel obstruction. [ 5 ] :\u200a850\u2013862"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1521", "text": "The normal thickness of the small  intestinal wall  is 3\u20135\u00a0mm, [ 8 ]  and 1\u20135\u00a0mm in the large intestine. [ 9 ]  Focal, irregular and asymmetrical gastrointestinal wall thickening on  CT scan  suggests a malignancy. [ 9 ]  Segmental or diffuse gastrointestinal wall thickening is most often due to ischemic, inflammatory or infectious disease. [ 9 ]  Though less common, medications such as  ACE inhibitors  can cause  angioedema  and small bowel thickening. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1522", "text": "The small intestine consists of the  duodenum ,  jejunum  and  ileum . Inflammation of the small intestine is called  enteritis , which if localised to just part is called  duodenitis ,  jejunitis  and  ileitis , respectively.  Peptic ulcers  are also common in the duodenum. [ 5 ] :\u200a879\u2013884"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1523", "text": "Chronic diseases of  malabsorption  may affect the small intestine, including the autoimmune  coeliac disease , infective  tropical sprue , and congenital or surgical  short bowel syndrome . Other rarer diseases affecting the small intestine include  Curling's ulcer ,  blind loop syndrome ,  Milroy disease  and  Whipple's disease . Tumours of the small intestine include  gastrointestinal stromal tumours ,  lipomas ,  hamartomas  and  carcinoid syndromes . [ 5 ] :\u200a879\u2013887"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1524", "text": "Diseases of the small intestine may present with symptoms such as  diarrhoea ,  malnutrition ,  fatigue  and  weight loss . Investigations pursued may include  blood tests  to monitor nutrition, such as  iron levels ,  folate  and  calcium ,  endoscopy  and  biopsy  of the duodenum, and  barium swallow . Treatments may include renutrition and  antibiotics  for infections. [ 5 ] :\u200a879\u2013887"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1525", "text": "Diseases that affect the  large intestine  may affect it in whole or in part.  Appendicitis  is one such disease, caused by inflammation of the  appendix . Generalised inflammation of the large intestine is referred to as  colitis , which when caused by the bacteria  Clostridioides difficile  is referred to as  pseudomembranous colitis .  Diverticulitis  is a common cause of abdominal pain resulting from outpouchings that particularly affect the colon.  Functional colonic diseases  refer to disorders without a known cause, including  irritable bowel syndrome  and  intestinal pseudoobstruction .  Constipation  may result from lifestyle factors,  impaction of a rigid stool  in the rectum, or in  neonates ,  Hirschprung's disease . [ 5 ] :\u200a913\u2013915"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1526", "text": "Diseases affecting the large intestine may cause blood to be passed with stool, may cause  constipation , or may result in  abdominal pain  or a fever. Tests that specifically examine the function of the large intestine include barium swallows,  abdominal x-rays , and  colonoscopy . [ 5 ] :\u200a913\u2013915"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1527", "text": "Diseases affecting the  rectum  and  anus  are extremely common, especially in older adults.  Hemorrhoids , vascular outpouchings of skin, are very common, as is  pruritus ani , referring to anal itchiness. Other conditions, such as  anal cancer  may be associated with  ulcerative colitis  or with  sexually transmitted infections  such as  HIV .  Inflammation of the rectum is known as  proctitis , one cause of which is radiation damage associated with  radiotherapy  to other sites such as the  prostate .  Faecal incontinence  can result from mechanical and neurological problems, and when associated with a lack of voluntary voiding ability is described as  encopresis . Pain on passing stool may result from  anal abscesses , small inflamed nodules,  anal fissures , and  anal fistulas . [ 5 ] :\u200a915\u2013916"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1528", "text": "Rectal and anal disease may be asymptomatic, or may present with pain when passing stools,  fresh blood in stool ,  a feeling of incomplete emptying , or pencil-thin stools. In addition to regular tests, medical tests used to investigate the anus and rectum include the  digital rectal exam  and  proctoscopy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1529", "text": "Hepatic diseases refers to those affecting the  liver .   Hepatitis  refers to inflammation of liver tissue, and may be  acute  or  chronic . Infectious  viral hepatitis , such as  hepatitis A ,  B  and  C , affect in excess of (X) million people worldwide. Liver disease may also be a result of lifestyle factors, such as  fatty liver  and  NASH .  Alcoholic liver disease  may also develop as a result of chronic alcohol use, which may also cause  alcoholic hepatitis .  Cirrhosis  may develop as a result of chronic  hepatic fibrosis  in a chronically inflamed liver, such as one affected by  alcohol  or viral hepatitis. [ 5 ] :\u200a947\u2013958"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1530", "text": "Liver abscesses  are often acute conditions, with common causes being  pyogenic  and  amoebic . Chronic liver disease, such as cirrhosis, may be a cause of  liver failure , a state where the liver is unable to compensate for chronic damage, and unable to meet the metabolic demands of the body.  In the acute setting , this may be a cause of  hepatic encephalopathy  and  hepatorenal syndrome . Other causes of chronic liver disease are genetic or autoimmune disease, such as  hemochromatosis ,  Wilson's disease ,  autoimmune hepatitis , and  primary biliary cirrhosis . [ 5 ] :\u200a959\u2013963,\u200a971"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1531", "text": "Acute liver disease rarely results in pain, but may result in  jaundice . Infectious liver disease may cause a fever. Chronic liver disease may result in  a buildup of fluid in the abdomen ,  yellowing of the skin  or  eyes , easy bruising,  immunosuppression , and feminization. [ 11 ]   Portal hypertension  is often present, and this may lead to the development of prominent veins in many parts of the body, such as  oesophageal varices , and  haemorrhoids . [ 5 ] :\u200a959\u2013963,\u200a971\u2013973"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1532", "text": "In order to investigate liver disease, a medical history, including regarding a person's  family history , travel to risk-prone areas, alcohol use and food consumption, may be taken. A  medical examination  may be conducted to investigate for symptoms of liver disease. Blood tests may be used, particularly  liver function tests , and other blood tests may be used to investigate the presence of the Hepatitis viruses in the blood, and ultrasound used. If ascites is present, abdominal fluid may be tested for protein levels. [ 5 ] :\u200a921,\u200a926\u2013927"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1533", "text": "Pancreatic diseases that affect digestion refers to disorders affecting the  exocrine pancreas , which is a part of the pancreas involved in digestion. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1534", "text": "One of the most common conditions of the exocrine pancreas is  acute pancreatitis , which in the majority of cases relates to  gallstones  that have impacted in the pancreatic part of the  biliary tree , or due to acute or chronic  hazardous alcohol use  or as a side-effect of  ERCP . Other forms of pancreatitis include  chronic  and  hereditary  forms. Chronic pancreatitis may predispose to  pancreatic cancer  and is strongly linked to alcohol use. Other rarer diseases affecting the pancreas may include  pancreatic pseudocysts ,  exocrine pancreatic insufficiency , and  pancreatic fistulas . [ 5 ] :\u200a888\u2013891"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1535", "text": "Pancreatic disease may present with or without symptoms. When symptoms occur, such as in  acute pancreatitis , a person may experience acute-onset, severe mid-abdominal pain, nausea and vomiting. In severe cases, pancreatitis may lead to rapid blood loss and  systemic inflammatory response syndrome . When the pancreas is unable to secrete digestive  enzymes , such as with a pancreatic cancer occluding the  pancreatic duct , result in jaundice. Pancreatic disease might be investigated using  abdominal x-rays ,  MRCP  or  ERCP ,  CT scans , and through blood tests such as measurement of the  amylase  and  lipase  enzymes. [ 5 ] :\u200a888\u2013894"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1536", "text": "Diseases of the  hepatobiliary system  affect the  biliary tract  (also known as the  biliary tree ), which secretes  bile  in order to aid digestion of fats. Diseases of the  gallbladder  and bile ducts are commonly diet-related, and may include the  formation of   gallstones  that impact in the gallbladder ( cholecystolithiasis ) or in the  common bile duct  ( choledocholithiasis ). [ 5 ] :\u200a977\u2013978"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1537", "text": "Gallstones are a common cause of inflammation of the gallbladder, called  cholecystitis . Inflammation of the  biliary duct  is called  cholangitis , which may be associated with  autoimmune  disease, such as  primary sclerosing cholangitis , or a result of bacterial infection, such as  ascending cholangitis . [ 5 ] :\u200a977\u2013978,\u200a963\u2013968"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1538", "text": "Disease of the biliary tree may cause pain in the upper right abdomen,  particularly when pressed . Disease might be investigated using  ultrasound  or  ERCP , and might be treated with drugs such as  antibiotics  or  UDCA , or by the surgical  removal of the gallbladder . [ 5 ] :\u200a977\u2013979"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1539", "text": "The Wikipedia article \" Gastrointestinal cancer \" describes the specific malignant conditions of the gastrointestinal tract. In general, a significant factor in the etiology of gastrointestinal cancers appears to be excessive exposure of the digestive organs to  bile acids . [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1540", "text": "Hemorrhoids  (or  haemorrhoids ), also known as  piles , are  vascular  structures in the  anal canal . [ 7 ] [ 8 ]  In their normal state, they are cushions that help with  stool  control. [ 2 ]  They become a disease when  swollen  or  inflamed ; the unqualified term  hemorrhoid  is often used to refer to the disease. [ 8 ]  The signs and symptoms of hemorrhoids depend on the type present. [ 4 ]  Internal hemorrhoids often result in painless, bright red  rectal bleeding  when  defecating . [ 3 ] [ 4 ]  External hemorrhoids often result in pain and swelling in the area of the  anus . [ 4 ]  If bleeding occurs, it is usually darker. [ 4 ]  Symptoms frequently get better after a few days. [ 3 ]  A  skin tag  may remain after the healing of an external hemorrhoid. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1541", "text": "While the exact cause of hemorrhoids remains unknown, a number of factors that increase pressure in the abdomen are believed to be involved. [ 4 ]  This may include  constipation ,  diarrhea , and sitting on the  toilet  for long periods. [ 3 ]  Hemorrhoids are also more common during  pregnancy . [ 3 ]  Diagnosis is made by looking at the area. [ 3 ]  Many people incorrectly refer to any symptom occurring around the anal area as hemorrhoids, and serious causes of the symptoms should not be ruled out. [ 2 ]   Colonoscopy  or  sigmoidoscopy  is reasonable to confirm the diagnosis and rule out more serious causes. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1542", "text": "Often, no specific treatment is needed. [ 9 ]  Initial measures consist of increasing  fiber  intake, drinking fluids to maintain hydration,  NSAIDs  to help with pain, and rest. [ 1 ]  Medicated creams may be applied to the area, but their effectiveness is poorly supported by evidence. [ 9 ]  A number of minor procedures may be performed if symptoms are severe or do not improve with conservative management. [ 6 ]   Hemorrhoidal artery embolization (HAE)  is a safe and effective  minimally invasive procedure  that can be performed and is typically better tolerated than traditional therapies. [ 10 ] [ 11 ] [ 12 ]  Surgery is reserved for those who fail to improve following these measures. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1543", "text": "Approximately 50% to 66% of people have problems with hemorrhoids at some point in their lives. [ 1 ] [ 3 ]  Males and females are both affected with about equal frequency. [ 1 ]  Hemorrhoids affect people most often between 45 and 65\u00a0years of age, [ 5 ]  and they are more common among the wealthy, [ 4 ]  although this may reflect differences in healthcare access rather than true prevalence. [ 13 ]  Outcomes are usually good. [ 3 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1544", "text": "The first known mention of the disease is from a 1700 BC Egyptian  papyrus . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1545", "text": "In about 40% of people with pathological hemorrhoids, there are no significant symptoms. [ 4 ]  Internal and external hemorrhoids may present differently; however, many people may have a combination of the two. [ 8 ]  Bleeding enough to cause  anemia  is rare, [ 5 ]  and life-threatening bleeding is even more uncommon. [ 15 ]  Many people feel embarrassed when facing the problem [ 5 ]  and often seek medical care only when the case is advanced. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1546", "text": "If not  thrombosed ,  external hemorrhoids  may cause few problems. [ 16 ]  However, when thrombosed, hemorrhoids may be very painful. [ 1 ] [ 8 ]  Nevertheless, this pain typically resolves in two to three days. [ 5 ]  The swelling may, however, take a few weeks to disappear. [ 5 ]  A  skin tag  may remain after healing. [ 8 ]  If hemorrhoids are large and cause issues with hygiene, they may produce irritation of the surrounding skin, and thus itchiness around the anus. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1547", "text": "Internal hemorrhoids usually present with painless, bright red  rectal bleeding  during or following a bowel movement. [ 8 ]  The blood typically covers the stool (a condition known as  hematochezia ), is on the toilet paper, or drips into the toilet bowl. [ 8 ]  The stool itself is usually normally coloured. [ 8 ]  Other symptoms may include mucous discharge, a perianal mass if they  prolapse  through the anus,  itchiness , and  fecal incontinence . [ 15 ] [ 17 ]  Internal hemorrhoids are usually painful only if they become thrombosed or  necrotic . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1548", "text": "The exact cause of symptomatic hemorrhoids is unknown. [ 18 ]  A number of factors are believed to play a role, including irregular bowel habits ( constipation  or  diarrhea ), lack of exercise, nutritional factors (low-fiber diets), increased intra-abdominal pressure (prolonged straining,  ascites , an intra-abdominal mass, or  pregnancy ), genetics, an absence of valves within the hemorrhoidal veins, and aging. [ 1 ] [ 5 ]  Other factors believed to increase risk include  obesity , prolonged sitting, [ 8 ] [ dubious  \u2013  discuss ]  a  chronic   cough , and  pelvic floor dysfunction . [ 2 ]  Squatting while defecating may also increase the risk of severe hemorrhoids. [ 19 ]  Evidence for these associations, however, is poor. [ 2 ]  Being a receptive partner in  anal intercourse  has been listed as a cause. [ 20 ] [ 21 ] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1549", "text": "During pregnancy, pressure from the  fetus  on the abdomen and hormonal changes cause the hemorrhoidal vessels to enlarge. The birth of the baby also leads to increased intra-abdominal pressures. [ 23 ]  Pregnant women rarely need surgical treatment, as symptoms usually resolve after delivery. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1550", "text": "Hemorrhoid cushions are a part of normal human anatomy and become a pathological disease only when they experience abnormal changes. [ 8 ]  There are three main cushions present in the normal  anal canal . [ 1 ]  These are located classically at left lateral, right anterior, and right posterior positions. [ 5 ]  They are composed of neither  arteries  nor  veins , but blood vessels called  sinusoids ,  connective tissue , and  smooth muscle . [ 2 ] :\u200a175\u200a  Sinusoids do not have  muscle tissue  in their walls, as veins do. [ 8 ]  This set of blood vessels is known as the  hemorrhoidal plexus . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1551", "text": "Hemorrhoid cushions are important for  continence . They contribute to 15\u201320% of anal closure pressure at rest and protect the  internal  and  external anal sphincter  muscles during the passage of stool. [ 8 ]  When a person bears down, the intra-abdominal pressure grows, and hemorrhoid cushions increase in size, helping maintain anal closure. [ 5 ]  Hemorrhoid symptoms are believed to result when these vascular structures slide downwards or when venous pressure is excessively increased. [ 15 ]  Increased  internal  and  external anal sphincter  pressure may also be involved in hemorrhoid symptoms. [ 5 ]  Two types of hemorrhoids occur: internals from the  superior hemorrhoidal plexus  and externals from the inferior hemorrhoidal plexus. [ 5 ]  The  pectinate line  divides the two regions. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1552", "text": "Hemorrhoids are typically diagnosed by physical examination. [ 6 ]  A visual examination of the anus and surrounding area may diagnose external or prolapsed hemorrhoids. [ 8 ]  Visual confirmation of internal hemorrhoids, on the other hand, may require  anoscopy , insertion of a hollow tube device with a light attached at one end. [ 5 ]  A  digital rectal exam  (DRE) can also be performed to detect possible rectal  tumors ,  polyps , an enlarged  prostate , or  abscesses . [ 8 ]  This examination may not be possible without appropriate  sedation  because of pain, although most internal hemorrhoids are not associated with pain. [ 1 ]  If pain is present, the condition is more likely to be an  anal fissure  or external hemorrhoid rather than internal hemorrhoid. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1553", "text": "Internal hemorrhoids originate above the pectinate line. [ 16 ]  They are covered by  columnar epithelium , which lacks pain  receptors . [ 2 ]  They were classified in 1985 into four grades based on the degree of  prolapse : [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1554", "text": "External hemorrhoids  occur below the dentate (or pectinate) line. [ 16 ]  They are covered proximally by  anoderm  and distally by skin, both of which are sensitive to pain and temperature. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1555", "text": "Many anorectal problems, including  fissures ,  fistulae , abscesses,  colorectal cancer ,  rectal varices , and  itching  have similar symptoms and may be incorrectly referred to as hemorrhoids. [ 1 ]   Rectal bleeding  may also occur owing to colorectal cancer,  colitis  including  inflammatory bowel disease ,  diverticular disease , and  angiodysplasia . [ 6 ]  If  anemia  is present, other potential causes should be considered. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1556", "text": "Other conditions that produce an anal mass include  skin tags ,  anal warts ,  rectal prolapse ,  polyps , and enlarged anal papillae. [ 5 ]   Anorectal varices  due to  portal hypertension  (blood pressure in the  portal venous system ) may present similar to hemorrhoids but are a different condition. [ 5 ]  Portal hypertension does not increase the risk of hemorrhoids. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1557", "text": "A number of preventative measures are recommended, including avoiding straining while attempting to defecate, avoiding constipation and diarrhea either by eating a high-fiber diet and drinking plenty of fluid or by taking fiber supplements and getting sufficient exercise. [ 5 ] [ 24 ]  Spending less time attempting to  defecate , avoiding reading while on the toilet, [ 1 ]  and losing weight for overweight persons and avoiding heavy lifting are also recommended. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1558", "text": "Conservative treatment typically consists of foods rich in  dietary fiber , intake of oral fluids to maintain hydration,  nonsteroidal anti-inflammatory drugs ,  sitz baths , and rest. [ 1 ]  Increased fiber intake has been shown to improve outcomes [ 26 ]  and may be achieved by dietary alterations or the consumption of  fiber supplements . [ 1 ] [ 26 ]  Evidence for benefits from sitz baths during any point in treatment, however, is lacking. [ 27 ]  If they are used, they should be limited to 15 minutes at a time. [ 2 ] :\u200a182\u200a  Decreasing time spent on the toilet and not straining is also recommended. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1559", "text": "While many  topical agents  and  suppositories  are available for the treatment of hemorrhoids, little evidence supports their use. [ 1 ]  As such, they are not recommended by the  American Society of Colon and Rectal Surgeons . [ 29 ]   Steroid -containing agents should not be used for more than 14 days, as they may cause thinning of the skin. [ 1 ]  Most agents include a combination of active ingredients. [ 2 ]  These may include a barrier cream such as  petroleum jelly  or  zinc oxide , an analgesic agent such as  lidocaine , and a  vasoconstrictor  such as  epinephrine . [ 2 ]  Some contain  Balsam of Peru  to which certain people may be allergic. [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1560", "text": "Flavonoids  are of questionable benefit, with potential side effects. [ 2 ] [ 32 ]  Symptoms usually resolve following pregnancy; thus active treatment is often delayed until after delivery. [ 33 ]  Evidence does not support the use of  traditional Chinese herbal treatment . [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1561", "text": "The use of  phlebotonics  has been investigated in the treatment of low-grade hemorrhoids, [ 29 ] [ 35 ] [ 36 ] [ 37 ]  although these drugs are not approved for such use in the United States or Germany. [ 38 ] [ 39 ]  The use of phlebotonics for the treatment of chronic venous diseases is restricted in Spain. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1562", "text": "A number of office-based procedures may be performed. While generally safe, rare serious side effects such as  perianal sepsis  may occur. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1563", "text": "Hemorrhoidal artery embolization (HAE)  is an additional minimally invasive procedure performed by an  interventional radiologist . [ 10 ]  HAE involves the blockage of abnormal blood flow to the rectal (hemorrhoidal) arteries using microcoils and/or  microparticles  to decrease the size of the hemorrhoids and improve hemorrhoid related symptoms, especially bleeding. [ 11 ]  HAE is very effective at stopping bleeding related symptom with success rate of approximately 90%. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1564", "text": "A number of surgical techniques may be used if conservative management and simple procedures fail. [ 6 ]  All surgical treatments are associated with some degree of complications, including bleeding, infection,  anal strictures , and  urinary retention , due to the close proximity of the rectum to the nerves that supply the bladder. [ 1 ]  Also, a small risk of  fecal incontinence  occurs, particularly of liquid, [ 2 ] [ 42 ]  with rates reported between 0% and 28%. [ 43 ]  Mucosal  ectropion  is another condition which may occur after hemorrhoidectomy (often together with anal stenosis). [ 44 ]  This is where the anal mucosa becomes everted from the anus, similar to a very mild form of  rectal prolapse . [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1565", "text": "It is difficult to determine how common hemorrhoids are as many people with the condition do not see a healthcare provider. [ 15 ] [ 18 ]  However, symptomatic hemorrhoids are thought to affect at least 50% of the US population at some time during their lives, and around 5% of the population is affected at any given time. [ 1 ]  Both sexes experience about the same incidence of the condition, [ 1 ]  with rates peaking between 45 and 65\u00a0years. [ 5 ]  Some studies have found that they are common in people of higher  socioeconomic status , [ 2 ]  however this may reflect differences in healthcare access rather than true prevalence. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1566", "text": "Long-term outcomes are generally good, though some people may have recurrent symptomatic episodes. [ 15 ]  Only a small proportion of persons end up needing surgery. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1567", "text": "The first known mention of this disease is from a 1700 BC Egyptian  papyrus , which advises: \"Thou shouldest give a recipe, an ointment of great protection;  acacia  leaves, ground, titurated and cooked together. Smear a strip of fine linen there-with and place in the anus, that he recovers immediately.\" [ 14 ]  In 460 BC, the  Hippocratic corpus  discusses a treatment similar to modern rubber band ligation: \"And hemorrhoids in like manner you may treat by transfixing them with a needle and tying them with very thick and woolen thread, for application, and do not foment until they drop off, and always leave one behind; and when the patient recovers, let him be put on a course of  Hellebore .\" [ 14 ]  Hemorrhoids may have been described in the  Bible , with earlier English translations using the now-obsolete spelling \" emerods \". [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1568", "text": "Celsus  (25 BC \u2013 14 AD) described ligation and excision procedures and discussed the possible complications. [ 48 ]   Galen  advocated severing the connection of the arteries to veins, claiming it reduced both pain and the spread of gangrene. [ 48 ]  The  Susruta Samhita  (4th\u20135th century BC) is similar to the words of Hippocrates, but emphasizes wound cleanliness. [ 14 ]  In the 13th century, European surgeons such as  Lanfranc of Milan ,  Guy de Chauliac ,  Henri de Mondeville , and John of Ardene made great progress and development of the surgical techniques. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1569", "text": "In medieval times, hemorrhoids were also known as  Saint Fiacre 's curse after a sixth-century saint who developed them following tilling the soil. [ 49 ]  The first use of the word \"hemorrhoid\" in English occurs in 1398, derived from the  Old French  \"emorroides\", from  Latin   h\u00e6morrhoida , [ 50 ]  in turn from the Greek \u03b1\u1f31\u03bc\u03bf\u03c1\u03c1\u03bf\u0390\u03c2 ( haimorrhois ), \"liable to discharge blood\", from \u03b1\u1f37\u03bc\u03b1 ( haima ), \"blood\" [ 51 ]  and \u1fe5\u03cc\u03bf\u03c2 ( rhoos ), \"stream, flow, current\", [ 52 ]  itself from \u1fe5\u03ad\u03c9 ( rheo ), \"to flow, to stream\". [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1570", "text": "Chest pain (angina) or tightness\nShortness of breath, especially during exertion or when lying down\nFatigue or weakness\nIrregular heartbeat or heart palpitations\nDizziness or fainting episodes\nGastrointestinal bleeding symptoms:\nOccult (hidden) or overt (visible) blood in the stool\nBlack, tarry stools (melena)\nBlood in vomit (hematemesis)\nFatigue or weakness due to chronic blood loss"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1571", "text": "Heyde's syndrome  is a syndrome of  gastrointestinal bleeding  from  angiodysplasia  in the presence of  aortic stenosis . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1572", "text": "It is named after Edward C. Heyde, MD, who first noted the association in 1958. [ 3 ]  It is caused by cleavage of  Von Willebrand factor  (vWF) due to high shear stress forces from aortic valvular  stenosis . This results in  Von Willebrand disease type IIA  (acquired). [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1573", "text": "Von Willebrand factor is synthesized in the  walls  of the  blood vessels  and circulates freely in the blood in a folded form. When it encounters damage to the wall of a blood vessel, particularly in situations of high velocity blood flow, it binds to the collagen beneath the damaged endothelium and uncoils into its active form.  Platelets  are attracted to this activated form of von Willebrand factor and they accumulate and block the damaged area, preventing bleeding  [ citation needed ] ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1574", "text": "In people with aortic valve stenosis, the stenotic aortic valve becomes increasingly narrowed resulting in an increase in speed of the blood through the valve in order to maintain  cardiac output . This combination of a narrow opening and a higher flow rate results in an increased  shear stress  on the blood.  This higher stress causes von Willebrand factor to unravel in the same way it would on encountering an injury site. [ 6 ] [ 7 ] [ 8 ]  As part of the normal  hemostasis  of the blood, when von Willebrand factor changes conformation into its active state, it is degraded by its natural  catabolic  enzyme  ADAMTS13 , rendering it incapable of binding the collagen at an injury site. [ 4 ] [ 6 ]   As the quantity of von Willebrand factor in the blood decreases, the rate of bleeding dramatically increases. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1575", "text": "The unraveling of high molecular weight von Willebrand factor in conditions of high shear stress is essential in the prevention of bleeding in the vasculature of the  gastrointestinal system  where small arterioles are common, as platelets cannot bind to damaged blood vessel walls well in such conditions. [ 7 ]  This is particularly true in the presence of  intestinal angiodysplasia , where  arteriovenous malformations  lead to very high blood flow, and so the loss of von Willebrand factor can lead to much more extensive bleeding from these lesions. [ 9 ] [ 10 ]   When people with aortic stenosis also have gastrointestinal bleeding, it is invariably from angiodysplasia. [ 4 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1576", "text": "It has been hypothesized that defects in high molecular weight von Willebrand factor could actually be the cause of the arteriovenus malformations in intestinal angiodysplasia, rather than just making existing angiodysplasic lesions bleed. This hypothesis is complicated by the extremely high rates of intestinal angiodysplasia in older people (who also have the highest rate of aortic stenosis), and thus requires further research for confirmation. [ 4 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1577", "text": "Heyde's syndrome is now known to be gastrointestinal bleeding from angiodysplasic lesions due to acquired vWD-2A deficiency secondary to aortic stenosis, and the diagnosis is made by confirming the presence of those three things. Gastrointestinal bleeding may present as  bloody vomit ,  dark, tarry stool from metabolized blood , or  fresh blood in the stool . In a person presenting with these symptoms,  endoscopy ,  gastroscopy , and/or  colonoscopy  should be performed to confirm the presence of  angiodysplasia . [ 12 ] [ 13 ]  Aortic stenosis can be diagnosed by  auscultation  for characteristic  heart sounds , particularly a  crescendo-decrescendo (i.e., 'ejection')  murmur , followed by  echocardiography  to measure aortic valve area (see  diagnosis of aortic stenosis ). While Heyde's syndrome may exist alone with no other symptoms of aortic stenosis, [ 2 ]  the person could also present with  evidence of  heart failure ,  fainting , or  chest pain . Finally, Heyde's syndrome can be confirmed using blood tests for vWD-2A, although traditional blood tests for von Willebrand factor may result in false negatives due to the subtlety of the abnormality. [ 13 ]  The gold standard for diagnosis is gel electrophoresis; in people with vWD-2A, the large molecular weight von Willebrand factors will be absent from the SDS-agarose electrophoresis plate. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1578", "text": "The definitive treatment for Heyde's syndrome is surgical replacement of the aortic valve. [ 10 ] [ 14 ]  Recently, it has been proposed that  transcatheter aortic valve implantation (TAVI)  can also be used for definitive management. [ 15 ]  Direct surgical treatment of the bleeding (e.g. surgical resection of the bleeding portion of the bowel) is only rarely effective. [ 14 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1579", "text": "Medical management of symptoms is possible also, although by necessity temporary, as definitive surgical management is required to bring levels of von Willebrand factor back to normal. [ 4 ]  In severe bleeding,  blood transfusions  and  IV fluid infusions  can be used to maintain blood pressure. In addition,  desmopressin  (DDAVP) is known to be effective in people with von Willebrand's disease, [ 17 ] [ 18 ]  including people with valvular heart disease. [ 19 ] [ 20 ]  Desmopressin stimulates release of von Willebrand factor from blood vessel endothelial cells by acting on the V2 receptor, which leads to decreased breakdown of  Factor VIII . Desmopressin is thus sometimes used directly to treat mild to moderate acquired von Willebrand's disease and is an effective  prophylactic  agent for the reduction of bleeding during heart valve replacement surgery. [ 19 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1580", "text": "The exact prevalence of the syndrome is unknown, because both aortic stenosis and angiodysplasia are common diseases in the elderly. A retrospective chart review of 3.8 million people in Northern Ireland found that the incidence of gastrointestinal bleeding in people with any diagnosis of aortic stenosis (they did not subgroup people by severity) was just 0.9%. They also found that the reverse correlation\u2014the incidence of aortic stenosis in people with gastrointestinal bleeding\u2014was 1.5%. [ 21 ]   However, in 2003 a study of 50 people with aortic stenosis severe enough to warrant immediate valve replacement found GI bleeding in 21% of people, [ 10 ]  and another study done in the USA looking at angiodysplasia rather than GI bleeding found that the prevalence of aortic stenosis was 31% compared to 14% in the control group. [ 4 ] [ 22 ] \nIt is a disease mainly found in older adults but a rare case of Heyde's syndrome has been reported in children. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1581", "text": "The American internist Edward C. Heyde originally described the syndrome in a 1958 letter to the  New England Journal of Medicine , reporting on ten patients with the association. [ 3 ]  Heyde graduated from Johns Hopkins School of Medicine in 1938, served three years in the Army Medical Corps in World War II and joined the Vancouver Clinic, Vancouver, Washington in 1948, practicing medicine there for 31 years. He died on October 13, 2004. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1582", "text": "In the 45 years following its initial description, no plausible explanations could be found for the association between aortic valve stenosis and gastrointestinal bleeding. Indeed, the association itself was questioned by a number of researchers. [ 5 ] [ 24 ]  Several studies demonstrated a statistically significant association between aortic stenosis and gastrointestinal bleeding, [ 25 ] [ 26 ] [ 27 ]  and in 1987 King et al. even noted the successful resolution of bleeding symptoms with aortic valve replacement in 93% of people, compared to just 5% in people where the bleeding was treated surgically. [ 16 ]  However, the potential causal  association  between the two conditions remained elusive and controversial. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1583", "text": "Several hypotheses for the association were proposed, the most prominent being the idea that there is no causal relationship between aortic stenosis and gastrointestinal bleeding, they are both just common conditions in the elderly, and they sometimes overlap. Other hypotheses included hypoxia of the colonic mucosa and bowel ischemia due to low blood flow, both of which were discounted by later research. [ 4 ] [ 5 ]  Another early hypothesis of note was proposed by Greenstein et al. in 1986. [ 27 ]  They suggested that GI bleeding could be caused by thinning of the wall of the  cecum  due to abnormal pulse waves in the  ileocolic artery  (an  artery  that supplies blood to the cecum) causing dilation of that artery. Specifically, they note that the usual anacrotic and dicrotic notches were absent from the pulse waves of their people with aortic stenosis. There has been no further research investigating this hypothesis, however, as it has been eclipsed by newer research into acquired von Willebrand's disease. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1584", "text": "The important role of depletion of von Willebrand factor in aortic stenosis was first proposed in 1992 by Warkentin et al. [ 7 ]  They noted a known association between aortic stenosis (in addition to other cardiac diseases) and acquired von Willebrand's disease type IIA, [ 20 ]  which is corrected by surgical replacement of the aortic valve. They also noted that von Willebrand's disease is known to cause bleeding from angiodysplasia. Based on these facts, they hypothesized that acquired von Willebrand's disease is the true culprit behind gastrointestinal bleeding in aortic stenosis. They also proposed a possible mechanism for the acquired von Willebrand's disease, noting that von Willebrand factor is most active in 'high shear' vessels (meaning small vessels in which blood flows rapidly). They used this fact to hypothesize that this may mean that von Willebrand factor is activated in the narrowed stenotic aortic valve and thus cleared from circulation at a much higher rate than in healthy individuals. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1585", "text": "This hypothesis received strong support in 2003 by the publication of a report by Vincentelli et al. that demonstrated a strong association between von Willebrand factor defects and the severity of aortic valve stenosis. [ 10 ]  They also showed these defects resolved within hours following  aortic valve replacement surgery  and remained resolved in most people, although in some people the von Willebrand factor defects had returned at six months. Following this observation the shear stress dependent depletion of von Willebrand factor was confirmed, and the protease responsible, ADAMTS13, was identified. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1586", "text": "Lymphocytic esophagitis  is a rare and poorly understood medical disorder involving  inflammation  in the  esophagus . The disease is named from the primary inflammatory process, wherein  lymphocytes  are seen within the esophageal mucosa. Symptoms of the condition include  difficulty swallowing ,  heartburn  and  food bolus obstruction . The condition was first described in 2006 by Rubio and colleagues. Initial reports questioned whether this was a true medical disorder, or whether the inflammation was secondary to another condition, such as  gastroesophageal reflux disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1587", "text": "The cause of lymphocytic esophagitis is unknown. The disease may cause different symptoms and be caused by different processes in childhood as compared to adulthood. Some studies have shown that it is associated with either other medical conditions involving the esophagus, including  gastroesophageal reflux disease  and  achalasia , or other inflammatory conditions such as  Crohn's disease ,  coeliac disease , and  allergic conditions . The diagnosis is based upon a  biopsy  of the  mucosa  of the esophagus, showing a characteristic appearance of inflammation involving  lymphocytes , and the relative absence of another group of inflammatory cells,  granulocytes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1588", "text": "Complications of the disorder include  stricture of the esophagus , which can lead to  food bolus obstruction , and weight loss. Treatment of lymphocytic esophagitis includes medications meant to target the esophagus topically, such as  budesonide , but also procedures to deal with complications, such as  esophageal dilation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1589", "text": "The most common symptom of lymphocytic esophagitis is  dysphagia , or difficulty swallowing, prevalent in 53 to 57% of individuals with the condition [ 1 ] [ 2 ]  due to inflammation, narrowing or altered movement of the esophagus. Other symptoms include  heartburn ,  abdominal pain ,  nausea  and  food bolus obstruction . [ 1 ] [ 2 ]  Some patients may have no symptoms, as was found in a significant percentage of patients in the first description of the condition, [ 3 ]  although more recent reports indicate that the absence of symptoms is uncommon. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1590", "text": "Food bolus impaction  is a common complication of lymphocytic esophagitis. [ 1 ]  This occurs when food is acutely obstructing the esophagus at an area of narrowing and may require an endoscopic procedure in order to remove or dislodge the obstructing food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1591", "text": "The cause of lymphocytic esophagitis is unknown. [ 4 ]  Attempts to better understand the cause of lymphocytic esophagitis include identification of other diseases that associate with the condition. [ 4 ]  These conditions include other esophageal conditions including  gastroesophageal reflux disease [ 1 ] [ 4 ] [ 5 ]  and  achalasia , [ 5 ]  as well as other inflammatory diseases such as  Crohn's disease , [ 4 ] [ 5 ]   coeliac disease , [ 4 ]  and allergic conditions such as  eczema . [ 4 ]  Additionally use of tobacco may associate with lymphocytic esophagitis. [ 1 ] [ 4 ]  Lymphocytic esophagitis does not occur with high frequency in other gastrointestinal conditions where lymphocytosis is found in the  mucosa , including  lymphocytic colitis  and lymphocytic  gastritis ; however, there is a disease association with  coeliac disease  wherein lymphocytic inflammation occurs in the  small bowel  after exposure to  gluten . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1592", "text": "Little is known about the pathophysiology of lymphocytic esophagitis. [ 4 ]  It has been hypothesized that lymphocytic esophagitis may be either a primary inflammatory disorder, or that the inflammation is triggered by an external stimulus leading to injury of the mucosal lining of the esophagus, such as gastric acid in  GERD . [ 4 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1593", "text": "The diagnosis of lymphocytic esophagitis is made by  biopsy  of the  mucosal lining  of the  esophagus . This is typically achieved at the time of  esophagogastroduodenoscopy , a medical procedure wherein an  endoscope  is inserted through the mouth, into the esophagus, in order to visualize and biopsy the mucosa. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1594", "text": "While the  histologic  changes in the biopsies are characterized by the presence of an inflammatory infiltrate, consisting primarily of  lymphocytes  in the absence of other inflammatory cells such as  granulocytes , the criteria for making the diagnosis are still unclear. [ 1 ] [ 4 ]  The location of the biopsies, cutoff of number of  lymphocytes  found in each high-power field of view of the microscope, the presence of  spongiosis , and the need for  immunohistochemical staining  to define lymphocytes are all unclear still. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1595", "text": "While the diagnosis of lymphocytic esophagitis depends on the biopsy results, certain changes can be visualized directly at the time of  endoscopy . The esophagus may be narrow in calibre, [ 5 ]  may show multiple rings, [ 5 ]  redness, [ 5 ]  linear furrows [ 1 ]  or the mucosal lining may slide demonstrating a \"crepe-paper\" appearance. [ 1 ]  Complications such as strictures of the esophagus can also be detected with endoscopy. [ 5 ]  These changes are very similar to those found in  eosinophilic esophagitis , a more common and better understood esophageal disorder thought to be of allergic origin. [ 5 ]   Narrow-band imaging  with  magnification endoscopy  is another imaging modality that can show characteristic changes of lymphocytic esophagitis. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1596", "text": "The treatment of lymphocytic esophagitis is still undefined. [ 5 ]  Treatment either targets symptoms, inflammation or complications. For example,  heartburn  is a symptom in lymphocytic esophagitis, and  proton pump inhibitors , which reduce acidity in the stomach, are consequently used for treatment. With respect to treatment of inflammation, steroids that are topical and coat the lining of the esophagus, such as  budesonide  have been used to treat the condition, in one German study. [ 8 ]   Prednisone  has also been used to treat the inflammation of lymphocytic esopahgitis. [ 5 ]  With respect to complications, strictures of the esophagus can be treated with  esophageal dilation . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1597", "text": "There has been little studied about the natural history of lymphocytic esophagitis. [ 4 ]  The longest study of the condition involved a median follow-up of 3.3 years, wherein participants were surveyed, and demonstrated that 87% of patients were alive but that the vast majority (97%) of patients still had symptoms. [ 4 ] [ 9 ]  There have been two reports of  esophageal perforation  associated with the condition, one case occurring during endoscopic treatment of complications. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1598", "text": "The  percentage of individuals  with lymphocytic esophagitis is uncertain. [ 1 ]  Early studies indicated that the prevalence was 0.1% in adults. [ 3 ]  However, reports in children indicate a higher prevalence of 8.5%, [ 10 ]  perhaps suggestive of incidental findings of lymphocytes in endoscopies performed for other reasons. [ 1 ]  The disease may occur more frequently in women over the age of 60. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1599", "text": "There is increasing awareness of lymphocytic esophagitis among physicians, perhaps affecting the prevalence over time. [ 1 ]  The majority of the studies on lymphocytic esophagitis are after 2015. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1600", "text": "The condition was first described in a series of 20 patients at the  Karolinska Institutet  by Carlos Rubio in 2006. [ 3 ]  Much of the reports of the condition over the subsequent several years were focused on ascertaining whether lymphocytic esophagitis was a true condition, and if it was, establishing uniform criteria for its diagnosis. [ 1 ] [ 2 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1601", "text": "The majority of the research into lymphocytic esophagitis has been performed after 2015. [ 1 ]  There remain many questions unanswered about the condition, such as establishing its natural history, [ 4 ]  clarifying its diagnostic criteria, [ 1 ]  and ascertaining the best treatment for the condition. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1602", "text": "The  National Digestive Diseases Information Clearinghouse  (NDDIC [ 1 ] ) is an information dissemination service of the  National Institute of Diabetes and Digestive and Kidney Diseases  (NIDDK). The NIDDK is part of the  National Institutes of Health , which is under the  U.S. Department of Health and Human Services ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1603", "text": "Established in 1980, the Clearinghouse provides information about digestive diseases to people with digestive disorders and to their families, health care professionals, and the public. The NDDIC answers inquiries, develops and distributes publications, and works closely with professional and patient organizations and Government agencies to coordinate resources about digestive diseases."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1604", "text": "Publications produced by the Clearinghouse are carefully reviewed by both NIDDK scientists and outside experts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1605", "text": "This article about a United States health organization is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1606", "text": "A  rectus sheath hematoma  is an accumulation of blood in the sheath of the  rectus abdominis muscle . It causes  abdominal pain  with or without a mass."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1607", "text": "The  hematoma  may be caused by either rupture of the  epigastric artery  or by a muscular tear. Several factors have been identified as predisposing risks for rectus sheath hematoma, including coughing, straining, exercise,  hypertension ,  obesity , previous  abdominal surgery ,  subcutaneous injection ,  trauma  and  anticoagulant therapy . With an ageing population and the widespread use of anticoagulant medications, there is evidence that this historically benign condition is becoming more common and more serious. [ 1 ]  Anticoagulant therapy is used to treat many diseases. However, in the COVID-19 pandemic, anticoagulant therapy was frequently used and therefore the incidence of rectus sheath hematoma increased. [ 2 ] [ 3 ]  Given that thrombotic events have been documented in numerous studies, it is advisable to initiate prophylactic and anticoagulant treatment during the early phase of COVID-19 disease.  [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1608", "text": "On  abdominal examination , people may have a  positive   Carnett's sign ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1609", "text": "Most hematomas resolve without treatment, but they may take several months to resolve."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1610", "text": "Reynolds syndrome  is a rare secondary  laminopathy , consisting of the combination of  primary biliary cirrhosis  and  progressive systemic sclerosis .  In some patients this syndrome has also been associated with  Sj\u00f6gren's syndrome  and  hemolytic anemia .  Typical clinical features include  jaundice , elevated blood levels of  alkaline phosphatase ,  calcinosis cutis ,  telangiectasias , and  pruritus . This disease may cause white or yellow-ish spots on the arms or legs. The syndrome, a special case of scleroderma, is named after the American physician, Telfer B. Reynolds, MD (1921\u20132004), who first described it.  He is also known for creating one of the world's first  hepatology  programs at the  University of Southern California ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1611", "text": "It should not be confused with the more common  Raynaud's phenomenon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1612", "text": "This  genetic disorder  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1613", "text": "Roemheld syndrome  ( RS ), or  gastrocardiac syndrome , [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ]  or  gastric cardiac syndrome [ 6 ]  or  Roemheld\u2013Techlenburg\u2013Ceconi syndrome [ 7 ]  or  gastric-cardia , [ 7 ]  was a medical syndrome first coined by  Ludwig von Roemheld  (1871\u20131938) describing a cluster of cardiovascular symptoms stimulated by gastrointestinal changes. Although it is currently considered an obsolete medical diagnosis, recent studies have described similar clinical presentations and highlighted potential underlying mechanisms. [ 3 ] [ 8 ] [ 9 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1614", "text": "Symptoms can be as follows. [ 10 ] [ 11 ]  They are periodic, and occur only during an \"episode\", usually after eating."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1615", "text": "Mechanically induced Roemheld syndrome is characterized by  pressure  in the epigastric and left  hypochondriac  region. Often the pressure is in the  fundus  of the stomach, the  esophagus  or distention of the bowel. It is believed this leads to elevation of the  diaphragm , and secondary displacement of the heart. This reduces the ability of the heart to fill and increases the  contractility of the heart  to maintain homeostasis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1616", "text": "The cranium dysfunction mechanical changes in the gut can compress the  vagus nerve  at any number of locations along the vagus, slowing the heart. As the heart slows, autonomic reflexes are triggered to increase blood pressure and heart rate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1617", "text": "This is complemented by gastro-coronary reflexes [ 12 ]  whereby the coronary arteries constrict with \"functional  cardiovascular  symptoms\" similar to chest-pain on the left side and radiation to the left shoulder, dyspnea, sweating, up to angina pectoris-like attacks with  extrasystoles , drop of blood pressure, and tachycardia (high heart rate) or sinus bradycardia (heart rate below 60 bpm). Typically, there are no changes/abnormalities related in the  EKG  detected. This can actually trigger a heart attack in people with cardiac structural abnormalities i.e.  coronary bridge , missing coronary, and  atherosclerosis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1618", "text": "If the heart rate drops too low for too long,  catecholamines  are released to counteract any lowering of blood pressure. Catecholamines bind to  alpha receptors  and  beta receptors , decreasing  vasodilation  and increasing  contractility of the heart . Sustaining this state causes  heart fatigue  which can lead to a decline in systolic and  diastolic function , resulting in fatigue and chest pain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1619", "text": "There is significant scope of misdiagnosis of Roemheld syndrome. Diagnosis of Roemheld syndrome usually begins with a cardiac workup, as the gastric symptoms may go unnoticed, and the cardiac symptoms are frightening and can be quite severe. After an  EKG ,  Holter monitor ,  tilt table test ,  cardiac MRI ,  cardiac CT ,  heart catheterization ,  electrophysiology study ,  echocardiogram , and extensive blood work, and possibly a  sleep study , a cardiologist may rule out a heart condition."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1620", "text": "Often a  psychiatric evaluation  may follow, as conversion disorder may be suspected in the absence of heart disease or structural heart abnormalities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1621", "text": "In the absence of heart abnormalities, the diagnosis is often made on the basis of symptoms. A  gastroenterologist  will perform a  colonoscopy ,  endoscopy , and  abdominal ultrasound  to locate or rule out problems in the abdomen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1622", "text": "Determining the cause of Roemheld syndrome is still not an exact science. If you have an ultrasound or sleep study, ensure that you know how to reproduce the symptoms, as it is difficult to detect any abnormalities when symptoms have subsided."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1623", "text": "Treatment of the primary gastroenterological distress is the first concern, mitigation of gastric symptoms will also alleviate cardiac distress."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1624", "text": "Roemheld syndrome is characterized strictly by abdominal maladies triggering reflexes in the heart. There are a number of pathways through which cardiac reflexes can occur: hormones, mechanical, neurological and immunological. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1625", "text": "Ludwig Roemheld characterized this particular syndrome shortly before his death; one of his research topics around this time was the effects of calorie intake on the heart. In  Elsevier  publications, there is no current research or publishing under the name Roemheld syndrome, and as a result, many cases go undiagnosed. German publishing on the subject remains untranslated as of 2009."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1626", "text": "Saint's triad  is a medical condition of concurrence of the following:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1627", "text": "Saint's triad is named after the British surgeon Hunterian and Emeritus Professor Charles Frederick Morris Saint CBE (14 August 1886 \u2013 15 February 1973), who established the first school of surgery in South Africa. He emphasised  the importance of considering the possibility of multiple separate diseases in a patient whenever his or her history and the results of the physical examination were atypical of any single condition. [ 2 ]  Traditionally, there is thought to be no pathophysiological basis for the coexistence of these three diseases. Saint emphasized that more than one disease may be responsible for a patient's clinical signs and symptoms, and his  triad  provides a counterexample to the commonly used diagnostic principle that \"the explanation of any phenomenon should make as few assumptions as possible,\" also known as  Occam's Razor . [ 3 ]  The principle underlying Saint's triad is also expressed as  Hickam's dictum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1628", "text": "A twist to this philosophic discussion on the art of diagnosis is that, in recent times, the possibility of an underlying pathophysiology has been considered\u2014obesity is associated with  gallstones ,  hiatal hernia , and  diverticular disease , and there is the suggestion of an underlying  connective tissue  defect such as a \"herniosis.\" [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1629", "text": "Gastroenterology  (from the Greek gast\u1e17r- \"belly\", -\u00e9nteron \"intestine\", and -log\u00eda \"study of\") is the branch of  medicine  focused on the  digestive system  and its disorders. [ 1 ]  The digestive system consists of the  gastrointestinal tract , sometimes referred to as the  GI tract,  which includes the  esophagus ,  stomach ,  small intestine  and  large intestine  as well as the accessory organs of digestion which include the  pancreas ,  gallbladder , and  liver . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1630", "text": "The digestive system functions to move material through the GI tract via  peristalsis , break down that material via  digestion , absorb nutrients for use throughout the body, and remove waste from the body via  defecation . [ 3 ]  Physicians who specialize in the medical specialty of gastroenterology are called gastroenterologists or sometimes  GI doctors ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1631", "text": "Some of the most common conditions managed by gastroenterologists include  gastroesophageal reflux disease ,  gastrointestinal bleeding ,  irritable bowel syndrome , inflammatory bowel disease (IBD) which includes  Crohn's disease  and  ulcerative colitis ,  peptic ulcer disease , gallbladder and biliary tract disease,  hepatitis ,  pancreatitis ,  colitis ,  colon polyps and cancer , nutritional problems, and many more. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1632", "text": "Citing from  Egyptian   papyri ,  John F. Nunn  identified significant knowledge of gastrointestinal diseases among practicing physicians during the periods of the  pharaohs .  Irynakhty , of the tenth dynasty,  c.  2125 B.C., was a  court physician  specializing in gastroenterology, sleeping, and  proctology . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1633", "text": "Among  ancient Greeks ,  Hippocrates  attributed  digestion  to  concoction .  Galen 's concept of the  stomach  having four  faculties  was widely accepted up to modernity in the seventeenth century. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1634", "text": "1.  International Classification of Disease ( ICD  2007)/WHO classification :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1635", "text": "2.  MeSH  subject Heading :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1636", "text": "3.  National Library of Medicine  Catalogue (NLM classification 2006) :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1637", "text": "A procedure using a  long thin tube with a camera  that is passed through the  anus  to visualize the  rectum  and the entire length of the colon. The procedure is performed either to look for  colon polyps  and/or  colon cancer  in somebody without symptoms, referred to as  screening , or to further evaluate symptoms including  rectal bleeding ,  dark tarry stools , change in bowel habits or stool consistency (diarrhea, pencil-thin stool), abdominal pain, and unexplained weight loss. Before the procedure, the physician might ask the patient to stop taking certain medications including blood thinners, aspirin, diabetes medications, or  nonsteroidal anti-inflammatory drugs . A  bowel prep  is usually taken the night before and into the morning of the procedure which consists of an  enema  or  laxatives , either pills or powder dissolved in liquid, that will cause diarrhea. The procedure might need to be stopped and rescheduled if there is stool remaining in the colon due to an incomplete bowel prep because the physician can not adequately visualize the colon. During the procedure, the patient is  sedated  and the scope is used to examine the entire length of the colon looking for polyps, bleeding, or abnormal tissue. A  biopsy  or  polyp removal  can then be performed and the tissue sent to the lab for evaluation. The procedure usually takes thirty minutes to an hour followed by a one to two hour observation period. Complications include bloating, cramping, a reaction to anesthesia, bleeding, and a  hole through the wall  of the colon that may require repeat colonoscopy or surgery. Signs of a serious complication requiring urgent or emergent medical attention include severe pain in the abdomen, fever, bleeding that does not improve, dizziness, and weakness. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1638", "text": "A procedure similar to a colonoscopy using a long thin tube with a camera (scope) passed through the  anus  but only intended to visualize the  rectum  and the  last part of the colon  closest to the rectum. All aspects of the procedure are the same as for a colonoscopy with the exception that this procedure only lasts ten to twenty minutes and is done without sedation. This usually allows for the patient to return to normal activities immediately after the procedure is finished. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1639", "text": "A procedure using a  long thin tube with a camera  that is passed through the mouth to view the  esophagus  (\"esophago-\"),  stomach  (\"gastro-\"), and the  duodenum  (\"duodeno-\"). It is also referred to as upper endoscopy or just endoscopy. The procedure is performed for further evaluation of symptoms including persistent  heartburn ,  indigestion ,  vomiting blood ,  dark tarry stools , persistent nausea and vomiting, pain,  difficulty swallowing ,  painful swallowing , and unexplained weight loss. It is also performed for further testing following a lab test that shows  low hemoglobin levels  without a known cause or an abnormal  barium swallow . The procedure can be used to diagnose many disorders through direct visualization or tissue biopsy including  esophageal varices ,  esophageal strictures ,  gastroesophageal reflux disease ,  Barrett's esophagus , cancer,  celiac disease ,  gastritis ,  peptic ulcer disease , and a  H. pylori  infection. Intra-operative techniques can then be used for treatment of certain disorders like  banding  esophageal varices or  dilating  esophageal strictures. The patient will likely be required to not eat or drink anything starting 4 hours prior to the procedure. Sedation is usually required for patient comfort. This procedure usually lasts around thirty minutes followed by a one to two hour observation period. Side effects include  bloating , nausea, and a sore throat for 1 to 2 days. Complications are rare but include reaction to the anesthesia, bleeding, and a  hole through the wall  of the esophagus, stomach, or small intestine which could require surgery. Signs of a serious complication requiring urgent or emergent medical attention include chest pain, problems breathing, problems swallowing, throat pain that gets worse, vomiting with blood or the appearance of \" coffee-grounds \", worsening abdominal pain,  bloody  or black tarry stool, and fever. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1640", "text": "A procedure using a  long thin tube with a camera  passed through the mouth into the  first part of the small intestine  to locate, diagnose, and treat disorders related to the  bile  and  pancreatic ducts . These ducts carry fluids that help with digesting food from the liver, gallbladder, and pancreas and can become narrowed or blocked as a result of  gallstones , infection, inflammation,  pancreatic pseudocysts , and tumors of the bile ducts or pancreas. As a result, one may experience back pain,  yellowing of the skin , and an abnormal lab test showing an elevated  bilirubin  level which could necessitate this procedure. However, the procedure is not recommended if the patient has  acute pancreatitis  unless the level of bilirubin remains high or is increasing which could suggest the blockage is still present. The patient will likely be required to not eat or drink anything starting 8 hours prior to the procedure. After the patient is sedated, the physician will pass the scope through the mouth, esophagus, stomach, and into the duodenum to locate the  opening  where the ducts  drain into the small intestine . The physician can then inject dye into these ducts and take X-rays which show a real time view, via  fluoroscopy , allowing the physician to locate and relieve the blockage. This is done through multiple techniques including  cutting the opening  and creating a bigger hole for drainage, removing gallstones and other debris, dilating narrow parts of the ducts, or placing a stent which keeps the ducts open. The physician can also take a  biopsy  of the ducts to evaluate for cancer, infection, or inflammation. Side effects include bloating, nausea, or a sore throat for one to two days. Complications include  pancreatitis , infection of the  bile ducts  or  gallbladder , bleeding, reaction to the anesthesia, and perforation of any structures that the scope or its instruments pass but particularly the duodenum, bile duct, and pancreatic duct. Signs of a serious complication requiring urgent or emergent medical attention include bloody or  black tarry stool , chest pain, fever, worsening abdominal pain, worsening throat pain, problems breathing, problems swallowing, vomit that is bloody or looks like  coffee-grounds . Most of the time complications from this procedure require hospitalization for treatment. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1641", "text": "A condition that is a result of stomach contents consistently coming back up into the esophagus causing troublesome symptoms or complications. [ 19 ]  Symptoms are considered troublesome based on how disruptive they are to a patient's daily life and well-being. This definition was standardized by the Montreal Consensus in 2006. [ 20 ]  Symptoms include a  painful feeling  in the middle of the chest and feeling stomach contents  coming back up  into the mouth. Other symptoms include chest pain, nausea,  difficulty swallowing ,  painful swallowing , coughing, and hoarseness. [ 21 ]  Risk factors include obesity, pregnancy, smoking,  hiatal hernia , certain medications, and certain foods. Diagnosis is usually based on symptoms and medical history, with further testing only after treatment has been ineffective. Further diagnosis can be achieved by  measuring  how much acid enters the esophagus or looking into the esophagus with a  scope . Treatment and management options [ 19 ]  include lifestyle modifications, medications, and surgery if there is no improvement with other interventions. Lifestyle modifications include not lying down for three hours after eating, lying down on the left side, elevating head while laying by elevating head of the bed or using extra pillows, losing weight, stopping smoking, and avoiding coffee, mint, alcohol, chocolate, fatty foods, acidic foods, and spicy foods. Medications include  antacids ,  proton pump inhibitors ,  H2 receptor blockers . Surgery is usually a  Nissen fundoplication  and is performed by a surgeon. Complications of longstanding GERD can include  inflammation of the esophagus  that may cause bleeding or ulcer formation,  narrowing of the esophagus  leading to swallowing issues, a change in the lining of the esophagus that can increase the chances of developing cancer ( Barrett's esophagus ), chronic cough, asthma,  inflammation of the larynx  leading to hoarseness, and  wearing away  of tooth enamel leading to dental issues. [ 19 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1642", "text": "A condition in which the lining of the esophagus changes to look more like the lining of the intestine and increases the risk of developing  esophageal cancer . [ 22 ]  There are no specific symptoms although symptoms of GERD may be present for years prior as it is associated with a 10\u201315% risk of Barrett's esophagus. [ 22 ]  Risk factors include chronic GERD for more than 5 years, being age 50 or older, being non-Hispanic white, being male, having a family history of this disorder,  belly fat , and a history of smoking. [ 23 ]  Protective factors include  H. pylori infection , frequent use of aspirin or other  non-steroidal anti-inflammatory drugs , and diets high in fruits and vegetables. [ 24 ]  Diagnosis can be made by looking into the esophagus with a  scope  and possibly taking a  biopsy  of the lining of the esophagus. Treatment includes managing GERD,  destroying  abnormal parts of the esophagus,  removing abnormal tissue  in the esophagus, and  removing part of the esophagus  as performed by a general surgeon. [ 22 ]  Further management could include periodic surveillance with repeat scopes at certain intervals determined by the physician, likely not more frequently than every three to five years. [ 23 ]  Complications from this disorder can result in a type of cancer called  esophageal adenocarcinoma . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1643", "text": "Gastroenterology is a subspecialty of internal medicine and therefore requires three years of  internal medicine   residency training  followed by three additional years in a dedicated gastroenterology  fellowship . [ 1 ]  This training is certified by the  American Board of Internal Medicine  (ABIM) and the  American Osteopathic Board of Internal Medicine  (AOBIM) and must be completed at a program accredited by the  Accreditation Council for Graduate Medical Education  (ACGME). [ 25 ] [ 26 ] [ 27 ]  Other national societies that oversee training include the  American College of Gastroenterology  (ACG), the  American Gastroenterological Association  (AGA), and the  American Society for Gastrointestinal Endoscopy  (ASGE). [ 28 ] [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1644", "text": "Gastroenterologists see patients both in the clinic and the hospital setting. They can order diagnostic tests, prescribe medications, and perform a number of diagnostic and  therapeutic  procedures including  colonoscopy ,  esophagogastroduodenoscopy  (EGD),  endoscopic retrograde cholangiopancreatography  (ERCP),  endoscopic ultrasound  (EUS), and  liver biopsy . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1645", "text": "Some gastroenterology trainees will complete a \"fourth-year\" (although this is often their seventh year of graduate medical education) in transplant  hepatology , advanced interventional  endoscopy ,  inflammatory bowel disease ,  motility , or other topics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1646", "text": "Advanced endoscopy, sometimes called interventional or surgical endoscopy, is a sub-specialty of gastroenterology that focuses on advanced endoscopic techniques for the treatment of  pancreatic ,  hepatobiliary , and  gastrointestinal disease . Interventional gastroenterologists typically undergo an additional year of rigorous training in advanced endoscopic techniques including endoscopic retrograde cholangiopancreatography, endoscopic ultrasound-guided diagnostic and interventional procedures, and advanced  resection  techniques including  endoscopic mucosal resection  and  endoscopic submucosal dissection . Additionally, the performance of endoscopic bariatric procedures is also performed by some advanced endoscopists."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1647", "text": "Hepatology , or  hepatobiliary medicine , encompasses the study of the  liver ,  pancreas , and  biliary tree , and is traditionally considered a sub-specialty of gastroenterology, while  proctology  encompasses disorders of the  anus ,  rectum , and  colon  and is considered a sub-specialty of  general surgery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1648", "text": "This is a list of  allergies , which includes the  allergen , potential reactions, and a brief description of the cause where applicable."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1649", "text": "Many substances can cause an allergic reaction when in contact with the human  integumentary system ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1650", "text": "An  anal plug  ( anal tampon  or  anal insert ) is a  medical device  that is often used to treat  fecal incontinence , the accidental passing of bowel moments, by physically blocking involuntary loss of  fecal material . [ 1 ]  Fecal material such as feces are solid remains of food that does not get digested in the small intestines; rather, it is broken down by bacteria in the large intestine. Anal plugs vary in design and composition, but they are typically single-use, intra-anal, disposable devices made out of soft materials to contain fecal material and prevent it from leaking out of the rectum. The idea of an anal insert for fecal incontinence was first evaluated in a study of 10 participants with three different designs of anal inserts. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1651", "text": "Anal plugs may be beneficial to certain risk groups including, but not limited to, frail older people, women following childbirth, people with some neurological or spinal diseases, severe cognitive impairment, urinary incontinence, pelvic organ prolapse, and so on. Typically, anal plugs are used in people whose symptoms do not improve with to typical treatments: this may include changes in diet, physical therapy,  nerve stimulation  targeting the  sacral  and  tibial  nerves, surgical repair of the anus, and utilization of a  colostomy bag . [ 2 ]  Nerve stimulation involves the placement of electrodes near the nerves that travel through a person's hips and down their legs. [ 3 ]  Colostomy bags are bags that collect feces from their intestines through a surgically created hole in a person's belly. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1652", "text": "Children with certain conditions, including  spina bifida  and  anal atresia , may struggle with leaks even after physical therapy and other interventions, so they may benefit from using anal plugs. [ 5 ] [ 6 ]  Spina bifida is a birth defect where a part of the spinal cord is not surrounded by the  vertebrae ; either the spinal cord is still in the back, just not surrounded by the vertebral bones, or it can be bulging out in a sac. [ 7 ]  Anal atresia is another birth defect where the rectum and/or anus is deformed: fecal incontinence is a side effect. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1653", "text": "The one common feature of people who use anal plugs is they all experience fecal incontinence, which is both uncomfortable and embarrassing. Some people may use it temporarily during certain events or while they have certain temporary medical conditions, such as women recovering from childbirth; others may need to use anal plugs for the rest of their lives. Others may opt to also use perineal pads or undergarments such as  diapers  to prevent the soiling of oneself. Management of fecal incontinence is very person-dependent, as anally inserted devices may not be for everyone."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1654", "text": "The plug allows individuals control over their bowel movements and may decrease negative side effects due to leakage. People have reported suffering from fewer of anal rashes, decreased soreness, and improved hygiene. [ 2 ]  Anal plugs can also be an affordable option: some countries with universal healthcare, like Germany, buy anal plugs for people who need them. [ 9 ]  During the development and approval of the Renew Insert, which is one of the types of anal plugs that have been developed, researchers found that on average people used 2.6 inserts per day. [ 2 ]  However, this plug is designed to be worn for twelve-hours; the number of inserts needed per day increases when products that have to be changed four times a day are considered. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1655", "text": "Whether anal plugs are a good choice varies based on the person. Trials have shown anywhere from 25 to 80% of people were satisfied enough with plug to continue using it. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1656", "text": "People who have to pay for anal plugs out of pocket may find them to be expensive. Although some countries, such as Germany, may subsidize the cost for people, private insurance may not cover anal plugs. [ 9 ]  Plugs have to be changed a minimum of twice a day, some up to four times per day."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1657", "text": "At the same time, discomfort, side effects, and occasional leaks from using anal plugs have been reported. [ 2 ]  A 2015  systematic review  found that anal plugs may be helpful in treating fecal incontinence, provided that they are tolerated and that people actually use them. [ 11 ] [ 12 ]  A 2001 study found that a majority of people could not tolerate an anal plug due to discomfort. Although only 20% decided to continue using the plug on a regular basis, anal plugs were generally successful at controlling fecal incontinence. Since anal plugs are considered an invasive strategy, they can result in pain, soreness, irritation, fecal urgency, and societal embarrassment. [ 2 ]  Bleeding  hemorrhoids  were a rare  adverse event . [ 13 ]  There is not a lot of evidence reported on the efficacy on the different types of anal plugs, so the choice of plug can be up to people and their doctors. [ 2 ]  Some other challenges of the plug include occasional slippage with decreases the efficacy and increases discomfort, but people report more usage for occasions where anal leakage would be publicly troublesome. [ 2 ] [ 13 ]  Anal plugs of smaller volume may resolve some people's discomfort, but still provide coverage for leakage. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1658", "text": "Due to the complexity of fecal incontinence, the use of anal plugs are not well defined in guidelines and treatment pathways, which decrease the comfortability of medical professional on prescribing and usage of anal plugs. [ 2 ]  Therefore, more studies are needed in order for healthcare providers and regular people to understand when anal plugs are an option worth considering."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1659", "text": "Anal plugs may come as tampons or inserts as detailed below. Tampons are similar to  menstruation   tampons , which can expand and absorb substances to prevent leakage. Inserts provide a physical blockage, and are inserted into the rectal cavity to stop feces from escaping. Plugs come in a variety of shapes, sizes, and materials.  Polyurethane  plugs have been found to be preferred over  polyvinyl-alcohol  plugs, and are also associated with less plug loss. [ 11 ]  For all plugs that become stuck in the rectum, it is recommended to see a doctor if it does not come out in the next bowel movement."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1660", "text": "The Peristeen (formerly Conveen) Anal Plug produced by  Coloplast  is a disposable polyurethane insert coated in a water-soluble film. [ 15 ]  When exposed to warmth and moisture in the  anal canal , the film dissolves, allowing the plug to expand. It has a conical tip and a cord to tug on for removal. [ 16 ]  It comes in two sizes, and is inserted similarly to a  suppository . This plug may remain inside the rectum for up to 12 hours."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1661", "text": "The polyvinyl-alcohol anal tampons A-tam produced by Med SSE-System in Germany come in various sizes and shapes including cone, cylindrical, spiral, concave, convex, and ball-headed. [ 9 ]  The different shapes can address different concerns, based on anal sphincter muscle function, remaining muscle tissue, and gassiness. The plug should be soaked in warm water before inserted, similar to some rectal  suppositories . While the plugs are single-use, the applicator may be used multiple times. Changing out the plug three times a day every 6-8 hours and anal hygiene are also recommended. A prescription is needed for this product."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1662", "text": "Renew Inserts are single-use  silicone  plugs that come in two sizes and require a prescription. [ 10 ]  The large size is recommended for adults, while the regular size may be used for children and young adults. Each plug is made of two attached disks and comes connected to a fingertip applicator which is disposed after insertion. The top disk blocks the stool, while the bottom disk secures the insert in place to prevent displacement. It can be removed either by pulling it out or through defecation, removing the concern of losing the plug in the anal canal. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1663", "text": "The ProCon2 device by Incontinent Control Devices, Inc is composed of a blow-up balloon cuff attached to the end of a silicon  catheter  with vent holes at the tip for  flatulence  to escape. [ 17 ]  The catheter is inserted into the anal canal and the balloon cuff is inflated with water or air through a syringe attached to the exposed portion of the catheter. Once inflated, the exposed end of the catheter is pulled until the balloon cuff is met with resistance within the anus. An infrared photo-interruptor sensor in the catheter senses stool in the anal canal, sending a notification to a pager. To remove the device, the catheter is cut to allow the balloon to deflate before pulling it out. Each device is made for single-use only."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1664", "text": "The SURGISPON anal tampon is made of a gamma-sterilized gelatin sponge and, unlike the previously mentioned products, is used to stop bleeding in anal and rectal surgeries and post-surgery bleeding and pain. [ 18 ]  The sponge can absorb up to 45 times its weight, liquefying and eventually being excreted in a bowel movement within 1-2 days. It also has an opening in the middle for gas to escape, and may be used as a carrier for delivery of antibiotics,  thrombin , or chemotherapeutics. It is inserted either dry or wet, but for surgeries, it is inserted dry using a  proctoscope ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1665", "text": "Anal cleansing is the practice of proper  sanitization  and maintaining healthy hygiene in a person's rectal area. It is usually done post defecation. [ 19 ]  From a science perspective, it helps prevent pathogen exposure, which could lead to infections or diseases. The cleansing process involves rinsing the rectal cavity with water and usually wiping the area with toilet paper or baby wipes. Sometimes, a hand is used for rubbing the area while rinsing it with water. Other times,  bidet system  could be used instead. [ 19 ]  A bidet is a plumbing device that is usually installed as a separate unit beside the bathroom tub to wash one's inner buttocks and anal area."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1666", "text": "Reasons to maintain anal hygiene:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1667", "text": "Maintaining good anal hygiene contributes to an individual overall health. [ 20 ]  Some of the key benefits include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1668", "text": "Astroviruses  ( Astroviridae ) are a type of  virus  that was first discovered in 1975 using  electron microscopes  following an outbreak of  diarrhea  in humans. [ 1 ]  In addition to humans, astroviruses have now been isolated from numerous mammalian animal species (and are classified as genus  Mamastrovirus ) and from avian species such as ducks, chickens, and turkey poults (classified as genus  Avastrovirus ). Astroviruses are 28\u201335\u00a0nm diameter,  icosahedral  viruses that have a characteristic five- or six-pointed star-like surface structure when viewed by electron microscopy. Along with the  Picornaviridae  and the  Caliciviridae , the Astroviridae comprise a third family of nonenveloped viruses whose  genome  is composed of plus- sense , single-stranded RNA. [ 2 ]  Astrovirus has a non-segmented, single stranded, positive sense  RNA  genome within a  non-enveloped  icosahedral  capsid . [ 3 ]  Human astroviruses have been shown in numerous studies to be an important cause of  gastroenteritis  in young children worldwide. [ 2 ]  In animals, Astroviruses also cause infection of the gastrointestinal tract but may also result in  encephalitis  (humans and cattle), hepatitis (avian) and nephritis (avian). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1669", "text": "This family of viruses consists of two genera,  Avastrovirus  (AAstV) and  Mamastrovirus  (MAstV). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1670", "text": "The  International Committee on Taxonomy of Viruses  (ICTV) established  Astroviridae  as a viral family in 1995. [ 6 ]  There have been over 50 astroviruses reported, although the ICTV officially recognizes 22 species. [ 7 ]  The genus  Avastrovirus  comprises three species; Chicken astrovirus (Avian nephritis virus types 1\u20133), Duck astrovirus (Duck astrovirus C-NGB), and Turkey astrovirus (Turkey astrovirus 1). The genus  Mamastrovirus  includes Bovine astroviruses 1 and 2, Human astrovirus (types 1\u20138), Feline astrovirus 1, Porcine astrovirus 1, Mink astrovirus 1 and Ovine astrovirus 1. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1671", "text": "Astroviruses have a star-like appearance with five or six points. Their name is derived from the Greek word \"astron\" meaning star. They are  non-enveloped   RNA  viruses with cubic  capsids , approximately 28\u201335\u00a0nm in diameter with T=3 symmetry. [ 8 ] [ 9 ]  Human astroviruses are part of the Mammastrovirus genus and contains 8 serotypes. The human astrovirus capsid spikes have a distinct structure. The spike domain in particular has a 3-layered beta-sandwiches fold and a core, 6-stranded beta-barrel structure. The beta-barrel has a hydrophobic core. The triple-layered beta-sandwich is packed outside the beta-barrel. The spike also forms a dimer. This unique structure was found to be similar to the protein projections found on the capsid of the hepatitis E virus. The projection domain of the human astrovirus contains a receptor binding site for polysaccharides. The amino acid sequence of the astrovirus capsid protein does not have similar homology to other known viral proteins, but the closest would be hepatitis E virus. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1672", "text": "Astroviruses infect birds and mammals through the  fecal-oral route . They have a  tissue tropism  for  enterocytes . Entry into the host cell is achieved by attachment to host receptors, which mediates endocytosis. Replication follows the  positive-strand RNA virus  replication model. [ 11 ]  Astrovirus RNA is infectious and functions as a  messenger RNA  for ORF1a and ORF1b. [ 12 ]  A frame-shifting mechanism between these two nonstructural polypeptides translates  RNA-dependent RNA polymerase . [ 13 ]  In replication complexes near intracellular membranes, ORF1a and ORF1b are cleaved to generate individual nonstructural proteins that are involved in replication. The resulting subgenomic RNA contains ORF2 and encodes precursor capsid protein (VP90). VP90 is proteolytically cleaved during packaging and produces immature capsids made of VP70. Following encapsidation, immature capsids are released from the cell without lysis. [ 6 ]  Extracellular virions are cleaved by Trypsin and form mature infectious virions. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1673", "text": "Astroviruses are 28-30\u00a0nm non-enveloped viruses with T-3 icosahedral symmetry. They have spherical shapes and consist of a capsid protein shell. Astroviruses have distinctive five or six pointed star-like projections on 10% of the virions (the other virions have smooth surfaces). [ 4 ]  The virion capsid is expressed from a subgenomic mRNA and its precursor undergoes multiple cleavages to make the VP70 protein. Capsids that are made of the VP70 protein are cleaved by trypsin to make particles that are very infectious (VP25/26, VP27/29 and VP34). The spikes that create the star-like appearance on the virion surface are made by two structural proteins (VP25 and VP27) while the capsid shell is made from VP34. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1674", "text": "Astroviruses have a  genome  composed of a single strand of positive sense  RNA . The strand has a  poly A  tail at the  3' end , but no  5' cap  but instead is linked to a  VPg  protein. With the exclusion of polyadenylation at the  3' end , the genome is between 6.8 and 7.9 kb long. The genome is arranged into three  open reading frames  (ORFs), with an overlap of approximately 70 nucleotides between ORF1a and ORF1b. The remaining ORF is known as ORF2. [ 16 ]  ORF2 encode the structural proteins, [ 17 ]  which are -at least- VP26, VP29 and VP32, the most antigenic and immunogenic of these being VP26. This protein is probably involved in the first steps of viral infection, being a key factor in the biological cycle of astroviruses. [ 18 ]  The human astrovirus genome mutation rate has been estimated to be 3.7\u00d710 \u22123  nucleotide substitutions per site per year with the synonymous changes rate of 2.8\u00d710 \u22123  nucleotide substitutions per site per year. [ 19 ]  The capability for  genetic recombination  appears to be present in type-3 and type-4 human astroviruses, [ 20 ] [ 21 ]  and in porcine astrovirus strains. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1675", "text": "Replication of astroviruses occur in the cytoplasm. [ 23 ]  Astrovirus RNA is infectious and functions as a  messenger RNA  for ORF1a and ORF1b, with translation initiation thought to be mediated by  VPg  similar to  Caliciviridae . [ 24 ] [ 25 ]  A frame-shifting mechanism between these two nonstructural polypeptides translates  RNA-dependent RNA polymerase  (RdRp). [ 26 ]  In replication complexes near intracellular membranes, ORF1a and ORF1b are cleaved to generate individual nonstructural proteins that are involved in replication. RdRp transcribes subgenomic RNA from the subgenomic promoter, which enables higher production of structural proteins. Subgenomic RNA contains ORF2 which encodes precursor capsid protein (VP90). VP90 is proteolytically cleaved during packaging and produces immature capsids made of VP70. Following encapsidation, immature capsids are released from the cell without lysis. [ 6 ]  Extracellular virions are cleaved by Trypsin and form mature infectious virions. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1676", "text": "The  Astroviridae  capsid is related to those of the  Tymoviridae . The non-structural region is related to the  Potyviridae . It appears that this group of viruses may have arise at some point in the past as a result of recombination event between two distinct viruses and that this even occurred at the junction of the structural and non-structural coding regions. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1677", "text": "Avastrovirus 1\u20133 are associated with enteric infections in turkeys, ducks, chicken and guinea fowl. In turkey poults 1\u20133 weeks of age, some symptoms of enteritis include diarrhea, listlessness, liver eating and nervousness. These symptoms are usually mild but in cases of poult enteritis and mortality syndrome (PEMS), which has dehydration, immune dysfunction and anorexia as symptoms, mortality is high. [ 29 ]   Post mortem  examination of the intestines of infected birds show fluid filled intestines. Hyperplasia of enterocytes is also observed in histopathology studies. However, in contrast to other enteric viruses, there isn't villous supply. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1678", "text": "Avastrovirus species often infect extraintestinal sites such as the kidney or liver resulting in hepatitis and nephritis. [ 4 ]  Birds infected by  avian nephritis virus  typically die within 3 weeks of infection. The viral particles can be detected in fecal matter within 2 days and peak virus shedding occurs 4\u20135 days after infection. [ 30 ]  The virus can be found in the kidney, jejunum, spleen, liver and bursa of infected birds. Symptoms of this disease include diarrhea and weight loss. Necropsies show swollen and discolored kidneys and there is evidence of death of the epithelial cells and lymphocytic interstitial nephritis. [ 4 ]  Another extraintestinal  avastrovirus  is avian hepatitis virus which infects ducks. Hepatitis in ducks caused by this duck astrovirus (DAstV) is often fatal. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1679", "text": "In birds,  Avastroviruses  are detected by antigen-capture ELISA. In the absence of vaccines, sanitation is the prevalent way to prevent  Avastrovirus  infections. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1680", "text": "Mamastroviruses often cause  gastroenteritis  in infected mammals. In animals,  gastroenteritis  is usually undiagnosed because most astrovirus infections are asymptomatic. However, in mink and humans, astroviruses can cause diarrhea and can be fatal. The incubation period for  Mamastrovirus  is 1\u20134 days. When symptoms occur, the incubation period is followed by diarrhea for several days. In mink, symptoms include increased secretion from  apocrine glands . [ 4 ]  Human astroviruses are associated with gastroenteritis in children and immunocompromised adults. [ 32 ]  2\u20138% of acute non-bacterial gastroenteritis in children is associated with human astrovirus. These viral particles are usually detected in epithelial cells of the duodenum. [ 4 ]  In sheep, ovine astroviruses were found in the villi of the small intestine. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1681", "text": "Mamastroviruses  also cause diseases of the nervous system. [ 34 ]  These diseases most commonly occur in cattle, mink and humans. In cattle, this occurs sporadically and infects individual animals. Symptoms of this infection include seizure, lateral recumbency and impaired coordination. Histological examinations showed neuronal necrosis and gliosis of the cerebral cortex, cerebellum, spinal cord and brainstem. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1682", "text": "Members of a relatively new virus family, the astroviridae, astroviruses are now recognised as a cause of  gastroenteritis  in children, whose immune systems are underdeveloped, and elderly adults, whose immune systems are generally somewhat compromised. Presence of viral particles in fecal matter and in epithelial intestinal cells indicate that the virus replicates in the gastrointestinal tract of humans. [ 36 ]  The main symptoms are  diarrhoea , followed by nausea,  vomiting ,  fever , malaise and abdominal pain. Some research studies have shown that the incubation period of the disease is approximately three to four days. Astrovirus infection is not usually a severe situation and only in some rare cases leads to  dehydration . The severity and variation in symptoms correlates with the region the case develops in. This could be due to climatic factors influencing the life cycle or transmission method for that particular strain of Astrovirus. Malnutrition and immunodeficiency tend to exacerbate the condition, leading to more severe cases or secondary conditions that could require hospital care. [ 37 ]  Otherwise, infected people do not need hospitalization because symptoms will reduce by themselves, after 2 to 4 days. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1683", "text": "Human infections are usually self-limiting but may also spread systematically and infect immunocompromised individuals. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1684", "text": "Astroviruses most frequently cause infection of the gastrointestinal tract but in some animals they may result in encephalitis (humans and cattle), hepatitis (avian) and nephritis (avian). [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1685", "text": "Electron microscopy , enzyme-immunoassay ( ELISA ),  immunofluorescence , and  polymerase chain reaction  have all been used for detecting virus particle, antigens or viral nucleic acid in the stools of infected people. [ 41 ]  A method using real-time RT-PCR, which can detect all human astrovirus genotypes, has been reported. [ 42 ]  Some  RT-qPCR  techniques are able to simultaneously detect human astroviruses and other enteric viruses associated with  gastroenteritis . [ 43 ]  Microarrays are also used to differentiate between the eight different human astrovirus serotypes. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1686", "text": "Astroviruses cause gastroenteritis by causing destruction of the intestinal epithelium, leading to the inhibition of usual absorption mechanism, loss of secretory functions, and decrease in epithelial permeability in the intestines. Inflammatory responses were seen to not affect astrovirus pathogenesis. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1687", "text": "Astroviruses are associated with 5\u20139% of the cases of gastroenteritis in young children. [ 45 ]  Humans of all ages are susceptible to astrovirus infection, but children, the elderly, and those that are  immunocompromised  are most prone. A study of intestinal disease in the UK, published in 1999, determined incidence as 3.8/1000 patient years in the community (95%  CI , range 2.3\u20136.4), the fourth most common known cause of viral gastroenteritis. [ 46 ]  Studies in the USA have detected astroviruses in the stools of 2\u20139% of children presenting symptoms; illness is most frequent in children younger than two years, although outbreaks among adults and the elderly have been reported. Early studies carried out in  Glasgow  demonstrated that a significant proportion of babies excreting virus particles did not exhibit gastrointestinal symptoms. [ 47 ]   Seroprevalence  studies carried out in the  US  have shown that 90% of children have antibody to  HastV-1  by age 9, suggesting that (largely asymptomatic) infection is common. Looking at the pattern of disease, it suggests that antibodies provide protection through adult life until the antibody titre begins to decline later in life. [ 48 ] [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1688", "text": "The occurrence of astrovirus infections vary depending on the season. In  temperate  climates, infection is highest during winter months possibly due to lower temperatures which enhance the stability of the virus. [ 50 ]  This is in contrast to  tropical  regions where prevalence is highest during the rainy season. The seasonal distribution in tropical climates can be explained by the effect of rain particularly on the breakdown of  sanitation  in developing countries. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1689", "text": "Human astroviruses are transmitted by the  fecal\u2013oral route . The main mode of astrovirus transmission is by contaminated food and water. Young children in childcare backgrounds or adults in military barracks are most likely to develop the disease. Human astroviruses may be released in large quantities in the stool of infected individuals and contaminate  groundwater ,  fresh water  and  marine water  due to inadequate  wastewater treatment . Fruits and vegetables grown in such contaminated water may also act as sources of viral infection. Poor food handling practices, poor hand hygiene and contamination of inanimate objects are other factors that encourage  enteric  virus transmission. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1690", "text": "Astroviruses can also be transmitted to humans from other animal species. In comparison to individuals who had no contact with turkey, turkey  abattoir  workers were three times more likely to test positive for antibodies against turkey astroviruses. [ 52 ]  Furthermore, some human, duck, chicken and turkey astroviruses are  phylogenetically  related and share genetic features. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1691", "text": "Human astroviruses can be prevented by detection and inactivation in contaminated food and water in addition to disinfection of contaminated fomites. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1692", "text": "In a study by Bjorkholm et al., a 78-year-old patient diagnosed with Waldenstrom's macroglobulinemia was given 0.4 g/kg of astrovirus immunoglobulin for four days, and the symptoms dissolved leading to a full recovery from astrovirus; however, further testing has yet to be completed. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1693", "text": "In a study by Tellez et al., extracts from a plant  Achyrocline bogotensis  was used to develop an antiviral therapy for both rotavirus and astrovirus.  Achyrocline bogotensis  was commonly used for skin and urinary infections. Drug testing methodology involved application of the extract to cell for pre-treatment (blocking), direct viral activity (evidence of killing the virus), and treatment (a decrease in the viral load after an infection is established). The extract demonstrated direct viral activity by killing astroviruses directly and treatment by leading to a decrease in the viral load after an established infection. A pre-treatment effect was not evident during the experiment. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1694", "text": "1975:  Appleton and Higgins first discovered astrovirus in stool samples of children suffering from gastroenteritis by using electron microscopy (EM)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1695", "text": "1975:  Madeley and Cosgrove named the 20\u201330\u00a0nm viral particle Astrovirus based on the star-like EM (electron microscopy) appearance"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1696", "text": "1976-1992:  Lee and Kurtz serotyped 291 astrovirus stool samples in Oxford; discovered serotypes 6 and 7"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1697", "text": "1981:  Lee and Kurtz were able to grow astrovirus in tripsin-dependent tissue culture by using human embryo kidney cells (HEK)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1698", "text": "1985:  Lee and Kurtz discover two serotypes of astrovirus that are used to type 13 strains of community-acquired astrovirus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1699", "text": "1987:  Gray et al. discovered that a 22-day long gastroenteritis outbreak in an elderly home was caused by astrovirus type 1 and calicivirus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1700", "text": "1988:  Hermann and Hudson use antigen characterization of HEK grown astroviruses to develop monoclonal antibodies"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1701", "text": "1992:  Cruz et al. analyzed 5,000 stool samples 7.5% of the diarrheal diseases found in Guatemalan ambulatory rural children were caused by astroviruses"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1702", "text": "1993:  Jiang et al. sequence astrovirus RNA and determine the presence of three ORFs and ribosomal frameshifting"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1703", "text": "1993:  Monroe et al. classify subgenomic data for astrovirus, providing support for astrovirus to be classified as a viral family"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1704", "text": "1994:  Oishi et al. determine astrovirus as the main cause of gastroenteritis in schools in Katano City, Osaka, Japan"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1705", "text": "1995:  Bjorkholm elt al. conducted a clinical study, and 78-year-old male Waldenstr\u00f6m's macroglobulinemia patient with astrovirus-associated gastroenteritis was successfully treated with intravenous immunoglobulin"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1706", "text": "1995:  Jonassen et al. uses PCR to detect all known serotypes (7) of astrovirus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1707", "text": "1995:  In their sixth report, ICTV establishes Astroviridae as a viral family"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1708", "text": "1996:  Glass et al. states an epidemiological shift regarding astrovirus due to improvements in RT-PCT (reverse transcription PCR), monoclonal antibodies, and enzyme immunoassays (EIA); astroviruses are now considered one of the main causes of diarrheal disease worldwide"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1709", "text": "1996:  Palombo and Bishop the epidemiology of astrovirus infections in children suffering from gastroenteritis in Melbourne, Australia (data collected include total incidence, genetic diversity, serotype characterization)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1710", "text": "1998:  Unicomb et al. conduct a clinical study in Bangladesh and conclude astrovirus infections involving nosocomial, acute, and persistent diarrheal diseases"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1711", "text": "1998:  Gaggero et al. identify human astrovirus type 1 to be the main cause of acute gastroenteritis in Chilean children"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1712", "text": "1999:  Bon et al. discover astrovirus in a gastroenteritis outbreak in Dijon, France"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1713", "text": "2001:  Dennehy et al. collected stool samples from hospitalized children suffering from acute gastroenteritis; astrovirus was determined the second leading cause of gastroenteritis after rotavirus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1714", "text": "2002:  Guix et al. completes an epidemiological study on the presence of astrovirus in Barcelona, Spain; the total incidence of astrovirus in 2,347 samples was 4.95 with a peak in the number of cases in the winter"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1715", "text": "2003:  Basu et al. discovered astrovirus in 2.7% of stool samples collected from 346 children suffering from gastroenteritis in Gaborone, Botswana"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1716", "text": "2009:  Finkbeiner et al. used Sanger sequencing to discover a novel astrovirus in stool samples from children suffering from an acute gastroenteritis outbreak at a childcare center"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1717", "text": "2009:  Using RT-PCR, Kapoor et al. discover novel astrovirus strains HMOAstV species A, B, C which are very similar to astroviruses found in mink and ovine species; this showed that the virus may have the ability to jump species"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1718", "text": "Balsalazide  is an anti-inflammatory drug used in the treatment of  inflammatory bowel disease . It is sold under the brand names  Giazo ,  Colazal  in the US and  Colazide  in the UK. It is also sold in generic form in the US by several generic manufacturers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1719", "text": "It is usually administered as the disodium salt. Balsalazide releases  mesalazine , also known as 5-aminosalicylic acid, or 5-ASA, [ 2 ]  in the large intestine. Its advantage over that drug in the treatment of  ulcerative colitis  is believed to be the delivery of the active agent past the small intestine to the large intestine, the active site of ulcerative colitis. It is in the category of  disease-modifying antirheumatic drugs  (DMARDs) family of medications. [ 3 ]  It is unclear exactly how it works. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1720", "text": "Ex 3 is actually for  Ipsalazide . See Ex 4 for Balsalazide proper. Same protocol but uses  \u03b2-Alanine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1721", "text": "A  barostat  is a device used to maintain constant pressure in a closed chamber. [ 1 ]  Its main principle is providing constant  pressures  in a  balloon  by means of a  pneumatic   pump . [ 2 ]   Barostats are frequently used in  neurogastroenterology  research, where they are used for measuring  gut wall   tension  or  sensory thresholds  in the gut. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1722", "text": "A specially designed instrument is needed in neurogastroenterology research since the gut wall has an outstanding capacity to expand and  contract  spontaneously and by  reflex . When this occurs, a balloon placed anywhere in the gut has to be inflated or deflated very rapidly in order to maintain a constant pressure in this balloon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1723", "text": "Barostat-balloon systems have been used anywhere in the gut, including the  esophagus , [ 4 ]   stomach , [ 5 ]   small bowel , [ 6 ]   colon , and the  rectum ampulla . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1724", "text": "Computer -driven barostats have widely been used to assess sensation and pain thresholds in the gut. Assessment of pain thresholds in the ampulla recti has been proposed as  diagnostic  measure in  irritable bowel syndrome . [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1725", "text": "Bowel management  is the process which a person with a bowel disability uses to manage  fecal incontinence  or  constipation . [ 1 ]  People who have a medical condition which impairs control of their  defecation  use bowel management techniques to choose a predictable time and place to evacuate. [ 1 ]  A simple bowel management technique might include diet control and establishing a toilet routine. [ 1 ]  As a more involved practice a person might use an  enema  to relieve themselves. [ 1 ]  Without bowel management, the person might either suffer from the feeling of not getting relief, or they might soil themselves. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1726", "text": "Bowel control is often a challenge for children who are born with anomalies in their  anus  or  rectum ,  Hirschsprung's disease , and/or  spina bifida . Medical providers can help anyone with long term bowel problems to develop a routine in such cases to assist children in managing their bowels so that they can otherwise live normally. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1727", "text": "Bowel management is achieved mainly through a daily  enema  which empties the  colon  to prevent unwanted and uncontrolled bowel movements that day. [ 2 ]  Some patients also use  laxatives  and a  controlled diet  as part of their bowel management regimen. Another alternative is  transanal irrigation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1728", "text": "Transanal irrigation of the rectum and colon is designed to assist the evacuation of faeces from the bowel by introducing water into rectum via the anus. [ 3 ]  By regularly emptying the bowel using transanal irrigation, controlled bowel function is often re-established to a high degree in patients with bowel incontinence and/or constipation. This enables the users to develop a consistent bowel routine by choosing the time and place of evacuation. [ 3 ]   An international consensus on when and how to use transanal irrigation for people with bowel problems was published 2013. The article offers practitioners a clear, comprehensive and simple guide to practice for the emerging therapeutic area of transanal irrigation. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1729", "text": "Determining the appropriate regimen to achieve successful bowel management is done under medical supervision. Care is tailored to suit each child and often requires a trial and error approach over the course of a week. The patient has an  X-ray  taken which is reviewed by their doctor. The doctor then recommends a course of action (e.g. enemas,  laxative , and/or controlled diet). The next day, the process is repeated with modifications to help the child achieve a completely empty colon. After the course of this week the doctor can determine the precise amount and combination of what the child needs to achieve bowel management. From then on the patient can continue the regimen on their own. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1730", "text": "Bowel management does not cure  fecal incontinence , but can greatly increase quality of life. With successful bowel management, a child may be more apt to establish independence in normal daily life. Children with severe incontinence may also be able to attend school and participate in activities they otherwise would never be able to. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1731", "text": "Depending on the prognosis, some patients will continue using these techniques for life while others may gain some degree of bowel control and become \"potty trained\". Children who practice bowel management often become unhappy as they age, especially at  puberty , due to feeling that the administration of enemas is an intrusion on their privacy, especially as it is difficult for them to administer the enema themselves. An operation called a continent appendicostomy or  Malone procedure  is available. This allows a person to give themselves an enema by inserting a  catheter  into a small orifice at the  navel . [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1732", "text": "The medical definition of  fecal incontinence  is the incapacity to voluntarily hold  feces  in the rectum. There are two subgroups to those with fecal incontinence: real fecal incontinence and pseudoincontinence. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1733", "text": "For a child with real fecal incontinence, the normal mechanism of bowel control is not working. An alteration of the muscles that surround the  anorectal canal  along with poor  sphincters  (the muscles that control the anus) are responsible for fecal incontinence in children operated on for  anorectal malformations  with a bad prognosis. Some patients operated on for Hirschsprung's disease have this anatomic problem as do those with spinal problems. The supply of  nerve  connections of these muscles is important for their correct function. A deficit of nerve connections occurs in anorectal anomalies as well as in other conditions. In cases of  spina bifida , or following  spinal cord  injury, the contraction and relaxation of the muscles, as well as sensation, are deficient. The presence and the passage of feces and the perception of the difference between solid and liquid feces and gas are limited."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1734", "text": "In cases of pseudoincontinence, a child is believed to have fecal incontinence. However, investigation shows that they have severe constipation and fecal impaction. When the  impaction  is treated and the patient receives enough laxatives to pass stool, they become continent."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1735", "text": "Children who have fecal incontinence after the repair of an  imperforate anus  are usually those born with a bad prognosis type of defect and severe associated defects (defect of the sacrum, poor muscle complex). However, such children can still achieve a good quality of life when treated with the bowel management program. Children operated on for imperforate anus and who have fecal incontinence can be divided into two groups that require individualized treatment plans:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1736", "text": "Children with constipation (colonic hypomotility) : No special diet or medications are necessary for children with  colonic hypomotility , a type of  constipation . Their tendency towards constipation helps them to remain clean between enemas. The real challenge is to find an enema capable of cleaning the colon completely. Soiling episodes or \"accidents\" occur when there is an incomplete cleaning of the bowel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1737", "text": "Children with loose stools and diarrhea (colonic hypermotility) : This group of children has an overactive colon. Rapid transit of stool results in frequent episodes of  diarrhea . This means that even when an enema cleans the colon rather easily, stool keeps on passing fairly quickly from the cecum to the  descending colon and the anus. To prevent this, a constipating diet and/or medications to slow down the colon are necessary. Eliminating foods that further loosen bowel movements will help the colon to slow down. Those who experience hypermotility may have to follow a constipating diet and avoid laxative foods. The diet is rigid and includes food such as banana, apple, baked bread, white pasta with no sauce, boiled meat, and others, while fried foods and  dairy products  are avoided. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1738", "text": "Buried bumper syndrome  ( BBS ) is a condition that affects feeding tubes placed into the stomach ( gastrostomy tubes ) through the abdominal wall.  Gastrostomy tubes include an internal bumper, which secures the inner portion of the tube inside the stomach, and external bumper, which secures the outer portion of the tube and opposes the abdomen. Buried bumper syndrome occurs when the internal bumper of a gastrostomy tube erodes into the wall of the stomach. The internal bumper may become entirely buried within the fistulous tract. The main causative factor is excessive tightening of the external bumper, leading to increased pressure of the internal bumper on the wall of the stomach.  Additional risk factors include:  obesity , weight gain,  malnutrition ,  corticosteroid  therapy, and poor wound healing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1739", "text": "Buried bumper syndrome may be entirely asymptomatic, though tube dysfunction is common.  The gastrostomy tube may leak around the entry site, or it may become difficult to infuse feeds, fluids or medications. Less often, bleeding, infection, abscess or peritonitis may occur. Diagnosis is achieved most often with  upper endoscopy .   Computed tomography  imaging may also confirm the diagnosis. Treatment consists of removal of the gastrostomy tube, either via simple external traction or endoscopic removal.  Surgery is rarely necessary."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1740", "text": "Buried bumper syndrome may be asymptomatic, especially early in the course.  Dysfunction of the tube occurs commonly, including leakage around the insertion site, inability to administer feedings or fluids, or need for more pressure when giving feeds. [ 1 ]   Buried bumper syndrome may cause abdominal pain or swelling ( erythema ) at the site of insertion of the PEG tube. Less commonly, buried bumper syndrome may also be complicated by acute infectious illness (sepsis), abscess formation, gastrointestinal bleeding or peritonitis. [ 2 ] [ 3 ]  In some cases, the internal bumper may be felt by palpating the abdomen. [ 2 ]  Inspection of the tube typically reveals an inability to easily rotate the tube. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1741", "text": "Buried bumper syndrome occurs when this internal bumper erodes into the wall of the stomach, sometimes becoming entirely buried within the wall of the stomach. Buried bumper syndrome tends to be a late complication of gastrostomy tube placement, but can rarely occur as early as 1 to 3 weeks after tube placement. [ 4 ] [ 5 ]   Most cases occur more than 1 year after initial placement of the PEG tube. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1742", "text": "Excessive tightening of the external bumper is the primary risk factor for buried bumper syndrome.  Maintaining the external bumper in a loose position may help prevent buried bumper syndrome. [ 6 ]  Additional risk factors include obesity, medications, poor wound healing, malnutrition, etc. Feeding tubes with soft balloon internal bumpers are less likely to cause buried bumper syndrome, compared with more firm or stiff polyurethane internal bumpers. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1743", "text": "Buried bumper syndrome may be suspected based on features consistent with this disorder.  The diagnosis is confirmed either endoscopically (via  upper endoscopy ) or with computed tomography. [ 8 ]  Upper endoscopy may reveal overgrowth of stomach tissue over the internal bumper (incomplete buried bumper syndrome). [ 1 ]  If the bumper has eroded deep into the gastric mucosa, it may not be visualized during endoscopic evaluation (complete buried bumper syndrome). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1744", "text": "Prevention consists of maintaining a space of 1\u20132\u00a0cm between the external bumper of the gastrostomy tube and the abdominal wall, which avoids excess pressure of the internal bumper onto the stomach wall. Mobilizing and rotating the tube may prevent mucosal overgrowth and aid in avoiding buried bumper syndrome. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1745", "text": "Treatment of buried bumper syndrome consists of removal of the gastrostomy tube.  For mild cases with externally removable tubes, simple external traction may be used to remove the tube.  Several different approaches may be utilized, including endoscopy. [ 9 ] [ 10 ]  If endoscopic removal is pursued, a new feeding tube may be placed during the same procedure. [ 11 ]  Where endoscopic removal is not possible, surgery may be necessary (laparoscopic or laparotomy)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1746", "text": "Buried bumper syndrome occurs in 0.3\u20132.4% of patients. Malnutrition, malignancy, chemoradiation, and corticosteroid therapy are additional risk factors. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1747", "text": "In 1980, the first percutaneous endoscopic gastrostomy (PEG) tube was reported, as an alternative to an open surgical placement of feeding tubes.  The first cases of buried bumper syndrome were reported in 1988 and 1989. [ 7 ]  The term \"buried bumper syndrome\" was first used in 1990. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1748", "text": "Burning mouth syndrome  ( BMS ) is a burning, tingling or scalding sensation in the mouth, lasting for at least four to six months, with no underlying known dental or medical cause. [ 3 ] [ 7 ]  No related  signs of disease  are found in the mouth. [ 3 ]   People with burning mouth syndrome may also have a subjective  xerostomia  (dry mouth sensation where no cause can be found such as reduced salivary flow),  paraesthesia  (altered sensation such as tingling in the mouth), or an altered sense of taste or smell. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1749", "text": "A burning sensation in the mouth can be a  symptom  of another disease when local or systemic factors are found to be implicated; this is not considered to be burning mouth syndrome, [ 3 ]   which is a syndrome of  medically unexplained symptoms. [ 3 ]   The  International Association for the Study of Pain  defines burning mouth syndrome as \"a distinctive  nosological  entity characterized by unremitting oral burning or similar pain in the absence of detectable  mucosal  changes\" [ 1 ]  and \"burning pain in the tongue or other oral mucous membranes\", [ 8 ]  and the  International Headache Society  defines it as \"an intra-oral burning sensation for which no medical or dental cause can be found\". [ 6 ]  To ensure the correct diagnosis of burning mouth syndrome, Research Diagnostic Criteria (RDC/BMS) have been developed. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1750", "text": "Insufficient evidence leaves it unclear if effective treatments exist. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1751", "text": "By definition, BMS has no signs. Sometimes affected persons will attribute the symptoms to sores in the mouth, but these are in fact normal anatomic structures (e.g.  lingual papillae ,  varices ). [ 10 ]  Symptoms of BMS are variable, but the typical clinical picture is given below, considered according to the  Socrates pain assessment method  (see table). If clinical signs are visible, then another explanation for the burning sensation may be present.  Erythema  (redness) and  edema  (swelling) of papillae on the tip of the tongue may be a sign that the tongue is being habitually pressed against the teeth. The number and size of  filiform papillae  may be reduced. If the tongue is very red and smooth, then there is likely a local or systemic cause (e.g. erythematous candidiasis,  anemia ). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1752", "text": "In about 50% of cases of burning mouth sensation  no identifiable cause is apparent; [ 1 ]  these cases are termed (primary) BMS. [ 11 ]  Several theories of what causes BMS have been proposed, and these are supported by varying degrees of evidence, but none is proven. [ 5 ] [ 11 ] \nAs most people with BMS are postmenopausal women, one theory of the cause of BMS is of  estrogen  or  progesterone  deficit, but a strong statistical correlation has not been demonstrated. [ 5 ]  Another theory is that BMS is related to  autoimmunity , as abnormal antinuclear antibody and rheumatoid factor can be found in the serum of more than 50% of persons with BMS, but these levels may also be seen in elderly people who do not have any of the symptoms of this condition. [ 5 ]  Whilst salivary flow rates are normal and there are no clinical signs of a dry mouth to explain a complaint of dry mouth, levels of salivary proteins and phosphate may be elevated and salivary pH or buffering capacity may be reduced. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1753", "text": "Depression and  anxiety  are strongly associated with BMS. [ 5 ] [ 13 ] [ 14 ]  It is not known if depression is a cause or result of BMS, as depression may develop in any setting of constant unrelieved irritation, pain, and sleep disturbance. [ 5 ] [ 12 ] [ 15 ]  It is estimated that about 20% of BMS cases involve  psychogenic factors , [ 14 ]  and some consider BMS a  psychosomatic illness , [ 5 ] [ 13 ]  caused by  cancerophobia , [ 13 ] [ 14 ]  concern about  sexually transmitted infections , [ 14 ]  or  hypochondriasis . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1754", "text": "Chronic low-grade trauma due to  parafunctional habits  (e.g. rubbing the tongue against the teeth or pressing it against the palate), may be involved. [ 12 ]  BMS is more common in persons with  Parkinson's disease , so it has been suggested that it is a disorder of reduced pain threshold and increased sensitivity. Often people with BMS have unusually raised taste sensitivity, termed  hypergeusia  (\"super tasters\"). [ 1 ]   Dysgeusia  (usually a bitter or metallic taste) is present in about 60% of people with BMS, a factor which led to the concept of a defect in sensory peripheral neural mechanisms. [ 12 ]  Changes in the oral environment, such as changes in the composition of saliva, may induce neuropathy or interruption of nerve transduction. [ 1 ] [ 11 ]  The onset of BMS is often spontaneous, although it may be gradual. There is sometimes a correlation with a major life event or stressful period in life. [ 10 ]  In women, the onset of BMS is most likely three to twelve years following menopause. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1755", "text": "Metals"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1756", "text": "Plastics"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1757", "text": "Several local and systemic factors can give a burning sensation in the mouth without any clinical signs, and therefore may be  misdiagnosed  as BMS. Some sources state that where there is an identifiable cause for a burning sensation, this can be termed \"secondary BMS\" to distinguish it from primary BMS. [ 16 ] [ 17 ]  However, the accepted definitions of BMS hold that there are no identifiable causes for BMS, [ 1 ] [ 3 ] [ 6 ]  and where there are identifiable causes, the term BMS should not be used. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1758", "text": "Some causes of a burning mouth sensation may be accompanied by clinical signs in the mouth or elsewhere on the body. For example, burning mouth pain may be a symptom of  allergic contact stomatitis . This is a contact sensitivity ( type IV hypersensitivity  reaction) in the oral tissues to common substances such as  sodium lauryl sulfate ,  cinnamaldehyde  or dental materials. [ 4 ]  However, allergic contact stomatitis is accompanied by visible lesions and gives positive response with patch testing. Acute (short term) exposure to the  allergen  (the substance triggering the allergic response) causes non-specific inflammation and possibly  mucosal ulceration . Chronic (long term) exposure to the allergen may appear as chronic inflammatory, lichenoid (lesions resembling oral  lichen planus ), or  plasma cell gingivitis , which may be accompanied by glossitis and  cheilitis . [ 12 ]  Apart from BMS itself, a full list of causes of an oral burning sensation is given below:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1759", "text": "BMS is a  diagnosis of exclusion , i.e. all other explanations for the symptoms are ruled out before the diagnosis is made. [ 1 ] [ 16 ]  There are no clinically useful investigations that would help to support a diagnosis of BMS [ 3 ]  (by definition all tests would have normal results), [ 1 ]  but  blood tests  and / or  urinalysis  may be useful to rule out anemia, deficiency states, hypothyroidism and diabetes. Investigation of a dry mouth symptom may involve  sialometry , which objectively determines if there is any reduction of the salivary flow rate (hyposalivation). Oral candidiasis can be tested for with use of a swabs, smears, an oral rinse or saliva samples. [ 11 ]   It has been suggested that allergy testing ( e.g. ,  patch test ) is inappropriate in the absence of a clear history and clinical signs in people with a burning sensation in the mouth. [ 11 ]  The diagnosis of a people with a burning symptom may also involve psychologic screening e.g. depression questionnaires. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1760", "text": "The second edition of the  International Classification of Headache Disorders  lists diagnostic criteria for \"Glossodynia and Sore Mouth\":"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1761", "text": "A burning sensation in the mouth may be primary (i.e. burning mouth syndrome) or secondary to systemic or local factors. [ 1 ]  Other sources refer to a \"secondary BMS\" with a similar definition, i.e. a burning sensation which is caused by local or systemic factors, [ 16 ]  or \"where oral burning is explained by a clinical abnormality\". [ 17 ]  However this contradicts the accepted definition of BMS which specifies that no cause can be identified. \"Secondary BMS\" could therefore be considered a misnomer. BMS is an example of  dysesthesia , or a distortion of sensation. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1762", "text": "Some consider BMS to be a variant of  atypical facial pain . [ 22 ]  More recently, BMS has been described as one of the 4 recognizable symptom complexes of chronic  facial pain , along with atypical facial pain,  temporomandibular joint dysfunction  and  atypical odontalgia . [ 23 ]  BMS has been subdivided into three general types, with type two being the most common and type three being the least common. [ 1 ]  Types one and two have unremitting symptoms, whereas type three may show remitting symptoms. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1763", "text": "Sometimes those terms specific to the tongue (e.g.  glossodynia ) are reserved for when the burning sensation is located only on the tongue. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1764", "text": "If a cause can be identified for a burning sensation in the mouth, then treatment of this underlying factor is recommended. If symptom persist despite treatment a diagnosis of BMS is confirmed. [ 11 ]  BMS has been traditionally treated by reassurance and with  antidepressants ,  anxiolytics  or  anticonvulsants . A 2016  Cochrane review  of treatment for burning mouth syndrome concluded that strong evidence of an effective treatment was not available, [ 3 ]  however,  a systematic review in 2018 found that the use of antidepressants and alpha-lipoic acids gave promising results. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1765", "text": "Other treatments which have been used include  atypical antipsychotics ,  histamine receptor antagonists , and  dopamine agonists . [ 26 ]  Supplementation with vitamin complexes and  cognitive behavioral therapy  may be helpful in the management of burning mouth syndrome. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1766", "text": "BMS is benign (importantly, it is not a symptom of  oral cancer ), but as a cause of chronic pain which is poorly controlled, it can detriment  quality of life , and may become a fixation which cannot be ignored, thus interfering with work and other daily activities. [ 10 ] [ 28 ]  Two thirds of people with BMS have a spontaneous partial recovery six to seven years after the initial onset, but in others the condition is permanent. [ 5 ] [ 15 ]  Recovery is often preceded by a change in the character of the symptom from constant to intermittent. [ 15 ]  No clinical factors predicting recovery have been noted. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1767", "text": "If there is an identifiable cause for the burning sensation, then psychologic dysfunctions such as anxiety and depression often disappear if the symptom is successfully treated. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1768", "text": "BMS is fairly uncommon worldwide, affecting up to five individuals per 100,000 general population. [ 3 ]  People with BMS are more likely to be middle aged or elderly, and females are three to seven times more likely to have BMS than males. [ 1 ] [ 29 ]  Some report a female to male ratio of as much as 33 to 1. [ 6 ]  BMS is reported in about 10\u201340% of women seeking medical treatment for  menopausal  symptoms, and BMS occurs in about 14% of postmenopausal women. [ 5 ] [ 15 ] [ contradictory ]  Males and younger individuals of both sexes are sometimes affected. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1769", "text": "Asian and Native American people have considerably higher risk of BMS. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1770", "text": "Sheila Chandra , a British singer of  Indian  heritage, retired due to this condition. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1771", "text": "Caustic ingestion  occurs when someone accidentally or deliberately ingests a  caustic or corrosive substance . Depending on the nature of the substance, the duration of exposure and other factors it can lead to varying degrees of damage to the  oral mucosa , the  esophagus , and the  lining of the stomach . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1772", "text": "The severity of the injury can be determined by  endoscopy  of the upper digestive tract, although  CT scanning  may be more useful to determine whether surgery may be required. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1773", "text": "During the healing process,  strictures  of the oesophagus may form, which may require  therapeutic dilatation  and insertion of a  stent . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1774", "text": "Immediate manifestations of caustic substance ingestions include erosions of mucosal surfaces of the gastrointestinal tract or airway (which can cause bleeding if the erosions extend to a blood vessel), mouth and tongue swelling, drooling or hypersalivation, nausea, vomiting,  dyspnea ,  dysphonia / aphonia , irritation of the eyes and skin. [ 1 ] [ 2 ]  Perforation of the esophagus can lead to  mediastinitis  or perforation of the stomach or bowel can lead to  peritonitis [ 1 ]  Swelling of the airway or  laryngospasm  can occur leading to compromised breathing. Injuries affecting the respiratory system include aspiration pneumonia and laryngeal sores. [ 3 ]  Signs of respiratory compromise include  stridor  and a change in a person's voice."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1775", "text": "Later manifestations of caustic substance ingestions include  esophageal strictures  or stenosis; which can result in chronic pain and malnutrition. [ 1 ]  Esophageal strictures more commonly occur after more severe mucosal injury, occurring in to 71% and 100% of grade 2b and 3 mucosal lesions respectively. [ 2 ]  Remote manifestations of caustic ingestions include esophageal cancer. People who have a history of caustic substance ingestion are 1000-3000 times more likely to develop esophageal cancer with most cases occurring 10\u201330 years after the ingestion. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1776", "text": "Acids  with a  pH  of less than 2 or  alkalis  with a pH above 12 are capable of causing the most extensive injuries in ingestions. [ 1 ]  Alkalis damage tissue by saponifying fats, leading to liquefaction necrosis which allows the alkalis to reach deeper tissues. Acids denature proteins via coagulation necrosis, this type of necrosis is thought to prevent the acid from reaching deeper tissues. [ 1 ] [ 2 ]  Clinically, the pH, concentration, volume of ingested substance in addition to the duration of time in contact with tissue as well as percentage of body surface area involved determine the severity of the injury. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1777", "text": "The severity of injuries to the mucosa of the gastrointestinal tract is commonly rated using the Zargar criteria. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1778", "text": "Common treatments used for toxic substance ingestions are ineffective, or are even harmful, when implemented in ingestions of caustic substances. Clinical attempts to empty the stomach can cause further injuries. [ 1 ]   Activated charcoal  does not neutralize caustics and can also obscure endoscopic visualization. [ 1 ]  There is no known clinical benefit of neutralization of the caustic substances; neutralization releases heat as well as causing gaseous distention and vomiting, all of which can worsen injuries. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1779", "text": "Signs of airway compromise including decreased level of consciousness, stridor, change in voice, inability to control oral secretions necessitate intubation and mechanical ventillation. [ 1 ]  IV fluids are often needed to maintain hydration and replace insensible water losses."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1780", "text": "Endoscopy should be done within the first 24\u201348 hours of ingestion as subsequent wound softening increases the risk of perforation. [ 1 ]  Endoscopically inserted nasogastric tubes can serve as a stent to prevent esophageal strictures as well as allow tube feedings. [ 1 ]  A CT scan, often enhanced with contrast, can also be used to evaluate injuries. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1781", "text": "The most common surgical methods of treatment in children include esophageal dilation and esophageal replacement as less commonly implantation of an esophageal stent. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1782", "text": "In general, most ingestions in children involve exploratory ingestions of small amounts of caustic substances, with the rare exception being cases of child abuse where larger amounts are often ingested. Caustic ingestions in adults usually involve larger amounts of ingested material during attempts of self harm. [ 1 ]  Due to the greater amount of material usually ingested; injuries are often more severe in the intentional ingestions of adolescents and adults as compared to those of children. [ 1 ]  Commonly ingested substances include  ammonium hydroxide  (found in general cleaner and grease remover),  sodium hydroxide  or  potassium hydroxide  (found in drain opener or oven cleaner),  sodium hypochlorite  (bleach),  oxalic acid  (metal polish) and  hydrochloric acid  (toilet bowl cleaner). [ 1 ]  Storage of caustic substances in water or drink containers is a risk factor for accidental ingestion of these materials, particularly in children. [ 2 ]  Boys of preschool age are at the greatest risk of accidental caustic ingestion. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1783", "text": "Preventative measures have been recommended that are intended to decrease the risk of accidental ingestion of caustic substances including: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1784", "text": "Cecal bascule  is a cause of  large bowel obstruction  where there is folding of the  cecum  anteriorly over the  ascending colon . It is one of two types of cecal  volvulus , the other being axial ileocolic.  It is caused by rotational torsion of the cecum or ascending colon along its own axis. In cecal bascule, the base of the cecum folds anteriorly over the ascending colon, creating a flap-valve, obstructing emptying of the cecum. [ 1 ]  The condition can be complicated by  necrosis  or  organ perforation  before the diagnosis is made, particularly if the  ileocecal valve  is competent, preventing retrograde decompression of the cecum into the  ileum . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1785", "text": "Checkpoint inhibitor induced colitis  is an inflammatory condition affecting the colon ( colitis ), which is caused by cancer  immunotherapy  ( checkpoint inhibitor therapy ). Symptoms typically consist of  diarrhea ,  abdominal pain  and  rectal bleeding . Less commonly,  nausea  and  vomiting  may occur, which may suggest the present of  gastroenteritis . The severity of diarrhea and colitis are graded based on the frequency of bowel movements and symptoms of colitis, respectively."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1786", "text": "The gold standard for the diagnosis of checkpoint inhibitor induced colitis is  colonoscopy  with evaluation of the  terminal ileum . However, in most cases, a  flexible sigmoidoscopy  is sufficient. Infection should be ruled out with stool studies, including  Clostridioides difficile , bacterial culture, ova and parasites. Symptoms of upper abdominal pain, nausea or vomiting warrant evaluation with  upper endoscopy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1787", "text": "Treatment of immune checkpoint inhibitor colitis is based on severity, as defined by the grade of diarrhea and colitis. Mild cases by managed with temporary interruption of immune checkpoint inhibitor therapy, dietary modification (low residue), and/or  loperamide . More severe cases require immune suppression with  corticosteroid therapy . If steroids are ineffective,  infliximab  may be considered. If colitis fails to improve with infliximab, then  vedolizumab  may be effective."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1788", "text": "The most common symptom is diarrhea, which occurs in 92 percent of cases, followed by abdominal pain (82%) and rectal bleeding (64%). [ 2 ]  About 46% of cases include fever and 36% involve nausea and vomiting. [ 2 ]  Less often, nausea and vomiting may be present. Weight loss has been reported. [ 1 ]  Onset of diarrhea generally occurs about 6\u20137 weeks after starting immune checkpoint inhibitor therapy. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1789", "text": "The extent of diarrhea is graded based on severity, from 1 to 5.  Grade 1 diarrhea is defined by an increase in the number of stools below four per day (compared with baseline). Grade 2 diarrhea is defined by an increase of 4\u20136 bowel movements per day.  Grade 3 diarrhea is defined by an increase by 7 or more bowel movements per day.  Grade 4 diarrhea involves life-threatening consequences, such as shock, whereas grade 5 results in death."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1790", "text": "The extent of colitis is also graded based on severity, from 1 to 5. Grade 1 colitis does not result in any symptoms, while grade 2 colitis leads to abdominal pain, mucous and blood in the stools.  Grade 3 colitis is defined by severe pain,  peritoneal signs  and  ileus .  Grade 4 colitis is defined by life-threatening consequences, including perforation, ischemia, necrosis, bleeding, or toxic megacolon.  Grade 5 colitis results in death."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1791", "text": "High grade colitis may lead to severe complications, including perforation, toxic megacolon and death. Bleeding may occur due to colitis. Treatment with corticosteroids may lead to infectious complications, including:  urinary tract infections ,  C. difficile infection , and  pneumonia . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1792", "text": "Immune checkpoints are important for the normal development of  T regulatory cells  (Tregs) in the intestine. Mice with the CTLA-4 gene removed (e.g. CTLA-4 knockout) develop severe autoimmune disease, with diffuse infiltration of T cells in multiple organs and fatal enterocolitis. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1793", "text": "Immune checkpoint inhibitor colitis is typically characterized by either diffuse mucosal inflammation or focal active colitis with patchy crypt abscesses. [ 4 ]  Common findings of acute colitis include: intraepithelial neutrophilic infiltrates, crypt abscesses, and increased apoptotic cells within crypts. However, the histologic appearance varies, and evidence of chronic inflammation is seen in some cases, including intraepithelial lymphocytes or basal lymphocytes and crypt architecture distortion. [ 4 ]  Histologic inflammation may occur as early as 1\u20132 weeks after immune checkpoint inhibitor therapy, well before the onset of symptoms. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1794", "text": "Anti-PD-1 induced colitis may lead to more CD8+ T cell inflammation, whereas Anti-CTLA4 induced colitis may involve more CD4+ T cell infiltration and higher mucosal levels of the inflammatory molecule  TNF alpha ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1795", "text": "Amongst people treated with immune checkpoint inhibitors, those with  Faecalibacterium  genus and other  Bacillota  present in the colonic flora have longer progression-free survival and overall survival.  In addition, a higher rate of checkpoint inhibitor induced colitis is associated with the presence of Faecalibacterium in the fecal microbiota. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1796", "text": "Colonoscopy  with evaluation of the  terminal ileum  is the gold standard in the diagnosis of checkpoint inhibitor induced colitis. [ 4 ] [ 2 ]  However, in most cases, a limited evaluation of the distal colon with  flexible sigmoidoscopy  is sufficient. [ 4 ] [ 2 ] [ 6 ]  Endoscopic findings may include loss of vascular pattern, erythema, edema, erosions, ulcers, exudates, granularity, and bleeding. [ 1 ] [ 7 ]  Biopsies should be taken even in endoscopic findings are normal, as inflammation may not be immediately apparent and may only be seen on histology ( microscopic colitis ). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1797", "text": "Symptoms of nausea, vomiting and epigastric pain may suggest involvement of the upper gastrointestinal tract. If present, evaluation with  upper endoscopy  is warranted. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1798", "text": "There are no stool tests or blood tests specific for checkpoint inhibitor induced colitis. [ 1 ]  However, diagnostic evaluation should include ruling out infectious causes for diarrhea and colitis. [ 4 ]  Stool studies should include:  Clostridioides difficile toxin , bacterial culture, ova and parasites. Testing for  CMV infection  should be considered. [ 4 ]   Fecal calprotectin  may be helpful, and is very sensitive and specific for inflammation in the intestines. [ 4 ]  Elevations in fecal calprotectin correlate with the extent of intestinal inflammation. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1799", "text": "Computed tomography  (CT) imaging may show evidence of colitis, though the sensitivity is relatively low (50%). [ 1 ]  Free air in the peritoneum indicates bowel perforation. [ 1 ]  Abdominal imaging may be necessary to rule out toxic megacolon or perforation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1800", "text": "Though rare, gastrointestinal metastases (rare) should be considered as a cause of symptoms. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1801", "text": "Treatment varies depending on the severity of disease.  For mild disease, supportive care may be sufficient, including  loperamide  and a low residue or bland diet.  For more severe disease, the immune checkpoint inhibitor should be discontinued.   Corticosteroid  therapy is used to decrease inflammation, at a dose of roughly  prednisone  1\u20132\u00a0mg per kg of body weight per day. In cases that do not respond to corticosteroid therapy,  infliximab  may be used.  For cases that fail to respond to infliximab, or where infliximab is contraindicated,  vedolizumab  may be used. [ 8 ]  Overall, response rates from treatment are 59% for corticosteroids, 81% for infliximab, and 85% for vedolizumab. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1802", "text": "Surgery with resection of the colon ( colectomy ) is necessary in some instances, [ 10 ]  particularly if severe complications occur, such as perforation [ 1 ]  or toxic megacolon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1803", "text": "Fecal calprotectin, a stool test and marker of inflammation, may be used to follow improvement in colitis. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1804", "text": "The prevalence of checkpoint inhibitor induced colitis varies depending on the regimen of immunotherapy. The incidence is 0.7 \u2013 1.6% for anti- programmed cell death protein 1  (PD1) agents, 5.7 \u2013 9.1% for anti- cytotoxic T-lymphocyte associated protein 4  (CTLA-4), and about 13.6% for combination therapy. [ 2 ]  The risk associated with  ipilimumab  is  dose dependent , such that higher doses are associated with higher rates of colitis. [ 11 ]  However, other agents ( nivolumab  and  pembrolizumab ) are not associated with a dose dependent effect on the risk of immune mediated colitis. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1805", "text": "Risk factors for immune mediated colitis include  Caucasian race , treatment with an anti-CTLA4 based regimen, melanoma as cancer type, [ 3 ]   nonsteroidal anti-inflammatory drug  (NSAID) use, [ 8 ]  and a prior history of checkpoint inhibitor induced colitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1806", "text": "Chromoendoscopy  is a medical procedure wherein  dyes  (often the same  stains  used in  histology ) are instilled into the  gastrointestinal tract  at the time of visualization with fibre-optic  endoscopy . The purpose of chromoendoscopy is chiefly to enhance the characterization of  tissues , although dyes may be used for other functional purposes. The detail achieved with chromoendoscopy can often allow for identification of the tissue type or pathology based upon the pattern uncovered. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1807", "text": "Stains used in chromoendoscopy have three major mechanisms. Absorptive stains have an affinity for particular mucosal elements, and include  Lugol's iodine ,  methylene blue ,  toluidine blue  and  crystal violet  (gentian violet) . Lugol's iodine specifically stains non- keratinized   squamous   epithelium , and consequently is useful for identifying squamous tissue, squamous  dysplasia  and  squamous cell carcinomas . Methylene blue stains absorptive  epithelium  and is useful for identifying abnormality in the  small intestine  and  colon .  Barrett's esophagus  involves change in the mucosa of the  esophagus  into a tissue that includes glands ( intestinal metaplasia ), and as a result, can be identified with  methylene blue  staining. [ 2 ]  Also, methylene blue has been used to identify  dysplasia  in patients with  ulcerative colitis . [ 1 ]  Toluidine blue stains nuclei of malignant cells blue, and is used in oral and esophageal squamous cell carcinoma. Crystal violet is absorbed into intestinal and neoplastic cells and is used to identify Barrett's esophagus and colonic neoplasms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1808", "text": "Contrast stains are not absorbed but rather provide contrast by permeating between irregularities in the  mucosa  to highlight irregularities. The primary contrast stain is  indigo carmine , administered at varying concentrations between 0.1% and 0.8%. The chief utility of indigo carmine is in the identification of  dysplastic cells  in individuals with chronic  ulcerative colitis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1809", "text": "Reactive stains undergo an observable change due to a chemical process related to the function of the gastrointestinal tract.  Congo red  is used as a test for  achlorhydria  in the stomach, to test adequacy of vagotomy ( post adequate vagotomy, gastric acid secretion is abolished) and to detect presence of ectopic gastric tissue, as it changes colour from red to black at a pH less than 3. Should acid not be present in the stomach, it would remain red. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1810", "text": "The most common applications for chromoendoscopy are the following: identification of  squamous cell carcinomas  or  dysplasia  of the  esophagus , identification of  Barrett's esophagus  and dysplasia, identification of early  gastric cancer , characterization of  colonic polyps  and  colorectal cancer , and in screening for  dysplasia  in individuals with  ulcerative colitis . [ 1 ]  A Cochrane review updated in 2016 found strong evidence that chromoscopy enhances the detection of cancerous tumours in the colon and rectum when compared to plain colonoscopy. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1811", "text": "The dyes used for chromoendoscopy are typically considered to be safe. Some dyes such as  indigo carmine  may discolour the feces temporarily. Lugol's iodine when applied to the esophagus can lead to discomfort, inflammation (of the esophagus or stomach) or rarely allergy.  Sodium thiosulfate  has been used to avert this. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1812", "text": "The stains are typically applied to the  mucosal  lining of the gastrointestinal tract using a device known as a spray catheter that is inserted into the endoscope. Before staining, the mucosa may need to be treated with an agent to remove excess mucus to enhance staining.  N-acetylcysteine  and  acetic acid  are typically used for this purpose. One or two minutes after staining with the dye, the mucosa typically is washed with water to remove excess amounts of the dye, which can obscure visualization. Depending on the reason for which chromoendoscopy is being performed, the dye can be sprayed directly on a suspected abnormality (such as for identification of  squamous cell carcinoma ) or diffusely to the mucosa (such as for screening for  dysplasia  in  ulcerative colitis [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1813", "text": "When the stain is applied diffusely in the colon, a complete  colonoscopy  is performed with the instrument lying in the  cecum . The mucosa is washed and the dye is applied to tissue while the  endoscope  is retracted by 20 to 30 centimetres. That area of mucosa is characterized, and then the procedure is repeated in the next area of the colon that is more distal, until the procedure is completed. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1814", "text": "Stains can be used in conjunction with other techniques that allow for better identification of mucosa, such as  magnification   endoscopy . [ 1 ]  Various classification of \"pit patterns\" in the mucosa have been used to attempt to correlate to tissue type. The most commonly used rubric is the Kudo classification. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1815", "text": "Various other techniques have been used to delineate the mucosa of the gastrointestinal tract without the use of dyes.  Narrow-band imaging  is a technique where ambient light of a blue and green wavelengths are used to highlight detail, particularly of vascular structures. It has the advantage requiring only a change in light source, and is less cumbersome than instillation of dye. [ 1 ]  A similar technique to narrow-band imaging using blue and green filters has been used in endoscopes manufactured by  Fujinon , termed Fuji Intelligent Chromoendoscopy (FICE), and has been referred to as virtual chromoendoscopy. [ 6 ]  Other techniques that can enhance detail of mucosa include  confocal microscopy ,  magnification   endoscopy  and  optical coherence tomography . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1816", "text": "The  CIOMS/RUCAM scale  is a tool to predict whether  liver  damage can be attributed to a particular  medication ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1817", "text": "Determining  hepatotoxicity  (toxic effects of a substance on the liver) remains a major challenge in clinical practice due to lack of reliable markers. [ 1 ]  Many other conditions lead to similar clinical as well as pathological picture. To diagnose hepatotoxicity, a causal relationship between the use of the toxin or drug and subsequent liver damage has to be established, but might be difficult, especially when idiosyncratic reaction is suspected. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1818", "text": "The  CIOMS /RUCAM scale has been proposed to establish causal relationship between offending drug and liver damage. The CIOMS/RUCAM scale involves a scoring system which categorizes the suspicion into \"definite or highly probable\" (score > 8), \"probable\" (score 6-8), \"possible\" (score 3-5), \"unlikely\" (score 1-2) and \"excluded\" (score \u2264 0). In clinical practice physicians put more emphasis on the presence or absence of similarity between the biochemical profile of the patient and known biochemical profile of the suspected toxicity ( e.g. cholestatic damage in  amoxycillin-clauvonic acid  ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1819", "text": "The  Clichy criteria  are a group of criteria proposed in determining the survival of individuals with  acute liver failure . It was based on a study of patients presenting with viral hepatitis, of which individuals with the lowest survival were identified."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1820", "text": "Two criteria predicted the prognosis of patients with poor survival:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1821", "text": "The positive predictive value of mortality was 82% and the negative predictive value of mortality was 98% in individuals meeting these criteria."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1822", "text": "The  kidney bean sign  (more commonly called the  coffee bean sign;  also  bent inner tube sign ) is a  radiologic sign  observed on  abdominal radiographs  that indicates the presence of a  sigmoid volvulus , a form of bowel obstruction. It is seen as an area of hyperlucency resembling a coffee bean. [ 1 ]  The opposed walls of adjacent bowel loops form the central cleft while the two sides of the bean represent gas\u2010filled segments of dilated bowel that form an inverted U\u2010shape. [ 2 ]  Air-fluid levels may also be seen in the segments of dilated bowel. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1823", "text": "This  medical  diagnostic article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1824", "text": "Cystica profunda  is a rare disease of the gut lining. It is characterized by formation of  mucin   cysts  in the muscle layers of the gut lining, and it can occur anywhere along the  gastrointestinal tract . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1825", "text": "When the condition occurs in the stomach, it may be termed  gastritis cystica profunda , and in the small intestine,  enteritis cystica profunda . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1826", "text": "When it occurs in the  colon , it is termed  colitis cystica profunda . Colitis cystica profunda is benign, but it may mimic a tumor. [ 2 ]   When it occurs in the rectum it may be termed  colitis cystica  profunda , or termed  proctitis cystica profunda . Some consider this synonymous, or closely related to  solitary rectal ulcer syndrome , a consequence of  internal rectal intussusception . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1827", "text": "It can have benign columnar epithelium and mucosal cysts deep to the muscularis mucosa on microscopy. Hence it can be mistaken for an invasive adenocarcinoma. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1828", "text": "This article about an endocrine, nutritional, or metabolic disease is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1829", "text": "The  De Simone Formulation  is a  probiotic  formula and manufacturing method developed by Claudio De Simone. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1830", "text": "The De Simone Formulation has been  clinically studied  for a variety of health conditions since the 1990s [ 2 ]  but it has been researched the most for its efficacy in the medical management of chronic intestinal conditions including  irritable bowel syndrome  (IBS) [ 3 ] [ 4 ]  and  inflammatory bowel disease  (IBD). [ 5 ] [ 6 ] [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1831", "text": "The De Simone Formulation has been the subject of lawsuits. In the United States, the 4th U.S. Circuit Court of Appeals upheld a  false advertising  verdict against the makers of the VSL#3 probiotic in February 2021 stating there was enough evidence to support a jury's November 2018 finding that the makers of VSL#3 had quote \"reverse-engineered an imperfect copy\" of De Simone's signature probiotic formulation that was sold under the brand name VSL#3 through May 2016 after he withdrew from their joint venture, VSL Pharmaceuticals Inc. According to the lawsuit, his departure was as a result of being pressured to substitute cheaper bacteria in the manufacturing process to lower production costs and raise profits. [ 9 ]  Court action states that De Simone apparently refused. [ 10 ]  The makers of VSL#3 were ordered to pay De Simone and ExeGi Pharma a combined total of $18 million (USD) in damages. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1832", "text": "The Court also issued a permanent  injunction  intended to prevent claims, implied or stated, of continuity between the two different formulations.  The court also cited public health and wellbeing concerns, when they blocked the makers of VSL#3 from linking their product with the original De Simone Formulation by referring to  clinical studies  that were executed using the De Simone Formulation prior to May 2016. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1833", "text": "On August 1, 2019, the American Gastroenterology Association (AGA), the medical association of gastroenterologists in the United States, issued a correction regarding the De Simone Formulation and VSL#3.  AGA's correction stated it had referenced studies referenced in its 2019 Technical Review on the Management of Mild-to-Moderate Ulcerative Colitis that were based on the probiotic formulation previously know by the brand name VSL#3 before May 2016, but was now known by the formulation name 'De Simone Formulation'. [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1834", "text": "On January 24, 2022, the European Crohn's and Colitis Organization (ECCO) issued a letter to the editor of Oxford Academic's Journal of Crohn's and Colitis (JCC) stating that as a result of a court injunction, the ECCO must provide a clarification note for changes relating to VSL#3 and the De Simone Formulation in their articles that reference or studied these probiotics. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1835", "text": "Intestinal desmosis  is a medical condition implicated in gut motility disorder and chronic  constipation . Desmosis can be observed as the absence of the  tendinous  plexus layer and connective tissue fibers. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1836", "text": "The absence of the tendinous plexus layer was first described in 1998 by Meier-Ruge. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1837", "text": "Desmosis is implicated in disturbed gut  motility . [ 4 ]  Normal  peristalsis  depends upon the interaction between muscles, nerve cells and tendinous connective tissue. A malfunction of any of these leads to intestinal motility disorders. Patients with desmosis demonstrate chronic constipation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1838", "text": "Desmosis may be congenital (aplastic form) or acquired (atrophic form). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1839", "text": "The  aplastic [ 5 ]  form is rare. Typical clinical findings are hypoperistalsis, and pseudo-obstruction. These are found in premature infants, associated with low birth weight."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1840", "text": "The  atrophic [ 6 ]  form is more frequent. Inflammation of the muscularis propria releases  enzymes  including  collagenases  which destroy the connective tissue of the bowel wall. Primarily newborns and small children are affected, although this manifestation can also be found in adults. The most common location is the colon with a necrotizing enterocolitis as well as  Crohn Disease  and  diverticulitis . If the taenia are also affected, the disease is defined as complete atrophic desmosis, all other forms without involvement of the taenia are referred to as incomplete. Clinically, patients demonstrate chronic  constipation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1841", "text": "As proposed by Giuseppe Martucciello, [ 7 ]  microscopic diagnosis requires laparoscopic intestinal full-thickness biopsies from colon. Histological findings are absence of the tendinous plexus layer and connective tissue fibers in longitudinal and circular muscle layer. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1842", "text": "Proton pump inhibitors  (PPIs) block the gastric  hydrogen potassium ATPase  (H + /K +  ATPase) and inhibit gastric acid secretion. These drugs have emerged as the treatment of choice for acid-related diseases, including  gastroesophageal reflux disease  (GERD) and  peptic ulcer disease .\nPPIs also can bind to other types of proton pumps such as  those that occur in cancer cells and are finding applications in the reduction of cancer cell acid efflux and reduction of chemotherapy drug resistance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1843", "text": "Evidence emerged by the end of the 1970s that the newly discovered proton pump (H + /K +  ATPase) in the secretory membrane of the  parietal cell  was the final step in acid secretion. [ 1 ]  Literature from anaesthetic screenings led attention to the potential antiviral compound pyridylthioacetamide which after further examination pointed the focus on an anti-secretory compound with unknown mechanisms of action called  timoprazole . [ 2 ] [ 3 ] [ 4 ]  Timoprazole is a pyridylmethylsulfinyl  benzimidazole  and appealed due to its simple chemical structure and its surprisingly high level of anti-secretory activity. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1844", "text": "Optimization of substituted benzimidazoles and their antisecretory effects were studied on the newly discovered proton pump to obtain higher  pKa  values of the  pyridine , thereby facilitating accumulation within the parietal cell and increasing the rate of acid-mediated conversion to the active mediate. As a result of such optimization the first proton pump inhibiting drug,  omeprazole , was released on the market. [ 4 ] [ 6 ] \nOther PPIs like  lansoprazole  and  pantoprazole  would follow in its footsteps, claiming their share of a flourishing market, after their own course of development. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1845", "text": "PPIs can be divided into two groups based on their basic structure. Although all members have a  substituted  pyridine part, one group has linked to various benzimidazoles, whereas the other has linked to a substituted imidazopyridine. All marketed PPIs (omeprazole, lansoprazole, pantoprazole) are in the benzimidazole group. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1846", "text": "Proton pump inhibitors are  prodrugs  and their actual inhibitory form is somewhat controversial. In acidic solution, the  sulfenic acid  is isolated before reaction with one or more cysteines accessible from the  luminar  surface of the  enzyme , a tetracyclic sulfenamide. This is a planar molecule thus any enantiomer of a PPI loses stereospecifity upon activation. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1847", "text": "The effectiveness of these drugs derives from two factors: their target, the H + /K +  ATPase which is responsible for the last step in acid secretion; therefore, their action on acid secretion is independent of the stimulus to acid secretion, of  histamine ,  acetylcholine , or other yet to be discovered stimulants. In addition, their mechanism of action involves  covalent binding  of the activated drug to the enzyme, resulting in a duration of action that exceeds their plasma  half-life . [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1848", "text": "Acid secretion by the human  stomach  results in a median  diurnal   pH  of 1.4. This very large (>10 6 -fold) H +   gradient  is generated by the gastric H + /K +  ATPase which is an ATP-driven proton pump. Hydrolysis of one ATP molecule is used to catalyse the electroneutral exchange of two luminal  potassium  ions for two  cytoplasmic   protons  through the gastric membrane. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1849", "text": "The proton pump, H + /K +  ATPase is a \u03b1,\u03b2-heterodimeric enzyme. The  catalytic  \u03b1 subunit has ten  transmembrane  segments with a cluster of intramembranal  carboxylic   amino acids  located in the middle of the transmembrane segments TM4, TM5, TM6 and TM8. The \u03b2 subunit has one transmembrane segment with  N terminus  in cytoplasmic region. The  extracellular   domain  of the \u03b2 subunit contains six or seven  N -linked  glycosylation  sites which is important for the enzyme assembly, maturation and sorting. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1850", "text": "The ion transport is accomplished by cyclical conformational changes of the enzyme between its two main  reaction  states, E1 and E2. The cytoplasmic-open E1 and luminal-open E2 states have high affinity for H +  and K + . [ 9 ]  The expulsion of the proton at 160  mM  (pH 0.8)  concentration  results from movement of  lysine  791 into the  ion  binding site in the E2P configuration. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1851", "text": "In the year 1975, timoprazole was found to inhibit acid secretion irrespective of stimulus, extracellular or intracellular. [ 7 ]  Studies on timoprazole revealed enlargement of the  thyroid gland  due to  inhibition  of  iodine  uptake as well as  atrophy  of the  thymus  gland. A literature search showed that some  substituted  mercapto-benzimidazoles had no effect on iodine uptake and introduction of such substituents into timoprazole resulted in an elimination of the toxic effects, without reducing the antisecretory effect. [ 6 ]  A derivative of timoprazole, omeprazole, was discovered in 1979, and was the first of a new class of drug that control acid secretion in the stomach, a proton pump inhibitor (PPI). [ 11 ] [ 12 ]  Addition of 5-methoxy-substitution to the benzimidazole moiety of omeprazole was also made and gave the compound much more stability at neutral pH. [ 6 ]  In 1980, an Investigational New Drug (IND) application was filed and omeprazole was taken into Phase III human trials in 1982. [ 6 ]  A new approach for the treatment of acid-related diseases was introduced, and omeprazole was quickly shown to be clinically superior to the  histamine H 2  receptor antagonists , and was launched in 1988 as Losec in Europe, and in 1990 as Prilosec in the United States. In 1996, Losec became the world's biggest ever selling pharmaceutical, and by 2004 over 800 million patients had been treated with the drug worldwide. During the 1980s, about 40 other companies entered the PPIs area, but few achieved market success:  Takeda  with lansoprazole, Byk Gulden (now  Nycomed ) with pantoprazole, and  Eisai  with rabeprazole, all of which were analogues of omeprazole. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1852", "text": "The story of pantoprazole's discovery is a good example of the stepwise development of PPIs. The main focus of modification of timoprazole was the benzimidazole part of its structure. Addition of a  trifluoromethyl  group to the benzimidazole  moiety  led to a series of very active compounds with varying solution-stability. In general fluoro substituents were found to block  metabolism  at the point where they were attached. Later the more balanced fluoroalkoxy substituent, instead of the highly  lipophilic  and strongly electron-withdrawing trifluoromethyl substituent, led to highly active compounds with supposed longer half-lives and higher solution stability. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1853", "text": "It was realized that activity was somehow linked to instability in solution and then came to the conclusion that the cyclic sulfenamides, formed in acidic conditions, were the active principle of the PPIs. Finally, it was understood that seemingly small alterations in the backbone of timoprazole led nowhere, and focus had to be centered on the substituents on the backbone. However, necessary intramolecular rearrangement of the benzimidazole into sulfenamide posed severe  geometric  constraints. Optimal compounds would be those that were stable at neutral pH but were quickly activated at low pH. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1854", "text": "A clear-cut design of active inhibitors was still not possible because in the complex multi-step chemistry the influence of a substituent on each step in the cascade could be different, and therefore not predictable for the overall rate of the prerequisite acid activation. Smith Kline and French, that entered into collaboration with Byk Gulden mid-1984, greatly assisted in determining criteria for further development. From 1985, the aim was to identify a compound with good stability at neutral pH, sustaining this higher level of stability down to pH 5 but being rapidly activateable at lower pHs, combined with a high level of H + /K +  ATPase inhibition. [ 13 ]  From the numerous already synthesized and tested compounds that fulfilled these criteria the most promising candidates were pantoprazole and its salt, pantoprazole sodium. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1855", "text": "In 1986 pantoprazole sodium sesquihydrate was synthesized and from 1987 onwards the development of pantoprazole was switched to the sodium salt which is more stable and has better compatibility with other excipients used in the drug formulation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1856", "text": "Pantoprazole was identified after nearly seven years of research and registered for clinical use after a further seven years of development, and finally reached its first market in 1994 in Germany. During the course of the studies on pantoprazole, more than 650 PPIs had been synthesized and evaluated. [ 5 ]  Pantoprazole obtained high selection criteria in its development process\u00a0\u2014\u00a0especially concerning the favorable low potential for interaction with other drugs. Good solubility of pantoprazole and a very high solution stability allowed it to become the first marketed PPI for intravenous use in critical care patients. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1857", "text": "Omeprazole showed an inter-individual variability and therefore a significant number of patients with acid-related disorders required higher or multiple doses to achieve symptom relief and healing. Astra started a new research program in 1987 to identify a new analogue to omeprazole with less interpatient variability. Only one compound proved superior to omeprazole and that was the ( S )-(\u2212)-isomer, esomeprazole, which was developed as the magnesium salt. Esomeprazole magnesium (brand name Nexium) received its first approval in 2000 and provided more pronounced inhibition of acid secretion and less inter-patient variation compared to omeprazole. In 2004, Nexium had already been used to treat over 200 million patients. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1858", "text": "Omeprazole was the first PPI on the market, in 1988. It is a 1:1 racemate drug with a backbone structure of timoprazole, but substituted with two methoxy and two methyl groups. One of the methoxy group is at position 6 of the bensoimidazole and the other at position 4 of the pyridine and the methyl groups are at position 3 and 5 of the pyridine.\nOmeprazole is available as enteric-coated  tablets ,  capsules , chewable tablets,  powder  for oral  suspensions  and powder for  intravenous injection . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1859", "text": "Lansoprazole was the second of the PPI drugs to reach the market, being launched in Europe in 1991 and the US in 1995.\nIt has no substitutions at the benzimidazole  but two substituents on the pyridine, methyl group at position 3 and a trifluoroethoxy group at position 4. The drug is a 1:1  racemate  of the  enantiomers  dexlansoprazole and levolansoprazole. It is available in gastroresistant capsules and tablets as well as chewable tablets. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1860", "text": "Pantoprazole was the third PPI and was introduced to the German market in 1994.\nIt has a difluoroalkoxy sidegroup on the benzimidazole part and two methoxy groups in position 3 and 4 on the pyridine.\nPantoprazole was first prepared in April 1985 by a small group of scale-up chemists. It is a dimethoxy-substituted pyridine bound to a fluoroalkoxy substituted benzimidazole. [ 5 ] \nPantoprazole sodium is available as gastroresistant or delayed release tablets and as lyophilized powder for intravenous use."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1861", "text": "Rabeprazole is a novel benzimidazole compound on market, since 1999 in USA. It is similar to lansoprazole in having no substituents on its benzimidazole part and a methyl group at site 3 on the pyridine, the only difference is the methoxypropoxy substitution at site 4 instead of the trifluoroethoxy group on lansoprazole.\nRabeprazole is marketed as rabeprazole sodium salt. It is available as enteric-coated tablets. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1862", "text": "In 2001 esomeprazole was launched in USA, as a follow-up of omeprazoles patent.\nEsomeprazole is the ( S )-(\u2212)-enantiomer of omeprazole and provides higher  bioavailability  and improved  efficacy , in terms of stomach acid control, over the ( R )-(+)-enantiomer of omeprazole. In theory, by using pure esomeprazole the effects on the proton pump will be equal in all patients, eliminating the \"poor metabolizer effect\" of the racemate omeprazole. It is available as delayed-release capsules or tablets and as esomeprazole sodium for intravenous injection/infusion. Oral esomeprazole preparations are enteric-coated, due to the rapid degradation of the drug in the acidic condition of the stomach. This is achieved by formulating capsules using the multiple-unit pellet system.\nAlthough the ( S )-(\u2212)- isomer  is more potent in humans, the ( R )-(+)-isomer is more potent in testings of rats, while the enantiomers are equipotent in dogs. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1863", "text": "Dexlansoprazole was launched as a follow up of lansoprazole in 2009.\nDexlansoprazole is an ( R )-(+)-enantiomer of lansoprazole, marketed as Dexilant. After oral appliance of the racemic lansoprazole, the circulating drug is 80% dexlansoprazole. Moreover, both enantiomers have similar effects on the proton pump. [ 15 ]  Consequently, the main advantage of Dexilant is not the fact that it is an enantiopure substance. The advantage is the pharmaceutical formulation of the drug, which is based on a dual release technology, with the first quick release producing a  blood plasma  peak concentration about one hour after application, and the second retarded release producing another peak about four hours later. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1864", "text": "Tenatoprazole (TU-199), an  imidazopyridine  proton pump inhibitor, is a novel compound that has been designed as a new chemical entity with a substantially prolonged plasma half-life (7 hours), but otherwise has similar activity as other PPIs. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1865", "text": "The difference in the structural backbone of tenatoprazole compared to benzimidazole PPIs, is its imidazo[4,5-b]pyridine moiety, which reduces the rate of metabolism, allowing a longer plasma residence time but also decreases the pKa of the fused imidazole  N  as compared to the current PPIs. [ 18 ]  Tenatoprazole has the same substituents as omeprazole, the methoxy groups at position 6 on the imidazopyridine and at position 4 on the pyridine part as well as two methyl groups at position 3 and 5 on the pyridine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1866", "text": "The bioavailability of tenatoprazole is double for the ( S )-(\u2212)-tenatoprazole sodium salt  hydrate  form when compared to the free form in dogs. This increased bioavailability is due to differences in the  crystal structure  and  hydrophobic  nature of the two forms, and therefore its more likely to be marketed as the pure ( S )-(\u2212)-enantiomer. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1867", "text": "The disulfide binding of the inhibitor takes place in the luminal sector of the H + /K +  ATPase were 2\u00a0mol of inhibitor is bound per 1\u00a0mol of active site H + /K +  ATPase. [ 19 ] [ 20 ] \nAll PPIs react with cysteine 813 in the loop between TM5 and TM6 on the H + /K +  ATPase, fixing the enzyme in the E2 configuration. Omeprazole reacts with cysteine 813 and 892. Rabeprazole binds to cysteine 813 and both 892 and 321. Lansoprazole reacts with cysteine 813 and cysteine 321, whereas pantoprazole and tenatoprazole react with cysteine 813 and 822. [ 18 ] [ 21 ] [ 22 ] [ 23 ] \n Reaction  with cysteine 822 confers a rather special property to the covalently inhibited enzyme, namely  irreversibility  to  reducing  agents. The likely first step is binding of the prodrug protonated on the pyridine of the compound with cysteine 813. Then the second proton is added with acid transport by the H + /K +  ATPase, and the compound is activated. Recent data suggest the hydrated sulfenic acid to be the reactive species forming directly from the mono-protonated benzimidazole bound on the surface of the pump. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1868", "text": "Even though consumption of food stimulates acid secretion and acid secretion activates PPIs, PPIs cannot inhibit all pumps. About 70% of pump enzyme is inhibited, as PPIs have a short half-life and not all pump enzymes are activated. It takes about 3 days to reach steady-state inhibition of acid secretion, as a balance is struck between covalent inhibition of active pumps, subsequent stimulation of inactive pumps after the drug has been eliminated from the blood, and  de novo  synthesis of new pumps. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1869", "text": "Although the drugs omeprazole, lansoprazole, pantoprazole, and rabeprazole share common structure and mode of action, each differs somewhat in its clinical pharmacology. [ 24 ] \nDiffering pyridine and benzimidazole substituents result in small, but potentially significant different physical and chemical properties.\nDirect comparison of pantoprazole sodium with other anti-secretory drugs showed that it was significantly more effective than H 2 -receptor antagonists and either equivalent or better than other clinically used PPIs. [ 5 ]  Another study states rabeprazole undergoes activation over a greater pH range than omeprazole, lansoprazole, and pantoprazole, and converts to the sulphenamide form more rapidly than any of these three drugs. [ 23 ] \nMost oral PPI preparations are enteric-coated, due to the rapid degradation of the drugs in the acidic conditions of the stomach. For example omeprazole is unstable in acid with a half-life of 2 min at pH 1\u20133, but is significantly more stable at pH 7 (half-life ca. 20 h).\nThe acid protective coating prevents conversion to the active principle in the lumen of the stomach, which then will react with any available sulfhydryl group in food and will not penetrate to the lumen of the secretory canaliculus [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1870", "text": "The oral bioavailability of PPIs is high; 77% for pantoprazole, 80\u201390% for lansoprazole and 89% for esomeprazole. All the PPIs except tenatoprazole are rapidly metabolized in the liver by CYP enzymes, mostly by  CYP2C19  and  CYP3A4 . PPIs are sensitive to CYP enzymes and have different pharmacokinetic profiles. Studies comparing the efficacy of PPIs indicate that esomeprazole and tenatoprazole have stronger acid suppression, with a longer period of intragastric pH (pH > 4). [ 25 ] [ 26 ] [ 27 ] [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1871", "text": "Studies of the effect of tenatoprazole on acid secretion in  in vivo  animal models, such as pylorus-ligated rats and acute gastric fistula rats, demonstrated a 2- to 4-fold more potent inhibitory activity compared with omeprazole. A more potent inhibitory activity was also shown in several models of induced gastric lesions. [ 30 ]  In Asian as well as Caucasian healthy subjects, tenatoprazole exhibited a seven-fold longer half-life than the existing H + /K +  ATPase inhibitors. [ 31 ]  It is thus hypothesized that a longer half-life results in a more prolonged inhibition of gastric acid secretion, especially during the night.\nA strong relationship has been stated between the degree and duration of gastric acid inhibition, as measured by monitoring of the 24-hour intragastric pH in pharmacodynamic studies, and the rate of healing and symptom relief reported.\nA clinical study showed that nocturnal acid breakthrough duration was significantly shorter for 40\u00a0mg of tenatoprazole than for 40\u00a0mg of esomeprazole, with the conclusion that tenatoprazole was significantly more potent than esomeprazole during the night. Although, the therapeutic relevance of this pharmacological advantage deserves further study. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1872", "text": "PPIs have been used successfully in triple-therapy regiments with  clarithromycin  and  amoxicillin  for the  eradication of  Helicobacter pylori  with no significant difference between different PPI-based regimens. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1873", "text": "Despite the fact that PPIs have revolutionized the treatment of  GERD , there is still room for improvement in the speed of onset of acid suppression as well as mode of action that is independent of an acidic environment and also better inhibition of the proton pump. [ 8 ]  Therefore, a new class of PPIs,  potassium-competitive acid blockers  (P-CABs) or  acid pump antagonists  (APAs), have been under development the past years and will most likely be the next generation of drugs that suppress gastric activity. [ 32 ]  These new agents can in a reversible and competitive fashion inhibit the final step in the gastric acid secretion with respect to K +  binding to the parietal cell gastric H + /K +  ATPase. That is, they block the action of the H + /K +  ATPase by binding to or near the site of the K +  channel. Since the binding is competitive and reversible these agents have the potential to achieve faster inhibition of acid secretion and longer duration of action compared to PPIs, resulting in quicker symptom relief and healing. [ 33 ] [ 34 ]  The  imidazopyridine -based compound SCH28080 was the prototype of this class, and turned out to be hepatotoxic. [ 35 ]  Newer agents that are currently in development include  CS-526 ,  linaprazan ,  soraprazan  and  revaprazan  in which the latter have reached clinical trials. Studies remain to determine whether these or other related compounds can become useful. [ 34 ] [ 36 ]  In June 2006,  Yuhan  obtained approval from the Korean FDA for the use of  revaprazan  (brand name Revanex) in the treatment of gastritis. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1874", "text": "Vonoprazan  is a newer agent with a faster and longer lasting action, first marketed in Japan, then in Russia, and in 2023 was approved for use in the US. It is still being trialed in the UK. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1875", "text": "Dolichocolon  is an abnormally long  large intestine . [ 1 ]  It should not be confused with an abnormally wide large intestine, which is called a  megacolon . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1876", "text": "Dolichocolon may predispose to abnormal rotation (see  volvulus ) and interposition between the diaphragm and the liver (see  Chilaiditi syndrome ). It is more commonly seen in the  elderly , some psychiatric patients or in institutionalised individuals. It is not, however, a part of normal aging. The exact cause remains unknown. Dolichocolon is often an incidental finding on  abdominal X-rays  or  colonoscopy . It is not by itself a disease and as such requires no treatment. The term is from  ancient Greek   dolichos , the long distance in running, and  colon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1877", "text": "Endoanal ultrasound  is a type of medical investigation which images the structures of the  anal canal . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1878", "text": "It is used in the investigation of some anorectal symptoms, e.g.  fecal incontinence  or  obstructed defecation . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1879", "text": "This article related to  medical imaging  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1880", "text": "An  endoclip  is a metallic mechanical device used in  endoscopy  in order to close two mucosal surfaces without the need for surgery and  suturing .  Its function is similar to a  suture  in gross surgical applications, as it is used to join together two disjointed surfaces, but, can be applied through the channel of an endoscope under direct visualization.  Endoclips have found use in treating  gastrointestinal bleeding  (both in the  upper  and  lower GI tract ), in preventing bleeding after therapeutic procedures such as  polypectomy , and in closing  gastrointestinal perforations .  Many forms of endoclips exist of different shapes and sizes, including two and three prong devices, which can be administered using single use and reloadable systems, and may or may not open and close to facilitate placement."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1881", "text": "The endoclip was first described by Hayashi and Kudoh in 1975, [ 1 ]   and was termed the \"staunch clip\".  Initial attempts to incorporate the clip into applications in endoscopy (such as clipping bleeding  blood vessels ) were limited by the applicator system of the clip. [ 1 ]   However, by 1988, an easy to use applicator delivery system was developed, and a functional reloadable endoclip system was described. [ 2 ]   This consisted of a stainless steel clip (of size approximately 6\u00a0mm long and 1.2\u00a0mm wide at the prongs) with a metal deployment device (that could be used to insert the clip into the endoscopic camera, and deployed outside the camera) enclosed in a plastic sheath. [ 1 ]   These clips were initially reloadable. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1882", "text": "Endoclips in use today have a variety of additional shapes and sizes than the original.  Clips with two and three prongs (TriClip,  Cook Medical [ 3 ] ) have been described and used for various applications. [ 4 ]   Rotatable clips have been devised to improve localization of deployment. [ 5 ]   Also, clips that open and close (as opposed to single-deployment) have also been developed (Resolution Clip,  Boston Scientific [ 6 ] ), and also facilitate the appropriate location of deployment. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1883", "text": "When a treatable lesion is identified on  endoscopy  (such as a bleeding vessel), an endoclip can be inserted through the channel of the endoscope until the sheathed clip is visible on the endoscopic image, and the handle for deployment handed to the  nurse  assistant.  The clip is unsheathed by retraction at the handle, positioned, and \"fired\" by the assistant to treat the lesion. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1884", "text": "Endoclips have found a primary application in  hemostasis  (or the stopping of bleeding) during  endoscopy  of the upper (through  gastroscopy ) or lower (through  colonoscopy ) gastrointestinal tract. [ 1 ]   Many bleeding lesions have been successfully clipped, including bleeding  peptic ulcers , [ 4 ]   Mallory-Weiss tears  of the  esophagus , [ 8 ]   Dieulafoy's lesions , [ 9 ]   stomach tumours , [ 10 ]  and bleeding after  removal of polyps . [ 11 ]   Bleeding peptic ulcers require endoscopic treatment if they show evidence of high risk stigmata of re-bleeding, such as evidence of active bleeding or oozing on  endoscopy  or the presence of a visible blood vessel around the ulcer. [ 12 ] [ 13 ]   The alternatives to endoscopic clipping of peptic ulcers are thermal therapy (such as  electrocautery  to burn the vessel causing the bleeding), or injection of  epinephrine  to constrict the blood vessel.  Comparative studies between endoclips and thermal therapy make the point that endoclips cause less trauma to the  mucosa  around the ulcer than electrocautery, [ 14 ]  but no definitive advantage to either approach has reached consensus by  gastroenterologists . [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1885", "text": "Endoclips have also found an application in preventing bleeding when performing complicated endoscopic procedures.  For example, prophylactic clipping of the base of a polyp has been found to be useful in preventing post- polypectomy  bleeding, especially in high-risk patients or patients on  anticoagulant  medications. [ 17 ]   In addition, clips can be used to close  gastrointestinal perforations  that may have been caused by complicated therapeutic endoscopy procedures, such as  polypectomy , or by the endoscopic procedure itself. [ 18 ]   Clips have also been used to secure the placement of endoscopic  feeding tubes , [ 19 ]  and to orient the  bile duct  to assist with  endoscopic retrograde cholangiopancreatography , a procedure used to image to bile duct. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1886", "text": "Endoclips have been seen to dislodge between 1 and 3 weeks from deployment, [ 21 ]  although lengthy clip retention intervals of as high as 26 months have been reported. [ 1 ] [ 9 ]   Endoclips are believed to be safe and no major complications (such as perforation or impaction) have been reported with them, although concern has been raised about blocking the outflow of the bile duct if clips are deployed in the  duodenum . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1887", "text": "An  endoscopy unit  refers to a dedicated area where medical procedures are performed with  endoscopes , which are cameras used to visualize structures within the body, such as the  digestive tract  and  genitourinary system .  Endoscopy units may be located within a  hospital , incorporated within other medical care centres, or may be stand-alone in nature."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1888", "text": "In the early days of endoscopy, when fewer procedures were carried out, facilities such as  operating theatres  tended to be used; as the number of procedures carried out and the complexity of the procedures and equipment increased, the need for specialised rooms and staff became apparent. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1889", "text": "An endoscopy unit consists of the following components: trained and accredited endoscopists (which are usually  gastroenterologists  or  surgeons ); trained nursing and additional staff; endoscopes and other equipment; preparation, procedural and recovery areas; a disinfection and cleaning area for equipment; emergency equipment and personnel; and, a program for quality assurance.  [ 2 ]   Procedures performed within an endoscopy unit may include gastrointestinal endoscopy (such as  gastroscopy ,  colonoscopy ,  ERCP , and  endoscopic ultrasound ),  bronchoscopy ,  cystoscopy , or other more specialized procedures.  Endoscopy units may be part of a hospital, where emergency procedures may be performed on ill patients admitted to hospital; however, most endoscopies are performed on ambulatory patients in the outpatient setting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1890", "text": "Endoscopy units consist of a number of areas: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1891", "text": "These are the rooms where the endoscopic procedures are performed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1892", "text": "Procedure rooms should to contain: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1893", "text": "Procedure rooms should be at least 200 square feet (19\u00a0m 2 ) in size, and hospitals should have at least two procedure rooms. Larger endoscopy units should contain one procedure room per 1,000 to 1,500 procedures performed annually. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1894", "text": "Since a number of patients undergoing endoscopy receive sedation, and a few emergency patients may be unstable, there must be an area available for the observation of patients until they have recovered. These areas also need to have piped oxygen, full monitoring facilities (including pulse oximetry), suction,  resuscitation equipment  and emergency drugs. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1895", "text": "An  enema , also known as a  clyster , is an injection of fluid into the rectum or into  lower bowel  by way of the  rectum . [ 1 ]  The word  enema  can also refer to the liquid injected, [ 2 ] [ 3 ]  as well as to a device for administering such an injection. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1896", "text": "In standard medicine, the most frequent uses of enemas are to relieve constipation and for bowel cleansing before a medical examination or procedure; [ 5 ]  also, they are employed as a  lower gastrointestinal series  (also called a barium enema), [ 6 ]  to treat  traveler's diarrhea , [ 7 ]  as a vehicle for the administration of food, water or medicine, as a stimulant to the general system, as a local application and, more rarely, as a means of reducing body temperature, [ 1 ]  as treatment for  encopresis , and as a form of  rehydration therapy  (proctoclysis) in patients for whom  intravenous therapy  is not applicable. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1897", "text": "The principal medical usages of enemas are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1898", "text": "As  bowel  stimulants, enemas are employed for the same purposes as orally administered  laxatives : to relieve  constipation ; to treat  fecal impaction ; to empty the colon prior to a medical procedure such as a  colonoscopy . When oral laxatives are not indicated or are not sufficiently effective, enemas may be a sensible and necessary measure. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1899", "text": "A large volume enema [ 10 ]  can be given to cleanse as much of the colon as possible of feces. [ 11 ] [ 12 ]  However, a low enema is generally useful only for stool in the rectum, not in the intestinal tract. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1900", "text": "Such enemas' mechanism consists of the volume of the liquid causing a rapid expansion of the intestinal tract in conjunction with, in the case of certain solutions, irritation of the intestinal  mucosa  which stimulates peristalsis and lubricates the stool to encourage a bowel movement. [ 14 ]  An enema's efficacy depends on several factors including the volume injected and the temperature and the contents of the infusion. [ 9 ]  In order for the enema to be effective the patient should retain the solution for five to ten minutes, as tolerated. [ 5 ] [ 14 ]  or, as some nursing textbooks recommend, for five to fifteen minutes or as long as possible. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1901", "text": "For emptying the entire colon as much as feasible [ 12 ]  deeper and higher enemas are utilized to reach large sections of the colon. [ 9 ]  The colon dilates and expands when a large volume of liquid is injected into it, and the colon reacts to that sudden expansion with general contractions,  peristalsis , propelling its contents toward the rectum. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1902", "text": "Soapsuds enema  is a frequently used synonym for a large volume enema (although soap is not necessary for effectivity). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1903", "text": "For relieving occasional constipation, a large volume enema may be used in a home setting, although for recurring or severe cases of constipation medical care may be required. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1904", "text": "Plain water can be used, simply functioning mechanically to expand the colon, thus prompting evacuation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1905", "text": "Normal saline  is least irritating to the colon. Like plain water, it simply functions mechanically to expand the colon, but having a neutral concentration gradient, it neither draws  electrolytes  from the body, as happens with plain water, nor draws water into the colon, as occurs with phosphates. Thus, a salt water solution can be used when a longer period of retention is desired, such as to soften an impaction."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1906", "text": "Castile soap  is commonly added because its irritation of the colon's lining increases the urgency to defecate. [ 15 ]  However, liquid handsoaps and detergents should not be used. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1907", "text": "Glycerol  is a specific bowel mucosa irritant serving to induce peristalsis via a  hyperosmotic effect . [ 16 ]  It is used in a dilute solution, e.g., 5%. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1908", "text": "Equal parts of milk and molasses heated together to slightly above normal body temperature have been used. [ 18 ]  Neither the milk sugars and proteins nor the molasses are absorbed in the lower intestine, thus keeping the water from the enema in the intestine. [ 19 ]  Studies have shown that milk and molasses enemas have a low complication rate when used in the  emergency department [ 20 ]  and are safe and effective with minimal side effects. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1909", "text": "Mineral oil  functions as a lubricant and stool softener, but may have side effects including rectal skin irritation and leakage of oil. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1910", "text": "ATC code A06   Drugs for constipation  is a therapeutic subgroup of the  Anatomical Therapeutic Chemical Classification System , a system of alphanumeric codes developed by the  World Health Organization  (WHO) for the classification of  drugs  and other medical products. [ 23 ] [ 24 ] [ 25 ]  Subgroup A06 is part of the anatomical group  A  Alimentary tract and metabolism . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1911", "text": "Codes for  veterinary  use ( ATCvet codes ) can be created by placing the letter Q in front of the human ATC code: for example,  QA06 . [ 27 ]   National issues of the ATC classification may include additional codes not present in this list, which follows the WHO version."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1912", "text": "In alphabetical order"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1913", "text": "In alphabetical order of the original brand names"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1914", "text": "Klyx contains  docusate sodium  1\u00a0mg/mL and sorbitol solution (70%)(crystallising) 357\u00a0mg/mL and is used for faecal impaction or constipation or for colon evacuation prior medical procedures, [ 44 ]  developed by  Ferring B.V."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1915", "text": "Micralax (not to be confused with MICROLAX\u00ae) [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1916", "text": "MICROLAX\u00ae  (not to be confused with Micralax) combines the action of  sodium citrate , a peptidising agent which can displace bound water present in the faeces, with sodium alkyl sulphoacetate, a wetting agent, and with glycerol, an anal mucosa irritant and hyperosmotic. However, also sold under the name \"Micralax\", is a preparation containing  sorbitol  rather than glycerol; [ 46 ]  which was initially tested in preparation for  sigmoidoscopy . [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1917", "text": "Micolette Micro-enema\u00ae contains 45\u00a0mg sodium lauryl sulphoacetate, 450\u00a0mg per 5 ml sodium citrate BP, and 625\u00a0mg glycerol BP [ 48 ]  and is a small volume stimulant enema suitable where large-volume enemas are contra-indicated. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1918", "text": "TAI , also termed  retrograde irrigation , is designed to assist evacuation using a water enema [ 49 ]  as a treatment for persons with bowel dysfunction, including  fecal incontinence  or constipation, especially  obstructed defecation . By regularly emptying the bowel using transanal irrigation, [ 50 ]  controlled bowel function is often re-established to a high degree, thus enabling development of a consistent bowel routine. [ 50 ]   Its effectiveness varies considerably, some individuals experiencing complete control of incontinence but others reporting little or no benefit. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1919", "text": "An international consensus on when and how to use transanal irrigation for people with bowel problems was published in 2013, offering practitioners a clear, comprehensive and simple guide to practice for the emerging therapeutic area of transanal irrigation. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1920", "text": "The term  retrograde irrigation  distinguishes this procedure from the  Malone antegrade continence enema , where irrigation fluid is introduced into the colon proximal to the anus via a surgically created irrigation port. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1921", "text": "Patients who have a bowel disability, a medical condition which impairs control of  defecation , e.g., fecal incontinence or constipation, [ 52 ]  can use bowel management techniques to choose a predictable time and place to evacuate. [ 52 ]  Without bowel management, such persons might either suffer from the feeling of not getting relief, or they might soil themselves. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1922", "text": "While simple techniques might include a controlled  diet  and establishing a toilet routine, [ 52 ]  a daily enema can be taken to empty the colon, thus preventing unwanted and uncontrolled bowel movements that day. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1923", "text": "In a  lower gastrointestinal series  an enema that may contain  barium sulfate  powder or a water-soluble  contrast agent  is used in the  radiological  imaging of the bowel. Called a  barium enema , such enemas are sometimes the only practical way to  view  the colon in a relatively safe manner. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1924", "text": "Failure to expel all of the barium may cause constipation or possible impaction [ 54 ]  and a patient who has no bowel movement for more than two days or is unable to pass gas rectally should promptly inform a physician and may require an enema or laxative. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1925", "text": "The administration of substances into the bloodstream. This may be done in situations where it is undesirable or impossible to deliver a medication by mouth, such as  antiemetics  given to reduce  nausea  (though not many antiemetics are delivered by enema). Additionally, several anti-angiogenic agents, which work better without digestion, can be safely administered via a gentle enema."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1926", "text": "The topical administration of medications into the rectum, such as  corticosteroids  and  mesalazine  used in the treatment of  inflammatory bowel disease . Administration by enema avoids having the medication pass through the entire  gastrointestinal tract , therefore simplifying the delivery of the medication to the affected area and limiting the amount that is absorbed into the bloodstream."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1927", "text": "Rectal corticosteroid enemas are sometimes used to treat mild or moderate ulcerative colitis. They also may be used along with systemic (oral or injection) corticosteroids or other medicines to treat severe disease or mild to moderate disease that has spread too far to be treated effectively by medicine inserted into the rectum alone."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1928", "text": "Improper administration of an enema can cause electrolyte imbalance (with repeated enemas) or ruptures to the bowel or rectal tissues which can be unnoticed as the rectum is insensitive to pain, [ 66 ]  resulting in internal  bleeding . However, these occurrences are rare in healthy,  sober  adults. Internal bleeding or rupture may leave the individual exposed to infections from intestinal bacteria. Blood resulting from tears in the colon may not always be visible, but can be distinguished if the feces are unusually dark or have a red hue. If intestinal rupture is suspected, medical assistance should be obtained immediately. [ 14 ]  Frequent use of enemas can cause laxative dependency. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1929", "text": "The enema tube and solution may stimulate the  vagus nerve , which may trigger an  arrhythmia  such as  bradycardia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1930", "text": "Enemas should not be used if there is an undiagnosed  abdominal pain  since the peristalsis of the bowel can cause an inflamed  appendix  to  rupture ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1931", "text": "There are arguments both for and against colonic irrigation in people with  diverticulitis ,  ulcerative colitis ,  Crohn's disease , severe or internal  hemorrhoids  or  tumors  in the rectum or  colon , and its usage is not recommended soon after bowel  surgery  (unless directed by one's  health care provider ). Regular treatments should be avoided by people with  heart disease  or  kidney failure . Colonics are inappropriate for people with bowel, rectal or anal  pathologies  where the pathology contributes to the risk of  bowel perforation . [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1932", "text": "Recent research has shown that ozone water, which is sometimes used in enemas, can immediately cause  microscopic colitis . [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1933", "text": "A recent case series [ 70 ]  of 11 patients with five deaths illustrated the danger of phosphate enemas in high-risk patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1934", "text": "Enema  entered the English language c. 1675 from Latin in which, in the 15th century, [ 3 ]  it was first used in the sense of a rectal injection, [ 2 ]  from Greek \u1f14\u03bd\u03b5\u03bc\u03b1 (\u00e9nema), \"injection\", itself from \u1f10\u03bd\u03b9\u03ad\u03bd\u03b1\u03b9 (enienai) \"to send in, inject\", from \u1f10\u03bd (en), \"in\" + \u1f31\u03ad\u03bd\u03b1\u03b9 (hienai), \"to send, throw\". [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1935", "text": "Clyster  entered the English language in the late 14th century from Old French or Latin, from Greek \u03ba\u03bb\u03c5\u03c3\u03c4\u03ae\u03c1 (klyster), \"syringe\", itself from \u03ba\u03bb\u03cd\u03b6\u03b5\u03b9\u03bd (klyzein), \"to wash out\", [ 72 ]  also spelled  glister  in the 18th century, [ 73 ]  is a generally archaic word used more particularly for enemas administered using a  clyster syringe ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1936", "text": "The first mention of the enema in medical literature is in the Ancient Egyptian  Ebers Papyrus  ( c. \u20091550  BCE). One of the many types of medical specialists was a Nery-Pehuyt, the Shepherd of the Anus. Many medications were administered by enemas. [ 74 ]  There was a Keeper of the Royal Rectum [ 75 ]  who may have primarily been the pharaoh's enema maker. The god  Thoth , according to Egyptian mythology, invented the enema. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1937", "text": "In parts of Africa the  calabash  gourd is used traditionally to administer enemas. On the Ivory Coast the narrow neck of the gourd filled with water is inserted the patient's rectum and the contents are then injected by means of an attendant's forcible oral inflation, or, alternatively, a patient may self-administer the enema by using suction to create a negative pressure in the gourd, placing a finger at the opening, and then upon anal insertion, removing the finger to allow atmospheric pressure to effect the flow. In South Africa,  Bhaca  people used an ox horn to administer enemas. [ 77 ]  Along the upper Congo River an enema apparatus is made by making a hole in one end of the gourd for filling it, and using a resin to attach a hollow cane to the gourd's neck. The cane is inserted into the anus of the patient who is in a posture that allows gravity to effect infusion of the fluid. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1938", "text": "The  Olmec  from their middle preclassic period (10th through 7th centuries BCE) through the Spanish Conquest used trance-inducing substances ceremonially, and these were ingested via, among other routes, enemas administered using jars."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1939", "text": "As further described below in  religious rituals , the  Maya  in their late classic age (7th through 10th centuries CE) used enemas for, at least, ritual purposes, Mayan sculpture and ceramics from that period depicting scenes in which, injected by syringes made of gourd and clay, ritual hallucinogenic enemas were taken. [ 79 ]  In the Xibalban court of the God D, whose worship included ritual cult paraphernal, the Maya illustrated the use of a characteristic enema bulb syringe by female attendants administering clysters ritually. [ 80 ] [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1940", "text": "For combating illness and discomfort of the digestive tract, the Mayan also employed enemas, as documented during the colonial period, e.g., in the  Florentine Codex . [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1941", "text": "The  indigenous peoples of North America  employed  tobacco smoke enemas  to stimulate respiration, injecting the smoke using a rectal tube. [ 82 ] [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1942", "text": "A rubber bag connected with a conical nozzle, at an early period, was in use among the  indigenous peoples of South America   as an enema syringe, [ 84 ]  and the rubber enema bag with a connecting tube and ivory tip remained in use by them while in Europe a syringe was still the usual means for conducting an enema. [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1943", "text": "In Babylonia, by 600 BCE, enemas were in use, although it appears that initially they were in use because of a belief that the demon of disease would, by means of an enema, be driven out of the body. [ 86 ]  Babylonian and Assyrian tablets c. 600 BCE bear cuneiform inscriptions referring to enemas. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1944", "text": "In China, c. 200 CE,  Zhang Zhongjing  was the first to employ enemas. \"Secure a large pig's bile and mix with a small quantity of vinegar. Insert a bamboo tube three or four inches long into the rectum and inject the mixture\" are his directions, according to  Wu Lien-teh . [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1945", "text": "In India, in the fifth century BCE,  Sushruta  enumerates the enema syringe among 121 surgical instruments described. Early Indian physicians' enema apparatus consisted of a tube of bamboo, ivory, or horn attached to the scrotum of a deer, goat, or ox. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1946", "text": "In Persia,  Avicenna  (980\u20131037 A. D.) is credited with the introduction of the \"clyster-purse\" or collapsible portion of an enema outfit made from ox skin or silk cloth and emptied by squeezing with the hands. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1947", "text": "Hippocrates  (460\u2013370 BCE) frequently mentions enemas, e.g., \"if the previous food which the patient has recently eaten should not have gone down, give an enema if the patient be strong and in the prime of life, but if he be weak, a suppository should be administered, should the bowels be not well moved on their own accord.\" [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1948", "text": "In the first century BCE the  Greek physician   Asclepiades of Bithynia  wrote \"Treatment consists merely of three elements: drink, food, and the enema\". [ 90 ]  Also, he contended that indigestion is caused by particles of food that are too big and his prescribed treatment was proper amounts of food and wine followed by an enema which would remove the improper food doing the damage. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1949", "text": "In the second century CE the Greek physician  Soranus  prescribed, among other  techniques , enemas as a safe  abortion  method, [ 92 ]  and the Greek philosopher  Celsus  recommended an enema of pearl barley in milk or rose oil with butter as a nutrient for those with dysentery and unable to eat, [ 93 ]  and also Galen mentions enemas in several contexts. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1950", "text": "In medieval times appear the first illustrations of enema equipment in the  Western world , a clyster syringe consisting of a tube attached to a pump action bulb made of a pig bladder. [ citation needed ] \nA simple piston  syringe  clyster was in use from the 15th through 19th centuries. This device had its rectal nozzle connected to a syringe with a plunger rather than to a bulb. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1951", "text": "Beginning in the 17th century enema apparatus was chiefly designed for self-administration at home and many were French as enemas enjoyed wide usage in France. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1952", "text": "In 1694  Fran\u00e7ois Mauriceau  in his early-modern treatise,  The Diseases of Women with Child,  records that both midwives and man-midwives commonly administered clysters to labouring mothers just prior to their delivery. [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1953", "text": "Clysters were administered for symptoms of constipation and, with more questionable effectiveness, stomach aches and other illnesses. [ when? ] [ citation needed ] [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1954", "text": "In 1753 an enema bag prepared from a pig's or beef's bladder attached to a tube was described by Johann Jacob Woyts as an alternative to a syringe. [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1955", "text": "In the 18th century Europeans began emulating the  indigenous peoples of North America's  use of tobacco smoke enemas to resuscitate drowned people. [ 97 ]  Tobacco resuscitation kits consisting of a pair of bellows and a tube were provided by the Royal Humane Society of London and placed at various points along the Thames. [ 93 ]  Furthermore, these enemas came to be employed for headaches, respiratory failure, colds, hernias, abdominal cramps, typhoid fever, and cholera outbreaks. [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1956", "text": "Clysters were a favourite medical treatment in the  bourgeoisie  and  nobility  of the Western world up to the 19th century. As medical knowledge was fairly limited at the time, purgative clysters were used for a wide variety of  ailments , the foremost of which were  stomach aches  and constipation. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1957", "text": "According to  the duc de Saint-Simon , clysters were so popular at the court of King  Louis XIV of France  that  the duchess of Burgundy  had her servant give her a clyster in front of the King (her modesty being preserved by an adequate posture) before going to the  comedy . However, he also mentions the astonishment of the King and Mme de Maintenon that she should take it before them. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1958", "text": "In the 19th century many new types of enema administration equipment were devised. Devices allowing gravity to infuse the solution, like those mentioned above used by South American indigenous people and like the enema bag described by Johann Jacob Woyts, came into common use. These consist of a nozzle at the end of a hose which connects a reservoir, either a bucket or a rubber bag, which is filled with liquid and held or hung above the recipient. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1959", "text": "In the early 20th century the disposable  microenema , a squeeze bottle, was invented by  Charles Browne Fleet . [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1960", "text": "The term \"colonic irrigation\" is commonly used in  gastroenterology  to refer to the practice of introducing water through a colostomy or a surgically constructed conduit as a treatment for constipation. [ 100 ]  The  Food and Drug Administration  has ruled that colonic irrigation equipment is not approved for sale for the purpose of general well-being [ 101 ]  and has taken action against many distributors of this equipment, including a  Warning Letter . [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1961", "text": "The same term is also used in  alternative medicine  where it may involve the use of substances mixed with water in order to  detoxify  the body. Practitioners believe the accumulation of fecal matter in the large intestine leads to ill health. [ 103 ]   This resurrects the old medical concept of  autointoxication  which was orthodox doctrine up to the end of the 19th century but which has now been discredited. [ 104 ] [ 105 ] [ 106 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1962", "text": "In the late 19th century Dr.  John Harvey Kellogg  made sure that the bowel of each and every patient was plied with water, from above and below. His favorite device was an enema machine (\"just like one I saw in Germany\") that could run fifteen gallons of water through a person's bowel in a matter of seconds. Every water enema was followed by a pint of yogurt\u2014half was eaten, the other half was administered by enema \"thus planting the protective germs where they are most needed and may render most effective service.\" The yogurt served to replace \"the intestinal flora\" of the bowel, creating what Kellogg claimed was a completely clean intestine. [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1963", "text": "Chlorine dioxide  enemas have been fraudulently marketed as a medical treatment, primarily for  autism . This has resulted, for example, in a six-year-old boy needing to have his colon removed and a colostomy bag fitted, [ 108 ] [ 109 ]  complaints to the FDA reporting life-threatening reactions, [ 110 ]  and even death. [ 111 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1964", "text": "Proponents falsely claim that administering autistic children these enemas results in the expulsion of parasitic worms (\" rope worms \"), which actually are fragments of damaged intestinal  epithelium  that are misinterpreted as being human pathogens. [ 112 ] [ 113 ]  Oral and rectal use of the solution has also been promoted as a cure for  HIV ,  malaria ,  viral hepatitis ,  influenza ,  common colds ,  acne ,  cancer ,  Parkinson's , and much more."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1965", "text": "Chlorine dioxide is a potent and toxic bleach [ 114 ]  that is relabeled for \"medicinal purposes\" to a variety of brand names including, but not limited, to MMS,  Miracle Mineral Supplement , and CD protocol. [ 115 ]  For oral use, the doses recommended on the labeling can cause nausea, vomiting, diarrhea, and potentially life-threatening dehydration. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1966", "text": "No clinical trials have been performed to test the health claims made for chlorine dioxide, which originate from former  Scientologist  Jim Humble [ 117 ]  in his 2006  self-published  book,  The Miracle Mineral Solution of the 21st Century [ 118 ]  and from anecdotal reports. The name MMS was coined by Humble. Sellers sometimes describe MMS as a  water purifier  so as to circumvent medical regulations. [ 119 ]  The  International Federation of Red Cross and Red Crescent Societies  rejected \"in the strongest terms\" reports by promoters of MMS that they had used the product to fight malaria. [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1967", "text": "Well documented as having no proven benefits and considered by medical authorities as rash and potentially dangerous is an enema of  coffee . [ 104 ] [ 121 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1968", "text": "A coffee enema can cause numerous maladies including  infections ,  sepsis  (including  campylobacter  sepsis), severe  electrolyte imbalance ,  colitis , polymicrobial enteric sepsis,  proctocolitis ,  salmonella ,  brain abscess , and heart failure, [ 122 ] [ 123 ] [ 124 ] [ 125 ] [ 126 ] [ 127 ] [ 128 ] [ 129 ] [ 130 ] [ excessive citations ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1969", "text": "and deaths related to coffee enemas have been documented. [ 131 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1970", "text": "Gerson therapy  includes administering enemas of coffee, [ 132 ]  as well as of  castor oil  and sometimes of  hydrogen peroxide  or of  ozone . [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1971", "text": "Some proponents of alternative medicine have claimed that coffee enemas have an anti- cancer  effect by \"detoxifying\" metabolic products of tumors [ 122 ]  but there is no medical scientific evidence to support this. [ 121 ] [ 123 ] [ 134 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1972", "text": "Enjoyment of enemas is known as  klismaphilia , which medically is classified as a  paraphilia . [ 135 ] [ 136 ]  A person with klismaphilia is a  klismaphile ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1973", "text": "Both women and men may enjoy sexual enema play, heterosexually and homosexually, experiencing  sexual arousal  from enemas which they find gratifying or sensual [ 137 ] [ 138 ]  and which can be an auxiliary to, or even a substitute for, genital  sexual activity . [ 137 ] [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1974", "text": "Klismaphiles may perceive pleasure from a large, water-distended belly, or the feeling of internal pressure. An enema fetish may include sexual attraction to the involved equipment, processes, environments, situations, or scenarios, [ 139 ]  Klismaphiles can gain satisfaction of enemas through fantasies, by actually receiving or giving one, or through the process of eliminating steps to being administered one (e.g., under the pretence of being constipated). [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1975", "text": "That some women use enemas while masturbating was documented by  Alfred Kinsey  in  Sexual Behavior in the Human Female : \"There were still other masturbatory techniques which were regularly or occasionally employed by some 11 percent of the females in the sample... Douches, streams of running water, vibrators, urethral insertions, enemas, other anal insertions, sado-masochistic activity, and still other methods were occasionally employed, but none of them in any appreciable number of cases.\" [ 140 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1976", "text": "Besides klismaphilia, the intrinsic enjoyment of enemas, there are other uses of enemas in sexual play. [ 141 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1977", "text": "Enemas are sometimes used in  sadomasochistic  activities [ 142 ] [ 143 ]  for  erotic humiliation [ 144 ]  or for physical discomfort. [ 145 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1978", "text": "Another sexual use for enemas is to empty the rectum as a prelude to other anal sexual activities such as  anal sex , [ 146 ]  possibly reducing risk of infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1979", "text": "This is different from klismaphilia, in which the enema is enjoyed for itself and as a part of sexual arousal and gratification. [ 146 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1980", "text": "Rectal douching is a common practice among people who take a receptive role in anal sex [ 147 ]  although rectal douching before anal sex may increase the risk of transferring  HIV , [ 148 ]   hepatitis B , [ 149 ]  and other diseases. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1981", "text": "Noting that deaths have been reported from  alcohol poisoning  via enemas, [ 151 ]  an  alcohol enema  can be used to very quickly instill alcohol into the bloodstream, absorbed through the membranes of the colon. However, great care must be taken as to the amount of alcohol used. Only a small amount is needed as the intestine absorbs the alcohol far more quickly than the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1982", "text": "Preceding an enema for administration of drugs or alcohol, a cleansing enema may first be used for cleaning the colon to help increase the rate of absorption. [ 152 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1983", "text": "All across  Mesoamerica  ritual enemas were employed to consume psychoactive substances, e.g.,  balch\u00e9 ,  alcohol ,  tobacco ,  peyote , and other  hallucinogenic drugs  and  entheogens , most notably by the  Maya , thus attaining more intense trance states more quickly, and Mayan classic-period sculpture and ceramics depict hallucinogenic enemas used in rituals. [ 79 ]  Some tribes continue the practice in the present day. [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1984", "text": "With historical roots in the  Indian subcontinent , enemas in  Ayurveda , called  Basti  or Vasti, form part of  Panchakarma  procedure in which  herbal medicines  are introduced rectally. [ 154 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1985", "text": "Enemas have also been forcibly applied as a means of punishment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1986", "text": "Political dissenters in post-independence Argentina were given enemas of  chili pepper  and  turpentine . [ 155 ]  Turpentine enemas are very harsh purgatives. [ 156 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1987", "text": "In the  Guantanamo Bay Detention Camp , the  Senate Intelligence Committee report on CIA torture  documented instances of enemas being used by the  Central Intelligence Agency  in order to ensure \"total control\" over detainees. [ 157 ]  Enemas, officials said, are uncomfortable and degrading, [ 158 ]  The CIA forced nutrient enema on detainees who attempted hunger strikes, documenting \"With head lower than torso \u2026 sloshing up the large intestines \u2026 [what] I infer is that you get a tube up as you can \u2026 We used the largest Ewal  [ sic ] tube we had\" wrote an officer, [ 159 ]  and \"violent enemas\" is how a detainee described what he received. [ 160 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1988", "text": "In the  Dionysus '  satyr play   Limos ,  Silenus  attempts to give an enema to  Heracles . [ 161 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1989", "text": "In  Cervantes '  Don Quixote , a narrative to Sancho includes \u201cThe Knight of the Sun ... bound hand and foot ... was administered a clyster of snow water and sand that almost disracted him\" [ 162 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1990", "text": "In the 17th century, satirists made physicians a favorite target, resembling  Moli\u00e8re 's caricature whose prescription for anything was \"clyster, bleed, purge,\" or \"purge, bleed, clyster\". [ 163 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1991", "text": "In Moli\u00e8re's play  The Imaginary Invalid , Argan, a severe  hypochondriac , is addicted to enemas as indicated by such lines as when B\u0115ralde asks, \"Can't you be one moment without a purge?\" [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1992", "text": "In  Grace Metalious 's novel  Peyton Place , the town doctor tells of \"a young boy with the worst case of dehydration I ever saw. It came from getting too many enemas that he didn't need. Sex, with a capital S-E-X.\". [ 165 ]  As a teenager, the boy enjoys receiving enemas from his mother. [ 166 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1993", "text": "In  Flora Rheta Schreiber 's book  Sybil , Sybil's psychiatrist asks her \"What's Mama been doing to you, dear?...I know she gave you the enemas.\" [ 167 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1994", "text": "In  The Right Stuff , during flight training astronaut  Alan Shepard  retains a barium enema, [ 168 ]  given two floors away from a toilet, embarrassedly riding a public elevator wearing a  hospital gown  and holding the enema bag with its tip still inserted in him. [ 169 ] [ 170 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1995", "text": "Water Power  is a film loosely based on the real-life exploits of  Michael H. Kenyon , an American criminal who pleaded guilty to a decade-long series of armed robberies of female victims, some of which involved sexual assaults in which he would give them enemas. [ 171 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1996", "text": "The lyrics of  Frank Zappa 's song  The Illinois Enema Bandit  are concerned with  Michael H. Kenyon 's  sexual assaults  which included administering involuntary enemas. [ 172 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1997", "text": "A 365-kilogram (805-pound) brass statue of a syringe enema bulb held aloft by three cherubs stands in front of the \"Mashuk\" spa in the settlement of  Zheleznovodsk  in Russia. Inspired by the 15th century Renaissance painter Botticelli, it was created by a local artist who commented that \"An enema is an unpleasant procedure as many of us may know. But when cherubs do it, it's all right.\" When unveiled on 19 June 2008, posted on one of the spa's wall was a banner declaring \"Let's beat constipation and sloppiness with enemas.\"  The spa lying in the Caucasus Mountains region, known for dozens of spas that routinely treat digestive and other complaints with enemas of mineral spring water, the director commented \"An enema is almost a symbol of our region.\" [ 173 ] [ 174 ]  It is the only known monument to the enema. [ 175 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1998", "text": "Sources"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_1999", "text": "\"A professional nursing instructional video demonstrating administering a cleansing enema\" .  Taber's Medical Dictionary . K. A. Davis Company . Retrieved  17 July  2014 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2000", "text": "In medicine  Enteroenteric circulation  is the secretion back into the  intestines  of substances previously taken up from it. It occurs when there is a negative relative concentration of substance in the\nintestines, making it passively diffuse from the  mesenteric circulation  into the  intestinal lumen  and is trapped. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2001", "text": "Examples of toxins that exhibit enteroenteric circulation include  theophylline ,  phenobarbital , and  phenytoin . [ 1 ]  Administration of  activated charcoal  inhibits the enteroenteric circulation of such substances, and is therefore useful in overdose or intoxication. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2002", "text": "The  enterogastric reflex  is one of the three extrinsic reflexes of the  gastrointestinal tract , the other two being the  gastroileal reflex  and the  gastrocolic reflex . [ 1 ]   The enterogastric reflex is stimulated by  duodenal  distension. [ 2 ]  It can also be stimulated by a pH of 3-4 in the  duodenum  and by a pH of 1.5 in the stomach.  Upon initiation of the reflex, the release of  gastrin  by G-cells in the antrum of the  stomach  is shut off.  This in turn inhibits  gastric motility  and the secretion of  gastric acid  ( HCl ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2003", "text": "The stomach's contents are inhibited from emptying into the small intestine by:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2004", "text": "The stomach's contents empty through the pylorus, allowing digestion to proceed, when there is:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2005", "text": "In  medicine , the  fecal fat test  is a diagnostic test for  fat   malabsorption  conditions, which lead to excess fat in the feces ( steatorrhea )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2006", "text": "In the  duodenum , dietary fat (primarily  triglycerides ) is digested by  enzymes  such as  pancreatic lipase  into smaller molecules of 1,2-Diacylglycerols and free fatty acids, which can be absorbed through the wall of the  jejenum  of the small intestine  [ 1 ]  and enter  circulation  for  metabolism  and storage. Since  fat  is a valuable nutrient,  human feces  normally contains very little undigested fat. However, a number of diseases of the pancreas and gastrointestinal tract are characterized by fat malabsorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2007", "text": "Examples of such diseases are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2008", "text": "In the simplest form of the fecal fat test, a random fecal specimen is submitted to the  hospital laboratory  and examined under a  microscope  after  staining  with a  Sudan III  or  Sudan IV  dye (\" Sudan staining \"). Visible amounts of fat indicate some degree of fat malabsorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2009", "text": "Quantitative fecal fat tests measure and report an amount of fat. This is usually done over a period of three days, the patient collecting all of their feces into a container."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2010", "text": "The container is thoroughly mixed to homogenize the feces, without using specific mixer equipment. A small sample from the feces is collected. The fat content is extracted with  solvents  and measured by  saponification  (turning the fat into  soap )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2011", "text": "Normally, up to 7  grams  of fat can be malabsorbed in people consuming 100 grams of fat per day. In patients with  diarrhea , up to 12 grams of fat may be malabsorbed since the presence of diarrhea interferes with fat absorption, even when the diarrhea is not due to fat malabsorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2012", "text": "Fish oil , sold under the brand name  Omegaven , is a  fatty acid  emulsion. [ 2 ]  It is used for  total parenteral nutrition  (feeding directly into a  venous  catheter), e.g. in  short bowel syndrome . [ 2 ]  It is rich in  omega-3 fatty acids . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2013", "text": "Fish oil triglycerides was approved for use in the United States in July 2018, [ 3 ]  and is available to people on the US market by prescription effective November 2018. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2014", "text": "In 2021, it was the 283rd most commonly prescribed medication in the United States, with more than 700,000 prescriptions. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2015", "text": "It has gained popularity in children in preference to the more commonly used  intralipid  after case reports that it reduced the risk of liver damage. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2016", "text": "A 2007, study indicated that the use of Omegaven may be an appropriate intervention strategy for newborns with a very  low birth weight ,  gastroschisis , and  intestinal atresia . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2017", "text": "A  clinical trial  exploring the use of fish oil as an adjunct to parenteral nutrition in surgical  intensive care units  at  National Taiwan University Hospital  completed in March 2007. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2018", "text": "Although the use of fish oil triglycerides in children in the United States is experimental, the use of it in adults in Europe is less controversial. [ 10 ]  In European studies, fish oil triglycerides have been associated with a reduction in  psoriasis , when contrasted to administration of  omega-6 fatty acid   Lipoven . [ 11 ]  Fish oil triglycerides have also been associated with reduced mortality and antibiotic use during hospital stays. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2019", "text": "FODMAPs  or  fermentable  oligosaccharides ,  disaccharides ,  monosaccharides , and  polyols [ 1 ]  are short-chain  carbohydrates  that are poorly absorbed in the  small intestine  and ferment in the colon. They include short-chain  oligosaccharide  polymers of  fructose  ( fructans ) and  galactooligosaccharides  (GOS,  stachyose ,  raffinose ),  disaccharides  ( lactose ),  monosaccharides  ( fructose ), and  sugar alcohols  ( polyols ), such as  sorbitol ,  mannitol ,  xylitol , and  maltitol . [ 1 ] [ 2 ]  Most FODMAPs are naturally present in food and the human diet, but the polyols may be added artificially in commercially prepared foods and beverages."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2020", "text": "FODMAPs cause digestive discomfort in some people. The reasons are hypersensitivity to  luminal  distension or a proclivity to excess water retention and gas production and accumulation, but they do not cause intestinal inflammation. Naturally occurring FODMAPs may help avert digestive discomfort for some people because they produce beneficial alterations in the  gut flora . [ 3 ] [ 4 ] [ 5 ] [ 6 ]  They are not the cause of these disorders, [ 7 ]  but a  low-FODMAP diet , restricting FODMAPs, might help to improve digestive symptoms in adults with  irritable bowel syndrome  (IBS) and other  functional gastrointestinal disorders  (FGID). [ 7 ] [ 8 ] [ 9 ] [ 10 ] [ 11 ]  Avoiding all FODMAPs long-term may have a detrimental impact on the  gut microbiota  and  metabolome . [ 2 ] [ 9 ] [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2021", "text": "FODMAPs, especially fructans, are present in small amounts in  gluten-containing grains  and have been identified as a possible cause of symptoms in people with  non-celiac gluten sensitivity . [ 13 ] [ 14 ] [ 15 ] [ 16 ] [ 3 ]  They are only minor sources of FODMAPs when eaten in the usual standard quantities in the daily diet. [ 13 ]  As of 2019, reviews conclude that although FODMAPs present in wheat and related grains may play a role in non-celiac gluten sensitivity, they only explain certain gastrointestinal symptoms, such as  bloating , but not the  extra-digestive symptoms  that people with non-celiac gluten sensitivity may develop, such as  neurological disorders ,  fibromyalgia , psychological disturbances, and  dermatitis . [ 3 ] [ 17 ] [ 13 ]  Consuming a low FODMAP diet without a previous medical evaluation could cause health risks because it can ameliorate and mask digestive symptoms of  celiac disease , delaying or avoiding its correct diagnosis and therapy. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2022", "text": "Some FODMAPs, such as fructose, are readily absorbed in the small intestine of humans via  GLUT receptors . [ 19 ]  Absorption thus depends on the appropriate expression and delivery of these receptors in the intestinal  enterocyte  to both the apical surface, contacting the lumen of the intestine (e.g.,  GLUT5 ), and to the basal membrane, contacting the blood (e.g.,  GLUT2 ). [ 19 ]  Improper absorption of these FODMAPS in the small intestine leaves them available for absorption by  gut flora . The resultant metabolism by the gut flora leads to the production of gas and potentially results in bloating and  flatulence . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2023", "text": "Although FODMAPs can cause certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they help prevent it because they produce beneficial alterations in the intestinal flora that contribute to maintaining good colon health. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2024", "text": "FODMAPs are not the cause of  irritable bowel syndrome  or other  functional gastrointestinal disorders , but rather a person develops symptoms when the underlying bowel response is exaggerated or abnormal. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2025", "text": "Fructose malabsorption  and  lactose intolerance  may produce IBS symptoms through the same mechanism, but unlike other FODMAPs, poor absorption of fructose is found in only a minority of people. Lactose intolerance is found in most adults, except for specific geographic populations, notably those of European descent. [ 20 ]  Many who benefit from a low FODMAP diet need not restrict fructose or lactose. It is possible to identify these two conditions with  hydrogen  and  methane   breath testing , thus eliminating the necessity for dietary compliance. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2026", "text": "The significance of sources of FODMAPs varies through differences in dietary groups such as geography, ethnicity, and other factors. [ 7 ]  Commonly used FODMAPs comprise the following: [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2027", "text": "Sources of fructans  include  wheat ,  rye ,  barley ,  onion ,  garlic ,  Jerusalem  and  globe artichoke ,  beetroot ,  dandelion leaves , the white part of  leeks , the white part of  spring onion ,  brussels sprouts ,  savoy cabbage , and  prebiotics  such as fructooligosaccharides ( FOS ),  oligofructose  and  inulin . [ 22 ] [ failed verification ] [ 7 ] [ 23 ]   Asparagus ,  fennel ,  red cabbage , and  radicchio  contain moderate amounts but may be eaten if the advised portion size is observed. [ 22 ] [ failed verification ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2028", "text": "Pulses  and  beans  are the main dietary sources (although  green beans , canned  lentils , sprouted  mung beans ,  tofu  (not silken), and  tempeh  contain comparatively low amounts). [ 22 ] [ failed verification ] [ 23 ]  Supplements of the enzyme  alpha-galactosidase  may reduce symptoms, [ 24 ]  assuming the enzyme product does not contain other FODMAPs, such as polyol  artificial sweeteners . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2029", "text": "Polyols are found naturally in  mushrooms , some fruit (particularly  stone fruits ), including  apples ,  apricots ,  avocados ,  blackberries ,  cherries ,  lychees ,  nectarines ,  peaches ,  pears ,  plums ,  prunes ,  watermelon , and in some vegetables, including  cauliflower ,  snow peas , and mange-tout peas. [ 25 ]   Cabbage ,  chicory , and fennel contain moderate amounts, but may be eaten in a low-FODMAP diet if the advised portion size is observed. [ 26 ] [ better\u00a0source\u00a0needed ] [ failed verification ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2030", "text": "Polyols, specifically  sugar alcohols , used as  artificial sweeteners  in commercially prepared food, beverages, and chewing gum, include  isomalt ,  maltitol ,  mannitol ,  sorbitol , and  xylitol . [ 7 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2031", "text": "People following a low-FODMAP diet may be able to tolerate moderate amounts of fructose and lactose, particularly if they have  lactase persistence . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2032", "text": "A  low-FODMAP diet  consists of the global restriction of all fermentable carbohydrates (FODMAPs), [ 7 ]  and is recommended only for a short time. A low-FODMAP diet is recommended for managing patients with  irritable bowel syndrome  (IBS) and can reduce digestive symptoms of IBS, including bloating [ 28 ]  and flatulence. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2033", "text": "Several studies have found a low-FODMAP diet to improve digestive symptoms in adults with irritable bowel syndrome, [ 8 ] [ 9 ] [ 10 ] [ 11 ]  but its long-term use can have negative effects, because it has a detrimental impact on the  gut microbiota  and  metabolome . [ 2 ] [ 9 ] [ 11 ] [ 12 ]  It should only be used for short periods and under the advice of a specialist. [ 30 ]  More study is needed to evaluate its effectiveness in children with irritable bowel syndrome. [ 8 ]  Small studies (which are susceptible to bias) show little evidence of its effectiveness in treating functional symptoms of  inflammatory bowel disease  (IBD). [ 31 ] [ 32 ]  More study is needed to assess the true impact of this diet on health. [ 9 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2034", "text": "FODMAPs present in  gluten-containing grains  have been identified as a possible cause of gastrointestinal symptoms in people with  non-celiac gluten sensitivity , either by themselves, [ 33 ]  or in combination effect with gluten and other proteins in gluten-containing cereals, such as amylase-trypsin inhibitors (ATIs). [ 14 ] [ 13 ]  The amount of fructans in these cereals is small. In rye, they account for 3.6\u20136.6% of dry matter, 0.7\u20132.9% in wheat, and barley contains only trace amounts. [ 3 ]  They are only minor sources of FODMAPs when eaten in common dietary amounts. [ 13 ]  Wheat and rye may comprise a major source of fructans when consumed in large amounts. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2035", "text": "In a 2018 double-blind, crossover research study on 59 persons on a  gluten-free diet  with challenges of  gluten ,  fructans , or  placebo , intestinal symptoms (specifically  bloating ) were (borderline) significantly higher after challenge with fructans, in comparison with gluten proteins (P=0.049). [ 3 ] [ 17 ]  Although the differences between the three interventions were small, the authors concluded that fructans are more likely to cause gastrointestinal symptoms in non-celiac gluten sensitivity than gluten. [ 3 ]  Fructans used in the study were extracted from  chicory  root, and the results may or may not apply to wheat fructans. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2036", "text": "A 2018 review concluded that although fructan intolerance may play a role in non-celiac gluten sensitivity, it only explains some gastrointestinal symptoms. Fructan intolerance does not explain the   extra-digestive symptoms  that people with non-celiac gluten sensitivity may develop, such as  neurological disorders ,  fibromyalgia , psychological disturbances, and  dermatitis . This review also found that FODMAPs may cause digestive symptoms when the person is hypersensitive to  luminal  distension. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2037", "text": "A 2019 review concluded that wheat fructans could cause certain IBS-like symptoms, such as  bloating , but that they are not likely to cause immune activation or extra-digestive symptoms, as many people with non-celiac gluten sensitivity reported resolution of their symptoms after removing gluten-containing cereals. These same participants continued to eat fruits and vegetables with high FODMAP content without issue. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2038", "text": "In  medicine ,  fragmentation  is an operation that breaks of solid matter in a body part into pieces. [ 1 ]   Physical force  (e.g.,  manual force ,  ultrasonic force ), applied directly or indirectly through intervening body parts, are used to break down the solid matter into pieces. The solid matter may be an abnormal  by-product of a biological function, or a  foreign body . The pieces of solid matter are not taken out, but are eliminated or absorbed through normal biological functions. Examples would be the fragmentation of  kidney  and  urinary bladder  stones ( nephrolithiasis  and  urolithiasis , respectively) by  shock-wave lithotripsy ,  laser   lithotripsy , or  transurethral lithotripsy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2039", "text": "The code for fragmentation in  ICD-10-PCS  is 0FF. [ 1 ] [ unreliable source? ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2040", "text": "This  medical treatment \u2013related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2041", "text": "2L71 ,  2B4N ,  2OBU ,  2QKH ,  2L70 ,  1T5Q"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2042", "text": "2695"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2043", "text": "14607"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2044", "text": "ENSG00000159224"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2045", "text": "ENSMUSG00000014351"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2046", "text": "P09681"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2047", "text": "P48756"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2048", "text": "NM_004123"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2049", "text": "NM_008119"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2050", "text": "NP_004114"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2051", "text": "NP_032145"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2052", "text": "Gastric inhibitory polypeptide   (GIP ), also known as  glucose-dependent insulinotropic polypeptide , is an  inhibiting hormone  of the  secretin family  of  hormones . [ 5 ]   While it is a weak inhibitor of  gastric acid  secretion, its main role, being an  incretin , is to stimulate  insulin  secretion. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2053", "text": "GIP, along with  glucagon-like peptide-1  (GLP-1), belongs to a class of molecules referred to as  incretins , [ 7 ]  which stimulate insulin release on oral food intake."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2054", "text": "GIP is derived from a 153-amino acid proprotein encoded by the GIP gene and circulates as a biologically active 42-amino acid peptide. It is synthesized by K cells, which are found in the  mucosa  of the  duodenum  and the  jejunum  of the  gastrointestinal tract . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2055", "text": "Like all  endocrine   hormones , it is transported by blood."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2056", "text": "Gastric inhibitory polypeptide receptors  are seven-transmembrane proteins ( GPCRs ) found on  beta-cells  in the  pancreas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2057", "text": "It has traditionally been named  gastrointestinal inhibitory peptide  or  gastric inhibitory peptide  and was found to decrease the secretion of  stomach acid [ 9 ]   to protect the  small intestine  from acid damage, reduce the rate at which  food  is transferred through the  stomach , and inhibit the GI motility and secretion of acid. However, this is incorrect, as it was discovered that these effects are achieved only with higher-than-normal physiological level, and that these results naturally occur in the body through a similar  hormone ,  secretin . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2058", "text": "It is now believed that the function of GIP is to induce  insulin  secretion, which is stimulated primarily by  hyperosmolarity  of  glucose  in the duodenum. [ 11 ]  After this discovery, some researchers prefer the new name of  glucose-dependent insulinotropic peptide , while retaining the  acronym  \"GIP.\"  The amount of insulin secreted is greater when glucose is administered orally than intravenously. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2059", "text": "In addition to its role as an incretin, GIP is known to inhibit  apoptosis  of the pancreatic beta cells and to promote their proliferation. It also stimulates  glucagon  secretion and fat accumulation. GIP receptors are expressed in many organs and tissues including the  central nervous system  enabling GIP to influence  hippocampal  memory formation and regulation of appetite and satiety. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2060", "text": "GIP recently appeared as a major player in  bone remodeling . Researchers at Universities of Angers and Ulster evidenced that genetic ablation of the GIP receptor in mice resulted in profound alterations of bone microarchitecture through modification of the adipokine network. [ 14 ]  Furthermore, the deficiency in GIP receptors has also been associated in mice with a dramatic decrease in bone quality and a subsequent increase in fracture risk. [ 15 ]  However, the results obtained by these groups are far from conclusive because their animal models give discordant answers and  these works should be analysed very carefully. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2061", "text": "It has been found that  type 2 diabetics  are not responsive to GIP and have lower levels of GIP secretion after a meal when compared to non-diabetics. [ 16 ]  In research involving  knockout mice , it was found that absence of the GIP receptors correlates with resistance to  obesity . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2062", "text": "Gelesis100 , sold under the brand name  Plenity , is an oral  hydrogel  used to treat  overweight  and  obesity . [ 1 ]  It absorbs water and expands in the  stomach  and  small bowel  thereby increasing feelings of fullness. Possible side effects include primarily gastrointestinal symptoms, [ 2 ]  such as  diarrhea ,  abdominal distention , infrequent bowel movements,  constipation ,  abdominal pain , and  flatulence . [ 3 ]  It is contraindicated in  pregnancy ,  chronic malabsorption syndromes , and  cholestasis . [ 1 ]  The  US Food and Drug Administration  approved it in 2019 as a medical device. Gelesis100 was developed by the company  Gelesis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2063", "text": "The US Food and Drug Administration approved the use of Gelesis100 in April 2019 as a  medical device . [ 4 ]  Gelesis100 is the first treatment of its kind for overweight and obesity. [ 2 ]  In 2022, the American Gastroenterology Association published a guideline for the management of obesity, which recommended the use of Gelesis100 be limited to clinical trials due to limited evidence. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2064", "text": "Gelesis100 is used to treat obesity and overweight as an  anti-obesity medication . [ 1 ]  Gelesis100 is taken as a pill before meals with water. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2065", "text": "Gelesis100 has been criticized for its small impact on weight loss relative to side effects. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2066", "text": "Gelesis100 is an oral superabsorbent hydrogel, which is produced from  carboxymethylcellulose  and  citric acid . [ 1 ] [ 9 ]  The cross-linked product forms a hydrophilic matrix, which absorbs water. [ 1 ]  Taken in capsule form by mouth, [ 10 ]  as Gelesis100 absorbs water, it expands in the stomach and small intestine. [ 3 ] [ 6 ]  After absorbing water, a semisolid gel structure forms, which may promote satiety and result in weight loss [ 1 ]  via reduced caloric intake. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2067", "text": "Gelesis100 is contraindicated in pregnancy, chronic malabsorption syndromes, and cholestasis. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2068", "text": "Side effects consist of minor gastrointestinal symptoms, [ 2 ]  including diarrhea, abdominal distention, infrequent bowel movements, constipation, abdominal pain, and flatulence. [ 3 ]  Gelesis100 is not associated with any severe adverse events. [ 11 ]  However, long-term safety data beyond 24 weeks is not available. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2069", "text": "Glycogen storage disease type 0  is a disease characterized by a deficiency in the  glycogen synthase  enzyme (GSY). Although glycogen synthase deficiency does not result in storage of extra glycogen in the liver, it is often classified as a  glycogen storage disease  because it is another defect of glycogen storage and can cause similar problems. There are two  isoforms  (types) of glycogen synthase enzyme; GSY1 in muscle and GSY2 in liver, each with a corresponding form of the disease. [ 1 ]  Mutations in the liver  isoform  (GSY2), causes  fasting   hypoglycemia , high blood  ketones , increased free fatty acids and low levels of  alanine  and  lactate .  Conversely, feeding in these patients results in  hyperglycemia  and  hyperlactatemia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2070", "text": "The most common clinical history in patients with glycogen-storage disease type 0 (GSD-0) is that of an infant or child with symptomatic hypoglycemia or seizures that occur before breakfast or after an inadvertent fast. In affected infants, this event typically begins after they outgrow their nighttime feeds. In children, this event may occur during acute GI illness or periods of poor enteral intake. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2071", "text": "Mild hypoglycemic episodes may be clinically unrecognized, or they may cause symptoms such as drowsiness, sweating, lack of attention, or pallor. Uncoordinated eye movements, disorientation, seizures, and coma may accompany severe episodes. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2072", "text": "Glycogen-storage disease type 0 affects only the liver. Growth delay may be evident with height and weight percentiles below average. Abdominal examination findings may be normal or reveal only mild hepatomegaly. [ citation needed ]  Signs of acute hypoglycemia may be present, including the following: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2073", "text": "Glycogen-storage disease type 0 is caused by genetic defects in the gene that codes for liver glycogen synthetase (GYS2), which is located on chromosome band 12p12.2. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2074", "text": "Glycogen synthetase catalyzes the rate-limiting reaction for glycogen synthesis in the liver by transferring glucose units from uridine 5'-diphosphate (UDP)-glucose to a glycogen primer. Its action is highly regulated by a mechanism of  phosphorylation  and dephosphorylation and modulated by counter-regulatory hormones including  insulin ,  epinephrine , and glucagon. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2075", "text": "Mutations in the gene for liver glycogen synthetase (GYS2, 138571) result in decreased or absent activity of liver glycogen synthetase and moderately decreased amounts of structurally normal glycogen in the liver. Mutational studies of patients with glycogen-storage disease type 0 do not demonstrate correlations between genotype and phenotype. [3] A different gene (GYS1, 138570) encodes muscle glycogen synthetase, which has normal activity in patients with glycogen-storage disease type 0A. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2076", "text": "In the early stages of fasting, the liver provides a steady source of glucose from glycogen breakdown (or glycogenolysis). With prolonged fasting, glucose is generated in the liver from noncarbohydrate precursors through gluconeogenesis. Such precursors include alanine (derived from the breakdown of proteins in skeletal muscle) and glycerol (derived from the breakdown of triacylglycerols in fat cells). In patients with glycogen-storage disease type 0, fasting hypoglycemia occurs within a few hours after a meal because of the limited stores of hepatic glycogen and inadequate  gluconeogenesis  to maintain normoglycemia. Feeding characteristically results in postprandial hyperglycemia and  glucosuria , in addition to increased blood lactate levels, because glycogen synthesis is limited, and excess glucose is preferentially converted to lactate by means of the  glycolytic pathway . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2077", "text": "Important clinical criteria to consider in the evaluation of a child with hypoglycemia and suspected glycogen-storage disease type 0 (GSD-0) include (1) the presence or absence of hepatomegaly; (2) the characteristic schedule of hypoglycemia, including unpredictable, postprandial, short fast, long fast, or precipitating factors; (3) the presence or absence of lactic acidosis; (4) any associated  hyperketosis  or hypoketosis; and (5) any associated liver failure or cirrhosis. The differential diagnosis also includes ketotic hypoglycemia. Patients with ketotic hypoglycemia have a normal response to glucagon in the fed state. Patients with glycogen-storage disease type 0 have normal-to-increased response to glucagon in the fed state, with hyperglycemia and lactic acidemia. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2078", "text": "Serum glucose levels are measured to document the degree of hypoglycemia. Serum electrolytes calculate the  anion gap  to determine presence of  metabolic acidosis ; typically, patients with glycogen-storage disease type 0 (GSD-0) have an  anion gap  in the reference range and no acidosis. See the Anion Gap calculator. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2079", "text": "Serum lipids (including triglyceride and total cholesterol) may be measured. In patients with glycogen-storage disease type 0,  hyperlipidemia  is absent or mild and proportional to the degree of fasting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2080", "text": "Urine (first voided specimen with dipstick test for ketones and reducing substances) may be analyzed. In patients with glycogen-storage disease type 0, urine ketones findings are positive, and urine-reducing substance findings are negative. However, urine-reducing substance findings are positive (fructosuria) in those with fructose 1-phosphate aldolase deficiency (fructose intolerance). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2081", "text": "Serum lactate is in reference ranges in fasting patients with glycogen-storage disease type 0. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2082", "text": "Liver function studies  provide evidence of mild hepatocellular damage in patients with mild elevations of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. [ citation needed ] Plasma amino-acid analysis shows plasma alanine levels as in reference ranges during a fast."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2083", "text": "Skeletal radiography may reveal  osteopenia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2084", "text": "Evaluation of a patient with suspected glycogen-storage disease type 0 requires monitored assessment of fasting adaptation in an inpatient setting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2085", "text": "Patients typically have hypoglycemia and  ketosis , with lactate and alanine levels in the low or normal part of the reference range approximately 5\u20137 hours after fasting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2086", "text": "A  glucagon tolerance test  may be needed if the fast fails to elicit the expected rise in plasma glucose. Lactate and alanine levels are in the reference range. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2087", "text": "By contrast, a glucagon challenge test after a meal causes hyperglycemia, with increased levels of plasma lactate and alanine. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2088", "text": "Oral loading of glucose,  galactose , or  fructose  results in a marked rise in blood lactate levels. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2089", "text": "Liver biopsy for microscopic analysis and enzyme assay is required for definitive diagnosis. Diagnosis may include linkage analysis in families with affected members and sequencing of the entire coding region of the GSY2 gene for mutations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2090", "text": "Histologic  analysis of liver tissue demonstrates moderately decreased amounts of periodic acid-Schiff (PAS)\u2013positive, diastase-sensitive glycogen stores. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2091", "text": "Evidence of increased fat accumulation in the liver may be observed, as in other glycogen-storage diseases. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2092", "text": "Electron microscopic analysis of liver sections shows normal glycogen structure. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2093", "text": "Muscle glycogen stores are normal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2094", "text": "There are two types of glycogen storage disease type 0 to be considered, they are: [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2095", "text": "The goal for treatment of Glycogen-storage disease type 0 is to avoid hypoglycemia. This is accomplished by avoiding fasting by eating every 1\u20132 hours during the day. At night, uncooked  corn starch  can be given because it is a complex glucose polymer. This will be acted on slowly by pancreatic amylase and glucose will be absorbed over a 6-hour period. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2096", "text": "The overall frequency of glycogen-storage disease is approximately 1 case per 20,000\u201325,000 people. Glycogen-storage disease type 0 is a rare form, representing less than 1% of all cases. The identification of asymptomatic and oligosymptomatic siblings in several glycogen-storage disease type 0 families has suggested that glycogen-storage disease type 0 is underdiagnosed. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2097", "text": "The major morbidity is a risk of fasting hypoglycemia, which can vary in severity and frequency. Major long-term concerns include growth delay, osteopenia, and neurologic damage resulting in developmental delay, intellectual deficits, and personality changes. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2098", "text": "No sexual predilection is observed because the deficiency of glycogen synthetase activity is inherited as an autosomal recessive trait. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2099", "text": "Glycogen-storage disease type 0 is most commonly diagnosed during infancy and early childhood. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2100", "text": "The  gut\u2013memory connection  is the relation between the  gastrointestinal tract  and  memory  performance. The phenomenon of the gut\u2013memory connection is based on and part of the idea of the  gut-brain axis , a complex communication network, linking the  central nervous system  to the gut. The  gut-brain axis  first gained significant momentum in research and formal recognition in the 20th century with advancements in  neuroscience  and  gastroenterology . The idea of a connection between the gut and emotion has been hinted at in various ancient traditions and medical practices for centuries. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2101", "text": "As a vital conduit for the communication between  gastrointestinal tract  and the brain, the gut-brain axis influences a variety of  physiological  processes. A prominent example of the gut\u2013memory connection is the effects that alterations in the gut microbiome can have on the  pathogenesis  of  neural diseases  like  Alzheimer's . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2102", "text": "Understanding the connections between the gut microbiome and cognitive health could aid researchers in developing novel strategies for slowing down cognitive decline in  neurodegenerative diseases . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2103", "text": "The  gut-brain axis  is a two-way communication network within human systems that correlates the  gut microbiome  and the brain, encompassing immune, endocrine and neural connections. There is an evident association between the  gastrointestinal tract  and enteric microbiota with functional changes highlighted in the nervous system evidenced in vivo and vitro studies. [ 5 ]  This relationship plays a role in maintaining brain health as a result of resident microbes in the GI tract, influencing pathophysiology and mental behaviours. [ 6 ]   [ 7 ]  This can be accomplished through neuronal function directly or indirectly via vitamins,  neurotransmitters  and  metabolites . [ 8 ]   [ 9 ]  The exact biochemical pathway for this has yet to be determined, while some experimental data may suggest afferent sensory neurons travel via neuroimmune and  endocrine systems  traveling over the  vagus nerve . [ 10 ]  This demonstrates a commensalistic relationship between bacteria that exist in the human GI tract reaping from a diverse source of nutrients while providing indigestible nutrients available to the host. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2104", "text": "It has also been hypothesized that  IBS  can originate as a result of brain-to-gut or gut-to-brain syndrome as well which emphasizes the importance of the gut-brain axis. [ 11 ]   Neurological disorders  could also be a result of microbiota factors explaining why the intestine is known as the second brain as opposed to having neural origin. [ 12 ]  This uncovers the link to discovering mental and neurological disorders such as  depression  and  anxiety  with gut microbiota health. While not much of the ancestral origin of these interactions is not well known, this has a long history based on the coevolution and ecological interactions between vertebrates and bacteria, tightly coupled in animal evolution. [ 13 ]  This can also be evidenced by observing the role of bacteria such as the Hydra holobiont in contractile behaviour necessary for gut motility, demonstrating the product of ancient interaction between bacteria and emerging metazoans. [ 12 ]   [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2105", "text": "The ancestral mammalian gut likely harboured a diverse array of microbes that played essential roles in metabolism, digestion and immune response, and as a result, has evolved and adapted in response to selection and dietary pressures. With the development of the vertebrate nervous system, the coordination of digestive processes in the  gastrointestinal tract  with external stimuli would\u2019ve allowed communication. [ 13 ]   [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2106", "text": "The anatomical basis of the gut\u2013memory connection includes the  gastrointestinal tract  (GIT), which has its own intrinsic nervous system, called the  enteric nervous system  (ENS). The ENS controls intestinal function and can theoretically operate independently from the  central nervous system  (CNS). [ 15 ]  More than 100 million  efferent neurons  are present in the human ENS. They are connected to the brain through the  vagus nerve , which seems to be the main mediator of  gut-brain communication . [ 16 ]  Around 90% of the vagus nerve fibers connecting the brain and the ENS are afferent, meaning that the brain receives more information from the digestive system than it sends out. [ 17 ]  Afferent vagus nerve fibers have cell bodies in the  nodose ganglia  that synapse with the CNS. The signals are then relayed to the medial  nucleus of the solitary tract  (NTS), which in turn relays them to various  brainstem  and  forebrain  regions, including the  hippocampus  and the  amygdala . [ 18 ]   [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2107", "text": "Signals from the GIT can activate the hippocampus, which was shown by directly stimulating the vagus nerve in human participants. [ 20 ]  The connection between the hippocampus and the medial NTS does not appear to be direct. Instead it seems to involve the  locus coeruleus  (LC) and the  medial septum  (MS), making the connection indirect. [ 21 ]  Studies have shown increased memory retention in both humans and rodents, following direct  vagus nerve stimulation . [ 22 ] [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2108", "text": "There are noradrenergic projections from the nucleus of the solitary tract to the amygdala, which is often associated with  emotional learning . [ 19 ]  Direct Vagus nerve stimulation increases the release of  noradrenaline  in the amygdala and has been linked to increased  fear depletion  and positive outcomes of preclinical treatments of  major depressive disorder  (MDD). [ 25 ] [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2109", "text": "Other factors that can indirectly influence memory function, include the  immune system  and  hormonal  processes. The ENS mediates  HPA-axis  function via  gastrointestinal hormones ,  cytokines  and  neuropeptides . Through the same pathways the HPA-axis can influence the ENS. Therefore, the gut can indirectly influence hippocampal functioning and other cortical structures related to memory, via the HPA-axis. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2110", "text": "Probiotics , living bacteria with health benefits, are emerging as a potential tool to influence the  microbiota-gut-brain  axis and improve mental well-being. [ 29 ]  This axis is a complex communication network linking the gut and the brain, primarily mediated by the  vagus nerve  and the production of neuromodulators, which influence nerve activity and brain function. [ 30 ]  Although the exact molecular mechanisms are still unclear, the gut microbiota has been demonstrated to influence behaviour and brain functions, including pain perception, [ 31 ]  stress response, [ 32 ]  prefrontal myelination, [ 33 ]  and brain biochemistry. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2111", "text": "Experimental manipulation of the gut microbial community composition has been shown to modify the host's neural function. For instance, long-term consumption of a probiotic  Lactobacillus  strain by  BALB/c  mice changed gamma-aminobutyric acid ( GABA ) expression in brain regions related to emotional processing. This alteration was associated with reduced anxiety and depression-like behaviour. [ 35 ]  A study found that consuming probiotics for 4\u20136 weeks altered neural activity in brain regions responsible for the central processing of emotion and sensation in healthy women, even without changes in gut microbial composition. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2112", "text": "Given the evidence that gut microbiota influences emotional processing and the connections between emotion, memory, and decision-making, researchers hypothesized that probiotic ingestion could impact brain mechanisms related to such contexts. Their study demonstrated that administering a multi-strain probiotic significantly impacts behavioural scores and  fMRI  measures in brain regions involved in emotional decision-making and memory. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2113", "text": "Probiotics contribute to the reduction of  oxidative stress , a cellular process that can damage brain cells. Accordingly, probiotics may protect brain cells in the  hippocampus , a region important for memory storage and retrieval while promoting a healthy gut lining. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2114", "text": "A study in middle-aged rats examined the effects of  probiotics ,  prebiotics  and a combination of both,  symbiotics , on memory. The study found that rats given the symbiotic supplement performed significantly better in spatial memory tests than the control groups. Improvement in memory was also accompanied by several positive changes in the brain. The symbiotic group showed lower levels of inflammation, a factor well known to impair memory. They also showed increased levels of  brain-derived neurotrophic factor  (BDNF), a protein important for memory formation, and higher levels of  butyrate , a fatty acid produced by gut bacteria that can improve memory and altered brain cell activity patterns that promote learning and memory. A mixture of probiotics and prebiotics could be a way to improve cognitive abilities, particularly spatial memory. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2115", "text": "Antibiotic medication  can disrupt the natural  gut microbiome , leading to an imbalance in the gut-brain axis. Some studies in mice have shown that probiotic treatment can reverse the negative effects of  antibiotics  on bacteria in the gut, called  dysbiosis  and can also improve memory function. They further found that probiotics not only reduced gut dysbiosis associated with memory loss but also reduced the activity of specific enzymes associated with memory deficits, such as  acetylcholinesterase  and  myeloperoxidase . [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2116", "text": "The link between gut bacteria and mental health, particularly  anxiety  and  depression  becomes a stronger focus in research. There exist studies on  germ-free  mice, devoid of any gut bacteria, that show the mice exhibit less anxiety compared to mice with a normal gut microbiome. [ 40 ]   [ 41 ]  Inflammations or infections of the gut tract of mice caused a change in certain behaviour associated with symptoms of anxiety, such as a less drive to explore [ 42 ]  and a stronger inhibition of behavioral responses. [ 43 ] [ 44 ]  This hints at the potential influence specific types of bacteria might have on behaviour and mental health. Studies with rodents have experimentally shown similar results. [ 45 ] [ 46 ] [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2117", "text": "Some certain probiotic strains, like  Lactobacillus rhamnosus [ 48 ]  and  Bifidobacterium infantis , [ 49 ]  have shown promise in reducing anxiety-like behaviour in animal models. These probiotics are being explored as potential so-called  psychobiotics  for treating mental health conditions, such as depression and anxiety. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2118", "text": "Further evidence comes from  microbiota  transfer experiments in mice, in which researchers transplanted gut bacteria from one strain of mice to another. It seems to influence their behaviour, suggesting the composition of the gut microbiome plays an important role. Stressful situations can also disrupt the delicate balance of gut bacteria and can lead to maternal separation and social defeat stress alters gut microbiota. [ 51 ]   [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2119", "text": "Some other studies of mice exposed to food deprivation or social disruption found changes in their gut bacteria composition. [ 53 ]  The influence seems to go both ways, since research using a depression model in mice revealed alterations in their gut bacteria compared to healthy mice. [ 54 ]  This, in turn, suggests that anxiety and depression might also affect the gut microbiome. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2120", "text": "The  gut-brain axis  acts as a communication network between the gastrointestinal tract and the brain. Due to this communication through neural, endocrine, and immune pathways, the  gut microbiota  and the brain can mutually influence their functions. [ 56 ]  Therefore, changes in the  gut microbiota  can influence the pathogenesis of various neurological diseases. There is rising evidence of a relationship between the  gut microbiome  and the neurodegenerative disease  Alzheimer\u2019s . [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2121", "text": "The development and progression of  Alzheimer\u2019s disease  are characterised by abnormal brain protein aggregation, inflammation, immune dysregulation, and impaired neuronal and synaptic activity of the brain. [ 56 ]  These abnormalities associated with  Alzheimer\u2019s disease  are also associated with a dysregulation of the gut microbiome. [ 56 ] [ 57 ]  There are different environmental factors such as diet, exercise and exposure to air pollution that have an impact on the  gut microbiome  and therefore could also have an influence on  Alzheimer\u2019s disease . [ 56 ] [ 57 ]  To have positive health outcomes the intestinal bacterial flora should be in an equilibrium. By consuming sufficient  probiotics  such as  Bifidobacteria  and  Lactobacillus  through a diet the achievement of this equilibrium is supported. [ 56 ]   Bifidobacteria  and  Lactobacillus  can be taken as supplements but are also contained in different types of foods. To ensure a variety of microbiota strains in the gut a large and diverse diet is required. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2122", "text": "Further research suggests a correlation between Alzheimer\u2019s disease, low insulin levels (diabetes type 1) and insulin resistance (diabetes type 2), that could be caused by amyloid beta-derived diffusible ligands (ADDLs). These ADDLs are  neurotoxins  that reduce synapse plasticity and provoke  oxidative damage  by altering the shape of insulin receptors. [ 58 ]  This inhibits the learning and memory mechanisms in the brain because Insulin usually supports the necessary regulation of processes like neuronal survival, energy metabolism, and  plasticity . Insulin resistance could therefore explain the memory loss in AD patients. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2123", "text": "There are different theories of the potential mechanisms through which the  gut microbiome  influences the pathogenesis of  Alzheimer\u2019s disease . A viral or bacterial infection can contribute to the development of  Alzheimer's disease . [ 56 ]  The  Heliobacter pylori infection  decreases the MMSE scores of patients with  Alzheimer's disease  through the release of inflammatory mediators. In addition, patients with  Alzheimer's disease  show higher serum levels of A\u00df40 and A\u00df42 if they are infected by a bacterial infection. The bacteria can alter the levels of specific neurotransmitters proteins and receptors which are responsible for synaptic plasticity. [ 56 ]  The theory of age-related dysbiosis associates the appearance of  Alzheimer's disease  with the ageing of the immune system. [ 56 ]  Through the process of ageing the levels of  proteobacteria  expand whereas the levels of  probiotics  decrease. These changes alter the composition of the  gut microbiota . [ 56 ] [ 57 ] [ 59 ]  As an alteration of the  gut microbiota  occurs it can lead to differences in the activity of the brain. This connection raises the possibility of a treatment for patients diagnosed with  Alzheimer\u2019s . Therapeutic treatment could manipulate the  gut microbiome  and therefore induce neuronal and synaptic changes in the patient's brain. [ 56 ] [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2124", "text": "Irritable bowel syndrome  or  IBS  is a gastrointestinal disorder with the disruption of the  gut-brain axis  as one of its characteristics. There are multiple ways in which this disorder impacts memory performance. IBS is a disorder that can cause  chronic pain ,  stress  and immune activity. [ 60 ] [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2125", "text": "Many of the people suffering from IBS have  visceral hypersensitivity . [ 62 ]  Pain disrupts attention which is a crucial factor for  memory  formation. [ 63 ]  The adverse effects of chronic pain also affect  executive functioning ,  working memory ,  episodic memory  and speed of information processing. [ 64 ]   Sleep deprivation  in IBS patients is common and can have adverse effects on memory consolidation, executive functions and mental health, which also impairs memory. [ 65 ] [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2126", "text": "IBS patients often show a higher response to stressors, causing dysregulation of the  hypothalamic-pituitary-adrenal ( HPA )  axis and the  autonomic nervous system ( ANS ) . [ 67 ]  The activation of the  HPA axis  leads to the release of  glucocorticoids ,  cortisol  in humans. In people with IBS, the amount of cortisol was found to be higher which is related to a decline in  hippocampus -dependent  episodic memory  performance. [ 68 ]  This also causes  hippocampus  deactivation and morphological changes which have been associated with spatial memory deficits. [ 69 ]  The decrease in blood flow to the  hippocampus  and other brain areas also seems to be involved in the effects of stress on the  hippocampus . [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2127", "text": "The  frontal lobes , which are involved in  executive functions  such as  working memory , are more sensitive than the  hippocampus  to  glucocorticoid  levels causing similar disruptive effects of IBS as in the  hippocampus . [ 71 ]  They are also affected by the  ANS . The disruption of the  ANS  in  IBS  causes an increase in  sympathetic nervous system  activation and a decrease in  parasympathetic nervous system  activation, resulting in higher  noradrenaline  levels. This activates  \u03b11 receptors  in the  prefrontal cortex  which impairs  working memory . [ 72 ]   Noradrenaline  and  cortisol  to the  amygdala  have the opposite effect and can enhance emotional memory formation which for  IBS  patients is shown as an enhanced memory for gastrointestinal-related words. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2128", "text": "IBS  patients have an abnormal immune activity which can be seen when measuring  cytokines . They have a higher-than-normal amount of the proinflammatory cytokines  IL6  and  IL8  and some also have elevated  TNF-\u03b1  and  IL1-\u03b1  levels. [ 74 ] [ 75 ]  (  IL6  is found to be related to cognitive abilities and  Alzheimer's disease  severity. [ 76 ] [ 77 ]  ) Too much of it can affect memory by reducing  neurogenesis  in the  dentate gyrus  and inhibiting  long term potentiation . [ 78 ] [ 79 ]  The high amount of  IL6  and  TNF-\u03b1  decreases  episodic memory  performance.  IL1-\u03b1  and  TNF-\u03b1  have these effects through  LTP  inhibition in the  dentate gyrus  and  TNF-a , through  excitotoxicity  through the modulation of  glutamate  transmission also. [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2129", "text": "Obesity  is associated with many adverse effects physically and mentally. These include memory deficits. Obesity causes an increase in inflammation throughout the body. [ 81 ]   Cytokines , the chemicals that regulate this, can cross the  blood-brain barrier  in certain cases and affect the brain, including memory related areas. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2130", "text": "Adipose tissue , which contains the fat, have certain neuroendocrine functions such as the production and release of  adipokines . In  obesity , the body is in a state of adiposopathy in which the secretion of  adipokines  changes. [ 83 ]   leptin , one of the  adipokines , also promotes  axonal  growth and modulates  NMDA  functioning, enhancing  LTP . [ 84 ]  In  obese  states, the body has  leptin  resistance, disrupting these effects of  leptin . [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2131", "text": "In adiposopathy, the secretion of  interleukin\u00a06  is increased. [ 86 ]  This leads to reduced  neurogenesis , the inhibition of  LTP  and impaired  working memory  performance as in  irritable bowel syndrome . Some studies also suggest that  cytokines  such as  interleukin 6  may reduce  hippocampal   grey matter  volume. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2132", "text": "In order to analyze the effects  gut microbiota  has on our learning of  spatial memory  and cognition,  animal studies  can be applied to human studies. This implies the use of rats, and mice in experiments in order to study the effects of a sucrose diet on cognitive skills. Experiments on lab animals demonstrated similar results in human experiments whereas sucrose diet has an impact on cognitive abilities.  [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2133", "text": "The excessive use of abundant sugar consumption has a significant impact on cognitive performance. Consistent consumption of foods rich in  cholesterol  shows that over a long duration decreases cognitive abilities, specifically spatial memory In order to study spatial learning using  animal models , rodents are placed into an experiment called  radial arm maze  where the  working memory  of  semantic memories  of animals are tested.  [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2134", "text": "This experiment uses  operant conditioning  such as rewards and punishments in order to measure working memory in rodents and motivate the animal towards a desired behaviour like figuring out where the food is located in the maze. Findings of high-fat diets include deficits in spatial memory and cognitive impairment. A study including obese mice which encompassed high levels of  palmitic acid  these high concentrations of acid demonstrated a change in the microbiota of the gut which shows deficits in cognition and spatial learning.  [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2135", "text": "This type of acid found in an animal study shows similarities with humans, therefore this finding can be applied to humans as well. According to animal studies, high-fat diets contribute to significant alterations in gut microbiota and in decrease of spatial learning.  [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2136", "text": "Hampton's line  is a thin,  radiolucent  line seen across the neck of a  gastric ulcer  filled with  barium sulphate  during a  barium meal . It is a sign of  mucosal   edema . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2137", "text": "It is named after  Aubrey Otis Hampton . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2138", "text": "Healthy digestion , also called  digestive health , results in the absorption of  nutrients  from food without distressing  symptoms . Healthy digestion follows having a  healthy diet , doing appropriate  self-care  including physical activity and exercise, minimizing activities like  smoking  or consuming  alcoholic drinks  which impair digestion, and managing any  medical condition  which disrupts digestion to the best of one's ability. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2139", "text": "A person with healthy digestion will have lower risk of experiencing  diarrhea ,  vomiting ,  constipation ,  heartburn ,  bloating ,  flatulence , and  indigestion . [ 2 ]  Additionally, a person with healthy digestion will have less need of digestive medications than a person who does not have healthy digestion. [ 2 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2140", "text": "Some foods like  Banana ,  Avocado ,  Melons ,  Oats ,  Yogurt  quickly or completely digested than others. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2141", "text": "Many events can disrupt digestion. [ 1 ]  Disrupted digestion can have many symptoms, including diarrhea, constipation, heartburn, bloating, flatulence, and indigestion. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2142", "text": "Some people have chronic medical conditions which disrupt their digestion. [ 1 ]  Other people might be taking a drug which disrupts their digestion. [ 1 ]  In those cases, the person's goals for healthy digestion might be to have their personal best possible digestion since they have other health problems to manage. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2143", "text": "Food intolerance  can disrupt digestion. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2144", "text": "Whenever possible, it is easier for a person to prevent digestive problems from happening rather than to seek to treat them after they begin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2145", "text": "Various drugs can relieve the symptoms of poor digestion.  Laxatives  counter  constipation .  Loperamide  counters  diarrhea .  Antacids  counter heartburn or indigestion.  Simethicone  counters  flatulence . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2146", "text": "Constipation can also be countered using  enemas  or  suppositories ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2147", "text": "Probiotics  have been shown to benefit gastrointestinal disorders and are a popular treatment to promote healthy digestion. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2148", "text": "Many people who seek healthcare for gastrointestinal problems are not satisfied with the treatment options which they find in conventional medicine. [ 6 ]  Because of this, people often use  alternative medicine  to promote healthy digestion. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2149", "text": "Various organizations observe a \"World Digestive Health Day\" to share information about promoting healthy digestion. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2150", "text": "See text"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2151", "text": "Helicobacter  is a  genus  of  gram-negative   bacteria  possessing a characteristic  helical  shape. They were initially considered to be members of the genus  Campylobacter , but in 1989, Goodwin  et al.  published sufficient reasons to justify the new genus name  Helicobacter . [ 2 ]  The genus  Helicobacter  contains about 35 species. [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2152", "text": "Some species have been found living in the lining of the  upper gastrointestinal tract , as well as the  liver  of  mammals  and some  birds . [ 6 ]  The most widely known species of the genus is  H. pylori , which infects up to 50% of the human population. [ 5 ]  It also serves as the  type species  of the genus. Some strains of this bacterium are  pathogenic  to humans, as they are strongly associated with  peptic ulcers , chronic  gastritis ,  duodenitis , and  stomach cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2153", "text": "Helicobacter  species are able to thrive in the very  acidic  mammalian  stomach  by producing large quantities of the  enzyme   urease , which locally raises the  pH  from about 2 to a more biocompatible range of 6 to 7. [ 7 ]  Bacteria belonging to this genus are usually susceptible to  antibiotics  such as  penicillin , are  microaerophilic  (optimal  oxygen  concentration between 5 and 14%)  capnophiles , and are fast-moving with their  flagella . [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2154", "text": "Comparative genomic analysis has led to the identification of 11 proteins that are uniquely found in the Helicobacteraceae. Of these proteins, seven are found in all species of the family, while the remaining four are not found in any  Helicobacter  strains and are unique to  Wollinella . Additionally, a rare genetic event has led to the fusion of the  rpoB  and  rpoC  genes in this family, which is characteristic of them. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2155", "text": "Recently, new gastric ( H. suis  and  H. baculiformis ) and enterohepatic ( H. equorum ) species have been reported.  H. pylori  is of primary importance for medicine, but non- H. pylori  species, which naturally inhabit mammals (except humans) and birds, have been detected in human clinical specimens. These encompass two (gastric and enterohepatic) groups, showing different organ specificity. Importantly, some species, such as  H. hepaticus, H. mustelae , and probably  H. bilis , exhibit carcinogenic potential in animals. They harbour many  virulence  genes and may cause diseases not only in animals, but also in humans. Gastric species such as  H. suis  (most often) , H. felis, H. bizzozeronii , and  H. salomonis  have been associated with chronic gastritis and peptic ulcers in humans, and importantly, with higher risk for MALT lymphoma compared to  H. pylori ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2156", "text": "Enterohepatic species e.g.,  H. hepaticus,   H. bilis , and  H. ganmani , have been detected by  PCR , but still are not isolated from specimens of patients with hepatobiliary diseases. Moreover, they may be associated with  Crohn's disease  and  ulcerative colitis . The significance of avian helicobacters ( H. pullorum, H. anseris , and  H. brantae)  also has been evaluated extensively.  H. cinaedi  and  H. canis  can cause severe infections, mostly in immunocompromised patients with animal exposure. Briefly, the role of these species in veterinary and human medicine is increasingly recognised. Several other topics such as isolation of still uncultured species,  antibiotic resistance , and treatment regimens for infections and pathogenesis and possible carcinogenesis in humans should be evaluated. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2157", "text": "Helicobacter heilmannii sensu lato  (i.e.  H. heilmanni s.l. ) is a grouping of non- H. pylori   Helicobacter  species that take as part of their definition a similarity to  H. pylori  in being associated with the development of stomach inflammation, stomach ulcers, [ 11 ]  duodenum ulcers, [ 12 ]  stomach cancers that are not lymphomas, and extranodal marginal B cell lymphoma of the stomach in humans and animals. [ 11 ]  Most clinical studies have not identified the exact species of  H. heilmanii  associated with these diseases, so designated these species as  H. heilmanni s.l.  However, investigative studies have identified these species in some patients with the cited  H. heilmanni s.l. -associated  upper gastrointestinal tract  diseases. The  H. heilmani species  identified to date in the stomachs of humans with the cited upper gastrointestinal tract diseases are:  Helicobacter bizzozeronii ,  Helicobacter felis ,  Helicobacter salomonis ,  Helicobacter suis , and  Helicobacter heilmannii s.s. [ 11 ]  It is important to recognize the association of  H. heilmannii sensu lato  with these  upper gastrointestinal tract diseases , particularly extranodal marginal zone lymphoma of the stomach, because some of them have been successfully treated using antibiotic-based drug regimens directed against the instigating  H. heilmannii sensu lato  species. [ 13 ]  The  H. heilmanni s.l. -associated human diseases appear to be acquired from pets and farm animals, so are considered to be  zoonotic diseases . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2158", "text": "The currently accepted taxonomy is based on the  List of Prokaryotic names with Standing in Nomenclature  (LPSN) [ 1 ]  and  National Center for Biotechnology Information  (NCBI) [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2159", "text": "Wolinella"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2160", "text": "H. valdiviensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2161", "text": "H. ganmani"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2162", "text": "H. mesocricetorum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2163", "text": "H. rodentium"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2164", "text": "H. enhydrae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2165", "text": "H. cholecystus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2166", "text": "H. brantae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2167", "text": "H. pametensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2168", "text": "H. kayseriensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2169", "text": "H. anseris"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2170", "text": "H. anatolicus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2171", "text": "H. mustelae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2172", "text": "H. canis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2173", "text": "H. bilis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2174", "text": "H. canicola   Kawamura et al. 2016"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2175", "text": "H. cinaedi"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2176", "text": "H. hepaticus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2177", "text": "H. trogontum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2178", "text": "H. japonicus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2179", "text": "H. muridarum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2180", "text": "H. typhlonius"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2181", "text": "H. mastomyrinus   Shen et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2182", "text": "H. apri   Zanoni et al. 2016"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2183", "text": "H. equorum   Moyaert et al. 2007"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2184", "text": "H. kumamotonensis   Kawamura et al. 2023"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2185", "text": "H. pullorum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2186", "text": "H. canadensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2187", "text": "H. colisuis   Gruntar et al. 2022"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2188", "text": "H. turcicus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2189", "text": "H. marmotae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2190", "text": "H. macacae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2191", "text": "H. himalayensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2192", "text": "H. fennelliae"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2193", "text": "H. jaachi"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2194", "text": "H. saguini"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2195", "text": "H. aurati"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2196", "text": "H. monodelphidis   Shen et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2197", "text": "H. didelphidarum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2198", "text": "H. acinonychis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2199", "text": "H. pylori"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2200", "text": "H. cetorum"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2201", "text": "H. delphinicola   Segawa et al. 2021"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2202", "text": "H. suis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2203", "text": "H. labacensis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2204", "text": "H. bizzozeronii"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2205", "text": "H. felis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2206", "text": "H. salomonis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2207", "text": "H. cynogastricus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2208", "text": "H. baculiformis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2209", "text": "H. ailurogastricus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2210", "text": "H. heilmannii"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2211", "text": "H. mehlei"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2212", "text": "H. vulpis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2213", "text": "\" Helicobacter burdigaliensis \"  Berthenet et al. 2019"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2214", "text": "Helicobacter valdiviensis   Collado, Jara & Gonzalez 2014"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2215", "text": "Helicobacter turcicus   Aydin et al. 2022"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2216", "text": "\" Helicobacter winghamensis \"  Melito et al."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2217", "text": "Helicobacter ganmani   Robertson et al. 2001"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2218", "text": "\" P. rodentium \"  (Shen et al. 1997) Waite, Chuvochina & Hugenholtz 2019"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2219", "text": "Helicobacter apodemus   Jeon et al. 2015"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2220", "text": "Helicobacter mesocricetorum   Simmons et al. 2000"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2221", "text": "\" P. canadensis \"  (Fox et al. 2002) Waite, Chuvochina & Hugenholtz 2019"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2222", "text": "\" P. pullorum \"  (Stanley et al. 1995) Waite, Chuvochina & Hugenholtz 2019"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2223", "text": "H. saguini   Shen et al. 2017"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2224", "text": "H. aurati   Patterson et al. 2002"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2225", "text": "H. muridarum   Lee et al. 1992"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2226", "text": "H. didelphidarum   Shen et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2227", "text": "H. trogontum   Mendes et al. 1996"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2228", "text": "H. bilis   Fox et al. 1997"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2229", "text": "\" H. rappini \"  Dewhirst et al. 2000"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2230", "text": "H. enhydrae   Shen et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2231", "text": "H. kayseriensis   Aydin et al. 2022"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2232", "text": "H. pametensis   Dewhirst et al. 1994"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2233", "text": "H. brantae   Fox et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2234", "text": "\" Ca.  H. avistercoris\"  Gilroy et al. 2021"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2235", "text": "H. cholecystus   Franklin et al. 1997"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2236", "text": "\" Ca.  H. avicola\"  Gilroy et al. 2021"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2237", "text": "H. himalayensis   Hu et al. 2015"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2238", "text": "\" H. labetoulli \"  Berthenet et al. 2019"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2239", "text": "H. cinaedi   (Totten et al. 1988) Vandamme et al. 1991"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2240", "text": "\" H. magdeburgensis \"  Traverso et al. 2010"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2241", "text": "H. jaachi   Shen et al. 2017"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2242", "text": "H. hepaticus   Fox et al. 1994"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2243", "text": "H. marmotae   Fox et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2244", "text": "H. japonicus   corrig. Shen et al. 2017"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2245", "text": "H. typhlonius   Franklin et al. 2002"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2246", "text": "H. fennelliae   (Totten et al. 1988) Vandamme et al. 1991"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2247", "text": "H. macacae   Fox et al. 2013"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2248", "text": "H. canis   Stanley et al. 1994"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2249", "text": "H. anseris   Fox et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2250", "text": "H. anatolicus   Aydin et al. 2023"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2251", "text": "H. mustelae   (Fox et al. 1988) Goodwin et al. 1989"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2252", "text": "H. cetorum   Harper et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2253", "text": "H. acinonychis   corrig. Eaton et al. 1993"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2254", "text": "H. pylori   (Marshall et al. 1985) Goodwin et al. 1989"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2255", "text": "H. bizzozeronii   Hanninen et al. 1996"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2256", "text": "H. mehlei   Gruntar et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2257", "text": "H. suis   Baele et al. 2008"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2258", "text": "H. ailurogastricus   Joosten et al. 2017"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2259", "text": "H. heilmannii   Smet et al. 2012"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2260", "text": "H. cynogastricus   Van den Bulck et al. 2006"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2261", "text": "H. felis   Paster et al. 1991"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2262", "text": "H. salomonis   Jalava et al. 1997"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2263", "text": "H. baculiformis   Baele et al. 2008"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2264", "text": "H. labacensis   Gruntar et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2265", "text": "H. vulpis   Gruntar et al. 2020"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2266", "text": "Species incertae sedis:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2267", "text": "Hemostatic Powder Spray TC-325  ( Hemospray  or  TC-325 ) is an inert, highly absorptive mineral agent which is used for the treatment of  gastrointestinal bleeding .  Applied during  endoscopy  to bleeding lesions, TC-325 is derived from  bentonite , and is used to achieve  hemostasis  (control of bleeding) by absorbing water and creating a barrier that leads to mechanical tamponade (pressure) and concentration of  clotting factors , resulting in enhanced  coagulation  (clotting of blood). [ 1 ]  TC-325 was approved for gastrointestinal bleeding from causes other than  gastric  or  esophageal varices  (e.g., nonvariceal bleeding). TC-325 results in immediate control of bleeding in 91-93% of cases. [ 2 ] [ 3 ]  Technical success has gradually increased between 2011 and 2019, which may be due to device improvements or physician familiarity with the application of TC-325. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2268", "text": "Hemostatic Powder Spray TC-325 was approved by the  United States   Food and Drug Administration  in 2018 for  gastrointestinal bleeding . [ 4 ] \nTechnical success has gradually increased between 2011 and 2019, which may be due to device improvements or physician familiarity with the application of TC-325. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2269", "text": "TC-325 is recommended for temporary control of gastrointestinal bleeding when other treatments are ineffective or not available. [ 5 ]  TC-325 may also be used for massive bleeding with poor visualization or diffuse bleeding due to cancer. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2270", "text": "The device is not FDA approved for the treatment of gastroesophageal variceal bleeding. [ 7 ]  However, TC-325 is 90.4% effective in achieving initial hemostasis in variceal bleeding, and its use was associated with a 4.2% rate of rebleeding. [ 8 ]  TC-325 use for variceal bleeding is safe. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2271", "text": "TC-325 is 91-93% effective in achieving initial control of bleeding, [ 3 ] [ 2 ]  but does not prevent re-bleeding from occurring. [ 3 ]  Rebleeding is most likely to occur if the initial bleed was brisk (spurting) or  hypotension  was present. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2272", "text": "Risks of TC-325 use include failure to control bleeding, gastrointestinal perforation, bowel obstruction, or malfunction of device or delivery system. If TC-325 is used for the control of bleeding at the site of a sphincterotomy or ampullary resection, there is a risk of biliary obstruction.  Additional risks include allergy to the TC-325 powder. The overall rate of adverse events to TC-325 is 0.7%. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2273", "text": "OR"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2274", "text": "AND"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2275", "text": "Hepatology  is the branch of  medicine  that incorporates the study of  liver ,  gallbladder ,  biliary tree , and  pancreas  as well as management of their disorders. Although traditionally considered a sub-specialty of  gastroenterology , rapid expansion has led in some countries to doctors specializing solely on this area, who are called  hepatologists ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2276", "text": "Diseases and complications related to  viral hepatitis  and alcohol are the main reason for seeking specialist advice. More than two billion people have been infected with  hepatitis B  virus at some point in their life, and approximately 350 million have become persistent carriers. [ 1 ]   Up to 80% of  liver cancers  can be attributed to either hepatitis B or  hepatitis C  virus. In terms of  mortality , the former is second only to smoking among known agents causing  cancer . With more widespread implementation of  vaccination  and strict  screening  before  blood transfusion , lower  infection  rates are expected in the future. [ citation needed ]  In many countries, however, overall alcohol consumption is increasing, and consequently the number of people with  cirrhosis  and other related complications is commensurately increasing. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2277", "text": "As for many medical specialties, patients are most likely to be referred by family physicians (i.e., GP) or by physicians from different disciplines. The reasons might be:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2278", "text": "Evidence from autopsies on Egyptian  mummies  suggests that liver damage from the  parasitic  infection  bilharziasis  was widespread in the ancient society. [ 2 ] \nIt is possible that the  Greeks  may have been aware of the liver's ability to exponentially duplicate as illustrated by the story of  Prometheus . However, knowledge about liver disease in  antiquity  is questionable. Most of the important advances in the field have been made in the last 50 years. [ when? ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2279", "text": "The word  hepatology  is from  Ancient Greek  \u1f27\u03c0\u03b1\u03c1 ( hepar ) or  \u1f21\u03c0\u03b1\u03c4\u03bf- ( hepato- ), meaning \"liver\", and -\u03bb\u03bf\u03b3\u03af\u03b1 ( -logia ), meaning \"study\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2280", "text": "1.  International Classification of Disease  ( ICD 2007) \u2013 WHO classification :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2281", "text": "2.  MeSH (medical subject heading) :sam"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2282", "text": "3.  National Library of Medicine Catalogue [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2283", "text": "Also see  Hepato-biliary diseases"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2284", "text": "Seven  cholera  pandemics have occurred in the past 200 years, with the first  pandemic  originating in  India  in 1817. The  seventh cholera pandemic  is officially a current pandemic and has been ongoing since 1961, according to a  World Health Organization  factsheet in March 2022. [ 1 ]   Additionally, there have been many documented major local cholera outbreaks, such as a 1991\u20131994 outbreak in South America and, more recently, the  2016\u20132021 Yemen cholera outbreak . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2285", "text": "Although much is known about the mechanisms behind the spread of  cholera , this has not led to a full understanding of what makes cholera outbreaks happen in some places and not others. Lack of treatment of human  feces  and lack of treatment of drinking water greatly facilitate its spread. Bodies of water have been found to serve as a  reservoir , and seafood shipped long distances can spread the disease."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2286", "text": "Between 1816 and 1923, the first six cholera pandemics occurred consecutively and continuously over time. Increased commerce, migration, and pilgrimage are credited for its transmission. [ 3 ]  Late in this period (particularly 1879\u20131883), major scientific breakthroughs toward the treatment of cholera develop: the first immunization by  Pasteur , the development of the first cholera vaccine, and identification of the bacterium  Vibrio cholerae  by  Filippo Pacini  and  Robert Koch . After a long hiatus, a  seventh cholera pandemic  spread in 1961. The pandemic subsided in the 1970s, but continued on a smaller scale. Outbreaks occur across the developing world to the current day. Epidemics occurred after wars, civil unrest, or natural disasters, when water and food supplies had become contaminated with  Vibrio cholerae , and also due to crowded living conditions and poor sanitation. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2287", "text": "Deaths in  India  between 1817 and 1860 in the first three pandemics of the nineteenth century, are estimated to have exceeded 15\u00a0million people. Another 23\u00a0million died between 1865 and 1917, during the next three pandemics. Cholera deaths in the  Russian Empire  during a similar time period exceeded 2\u00a0million. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2288", "text": "The  first cholera pandemic  occurred in the Bengal region of India, near  Calcutta  (now Kolkata), starting in 1817 through 1824. The disease dispersed from India to Southeast Asia, the Middle East, Europe, and Eastern Africa through trade routes. [ 6 ]  The  second pandemic  lasted from 1826 to 1837 and particularly affected North America and Europe, due to the result of advancements in transportation and global trade, and increased human migration, including soldiers. [ 7 ]   The  third pandemic  erupted in 1846, persisted until 1860, extended to North Africa, and reached South America, for the first time specifically affecting Brazil. The  fourth pandemic  lasted from 1863 to 1875, and spread from India to Naples and  Spain , and to the United States in 1873. The  fifth  pandemic was from 1881 to 1896 and started in India and spread to Europe, Asia, and South America. The  sixth pandemic  started in India and lasted from 1899 to 1923. These epidemics were less fatal due to a greater understanding of the cholera bacteria. Egypt, the Arabian peninsula, Persia, India, and the Philippines were hit hardest during these epidemics, while other areas, such as Germany in 1892 and Naples from 1910 to 1911, also suffered severe outbreaks. The  seventh pandemic  originated in 1961 in Indonesia and is marked by the emergence of a new strain, nicknamed  El Tor , which still persists (as of 2019 [ 8 ] ) in developing countries. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2289", "text": "Cholera did not occur in the  Americas  for most of the 20th century after the early 1900s in New York City. It reappeared in the Caribbean toward the end of that century and seems likely to persist. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2290", "text": "The  first cholera pandemic , though previously restricted, began in  Bengal , and then spread across  India  by 1820. Hundreds of thousands of Indians and ten thousand  British troops  died during this pandemic. [ 11 ]  The cholera outbreak extended as far as  China ,  Indonesia  (where more than 100,000 people succumbed on the island of  Java  alone) and the  Caspian Sea  in Europe, before receding. [ 12 ] [ 13 ]  In 1821, it is estimated that up to 100,000 deaths occurred in  Korea . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2291", "text": "A  second cholera pandemic  reached Russia (see  Cholera Riots ),  Hungary  (about 100,000 deaths) and  Germany  in 1831; [ 15 ]  it killed 130,000 people in  Egypt  that year. [ 16 ]   In 1832 it reached  London  and the United Kingdom (where more than 55,000 people died) [ 17 ]  and  Paris . In London, the disease claimed 6,536 victims and came to be known as \"King Cholera\"; in Paris, 20,000 died (of a population of 650,000), and total deaths in France amounted to 100,000. [ 18 ]  In 1833, a cholera epidemic killed many  Pomo , which are a Native American tribe. The epidemic reached  Quebec ,  Ontario ,  Nova Scotia , [ 19 ]  and  New York  in the same year, and the Pacific coast of North America by 1834. In the center of the country [ clarification needed ] , it spread through the cities linked by the rivers and steamboat traffic. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2292", "text": "In Washington D.C.  Michael Shiner , an enslaved laborer at the  Washington Navy Yard  recorded, \"The time the colery [cholera] broke out in about June and July August and September 1832 it Raged in the City of Washington and every day they wher [were] twelve or 13 carried out to they [their] graves a day.\" [ 21 ]  By late July 1832, cholera had spread to Virginia and on 7 August 1832, Commodore  Lewis Warrington  confirmed to the Secretary of the Navy  Levi Woodbury  cholera was at the  Gosport Navy Yard , \"Between noon of that day, [1 August] and the morning of Friday [3 August], when all work on board her  USS  Fairchild  stopped, several deaths by cholera occurred and fifteen or sixteen cases (of less violence) were reported.\" [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2293", "text": "The epidemic of cholera, cause unknown and prognosis dire, had reached its peak. [ 23 ]  Cholera afflicted Mexico's populations in 1833 and 1850, prompting officials to quarantine some populations and fumigate buildings, particularly in major urban centers, but nonetheless the epidemics were disastrous. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2294", "text": "In response to the  second cholera pandemic , the  Ottoman Empire  and  Egypt  reformed their quarantine systems, following the western Mediterranean model. In 1831, the Egyptian Quarantine Board was established. It constructed Egypt\u2019s first modern lazaretto in  Alexandria  in 1833. In 1831, the Ottoman government set up the first permanent quarantine complex in  Istanbul . In 1838, the Ottoman government established the Supreme Council of Health, which oversaw 59 quarantines. While largely useless against cholera, these quarantines shored up the two countries' epidemiological defenses against  bubonic plague . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2295", "text": "During this pandemic, the scientific community varied in its beliefs about the causes of cholera. In France, doctors believed cholera was associated with the poverty of certain communities or poor environment. Russians believed the disease was contagious, although doctors did not understand how it spread. The United States believed that cholera was brought by recent immigrants, specifically the Irish, and epidemiologists understand they were carrying disease from British ports. Lastly, some British thought the disease might rise from divine intervention. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2296", "text": "The  third cholera pandemic  deeply affected Russia, with over one million deaths.  Over 15,000 people died of cholera in  Mecca  in 1846. [ 27 ]  A two-year outbreak began in  England and Wales  in 1848, and claimed 52,000 lives. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2297", "text": "In 1849, a second major outbreak occurred in France. In London, it was the worst outbreak in the city's history, claiming 14,137 lives, over twice as many as the 1832 outbreak. Cholera hit  Ireland  in 1849 and killed many of the  Irish Famine  survivors, already weakened by starvation and fever. [ 28 ]  In 1849, cholera claimed 5,308 lives in the major port city of  Liverpool ,  England , an embarkation point for immigrants to North America, and 1,834 in  Hull , England. [ 18 ]  In Vietnam and Cambodia, cholera hit in summer 1849, killing approximately 589,000 to 800,000 people within one year, along with its consequential famine. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2298", "text": "An  outbreak in North America  took the life of former  U.S. President   James K. Polk . Cholera, believed spread from Irish immigrant ships from England, spread throughout the  Mississippi river system , killing over 4,500 in  St. Louis [ 18 ]  and over 3,000 in  New Orleans . [ 18 ]  Thousands died in  New York , a major destination for Irish immigrants. [ 18 ]  Cholera claimed 200,000 victims in  Mexico . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2299", "text": "That year, cholera was transmitted along the  California ,  Mormon , and  Oregon Trails  as 6,000 to 12,000 [ 32 ]  are believed to have died on their way to the  California Gold Rush ,  Utah  and  Oregon  in the cholera years of 1849\u20131855. [ 18 ]  It is believed more than 150,000 Americans died during the two pandemics between 1832 and 1849. [ 33 ] [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2300", "text": "In 1851, a ship coming from Cuba carried the disease to  Gran Canaria . [ 35 ]  It is considered that more than 6,000 people died in the island during summer, [ 36 ]  out of a population of 58,000."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2301", "text": "In 1852, cholera spread east to the Dutch East Indies and later was carried to Japan in 1854. The  Philippines  were infected in 1858 and  Korea  in 1859. In 1859, an outbreak in Bengal contributed to transmission of the disease by travelers and troops to  Iran ,  Iraq ,  Arabia , and Russia. [ 27 ]  Japan suffered at least seven major outbreaks of cholera between 1858 and 1902. Between 100,000 and 200,000 people died of cholera in  Tokyo  in an outbreak in 1858\u20131860. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2302", "text": "In 1854, an outbreak of cholera in  Chicago  took the lives of 5.5 percent of the population (about 3,500 people). [ 18 ] [ 38 ]   Providence, Rhode Island , suffered an outbreak so widespread that for the next thirty years, 1854 was known there as \"The Year of Cholera.\" [ 39 ]  In 1853\u20131854, London's epidemic claimed 10,739 lives. The  1854 Broad Street Cholera outbreak  in London ended after the physician  John Snow  identified a neighborhood  Broad Street pump  as contaminated and convinced officials to remove its handle to prevent people from drawing water there. [ 40 ]  His study proved contaminated water was the main agent spreading cholera, although he did not identify the contaminant. It would take many years for this message to be believed and fully acted upon. [ 41 ]   In Spain , over 236,000 died of cholera in the epidemic of 1854\u20131855. [ 42 ]  The disease reached South America in 1854 and 1855, with victims in Venezuela and Brazil. [ 31 ]  During the third pandemic, residents of  Tunisia , which had not been affected by the two previous pandemics, thought Europeans had brought the disease. They blamed their sanitation practices. Some United States scientists began to believe that cholera was somehow associated with African Americans, as the disease was prevalent in the South in areas of black populations. Current researchers note their populations were underserved in terms of sanitation infrastructure and health care, and they lived near the waterways by which travelers and ships carried the disease. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2303", "text": "From November 10, 1855, to December 1856, the disease spread through Puerto Rico, claiming 25,820 victims. [ 44 ]  Cemeteries were expanded to allow for the burial of victims of cholera. [ 45 ]  In  Arecibo , a large municipality of Puerto Rico, the number of people dying in the streets was so great that the city could not keep up. A man named Ulanga made it his responsibility to collect and carry the dead to the provisional  Cementerio de los Col\u00e9ricos . [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2304", "text": "The  fourth cholera pandemic  of the century began in the  Ganges Delta  of the  Bengal  region and traveled with Muslim pilgrims to  Mecca . In its first year, the epidemic claimed 30,000 of 90,000 Mecca pilgrims. [ 47 ]  Cholera spread throughout the Middle East and was carried to Russia, Europe, Africa and North America, in each case spreading from port cities and along inland waterways. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2305", "text": "The pandemic reached Northern Africa in 1865 and spread to sub-Saharan Africa, killing 70,000 in  Zanzibar  in 1869\u20131870. [ 48 ]  Cholera claimed 90,000 lives in Russia in 1866. [ 49 ]  The epidemic of cholera that spread with the  Austro-Prussian War  (1866) is estimated to have taken 165,000 lives in the  Austrian Empire , including 30,000 each in Hungary and Belgium and 20,000 in the Netherlands. [ 50 ]  Other deaths from cholera at the time included 115,000 in Germany, 90,000 in Russia, and 30,000 in Belgium. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2306", "text": "In London in June 1866, a localized epidemic in the East End claimed 5,596 lives, just as the city was completing construction of its major sewage and water treatment systems (see  London sewerage system ); the East End section was not quite complete. [ 52 ]  Epidemiologist  William Farr  identified the  East London Water Company  as the source of the contamination. Farr made use of prior work by  John Snow  and others pointing to contaminated drinking water as the likely cause of cholera in an  1854 outbreak . Quick action prevented further deaths. [ 18 ]  In the same year, the use of contaminated canal water in local water works caused a minor outbreak at  Ystalyfera  in South Wales. Workers associated with the company and their families were most affected, and 119 died. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2307", "text": "In 1867, Italy lost 113,000 lives; and 80,000 died of the disease in Algeria. [ 48 ]  Outbreaks in North America in the 1870s killed some 50,000 Americans as cholera spread from New Orleans to other ports along the Mississippi River and its tributaries. None of the cities had adequate sanitation systems, and cholera spread through the water supply and contact. [ 33 ] [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2308", "text": "According to A. J. Wall, the 1883\u20131887 part of the epidemic cost 250,000 lives in Europe and at least 50,000 in the Americas. Cholera claimed 267,890 lives in Russia (1892); [ 55 ]   120,000 in Spain ; [ 56 ]  90,000 in  Japan , and over 60,000 in  Persia . [ 55 ]  In  Egypt , cholera claimed more than 58,000 lives. The 1892 outbreak in  Hamburg  killed 8,600 people. Although the city government was generally held responsible for the virulence of the epidemic, it was not changed. This was the last serious European cholera outbreak, as cities improved their sanitation and water systems. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2309", "text": "From the Russian Empire, cholera most likely spread to European countries. In Russia, cholera vibrio was found in  Baku  in 1892. The authorities of the city, despite the mortality of the population from cholera for a long time did not recognize the outbreak of the epidemic. The residents of Baku left the city, including traveling to  Astrakhan , a city located in the delta of the Volga River. After quarantine measures were introduced in Astrakhan, rumors spread among the population that living people were being put in coffins, sprinkled with lime, and buried in cholera hospitals. These rumors provoked riots. During the riots, medical workers were killed, the cholera hospital was burned down, and the infected were sent home. The incidence of the disease increased dramatically after the riots. From June 14 to September 20, 1892, more than 3% of Astrakhan's population died of cholera, with 480 cases and 316 deaths per 10,000 inhabitants. This was the demographic maximum of the 1892 cholera epidemic. An estimate of excess mortality showed an increase of 278% in June and 555% in July over the same months in 1888\u20131894. Of all those admitted to Astrakhan hospitals, about 73% were workers living in hostels (shelters), about 5% were workers on ships, steamships, and barges, and 12% were artisans. The social composition by estates was as follows: 1983  peasants , 316 soldiers, 262  bourgeois , 12  Cossacks , 8  nobles  and 5 clergymen. Natives of Astrakhan and the province accounted for about 11% of the cases, 89% were seasonal migrants. Many children were orphaned due to the high mortality rate. Because cholera is characterized by waterborne transmission, cholera epidemics were observed in large cities along the Volga River. Much of the empire was infested with cholera vibrio. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2310", "text": "The  sixth cholera pandemic , which was due to the classical strain of O1, had little effect in western Europe because of advances in sanitation and  public health , but major Russian cities and the  Ottoman Empire  particularly suffered a high rate of cholera deaths. More than 500,000 people died of cholera in Russia from 1900 to 1925, which was a time of extreme social disruption because of revolution and warfare. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2311", "text": "Cholera broke out 27 times during the  hajj  at  Mecca  from the 19th century to 1930. [ 58 ]  The sixth pandemic killed more than 800,000 in  India . [ 12 ]  The 1902\u20131904 cholera epidemic claimed 200,000 lives in the  Philippines , [ 59 ]  including their revolutionary hero and first prime minister  Apolinario Mabini . A 1905 governmental report mentioned he reappearance of asiatic cholera, characterized that as noteworthy, and described a \"very strict marine quarantine\" and other measures being imposed in the archipelago to control it. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2312", "text": "The last outbreak of cholera in the United States was in 1910\u20131911, when the steamship  Moltke  brought infected people from Naples to New York City. Vigilant health authorities isolated the infected in quarantine on  Swinburne Island . Eleven people died, including a health care worker at the hospital on the island. [ 61 ] [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2313", "text": "In 1913, the  Romanian Army , while invading  Bulgaria  during the  Second Balkan War , suffered  a cholera outbreak  that resulted in 1,600 deaths. [ 64 ] [ 65 ] [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2314", "text": "During the outbreak, due to cholera frequently being spread by immigrants and tourists, the disease became associated with either outsiders or marginalized groups in societies. In Italy, some blamed  Jews  and  Romani , while in  British India  numerous  Anglo-Indians  ascribed the spread of cholera to  Hindu  pilgrims, and in the  United States  many accused  Filipino immigrants  of introducing the disease. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2315", "text": "As of March 2022, the  World Health Organization  (WHO) continues to define this outbreak as a current  pandemic , noting that cholera has become  endemic  in many countries. In 2017, WHO announced a global strategy aimed at this pandemic with the goal of reducing cholera deaths by 90% by 2030. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2316", "text": "The  seventh cholera pandemic  began in  Indonesia , called  El Tor [ 68 ]  after the strain, and reached  East Pakistan  (now  Bangladesh ) in 1963, India in 1964, and the  Soviet Union  in 1966. From  South America , it spread into Italy by 1973. In the late 1970s, there were small outbreaks in Japan and in the South Pacific. There was an outbreak in  Odessa  in July 1970, and there were also many reports of a cholera outbreak near  Baku  in 1972, but information about it was suppressed in the Soviet Union. [ 69 ]  In 1970, a cholera outbreak struck the  Sa\u011fmalc\u0131lar  district of  Istanbul , then an impoverished slum, claiming more than 50 lives. Because this incident was notorious, the district was renamed as Bayrampa\u015fa. Also in August 1970, a few cases were reported in  Jerusalem . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2317", "text": "Vibrio cholerae  has shown to be a very potent pathogenic bacterium causing many pandemics and epidemics over the past three centuries. However, most outbreaks are known to be self-limiting, meaning they come to an end after peaking, without human intervention. One of the mechanisms significantly determining the course of epidemics is phage predation. [ 70 ]  This process is strongly dependent on successful recognition of the bacteria by lytic phages, in which cell surface receptors play a crucial role. Bacteria can reduce their susceptibility by changing their surface receptors and  preventing phage adsorption. In the case of  V. cholerae , the changed receptor gene expression is due to an alteration in cell-density during its infection cycle, a process called quorum sensing (QS). The stool samples collected from patients contain clumps of bacterial cells, demonstrating the occurrence of cell-cell interaction in the latter stage of the infection cycle. QS is strongly regulated by two auto-inducer molecules, AI-2 and CAI-1. [ 71 ]  Evidently, these molecules will have a significant effect on the success of phage predation in  V. cholerae  infections. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2318", "text": "A previous study has unravelled the mode of action of auto-inducers on preventing predation on the level of phage entry. [ 72 ]  The study has shown that the aforementioned auto-inducers downregulate the ten biosynthetic genes of the surface O-antigen, which is primarily used as a phage receptor for Vibriophages. This mechanism results in an increased phage resistance. It can be stated that the loss of the ability to produce the receptor, reduces the possibility of a phage-dependent limitation or even elimination of  V. cholerae . This should be kept in mind when developing a treatment for enteric bacterial infections with phages as an intervention tool. Future approaches may include additional quorum regulators that operate as \u201cquorum quenchers\u201d to reduce quorum-mediated phage resistance. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2319", "text": "In 1992 a new strain appeared in Asia, a non-O1, nonagglutinable vibrio (NAG), which was named O139 Bengal. It was first identified in  Tamil Nadu , India, and for a while displaced El Tor in southern Asia. It decreased in prevalence from 1995 to around 10 percent of all cases. It is considered to be an intermediate between El Tor and the classic strain, and occurs in a new serogroup. Scientists warn of evidence of wide-spectrum resistance by cholera bacteria to drugs such as  trimethoprim ,  sulfamethoxazole  and  streptomycin . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2320", "text": "A persistent  urban myth  states 90,000 people died in Chicago of cholera and  typhoid fever  in 1885, but this story has no factual basis. [ 129 ]  In 1885, a torrential rainstorm flushed the  Chicago River  and its attendant pollutants into  Lake Michigan  far enough that the city's water supply was contaminated. But, as cholera was not present in the city, there were no cholera-related deaths. As a result of the pollution, the city made changes to improve its treatment of sewage and avoid similar events. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2321", "text": "Unlike  tuberculosis  (\"consumption\"), which in literature and the arts was often romanticized as a disease of denizens of the  demimondaine  or those with an artistic temperament, [ 130 ]  cholera is a disease that today almost entirely affects the lower-classes living in filth and poverty.  This, and the unpleasant course of the disease \u2013 which includes voluminous \"rice-water\" diarrhea, the hemorrhaging of liquids from the mouth, and violent muscle contractions which continue even after death \u2013 has discouraged the disease being romanticized. It is seldom presented at all in popular culture. [ 131 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2322", "text": "Human feces  ( American English ) or  faeces  ( British English ), commonly and in medical literature more often called  stool , [ 1 ]  are the solid or semisolid remains of food that could not be digested or absorbed in the  small intestine  of humans, but has been further broken down by bacteria in the  large intestine . [ 2 ] [ 3 ]  It also contains bacteria and a relatively small amount of  metabolic waste  products such as bacterially altered  bilirubin , and the dead epithelial cells from the lining of the gut. [ 2 ]  It is discharged through the  anus  during a process called  defecation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2323", "text": "Human feces has similarities to the feces of other animals and varies significantly in appearance (i.e. size, color, texture), according to the state of the  diet ,  digestive system , and general  health . Normally, human feces are semisolid, with a  mucus  coating. Small pieces of harder, less moist feces can sometimes be seen impacted in the  distal  (final or lower) end. This is a normal occurrence when a prior  bowel movement  is incomplete, and feces are returned from the  rectum  to the large  intestine , where water is further absorbed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2324", "text": "Human feces together with human  urine  are collectively called  human waste  or  excretion . Containing human feces and preventing spread of  pathogens  from human feces by the  fecal\u2013oral route  are the main goals of  sanitation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2325", "text": "The Bristol stool scale is a  medical  aid designed to classify the form of human feces into seven categories. Sometimes referred to in the UK as the Meyers Scale, it was developed by K.W. Heaton at the  University of Bristol  and was first published in the  Scandinavian Journal of Gastroenterology  in 1997. [ 4 ]  The form of the stool depends on the time it spends in the  colon . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2326", "text": "The seven types of stool are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2327", "text": "Types 1 and 2 indicate  constipation . Types 3 and 4 are optimal, especially the latter, as these are the easiest to  pass . Types 5\u20137 are associated with increasing tendency to  diarrhea  or urgency. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2328", "text": "Meconium  is a newborn  baby 's first feces."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2329", "text": "Human fecal matter varies significantly in appearance, depending on diet and health."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2330", "text": "Feces possesses physiological odor, which can vary according to diet and health status. For example, meat protein is rich in the amino acid  methionine , which is a precursor of the sulfur-containing odorous compounds listed below. [ 12 ] [ 13 ] [ 14 ] [ 15 ] [ 16 ]  The odor of human feces is suggested to be made up from the following odorant volatiles: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2331", "text": "(H 2 S) is the most common volatile sulfur compound in feces. [ 13 ]  The odor of feces may be increased when various pathologies are present, including: [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2332", "text": "Attempts to reduce the odor of feces (and  flatus ) are largely based on animal research carried out with industrial applications, such as reduced environmental impact of pig farming. See also:  Flatulence#Management , odor. Many dietary modifications/supplements have been researched, including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2333", "text": "On average, healthy humans eliminate 128 g of fresh feces per person per day with a  pH value  of around 6.6 as indicated by a  Fecal pH test . [ 23 ]  Fresh feces contains around 75% water and the remaining solid fraction is 84\u201393% organic solids along with some insoluble phosphate salts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2334", "text": "These organic solids consist of: 25\u201354% bacterial biomass, 2\u201325% protein or nitrogenous matter, 25% carbohydrate or undigested plant matter, and 2\u201315% fat. Protein and fat come from the colon due to secretion, epithelial shedding, and gut bacterial action. These proportions vary considerably depending on many factors but mainly  diet  and  body weight . [ 24 ]  The remaining solids are composed of insoluble calcium and iron phosphate salts, intestinal secretions, small amounts of dried  epithelial  cells, and  mucus . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2335", "text": "Sometimes undigested food may make an appearance in feces. Common undigested foods found in human feces are seeds, nuts, and corn, mainly because of their high  fiber  content. Beets may turn feces different hues of red. Artificial food coloring in some processed foods, such as highly colorful packaged breakfast cereals, can cause an unusual coloring of feces if eaten in sufficient quantities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2336", "text": "Undigested objects such as seeds can pass through the human digestive system, and later  germinate . One result of this is  tomato  plants growing where treated  sewage sludge  has been used as  fertilizer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2337", "text": "Clinical laboratory examination of feces, usually termed as stool examination or  stool test , is conducted for the sake of diagnosis; for example, to detect the presence of parasites such as  pinworms  and their eggs (ova) or to detect disease-spreading bacteria. A  stool culture \u2014the controlled growth of microbial organisms in  culture media  under laboratory conditions\u2014sometimes is performed to identify specific pathogens in stool. The  stool guaiac test  (or guaiac fecal occult blood test) is conducted to detect the presence of blood in stool that is not apparent to the unaided eye."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2338", "text": "The main pathogens that are commonly looked for in feces include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2339", "text": "Intestinal parasites  and their  ova  (eggs) can sometimes be visible to the  naked eye ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2340", "text": "Feces can be analyzed for various markers that are indicative of various diseases and conditions. For example,  fecal calprotectin  levels indicate an inflammatory process such as  Crohn's disease ,  ulcerative colitis , and  neoplasms  ( cancer )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2341", "text": "Also, feces may be analyzed for any  fecal occult blood , which is indicative of a  gastrointestinal bleeding ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2342", "text": "A quick test for fecal contamination of water sources or soil is a check for the presence of  E. coli   bacteria  performed with the help of  MacConkey agar  plates or  Petri dishes .  E. coli  bacteria uniquely develop red colonies at temperature of approximately 43\u00a0\u00b0C (109\u00a0\u00b0F) overnight. Although most strains of  E. coli  are harmless, their presence is indicative of fecal contamination, and hence an increased possibility of the presence of more dangerous organisms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2343", "text": "Fecal contamination of water sources is highly prevalent worldwide, accounting for the majority of unsafe  drinking water . In  developing countries  most sewage is discharged without treatment. Even in  developed countries  events of  sanitary sewer overflow  are not uncommon and regularly pollute the  Seine River  ( France ) and the  River Thames  ( England ), for example."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2344", "text": "Diarrhea (or diarrhoea in  British English ) is the condition of having three or more loose or liquid  bowel movements  per day. [ 26 ]  This condition can be a symptom of injury,  disease , or  foodborne illness  and is usually accompanied by abdominal pain. There are other conditions which involve some but not all of the symptoms of diarrhea, and so the formal medical definition of diarrhea involves defecation of more than 200 grams per day (though formal weighing of stools to determine a diagnosis is never actually carried out)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2345", "text": "It occurs when insufficient fluid is absorbed by the colon. As part of the  digestion  process, or due to fluid intake,  food  is mixed with large amounts of water. Thus, digested food is essentially liquid prior to reaching the colon. The colon absorbs water, leaving the remaining material as a semisolid stool. If the colon is damaged or inflamed, however, absorption is inhibited, and watery stools result."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2346", "text": "Diarrhea is most commonly caused by a myriad of  viral  infections but is also often the result of  bacterial  toxins and sometimes even infection. In sanitary living conditions and with ample food and water available, an otherwise healthy patient typically recovers from the common viral infections in a few days and at most a week. However, for ill or malnourished individuals diarrhea can lead to severe  dehydration  and can become life-threatening without treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2347", "text": "Constipation refers to  bowel movements  that are infrequent or hard to pass. [ 27 ]  Constipation is a common cause of painful defecation. Severe constipation includes obstipation (failure to pass stools or gas) and  fecal impaction , which can progress to  bowel obstruction  and become life-threatening."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2348", "text": "Bile  overload is very rare, and not a health threat. Problems as simple as serious  diarrhea  may cause blood in one's stool. Black stools caused by the presence of blood usually indicate a problem in the intestines (the black color is a sign of digested blood), whereas red streaks of blood in stool usually are caused by bleeding in the rectum or anus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2349", "text": "Human feces has historically been used as  fertilizer  for centuries in the form of  night soil ,  fecal sludge , and  sewage sludge . The use of untreated human feces in agriculture poses significant health risks and has contributed to widespread infection with  parasitic worms \u2014a disease called  helminthiasis , affecting over 1.5 billion people in developing countries."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2350", "text": "There are methods available to safely reuse human feces in  agriculture  as per the \"multiple barrier concept\" described by the  World Health Organization  in 2006. [ 28 ]  The approach to \"close the loop\" between human excreta ( sanitation ) and agriculture is also called  ecological sanitation . It may involve certain types of  dry toilets  such as  urine-diversion dry toilets  or  composting toilets ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2351", "text": "In humans, fecal transplants (or  stool transplant ) is the process of transplantation of fecal bacteria from a healthy individual into a recipient who has a certain disease, such as  irritable bowel syndrome . The resulting  inoculation  of healthy  gut flora  can sometimes improve the physiology of the recipient gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2352", "text": "Fecal bacteriotherapy \u2014also known as a fecal transplant\u2014is a medical procedure wherein fecal bacteria are transplanted from a healthy individual into a patient. [ 29 ] [ 30 ]  Recent research indicates that this may be a valuable method to re-establish normal gut cultures that have been destroyed through the use of antibiotics or some other medical treatments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2353", "text": "The  biogas  produced from feces when it is contained in  sewage  and treated in an  anaerobic digestion  process could be worth as much as US$9.5 billion. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2354", "text": "Washington DC plans to produce biogas from  sewage sludge , the by-product of  sewage treatment , which will save US$13 million a year. [ 32 ]  Teams from the Cambridge Development Initiative, led by Stanford researcher Maisam Pyarali, began a project in 2015 to convert sewage from the slums of  Dar Es Salaam  into biogas and fertilizer with solar concentrators. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2355", "text": "Paleofeces , also known as coprolites (though that name is more commonly used in reference to animal feces), are ancient human feces, often found as part of  archaeological  excavations or surveys. Intact feces of ancient people may be found in caves in arid climates and in other locations with suitable preservation conditions. These are studied to determine the diet and health of the people who produced them through the analysis of seeds, small bones, and parasite eggs found inside. They also may be analyzed chemically for more in-depth information on the individual who excreted them, using  lipid analysis  and  DNA analysis . The success rate of usable DNA extraction is relatively high in paleofeces, making it more reliable than skeletal DNA retrieval. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2356", "text": "In most human cultures, feces elicit varying degrees of  disgust . Disgust is experienced primarily in relation to the sense of taste (either perceived or imagined) and, secondarily to anything that causes a similar feeling by sense of smell, touch, or vision. As such, human feces are regarded as something to be avoided diligently: expelled in private and disposed of immediately and without a trace. It often is considered an unacceptable topic in polite conversation and its mere mention may cause offence in certain contexts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2357", "text": "An example of repulsion by feces from the  ancient world  is found in the writings called  Deuteronomy  used by  Jews  and  Christians :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2358", "text": "Designate a place outside the camp where you can go to relieve yourself. As part of your equipment have something to dig with, and when you relieve yourself, dig a hole and cover up your excrement. For the LORD your God moves about in your camp to protect you and to deliver your enemies to you. Your camp must be holy, so that he will not see among you anything indecent and turn away from you. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2359", "text": "Evolution can explain this disgust since feces are a significant disease vector, carrying many kinds of microorganisms that can sicken humans, including  E. coli ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2360", "text": "People from different cultures employ a variety of personal cleansing practices after defecation. The  anus  and  buttocks  may be either washed with liquids or wiped with  toilet paper  or other solid materials. In many  Muslim ,  Hindu  and  Sikh  cultures, as well as  Southeast Asia  and Southern Europe, water is usually used for anal cleansing using a jet, as with a  bidet , or most commonly, splashed and washed with the hand. In other cultures (such as many  Western countries ), cleaning after defecation is generally done with  toilet paper  only."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2361", "text": "There are many synonyms in informal  registers  for human feces. Many are  euphemistic ,  colloquial , or both; some are  profane  (such as  shit ), whereas most belong chiefly to  child-directed speech  (such as  poo  or  poop ) or to  crude humor  (such as  turd ). An example of an euphemistic term for feces is  number two ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2362", "text": "Human feces together with human  urine  are collectively referred to as  human waste  or human  excreta ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2363", "text": "In  medicine , the  ileal pouch\u2013anal anastomosis  ( IPAA ), also known as  restorative proctocolectomy  ( RPC ),  ileal-anal reservoir  ( IAR ), an  ileo-anal pouch ,  ileal-anal pullthrough , or sometimes referred to as a  J-pouch ,  S-pouch ,  W-pouch , or a  pelvic pouch , is an  anastomosis  of a reservoir pouch made from  ileum  (small intestine) to the  anus , bypassing the former site of the  colon  in cases where the colon and rectum have been removed. The pouch retains and restores functionality of the anus, with stools passed under voluntary control of the person, preventing  fecal incontinence  and serving as an alternative to a total proctocolectomy with  ileostomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2364", "text": "During a total proctocolectomy, a surgeon removes a person's diseased colon, rectum, and anus. [ citation needed ]   For the ileostomy, the end of the small intestine is brought to the surface of the body through an opening in the abdominal wall for waste to be removed.  People with ileostomies wear an external bag, also known as an  ostomy system  or stoma appliance, to collect waste which can be emptied and changed as needed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2365", "text": "With an optional ileo-anal pouch procedure, the pouch component is a surgically constructed internal intestinal reservoir; usually situated near where the  rectum  would normally be. It is formed by folding loops of small intestine (the  ileum ) back on themselves and stitching or stapling them together. The internal walls are then removed thus forming a reservoir often referred to as a 'pouch'. The reservoir is then stitched or stapled into anal area where the bottom of the rectum was.  The first pouch anal-anastomosis surgery in the world was performed by British surgeon  Sir Alan Parks  in 1976 at the London Hospital (called the  Royal London Hospital  since 1990).  After the first surgery, he continued to develop the procedure at  St Mark's Hospital  in London along with his colleague  John Nicholls . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2366", "text": "Pouch surgery is elective, meaning it is entirely optional, and should be done on the basis of choice by people who doctors deem suitable for a pouch after medical evaluations.  Pouch surgery is considered reconstructive with the benefit being for quality of life and not disease removal, similar in theory to a breast reconstruction after a mastectomy removes diseased breast tissue.  Before a pouch is created, a person's diseased colon and rectum are removed.  After disease removal, standard medical screening exams for pouch candidates include but are not limited to biopsies, radiology imaging, sphincter function tests, fertility consultations for people of childbearing age with the wish to get pregnant, and psychological support due to intensity of the pouch operations. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2367", "text": "A similar ileal pouch without the anal anastomosis is a  Kock pouch .  A Kock pouch is also called a 'continent ileostomy' because while a person has a pouch constructed inside their body, it is located near the abdominal wall and empties via a stoma from the ileum at the person's convenience. [ 3 ]   A Kock pouch does not restore the anal function.  The procedure was first premiered by Finnish surgeon  Nils Kock  in Sweden during 1969.  It was an evolution in bowel surgery because it created an ileum pouch for storage of waste inside the body eliminating the need for an external bag for waste collection.  An  ileostomy  without a Kock pouch functions constantly, meaning, a patient with ileostomy by itself is incontinent because waste is always moving down the bowel and thus the need for an external appliance bag.  Kock pouch surgery is also elective surgery that only provides a reconstructive benefit after disease removal.  It should be the patient's optional choice based on how a person wants to live their life."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2368", "text": "Ileo-anal pouches are constructed for people who have had their  colon  and  rectum  surgically removed due to disease, injury, or infection. Several diseases and conditions may trigger the need for surgical removal. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2369", "text": "There is debate about whether patients with  Crohn's disease  and  indeterminate colitis  are suitable candidates for an ileo-anal pouch due to the risk of the disease occurring in the pouch. Crohn's disease can manifest in many different parts of the digestive tract, so the removal of the colon and creation of a pouch, while alleviating symptoms that occurred in the large intestine plus possibly the rectum, does not eliminate Crohn's disease. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2370", "text": "Additional contradictions that may prevent a person from being able to undergo pouch surgery include but are not limited to weak sphincter muscles, advanced age (elderly) due to the higher risk of fecal incontinence, pelvic radiation therapy, and women with a history of obstetric complications. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2371", "text": "Ileum pouch surgery (Kock and IPAA) are  reconstructive procedures .  Reconstructive procedures do not cure disease.  Since they are not  curative , reconstructive surgeries are not medically necessary, meaning they are elective operations.  Several words can be used to describe an ' elective surgery ' including optional and patient's choice.  Pouch reconstruction should never be offered as the only option to a person because it is elective and should be a voluntary choice offered alongside other options that are safe for the person's individual circumstances. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2372", "text": "While both  ulcerative colitis  (UC) and  familial adenomatous polyposis  (FAP) patients and are sometimes controversially considered cured of problematic symptoms after pouch creation due to the removal of disease activity in the colon and rectum, there are still many complications that can arise. While life with a pouch is typically viewed by some people plus some medical professionals as a significant improvement compared to life with an ileostomy, patients living with a pouch may still face daily pains and discomforts including the inability to sleep through the night, a changed diet, severe or frequent gas pain, nutrient deficiencies, and the inability to digest certain foods."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2373", "text": "With regards to  ulcerative colitis  (UC), the disease is a systemic  immune mediated inflammatory disease , also often referred to as an  autoimmune  condition. [ 10 ]   The main risk UC presents is typically inflammation that causes ulcers in the lining of the colon and rectum.  This common expression happens in the mucosal layer of the intestine that is only present in the colon and rectum (not the small intestine), which is why the disease was named 'ulcerative colitis'.  Therefore, ulcerative colitis is considered 'cured' of the problematic disease activity in the colon and rectum only, after both the large intestine and rectum are removed.  Reasons to remove this mucosal layer include severe discomfort that reduces quality of life, bowel perforation from inflammation, and development of tumors that are cancerous from long-term inflammation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2374", "text": "Even after a person has their colon and rectum removed, the circumstances that created ulcerative colitis still lives on inside that person's body because it is a systemic  immune mediated  condition.  These conditions occasionally manifest in other ways including additional illnesses considered related to ulcerative colitis like  primary sclerosing cholangitis  (PSC) in the liver, the eye condition  uveitis , and certain forms of  arthritis  throughout the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2375", "text": "It is important to understand that pouch surgery does not cure a patient of ulcerative colitis, removal of the diseased mucosal layer in the colon and rectum cures the disease in the colon and rectum only, if the entire colon and full rectum are removed.  For example, if a rectal remnant remains, UC disease can be retained in the small remnant.  Active disease feels similar to ulcerative proctosis when the full natural rectum was in place.  It is also medically treated the same way ulcerative proctosis was before any surgery.  Even if the entire colon and rectum are removed to stop disease activity in this area, the underlying reasons for the expression of the disease in the large bowel and rectum's mucosal layer remain with the person. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2376", "text": "A pouch should never be offered as the only treatment option due to the fact it is  reconstructive  and not  curative .  People who need to have their colon and rectum removed are usually presented with several options including total proctocolectomy with end ileostomy (\"Barbie\" or \"Ken\" butt), colectomy with rectum left in place, pelvic pouch (ileo-anal pouch / IPAA), ileo-rectum anastomosis (IRA), or continent ileostomy such as a Kock pouch, for example, if someone has weak  sphincter  muscles or a diseased anus.  The end decision should always be the patient's choice, based on if their health permits the option to have a good outcome. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2377", "text": "Pouch surgery comes with a number of well known complications that a person will not be able to imagine as possibilities themselves, therefore, as part of the education and  informed consent  process before pouch creation surgery is scheduled, risks, complications, and safe alternatives need to be communicated. [ 14 ] [ 15 ]   If a person has  indeterminate colitis , they should also be informed before a pouch is recommended and created that their pathology is unknown due to the even higher risk indeterminate folks face. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2378", "text": "The most common complication of pouch surgery is an umbrella term called pouchitis that encompasses many causes of inflammation of the pouch.  The word 'pouchitis' simply means 'pouch inflammation' similar to 'tonsillitis' meaning 'tonsil inflammation' or 'sinusitis' meaning 'sinus inflammation'.  While ulcerative colitis pouch patients may experience a dysbiosis sparked type of inflammation more than people who get a pouch because of cancer or FAP, pouchitis can be caused by a number of factors in any pouch. [ 18 ]   Pouchitis is grouped into four main categories of origin: inflammatory, mechanical, surgical, or functional.  Pouchitis, meaning pouch inflammation from various root causes, can be a driver of pouch dysfunction for some. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2379", "text": "The surgical procedure for forming an ileal pouch-anal anastomosis (IPAA) was pioneered by  Sir Alan Parks  at the London Hospital, today called the  Royal London Hospital , in 1976."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2380", "text": "Parks' pouch surgery was originally envisioned as a quality of life enhancing procedure for people who needed to have their colon and rectum removed.  People who opted to have the procedure would be able to avoid an ileostomy by restoring intestinal continuity with elective, or optional, ileo-anal pouch surgery.  Shortly after performing the world's first few pouch procedures in 1976, Sir Alan along with  John Nicholls  joined  St Mark's Hospital  also in London where they continued to develop the intestinal pouch procedure.  The pair first published details of the procedure in the  British Medical Journal  in 1978 with the article \"Proctocolectomy without ileostomy for ulcerative colitis\". [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2381", "text": "Sir Alan Parks' ileo pouch-anal anastomosis (IPAA), was a surgical advancement from the ileoanal anastomosis procedure developed in the 1940s.  With an ileum-anal anastomosis, the entire colon and rectum were removed.  Next a surgical join (anastomosis) was used to connect the end of the small intestine (ileum) to the anus.  It was described by the German surgeon Nissen in 1934 and American surgeons Ravitch and Sabiston in 1947.  The ileum-anal anastomisis [ check spelling ]  was reported to have a high of frequency of liquid movements making it uncomfortable for many people. [ 21 ]   It was also a surgical advancement from the  Kock pouch  first performed in Sweden by Finnish surgeon  Nils Kock  in 1969 because Parks' ileum pouch-anal anastomosis (IPAA), unlike Kock's 'continent ileostomy' allowed for restoration of anal evacuation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2382", "text": "The original Sir Alan S-pouches had a bit of intestine at the bottom of the design that often made them difficult to evacuate.  Some patients later underwent advancement surgery to remove the extra tip of small intestine and lower the pouch directly onto the anus to remedy evacuation difficulties. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2383", "text": "In 1980, surgeons in Japan published the first study on the J-shaped pouch. J. Utunomiya is created with its creation. [ 23 ]   The J-shaped pouch design eliminated the 'conduit' or bit of intestine at the bottom of Sir Alan Parks' S-pouch formation making it easier for people to empty a J-pouch.  As intestinal pouch surgery became more common, the J-pouch eventually became the dominant shape.  J-pouches are easier for surgeons to construct than the hand sewn S or W formations because the Js are from two loops of ileum plus with the invention of the stapler, Js could be stapled, instead of hand-sewn.  J-pouches are considered faster and easier to make over Ss and Ws. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2384", "text": "The same year as Sir Alan Parks' unexpected death in 1982, his St Mark's Hospital colleague,  John Nicholls  premiered the W-pouch which was an augmentation of the J-pouch made to expand the pouch's capacity and reduce the person's frequency of bowel movements. [ 26 ]   Nicholls' W-pouch is explained as two J-pouches placed together to make the higher capacity W-pouch."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2385", "text": "The W-pouch was entirely hand-sewn and required a very experienced and highly skilled surgeon plus more time in the operating room. [ 27 ] [ 28 ]   A J-pouch was not as technical and therefore, more surgeons could perform the procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2386", "text": "In the United States, Australian born colorectal surgeon  Victor Warren Fazio  was a driving force behind the procedure's adaptation into American colorectal surgery offerings.  He established the  Cleveland Clinic 's prestigious pouch practice in 1983 when the clinic performed its first pouch surgery.  In 2002 the Cleveland Clinic opened the world's first pouch center with its \"Ileal Pouch Center\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2387", "text": "About the same time as the Cleveland Clinic began offering the restorative proctocolectomy procedure (RPC), surgeons at the  Mayo Clinic  in Minnesota also started offering it to suitable patients including Roger R. Dozois who published several early studies on the pouch operation in the United States. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2388", "text": "By the early 1980s, the ileal pouch procedure had become part of specialist colorectal surgical practices not just in the United Kingdom and United States but worldwide.  Following the unexpected death of  Sir Alan Parks  in 1982, his colleague  John Nicholls  along with the pouch surgery team at  St Marks Hospital  collaborated with a number of leading hospitals globally to share pouch surgery knowledge Zane Cohen is credited with being a leader in Canada's development of pouch surgery. [ 31 ] [ 32 ]  Rolland Parc was a force behind its early evolution in France. [ 33 ]  Gilberto Poggioli is credited with being at the forefront of establishing the pouch a surgical offering in Italy. [ 34 ] [ 35 ] [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2389", "text": "It is generally considered best practice to create and manage ileum pouches at a facility that has specialized and experienced clinicians specifically for intestinal pouch care.  Individual doctors and facilities can communicate their level of pouch experience to potential pouchees, people already living with a pouch interested in continued care, or loved ones who care for a person eligible for pouch construction surgery, or for loved ones already with a pouch.  Colorectal ,  coloproctology , and/or  proctology surgeons  should be able to communicate their pouch surgery success and failure rates.  Gastroenterologists  and surgeons should also be able to refer people to pouch specialists for a second opinion on an existing recommendation or for continued pouch care."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2390", "text": "Intestinal pouches are considered optional reconstructive procedures to be done by the patient's choice since pouch surgery itself does not cure disease.  Pouch surgery can only take place after disease is removed.  Many national gastroenterology associations including the  British Society of Gastroenterology  (BSG) [ 37 ]  and the European Crohn's and Colitis Organisation (ECCO) [ 38 ]  recommend that pouches should ideally be created at facilities that have specialized pouch centers when possible due to the high level of technical skill required for multidisciplinary management of a pouch.  Numerous studies also show that there is a direct relation between the success of a pouch and the experience a surgeon has with previous pouch creations. [ 39 ] [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2391", "text": "In addition to specialized doctors for colorectal surgery, gastroenterology, pathology, radiology, gynecology and urology, fertility, psychology, nutrition, and rehabilitation including physiotherapy, facilities with pouch centers often also have a specialized pouch nurse or pouch nursing team.  The pouch nurse is usually an extension of the IBD nursing team or stoma nurse team.  However, pouch nurses are also trained for pouches created from injury, infection, FAP, cancer and other reasons.  Pouch nurses provide healthcare, advice, and support specific to the concerns of pouch patients before and after surgery. [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2392", "text": "In this elective and reconstructive  surgical procedure , a pouch, or intestinal reservoir, made from  ileum  (small intestine) is attached to the  anus  after the  colon  (large intestine) and  rectum  have been removed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2393", "text": "The entire procedure can be performed in one operation, but is usually split into two or three procedures based on the person's overall health at the time of surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2394", "text": "If a colectomy is planned, and not done as an emergency due to severe injury or illness and the person is in good health, some surgeons will recommend a two-step procedure.  When done as a two-step, the first operation (step one) involves a  proctocolectomy  (removal of the large intestine and rectum), and fashioning of the pouch. The patient is given a temporary defunctioning  ileostomy  (also known as a \"loop ileostomy\"). After a healing period determined by the surgeon based on the individual patient, the second step is performed, in which the ileostomy is reversed. This step is referred to as ileostomy reversal or takedown.  The reason for the temporary ileostomy is to allow the newly constructed pouch to fully heal without waste passing through it, thus avoiding leaks that can lead to infection. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2395", "text": "When a colectomy is performed as an emergency (which can arise from  toxic megacolon  and other complications including infection), or when the patient is extremely ill, the colectomy and pouch construction are performed in separate stages, resulting in a three-part surgery. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2396", "text": "Outside of serious illness, some surgeons also prefer to perform a  subtotal colectomy  (removing all the colon except the  rectum ) first, since removal of the rectum can lead to complications with the anal  sphincters . After the subtotal colectomy, the second operation consists of pouch creation with installation of a double or loop ileostomy to protect the pouch while it heals.  Waste continues to exit through an opening in the abdominal wall.  Then usually three to six months later when surgeons feel the pouch has healed, the loop stoma is reversed and the pouch becomes fully operational restoring intestinal continuity. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2397", "text": "Just as debate continues on which formation of pouch functions best, there is also an ongoing discussion about the pouch's type of anal anastomosis - or method used to attach the pouch to the anal canal.  Both methods have risks and benefits."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2398", "text": "The pouch can also be formed as part of a three step procedure for people of childbearing age who have not completed their family planning.  When there is a wish for pregnancy, the process can be paused after subtotal colectomy until family planning is complete if doctors feel remaining disease in the rectum, if any, can be safely managed until removal during pouch creation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2399", "text": "A fall in female fertility was reported in a Danish study by Olsen et al. in 1999 showing a drop after pouch surgery to less than 50% of the normal population. [ 51 ]   There are well researched risks to fertility for both men and women.  Highly specialized pouch centers globally typically offer fertility counselling as part of their patient selection and informed consent process. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2400", "text": "A rare risk to male fertility is nerve damage that impairs or prevents ejaculation.  Risks to fertility for women include removal of the rectum reducing fertility by at least 50%, a dysfunctional pouch sparking a hostile environment in the pelvis preventing embryo implementation in the uterus and scar tissue formation over fallopian tubes blocking ovulation, although, scar tissue formation appears to be less likely with laparoscopic than open surgery. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2401", "text": "Women who choose the option to undergo pouch surgery before childbirth, should also undergo a fertility evaluation before surgery that includes an egg preservation consultation especially if she is over the age of 35 years.  With the pouch surgery potentially reducing fertility, the  in vitro  fertilization  (IVF) treatment a younger woman experiencing pouch related infertility may need to rely on to conceive, may not legally be available to the older woman if she later learns past the cutoff-age that her situation requires IVF to get pregnant.  Most women are not aware of age limits to IVF treatment using their own eggs - especially if they are living, studying, or working away from their hometown or abroad at the time of their operations. [ 54 ] [ 55 ] [ 56 ] [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2402", "text": "The general public's lack of widespread knowledge about IVF regulations also applies to child adoption laws.  Most men and women are not aware that some countries place age bans on adopting newborns.  For example, in Germany adoption of an infant is prohibited if a parent is over the age of 40 years.  These adoption age bans combined with the risk of pouch related fertility complications, plus potential IVF age cut-off limits then increases the need for a person to plan to preserve fertility before pouch surgery commences in order to improve chances of later completing a wish for a family. [ 58 ] [ 59 ] [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2403", "text": "While most people who undergo elective reconstructive pouch surgery have either no issues or occasional minor discomfort, some pouches experience more serious complications that need medical management with a variety of therapies including medication and/or additional surgery. \n [ 61 ] [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2404", "text": "Pouchitis  is a general term that refers to a wide spectrum of diseases and conditions that cause inflammation of the pouch. It is a common complication after IPAA/RPC. People report many symptoms including abdominal pain or cramps, increased bowel frequency, urgency of movements, strong evacuation urges, daytime incontinence, nocturnal seepage, and/or rectal bleeding. Studies show pouchitis occurs more often in people who got their pouch because of ulcerative colitis rather than familial adenomatous polyposis (FAP) which suggests that the pathogenic (microbial) background of UC may contribute to the development of pouchitis in some pouches. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2405", "text": "Diagnosis of pouchitis: \nPouchitis is diagnosed based on the presence of symptoms together with endoscopic and histological evidence of pouch inflammation. For example, biopsies may be taken during a pouchoscopy (a camera exam like a colonoscopy but for the pouch) to rule out infection from  Clostridioides difficile  infection  (C-diff) or  Cytomegalovirus  (CMV). Treatment of infections usually begins with antibiotics and may also include multi-strain probiotics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2406", "text": "After exams and tests, pouchitis is divided into two categories based on findings: idiopathic or secondary. In idiopathic pouchitis, the cause of inflammation is still unclear. With secondary pouchitis, there is an association with a specific causative or pathogenetic factor. Secondary pouchitis can be classified into subgroups. It is possible to have one or more causes of pouch inflammation at the same time. [ 64 ] [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2407", "text": "Antibiotic therapy for pouchitis: \nStandard treatment of pouchitis when first reported (acute pouchitis) without any other obvious cause identified such as infection or anal join leak (fistula) is oral antibiotics for two weeks, typically ciprofloxacin 500\u00a0mg every 12 hours.  Alternatives to ciprofloxacin for initial therapy include metronidazole 500\u00a0mg (twice daily) or tinidazole 500\u00a0mg (twice daily). [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2408", "text": "For pouches with acute idiopathic pouchitis, response to antibiotic therapy is typically examined clinically by asking the patient if they have experienced an improvement with their symptoms plus looking endoscopically using a pouchoscopy after completing antibiotic therapy. While endoscopic mucosal healing may lag behind symptomatic improvement, mucosal healing is a treatment target for patients with pouchitis. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2409", "text": "Cuffitis: \nCuffitis is inflammation of the retained rectal 'cuff' usually in a stapled pouch-anal anastomosis or the spot where the intestinal pouch was attached to the anus to restore anal evacuation.  Symptoms are typically similar to ulcerative proctosis for ulcerative colitis pouches including burning in the anal canal, a change in bowel movements, and sometimes rectal bleeding. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2410", "text": "Cuffitis diagnosis: \nMost expert pouch centers plus national gastroenterology society guidelines worldwide recommend a cuff be no longer than 2\u00a0cm with the aim to staple the pouch at the level of the anorectal junction, [ 48 ] [ 68 ]  leaving about 1\u00a0cm of rectum or mucus layer behind for the staple to attach the pouch to the anus. [ 69 ] [ 67 ] [ 70 ]   This retained 1 to 2\u00a0cm of rectum can therefore, sometimes retain ulcerative colitis in UC pouches.  In contrast, hand sewn pouch-anal anastomosis' typically do not retain any mucus layer but sometimes a cuff is also used and it might cause discomfort for some hand sewn pouches.  Cuffitis is clinically diagnosed by symptoms plus endoscopically (pouchoscopy)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2411", "text": "Treatment of cuffitis: \nFirst-line therapy for acute cuffitis due to retained rectal mucosal layer is usually similar to the treatment for ulcerative proctosis that ulcerative colitis patients would have likely used before pouch surgery.  Mesalazine  suppositories or enemas are sometimes prescribed first (brand names include Asacol, Canasa, and Pentasa).  If those do not provide enough relief then treatment might be escalated to corticosteroid suppositories or enemas such as Budesonide.  Biological therapy may be prescribed if all other medical therapies fail to manage cuffitis and the person either is not suitable for or does not want to undergo a revision operation to remove the retained cuff and hand sew the pouch on the level of the dentate line (spot where anal skin changes to rectal mucus layer). [ 67 ] [ 71 ] [ 72 ] [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2412", "text": "Crohn's disease of the pouch: \nSome people undergoing IPAA/RPC may be later diagnosed with underlying Crohn's disease because the disease likely had not fully expressed itself at the time of surgery.  Crohn's disease of the pouch is associated with high failure rates.  Pouches may experience fistula leaks that cause pelvic sepsis and other complications. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2413", "text": "Treatment of Crohn's disease of the pouch: \nIf a person later diagnosed with Crohn's disease of the pouch wishes to keep their pouch operational, in some circumstances medical management might be possible.  Typically this is done with the prescription of biologics.  It may take more than one drug prescription to find a suitable biologic that encourages the desired anti-inflammatory response."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2414", "text": "Celiac disease: \n Celiac disease  is an autoimmune condition that causes inflammation in the small intestine after gluten is eaten.  It can cause pouchitis symptoms and discomfort.  Some pouches that are celiac initially get misdiagnosed with Crohn's of the pouch.  Celiac disease is typically diagnosed by biopsy of the pouch. [ 75 ] [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2415", "text": "Treatment of Celiac disease: \nTypically, the first therapy approach to manage Celiac disease in person with an ileum pouch is dietary modification to reduce and/or eliminate gluten."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2416", "text": "Other inflammatory conditions including IgG and IgG4: \nImmunoglobulin related diseases can also cause problems for a pouch.  The two most common that are biopsied for are IgG and IgG4.  IgG molecules can initiate inflammatory reactions, both good and bad.  When the autoimmune reaction is inappropriate, a pouch might have problems with IgG.\nIgG4 is a subclass of IgG.  IgG4 disease is a chronic immune-mediated fibroinflammatory disorder that can manifest with painless enlargement of organs or tumor-like masses. [ 77 ] [ 78 ] [ 79 ] [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2417", "text": "Biopsies of the pouch should confirm if an infection is the root cause of pouch inflammation. If an infection from  Clostridioides difficile  (C-diff) or  Cytomegalovirus  (CMV) is found, initial therapy is usually antibiotics. [ 81 ] [ 82 ]  Certain infections such as a  Clostridioides difficile  (C-diff) might also be treated with probiotics just as a C-diff infection in a person who still has their colon would be treated. Probiotics that are prescribed for pouchitis (specifically pouchitis diagnosed as being caused by dysbiosis) are often also prescribed for C-diff. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2418", "text": "The pouch surgery itself can be the reason for some complications. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2419", "text": "Anastomotic leaks: \nAnastomotic leaks occur on the lines where the pouch was sutured or stapled.  They usually occur close to the time of surgery but can appear months or years later.  When an anastomotic leak occurs, it can form a fistula or tract of fluid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2420", "text": "Fistulas: \nMost fistulas will connect from an anastomotic leak to another area of the body such as a pouch-vagina fistula, perianal fistula, or presacral fistula with pelvic collection.  In some circumstances fistulas develop years after pouch creation due to the development of Crohn's disease.  Fistula's caused by Crohn's disease are often treated with biological therapy while a fistula from an anastomotic leak requires different therapies as biologics rarely help close a leak in a surgical suture or staple line of the pouch.  Different potential treatment options for an anastomotic fistula depend on the leak's location and include but are not limited to ENDO-Vac sponge, needle-knife therapy, draining seton, or cutting seton. [ 84 ] [ 85 ] [ 86 ] [ 87 ] [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2421", "text": "Pelvic collection/sinus: \nA pelvic collection or collection of fluid anywhere from a leak is called a sinus.  When an anastomotic leak is not treated promptly or does not heal it can cause pelvic sepsis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2422", "text": "Pelvic sepsis: \nPelvic sepsis also called peri pouch sepsis is a main cause of pouch failure and it creates conditions that make major revisionary surgery difficult."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2423", "text": "Large or small pouch: \nStandard guidelines for J-pouch construction is to use two loops of 15\u201320\u00a0cm ileum.  If the pouch is too small, the pouch will have a small volume.  This will increase the frequency of moments and could also be a cause of pouch failure. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2424", "text": "Pouch prolapse: \nA pouch can either tilt or twist when stapled onto the anus causing prolapse. Pouch prolapse is also sometimes referred to as a floppy pouch. [ 90 ]   Pouch prolapse from a pouch being tilted or twisted can also cause pouch fistulas to develop, especially pouch-vagina fistulas.  Prolapse can also happen after the pouch is already in use.  With symptoms for pouch prolapse, a person typically has evacuation difficulties, seepage, pain, nausea, abdominal pain, or overt external prolapse of tissue. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2425", "text": "Strictures or stenosis \nNarrowing of the anal canal under the pouch can cause evacuation difficulties.  Anal stricture can be a cause of pouch failure if not managed properly.  Anal stricture is a common complication of pouch surgery.  It is treated with dilatation or stretching under anesthesia.  Some people are also prescribed home dilatation routine using a  Hegar dilator  to manage chronic stenosis that keeps returning after dilatation. [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2426", "text": "U-bend: \nThis happens when the surgeon fires the linear stapler and it malfunctions.  Usually the flaw is not noticed until after surgery is complete during first pouchoscopy.  The pouch is called a \"U\" bend because instead of stapling the two full sections of ileum together into a \"J\", the stapler does not create the 'J' but instead retains the shape of a 'U'."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2427", "text": "Pelvic floor dysfunction and evacuation difficulties \nPelvic floor dysfunction is a common complication of pelvic surgery.  The Mayo Clinic believes it is an under reported complication of IPAA/RPC surgery with up to 75% of pouch patients experiencing non-relaxing pelvic floor dysfunction.  Biofeedback therapy is the main treatment for pelvic floor dysfunction. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2428", "text": "Cancer is a rare event after a pouch is created.  However, retained rectal mucosa can develop dysplasia over time especially if cuffitis is an ongoing complication.  Cancer can also develop in the pouch when there has been long-term pouchitis (inflammation of the pouch for any reason).  People who got their pouch as a result of bowel cancer may also experience cancer of the pouch. [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2429", "text": "Removal of the entire large intestine (colon) and amounts of the terminal ileum at the end of the small intestine leads to fluid and nutritional absorption issues for all pouches.  The colon absorbs water, salts, and some key nutrients.  Dehydration can occur if a person does not get enough fluids."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2430", "text": "The importance of ileum is that it absorbs key vitamins and minerals including  B12 ,  potassium , and  magnesium . In medical terms, low potassium is called  hypokalemia .  When a pouch is constructed small amounts of ileum are lost to the stomas and any stoma revisions.  The pouch itself is also made from ileum.  If a pouch is defunctioned (also explained as disconnected and/or pouch failure) the person also loses this extra amount of ileum when the pouch is disconnected from the digestive tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2431", "text": "People with a pouch are at a further health risk if they experience excessive potassium loss due to things like vomiting, diarrhea, and prescription medications that increase urination. This is because potassium is a key electrolyte that helps regulate the heart and if levels become too low, a person can quickly become life-threateningly ill.  When levels are dangerously low, medical intervention with supplementation either orally or intravenously becomes necessary. [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2432", "text": "Intestinal obstruction after ileal pouch-anal anastomosis (IPAA) surgery can occur due to various reasons such as adhesions (scar tissue ), strictures (narrowing at the anastomosis site), and Pouchitis (inflammation of the ileal pouch). [ 97 ]  Perforation at the site of attachment of the ileum to the rectum, or near the J-pouch, is a serious complication. [ 98 ] [ 99 ]  It can occur due to several reasons. But sometimes when pouchitis is not treated well, it gradually weakens the intestinal wall, which can eventually perforate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2433", "text": "When a pouch fails, suitable patients can choose to undergo surgery to repair the pouch or completely redo a pouch's anal-anastomosis or redo the entire pouch (if enough terminal ileum remains to produce a second pouch). [ 100 ] [ 101 ]   The cause of the problem that triggered a person's need for pouch salvage surgery will determine which method an experienced revision surgeon recommends as the surgical approach most likely to produce the best result possible.  Revisional surgeries are considered highly specialized. [ 102 ]   They require a skilled surgeon with complex revisional experience for the best chance at a good result.  Many expert pouch surgeons advocate for early referrals to specialists for best outcomes. [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2434", "text": "Sometimes the root cause of pouch dysfunction can be managed with more conservative methods such as using an ENDO-Vac sponge for an anastomotic defect that leaks, needle knife therapy for fistulas and sinuses, or cutting seton for a low lying peri-anal fistula that does not impact the pouch's anal anastomosis (and many not even be related to the pouch itself).  When a more conservative method will not work or an attempt fails, bigger surgicial salvage procedures are then recommended, if the operation will have a chance to succeed and restore quality of life. [ 104 ] [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2435", "text": "If a pouch has a troubled anal-anastomosis that leaks and causes sepsis or if a person retained more than the recommended amount of rectum (a rectal cuff of no more than 2\u00a0cm follows global colorectal surgery recommendations for an ulcerative colitis person), then an experience surgeon may be able to 'redo' the anal anastomosis by removing excess rectum.  Similarly, if a standard cuff of 1\u20132\u00a0cm was used, a revision surgeon still might be able to remove that and lower the pouch onto the anus.  In this scenario, the surgeon typically tries to save and reuse the existing pouch, but this is not always possible if the pouch is also damaged from complications or has technical flaws.  It might not be possible for an experienced salvage surgeon to redo an anal-anastomosis that has already been hand sewn or has a complication like a fistula or sepsis damage too close to the anus because this presents a surgical situation that is high risk to not heal properly and cause more complications. [ 106 ] [ 104 ] [ 107 ] [ 108 ] [ 109 ] [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2436", "text": "If a person's pouch body is troubled, then an experienced pouch surgeon may be able to make a second pouch if the person's previous surgeries retained enough ileum to still safely create a second pouch.  Experienced revision surgeons will not create a second pouch if it risks putting the person into nutritional difficulties (including  short bowel syndrome ) because too much small bowel would be lost. [ 106 ] [ 104 ] [ 107 ] [ 108 ] [ 109 ] [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2437", "text": "Occasionally, an experienced revision surgeon may need to alter the shape of the original pouch they are attempting to rescue.  For example, when there is not enough ileum to create a second pouch or if the person's anatomy (mesentery and/or vascular supply) does not allow for the pouch to reach to the anus.  This means the shape of a J-pouch may be transformed into an S, W, or even an H to repurpose functional ileum from the primary, or first pouch surgery, when retaining the original shape would not be successful but altering it could rescue the pouch situation. [ 110 ] [ 111 ] [ 112 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2438", "text": "People can also choose to convert their failed ileo pouch-anal anastomosis (IPAA) to a continent ileostomy such as a  Kock pouch  in some circumstances. [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2439", "text": "If a repair or redo can not be undertaken because of factors like severe disease, or a repeat surgery fails, or a patient wishes to have their pouch removed with undergoing additional surgery, a pouch excision operation can be performed to remove the pouch.  Removal of a pouch is a big operation that comes with complication risks. [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2440", "text": "Ileo pouch-anal anastomosis surgery (IPAA) also called Reconstructive Proctocolectomy (RPC) was originally designed and premiered to improve quality of life for people who needed to have their colon and rectum removed because it avoided the need for stool collection in an external bag and restored the anal evacuation route."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2441", "text": "The surgical evolution of the anal pouch also empowered people who were forced to lose their colon and rectum because of disease with choice: they could decide to live their life with an ileostomy or undergo reconstructive surgery to restore anal evacuation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2442", "text": "Ileo pouch-anal anastomosis (IPAA) surgery is generally viewed as providing benefits over living with an ileostomy from a total proctocolectomy.  However, not all people may consider extra surgery as a 'benefit' and therefore, some people opt to forgo the pouch option and remain living with an ileostomy after disease removal.  Pouches are the individual's choice based on how a person wants to live their life."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2443", "text": "After the colon is removed a person does not have the ability to form solid stool.  Because waste will always be liquid, people experience several movements per day when their pouch's capacity is full.  The aim of pouch surgery is 4-8 movements per day, although, some people experience many more.  The number of movements per day may seem similar to when someone was in an  ulcerative colitis  (UC) flare, for people who got their pouch as a result of UC.  People with a small volume pouch will likely experience more movements. [ 115 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2444", "text": "Additionally, liquid stool directly from the ileum no longer benefits from the colon removing digestive enzymes before a bowel movement.  This means liquid stool produced by the ileum can be aggressive on the skin around the anus.  Discomfort, including experiencing itching and/or burning around the anus' opening, can be treated with creams, by using a squirt water bottle or hand bidet after each movement to wash away enzymes, or by placing a piece of gauze between buttocks to prevent seepage from irritating the skin around the anus. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2445", "text": "The experience of learning how to use a newly functional anal pouch can be distressing for some.  Sharp pains, explosive moments, and anal seepage are common initial sensations.  Specialized pouch centers often have a pouch nurse that educates a person for how to safely empty the pouch without causing avoidable complications like incisional hernias after reversal or takedown surgery. [ 117 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2446", "text": "The process of adjusting to life with an anal pouch can take many months.  Mayo Clinic research estimates that up to 75% of people with a pouch might experience some level of pelvic floor dysfunction after pouch surgery. [ 118 ]  For pouches that are difficult to evacuate or experience anal seepage, biofeedback therapy can be prescribed. [ 119 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2447", "text": "Water and salts are typically reabsorbed into the body by the colon or  large intestine .  However, people with an ileum pouch have lost their entire colon and at least small amounts of  ileum .  Experiences like having sudden  diarrhea ,  vomiting  from sickness,  sweating  in hot weather, sweating from  physical exercise , or from not drinking enough  fluids  can all cause dehydration.  Having an episode of pouchitis, or pouch inflammation, can also cause dehydration for some if the episode causes an increase in bowel movements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2448", "text": "This experiences mean that people with pouches, like people with ileostomies, will require drinking more fluids and eating more salt to not become dehydrated.  Dehydration  can cause feelings of  dizziness ,  physical weakness , and/or  fatigue . People may also notice that urine has changed from light yellow and become darker and more concentrated. [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2449", "text": "It is important that people with pouches maintain healthy  fluid  and  salt levels  because chronic dehydration increases the risk for  kidney stones  and even  kidney failure .  If a person becomes severely dehydrated, hospital admission for intravenous administration of fluids to restore hydration safely may be required. [ 116 ] [ 121 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2450", "text": "Many people with a pouch eat their normal diet after surgery while others have to alter their diet due to discomfort when digesting certain foods.  Others experience more watery output after eating specific foods like processed sugary snacks which may require some people with pouches to use dietary or medical interventions like fiber products or doctor prescribed tablets to control watery stool and prevent dehydration. [ 122 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2451", "text": "People with a pouch can follow any diet they choose while monitoring their overall nutritional status due to the loss of bowel causing absorption issues.  People diagnosed with vitamin or mineral deficiencies may be prescribed injections or tablets.  Others may be referred to a nutritionist to design meals that provide additional amounts of needed vitamins and minerals. Studies show that some foods may also contribute to pouch inflammation. [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2452", "text": "Having an intestinal pouch is considered a rare condition.  Some national organizations and specialist charities usually associated with inflammatory bowel disease (IBD) or ostomies provide some information to people considering or who have chosen to undergo elective pouch surgery. Some of the larger national organizations globally include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2453", "text": "Implantable bulking agents  are self-expanding solid  prostheses  which are implanted in the tissues around the  anal canal . [ 1 ]  It is a  surgical treatment for fecal incontinence  and represents a newer evolution of the similar procedure which uses  perianal injectable bulking agents ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2454", "text": "The implantable bulking agents represent the most recent stage of development of a similar procedure which uses  perianal injectable bulking agents . That procedure in turn was developed from use of injectable bulking agents in urology to treat  urinary incontinence . Many different injectable materials have been used. The biggest problem with injectable materials is that they seem to have only a temporary effect. Over time, the material degrades and may migrate away from the injection site. For example, one study investigated the outcome and ultrasound appearance of 3 of the commonly used injectable bulking agents (Durasphere, PTQ, Solesta) after an average of 7 years. The researchers reported that typically about 14% of the original volume of material was still identifiable on ultrasound, and that complete disappearance of the materials on ultrasound was correlated with poorer clinical outcomes. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2455", "text": "Implantable bulking agents use multiple cylindrical HYEXPAN ( polyacrylonitrile ) implants. Marketed as \"Gatekeeper\" by Medtronic, Minneapolis, USA, it was first used to treat  gastro-esophageal reflux disease . [ 1 ]  Production of the implant system was transferred to THD S.p.A., Correggio, Italy. Gatekeeper now has a  CE marking , and was registered for the treatment of fecal incontinence in 2010. [ 4 ]  The first publication describing use of these implants in FI was in 2011. [ 5 ]  Several other publications appeared and the results were initially promising. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2456", "text": "In the original description, Gatekeeper used four self-expandable, solid, thin cylinders. [ 4 ]  Subsequently, six of the prostheses were used. [ 6 ]  An advancement of the procedure was described in 2016, marketed as \"SphinKeeper\". [ 4 ]  SphinKeeper uses 10 prostheses which are slightly thicker and longer compared to those used in the Gatekeeper implant system. [ 4 ]  One publication stated that new generation SphinKeeper implant system has replaced use of Gatekeeper, and that the use of 10 prostheses represents change in the paradigm of injectable and implantable bulking agents. [ 3 ]  SphinKeeper is a permanent implantable device rather than a bulking agent, and aims to create a kind of artificial neosphincter. [ 3 ]  Previous techniques aimed to simply augment the internal anal sphincter. [ 3 ]  The first systematic review on implantable bulking agents was published in 2022. [ 4 ]  However, no randomized placebo controlled trials have been published yet."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2457", "text": "The implants are made of  polyacrylonitrile  (HYEXPAN). This material is inert, non-allergenic, non-immunogenic, nondegradable and noncarcinogenic. [ 1 ]  The material is hydrophilic, which allows the implants to slowly absorb water and change in dimensions, which occurs within 48 hours once they are implanted in the tissues. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2458", "text": "This polyacrylonitrile material is thought to meet the criteria for the \"ideal bulking agent\", and therefore may overcome the disadvantages of other bulking agents. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2459", "text": "Implantable bulking agents are indicated for passive fecal incontinence, caused by interior anal sphincter dysfunction or damage. [ 1 ]  The onset of incontinence should be at least 6 months ago. [ 6 ]  It has been recommended that this procedure should be attempted only if non-surgical options have failed (such as pharmacologic, behavioral, pelvic floor rehabilitation), [ 6 ]  and also if injectable bulking agents were unsuccessful. [ 1 ]  Researchers are investigating the use of GK and SK in patients with a wider range of causes of fecal incontinence. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2460", "text": "Contraindications have been suggested by different authors, and include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2461", "text": "Diabetes mellitus ,  pudendal neuropathy , and previous implantation of  sacral nerve stimulation  device are not contraindications to the use of implantable bulking agents. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2462", "text": "The procedure is carried out under  local  or regional anesthesia ( Spinal anaesthesia ) with or without  sedation  or  general anesthesia . [ 1 ] [ 6 ] [ 3 ]  It takes 30-40 minutes and may be done as a  day case  on an outpatient basis. [ 1 ]  Intravenous  antibiotics  may given at the start of the procedure. [ 1 ]  The patient is usually put into the  lithotomy position . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2463", "text": "The surgeon identifies the interior anal sphincter and the intersphincteric groove while using an anal retractor such as the Eisenhammer retractor. 2 cm away from the anal verge a 2 mm incision is made in the perianal skin. [ 1 ]  This location may minimize the possibility of contamination of the wounds during bowel movements. [ 6 ]  The prostheses are implanted using a custom \"gun\" which consists of a delivery system and a dispenser which holds one prosthesis at a time. [ 1 ]  This device is specific to the type of implant being used: Gatekeeper or SphinKeeper. [ 6 ]  The needle (cannula / sheath) is inserted into the incision and pushed into the intersphincteric space through a short subcutaneous tunnel. [ 1 ] [ 6 ]  It is thought that the path of this created \"tunnel\" should not be a straight line, in order to prevent extrusion of the prosthesis along the insertion track. [ 6 ]  The needle is advanced to a depth just beyond the level of the  dentate line . [ 1 ]  This will correspond to the upper part of the anal canal, at the level of the  puborectalis muscle . [ 6 ]  The exact position of the needle tip is confirmed by direct vision or with the guidance of endoanal ultrasound. [ 1 ]  The procedure is described as relatively simple to perform from a technical perspective, [ 4 ]  and one author stated that ultrasound guidance during placement is not necessary if the surgeon is experienced. Firing the \"gun\" causes the cannula to retract completely into the delivery system, leaving the prosthesis in the target location. [ 6 ]  The prosthesis is then placed into the intersphincteric space. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2464", "text": "It is thought that placement of the implants in the intersphincteric space pushes the external anal sphincter outwards and the internal anal sphincter inwards. This may increase the length of the  sarcomeres , which theoretically increases the contractility of the muscle. In terms of physiological measurements, the resting anal pressure and the length of the high pressure zone in the anal canal may be improved. In other words, the bulking effect may improve the seal of the anal canal and the length of the anal canal. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2465", "text": "The surgical procedure is almost identical for Gatekeeper and SphinKeeper. The difference between Gatekeeper and SphinKeeper is in the size and number of the individual prostheses. Gatekeeper uses 4-6 prostheses. SphinKeeper uses up to 10 prostheses. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2466", "text": "Within 48 hours of implantation, the implant material absorbs water from the tissues because of its hydrophilic properties. Each prosthesis becomes thicker and shorter in shape. This rapid increase in volume allows the prostheses to self-fix in position and prevents displacement and migration (in most cases). [ 1 ]  The prostheses also become softer in consistency and compliant to external pressures, but are still able to maintain their original shape. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2467", "text": "In the dehydrated state, Gatekeeper prostheses are thin cylinders, 2 mm in diameter and 22 mm long. After implantation, they become 6.5 mm in diameter and 17 mm long. Their volume increases by 750% from 70 mm 3  to 500 mm 3 . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2468", "text": "SphinKeeper prostheses are slightly thicker and longer cylinders. In the dehydrated state, SphinKeeper prostheses are 3 mm in diameter and 29 mm long. After implantation, they become 7 mm in diameter and 23 mm long. [ 1 ]  SphinKeeper implants are long enough to restore the normal length of the anal canal. [ 6 ]  They are also wide enough to make sure there is good filling ability. Therefore, SphinKeeper allows for surgical correction of larger defects of the internal anal sphincter or external anal sphincter. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2469", "text": "The process is repeated for each individual prosthesis, placing them into incisions made at the intersphincteric groove at equidistant intervals depending upon the total number of prostheses to be deployed. [ 1 ]  For example, if 4 prostheses are to be used, incisions may be placed at 12, 3, 6, and 9 o\u2019clock. If 6 prostheses are to be used, incisions may be placed at 1, 3, 5, 7, 9, and 11 o\u2019clock. [ 6 ]  The exact number of prostheses used is arbitrary, but placing 10 prostheses enables the creation of a circumferential ring of prostheses around the anal canal in the intersphincteric space. This effectively creates a situation similar to an artificial anal sphincter. [ 1 ]  One publication reported improved outcome with Gatekeeper when more prostheses were used. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2470", "text": "Interestingly, it is thought that the exact spacing of the prostheses does not influence the outcome of the procedure, and the important factor appears to be that the prostheses are distributed equally around the anal canal. [ 6 ]  This is the case even in the presence of tears of the external anal sphincter or internal anal sphincter. [ 6 ]  Therefore, the implants are placed in the above locations for convenience of the surgeon, even for patients with a tear in a specific part of the sphincter. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2471", "text": "The incisions are closed with resorbable sutures. Endoanal ultrasound may be used to confirm the location of each prosthesis. A course of oral antibiotics (e.g. metronidazole) may be given after the procedure. Oral  laxatives  (e.g.  lactulose ) may be given, which prevents straining and constipation. Anal trauma (e.g. receptive anal intercourse) should be avoided for at least 72 hours after the procedure. [ 1 ]  Patients are usually advised to rest in bed, with the aim of reducing the risk of dislocation of the prostheses. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2472", "text": "After healing, the implants continue to be palpable and are visible on endoanal ultrasound. [ 1 ]  Each prosthesis appears as hyperechoic dot with a hypoechoic shadow behind it. [ 6 ]  Three dimensional endoanal ultrasound has also been used to visualize the implants, wherein the prostheses appear as a continuous hyperechoic line. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2473", "text": "Compared to other surgical treatment options for fecal incontinence, implantable bulking agents appear to be safe. [ 6 ]  Therefore, it is also suitable for elderly or frail patients. [ 6 ]  However, complications are sometimes reported. For example, acute sepsis (infection) at the implantation site has been rarely recorded. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2474", "text": "The most important complication is displacement of a prosthesis (also referred to as migration / dislocation / dislodgement / extrusion). [ 6 ]  The rate of displacement of at least 1 of the prostheses has been reported to be as low as 0%, or as high as 91% of cases. [ 4 ]  The patient may report pain, swelling and/or no improvement in symptoms when there is prosthesis displacement. [ 6 ]  This is potentially noteworthy, [ 7 ]  since improved symptoms after use of injectable bulking agents have been attributed at least in part to the  placebo effect . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2475", "text": "Placement in the intersphincteric space is thought to be less liable to extrusion or migration of the prostheses or other complications such as erosion, ulceration or fistula formation in the anal canal. [ 1 ] [ 6 ]  If the implants were in the submucosal layer, they would be more vulnerable to such complications. [ 1 ]  Furthermore, displacement is less likely because of the rapid increase in size of the prostheses, [ 4 ]  allowing them self-fix in position in most cases. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2476", "text": "A systematic review found that in total, migration / dislodgement / dislocation was reported in 41 out of 154 patients (26.6%) across 7 studies. [ 4 ]  The same researchers reported that some kind of adverse event occurred in 48 out of 166 patients (28.9%). [ 4 ]  Sometimes, a prosthesis had to be removed, [ 4 ]  however it is possible to implant a new one in the correct position. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2477", "text": "The first systematic review on GK and SK was published in 2022. It combined results from 8 studies published before 2020 \u2013 a total of 166 patients. All studies were judged to be at moderate to high risk of bias. The reviewers reported that severity of FI improved in 5 out of 7 of the studies which used the Cleveland Clinic FI Score and in 3 out of 5 of the studies which used the Vaizey score. Quality of life improved in 2 studies which measured that outcome. They concluded that GK and SK may be effective, safe and minimally invasive options for fecal incontinence in those cases where non surgical treatments have failed. The reviewers called for controlled trials to be conducted. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2478", "text": "This is a list of instruments used specially in  Gastroenterology ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2479", "text": "This article related to  medical equipment  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2480", "text": "Intestine transplantation  ( intestinal transplantation,  or  small bowel transplantation ) is the  surgical   replacement  of the  small intestine  for  chronic  and  acute  cases of intestinal  failure . While intestinal failure can oftentimes be treated with alternative therapies such as  parenteral nutrition  (PN), complications such as PN-associated  liver disease  and  short bowel syndrome  may make transplantation the only viable option. One of the rarest type of  organ  transplantation performed, intestine transplantation is becoming increasingly prevalent as a therapeutic option due to improvements in  immunosuppressive regimens , surgical technique, PN, and the clinical management of pre and post-transplant patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2481", "text": "Intestine transplantation dates back to 1959, when a team of surgeons at the  University of Minnesota  led by Richard C. Lillehei reported successful transplantation of the small intestine in dogs. Five years later in 1964, Ralph Deterling in  Boston  attempted the first human intestinal transplant, albeit unsuccessfully. For the next two decades, attempts at transplanting the small intestine in humans were met with universal failure, and patients died of technical complications,  sepsis , or  graft rejection . However, the discovery of the immunosuppressant  ciclosporin  in 1972 triggered a revolution in the field of transplant medicine. Due to this discovery, in 1988, the first successful intestinal transplant was performed in Germany by E. Deltz, followed shortly by teams in France and Canada. Intestinal transplantation was no longer an experimental procedure, but rather a life-saving therapy. In 1990, a newer immunosuppressant drug,  tacrolimus , appeared on the market as a superior alternative to ciclosporin. In the two decades since, intestine transplant efforts have improved tremendously in both number and outcomes. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2482", "text": "Failure of the small intestine is life-threatening due to the inability to absorb  nutrients ,  fluids , and  electrolytes  from food. Without these essential substances and the ability to maintain  energy balances ,  homeostasis  cannot be maintained and one's  prognosis  will be dismal. Causes of intestinal failure may be clinically complex, and may result from a combination of nutritional,  infectious ,  traumatic , and  metabolic  complications that affect ordinary  anatomy  and  physiology . [ 3 ]  Many underlying conditions that serve as precursors to failure are genetic or congenital in nature. For example, severe  inflammation ,  ulceration ,  bowel obstruction ,  fistulation ,  perforation , or other pathologies of  Crohn's disease  may severely compromise intestinal function. [ 4 ]  Despite the danger these conditions may pose in themselves, they may lead to even further, more serious complications that necessitate replacement of the diseased intestine. The single leading cause for an intestinal transplant is affliction with  short bowel syndrome , oftentimes a secondary condition of some other form of intestinal disease. [ 5 ] [ 6 ]  Short-bowel syndrome was the cause for 73% of American intestinal transplantations in 2008, followed by functional bowel problems for 15% and other causes representing 12% of cases. [ 7 ]  Natural SBS is mercifully rare, estimated to be 3 per 100,000 births. [ 8 ]  Surgical removal is the most common cause, performed as a treatment for various  gastroenterological  and  congenital  conditions such as Crohn's disease,  necrotizing enterocolitis ,  mesenteric ischemia ,  motility disorder ,  omphalocele / gastroschisis ,  tumors , and  volvulus . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2483", "text": "Regardless of the underlying condition, the loss of intestinal function does not necessarily necessitate a transplant. Several conditions, such as necrotizing enterocolitis or volvulus, may be adequately resolved by other surgical and nonsurgical treatments, especially if SBS never develops. An individual can obtain nutrients intravenously through PN, bypassing food consumption entirely and its subsequent  digestion . Long-term survival with SBS and without PN is possible with  enteral nutrition , but this is inadequate for many patients as it depends on the remaining intestine's ability to adapt and increase its absorptive capacity. [ 3 ]  Although more complicated and expensive to perform, any person may receive PN. Although PN can meet all energy, fluid, and nutrient needs and can be performed at home,  quality of life  can be significantly decreased. On average, PN takes 10 to 16 hours to administer but can take up to 24. Over this time frame, daily life can be significantly hindered as a consequence of attachment to the  IV pump . [ 5 ] [ 10 ]  Over long periods of time, PN can lead to numerous health conditions, including severe  dehydration ,  catheter -related infections, and liver disease. [ 2 ] [ 11 ]  PN-associated liver disease strikes up to 50% of patients within 5\u20137 years, correlated with a mortality rate of 2\u201350%. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2484", "text": "Another alternative treatment to transplant for patients with SBS is surgical bowel lengthening via either  serial transverse enteroplasty  (STEP) or the older  longitudinal intestinal lengthening and tailoring  (LILT) technique. Although both procedures contribute to an approximate 70% increase in length, STEP appears somewhat more favorable in terms of lower mortality and progression to transplant. [ 12 ]  Nevertheless, a positive reception to either procedure may reduce the level of PN required, if not negate its required use altogether. [ 8 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2485", "text": "There are four  Medicare  and  Medicaid -approved  indications  for intestine transplantation: a loss of two of the six major routes of  venous access , multiple episodes of  catheter -associated life-threatening sepsis, fluid and electrolyte abnormalities in the face of maximal medical therapy, and PN-associated liver disease. Transplants may also be performed if the growth and development of a  pediatric  patient fails to ensue, or in extreme circumstances for patients with an exceptionally low quality of life on PN. [ 14 ] [ 15 ]  A multidisciplinary team consisting of  transplant surgeons ,  gastroenterologists ,  dieticians ,  anesthesiologists ,  psychiatrists , financial representatives, and other  specialists  should be consulted to evaluate the treatment plan and ensure transplantation is the patient's best option.  Psychological  preparations should be made for the transplant team and patient as well. Early referral requires trust between all parties involved in the operation to ensure that a rush to judgment does not lead to a premature transplant. [ 11 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2486", "text": "Other  absolute contraindications  to receiving an intestinal transplant include the presence of  systemic  and untreated local infections, malignant cancer, severe  neurological impairment , and severe  cardiac  and/or  pulmonary disease .  These criteria are similar to established guidelines for transplants of other organ types. [ 17 ]  HIV infection is a  relative contraindication  for intestine transplantation; desperate terminal patients may accept a transplant from a HIV-positive donor if they are willing to expose themselves to HIV. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2487", "text": "There are three major types of intestine transplants: an isolated intestinal  graft , a combined intestinal-liver graft, and a  multivisceral graft  in which other  abdominal  organs may be transplanted as well. In the most basic and common graft, an isolated intestinal graft, only sections of the  jejunum  and  ileum  are transplanted. [ 18 ]  These are performed in the absence of liver failure. In the event of severe liver dysfunction due to PN,  enzyme  deficiencies, or other underlying factors, the liver may be transplanted along with the intestine. In a multivisceral graft, the  stomach ,  duodenum ,  pancreas , and/or  colon  may be included in the graft. Multivisceral grafts are considered when the underlying condition significantly compromises other sections of the digestive system, such as intra-abdominal tumors that have not yet  metastasized , extensive venous  thrombosis  or  arterial   ischemia  of the  mesentery , and motility syndromes. [ 11 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2488", "text": "Donated  intestines, like all organs, should be matched to a recipient prior to recovery, as to prepare him or her and minimize the time the organ spends outside the  body . [ 5 ]  Potential recipients are placed on the  International Intestinal Transplant Registry  (ITR), where they contribute to the world's growing understanding of intestine transplantation. Before a transplant may be performed, an organ must first be located. In the United States, the matching of all organs is coordinated by the  United Network for Organ Sharing  (UNOS). The standard intestinal donor is deceased with a diagnosis of  brain death . [ 19 ]  In terms of transplant outcomes, brain-dead donors are highly preferable to donors who have suffered  cardiopulmonary death . If respiration can be assisted by a  ventilator , brain-dead donors may exhibit maintainable  cardiac ,  endocrine , and  excretory  function. If appropriately managed, the continuation of  blood flow  and bodily metabolism allows for healthier organs for procurement and additional time to prepare recipients for transplant. [ 20 ]  Furthermore, terminal ileum recovery from living donors is possible., [ 21 ]  and a  laparoscopic technique  is being developed to harvest limited sections of small bowel from living donors. [ 22 ]  When determining potential donor-recipient matches, important characteristics include donor size, age,  tissue  quality, and  ABO  and  histo-compatibility . [ 11 ] [ 21 ]  If the intestine is too large, it may be not transplantable into young or small patients. Ideally, intestines should be selected from donors of lighter weight than the proposed recipients to ensure simple closure of the abdominal wound. [ 23 ]  If a patient is too young or too old, they may not be hardy enough to survive the operation and recovery period. [ 11 ]  If the donor and recipient organs do not meet compatibility requirements, the threat of  organ rejection  by the body is all but certain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2489", "text": "Organ rejection is the unfortunate circumstance of the host  immune system  recognizing the transplanted organ as foreign. This is the most notable complication facing transplant recipients. Through  T-cell receptors ,  T-lymphocytes  are able to distinguish between self and non-self by recognizing  human leukocyte antigens  (HLA) bound to the  major histocompatibility complex  (MHC)  protein  located on the surface of organ  cells . Once identified as foreign, the immune system proceeds to destroy the transplanted tissue. The  panel-reactive antibody  (PRA) test measures the proportion of the population to which a recipient will react via pre-existing  antibodies  to various HLA  antigens ; in other words, how likely a patient is to acutely reject their new transplant. Therefore, it is essential that HLA and PRA statuses are tested for and demonstrate low immunoreactivity of the patient to the graft. [ 2 ] [ 21 ] [ 24 ]  In some cases, a recipient may suffer from  graft-versus-host disease , in which cells of the transplanted organ attack the recipient's cells. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2490", "text": "To ensure proper histocompatibility, tissue quality, and safety from infection,  blood work  should be collected and tested in the laboratory. In addition to HLA and PRA typing, the  complete blood count  (CBC),  coagulation  profile,  complete metabolic panel , and  ABO blood group  determination tests should be performed for both the donor and recipient. [ 2 ]  ABO-incompatible grafts can sometimes be performed on very young pediatric patients, as their immune systems have not fully developed and for whom waiting list mortality remains high. [ 14 ]  Additionally, blood  serum  should be  tested  for the presence of  viruses , including HIV,  hepatitis B  and  C ,  cytomegalovirus  (CMV), and  Epstein\u2013Barr virus  (EBV) antibodies to prevent infection. [ 24 ]  Particularly in the immunocompromised system necessitated by the transplant, these viruses can wreak havoc on the body and become extremely dangerous, even fatal. Even with healthy physiological levels, ABO and HLA compatibilities, and no signs of bacterial, viral, and  fungal  infections, organ transplantation is not without extrasurgical risk. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2491", "text": "A major challenge facing the intestinal transplant enterprise is meeting the need for transplantable intestines, particularly in the United States where the majority of intestinal transplants take place. [ 9 ]  There exists a narrow timeslot between procurement and transplantation that any organ remains viable, and logistical challenges are faced regarding bringing organ and recipient together. During procurement, organs that are being recovered are cooled and  perfused  with preservation solution. This slows organ activity and increases the time they remain viable for transplant. [ 2 ]  Although chilling and perfusion may extend intestinal lifespans by several hours, failure is still imminent unless transplanted. This duration between the cooling of the organ during procurement and the restoration of physiological temperature during implantation is the  cold ischemic time . Due to the sensitivity of the intestine to ischemic injury, many potential donor intestines are lost to the events following brain death and trauma. Furthermore, irreversible intestinal damage is seen after approximately only 5 hours of cold ischemia in the form of  mucosal  damage and bacterial translocation outside the  gastrointestinal tract . Therefore, ensuring cardiac survival and nearby donor-recipient proximity before procurement are essential so organs do not wait too long outside the body and without blood flow. [ 11 ]  Not only is there a lack of transplantable intestines, but a deficiency in the number of centers possessing the capability to carry out the complicated transplant procedure as well. As of 2005 [update] , there were only 61 medical centers in the world capable of executing an intestinal transplant. [ 9 ]  Furthermore, many young, small children, particularly those weighing less than 5  kg , cannot find a transplant due to the lack of size-matched donors. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2492", "text": "Despite these challenges, obtaining an intestine for transplant is rather probable in the United States. In 2008, there were 212 people on the U.S. intestinal transplant waitlist, 94% of whom were U.S. citizens. [ 7 ]  Regardless of transplant type, over half of new registrants are 5 years of age or younger.  Adults  compromise the next largest cohort, followed by pediatric patients aged 6 and older. In 2008, the  ethnic  composition of the intestinal transplant waitlist was 65%  White , 18%  Black , 16%  Hispanic , 1%  Asian , and 0.5% other or  mixed race , resembling the  demographics  of the American general population at the time aside from a below-average Asian cohort. ABO blood types also matched the general population, with 31% A, 14% B, 5% AB, and 50% O. [ 7 ]  In 2004, the average waiting period to receive a transplant was 220 days, [ 21 ]  with a  median  of 142 days in 2008. [ 7 ]  The rate of waitlist additions has shifted from year to year; gains increased until 2006 (with 317 added), but then decreased in 2012 (to 124 added). [ 26 ]  In 2007, only 9% of patients on the U.S. waitlist died while waiting for a transplant. [ 7 ]  Waitlist mortality peaked around 2002 and was highest for liver-intestine (pediatric) patients. Deaths among all pediatric groups awaiting intestine-liver transplants have decreased in the years leading up to 2014 whereas adult intestine-liver deaths have dropped less dramatically. The decrease in recent years is likely due to improved care of infants with intestinal failure and subsequently a decrease in referrals for transplant. [ 26 ]  Although many improvements have been made in the States, outcomes everywhere still demonstrate much room for improvement. Worldwide, 25% of pediatric patients on the waitlist for an intestinal transplant die before they can receive one. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2493", "text": "Following matching of the organ, the complicated procurement of the small bowel can be performed by a team of abdominal transplant surgeons. Once a donor has been selected and approved for donation, several pretreatments may be initiated to destroy  microorganisms  and  immune cells . The donor intestine must be  decontaminated  with several  antibiotics , including  neomycin ,  erythromycin ,  amphotericin B , and  cephalosporin . [ 18 ]  They may also be treated with anti- lymphocyte  antibodies ( anti-thymocyte globulin ,  alemtuzumab ),  irradiation  directed against excessive mesenteric  lymphatic tissue , and have their bowel  irrigated . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2494", "text": "Once donor preparation is accomplished, procurement can begin by utilizing the same standard techniques for all abdominal organ procurements. The team exposes the abdominal cavity and inserts two  cannulae  for the  infusion  of  University of Wisconsin   organ preservation solution  into the  aorta  and  inferior mesenteric vein . As the abdominal organs are cooled  in situ , the surrounding tissue is  dissected  so that they may be quickly extracted. In the next step, the aorta is  cross-clamped , cutting off blood supply to the organs. Once blood and oxygen supply to an organ is cut off, organ death will approach swiftly unless steps are taken to preserve them until transplant. Organs are therefore fully  drained of blood , flushed with cool preservation solution, and removed from the body. [ 2 ] [ 18 ]  In an isolated intestinal transplant, the  colon will be detached  from the small intestine. The  cecum  and  ascending colon  are devascularized, while care is taken to preserve major  vasculature  in the ileum. The jejunum will be separated from the duodenum while preserving the vasculature of the jejunum, ileum, mesentery, and the pancreas. If healthy, the pancreas can oftentimes be retrieved as an additional isolated procurement. The intestinal allograft, when ready to be extracted, is attached by the mesenteric  pedicle , where the vessels converge out of the intestinal system. This pedicle will be  stapled  closed, and can be separated from the body via a  transverse  cut to create a vascular cuff. The complete intestinal allograft can then be removed and wrapped in a surgical  towel . [ 18 ]  The protocols for combined liver and multivisceral procurements are far more complicated and meticulous than isolated intestine alone. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2495", "text": "First, any abdominal  scar tissue  from previous surgeries must be removed. The aorta and  vena cava  are dissected in preparation for vascular  anastomosis , followed by dissection of the  proximal  and  distal  ends of the digestive tract. Anastomosis is then performed to revascularize the graft. Arterial vessels are connected to the abdominal aorta, below the  kidneys . However, venous drainage, or the reattachment of the transplanted organ to the venous system, may be performed differently depending on the unique intra-abdominal vasculature of the recipient. The graft is usually drained systemically into the  infrarenal  vena cava, [ 15 ]  but may also be drained  portally  into the  hepatic portal  or  superior mesenteric vein . [ 17 ]  The graft is then reperfused with blood and any bleeding is stopped before the proximal and distal ends of the transplant bowel are connected to the original digestive tract. A loop  ileostomy  is then created as to provide easy access for future  endoscopic  observation and  biopsies . A  gastronomy  or  jejunostomy   feeding tube  may be placed before the abdominal wall is closed. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2496", "text": "When a liver is being transplanted in conjunction with the intestine, the recipient must first have their own  liver removed . Following this, the aorta, cava, and portal veins of the donor and recipient are anastomosed. The graft is then flushed before the caval  clamps  are removed. The intestine is then reconstructed as in an isolated intestinal transplant, before being connected to the  bile duct  servicing the new liver. [ 17 ]   Multivisceral transplants  are especially difficult and susceptible to complications because all organs must survive a conjoined procurement, transport, and transplantation. All three of these measures are tailored to the individual needs of the recipient. [ 18 ]  Preservation of the native  spleen , pancreas, and duodenum during a multivisceral transplant can reduce the risk of additional complications related to these structures. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2497", "text": "Following the procedure, the patient is actively monitored in an  intensive care unit  (ICU).  Broad-spectrum antibiotics  are administered, bleeding monitored, and serum  pH  and  lactate  levels measured for evidence of intestinal ischemia. The patient's immune system is strongly modulated immediately post-operation. The  initial phase of treatment  consists of the administration of tacrolimus with  corticosteroids  to suppress T-lymphocyte activation. Next, various assortments of  interleukin-2  (IL-2)  receptor   antagonists  ( daclizumab ,  basiliximab ), anti-proliferation agents ( azathioprine ,  mycophenolate mofetil ), and the drugs  cyclophosphamide  and  sirolimus  are administered on an individual patient basis to further suppress the immune system. [ 11 ]  The  bioavailability  of these drugs is dependent on intestinal  surface area  and transit time, and therefore the length of the allograft determines the immunosuppression regimen. [ 2 ]  Intravenous administration of  prostaglandin E1  is occasionally performed for the first 5 to 10 days following transplant to improve intestinal circulation and a potential dispensing of immunosuppressive effects. [ 2 ] [ 11 ]  The gut is selectively decontaminated against high-risk  flora  and  preventative care  is taken against CMV and fungal infections. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2498", "text": "It is ideal to commence enteral nutrition as early as possible following transplantation. Therefore, a feeding tube connecting to the stomach or jejunum is quickly placed to facilitate rehabilitation. [ 11 ]  If gastrointestinal function is restored, a diet can be reestablished and cautiously advanced as tolerated. Most patients are weaned from PN within 4 weeks of transplantation, and nearly all are free from additional enteral supplementation by one year. [ 14 ]  Evidence for the restoration of function includes decreasing gastrostomy tube returns and increasing  gas  and enteric contents in the ileostomy. [ 2 ]  Routine surveillance endoscopy and biopsies via the ileostomy should be performed with decreasing frequency over several months to observe signs of rejection, ideally before clinical symptoms present themselves. Should the patient continue to perform well through the first post-transplant year, the ileostomy would generally be closed. Should rejection be suspected in the future, endoscopies would be performed and an appropriate antirejection therapy will be tailored. The median time for hospital  discharge  varies between procedures. The median times for isolated intestine, intestine-liver, and multivisceral transplants are 30, 60, and 40 days post-operation respectively. [ 14 ]  Within the first several months,  carbohydrate  and  amino acid  absorptive capacity should normalize, followed by the absorptive capacity for fats. Once enteral nutrition is capable of providing all nutritional needs, PN can be discontinued. [ 2 ]  Nearly all patients with a successful transplant are free of PN within one year. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2499", "text": "Intestinal transplantation is the least performed type of transplant due to a number of unique obstacles. The most major of these is the profound immunosuppression required due to the ability of the intestine to elicit strong immune responses. Because of exposure to a wide range of gut flora and material consumed by the body, the intestinal  epithelium  possesses a highly developed  innate immune system  and  antigen-presenting  abilities. Immunosuppression is the primary determinant of outcome in small bowel transplantation; the risk for graft rejection is increased by under-immunosuppression and for local and systemic infection with over-immunosuppression. [ 11 ]  Ensuring an appropriate dose of immunosuppressant can therefore be difficult, especially as both ciclosporin (14\u201336%) and tacrolimus (8.5\u201322%) have generally low bioavailabilities. [ 27 ]  A major problem due to immunosuppression in intestinal transplant patients is post-transplant  lymphoproliferative disorder , in which B-lymphocytes excessively proliferate due to infection by EBV and result in infectious  mononucleosis -like lesions. [ 7 ]  Intestinal transplant recipients are also at risk for chronic  renal failure  because  calcineurin  inhibitors are  toxic  to the kidneys. A transplant recipient must remain on immunosuppressants for the rest of his or her life. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2500", "text": "Intestinal transplants are highly susceptible to infection even more so than the standard immunocompromised recipient of other organs due to the great composition and variety of the gut flora. [ 11 ]  A complex assortment of microorganisms inhabits the human digestive tract, with concentrations of up to 10 4 \u201310 7   CFU /mL in the jejunoileum and 10 11 \u201310 12  CFU/mL in the colon. [ 28 ]  While suppression of the immune system may prevent immune attack on the new allograft, it may also prevent the immune system's ability to keep certain gut microbial populations in line. Despite pre and post-decontamination of the transplant, recipients are at risk of local and systemic infection by both natural and external flora. The common symptom of graft dysfunction, whether due to infection, rejection, or some other condition, is  diarrhea . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2501", "text": "Intestinal transplant outcomes have improved significantly in recent years. Despite mild incongruities in survival rate percentages between centers in North America, Europe, Australia, and elsewhere, intestinal transplantations mostly approach survivorship rates of  lung transplantation . [ 11 ]  At one-year, graft survival rates for isolated intestine currently waver around 80%, and 70% for intestine-liver and multivisceral. Over the same time period, patient survival for isolated intestine patients may even exceed 90%, while the more complicated multiorgan transplants do not show any increase in patient survival when compared to patients surviving with the intestinal graft alone. [ 14 ]  The five-year survival rate for patients and transplants ranges from 50 to 80% (overall mean 60%), depending on underlying disease and presurgical  morbidity . Very young (<1 year) and very old (>60 years) patients receiving a transplant have pronounced rates of mortality. [ 14 ] [ 15 ]  After 4 years, pediatric survival significantly worsens compared to adults. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2502", "text": "Several factors relating to superior patient and graft prognosis have proven to be statistically significant. Patients who have been admitted for transplant directly from home rather than the hospital, younger patients over one year of age, those receiving their first transplant, those receiving transplants at experienced transplant centers, and who receive antibody or sirolimus-based induction therapies have increased rates of survival. [ 9 ] [ 15 ]  Furthermore, underlying  etiology , [ 29 ]  the presence of  comorbidity , the frequency of previous surgery, nutritional status, and the level of liver function have been found to affect patient-graft survival . [ 30 ]  Patients with a pre-transplant diagnosis of volvulus were found to possess a lower risk of mortality. [ 29 ]  As of 2008, the longest recorded surviving transplant survived for 18 years. [ 14 ]  Between 1999 and 2008, 131 retransplant procedures were performed in the United States. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2503", "text": "The improvement to quality of life following an intestinal transplantation is significant. Of living patients 6 months after transplant, 70% are considered to have regained full intestinal function, 15% are at partial function, and 15% have had their grafts removed. [ 9 ] [ 14 ]  For those with full function, enteral nutritional  autonomy  is high. [ 7 ]  The ability to resume regular activities such as the ability to consume food and exert control over digestive function is certainly a welcome return for patients. The low quality of life induced by intestinal failure is oftentimes further supplemented by significant  psychosocial   disability  and  narcotic   dependence . Following transplantation, these have been found to generally decrease. [ 15 ]  According to surveys comparing patients who have undergone transplants and those that have not, there seems to be a remarkable improvement for transplant recipients in such areas as  anxiety , depression,  appearance ,  stress ,  parenting ,  impulsiveness ,  optimism ,  medical compliance , and the quality of  relationships . [ 14 ] [ 15 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2504", "text": "Receiving an organ transplant of any kind is a highly significant investment financially, but a successful, well-functioning transplant can be very  cost-efficient  relative to alternate therapies. Total charges to maintain PN at home can reach upwards of $150,000 a year, even though the actual cost of nutrition is typically only $18 to $22 a day. [ 5 ] [ 14 ]  This excludes the cost for additional home support, equipment, and the care of PN-related complications. The cost involved in undergoing intestinal transplantation, including the initial hospitalization for the transplant, can range from $150,000 to $400,000, and reoccurring hospitalizations are common up through the second year. Two to three years post-transplant, the financial cost of transplantation reaches parity with PN and is more cost-effective thereafter. [ 11 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2505", "text": "2PMV ,  3KQ4"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2506", "text": "2694"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2507", "text": "14603"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2508", "text": "ENSG00000134812"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2509", "text": "ENSMUSG00000024682"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2510", "text": "P27352"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2511", "text": "P52787"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2512", "text": "NM_005142"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2513", "text": "NM_008118"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2514", "text": "NP_005133"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2515", "text": "NP_032144"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2516", "text": "Intrinsic factor  ( IF ),  cobalamin binding intrinsic factor , [ 5 ]  also known as  gastric intrinsic factor  ( GIF ), is a  glycoprotein  produced by the  parietal cells  (in humans) or chief cells (in rodents) of the  stomach . It is necessary for the absorption of  vitamin B 12  later on in the distal  ileum  of the  small intestine . [ 6 ]  In humans, the gastric intrinsic factor  protein  is encoded by the  CBLIF   gene . [ 5 ]   Haptocorrin  ( transcobalamin I ) is another glycoprotein secreted by the  salivary glands  which binds to  vitamin B 12 . Vitamin B 12  is acid-sensitive and in binding to haptocorrin it can safely pass through the acidic stomach to the duodenum. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2517", "text": "In the less acidic environment of the  small intestine , pancreatic enzymes digest the glycoprotein carrier and vitamin B 12  can then bind to intrinsic factor. [ 7 ]  This new complex is then absorbed by the epithelial cells ( enterocytes ) of the  ileum . [ 7 ]  Inside the cells, vitamin B 12  dissociates once again and binds to another protein,  transcobalamin II ; the new complex can then exit the epithelial cells to be carried to the liver. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2518", "text": "Intrinsic factor is secreted by  parietal cells  within the stomach, and so is present in the gastric juice as well as in the  gastric mucous membrane . [ 9 ]  The optimum pH for its action is approximately 7. [ 10 ]  Its concentration does not correlate with the amount of  HCl  or  pepsin  in the gastric juice, e.g., intrinsic factor may be present even when pepsin is largely absent. [ 11 ]  The site of formation of the intrinsic factor varies in different species. In pigs it is obtained from the  pylorus  and beginning of the  duodenum ; [ 12 ]   in human beings it is present in the  fundus  and body of the  stomach . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2519", "text": "The limited amount of normal human gastric intrinsic factor limits normal efficient absorption of B 12  to about 2\u00a0\u03bcg per meal, a nominally adequate intake of B 12 . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2520", "text": "In  pernicious anemia , which is usually an  autoimmune disease ,  autoantibodies  directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency,  malabsorption  of vitamin B 12 , and subsequent  megaloblastic anemia . [ 15 ]   Atrophic gastritis  can also cause intrinsic factor deficiency and anemia through damage to the parietal cells of the stomach wall. [ 16 ]   Pancreatic exocrine insufficiency  can interfere with normal dissociation of vitamin B 12  from its binding proteins in the small intestine, preventing its absorption via the intrinsic factor complex. [ 17 ]  Other risk factors contributing to pernicious anemia are anything that damages or removes a portion of the stomach's parietal cells, including  bariatric surgery , gastric tumors, gastric ulcers, and excessive consumption of alcohol. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2521", "text": "Mutations in the  GIF  gene are responsible for a rare inheritable disease called  intrinsic factor deficiency [ 18 ]  which results in malabsorption of vitamin B 12 . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2522", "text": "In most countries,  intramuscular injections  of vitamin B 12  are used to treat  pernicious anemia . [ 20 ]  Orally administered vitamin B 12  is absorbed without intrinsic factor, but at levels of less than one percent than if intrinsic factor is present. [ 21 ]   Despite the low amounts absorbed, oral vitamin B 12  therapy is effective at reducing symptoms of pernicious anemia. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2523", "text": "Vitamin B 12  can also be given  sublingually , but there is no evidence that this route of administration is superior to the oral route, [ 23 ]  and only Canada and Sweden routinely prescribe this route of administration. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2524", "text": "Because vitamin B 12  absorption is a multistep process that involves the stomach, pancreas and small intestine, and is mediated by two carriers:  Haptocorrin  and intrinsic factor, and because  Haptocorrin  ( transcobalamin I ) binds to vitamin B 12 , and  Vitamin B 12  is acid-sensitive, when vitamin B 12  binds to  Haptocorrin  it can safely pass through the acidic stomach to the duodenum, given time in the mouth. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2525", "text": "Divisions"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2526", "text": "John Harvey Kellogg  (February 26, 1852 \u2013 December 14, 1943) was an American businessman,  inventor , physician, [ 1 ]  and advocate of the  Progressive Movement . [ 2 ]  He was the director of the  Battle Creek Sanitarium  in  Battle Creek, Michigan , founded by members of the  Seventh-day Adventist Church . It combined aspects of a European spa, a  hydrotherapy  institution, a hospital and high-class hotel. Kellogg treated the rich and famous, as well as the poor who could not afford other hospitals. According to  Encyclop\u00e6dia Britannica , his \"development of dry breakfast cereals was largely responsible for the creation of the  flaked-cereal industry , with the founding and the culmination of the global conglomeration brand of  Kellogg's (now Kellanova) .\" [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2527", "text": "An early proponent of the  germ theory of disease , Kellogg was well ahead of his time in relating  intestinal flora  and the presence of bacteria in the intestines to health and disease. The sanitarium approached treatment in a  holistic  manner, actively promoting vegetarianism, nutrition, the use of yogurt  enemas  to clear \"intestinal flora\", exercise, sun-bathing, and  hydrotherapy , as well as abstinence from smoking tobacco, drinking alcoholic beverages, and sexual activity. Kellogg dedicated the last 30 years of his life to promoting  eugenics  and  segregation . [ 3 ]  Kellogg was a major leader in progressive health reform, particularly in the second phase of the  clean living movement . [ 4 ] [ 5 ]  He wrote extensively on science and health. His approach to \"biologic living\" combined scientific knowledge with Adventist beliefs, promoting health reform, and  temperance . [ 6 ]  Many of the vegetarian foods that Kellogg developed and offered his patients were publicly marketed: Kellogg's brother,  Will Keith Kellogg , is best known today for the invention of the  breakfast cereal   corn flakes . [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2528", "text": "Kellogg held  liberal theological beliefs  radically different from mainstream  Nicene Christianity  and emphasized what he saw as the importance of  human reason  over many aspects of  traditional doctrinal authority . He strongly rejected  fundamentalist  and  conservative  notions of  original sin ,  human depravity , and  the atonement of Jesus , viewing the last in terms of \"his exemplary life\" on Earth rather than  death . [ 2 ] [ 9 ]  Becoming a  Seventh-day Adventist  as their beliefs shifted towards  Trinitarianism  during the 1890s, Adventists were \"unable to accommodate the essentially  liberal  understanding of Christianity\" exhibited by Kellogg, viewing his theology as  pantheistic  and unorthodox. [ 2 ] [ 9 ]  Disagreements with other members of the SDA led to a major schism: he was  disfellowshipped  in 1907, but continued to follow many of their beliefs and directed the sanitarium until his death. Kellogg helped to establish the  American Medical Missionary College  in 1895. [ 10 ]   Popular misconceptions  have wrongly attributed various cultural practices, inventions, and historical events to Kellogg. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2529", "text": "John Harvey Kellogg was born in  Tyrone, Michigan , on February 26, 1852, [ 13 ]  to John Preston Kellogg (1806\u20131881) and his second wife Ann Janette Stanley (1824\u20131893). [ 7 ]  His father, John Preston Kellogg, was born in  Hadley, Massachusetts ; his ancestry can be traced back to the founding of Hadley, Massachusetts, where a great-grandfather operated a ferry. [ 14 ]  \nJohn Preston Kellogg and his family moved to Michigan in 1834, and after his first wife's death and his remarriage in 1842, to a farm in Tyrone Township. [ 15 ] :\u200a9\u200a [ 16 ] :\u200a14\u201318\u200a \nIn addition to six children from his first marriage, John Preston Kellogg had 11 children with his second wife Ann, including John Harvey and his younger brother,  Will Keith Kellogg . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2530", "text": "John Preston Kellogg became a member of several  revivalist  movements, including the  Baptists , the  Congregationalist Church , and finally the  Seventh-day Adventist Church . [ 15 ] :\u200a9\u200a  He was one of four adherents who pledged substantial sums to convince Seventh-day Adventists  Ellen G. White  and her husband  James Springer White  to relocate to  Battle Creek, Michigan , with their publishing business, in 1855. [ 15 ] :\u200a10\u200a  He persuaded a Seventh-day Adventist couple,  Daniel H. Kress  and  Lauretta E. Kress , to become doctors at Michigan where he had studied; they were early founders of what became  Washington Adventist Hospital . In 1856, the Kellogg family moved to Battle Creek to be near other members of the denomination. There John Preston Kellogg established a  broom  factory. [ 15 ] :\u200a9\u200a  The Kelloggs believed that the  Second Coming  of Christ was imminent, and that formal education of their children was therefore unnecessary. Originally a sickly child, John Harvey Kellogg attended Battle Creek public schools only briefly, from ages 9\u201311. He left school to work sorting brooms in his father's broom factory. Nonetheless, he read voraciously and acquired a broad but largely self-taught education. At age 12, John Harvey Kellogg was offered work by the Whites. He became one of their prot\u00e9g\u00e9s, [ 18 ] :\u200a111\u2013112\u200a  rising from errand boy to  printer's devil , and eventually doing proofreading and editorial work. [ 19 ]  He helped to set articles for  Health, or how to live  and  The Health Reformer , becoming familiar with Ellen G. White's theories of health, and beginning to follow recommendations such as a vegetarian diet. [ 16 ] :\u200a28\u200a  Ellen White described her husband's relationship with John Harvey Kellogg as closer than that with his own children. [ 18 ] :\u200a111\u2013112"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2531", "text": "Kellogg hoped to become a teacher, and at age 16 taught a district school in Hastings, Michigan. [ 16 ] :\u200a29\u201330\u200a  By age 20, he had enrolled in a teacher's training course offered by  Michigan State Normal School . [ 20 ]  The Kelloggs and the Whites, however, convinced him to join his half-brother Merritt,  Edson White ,  William C. White , and Jennie Trembley, as students in a six-month medical course at Russell Trall's  Hygieo-Therapeutic College  in  Florence Township, New Jersey . Their goal was to develop a group of trained doctors for the Adventist-inspired Western Health Reform Institute in Battle Creek. [ 16 ] :\u200a30\u200a  Under the Whites' patronage, John Harvey Kellogg went on to attend medical school at the  University of Michigan  and the  Bellevue Hospital Medical College  in New York City. He graduated in 1875 with a medical degree. [ 20 ]  In October 1876, Kellogg became director of the Western Health Reform Institute. [ 20 ]  In 1877, he renamed it the  Battle Creek Medical Surgical Sanitarium , [ 8 ]  cleverly coining the term \"sanitarium\" to suggest both hospital care and the importance of sanitation and personal health. [ 21 ] \nKellogg would lead the institution until his death in 1943. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2532", "text": "Kellogg was brought up in the  Seventh-day Adventist Church  from childhood. Selected as a prot\u00e9g\u00e9 of the Whites and trained as a doctor, Kellogg held a prominent role as a speaker at church meetings. [ 15 ] :\u200axiii\u2013xv\u200a  Throughout his lifetime, Kellogg experienced pressure from both science and religion regarding his theological views. [ 15 ] :\u200axiii\u2013xv"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2533", "text": "At the Seventeenth Annual Session of the General Conference of Seventh-day Adventists, October 4, 1878, the following action was taken:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2534", "text": "WHEREAS, The impression has gone out from some unknown cause that J. H. Kellogg, M.D., holds infidel sentiments, which does him great injustice, and also endangers his influence as physician-in-chief of the Sanitarium; therefore\n \nRESOLVED, That in our opinion justice to the doctor and the Institute under his medical charge, demand that he should have the privilege of making his sentiments known, and that he be invited to address those assembled on this ground, upon the harmony of science and the Sacred Scriptures.\n \nThis resolution was unanimously adopted, after which the Conference adjourned to the call of the chair."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2535", "text": "[Note. \u2013 In accordance with the foregoing resolution, Dr. Kellogg gave, before a large audience, October 6, an able address on the harmony of science and the Bible, for which the congregation tendered him a vote of thanks.] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2536", "text": "Kellogg rejected  Christian fundamentalism  and promoted the tenets of theological modernism. He rejected many of the traditional tenets of  Nicene Christianity , viewing the  atonement of Jesus  as \"his exemplary life\" on Earth rather than the Cross. [ 2 ]  Kellogg mocked the concepts of  original sin  and  inherent human depravity , frequently joking that \"the total depravity which we often hear talked about is, half the time at least, nothing more nor less than total indigestion\". [ 2 ]  Historian Brian C. Wilson writes: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2537", "text": "One of the most controversial aspects of Kellogg's developing theology... was its decidedly non-Christocentric focus. While \"God\" is mentioned one hundred times, \"Jesus Christ\" is mentioned only briefly, twelve times, and is treated as something of a peripheral character."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2538", "text": "Kellogg defended \"the harmony of science and the Bible\" throughout his career, but he was active at a transitional time, when both science and medicine were becoming increasingly  secularized . White and others in the Adventist ministry worried that Kellogg's students and staff were in danger of losing their religious beliefs, while Kellogg felt that many ministers failed to recognize his expertise and the importance of his medical work. There were ongoing tensions between his authority as a doctor, and their authority as ministers. [ 23 ]  \nNonetheless, Kellogg attempted to reconcile science and medicine with religion, rejecting their separation, and emphasizing the presence of God within God's creation of living things. [ 15 ] :\u200axiii\u2013xv"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2539", "text": "The heart is a muscle. The heart beats. My arm will contract and cause the fist to beat; but it beats only when my will commands. But here is a muscle in the body that beats when I am asleep. It beats when my will is inactive and I am utterly unconscious. It keeps on beating all the time. What will is it that causes this heart to beat? The heart can not beat once without a command. To me it is a most wonderful thing that a man's heart goes on beating. It does not beat by means of my will; for I can not stop the heart's beating, or make it beat faster or slower by commanding it by my will. But there is a will that controls the heart. It is the divine will that causes it to beat, and in the beating of that heart that you can feel, as you put your hand upon the breast, or as you put your finger against the pulse, an evidence of the divine presence that we have within us, that God is within, that there is an intelligence, a power, a will within, that is commanding the functions of our bodies and controlling them\u2026 [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2540", "text": "He further elaborated these ideas in his book  The Living Temple  (1903):"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2541", "text": "There is a clear, complete, satisfactory explanation of the most subtle, the most marvelous phenomena of nature, \u2013 namely, an infinite Intelligence working out its purposes. God is the explanation of nature, \u2013 not a God outside of nature, but in nature, manifesting himself through and in all the objects, movements, and varied phenomena of the universe. ... The tree does not create itself; a creative power is constantly going forward in it. Buds and leaves come forth from within the tree ... So there is present in the tree a power which creates and maintains it, a tree-maker in the tree, a flower-maker in the flower, \u2013 a divine architect who understands every law of proportion, an infinite artist who possesses a limitless power of expression in color and form; there is, in all the world about us, an infinite, divine, though invisible Presence, to which the unenlightened may be blind, but which is ever declaring itself by its ceaseless, beneficent activity. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2542", "text": "At the same time that Kellogg defended the presence of God in nature against  secularization , his co-religionists saw his descriptions of the presence of God in nature as evidence of\n panentheistic  tendencies (Everything is in God). [ 26 ]  \nKellogg rejected their religious criticisms, asserting that his views on indwelling divinity were simply a restatement of the omnipresence of God, and not pantheism. [ 15 ] :\u200axiii\u2013xv\u200a [ 16 ] :\u200a189"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2543", "text": "His theological views went against many of the traditional tenets of  Nicene Christianity . As  Seventh-day Adventist  beliefs shifted towards orthodox Trinitarianism during the 1890s, Adventists within the denominations were \"unable to accommodate the essentially  liberal  understanding of Christianity\" exhibited by Kellogg, viewing his theology as  pantheistic  and unorthodox. [ 9 ]  What came to be referred to as the \"Pantheism Crisis\" of 1903 was a pivotal moment in the church's history. Kellogg's theological views were only one of the issues involved: operation of the sanitarium was equally if not more important. [ 15 ] :\u200axiii\u2013xv\u200a  \nControl of the sanitarium and its finances had been a source of contention for some time, especially as the institution expanded and attracted more affluent patients. [ 27 ]  \nTensions came to a head when the Battle Creek Sanitarium, originally owned by the Seventh-day Adventist Church but run by Kellogg, was destroyed by fire on February 18, 1902. Although almost all of the guests escaped safely, property loss was estimated at $300,000 to $400,000, about twice the insured value. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2544", "text": "Ellen G. White , who had proclaimed that a cleansing sword of fire was poised over the increasingly \"worldly\" and business-oriented Battle Creek, was against rebuilding the large institution. [ 29 ] [ 30 ]  Although she apparently wrote a manuscript testifying against the rebuilding in 1902, it was not sent to Kellogg at that time, [ 29 ]  and Kellogg did not directly consult her about his plans. [ 23 ] :\u200a38\u200a  With support of the board of directors, he not only rebuilt the institution, but doubled its size. The new building was designed by architect  Frank Mills Andrews  of Ohio [ 31 ]  and opened on May 31, 1903. [ 15 ] :\u200axiii\u2013xv\u200a [ 26 ] :\u200a189\u200a  Designed to be fireproof, the new brick building was six stories high, with an elegant frontage extending 550 feet along Washington Avenue, and three wings opening out behind. It included, among other things, a solarium and palm court, and it cost more than $700,000. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2545", "text": "Kellogg used proceeds from his book  The Living Temple  to help pay the costs of reconstruction. The book's printing was opposed by a commission of the General Council of the Adventists after  W. W. Prescott , one of the four members of the commission, argued that it was heretical. When Kellogg arranged to print it privately, the book went through its own trial by fire: on December 30, 1902, fire struck the  Herald  where the book was typeset and ready to print. [ 26 ]  When it finally appeared in 1903, the book was sharply criticized by White for what she considered its many statements of pantheism. [ 15 ] :\u200a84\u201389\u200a  Over the next few years, there was increasing conflict between Kellogg, General Conference President  A. G. Daniells  and others. [ 29 ]  In 1907, Kellogg was \"disfellowshipped\", as part of a schism that split the church. Kellogg retained control of the Battle Creek Sanitarium and the American Medical Missionary College, and continued to promote Adventist ideas of health and well-being at those institutions. [ 23 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2546", "text": "In later life, Kellogg spoke positively of Seventh-day Adventists and Ellen G. White's prophetic ministry, despite their struggles. In 1941, in response to critic E. S. Ballenger, Kellogg admonished Ballenger for his critical attitude to Mrs. White. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2547", "text": "Mrs. White was unquestionably an inspired woman. In spite of this fact, she was human and made many mistakes and probably suffered more from those mistakes than any person ever did. Nevertheless, I knew the woman was sincere and honest and that the influence of her life was immensely helpful to a vast multitude of people, and I have not the slightest desire in any way to weaken in the smallest degree the good influence of her life and work. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2548", "text": "Kellogg was a  Seventh-day Adventist  until mid-life, and gained fame while being the chief medical officer of the Battle Creek Sanitarium, which was owned and operated by the Seventh-day Adventist Church. The sanitarium was operated based on the church's health principles. Adventists believe in promoting a vegetarian diet, abstinence from alcohol and tobacco, and a regimen of exercise, all of which Kellogg followed. He is remembered as an advocate of vegetarianism [ 35 ]  and wrote in favor of it, even after leaving the Adventist Church. [ 36 ]  His dietary advice in the late 19th century discouraged meat-eating, but not emphatically so. His development of a bland diet was driven in part by the Adventist goal of reducing sexual stimulation. [ 37 ] [ failed verification ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2549", "text": "Kellogg was an especially strong proponent of  nuts , which he believed would save humanity in the face of decreasing food supplies. [ 38 ]  Though mainly renowned nowadays for his development of  corn flakes , Kellogg also invented a process for making  peanut butter [ 39 ] [ 40 ]  and developed healthy \"granose biscuits\" which became popular as far away as Australia [ 41 ]  and England. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2550", "text": "The Battle Creek Sanitarium had its own experimental kitchen. There, Ella Eaton Kellogg helped to develop vegetarian foods, and supervised a \"school of cookery\" which taught classes in food preparation for homemakers. [ 43 ]  She published a cookbook,  Science in the Kitchen , containing hundreds of recipes along with discussions of nutrition and household and diet management. Some of its inventive vegetarian recipes use food products created at the sanitarium, such as Nuttolene (a meat p\u00e2t\u00e9 made from peanuts), [ 42 ]  \nProtose (a combination of nuts and grains), [ 8 ]  and various types of nut butters. [ 40 ] [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2551", "text": "Kellogg believed that most disease is alleviated by a change in  intestinal flora . He posited that bacteria in the intestines can either help or hinder the body; that pathogenic bacteria produce  toxins  during the digestion of protein which poison the blood; that a poor diet favors harmful bacteria that can then infect other tissues in the body; that the intestinal flora is changed by diet and is generally changed for the better by a well-balanced vegetarian diet favoring low- protein ,  laxative , and high- fiber  foods. He recommended various regimens of specific foods designed to heal particular ailments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2552", "text": "Kellogg further believed that natural changes in intestinal flora could be sped by enemas seeded with favorable bacteria. He advocated the frequent use of an enema machine to cleanse the bowel with several gallons of water. Water enemas were followed by the administration of a pint of  yogurt  \u2013 half was eaten, the other half was administered by enema, \"thus planting the protective germs where they are most needed and may render most effective service.\" The yogurt served to replace the intestinal flora of the bowel, creating what Kellogg claimed was a squeaky-clean  intestine . [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2553", "text": "Sanitarium visitors also engaged in breathing exercises and mealtime marches, to promote proper  digestion  of food throughout the day. Because Kellogg was a staunch supporter of  phototherapy , the sanitarium made use of artificial  sunbaths . [ 8 ]  Kellogg was a skilled surgeon, who often donated his services to indigent patients at his clinic. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2554", "text": "He had many notable patients, such as former president  William Howard Taft , composer and pianist  Percy Grainger , arctic explorers  Vilhjalmur Stefansson  and  Roald Amundsen , world travellers  Richard Halliburton  and  Lowell Thomas , aviator  Amelia Earhart , economist  Irving Fisher , Nobel prize winning playwright  George Bernard Shaw , actor and athlete  Johnny Weissmuller , founder of the Ford Motor Company  Henry Ford , inventor  Thomas Edison , [ 47 ]  African-American activist  Sojourner Truth , and actress  Sarah Bernhardt . [ 48 ] [ 49 ] [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2555", "text": "John Harvey Kellogg developed and marketed a wide variety of vegetarian foods. Many of them were meant to be suitable for an invalid diet, and were intentionally made easy to chew and to digest. Starchy foods such as grains were ground and baked, to promote the conversion of  starch  into  dextrin . Nuts were ground and boiled or steamed. [ 16 ] :\u200a114\u2013115,\u200a119"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2556", "text": "The foods Kellogg developed also tended to be bland. In this, Kellogg followed the teachings of  Ellen G. White  and  Sylvester Graham  who recommended a diet of bland foods to minimize excitement, sexual arousal, and masturbation. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2557", "text": "Around 1877, John H. Kellogg began experimenting to produce a softer breakfast food, something easy to chew. He developed a dough that was a mixture of wheat,  oats , and corn. It was baked at high temperatures for a long period of time, to break down or \"dextrinize\" starch molecules in the grain. After it cooled, Kellogg broke the bread into crumbs. The cereal was originally marketed under the name \" Granula \" but this led to legal problems with  James Caleb Jackson  who already sold a wheat cereal under that name. In 1881, under threat of a lawsuit by Jackson, Kellogg changed the sanitarium cereal's name to \"Granola\". [ 52 ]  \nIt was used initially by patients at the sanitarium, but slowly began to build up a following among former patients. [ 16 ] :\u200a115\u200a  In 1890, John formed the Sanitas Food Company to develop and market food products. [ 4 ] :\u200a53"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2558", "text": "The Kelloggs are best known for the invention of the famous breakfast cereal  corn flakes . The development of the flaked cereal in 1894 has been variously described by those involved: Ella Eaton Kellogg, John Harvey Kellogg, his younger brother Will Keith Kellogg, and other family members. There is considerable disagreement over who was involved in the discovery, and the role that they played. According to some accounts, Ella suggested rolling out the dough into thin sheets, and John developed a set of rollers for the purpose. According to others, John had the idea in a dream, and used equipment in his wife's kitchen to do the rolling. It is generally agreed that upon being called out one night, John Kellogg left a batch of wheat-berry dough behind. Rather than throwing it out the next morning, he sent it through the rollers and was surprised to obtain delicate flakes, which could then be baked. Will Kellogg was tasked with figuring out what had happened, and recreating the process reliably. Ella and Will were often at odds, and their versions of the story tend to minimize or deny each other's involvement, while emphasizing their own part in the discovery. [ 52 ]  The process that Kellogg had discovered, tempering, was to be a fundamental technique of the flaked cereal industry. [ 16 ] :\u200a116"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2559", "text": "A patent for \"Flaked Cereals and Process of Preparing Same\" was filed on May 31, 1895, and issued on April 14, 1896, to John Harvey Kellogg as Patent No. 558,393. Significantly, the patent applied to a variety of types of grains, not just to wheat. John Harvey Kellogg was the only person named on the patent. [ 53 ]  Will later insisted that he, not Ella, had worked with John, and repeatedly asserted that he should have received more credit than he was given for the discovery of the flaked cereal. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2560", "text": "During their first year of production, the Kelloggs sold tens of thousands of pounds of flaked cereal, marketing it as \"Granose\". They continued to experiment using rice and corn as well as wheat, and in 1898 released the first batch of Sanitas Toasted Corn Flakes. A modified version with a longer shelf life was released in 1902. [ 8 ]  By that time, both \"Granose Biscuits\" and \"Granose Flakes\" were available. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2561", "text": "Will Kellogg continued to develop and market flaked cereal. When he proposed adding sugar to the flakes, John would not agree to the change. \nSo, in 1906, Will started his own company, the Battle Creek Toasted Corn Flake Company. This marked the start of a decades-long feud between the brothers. Will's Battle Creek Toasted Corn Flake Company eventually became the  Kellogg Company , while John was denied the right to use the Kellogg name for his cereals. [ 8 ] [ 4 ] :\u200a53\u200a [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2562", "text": "They had other competitors as well, including  C. W. Post . Post was treated at the Battle Creek Sanitarium between February 6 and November 9, 1891, and later by  Christian Scientists  whom he credited with his successful treatment. He settled in Battle Creek, opened his own sanitarium, the LaVita Inn, in March 1892, and founded his own dry foods company,  Post Holdings . [ 56 ] \nPost started selling  Postum  coffee substitute in 1895. [ 57 ]  \nHe issued  Grape-Nuts  breakfast cereal, a mixture of yeast, barley and wheat, in January 1898. [ 56 ]  \nIn January 1906, Post introduced \"Elijah's Manna\", later renaming it  Post Toasties  Double-Crisp Corn Flakes, and marketing it as a direct competitor to Kellogg's Corn Flakes. [ 55 ] [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2563", "text": "John Harvey Kellogg was inducted into the  National Inventors Hall of Fame  in 2006 for the discovery of tempering and the invention of the first dry flaked breakfast cereal, which \"transformed the typical American breakfast\". [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2564", "text": "John H. Kellogg is one of several people who have been credited with the invention of peanut butter. [ 60 ] [ 39 ]  \nRose Davis of  Alligerville, New York  has been reported to have made a peanut spread as early as 1840, after her son described Cuban women grinding peanuts and eating the paste on bread. [ 39 ] :\u200a30\u200a  \nIn 1884,  Marcellus Gilmore Edson  (1849\u20131940) of  Montreal , Canada obtained a patent for the \"Manufacture of peanut-candy\", combining 1 part of a \"flavoring paste\" made from roasted peanuts with 7 parts of sugar. [ 61 ]  \nBy 1894, George A. Bayle of St. Louis was selling a \"Cheese Nut\" snack food containing peanuts and cheese; a peanut-only version was apparently more successful. [ 60 ] [ 62 ] \n George Washington Carver  is often credited because of his scientific work with peanuts and promotion of their use. [ 63 ] :\u200a357\u200a  Carver and Kellogg corresponded in the 1920s and 30s about the use of both peanuts and  sweet potatoes . [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2565", "text": "Some form of nut butter, likely made with peanuts, was served to patients at the Battle Creek Sanitarium before October 1895, when Kellogg wrote to Ellen White that \"some very excellent preparations from nuts\" had entirely replaced butter. [ 63 ] :\u200a357\u200a \nKellogg did not patent peanut butter explicitly, and later stated that this was intentional: \"Let everybody that wants it have it, and make the best use of it\". [ 39 ] :\u200a32\u200a  Kellogg did, however, apply for two patents relating to \"nut butters\" in 1895, before anyone else did so. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2566", "text": "On November 4, 1895, John H. Kellogg applied for two patents that are relevant to the production of peanut butter. [ 63 ]  Patent No. 567901, granted September 15, 1896, was for a \"Food Compound\" which produced \"an improved article of manufacture, the alimentary product composed of completely digested starch, completely-emulsified vegetable oil such as described, and thoroughly cooked and finely-divided vegetable proteins derived from nuts, as specified.\" \nThe process described involved taking raw edible nuts, preferably peanuts or almonds, blanching them to remove their skins, and then boiling them for several hours. The nuts were then crushed and passed through rollers to separate out \"a fine and comparatively dry and nearly white nutmeal\" and a \"moist, pasty, adhesive, and brown\" butter or paste. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2567", "text": "The second patent, No. 604493, granted on May 24, 1898, was for a \"Process of Producing Alimentary Products\" from \"edible nuts, preferably peanuts\". The process for making the paste again involved boiling the peanuts, but noted that roasting was a possible alternative. The final substance was heated in sealed cans to obtain \"a product differing in many ways from the original paste\" with a consistency resembling cheese. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2568", "text": "By 1898, the Kelloggs were marketing a wide variety of nut-based foods through the Sanitas Nut Food Company. [ 67 ] \nKellogg marketed nut butters as a nutritious protein substitute for people who had difficulty chewing on solid food. Because peanuts were the least expensive nut available, they rapidly dominated the nut butter market. [ 63 ] \n [ 39 ] [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2569", "text": "Joseph Lambert, who had worked for Kellogg at the sanitarium, began selling a hand-operated peanut butter grinder in 1896. [ 68 ]  In 1899, his wife Almeida Lambert published a  Guide for Nut Cookery . [ 39 ] :\u200a33"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2570", "text": "Kellogg credited his interest in  meat substitutes  to  Charles William Dabney , an agricultural chemist and the Assistant Secretary of Agriculture. Dabney wrote to Kellogg on the subject around 1895. [ 16 ] :\u200a119"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2571", "text": "In 1896, Kellogg introduced but did not patent \"Nuttose\", the first commercially produced alternative to meat. Nuttose was made primarily from peanuts and resembled \"cold roast  mutton \". [ 42 ] :\u200a6\u200a \nBy seasoning or marinating, Nuttose could be made to taste like fried chicken or barbeque. Served with mashed potatoes and vegetables, it could mimic a traditional American meal. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2572", "text": "On March 19, 1901, Kellogg was granted the first United States Patent for a \"vegetable substitute for meat\", for a blend of nuts and grain cereals called \"Protose\".\nIn applying for  US patent 670283A , John Harvey Kellogg, \"Vegetable-food Compound\", issued June 8, 1899 \u00a0 , Kellogg described Protose as a product \"which shall possess equal or greater nutritive value in equal or more available form... By proper regulation of the temperature and proportions of the ingredients, various meat-like flavors are developed, which give the finished product very characteristic properties.\" [ 42 ] :\u200a6\u200a [ 70 ] \nNuttose and Protose were the first of many meat alternatives. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2573", "text": "In addition to developing  imitation meats  variously made from nuts, grains, and soy, Kellogg also developed the first  acidophilus   soy milk , [ 71 ]  which was patented in 1934. [ 72 ] \nKellogg advocated that it be administered to bottle-fed babies, to improve their intestinal fauna and combat bowel infections. Perhaps his most famous patients were the  Dionne quintuplets . When he learned that Marie had a bowel infection, Kellogg sent a case of his soy acidophilus to their doctor,  Allan Roy Dafoe . When Marie's infection cleared up, Dafoe requested that Kellogg send an ongoing supply for the quintuplets. By 1937, each one consumed at least a pint per day. Another famous patient who benefited from soy acidophilus was polar explorer  Richard E. Byrd . [ 52 ] :\u200a330\u2013333\u200a \nKellogg also sold yogurt, soy flour, and soy bread. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2574", "text": "Although they are less discussed than his food creations, Kellogg designed and improved upon a number of medical devices that were regularly used at the Battle Creek Sanitarium in surgical operations and in treatment modalities falling under the term \" physiotherapy \".\nMany of the machines invented by Kellogg were manufactured by the Battle Creek Sanitarium Equipment Company, which was established in 1890. [ 32 ] \nDr. Kellogg attempted to popularize these treatment methods, including  electrotherapy ,  hydrotherapy , and motor therapy, in his work  The Home Handbook of Domestic Hygiene and Rational Medicine , first published in 1881. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2575", "text": "As he specialized in certain gynecological surgeries (particularly  hemorrhoidectomies  and  ovariotomies ) and  gastrointestinal  surgeries, he developed various instruments for these operations. These included specialized hooks and  retractors , a heated operating table, and an aseptic drainage tube used in abdominal surgery. [ 16 ] :\u200a116\u2013127"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2576", "text": "Additionally, Kellogg took keen interest in devising instruments for  light therapy , mechanical exercising, proper breathing, and  hydrotherapy . His medical inventions spanned a wide range of applications and included a hot air bath, vibrating chair, oscillomanipulator, window tent for fresh air,  pneumograph  to graphically represent respiratory habits, [ 16 ]   loofah  mitt, and an apparatus for home sterilization of milk. [ 16 ]  Some of his inventions were fashionable enough to be included in the first class gymnasium of the  RMS Titanic . [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2577", "text": "Kellogg did not make concerted efforts to profit from his medical inventions. Kellogg's statement in 1916 about his food company sheds light on his general motivations: \"I desire to make clear...that the food business I have been carrying on is a part of my general scheme to propagate the ideas of health and biological living. Otherwise, I should not have engaged in it as a commercial enterprise, but I have carried it on as a part of the general philanthropic work in which I was engaged.\" [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2578", "text": "Partly motivated by the overcast skies of Michigan winters, Kellogg experimented with and worked to develop light therapies, as he believed in the value of the  electric light bulb  to provide heat penetration for treating bodily disorders. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2579", "text": "He constructed his first incandescent light bath in 1891, claiming to treat thousands of patients at the Battle Creek Sanitarium before exhibiting the bath at the  World's Columbian Exposition  in Chicago in 1893. [ 75 ]  The invention reportedly aroused little attention there but was brought back to Germany, where it began to be manufactured and sold. [ 75 ]  It was spread to Vienna by Kellogg's friend Dr.  Wilhelm Winternitz ; installed in royal palaces across Europe; and popularly replaced old Turkish steam baths at athletic clubs. [ 16 ]  Only after cabinet baths became popular in Europe did demand within the United States develop. It was imported from  Berlin  to New York \"as a therapeutic novelty\". [ 75 ]  In 1896, Kellogg patented the radiant-heat bath in the United States (US558394)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2580", "text": "In order \"to make a record of his work and experience as a pioneer in this branch of physiotherapeutics\", Kellogg published his book  Light Therapeutics: a practical manual of phototherapy for the student and the practitioner, with special reference to the incandescent electric-light bath  in 1910. [ 76 ]  In the short work, Kellogg describes the application of the arc light to the spine, chest, abdominal region, loins, shoulders, hip and thigh, knees and other joints. He also goes into detail about combining electrotherapies with hydrotherapies, e.g. the electric light bath with shower and shampoo. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2581", "text": "Though Kellogg stated that \"electricity is not capable of accomplishing half the marvels that are claimed for it by many enthusiastic electrotherapists,\" he still believed electric currents to be \"an extremely valuable therapeutic agent, especially when utilized in connection with hydrotherapy, thermotherapy, and other physiologic methods.\" [ 78 ]  As a result, electrotherapy coils were used in the Static Electrical Department of the Battle Creek Sanitarium especially for cases of paresthesias of neurasthenia, insomnia, and certain forms of neuralgia. [ 78 ]  Devices were also used to administer electric shocks to various parts of a patient's body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2582", "text": "Vibrational therapy by way of sinusoidal (high-frequency oscillating) electric current was discovered by Kellogg in 1884 to have medical use for increasing blood circulation and passive exercise. [ 16 ]  In particular, Kellogg invented a vibrating chair used to stimulate vital organs in the lower abdomen. [ 16 ]  Even today one can visit the Kellogg Discovery Center in Battle Creek, Michigan, and sit on Kellogg's vibrating chair, which is equipped to mechanically oscillate 20 times per second. [ 79 ]  Furthermore, Kellogg devised an electrotherapy exercise bed in which a sinusoidal current that produced muscular contraction could be delivered without pain for twenty minutes and reportedly achieve the stimulation of a brisk four-mile walk. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2583", "text": "Massage devices included two- or four-person foot vibrators, a mechanical slapping massage device, and a kneading apparatus that was advertised in 1909 to sell for  $150.00  (equivalent to about $5,100 in 2023). [ 80 ]  Kellogg advocated mechanical massage, a branch of  mechanotherapy , for cases of  anemia , general debility, and muscular or nervous weakness. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2584", "text": "In 1936, Kellogg filed a petition for his invention of improvements to an \"irrigating apparatus particularly adaptable for colonic irrigating, but susceptible of use for other irrigation treatments.\" [ 82 ]  The improved irrigator included features such as measuring the amount of liquid entering and exiting the colon as well as indicating and regulating the positive pressure of the pumped liquid. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2585", "text": "At the Battle Creek Sanitarium, these colonic irrigators were often used to shoot gallons of water up patients' rectums into their colons, sometimes followed by a half-pint yogurt enema to aid in further cleaning. It has been suggested that multiple people would get this treatment at one time. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2586", "text": "Synthesizing his Adventist beliefs with his scientific and medical knowledge, Kellogg created his idea of \"biologic living\". [ 15 ]  This was the idea that appropriate diet, exercise, and recreation was required to maintain a healthy body, mind, and soul. As such, the policies and therapies at the Battle Creek Sanitarium were very much in line with these principles of biologic living, such as the focus on vegetarianism or drinking 8\u201310 glasses of water a day. [ 83 ]  In fact, his belief that biologic living would protect his health was so strong that he did not even feel it necessary to get vaccinated against smallpox. [ 16 ] :\u200a59"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2587", "text": "Kellogg's philosophy was presented in seven textbooks that were prepared for Adventist schools and colleges. In these, Kellogg put his main emphasis on the value of fresh air, exercise, and sunshine, and the dangers of alcohol and tobacco. [ 16 ] :\u200a91\u200a  In terms of practice, Kellogg's biologic living was very similar to the methods of Christian physiologists, requiring sexual restraint, total abstinence from drugs, and a vegetarian diet. [ 16 ] :\u200a44"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2588", "text": "Kellogg was a prominent member of the anti-tobacco consumption campaign, speaking out often on the issue. [ 84 ]  He believed that consumption of tobacco not only caused physiological damage, but also pathological, nutritional, moral, and economic devastation onto society. His belief was that \"tobacco has not a single redeeming feature\u2026 and is one of the most deadly of all the many poisonous plants known to the botanist.\" [ 85 ]  His beliefs were very much in line with the prevailing view of the Adventists, who had become some of the most important supporters of the anti-tobacco movement."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2589", "text": "In his 1922 book  Tobaccoism, or How Tobacco Kills , Kellogg cited many studies on the negative impacts of smoking, and went so far as to attribute the longer lifespan of women to the observation that they partook in tobacco less than their male counterparts. [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2590", "text": "Kellogg also served as the president of the Michigan Anti-Cigarette Society, and after the First World War, he served as a member of the Committee of Fifty to Study the Tobacco Problem. This latter group included Henry Ford, George Peabody, and John Burroughs, and ended with the production of one of the first educational motion pictures against smoking. [ 16 ] :\u200a107\u200a  Kellogg's work on several committees against smoking culminated in Utah Senator Reed Smoot introducing a bill to Congress in 1929 that aimed to put tobacco under the purview of the Pure Food and Drug Act. In the end, however, this measure failed to pass. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2591", "text": "Though alcoholic beverages were commonly used as a stimulant by the medical community during the time that Kellogg began his medical practice, he was firm in his opposition to the practice. [ 16 ]  The usage of alcohol as a remedy to anything was \"an evil of stupendous proportions.\" [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2592", "text": "Kellogg went against the prevailing notion of the time that alcohol was a stimulant. Citing contemporary research, Kellogg believed that alcohol could not be a stimulant because it lessened vital activity and depressed vital forces. [ 87 ]  Seeing its effects on plants, animals, and humans, he felt that alcohol was a poison. [ 87 ]  Kellogg noticed deleterious effects that alcohol had on both the brain, the digestive system, and the liver, among other organs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2593", "text": "In addition to the idea that alcohol was an unsuitable therapeutic tool, Kellogg also considered it to lead to mental and moral bankruptcy. [ 87 ]  Alcohol was \"one of the devil's most efficient agents for destroying the happiness of man, both for the present and the hereafter.\" [ 87 ]  Even moderate drinkers were subject to these effects, as Kellogg felt that a poison was a poison in all doses."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2594", "text": "Kellogg also opposed tea and coffee due to the  caffeine  content of those beverages. His view was that caffeine was a poison. [ 88 ]  Not only did he detail numerous physiological and developmental problems caused by caffeine, but he also suggested that caffeine usage could lead to moral deficiencies. He blamed the prevalence of these beverages not only on the prohibition of alcoholic beverages at the time, but also on the extensive marketing efforts organized by the producers of these products. Kellogg's view was that \"nature has supplied us with pure water, with a great variety of fruit juices and wholesome and harmless flavors quite sufficient to meet all our needs.\" [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2595", "text": "As early as the 1880s, Kellogg had prepared charts and lectures on the dangers of tobacco and alcohol, which were used widely by lecturers who encouraged temperance in their students. [ 16 ] :\u200a106\u200a  In 1878, John Harvey Kellogg, along with Ellen G. White, the founder of the Seventh-day Adventists, and several others, had organized the American Health and Temperance Association. [ 16 ] :\u200a107\u200a  The goal of this organization was to expose the far-reaching dangers of tobacco, alcohol, tea, and coffee. For the 15 years that the organization persisted, Kellogg remained as its president. [ 16 ] :\u200a107"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2596", "text": "Kellogg has labeled the various uses of hydropathy as being byproducts of the many properties of water. In his 1876 book,  The Uses of Water in Health & Disease , he acknowledges both the chemical composition and physical properties of water. Hydrogen and oxygen, when separate, are two \"colorless, transparent, and tasteless\" gases, which are explosive when mixed. [ 90 ]  More importantly, water, he says, has the highest specific heat of any compound (although in actuality it does not). As such, the amount of heat and energy needed to elevate the temperature of water is significantly higher than that of other compounds like mercury. Kellogg addressed water's ability to absorb massive amounts of energies when shifting phases. He also highlighted water's most useful property, its ability to dissolve many other substances. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2597", "text": "According to Kellogg, water provides remedial properties partly because of vital resistance and partly because of its physical properties. For Kellogg, the medical uses of water begin with its function as a refrigerant, a way to lower body heat by way of dissipating its production as well as by conduction. \"There is not a drug in the whole materia medica that will diminish the temperature of the body so readily and so efficiently as water.\" [ 92 ]  Water can also serve as a sedative. While other substances serve as sedatives by exerting their poisonous influences on the heart and nerves, water is a gentler and more efficient sedative without any of the negative side-effects seen in these other substances. Kellogg states that a cold bath can often reduce one's pulse by 20 to 40 beats per minute quickly, in a matter of a few minutes. Additionally, water can function as a tonic, increasing both the speed of circulation and the overall temperature of the body. A hot bath accelerates one's pulse from 70 to 150 beats per minute in 15 minutes. Water is also useful as an anodyne since it can lower nervous sensibility and reduce pain when applied in the form of hot fomentation. Kellogg argues that this procedure will often give one relief where every other drug has failed to do so. He also believed that no other treatment could function as well as an antispasmodic, reducing infantile convulsions and cramps, as water. Water can be an effective astringent as, when applied cold, it can arrest hemorrhages. Moreover, it can be very effective in producing bowel movements. Whereas purgatives would introduce \"violent and unpleasant symptoms\", water would not. Although it would not have much competition as an emetic at the time, Kellogg believed that no other substance could induce vomiting as well as water did. Returning to one of Kellogg's most admired qualities of water, it can function as a \"most perfect eliminative\". Water can dissolve waste and foreign matter from the blood. These many uses of water led Kellogg to belief that \"the aim of the faithful physician should be to accomplish for his patient the greatest amount of good at the least expence  of vitality; and it is an indisputable fact that in a large number of cases water is just the agent with which this desirable end can be obtained.\" [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2598", "text": "Although Kellogg praised hydropathy for its many uses, he did acknowledge its limits. \"In nearly all cases, sunlight, pure air, rest, exercise, proper food, and other hygienic agencies are quite as important as water. Electricity, too, is a remedy which should not be ignored; and skillful surgery is absolutely indispensable in not a small number of cases.\" [ 94 ]  With this belief, he went on to criticize many medical figures who misused or overestimated hydropathy in the treating of disease. Among these, he criticized what he referred to as \"Cold-Water Doctors\" who would recommend the same remedy regardless of the type of ailment or temperament of the patient. [ 95 ]  These doctors would prescribe ice-cold baths in unwarmed rooms even during the harshest winters. In his opinion, this prejudicial approach to illness resulted in converting hydropathy to a more heroic type of treatment where many became obsessed with taking baths in ice-cold water. He addresses the negative consequences that resulted from this \"infatuation\", among them tuberculosis and other diseases. [ 96 ]  This dangerous habit was only exacerbated by physicians who used hydropathy in excess. Kellogg recounts an instance where a patient with a low typhus fever was treated with 35 cold packs while in a feeble state and, not to the surprise of Kellogg, died. Kellogg posits this excessive and dangerous use of hydropathy as a return to the \"violent processes\" of bloodletting, antimony, mercury and purgatives. [ 97 ]  Kellogg also criticizes the ignorance in \"Hydropathic Quacks\" as well as in Preissnitz, the founder of modern hydropathy, himself. Kellogg states that the \"Quacks\" as well as Preissnitz are ignorant for overestimating the hydropathy as a \"cure-all\" remedy without understanding the true nature of disease. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2599", "text": "Kellogg would live for over 60 years after writing  Plain Facts . He continued to work on healthy eating advice and run the sanitarium, although this was hit by the  Great Depression  and had to be sold. He ran another institute in Florida, which was popular throughout the rest of his life, [ 99 ]  although it was a distinct step down from his Battle Creek institute. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2600", "text": "In 1937, Kellogg received an honorary degree in Doctor of Public Service from  Oglethorpe University . [ 101 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2601", "text": "Pulitzer Prize -winning historian  Will Durant , who had been a vegetarian since the age of 18, called Dr. Kellogg \"his old mentor\", [ 102 ]  and said that Dr. Kellogg, more than any other person since his high school days, had influenced his life. [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2602", "text": "Kellogg became editor of the  Health Reformer  journal in 1874. The journal changed its name to  Good Health  in 1879 and Kellogg held his editorial position for many years until his death. [ 104 ]  The  Good Health  journal had more than 20,000 subscribers and was published until 1955. [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2603", "text": "Kellogg was outspoken about his  views  on  race  and his belief in  racial segregation , regardless of the fact that he himself raised several  black  foster children. In 1906, together with  Irving Fisher  and  Charles Davenport , Kellogg founded the  Race Betterment Foundation , which became a major center of the new  eugenics movement in America . Kellogg was in favor of  racial segregation in the United States  and he also believed that immigrants and non-whites would damage the white American population's gene pool. [ 106 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2604", "text": "He co-founded the  Race Betterment Foundation , [ 107 ]  co-organized several National Conferences on Race Betterment and attempted to create a 'eugenics registry'. Alongside discouraging 'racial mixing', Kellogg was in favor of sterilizing 'mentally defective persons', promoting a eugenics agenda while working on the Michigan Board of Health [ 108 ]  and helping to enact authorization to sterilize those deemed 'mentally defective' into state laws during his tenure. [ 109 ] [ 110 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2605", "text": "Kellogg had a long personal and business split with his brother, after fighting in court for the rights to cereal recipes. The  Foundation for Economic Education  records that the nonagenarian J.H. Kellogg prepared a letter seeking to reopen the relationship. His secretary decided her employer had demeaned himself in it and refused to send it. The younger Kellogg did not see it until after his brother's death. [ 52 ] :\u200a381\u2013382"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2606", "text": "John Harvey Kellogg married  Ella Ervilla Eaton  of  Alfred Center, New York , on February 22, 1879. The couple maintained separate bedrooms and did not have any biological children. However, they were foster parents to 42 children, legally  adopting  8 of them, before Ella died in 1920. [ 111 ]  The adopted children included Agnes Grace, Elizabeth Ella, Harriett Eleanor, John William, Ivaline Maud, Paul Alfred, Robert Mofatt, and Newell Carey. [ 112 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2607", "text": "Kellogg died on December 14, 1943, in  Battle Creek, Michigan . [ 7 ]  He was buried in Oak Hill Cemetery in Battle Creek. [ 52 ] :\u200a385\u200a  In his will, Kellogg left his entire estate to the  Race Betterment Foundation . [ 52 ] :\u200a321"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2608", "text": "British actor  Anthony Hopkins  plays a highly fictionalized Dr. J.H. Kellogg in the American 1994 film  The Road to Wellville  by Alan Parker. [ 113 ]  This film depicts the fire of the sanitarium building complex, and ends with Dr. Kellogg, years after, dying of a heart attack while diving from a high board."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2609", "text": "Several  popular controversies  attribute various cultural practices, inventions, and historical events to Kellogg. [ 11 ] [ 12 ]  These include claims that  Kellogg's corn flakes  were invented and/or marketed to prevent masturbation. They were promoted to prevent indigestion, while the reason for their invention is, as of yet, inconclusive. [ 12 ]  Another  common claim  credits Kellogg with popularizing routine infant  circumcision  in the  United States  and broader  Anglosphere . [ 11 ]  This is a potential overstatement, [ 114 ]  although Kellogg did advocate circumcision, without anaesthetic, as an eficacious cure for masturbation. [ 115 ] :\u200a659\u200a  He wrote in  Plain facts for old and young  that \"Eminent physicians have expressed the opinion that the practice would be a salutary one for all men.\" [ 116 ] :\u200a114\u200a  However in later editions, Kellogg came to criticize this growing belief among medical professionals, arguing that routine circumcision provided doubtful medical benefit, citing  iatrogenically  created  meatal stenosis  among the  Jewish  male population:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2610", "text": "Eminent physicians have expressed the opinion that the practice would be a salutary one for all men...It is doubtful, however, whether as much harm as good does not result from circumcision, since it has been shown by extensive observation among the Jews that very great contraction of the meatus, or external orifice of the urethra, is exceedingly common among them, being undoubtedly the result of the prolonged irritation and subsequent cicatricial contraction resulting from circumcision in infancy. [ 117 ] :\u200a107"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2611", "text": "The  King's College Criteria  or the  King's College Hospital criteria  were devised in 1989 to determine if there were any early indices of poor prognosis in patients with  acute liver failure .  Acute liver failure is defined as the onset of  encephalopathy  (altered mental status) or  coagulopathy  (altered bleeding tendencies) within 26 weeks of a patient diagnosed with liver disease.  Patients with  hepatitis B  acquired at birth,  Wilson's disease  and  autoimmune hepatitis  are included if their disease was identified within the past 26 weeks.  These patients are very ill, and have a very high risk of dying of their illness without adequate treatment which may include  liver transplantation .  It is important that physicians find ways of identifying patients with acute liver failure early in their course who will do poorly, and may require liver transplantation.  The King's College Criteria have consistently shown excellent  operating characteristics  for determining prognosis in these patients.  As  liver transplantation  becomes a more accessible option for patients with acute liver failure, the King's College Criteria serve a role in determining which patients may require transplantation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2612", "text": "The King's College criteria were described in a seminal publication in 1989 by J.G. O'Grady and colleagues from  King's College School of Medicine . [ 2 ]   588 patients with acute liver failure who presented to King's College Hospital from 1973 to 1985 were assessed retrospectively to determine if there were particular clinical features or tests that correlated poorly with prognosis.  The criteria were stratified into acetaminophen and non-acetaminophen causes of acute liver failure, due to the different operating characteristics of parameters correlating with prognosis in the two causes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2613", "text": "Acetaminophen  (or  paracetamol ) is an  analgesic  medication that can affect the liver when administered in high doses.  Acetaminophen is predominantly conjugated into  glucuronate  and  sulfate  moieties by  Phase II metabolism .  A small percentage is metabolized by the  cytochrome P450  pathway to a toxic metabolite, NAPQI.  NAPQI is conjugated by  glutathione  to non-toxic cysteine and mercapturic acid moieties.  In cases of acetaminophen toxicity, the Phase II conjugation enzymes are saturated, and a higher fraction is converted to NAPQI.  The conjugation of NAPQI to glutathione occurs until glutathione is depleted from hepatic reserves, after which the toxic NAPQI accumulates and causes damage to the hepatocytes.  This occurs primarily in areas of the liver that are relatively poorly perfused with oxygen, or furthest away from the  hepatic artery , termed  Zone 3 .  Acetaminophen overdose is associated with Zone 3 necrosis, to the point that acute liver failure may result. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2614", "text": "The King's College Criteria identify two groups of patients that have a poor prognosis with acetaminophen induced liver failure:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2615", "text": "There are many causes of acute liver failure aside from acetaminophen toxicity; these include viral hepatitis\u2014including  hepatitis A  (rarely), [ 4 ]   hepatitis B , [ 1 ]   hepatitis C  (rarely), [ 5 ]   hepatitis E  (especially in pregnant women),  [ 6 ]   Epstein\u2013Barr virus ,  cytomegalovirus  and  varicella zoster virus [ 1 ]  --  Wilson's disease , the toxin of the  death cap  mushroom ( Amanita phalloides ),  alcohol ,  autoimmune hepatitis ,  Budd\u2013Chiari syndrome , other medications (including  halothane ,  hormonal contraception , and  isoniazid ), recreational drugs (including  ecstasy   [1] ) and, rarely, tumours infiltrating the liver. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2616", "text": "In patients with non-acetaminophen acute liver failure, the following criteria were identified as being associated with a poor prognosis: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2617", "text": "The utility of the criteria in determining the prognosis of patients with acute liver failure is defined by their operating characteristics.  The  positive predictive value  of the criteria in predicting death from acute liver failure has ranged from 70% to 100%. [ 1 ] [ 7 ] [ 8 ]   A Canadian  meta-analysis  assessing various prognostic indices found that the  specificity  of the King's College criteria in predicting  mortality  exceeded 90%, with a  sensitivity  of 69%. [ 9 ]   As a result, the American Society for Study of Liver Diseases has recommended the King's College Criteria as being helpful early parameters in ascertaining the need for  liver transplantation  in patients with acute liver failure. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2618", "text": "A variety of other calculations have been done based on similar parameters to determine the risk of mortality in acute liver failure. [ 1 ]   The Acute Physiology and Chronic Health Evaluation II ( APACHE II ) score has a comparable sensitivity to the King's College Criteria in determining prognosis. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2619", "text": "Lactulose  is a non-absorbable  sugar  used in the treatment of  constipation  and  hepatic encephalopathy . [ 3 ] [ 4 ]  It is administered  orally  for constipation, and either orally or  rectally  for  hepatic encephalopathy . [ 3 ]  It generally begins working after 8\u201312 hours, but may take up to 2 days to improve constipation. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2620", "text": "Common  side effects  include abdominal  bloating  and cramps. [ 3 ]  A potential exists for  electrolyte problems  as a result of the  diarrhea  it produces. [ 3 ]  No evidence of harm to the fetus has been found when used during  pregnancy . [ 3 ]  It is generally regarded as safe during breastfeeding. [ 5 ]  It is classified as an  osmotic laxative . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2621", "text": "Lactulose was first made in 1929, and has been used medically since the 1950s. [ 7 ] [ 8 ]  Lactulose is made from the milk sugar  lactose , which is  composed of two simple sugars ,  galactose  and  glucose . [ 9 ] [ 3 ]  It is on the  World Health Organization's List of Essential Medicines . [ 10 ]  It is available as a  generic medication . [ 4 ]  In 2022, it was the 267th most commonly prescribed medication in the United States, with more than 900,000 prescriptions. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2622", "text": "Lactulose is used in the treatment of chronic constipation in patients of all ages as a long-term treatment. [ 13 ]  The dosage of lactulose for chronic idiopathic constipation is adjusted depending on the constipation severity and desired effect, from a mild stool softener to causing diarrhea. Lactulose is contraindicated in case of  galactosemia , as most preparations contain the monosaccharide galactose due to its synthesis process. [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2623", "text": "Lactulose may be used to counter the constipating effects of  opioids , and in the symptomatic treatment of  hemorrhoids  as a stool softener. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2624", "text": "Lactulose is commonly prescribed for children who develop fear of their bowel movements and are withholders. This is because lactulose, when dosed in the proper amount, causes a bowel movement that is impossible to retain for very long. Lactulose is also used for the elderly because of its gentle and consistent results. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2625", "text": "Lactulose is useful in treating  hyperammonemia  (high blood ammonia), which can lead to  hepatic encephalopathy . Lactulose helps trap the  ammonia  (NH 3 ) in the colon and bind to it. [ 16 ]   It does this by using gut flora to acidify the colon, transforming the freely diffusible ammonia into  ammonium  ions ( NH + 4 ), which can no longer diffuse back into the blood. [ 17 ]  It is also useful for preventing hyperammonemia caused as a side effect of administration of  valproic acid . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2626", "text": "Lactulose is used as a test of  small intestine bacterial overgrowth  (SIBO). Recently, the reliability of it for diagnosing SIBO has been seriously questioned. [ 19 ] [ 20 ] [ 21 ] [ 22 ]  A large amount of it is given with subsequent testing of molecular  hydrogen gas in the breath . The test is positive if an increase in exhaled hydrogen occurs before that which would be expected by normal  digestion by the normal  gut flora  in the colon. An earlier result has been hypothesized to indicate digestion occurring within the small intestine. An alternate explanation for differences in results is the variance in small bowel transit time among tested subjects. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2627", "text": "No evidence of harm to the fetus has been found when used during  pregnancy . [ 3 ]  It is generally regarded as safe during breastfeeding. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2628", "text": "Common side effects of lactulose are abdominal cramping,  borborygmus , and  flatulence . In normal individuals, overdose is considered uncomfortable, but not life-threatening. [ 23 ]  Uncommon side effects are  nausea  and  vomiting .  In sensitive individuals, such as the elderly or people with reduced  kidney  function, excess lactulose dosage can result in  dehydration  and electrolyte disturbances such as  low magnesium levels .  Ingestion of lactulose does not cause a weight gain because it is not digestible, with no nutritional value. Although lactulose is less likely to cause  dental caries  than sucrose, as a sugar, a potential for this exists, which is relevant when taken by people with a high susceptibility to this condition. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2629", "text": "Lactulose is not absorbed in the  small intestine  nor broken down by human enzymes, thus stays in the digestive bolus through most of its course, causing retention of water through  osmosis  leading to softer, easier-to-pass stool. It has a secondary laxative effect in the colon, where it is  fermented  by the  gut flora , producing  metabolites  which have osmotic powers and  peristalsis -stimulating effects (such as  acetate ), but also  methane  associated with  flatulence . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2630", "text": "Lactulose is metabolized in the  colon  by  bacterial flora  into short-chain fatty acids, including  lactic acid  and  acetic acid . These partially dissociate, acidifying the colonic contents (increasing the H +  concentration in the gut). [ 17 ]  This favors the formation of the nonabsorbable  NH + 4  from NH 3 , trapping NH 3  in the colon and effectively reducing plasma NH 3  concentrations. Lactulose is therefore effective in treating hepatic encephalopathy. [ 24 ]  Specifically, it is effective as secondary prevention of hepatic encephalopathy in people with cirrhosis. [ 25 ]  Moreover, research showed improved cognitive functions and health-related quality of life in people with cirrhosis with minimal hepatic encephalopathy treated with lactulose. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2631", "text": "Lactulose is a  disaccharide  formed from one molecule each of the  simple sugars  ( monosaccharides )  fructose  and  galactose . Lactulose is not normally present in raw milk, but is a product of heat processes: [ 27 ]  the greater the heat, the greater amount of this substance (from 3.5 mg/L in low-temperature  pasteurized  milk to 744 mg/L in in-container sterilized milk). [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2632", "text": "Lactulose is produced commercially by  isomerization  of  lactose . A variety of reaction conditions and catalysts can be used. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2633", "text": "Lactulose  is its  international nonproprietary name  (INN). [ 29 ]  It is sold under various brand names. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2634", "text": "Lactulose is available as a  generic medication . [ 4 ]  It is available without prescription in most countries, but a prescription is required in the United States, [ 3 ]  Philippines, and Austria. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2635", "text": "In some countries where lactulose may be obtained without a prescription, lactulose is commonly used as a  food additive  to improve taste and promote intestinal transit. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2636", "text": "Lactulose is used in veterinary medicine. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2637", "text": "Laminarid  is a blend of  polysaccharides , proteins and salts of  alginic acid  obtained from  sea cabbage  (Laminariae thalli [ citation needed ] ). It is an  osmotic laxative . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2638", "text": "This  drug  article relating to the  gastrointestinal system  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2639", "text": "Laparoscopic hernia repair  is the repair of a  hiatal hernia  using a  laparoscope , which is a tiny telescope-like instrument. [ 1 ] [ 2 ] [ 3 ] [ 4 ]  A hiatal hernia is the protrusion of an organ through its wall or cavity. [ 5 ]  There are several different methods that can be used when performing this procedure. Among them are the Nissen Fundoplication and the general laparoscopic hernia repair."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2640", "text": "There are two types of hiatal hernias. The two different types of hiatal hernias that are relevant to this surgery are rolling hiatal hernias and sliding hiatal hernias. A type II, rolling hiatal hernia, is when the  gastric fundus  is herniated, but the cardia portion of the stomach remains still. A type 1, or sliding hiatal hernia, is when the gastroesophageal junction and the cardia portion of the stomach move through the posterior  mediastinum . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2641", "text": "There are several different methods when performing a laparoscopic hernia repair. A few of these are the fundoplication and the general laparoscopic hernia repair."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2642", "text": "In  bariatric surgery , hernias are repaired  laparoscopically  anteriorly, rather than posteriorly as in the  fundoplication  procedure.  This general laparoscopic procedure was introduced by Sami Salem Ahmad from Germany.\nThe  Nissen fundoplication  procedure was first performed by  Rudolph Nissen  in 1955. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2643", "text": "A laparoscopic hernia repair is when the hiatal hernia is corrected using a covering for the mesh that is used to repair the weakened area. The defect is then measured and the mesh is stapled into place. [ 6 ]  A benefit of performing Laparoscopic hernia repair is shorter recovery times compared to other methods. However, it is a longer procedure than most other methods of repair. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2644", "text": "The  Nissen fundoplication  procedure consists of a 360 degree transabdominal  fundoplication . A fundoplication is the suturing of the fundus located in the stomach and around the esophagus. [ 5 ]  The procedure itself is performed with the patient in a low lithotomy position at approximately 25 degrees. After the esophagus is mobilized, the  crura  is moved posteriorly using sutures to make room for a French bougie. When in place, a wrap is created and sutured to the esophagus and to the right  crus  at the hiatus as well. After this is performed, the bougie is removed and the wrap is further anchored with additional sutures. The  trocar  sites are then closed. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2645", "text": "When performing a laparoscopic hernia repair, patients undergoing the procedure face complications such as postoperative urinary retention (PUR).\nAnother potential complication is requiring a second hernia repair after previously having one at an earlier time. [ 8 ] \nSome complications can arise from the need for general anesthesia in having an open ventral hernia repair. [ 9 ]  Inherent risks are associated with the use of anesthesia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2646", "text": "General complications that can occur using any method of hernia repair are: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2647", "text": "Some complications that can arise from the general laparoscopic procedure are PUR (postoperative urinary retention)  [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2648", "text": "Other complications that can arise during this procedure are: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2649", "text": "Complications that can arise form this procedure are: [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2650", "text": "Overall, the complication rate for this procedure is about 10% to 20%. The failure rate, or inability to repair the hernia, is approximately 5%. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2651", "text": "The outcomes of laparoscopic hernia repair versus open hernia repair support laparoscopic hernia repair as the method of choice.\nOutcomes from having laparoscopic hernia repair are: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2652", "text": "A laparoscopic hiatal hernia repair results in a hospital stay of approximately 36 to 48 hours after the procedure has been performed  [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2653", "text": "Laparoscopic hernia repair has several benefits compared to performing Open hernia repairs. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2654", "text": "Benefits are: [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2655", "text": "Laxatives ,  purgatives , or  aperients  are substances that loosen  stools [ 1 ]  and increase  bowel movements . They are used to treat and prevent  constipation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2656", "text": "Laxatives vary as to how they work and the side effects they may have. Certain  stimulant ,  lubricant , and  saline  laxatives are used to evacuate the  colon  for  rectal  and bowel examinations, and may be supplemented by  enemas  under certain circumstances. Sufficiently high doses of laxatives may cause  diarrhea . Some laxatives combine more than one active ingredient, and may be administered  orally  or  rectally ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2657", "text": "Bulk-forming laxatives, also known as  roughage , are substances, such as  fiber  in food and  hydrophilic  agents in  over-the-counter drugs , that add bulk and water to  stools  so they can pass more easily through the  intestines  (lower part of the  digestive tract ). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2658", "text": "Properties"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2659", "text": "Bulk-forming agents generally have the gentlest of effects among laxatives, [ 1 ]  making them ideal for long-term maintenance of regular bowel movements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2660", "text": "Foods that help with laxation include fiber-rich foods.  Dietary fiber  includes  insoluble fiber  and  soluble fiber , such as: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2661", "text": "Emollient laxatives, also known as stool softeners, are  anionic surfactants  that enable additional water and fats to be incorporated in the stool, making movement through the bowels easier."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2662", "text": "Emollient agents prevent constipation rather than treating long-term constipation. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2663", "text": "Lubricant  laxatives are substances that coat the stool with slippery lipids and decrease colonic absorption of water so the stool slides through the colon more easily. Lubricant laxatives also increase the weight of stool and decrease intestinal transit time. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2664", "text": "Mineral oils , such as  liquid paraffin , are generally the only nonprescription lubricant laxative available, but due to the risk of lipid pneumonia resulting from accidental aspiration, mineral oil is not recommended, especially in children and infants. [ 10 ] [ 11 ]  Mineral oil may decrease the absorption of fat-soluble vitamins and some minerals. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2665", "text": "Hyperosmotic  laxatives cause the intestines to hold more water, creating an  osmotic gradient , which adds more pressure and stimulates bowel movement. [ 12 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2666", "text": "Lactulose  works by the  osmotic  effect, which retains water in the colon; lowering the  pH  through bacterial fermentation to lactic, formic, and acetic acids; and increasing colonic  peristalsis . Lactulose is also indicated in  portal-systemic encephalopathy . Glycerin suppositories work mostly by hyperosmotic action, but the  sodium stearate  in the preparation also causes local irritation to the colon. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2667", "text": "Solutions of  polyethylene glycol  and electrolytes ( sodium chloride ,  sodium bicarbonate ,  potassium chloride , and sometimes  sodium sulfate ) are used for  whole bowel irrigation , a process designed to prepare the bowel for surgery or  colonoscopy  and to treat certain types of  poisoning . Brand names for these solutions include GoLytely, GlycoLax, Cosmocol, CoLyte, Miralax, Movicol, NuLytely, Suprep, and Fortrans. Solutions of  sorbitol  (SoftLax) have similar effects. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2668", "text": "Saline laxatives are nonabsorbable, osmotically active substances that attract and retain water in the intestinal lumen, increasing intraluminal pressure that mechanically stimulates evacuation of the bowel. Magnesium-containing agents also cause the release of  cholecystokinin , which increases intestinal motility and fluid secretion. [ 3 ]  Saline laxatives may alter a patient's fluid and electrolyte balance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2669", "text": "Stimulant laxatives are substances that act on the intestinal  mucosa  or  nerve plexus , altering water and  electrolyte  secretion. [ 13 ]  They also stimulate peristaltic action and can be dangerous under certain circumstances. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2670", "text": "Prolonged use of stimulant laxatives can create drug dependence by damaging the colon's  haustral folds , making users less able to move feces through their colon on their own. A study of patients with chronic constipation found that 28% of chronic stimulant laxative users lost haustral folds over the course of one year, while none of the control group did. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2671", "text": "Castor oil  is a glyceride that is hydrolyzed by pancreatic lipase to  ricinoleic acid , which produces laxative action by an unknown mechanism."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2672", "text": "Long-term use of castor oil may result in loss of fluid, electrolytes, and nutrients. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2673", "text": "These are motility stimulants that work through activation of  5-HT 4  receptors of the  enteric nervous system  in the  gastrointestinal tract . However, some have been discontinued or restricted due to potentially harmful cardiovascular side effects."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2674", "text": "Tegaserod  (brand name  Zelnorm ) was removed from the general U.S. and Canadian markets in 2007, due to reports of increased risks of heart attack or stroke. It is still available to physicians for patients in emergency situations that are life-threatening or require hospitalization. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2675", "text": "Prucalopride  (brand name Resolor) is a current drug approved for use in the EU since October 15, 2009, [ 17 ]  in Canada (brand name Resotran) since December 7, 2011, [ 18 ]  and in the United States since December 2018."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2676", "text": "Lubiprostone  is used in the management of chronic idiopathic constipation and irritable bowel syndrome. It causes the intestines to produce a chloride-rich fluid secretion that softens the stool, increases motility, and promotes spontaneous bowel movements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2677", "text": "For adults, a  randomized controlled trial  found  PEG  (MiraLax or GlycoLax) 17\u00a0grams once per day to be superior to  tegaserod  at 6\u00a0mg twice per day. [ 21 ]  A randomized controlled trial found greater improvement from two sachets (26\u00a0g) of PEG versus two sachets (20\u00a0g) of lactulose. [ 22 ]  17\u00a0g per day of PEG has been effective and safe in a randomized, controlled trial for six months. [ 23 ]  Another randomized, controlled trial found no difference between sorbitol and lactulose. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2678", "text": "For children, PEG was found to be more effective than lactulose. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2679", "text": "Some of the less significant adverse effects of laxative abuse include  dehydration  (which causes tremors, weakness, fainting, blurred vision, kidney damage),  low blood pressure ,  fast heart rate , postural dizziness and  fainting ; [ 26 ]  however, laxative abuse can lead to potentially fatal  acid-base , and  electrolyte imbalances . [ 26 ]  For example, severe  hypokalaemia  has been associated with  distal renal tubular acidosis  from laxative abuse. [ 26 ]   Metabolic alkalosis  is the most common acid-base imbalance observed. [ 26 ]  Other significant adverse effects include  rhabdomyolysis , [ 26 ]   steatorrhoea , [ 26 ]   inflammation  and  ulceration  of colonic mucosa, [ 26 ]   pancreatitis , [ 26 ] [ 27 ]   kidney failure , [ 26 ] [ 28 ] [ 29 ]   factitious diarrhea [ 26 ] [ 30 ]  and other problems. [ 26 ]  The colon will need more quantities of laxatives to keep functioning, this will result in a lazy colon, infections, irritable bowel syndrome, and potential liver damage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2680", "text": "Although some patients with eating disorders such as  anorexia nervosa  and  bulimia nervosa  abuse laxatives in an attempt to lose weight, laxatives act to speed up the transit of feces through the large intestine, which occurs after the absorption of nutrients in the small intestine is already complete. Thus, studies of laxative abuse have found that effects on body weight reflect primarily temporary losses of body water rather than energy (calorie) loss. [ 26 ] [ 31 ] [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2681", "text": "Physicians warn against the chronic use of stimulant laxatives due to concern that chronic use could cause the colonic tissues to get worn out over time and not be able to expel feces due to long-term overstimulation. [ 33 ]   A common finding in patients having used stimulant laxatives is a brown pigment deposited in the intestinal tissue, known as  melanosis coli . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2682", "text": "Laxatives, once called \"physicks\" or \"purgatives\", were used extensively in  historic medicine  to treat many conditions for which they are now generally regarded as ineffective in  evidence-based medicine . [ 34 ]  Likewise, laxatives (often termed  colon cleanses ) may be promoted in  alternative medicine  for various conditions of  quackery , such as \" mucoid plaque \". [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2683", "text": "Leaky gut syndrome  is a hypothetical and medically unrecognized condition [ 1 ] [ 2 ]  that is distinct from the scientific phenomenon of  increased intestinal permeability  commonly known as \"leaky gut\". [ 1 ] [ 3 ]  Claims for the existence of \"leaky gut syndrome\" as a distinct medical condition come mostly from nutritionists and practitioners of  alternative medicine . [ 1 ] [ 4 ] [ 5 ]  Proponents claim that a \"leaky gut\" causes  chronic inflammation  throughout the body that results in a wide range of conditions, including  myalgic encephalomyelitis/chronic fatigue syndrome ,  rheumatoid arthritis ,  lupus ,   migraines ,  multiple sclerosis , and  autism . [ 1 ] [ 4 ]  There is little evidence to support this hypothesis. [ 1 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2684", "text": "Stephen Barrett  has described \"leaky gut syndrome\" as a  fad  diagnosis and says that its proponents use the alleged condition as an opportunity to sell a number of alternative-health remedies \u2013 including diets, herbal preparations, and dietary supplements. [ 5 ]  Promoters of  pseudoscience  have claimed that the passage of proteins through a \"leaky\" gut is the cause of autism. [ 7 ]  Evidence for claims that a leaky gut causes autism is weak and conflicting. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2685", "text": "Advocates tout various treatments for \"leaky gut syndrome\", such as  dietary supplements ,  probiotics , herbal remedies,  gluten -free foods, and low- FODMAP , low-sugar, and/or antifungal diets, but there is little evidence that the treatments offered are of benefit. [ 1 ] \nNone have been adequately tested to determine whether they are safe and effective for this purpose. [ 4 ]  The U.K.  National Institute for Health and Care Excellence  (NICE) does not recommend the use of any special diets to manage the main symptoms of autism or leaky gut syndrome. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2686", "text": "The  Lichtiger Colitis Activity Index  is a tool used in clinical research to measure quantify the impact of symptoms of  ulcerative colitis . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2687", "text": "The  Lille Model  is a medical modeling tool for predicting mortality in patients with  alcoholic hepatitis  who are not responding to steroid therapy. The model risk stratifies patients who have been receiving steroid treatment for seven days to predict who will improve and who should be considered for alternative treatment options including early referral for transplant. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2688", "text": "The model is based on:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2689", "text": "Initial model was based on a study of 238 patients and published in the Journal of Hepatology in 2003. [ 1 ]   Recent cohort studies demonstrate that those with a Lille score above 0.45 are likely non-responders to steroid therapy. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2690", "text": "Lipoprotein-X  ( Lp-X ) is an abnormal  low density lipoprotein  found in  cholestasis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2691", "text": "Lipoprotein-X is a lamellar particle of 30 to 70\u00a0nm in diameter as revealed by  electron microscopy . It is characterized by its high content of  phospholipids  (66% by weight) and unesterified  cholesterol  (22%), and its low content of  protein  (6%), cholesterol esters (3%), and  triglycerides  (3%). The protein component is dominated by  albumin , located in the core, and by  apolipoprotein  C, located on the surface of the particle. Using zonal ultracentrifugation, lipoprotein-X can be divided into three distinct populations: Lp-X1, Lp-X2, and Lp-X3, differing in density and apolipoprotein composition."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2692", "text": "The pathogenesis of lipoprotein-X in cholestasis is not totally resolved. Normally, the  liver  excretes lipoprotein complexes into the bile showing phospholipid and unesterified cholesterol concentrations similar to Lipoprotein-X. The in vitro incubation of these  bile  lipoproteins with serum or albumin leads to the appearance of Lp-X\u2013like particles. These findings suggest that the reflux of  bile  into the plasma compartment causes the formation of lipoprotein-X in  cholestasis  as a result of a physicochemical, nonmetabolic process. On the other hand, lipoprotein-X particles found in familial LCAT deficiency are identical to those in cholestasis regarding ultrastructure and biochemical composition. It has been supposed that reduced LCAT activities, common in patients with hepatocellular disease, cause, alone or in combination with other factors, the formation of Lipoprotein-X in cholestasis. Lipoprotein-X is mainly removed by the reticuloendothelial system of the liver and the  spleen , as shown by studies using radioactively labeled lipoprotein-X in rats. Other organs, such as the  kidney , also actively clear Lipoprotein-X from the plasma."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2693", "text": "Liver function tests  ( LFTs  or  LFs ), also referred to as a hepatic panel or liver panel, are groups of blood tests that provide information about the state of a patient's  liver . [ 1 ]  These tests include  prothrombin time  (PT/INR),  activated partial thromboplastin time  (aPTT),  albumin ,  bilirubin  (direct and indirect), and others. The liver transaminases  aspartate transaminase (AST or SGOT)  and  alanine transaminase (ALT or SGPT)  are useful biomarkers of liver injury in a patient with some degree of intact liver function. [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2694", "text": "Most  liver diseases  cause only mild symptoms initially, but these diseases must be detected early. Hepatic (liver) involvement in some diseases can be of crucial importance.  This testing is performed on a patient's blood sample. Some tests are associated with functionality (e.g., albumin), some with cellular integrity (e.g.,  transaminase ), and some with conditions linked to the biliary tract ( gamma-glutamyl transferase  and  alkaline phosphatase ). Because some of these tests do not measure function, it is more accurate to call these liver chemistries or liver tests rather than liver function tests. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2695", "text": "Several biochemical tests are useful in the evaluation and management of patients with hepatic dysfunction. These tests can be used to detect the presence of liver disease. They can help distinguish among different types of liver disorders, gauge the extent of known liver damage, and monitor the response to treatment. Some or all of these measurements are also carried out (usually about twice a year for routine cases) on individuals taking certain medications, such as anticonvulsants, to ensure that these medications are not adversely impacting the person's liver. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2696", "text": "Standard liver tests for assessing liver damage include alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP). Bilirubin may be used to estimate the excretory function of the liver and coagulation tests and albumin can be used to evaluate the metabolic activity of the liver. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2697", "text": "Although example reference ranges are given, these will vary depending on method of analysis used at the administering laboratory, as well as age, gender, ethnicity, and potentially unrelated health factors. Individual results should always be interpreted using the reference range provided by the laboratory that performed the test. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2698", "text": "Measurement of total  bilirubin  includes both unconjugated (indirect) and conjugated (direct) bilirubin. Unconjugated bilirubin is a breakdown product of  heme  (a part of  hemoglobin  in red blood cells). The liver is responsible for clearing the blood of unconjugated bilirubin, by 'conjugating' it (modified to make it water-soluble) through an enzyme named  UDP-glucuronyl-transferase . When the total bilirubin level exceeds 17 \u03bcmol/L, it indicates liver disease. When total bilirubin levels exceed 40 \u03bcmol/L, bilirubin deposition at the sclera, skin, and mucous membranes will give these areas a yellow colour, thus it is called  jaundice . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2699", "text": "The increase in predominantly unconjugated bilirubin is due to overproduction, reduced hepatic uptake of the unconjugated bilirubin and reduced conjugation of bilirubin. Overproduction can be due to the reabsorption of a  haematoma  and ineffective  erythropoiesis  leading to increased red blood cell destruction.  Gilbert's syndrome  and  Crigler\u2013Najjar syndrome  have defects in the  UDP-glucuronyl-transferase  enzyme, affecting bilirubin conjugation. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2700", "text": "The degree of rise in conjugated bilirubin is directly proportional to the degree of hepatocyte injury. Viral  hepatitis  can also cause the rise in conjugated bilirubin. In parenchymal liver disease and incomplete extrahepatic obstruction, the rise in conjugated bilirubin is less than the complete  common bile duct  obstruction due to malignant causes. In  Dubin\u2013Johnson syndrome , a mutation in  multiple drug-resistance protein 2 (MRP2)  causes a rise in conjugated bilirubin. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2701", "text": "In  acute appendicitis , total bilirubin can rise from 20.52 \u03bcmol/L to 143 \u03bcmol/L. In pregnant women, the total bilirubin level is low in all three trimesters. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2702", "text": "The measurement of bilirubin levels in the newborns is done through the use of bilimeter or transcutanoeus bilirubinometer instead of performing LFTs. When the total serum bilirubin increases over 95th percentile for age during the first week of life for high risk babies, it is known as hyperbilirubinemia of the newborn ( neonatal jaundice ) and requires  light therapy  to reduce the amount of bilirubin in the blood. Pathological jaundice in newborns should be suspected when the serum bilirubin level rises by more than 5\u00a0mg/dL per day, serum bilirubin more than the physiological range, clinical jaundice more than 2 weeks, and conjugated bilirubin (dark urine staining clothes).  Haemolytic jaundice  is the commonest cause of pathological jaundice. Those babies with Rh hemolytic disease, ABO incompatibility with the mother,  Glucose-6-phosphate dehydrogenase  (G-6-PD) deficiency and minor blood group incompatibility are at increased risk of getting haemolytic jaundice. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2703", "text": "Apart from being found in high concentrations in the liver, ALT is found in the kidneys, heart, and muscles. It catalyses the  transamination  reaction, and only exists in a cytoplasmic form. Any kind of liver injury can cause a rise in ALT. A rise of up to 300 IU/L is not specific to the liver, but can be due to the damage of other organs such as the kidneys or muscles. When ALT rises to more than 500 IU/L, causes are usually from the liver. It can be due to hepatitis, ischemic liver injury, and toxins that causes liver damage. The ALT levels in  hepatitis C  rises more than in hepatitis A and B. Persistent ALT elevation more than 6 months is known as  chronic hepatitis .  Alcoholic liver disease ,  non-alcoholic fatty liver disease  (NAFLD), fat accumulation in liver during childhood obesity,  steatohepatitis  (inflammation of fatty liver disease) are associated with a rise in ALT. Rise in ALT is also associated with reduced insulin response, reduced glucose tolerance, and increased free  fatty acids  and  triglycerides . Bright liver syndrome (bright liver on ultrasound suggestive of fatty liver) with raised ALT is suggestive of  metabolic syndrome . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2704", "text": "In pregnancy, ALT levels would rise during the second trimester. In one of the studies, measured ALT levels in pregnancy-related conditions such as  hyperemesis gravidarum  was 103.5 IU/L,  pre-eclampsia  was 115,  HELLP syndrome  was 149. ALT levels would reduce by greater than 50% in three days after child delivery. Another study also shows that  caffeine  consumption can reduce the risk of ALT elevation in those who consume alcohol, overweight people, impaired glucose metabolism, and viral hepatitis. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2705", "text": "AST exists in two  isoenzymes  namely mitochondrial form and cytoplasmic form. It is found in highest concentration in the liver, followed by heart, muscle, kidney, brain, pancreas, and lungs. [ 10 ]  This wide range of AST containing organs makes it a relatively less specific indicator of liver damage compared to ALT. An increase of mitochondrial AST in bloods is highly suggestive of tissue  necrosis  in  myocardial infarction  and chronic liver disease. More than 80% of the liver AST activity are contributed by mitochondrial form of the isoenzymes, while the circulating AST in blood are contributed by cytoplasmic form of AST. AST is especially markedly raised in those with  liver cirrhosis . [ 6 ]  AST can be released from a variety of other tissues and if the elevation is less than two times the normal AST, no further workup needs to be performed if a patient is proceeding to surgery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2706", "text": "In certain pregnancy related conditions such as hyperemesis gravidarum, AST can reach as high as 73 IU/L, 66 IU/L in pre-eclampsia, and 81 IU/L in HELLP syndrome. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2707", "text": "The AST/ALT ratio increases in liver functional impairment. In alcoholic liver disease, the mean ratio is 1.45, and mean ratio is 1.33 in post necrotic liver cirrhosis. Ratio is greater than 1.17 in viral cirrhosis, greater than 2.0 in alcoholic hepatitis, and 0.9 in non-alcoholic hepatitis. Ratio is greater than 4.5 in  Wilson disease  or  hyperthyroidism . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2708", "text": "Alkaline phosphatase  (ALP) is an enzyme in the cells lining the  biliary ducts  of the liver.  It can also be found on the mucosal epithelium of the small intestine,  proximal convoluted tubule  of the kidneys, bone, liver, and placenta. It plays an important role in lipid transposition in small intestines and calcification of bones. 50% of all the serum ALP activities in blood are contributed by bone. Acute viral hepatitis usually has normal or increased ALP. For example, hepatitis A has increased ALP due to  cholestasis  (impaired bile formation or bile flow obstruction) and would have the feature of prolonged itching. Other causes include: infiltrative liver diseases, granulomatous liver disease, abscess,  amyloidosis  of the liver and  peripheral arterial disease . Mild elevation of ALP can be seen in liver cirrhosis, hepatitis, and  congestive cardiac failure . Transient  hyperphosphataemia  is a benign condition in  infants , and can reach normal level in 4 months. In contrast, low levels of ALP is found in  hypothyroidism ,  pernicious anemia ,  zinc deficiency , and  hypophosphatasia . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2709", "text": "ALP activity is significantly increased in the third trimester of  pregnancy . [ 11 ]  This is due to increased synthesis from the  placenta  as well as increased synthesis in the  liver  induced by large amounts of estrogens. [ 11 ] [ 12 ] [ 13 ]  Levels in the third trimester can be as much as 2-fold greater than in non-pregnant women. [ 11 ]  As a result, ALP is not a reliable marker of hepatic function in pregnant women. [ 11 ]  In contrast to ALP, levels of ALT, AST, GGT, and  lactate dehydrogenase  are only slightly changed or largely unchanged during pregnancy. [ 11 ]   Bilirubin  levels are significantly decreased in pregnancy. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2710", "text": "In pregnancy conditions such as hyperemesis gravdirum, ALP levels can reach 215 IU/L, meanwhile, in pre-eclampsia, ALP can reach 14 IU/L, and in HELLP syndrome ALP levels can reach 15 IU/L. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2711", "text": "GGT is a microsomal enzyme found in hepatocytes, biliary epithelial cells, renal tubules, pancreas, and intestines. It helps in  glutathione  metabolism by transporting peptides across the cell membrane. Much like ALP, GGT measurements are usually elevated if cholestasis is present. [ 10 ]  In acute viral hepatitis, the GGT levels can peak at 2nd and 3rd week of illness, and remained elevated at 6 weeks of illness. GGT is also elevated in 30% of the hepatitis C patients. GGT can increase by 10 times in alcoholism. GGT can increase by 2 to 3 times in 50% of the patients with non-alcoholic liver disease. When GGT levels is elevated, the  triglyceride  level is elevated also. With insulin treatment, the GGT level can reduce. Other causes of elevated GGT are: diabetes mellitus,  acute pancreatitis , myocardial infarction,  anorexia nervosa ,  Guillain\u2013Barr\u00e9 syndrome , hyperthyroidism, obesity and  myotonic dystrophy . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2712", "text": "In pregnancy conditions GGT activity is reduced in 2nd and 3rd trimesters. In hyperemesis gravidarum, GGT level value can reach 45 IU/L, 17 IU/L in pre-eclampsia, and 35 IU/L in HELPP syndrome. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2713", "text": "Albumin  is a protein made specifically by the liver, and can be measured cheaply and easily. It is the main constituent of total protein (the remaining constituents are primarily  globulins ). Albumin levels are decreased in chronic liver disease, such as  cirrhosis . It is also decreased in  nephrotic syndrome , where it is lost through the urine.  The consequence of low albumin can be edema since the intravascular  oncotic pressure  becomes lower than the extravascular space. An alternative to albumin measurement is prealbumin, which is better at detecting acute changes (half-life of albumin and prealbumin is about 2 weeks and about 2 days, respectively). [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2714", "text": "Other tests are requested alongside LFT to rule out specific causes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2715", "text": "5'  Nucleotidase  (5NT) is a  glycoprotein  found throughout the body, in the cytoplasmic membrane, catalyzing the conversion to inorganic phosphates from nucleoside-5-phosphate. Its level is raised in conditions such as obstructive jaundice, parenchymal liver disease, liver metastases, and bone disease. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2716", "text": "Serum NT levels are higher during 2nd and 3rd trimesters in pregnancy. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2717", "text": "Ceruloplasmin is an  acute phase protein  synthesized in the liver. It is the carrier of the copper ion. Its level is increased in infections,  rheumatoid arthritis , pregnancy, non-Wilson liver disease and obstructive jaundice. In Wilson disease, the ceruloplasmin level is depressed which lead to copper accumulation in body tissues. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2718", "text": "Alpha-fetoprotein (AFP) is significantly expressed in foetal liver. However, the mechanism that led to the suppression of AFP synthesis in adults is not fully known. Exposure of the liver to cancer-causing agents and arrest of liver maturation in childhood can lead to the rise in AFP. AFP can reach until 400\u2013500 \u03bcg/L in  hepatocellular carcinoma . AFP concentration of more than 400 \u03bcg/L is associated with greater tumour size, involvement of both lobes of liver, portal vein invasion and a lower median survival rate. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2719", "text": "The liver is responsible for the production of the vast majority of  coagulation  factors. In patients with liver disease,  international normalized ratio  (INR) can be used as a marker of liver synthetic function as it includes  factor VII , which has the shortest half life (2\u20136 hours) of all coagulation factors measured in INR. An elevated INR in patients with liver disease, however, does not necessarily mean the patient has a tendency to bleed, as it only measures procoagulants and not anticoagulants. In liver disease the synthesis of both are decreased and some patients are even found to be hypercoagulable (increased tendency to clot) despite an elevated INR. In liver patients, coagulation is better determined by more modern tests such as  thromboelastogram  (TEG) or thomboelastrometry (ROTEM). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2720", "text": "Prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and INR are measures of the  extrinsic pathway  of  coagulation . This test is also called \"ProTime INR\" and \"INR PT\". They are used to determine the clotting tendency of blood, in the measure of  warfarin  dosage, liver damage, and  vitamin K  status. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2721", "text": "The serum glucose test, abbreviated as \"BG\" or \"Glu\", measures the liver's ability to produce glucose ( gluconeogenesis ); it is usually the last function to be lost in the setting of  fulminant liver failure . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2722", "text": "Lactate dehydrogenase  (LDH) is found in many body tissues, including the liver. Elevated levels of LDH may indicate liver damage. [ 18 ]  LDH isotype-1 (or cardiac) is used for estimating damage to cardiac tissue, although troponin and creatine kinase tests are preferred. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2723", "text": "A  low-FODMAP diet  is a person's global restriction of consumption of all  fermentable   carbohydrates  ( FODMAPs ), [ 1 ]  recommended only for a short time. A low-FODMAP diet is recommended for managing patients with  irritable bowel syndrome  (IBS) and can reduce digestive symptoms of IBS including  bloating  and  flatulence . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2724", "text": "If the problem lies with indigestible  fiber  instead, the patient may be directed to a  low-residue diet ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2725", "text": "A low-FODMAP diet might help to improve short-term digestive symptoms in adults with functional abdominal  bloating [ 3 ]  and  irritable bowel syndrome , [ 4 ] [ 5 ] [ 6 ] [ 7 ]  but its long-term use can have negative effects because it causes a detrimental impact on the  gut microbiota  and  metabolome . [ 8 ] [ 5 ] [ 7 ] [ 9 ]  It should only be used for short periods of time and under the advice of a specialist. [ 10 ]  More studies are needed to evaluate its effectiveness in children with irritable bowel syndrome. [ 4 ] \nThere is only a little evidence of its effectiveness in treating functional symptoms in  inflammatory bowel disease  from small studies that are susceptible to bias. [ 11 ] [ 12 ]  More studies are needed to assess the true impact of this diet on health. [ 5 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2726", "text": "In addition, the use of a low-FODMAP diet without medical advice can lead to serious health risks, including nutritional deficiencies and misdiagnosis, so it is advisable to conduct a complete medical evaluation before starting a low-FODMAP diet to ensure a correct diagnosis and that the appropriate therapy may be undertaken. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2727", "text": "Since the consumption of  gluten  is suppressed or reduced with a low-FODMAP diet, the improvement of the digestive symptoms with this diet may not be related to the withdrawal of the FODMAPs, but of gluten, indicating the presence of an unrecognized  celiac disease , avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2728", "text": "A low-FODMAP diet is highly restrictive in various groups of nutrients, can be impractical to follow in the long-term and may add an unnecessary financial burden. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2729", "text": "Below are low-FODMAP foods categorized by group according to the  Monash University  \"Low-FODMAP Diet\". [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2730", "text": "Other sources confirm the suitability of these and suggest some additional foods. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2731", "text": "The basis of many  functional gastrointestinal disorders  (FGIDs) is distension of the  intestinal lumen . Such luminal distension may induce pain, a sensation of  bloating ,  abdominal distension  and  motility  disorders. Therapeutic approaches seek to reduce factors that lead to distension, particularly of the distal  small  and proximal  large intestine . Food substances that can induce distension are those that are poorly absorbed in the proximal small intestine,  osmotically  active, and fermented by intestinal bacteria with  hydrogen  (as opposed to  methane ) production. The small molecule FODMAPs exhibit these characteristics. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2732", "text": "Over many years, there have been multiple observations that ingestion of certain short-chain carbohydrates, including lactose, fructose and sorbitol, fructans and  galactooligosaccharides , can induce gastrointestinal discomfort similar to that of people with irritable bowel syndrome. These studies also showed that dietary restriction of short-chain carbohydrates was associated with symptoms improvement. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2733", "text": "These short-chain carbohydrates (lactose, fructose and sorbitol, fructans and GOS) behave similarly in the intestine. Firstly, being small molecules and either poorly absorbed or not absorbed at all, they drag water into the intestine via osmosis. [ 19 ]  Secondly, these molecules are readily fermented by colonic bacteria, so upon malabsorption in the small intestine they enter the large intestine where they generate gases (hydrogen, carbon dioxide and methane). [ 1 ]  The dual actions of these carbohydrates cause an expansion in volume of intestinal contents, which stretches the intestinal wall and stimulates nerves in the gut.  It is this 'stretching' that triggers the sensations of pain and discomfort that are commonly experienced by people with IBS. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2734", "text": "The FODMAP concept was first published in 2005 as part of a hypothesis paper. [ 20 ]  In this paper, it was proposed that a collective reduction in the dietary intake of all indigestible or slowly absorbed, short-chain carbohydrates would minimise stretching of the intestinal wall. This was proposed to reduce stimulation of the gut's nervous system and provide the best chance of reducing symptom generation in people with IBS (see below). At the time, there was no collective term for indigestible or slowly absorbed, short-chain carbohydrates, so the term 'FODMAP' was created to improve understanding and facilitate communication of the concept. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2735", "text": "The low FODMAP diet was originally developed by a research team at  Monash University  in Melbourne, Australia. [ 15 ]  The Monash team undertook the first research to investigate whether a low FODMAP diet improved symptom control in patients with IBS and established the mechanism by which the diet exerted its effect. [ 8 ] [ 21 ]  Monash University also established a rigorous food analysis program to measure the FODMAP content of a wide selection of Australian and international foods. [ 22 ] [ 23 ] [ 24 ]  The FODMAP composition data generated by Monash University updated previous data that was based on limited literature, with guesses (sometimes wrong) made where there was little information. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2736", "text": "The  Manning criteria  are a  diagnostic algorithm  used in the diagnosis of  irritable bowel syndrome  (IBS).  The criteria consist of a list of questions the physician can ask the patient. [ 1 ]  The answers are used in a process to produce a diagnostic decision regarding whether the patient can be considered to have IBS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2737", "text": "The Manning criteria have been compared with other diagnostic algorithms for IBS, such as the  Rome I criteria , the  Rome II process , and the Kruis criteria. [ 2 ]   A 2013 validation study found the Manning criteria to have less sensitivity but more specificity than the Rome criteria. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2738", "text": "The threshold for a positive diagnosis varies from two to four of the Manning criteria below. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2739", "text": "Mesalazine , also known as  mesalamine  or  5-aminosalicylic acid  ( 5-ASA ), is a medication used to treat  inflammatory bowel disease , including  ulcerative colitis  and  Crohn's disease . [ 1 ]  It is generally used for mildly to moderately severe disease. [ 1 ]  It is taken by mouth or  rectally . [ 1 ]  The formulations which are taken by mouth appear to be similarly-effective. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2740", "text": "Common side-effects include headache, nausea, abdominal pain, and fever. [ 1 ]  Serious side-effects may include  pericarditis ,  liver problems , and  kidney problems . [ 1 ] [ 12 ]  Use in  pregnancy  and  breastfeeding  appears safe. [ 12 ]  In people with a  sulfa allergy  certain formulations may result in problems. [ 1 ]  Mesalazine is an  aminosalicylate  and  anti-inflammatory . [ 1 ] [ 12 ]  It works by direct contact with the  intestines . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2741", "text": "Mesalazine was approved for medical use in the United States in 1987. [ 1 ] [ 8 ]  It is on the  World Health Organization's List of Essential Medicines . [ 13 ]  It is available as a  generic medication . [ 1 ] [ 14 ] [ 15 ] [ 16 ]  In 2021, it was the 239th most commonly prescribed medication in the United States, with more than 1 \u00a0 million prescriptions. [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2742", "text": "It is used to treat  inflammatory bowel disease , including  ulcerative colitis  and  Crohn's disease  (effective only in colonic diseases). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2743", "text": "In 2022 Germany introduced guidance to use mesalamine to treat acute uncomplicated  diverticulitis . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2744", "text": "Most often reported side-effects are gastrointestinal (GI) (but may also include headache), including: nausea, diarrhea, and abdominal pain. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2745", "text": "Very rarely, use of mesalazine has been associated with an exacerbation of the symptoms of  colitis ,  Stevens Johnson syndrome , and  erythema multiforme . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2746", "text": "There is no data on use in pregnant women, but the drug does cross the placenta and is excreted in  breast milk . The drug should not be used in children under two years of age, [ 7 ]  people with  kidney disease , [ 7 ]  or people who are allergic to  aspirin . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2747", "text": "Mesalazine is the active  moiety  of  sulfasalazine , which is metabolized to  sulfapyridine  and mesalazine. [ 20 ]  It is also the active component of the prodrug  balsalazide  along with the inert carrier molecule 4-aminobenzoyl-beta-alanine. [ 21 ]  It is in the category of  disease-modifying antirheumatic drugs  (DMARDs) family of medications. [ 22 ]  It is unclear exactly how it works. [ 22 ]  Mesalazine is claimed to be a  PPAR-\u03b3 agonist . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2748", "text": "Exact mechanism of mesalazine is unknown, but is speculated that mesalazine decreases synthesis of  prostaglandin  and  leukotriene , modulating the inflammatory response derived from the  cyclooxygenase  and  lipooxygenase  pathways. [ 24 ]  It appears to act locally on colonic mucosa. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2749", "text": "Mesalazine is sold under various names including Apriso, Asacol, Asacol HD, Canasa, Delzicol, Fivasa, Lialda, Salofalk, Pentasa, Rowasa, Octasa, and Sfrowasa. In Europe, it is sold under the name Salofalk (rectal suppository).  [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2750", "text": "Misoprostol  is a synthetic  prostaglandin  medication used to prevent and treat  stomach and duodenal ulcers ,  induce labor , cause an  abortion , and treat  postpartum bleeding  due to poor contraction of the  uterus . [ 10 ] [ 11 ]  It is taken  by mouth  when used to prevent gastric ulcers in people taking  nonsteroidal anti-inflammatory drugs  (NSAID). [ 11 ]  For abortions it is used by itself or in conjunction with  mifepristone  or  methotrexate . [ 12 ]  By itself, effectiveness for abortion is between 66% and 90%. [ 13 ] [ 14 ]  For labor induction or abortion, it is taken by mouth, dissolved in the mouth, or  placed in the vagina . [ 12 ] [ 15 ] [ 16 ] [ 17 ] [ 18 ]  For postpartum bleeding it may also be  used rectally . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2751", "text": "Common side effects include  diarrhea  and abdominal pain. [ 11 ]  It is in  pregnancy category  X, meaning that it is known to result in negative outcomes for the fetus if taken during  pregnancy . [ 11 ]  In rare cases,  uterine rupture  may occur. [ 11 ]  It is a  prostaglandin analogue \u2014specifically, a synthetic  prostaglandin E 1  (PGE 1 ). [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2752", "text": "Misoprostol was developed in 1973. [ 20 ]  It is on the  World Health Organization's List of Essential Medicines . [ 21 ]  It is available as a  generic medication . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2753", "text": "Misoprostol is used for the prevention of  NSAID -induced gastric ulcers. It acts upon gastric  parietal cells , inhibiting the secretion of  gastric acid  by  G-protein coupled receptor -mediated inhibition of  adenylate cyclase , which leads to decreased intracellular  cyclic AMP  levels and decreased  proton pump  activity at the  apical  surface of the parietal cell. Misoprostol is sometimes coprescribed with NSAIDs to prevent their common adverse effect of  gastric ulceration  (e.g., with  diclofenac  in  Arthrotec ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2754", "text": "However, even in the treatment of NSAID-induced ulcers,  omeprazole  proved to be at least as effective as misoprostol, [ 22 ]  but was significantly better tolerated, so misoprostol should not be considered a first-line treatment. Misoprostol-induced diarrhea and the need for multiple daily doses (typically four) are the main issues impairing compliance with therapy. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2755", "text": "Misoprostol is commonly used for  labor induction . It causes  uterine  contractions and the ripening ( effacement  or thinning) of the  cervix . [ 23 ]  It can be less expensive than the other commonly used ripening agent,  dinoprostone . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2756", "text": "Oxytocin  has long been used as the standard agent for labor induction, but does not work well when the cervix is not yet ripe. Misoprostol also may be used in conjunction with oxytocin. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2757", "text": "Between 2002 and 2012, a misoprostol vaginal insert was studied, and was approved in the EU. [ 25 ] [ 26 ] [ 27 ]  It was not approved for use in the United States, and the US FDA still considers cervical ripening and labor induction to be outside of the approved uses for misoprostol. [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2758", "text": "When administered prior to  myomectomy  in women with uterine fibroids, misoprostol reduces operative blood loss and requirement of blood transfusion. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2759", "text": "Misoprostol is used either alone or in conjunction with another medication ( mifepristone  or  methotrexate ) for  medical abortions  as an alternative to  surgical abortion . [ 31 ]  Medical abortion has the advantage of being less invasive, and more autonomous, self-directed, and discreet. It is preferred by some women because it feels more natural, as the drugs induce a miscarriage. [ 32 ]  It is also more easily accessible in places where abortion is illegal. [ 33 ]  The  World Health Organization  (WHO) provides clear guidelines on the use, benefits and risks of misoprostol for abortions. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2760", "text": "Misoprostol is most effective when it is used in combination with methotrexate or mifepristone (RU-486). [ 35 ]  Mifepristone blocks signaling by  progesterone , causing the uterine lining to degrade, the blood vessels of the  cervix  and  uterus  to dilate and causing uterine contraction, similar to a  menstrual period , which causes the embryo to detach from the uterine walls. [ 36 ]  Misoprostol then dilates the cervix and induces muscle contractions which clear the uterus. [ citation needed ]  Misoprostol alone is less effective (typically 88% up to eight-weeks gestation). It is not inherently unsafe if medically supervised, but 1% of women will have heavy bleeding requiring medical attention, some women may have  ectopic pregnancy , and the 12% of pregnancies that continue after misoprostol failure are more likely to have birth defects and are usually followed up with a more effective method of abortion. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2761", "text": "Most large studies recommend a protocol for the use of misoprostol in combination with mifepristone. [ 38 ] [ 39 ]  Together they are effective in around 95% for early pregnancies. [ 40 ]  Misoprostol alone may be more effective in earlier gestation. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2762", "text": "Misoprostol can also be used to  dilate the cervix  in preparation for a surgical abortion, particularly in the second trimester (either alone or in combination with  osmotic dilators ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2763", "text": "Misoprostol by mouth is the least effective treatment for producing complete abortion in a period of 24 hours due to the liver's  first-pass effect  which reduces the  bioavailability  of the misoprostol. Vaginal and sublingual routes result in greater efficacy and extended duration of action because these routes of administration allow the drug to be directly absorbed into circulation by bypassing the liver first-pass effect. [ 42 ] [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2764", "text": "Hematocrit  or Hb tests and Rh testing are recommended before use for abortion confirmation of pregnancy. [ 43 ]  Following use, it is recommended that people attend a follow-up visit 2 weeks after treatment. If used for treatment of complete abortion, a pregnancy test, physical examination of the uterus, and ultrasound should be performed to ensure success of treatment. Surgical management is possible in the case of failed treatment. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2765", "text": "Misoprostol may be used to complete a  miscarriage  or  missed abortion  when the body does not expel the embryo or fetus on its own. Compared to no medication or placebo, it could decrease the time to complete expulsion. [ 44 ]  Use of a single dose of misoprostol vaginally or buccally is preferred, with additional doses as needed. It also can be used in combination with mifepristone, with a similar regimen to medical abortion. [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2766", "text": "Misoprostol is regularly used in some Canadian hospitals for labour induction for fetal deaths early in pregnancy, and for termination of pregnancy for fetal anomalies. A low dose is used initially, then doubled for the remaining doses until delivery. In the case of a previous Caesarian section, however, lower doses are used."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2767", "text": "Misoprostol is also used to prevent and treat  post-partum bleeding . Orally administered misoprostol was marginally less effective than  oxytocin . [ 45 ]  The use of rectally administered misoprostol is optimal in cases of bleeding; it was shown to be associated with lower rates of side effects compared to other routes. Rectally administered misoprostol was reported in a variety of case reports and randomised controlled trials. [ 46 ] [ 47 ]  However, it is inexpensive and thermostable (thus does not require refrigeration like oxytocin), making it a cost-effective and valuable drug to use in the developing world. [ 48 ]  A randomised control trial of misoprostol use found a 38% reduction in maternal deaths due to  post partum  haemorrhage in resource-poor communities. [ 49 ]  Misoprostol is recommended due to its cost, effectiveness, stability, and low rate of side effects. [ 50 ]  Oxytocin must also be given by injection, while misprostol can be given orally or rectally for this use, making it much more useful in areas where nurses and physicians are less available. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2768", "text": "In women with prior caesarean section or prior failure of insertion of an intrauterine contraceptive device, pre-procedure administration of misoprostol reduces the rate of failure of insertion of intrauterine contraceptive device. However, due to a higher rate of adverse effects, routine use of misoprostol for this purpose in other women is not supported by the data. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2769", "text": "For  cervical ripening  in advance of endometrial biopsy to reduce the need for use of a tenaculum or cervical dilator. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2770", "text": "There is limited evidence supporting the use of misoprostol for the treatment of  trigeminal neuralgia  in patients with  multiple sclerosis . [ 53 ] [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2771", "text": "The most commonly reported  adverse effect  of taking misoprostol by mouth for the prevention of stomach ulcers is  diarrhea . In clinical trials, an average 13% of people reported diarrhea, which was dose-related and usually developed early in the course of therapy (after 13 days) and was usually self-limiting (often resolving within 8 days), but sometimes (in 2% of people) required discontinuation of misoprostol. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2772", "text": "The next most commonly reported adverse effects of taking misoprostol by mouth for the prevention of gastric ulcers are:  abdominal pain ,  nausea ,  flatulence ,  headache ,  dyspepsia ,  vomiting , and  constipation , but none of these adverse effects occurred more often than when taking  placebos . [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2773", "text": "There are increased side effects with sublingual or oral misoprostol, compared to a low dose (400\u00a0\u03bcg) vaginal misoprostol. However, low dose vaginal misoprostol was linked with low complete abortion rate. [ 42 ]  The study concluded that sublingually administered misoprostol dosed at 600\u00a0\u03bcg or 400\u00a0\u03bcg had greater instances of fever and diarrhea due to its quicker onset of action, higher peak concentration and bioavailability in comparison to vaginal or oral misoprostol. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2774", "text": "For the indication of medical abortion, bleeding and cramping is commonly experienced after administration of misoprostol. Bleeding and cramping is likely to be greater than that experienced with menses, however, emergency care is advised if bleeding is excessive. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2775", "text": "Misoprostol should not be taken by pregnant women with wanted pregnancies to reduce the risk of NSAID-induced gastric ulcers because it increases uterine tone and contractions in pregnancy, which may cause partial or complete abortions, and because its use in pregnancy has been associated with birth defects. [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2776", "text": "All cervical ripening and induction agents can cause  uterine hyperstimulation , which can negatively affect the blood supply to the fetus and increases the risk of complications such as uterine rupture. [ 57 ]  Concern has been raised that uterine hyperstimulation that occurs during a misoprostol-induced labor is more difficult to treat than hyperstimulation during labors induced by other drugs. [ 58 ]  Because the complications are rare, it is difficult to determine if misoprostol causes a higher risk than do other cervical ripening agents. One estimate is that it would require around 61,000 people enrolled in randomized controlled trials to detect a difference in serious fetal complications and about 155,000 people to detect a difference in serious maternal complications. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2777", "text": "It is recommended that medical treatment for  missed abortion  with misoprostol should only be considered in people without the following contraindications: suspected ectopic pregnancy, use of non-steroidal drugs, signs of pelvic infections or sepsis, unstable hemodynamics, known allergy to misoprostol, previous caesarean section, mitral stenosis, hypertension, glaucoma, bronchial asthma, and remote areas without a hospital nearby. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2778", "text": "Misoprostol, a  prostaglandin analogue , binds to myometrial cells to cause strong myometrial contractions leading to expulsion of tissue. This agent also causes cervical ripening with softening and dilation of the cervix. Misoprostol binds to and stimulates  prostaglandin EP 2  receptors ,  prostaglandin EP 3  receptor  and  prostaglandin EP 4  receptor  but not  prostaglandin EP 1  receptor  and therefore is expected to have a more restricted range of physiological and potentially toxic actions than prostaglandin E 2  or other analogs which activate all four prostaglandin receptors. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2779", "text": "In August 2000, a letter from  G.D. Searle, LLC , the inventor of the drug, [ 61 ] [ 62 ]  generated controversy by warning against its use by pregnant women because of its ability to induce abortion, citing reports of maternal and fetal deaths when it was used to induce labor. [ 63 ]  The  American College of Obstetricians and Gynecologists  holds that substantial evidence supports the use of misoprostol for induction of labor, a position it reaffirmed in response to the Searle letter. [ 64 ]  It is on the  World Health Organization's List of Essential Medicines . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2780", "text": "A vaginal form of the medication is sold in the EU under the names Misodel [ 65 ]  and Mysodelle [ 66 ]  for use in labor induction. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2781", "text": "Misoprostol is used for  self-induced abortions  in Brazil, where  black market  prices exceed US$100 per dose. Illegal medically unsupervised misoprostol abortions in Brazil are associated with a lower complication rate than other forms of illegal self-induced abortion, but are still associated with a higher complication rate than legal, medically supervised surgical and medical abortions. Failed misoprostol abortions are associated with birth defects in some cases. [ 67 ] [ 68 ] [ 69 ] [ 70 ] [ 71 ]  Low-income and immigrant populations in  New York City  have also been observed to use self-administered misoprostol to induce abortions, as this method is much cheaper than a surgical abortion (about $2 per dose). [ 72 ]  The drug is readily available in Mexico. [ 73 ]  Use of misoprostol has also increased in Texas in response to increased regulation of abortion providers. [ 74 ]  Following the United States Supreme Court decision of  Dobbs v. Jackson Women's Health Organization , many states restricted access to legal abortion services, including medication abortion using misoprostol. As a result of these restrictions, it was reported that there was an increase in self-managed abortions by women in the United States. Many women purchased the pills from overseas online pharmacies or obtained misoprostol from Mexico. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2782", "text": "Maddrey's discriminant function  (DF) is the traditional model for evaluating the severity and prognosis in alcoholic hepatitis and evaluates the efficacy of using alcoholic hepatitis steroid treatment.  The Maddrey DF score is a predictive statistical model compares the subject's DF score with mortality prognosis within 30-day or 90-day scores. [ clarification needed ]   The subject's Maddrey DF score is determined by blood analysis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2783", "text": "The  modified Maddrey's discriminant function  was originally described by Maddrey and Boitnott [ 1 ]  to predict  prognosis  in  alcoholic hepatitis .  It is calculated by a simple formula using  prothrombin time  and serum  bilirubin  concentration: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2784", "text": "( \n \n 4.6 \n \u00d7 \n \n ( \n \n \n \n prothrombin time \n \n \n \u2212 \n \n \n control time \n \n \n \n ) \n \n \n ) \n \n + \n \n \n serum bilirubin in mg/dl \n \n \n \n \n {\\displaystyle \\left(4.6\\times \\left({\\hbox{prothrombin time}}-{\\hbox{control time}}\\right)\\right)+{\\hbox{serum bilirubin in mg/dl}}} \n \n [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2785", "text": "Prospective studies  have shown that it is useful in predicting short term prognosis, especially mortality within 30 days. [ 3 ]   A value more than 32 implies poor outcome with one month mortality ranging between 35% and 45%. [ 4 ]   Corticosteroid therapy or pentoxifylline have been used with mixed results for patients whose increased mortality is indicated with a value greater than 32. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2786", "text": "To calculate Maddrey discriminant function using SI units, such as  micromoles  per litre, divide bilirubin value by 17."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2787", "text": "A  Murphy drip  is a  rectal infusion  apparatus to administer the medical procedure of  proctoclysis , also known as rectoclysis. [ 2 ] [ 3 ]  During the procedure, an end of the Murphy drip is inserted into the  rectum  and large quantities of liquid are infused into the rectum drop by drop. [ 4 ]  Prior to fluids or medicines being given  intravenously , the Murphy drip and  hypodermoclysis  were the prime routes to administer fluids such as for  replacement  when patients could not be fed by mouth. [ 5 ]  American surgeon  John Benjamin Murphy  introduced the drip method of  saline  infusion per rectum in the treatment of  peritonitis . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2788", "text": "The Murphy drip was invented by  Wisconsin  surgeon  John Benjamin Murphy , for the purpose of administering a proctoclysis for  hydration  and replenishment of  electrolytes , via a  sodium  and  calcium chloride  solution. This would be used when administration by mouth was not possible because of the condition of the patient. [ 7 ]  The Murphy drip was described in the April 1909 issue of the  Journal of the American Medical Association . [ 8 ]  By as early as July 1928, the Murphy drip was considered an auxiliary method of injection behind  intravenous therapy  and  subcutaneous injection , the two principal methods of  injection  at that time. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2789", "text": "The Murphy drip can be used for administering drugs by this route and the apparatus is also used in conjunction with a  catheter  for  bladder  irrigation.\nThe term can even be applied to apparatus used to administer fluids intravenously. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2790", "text": "A curious anecdote involving the Murphy drip is related by  Walter Lord  in his book on the  Battle of Midway . On 4 June 1942 Pharmacist's Mate Edwin Miller was stationed on Sand Island (part of the  Midway Atoll ) and was making ready for the expected Japanese attack. Miller prepared undrinkably strong coffee which, he claimed, was to be used in an \"old fashioned\" treatment for  shock  \u2013 administration of  strong coffee through the rectum  via a Murphy drip. When the attack got underway, Miller was joined by his commanding officer and doctor in charge, Lieutenant Commander A. E. Ady, who did not appear to know the medical purpose of the coffee and asked for some to be poured. Miller thought that it would be amusing to let his commander drink it, but made the mistake of also drinking some himself. Dr. Ady continued to tell jokes throughout the attack. Miller, however, paid for his practical joke and was sick. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2791", "text": "A description of a Murphy drip set-up is contained in the 1932  Kansas Supreme Court  legal case  Ratliffe v. Wesley Hospital and Nurses' Training School: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2792", "text": "On February 14, 1929, \"Dr. Horn directed the nurse to use the proctoclysis, known as the \u201cMurphy drip.\u201d While the operation was in progress a student nurse in the employ of the hospital prepared the room for the return of the appellant. The proctoclysis set was a part of the equipment of the hospital and was assembled and placed at or near the foot of the bed by the student nurse. The proctoclysis set consists of a standard which is an iron pole setting on a tripod containing hooks at intervals, and on these hooks by means of a chain, tape, string, or piece of gauze is hung a can containing hot water and soda solution. From this can a tube extends which is inserted in the rectum of the patient to whom the proctoclysis is administered. It was necessary to keep the solution hot in order that it would have a body temperature after dropping through the tube and entering the body. ... It was not unusual for the vessel holding the water to be fastened to the standard by gauze, string, or other bandage, although a part of the vessels were equipped with chains.\" [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2793", "text": "Olsalazine  is an anti-inflammatory medication used in the treatment of  ulcerative colitis . [ 2 ] [ 3 ]  It is sold under the brand name  Dipentum . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2794", "text": "Olsalazine itself is a pro-drug of  mesalazine  (5-aminosalicyclic acid or 5-ASA) and is not absorbed in the small intestine. Instead it continues through to the colon where it is cleaved into two molecules of 5-ASA by  azoreductases  produced by colonic bacteria. Olsalazine thus exerts its anti-inflammatory effect by its colonic breakdown into 5-ASA which inhibits cyclooxygenase and lipoxygenase thereby reducing prostaglandin and leukotriene production. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2795", "text": "Olsalazine gained  Food and Drug Administration  (FDA) approval in 1990."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2796", "text": "The drug is supplied by  UCB Pharma ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2797", "text": "In 2006 the Australian biotech company  Giaconda  received a European patent for a combination therapy for treating constipation-predominant  irritable bowel syndrome  that uses olsalazine and the anti- gout  drug  colchicine , for trials the following year. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2798", "text": "Oral rehydration therapy  ( ORT ) is a type of  fluid replacement  used to prevent and treat  dehydration , especially due to  diarrhea . [ 1 ]  It involves drinking water with modest amounts of sugar and salts, specifically  sodium  and  potassium . [ 1 ]  Oral rehydration therapy can also be given by a  nasogastric tube . [ 1 ]  Therapy can include the use of  zinc supplements  to reduce the duration of diarrhea in infants and children under the age of 5. [ 1 ]  Use of oral rehydration therapy has been estimated to decrease the risk of death from diarrhea by up to 93%. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2799", "text": "Side effects may include  vomiting ,  high blood sodium , or  high blood potassium . [ 1 ]  If vomiting occurs, it is recommended that use be paused for 10 minutes and then gradually restarted. [ 1 ]  The recommended formulation includes  sodium chloride ,  sodium citrate ,  potassium chloride , and  glucose . [ 1 ]  Glucose may be replaced by  sucrose  and sodium citrate may be replaced by  sodium bicarbonate , if not available, although the resulting mixture is not shelf stable in high-humidity environments. [ 1 ] [ 3 ]  It works as glucose increases the uptake of sodium and thus water by the  intestines , and the potassium chloride and sodium citrate help prevent  hypokalemia  and  acidosis , respectively, which are both common side effects of diarrhea. [ 4 ] [ 3 ] [ 5 ]  A number of other formulations are also available including versions that can be made at home. [ 4 ] [ 2 ]  However, the use of homemade solutions has not been well studied. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2800", "text": "Oral rehydration therapy was developed in the 1940s using electrolyte solutions with or without glucose on an empirical basis chiefly for mild or convalescent patients, but did not come into common use for rehydration and maintenance therapy until after the discovery that glucose promoted sodium and water absorption during cholera in the 1960s. [ 6 ]  It is on the  World Health Organization's List of Essential Medicines . [ 7 ]  Globally, as of 2015 [update] , oral rehydration therapy is used by 41% of children with diarrhea. [ 8 ]  This use has played an important role in reducing the  number of deaths in children under the age of five . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2801", "text": "ORT is less invasive than the other strategies for fluid replacement, specifically  intravenous  (IV) fluid replacement. Mild to moderate dehydration in children seen in an  emergency department  is best treated with ORT. Persons taking ORT should eat within six hours and return to their full diet within 24\u201348 hours. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2802", "text": "Oral rehydration therapy may also be used as a treatment for the symptoms of  dehydration  and rehydration in  burns  in resource-limited settings. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2803", "text": "ORT may lower the mortality rate of diarrhea by as much as 93%. [ 2 ]  Case studies in four developing countries also have demonstrated an association between increased use of ORS and reduction in mortality. [ 11 ] \nORT using the original ORS formula has no effect on the duration of the diarrheic episode or the volume of fluid loss, [ 12 ]  although reduced osmolarity solutions have been shown to reduce stool volume. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2804", "text": "The degree of dehydration should be assessed before initiating ORT. ORT is suitable for people who are not dehydrated and those who show signs and symptoms of mild to moderate dehydration. People who have severe dehydration should seek professional medical help immediately and receive intravenous rehydration as soon as possible to rapidly replenish fluid volume in the body. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2805", "text": "ORT should be discontinued and fluids replaced intravenously when vomiting is protracted despite proper administration of ORT; or signs of dehydration worsen despite giving ORT; or the person is unable to drink due to a decreased level of consciousness; or there is evidence of intestinal blockage or  ileus . ORT might also be contraindicated in people who are in hemodynamic shock due to impaired airway protective reflexes. [ 15 ]  Short-term vomiting is not a contraindication to receiving oral rehydration therapy. In persons who are vomiting, drinking oral rehydration solution at a slow and continuous pace will help resolve vomiting. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2806", "text": "WHO  and  UNICEF  have jointly developed official guidelines for the manufacture of oral rehydration solution and the oral rehydration salts used to make it (both often abbreviated  ORS ). They also describe other acceptable solutions, depending on material availability. Commercial preparations are available as prepared fluids and as packets of powder ready to mix with water. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2807", "text": "A basic oral rehydration therapy solution can also be prepared when packets of oral rehydration salts are not available. [ 18 ] [ 19 ]  The  molar   ratio  of sugar to salt should be 1:1 and the solution should not be  hyperosmolar . [ 20 ]  The Rehydration Project states, \"Making the mixture a little diluted (with more than 1 litre of clean water) is not harmful.\" [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2808", "text": "The optimal fluid for preparing oral rehydration solution is clean water. However, if this is not available, the usually available water should be used. Oral rehydration solution should  not   be withheld simply because the available water is potentially unsafe; rehydration takes precedence. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2809", "text": "When oral rehydration salts packets and suitable teaspoons for measuring sugar and salt are not available, the WHO has recommended that homemade gruels, soups, etc., may be considered to help maintain hydration. [ 23 ]  A Lancet review in 2013 emphasized the need for more research on appropriate home made fluids to prevent dehydration. [ 24 ]   Sports drinks  are not optimal oral rehydration solutions, but they can be used if optimal choices are not available. They should not be withheld for lack of better options; again, rehydration takes precedence. But they are not replacements for oral rehydration solutions in nonemergency situations. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2810", "text": "In 2003, WHO and UNICEF recommended that the  osmolarity  of oral rehydration solution be reduced from 311 to 245 mOsm/L. [ 26 ] [ 27 ]  These guidelines were also updated in 2006. This recommendation was based on multiple clinical trials showing that the reduced osmolarity solution reduces stool volume in children with diarrhea by about twenty-five percent and the need for IV therapy by about thirty percent when compared to standard oral rehydration solution. The incidence of vomiting is also reduced. The reduced osmolarity oral rehydration solution has lower concentrations of glucose and sodium chloride than the original solution, but the concentrations of potassium and  citrate  are unchanged. [ 28 ] [ 13 ] [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2811", "text": "The reduced osmolarity solution has been criticized by some for not providing enough sodium for adults with cholera. [ 31 ]  Clinical trials have, however, shown reduced osmolarity solution to be effective for adults and children with cholera. [ 30 ]  They seem to be safe but some caution is warranted according to the  Cochrane review . [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2812", "text": "ORT is based on evidence that water continues to be absorbed from the  gastrointestinal tract  even while fluid is lost through diarrhea or vomiting. The  World Health Organization  specify indications, preparations and procedures for ORT. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2813", "text": "WHO/UNICEF guidelines suggest ORT should begin at the first sign of diarrhea in order to prevent dehydration. [ 28 ] [ 33 ]  Babies may be given ORS with a dropper or a syringe. Infants under two may be given a teaspoon of ORS fluid every one to two minutes. Older children and adults should take frequent sips from a cup, with a recommended intake of 200\u2013400 mL of solution after every loose movement. [ 1 ]  The WHO recommends giving children under two a quarter- to a half-cup of fluid following each loose  bowel movement  and older children a half- to a full cup. If the person vomits, the caregiver should wait 5\u201310 minutes and then resume giving ORS. [ 22 ] :\u200aSection 4.2\u200a  ORS may be given by  aid workers  or health care workers in  refugee  camps, health clinics and hospital settings. [ 34 ]  Mothers should remain with their children and be taught how to give ORS. This will help to prepare them to give ORT at home in the future. Breastfeeding should be continued throughout ORT. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2814", "text": "As part of oral rehydration therapy, the WHO recommends supplemental zinc (10 to 20\u00a0mg daily) for ten to fourteen days, to reduce the severity and duration of the illness and make recurrent illness in the following two to three months less likely. Preparations are available as a  zinc sulfate  solution for adults, a modified solution for children and in tablet form. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2815", "text": "After severe dehydration is corrected and appetite returns, feeding the person speeds the recovery of normal intestinal function, minimizes weight loss and supports continued growth in children. Small frequent meals are best tolerated (offering the child food every three to four hours). Mothers should continue to  breastfeed . [ 22 ] [ 11 ] [ 36 ]  A child with watery diarrhea typically regains their appetite as soon as dehydration is corrected, whereas a child with bloody diarrhea often eats poorly until the illness resolves. Such children should be encouraged to resume normal feeding as soon as possible. Once diarrhea is corrected, the WHO recommends giving the child an extra meal each day for two weeks, and longer if the child is malnourished. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2816", "text": "Dehydration may be overestimated in  wasted  children and underestimated in  edematous  children. [ 37 ]  Care of these children must also include careful management of their  malnutrition  and treatment of other infections. Useful signs of dehydration include an eagerness to drink, lethargy, cool and moist extremities, weak or absent  radial pulse  (wrist), and reduced or absent  urine  flow.  In children with severe malnutrition, it is often impossible to reliably distinguish between moderate and severe dehydration. A severely malnourished child who has signs of severe dehydration but who does not have a history of watery diarrhea should be treated for  septic shock . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2817", "text": "The original ORS (90\u00a0mmol sodium/L) and the current standard reduced-osmolarity ORS (75\u00a0mmol sodium/L) both contain too much sodium and too little potassium for severely malnourished children with dehydration due to diarrhea. ReSoMal ( Re hydration  So lution for  Mal nutrition) is recommended for such children. It contains less sodium (45\u00a0mmol/L) and more potassium (40\u00a0mmol/L) than reduced osmolarity ORS. [ 38 ]  It can be obtained in packets produced by UNICEF or other manufacturers. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2818", "text": "An exception is if the severely malnourished child also has severe diarrhea (in which case ReSoMal may not provide enough sodium), in which case standard reduced-osmolarity ORS (75\u00a0mmol sodium/L) is recommended. [ 22 ]  Malnourished children should be rehydrated slowly. The WHO recommends 10 milliliters of ReSoMal per kilogram body weight for each of the first two hours (for example, a 9-kilogram child should be given 90 mL of ReSoMal over the course of the first hour, and another 90 mL for the second hour) and then continuing at this same rate or slower based on the child's thirst and ongoing stool losses, keeping in mind that a severely dehydrated child may be lethargic.  If the child drinks poorly, a nasogastric tube should be used. The IV route should not be used for rehydration except in cases of shock and then only with care, infusing slowly to avoid flooding the circulation and overloading the heart. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2819", "text": "Feeding should usually resume within 2\u20133 hours after starting rehydration and should continue every 2\u20133 hours, day and night. For an initial cereal diet before a child regains his or her full appetite, the WHO recommends combining 25 grams skimmed milk powder, 20 grams vegetable oil, 60 grams sugar, and 60 grams rice powder or other cereal into 1,000 milliliters water and boiling gently for five minutes. Give 130 mL per kilogram of body weight during per 24 hours. A child who cannot or will not eat this minimum amount should be given the diet by nasogastric tube divided into six equal feedings. Later on, the child should be given cereal made with a greater amount of skimmed milk product and vegetable oil and slightly less sugar. As appetite fully returns, the child should be eating 200 mL per kilogram of body weight per day. Zinc, potassium, vitamin A, and other vitamins and minerals should be added to both recommended cereal products, or to the oral rehydration solution itself. Children who are breastfed should continue breastfeeding. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2820", "text": "The WHO recommends that all severely malnourished children admitted to hospital should receive  broad-spectrum antibiotics  (for example,  gentamicin  and  ampicillin ). In addition, hospitalized children should be checked daily for other specific infections. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2821", "text": "If cholera is suspected give an antibiotic to which  V. cholera e are susceptible. This reduces the volume loss due to diarrhea by 50% and shortens the duration of diarrhea to about 48 hours. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2822", "text": "Fluid from the body enters the  intestinal   lumen  during  digestion . This fluid is  isosmotic  with the blood and contains a high quantity, about 142 mEq/L, of  sodium . A healthy individual secretes 2000\u20133000 milligrams of sodium per day into the intestinal lumen. Nearly all of this is reabsorbed so that sodium levels in the body  remain constant . In a diarrheal illness, sodium-rich intestinal secretions are lost before they can be reabsorbed. This can lead to life-threatening  dehydration  or  electrolyte imbalances  within hours when fluid loss is severe. The objective of therapy is the replenishment of sodium and water losses by ORT or intravenous infusion. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2823", "text": "Sodium absorption occurs in two stages. The first is via intestinal  epithelial  cells ( enterocytes ). Sodium passes into these cells by  co-transport  with glucose, via the  SGLT1  protein. From the intestinal epithelial cells, sodium is pumped by  active transport  via the  sodium-potassium pump  through the  basolateral cell membrane  into the  extracellular space . [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2824", "text": "The  sodium\u2013potassium ATPase pump  at the basolateral  cell membrane  moves three sodium ions into the extracellular space, while pulling into the enterocyte two  potassium  ions. This creates a \"downhill\" sodium  gradient  within the cell.  SGLT proteins  use energy from this downhill sodium gradient to transport  glucose  across the  apical membrane  of the cell against the glucose gradient. The co-transporters are examples of  secondary active transport . The GLUT  uniporters  then transport glucose across the basolateral membrane. Both SGLT1 and SGLT2 are known as  symporters , since both sodium and glucose are transported in the same direction across the membrane. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2825", "text": "The co-transport of glucose into epithelial cells via the  SGLT1  protein requires sodium. Two sodium ions and one molecule of glucose (or  galactose ) are transported together across the  cell membrane  via the SGLT1 protein. Without glucose, intestinal sodium is not absorbed. This is why oral rehydration salts include both sodium and glucose. For each cycle of the transport, hundreds of water molecules move into the epithelial cell to maintain osmotic equilibrium. The resultant absorption of sodium and water can achieve rehydration even while diarrhea continues. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2826", "text": "In the early 1980s, \"oral rehydration therapy\" meant only the preparation prescribed by the  World Health Organization  (WHO) and  UNICEF . In 1988, the definition was changed to include recommended home-made solutions, because the official preparation was not always available. The definition was also amended in 1988, to include continued feeding as associated therapy. In 1991, the definition became \"an increase in administered  hydrational fluids \"; in 1993, \"an increase in administered fluids and continued feeding\". [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2827", "text": "Dehydration was a major cause of death during the 1829  cholera  pandemic in Russia and Western Europe. In 1831,  William Brooke O'Shaughnessy  noted the changes in blood composition and loss of water and salt in the stool of people with cholera and prescribed  intravenous fluid therapy  (IV fluids). The prescribing of  hypertonic  IV therapy decreased the mortality rate of cholera to 40%, from 70%. In the West, IV therapy became the \"gold standard\" for the treatment of moderate and severe dehydration. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2828", "text": "In 1953,  Hemendra Nath Chatterjee  published in  The Lancet  the results of using ORT to treat people with mild cholera. [ 44 ]  He gave the solution orally and rectally, along with Coleus extract, antihistamines, and antiemetics, without controls. The formula of the fluid replacement solution was 4\u00a0g of  sodium chloride , 25\u00a0g of  glucose , and 1000\u00a0mL of  water . [ 44 ] [ 45 ]  He did not publish any balance data, and his exclusion of patients with severe dehydration did not lead to any confirming study; his report remained anecdotal. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2829", "text": "Robert Allan Phillips  tried to make an effective ORT solution based on his discovery that, in the presence of glucose, sodium, and chloride could be absorbed in patients with cholera; but he failed because his solution was too hypertonic and he used it to try to stop the diarrhea rather than to rehydrate patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2830", "text": "In the early 1960s,  Robert K. Crane  described the  sodium-glucose co-transport mechanism  and its role in intestinal glucose absorption. [ 46 ]  This, along with evidence that the intestinal  mucosa  appears undamaged in cholera, suggested that intestinal absorption of glucose and sodium might continue during the illness. This supported the notion that oral rehydration might be possible even during severe diarrhea due to cholera. In 1967\u20131968,  Norbert Hirschhorn  and Nathaniel F. Pierce showed that people with severe cholera can absorb glucose, salt, and water and that this can occur in sufficient amounts to maintain hydration. [ 47 ] [ 48 ]  In 1968,  David R. Nalin  and  Richard A. Cash , helped by  Rafiqul Islam  and Majid Molla, reported that giving adults with cholera an oral glucose-electrolyte solution in volumes equal to those of the diarrhea losses reduced the need for IV fluid therapy by eighty percent. [ 49 ] [46]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2831", "text": "In 1971, fighting during the  Bangladesh Liberation War  displaced millions and an epidemic of cholera ensued among the refugees. When IV fluid ran out in the  refugee camps ,  Dilip Mahalanabis , a physician working with the Johns Hopkins International Center for Medical Research and Training in Calcutta, issued instructions to prepare an oral rehydration solution and to distribute it to family members and caregivers. Over 3,000 people with cholera received ORT in this way. The  mortality rate  was 3.6% among those given ORT, compared with 30% in those given IV fluid therapy. [ 43 ] [ 45 ]  After Bangladesh won independence, there was a wide campaign to promote the use of saline in the treatment of diarrhea.  In 1980, the World Health Organization recognized ORT and began a global program for its dissemination. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2832", "text": "In the 1970s,  Norbert Hirschhorn  used oral rehydration therapy on the  White River Apache Indian Reservation  with a grant from the National Institute of Allergy and Infectious Diseases. [ 50 ] [ 51 ] [ 52 ]  He observed that children voluntarily drank as much of the solution as needed to restore hydration, and that rehydration and early re-feeding would protect their nutrition. This led to increased use of ORT for children with diarrhea, especially in developing countries. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2833", "text": "In 1980, the Bangladeshi nonprofit BRAC created a door-to-door and person-to-person sales force to teach ORT for use by mothers at home. A  task force  of fourteen women, one cook, and one male supervisor traveled from village to village. After visiting with women in several villages, they hit upon the idea of encouraging the women in the village to make their own oral rehydration fluid. They used available household equipment, starting with a \"half a seer\" (half a quart) of water and adding a fistful of sugar and a three-finger pinch of salt. Later on, the approach was broadcast over television and radio, and a market for oral rehydration salts packets developed. Three decades later, national surveys have found that almost 90% of children with severe diarrhea in Bangladesh are given oral rehydration fluids at home or in a health facility. [ 53 ]  ORT is known in Bangladesh as Orosaline or Orsaline. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2834", "text": "From 2006 to 2011, UNICEF estimated that worldwide about a third of children under 5 who had diarrhea received an oral rehydration solution, with estimates ranging from 30% to 41% depending on the region. [ 54 ] [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2835", "text": "ORT is one of the principal elements of the UNICEF \"GOBI FFF\" program (growth monitoring; ORT; breast feeding; immunization; female education; family spacing and  food supplementation ). The program aims to increase child survival in developing nations through proven low-cost interventions. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2836", "text": "An  ostomy pouching system [ 1 ]  is a  prosthetic   medical device  that provides a means for the collection of waste from a surgically diverted biological system ( colon ,  ileum ,  bladder ) and the creation of a  stoma . Pouching systems are most commonly associated with  colostomies ,  ileostomies , and  urostomies . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2837", "text": "Pouching systems usually consist of a collection pouch, a barrier on the skin, and connect with the stoma itself, which is the part of the body that has been diverted to the skin. The system may be a one-piece system consisting only of a bag or, in some instances involve a device placed on the skin with a collection pouch that is attached mechanically or with an  adhesive  in an  airtight  seal, known as a two-piece system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2838", "text": "The system used varies between individuals and is often based on the medical reason, personal preference and lifestyle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2839", "text": "Ostomy pouching systems collect  waste  that is output from a stoma. The pouching system allows the stoma to drain into a sealed collection pouch, while protecting the surrounding  skin  from  contamination . [ 3 ]  They are used to maintain independence, so that a wearer can continue to lead an active lifestyle that can include all forms of sports and recreation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2840", "text": "Ostomy barriers sit on the skin and separate the ostomy pouch from the internal conduit. They are not always present. These barriers, also called flanges, wafers, or baseplates are manufactured using  pectin  or similar organic material and are available in a wide variety of sizes to accommodate a person's particular anatomy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2841", "text": "The internal opening must be the correct size to accommodate the individual's  stoma  while protecting the skin from contact with waste. The methods for sizing this opening vary depending on the type of wafer/baseplate; some pre-cut sizes are available, some users customize the opening using  scissors . Manufacturers have recently [ when? ]  introduced moldable wafers that can be shaped by hand without the need for scissors. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2842", "text": "Skin adhesion for modern wafers/baseplates/flanges are optimized on all the five parameters required in an adhesive:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2843", "text": "In addition, barriers with adhesive border can provide additional security that the system stays in place. Using a barrier film spray before applying a new flange will improve adhesion, soothe irritated skin and protect the skin from irritation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2844", "text": "A barrier may last between one and many days before it needs to be replaced; this is highly dependent on the individual's lifestyle, ostomy type, and anatomy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2845", "text": "The method of attachment to the barrier varies between manufactures and includes permanent (one-piece), press-on/click (\" Tupperware \" type), turning locking rings and \"sticky\" adhesive mounts. The two-piece arrangement allows pouches to be exchanged without removing the wafer; for example, some people prefer to temporarily switch to a \"mini-pouch\" for swimming, intimate and other short-term activities. Mini-pouches are suitable for minimum usage only."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2846", "text": "Pouches can be divided into two basic types: open-end (drainable) and closed-end (disposable)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2847", "text": "The use of open-end vs. closed-end pouches is dependent on the frequency in which an individual needs to empty the contents, as well as  economics . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2848", "text": "Gas  is created during  digestion , and an airtight pouch will collect this and inflate. To prevent this some pouches are available with special  charcoal filtered  vents that will allow the gas to escape, and prevent ballooning at night. Some odor can be expelled through the charcoal filter especially if  sufficient deodorant is not used in the pouch."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2849", "text": "Pouch covers are helpful to disguise the plastic pouch when it is exposed when reaching or other physical activity. These are usually made of cloth and can be decorative or plain to blend in with clothing. Various sources stock sizes for most manufacturers pouches. There are flexible elastic pouch belts available for extreme physical activity but some of these require the pouch to be worn sideways so it does not fill properly and the tight fit causes pancaking of the effluent."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2850", "text": "People with colostomies must wear an ostomy pouching system to collect intestinal waste.  Ordinarily the pouch must be emptied or changed a couple of times a day depending on the frequency of activity; in general the further from the  anus  (i.e., the further 'up' the intestinal tract) the ostomy is located the greater the output and more frequent the need to empty or change the pouch. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2851", "text": "People with colostomies who have ostomies of the  sigmoid colon  or  descending colon  may have the option of irrigation, which allows for the person to not wear a pouch, but rather just a gauze cap over the stoma, and to schedule irrigation for times that are convenient. [ 5 ]  To irrigate, a  catheter  is placed inside the stoma, and flushed with water, which allows the feces to come out of the body into an irrigation sleeve. [ 6 ]  Most colostomates irrigate once a day or every other day, though this depends on the person, their food intake, and their health."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2852", "text": "Ostomy systems often take some time for a person to adjust to, including requiring time to learn how to use them and change the pouch, as well as psychologically adjust. [ 7 ]  The time taken to adjust may last for more than a year. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2853", "text": "Because of embarrassment or stigma associated with an ostomy system, a person who has an ostomy system can experience  social isolation ,  depression , and change in  sexual function  as well as physical complications such as weight change. In various online ostomy groups and ostomy societies, ostomates share their experiences and help each other. One of the largest is MeetAnOstoMate, a community where people with similar experiences share information, ask questions, and receive support.  [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2854", "text": "Pancreatic elastase  is a form of  elastase  that is produced in the  acinar  cells of the  pancreas , initially produced as an inactive  zymogen  and later activated in the duodenum by  trypsin . Elastases form a subfamily of  serine proteases , characterized by a distinctive structure consisting of two  beta barrel  domains converging at the active site that hydrolyze amides and esters amongst many proteins in addition to  elastin , a type of connective tissue that holds organs together. Pancreatic elastase 1 is a serine endopeptidase, a specific type of protease that has the amino acid  serine  at its active site. Although the recommended name is pancreatic elastase, it can also be referred to as elastase-1, pancreatopeptidase, PE, or serine elastase."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2855", "text": "The first  isozyme , pancreatic elastase 1, was initially thought to be expressed in the pancreas. However it was later discovered that it was the only  chymotrypsin -like elastase that was not expressed in the pancreas. In fact, pancreatic elastase is expressed in basal layers of  epidermis  (at protein level). Hence pancreatic elastase 1 has been renamed  elastase 1  (ELA1) or  chymotrypsin-like elastase family, member 1  ( CELA1 ). [ 1 ]  For a period of time, it was thought that ELA1 / CELA1 was not  transcribed  into a protein. [ 2 ]   However it was later discovered that it was expressed in skin  keratinocytes . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2856", "text": "Clinical literature that describes human elastase 1 activity in the pancreas or fecal material is actually referring to chymotrypsin-like elastase family, member 3B ( CELA3B ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2857", "text": "Pancreatic elastase is a compact globular protein with a  hydrophobic  core. This enzyme is formed by three subunits. Each subunit binds one calcium ion ( cofactor ). There are three important metal-binding sites in  amino acids  77, 82, 87. [ 4 ]  The  catalytic triad , located in the active site is formed by three hydrogen-bonded amino acid residues (H71, D119, S214), and plays an essential role in the cleaving ability of all proteases. It is composed of a single  peptide  chain of 240 amino acids and contains 4 disulfide bridges. It has a high degree of sequence identity with pancreatic elastases that correspond to other species, such as the rat's, with whom it shares 86% of its sequence. [ 5 ]  Its enzymatic activity is a result of the specific three-dimensional conformation which its single polypeptide chain adopts, and therefore, activity is lost by  denaturation  and/or conformational changes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2858", "text": "Elafin, the skin-derived elastase inhibitor, has been shown to be a potent and specific inhibitor of both the porcine homolog of ELA1 and human leukocyte elastase in vitro. Elafin is expressed by epidermal keratinocytes under hyperproliferative conditions such as psoriasis and wound healing. It has also been reported to be present in many other adult epithelia that are exposed to environmental stimuli: tongue, plate, lingual tonsils, gingiva, pharynx, epiglottis, vocal fold, esophagus, uterine cervix, vagina, and hair follicles. In all these tissues, the presence of inflammatory cells is physiologic and elafin expression is believed to protect against leukocyte proteases, thereby helping to maintain epithelial integrity. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2859", "text": "Elafin on the contrary has never been found in the basal layer in any type of epithelial tissue. Indeed, elafin is virtually absent in normal human epidermis. The other known elastase inhibitor,  SLPI , however, has been reported to be expressed in the basal keratinocytes suggesting that this may be the major elastase inhibitor in normal epidermis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2860", "text": "Alpha 1-antitrypsin  and  alpha-2-macroglobulin  are human serum protease inhibitors that completely inhibit the general proteolytic activity of pancreatic elastase 1 and 2. It has been observed that a protease must be active in order to bind to these two inhibitors. Studies proved that the activity of elastase 2 was enhanced in 25-250 mM NaCl. The activity of elastase 2 in NaCl approached approximately twice the activity without NaCl.\nElastase 1 is slightly inhibited above 150 mM NaCl [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2861", "text": "Mutations of the CELA1 gene were suspected to be associated with  diffuse nonepidermolytic palmoplantar keratoderma  (diffuse NEPPK). [ 3 ]  However the suspected sequence variant was fully functional and did not strongly associate with the disease.  More recently, a specific mutation in the  KRT6C  gene has been linked to some cases of diffuse NEPPK. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2862", "text": "A possible  polymorphism  of the CELA1 gene coding this protein was found. On a secondary structure level, this polymorphism manifests itself in an excision of a short sequence of CELA1. The disappeared sequence carries the key amino acid residues Val-227 and Thr-239, which contribute to the  substrate specificity  of elastase I (highlighted in Figure 3), as well as five of the eight amino acids involved in the primary contact of the  elafin (inhibitor)/elastase complex formation. These observations imply that the sequence variant might modify the substrate specificity of the enzyme and abolish the  inhibitor  binding capability. Though there were no obvious pathogenic epidermal abnormalities associated with the truncated ELA1 variant, it is possible that carriers of the polymorphism may be at greater risk of developing the common skin diseases such as psoriasis and eczema (genetic and histologic studies will be required to investigate the role of ELA1 in these common epidermal disorders.). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2863", "text": "Pancreatic elastase is formed by activation of  proelastase  from mammalian pancreas by  trypsin . After processing to proelastase, it is stored in the zymogen granules and then activated to elastase in the  duodenum  by the tryptic cleavage of a peptide bond in the inactive form of the precursor molecule. [ 8 ]  This process results in the removal of an activation peptide from the N-terminal, that enables the  enzyme  to adopt its native conformation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2864", "text": "Humans have five chymotrypsin-like elastase genes which encode the structurally similar proteins:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2865", "text": "Glycosylation  at Asn79 and Asn233. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2866", "text": "The gene that codes for pancreatic elastase 1 is  CELA1  (synonym: ELA1)\nPancreatic elastase 1 is encoded by a single genetic locus on chromosome 12. Studies of human pancreatic elastase 1 have shown that this serine protease maps to the chromosomal region 12q13 [ 10 ]  and it is close to a locus for an autosomal dominant skin disease,  Diffuse nonepidermolytic palmoplantar keratoderma . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2867", "text": "The hydrolysis that elastases bring about occur in several steps, starting with the formation of a complex between elastase and its substrate, with the carbonyl carbon positioned near the nucleophilic serine, followed by a nucleophillic attack that forms an acyl-enzyme intermediate (a pair of electrons from the double bond of the carbonyl oxygen moves to the oxygen) while the first product is released. The intermediate is then hydrolyzed in a deacylation step, regenerating the active enzyme and resulting in the release of the second product ( the electron-deficient carbonyl carbon re-forms the double bond with the oxygen and the  C-terminus  of the peptide is released.  It preferentially cleaves peptide bonds at the carbonyl end of amino acid residues with small hydrophobic side chains such as  glycine ,  valine ,  leucine ,  isoleucine  and  alanine . The wide specificity of elastases for non-aromatic uncharged side chains can explain its ability to break down native elastin. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2868", "text": "Human pancreatic elastase 1 (E1) is not degraded in intestinal transit, so that its concentration in feces reflects exocrine pancreatic function. In inflammation of the pancreas, E1 is released into the bloodstream. Thus the quantification of pancreatic elastase 1 in serum allows diagnosis or exclusion of acute pancreatitis. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2869", "text": "Main indications:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2870", "text": "Method of detection:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2871", "text": "Reference concentration to interpret Pancreatic Elastase results:\nFor adults and children after the first month of life"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2872", "text": "This article incorporates text from the  United States National Library of Medicine , which is in the  public domain ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2873", "text": "Paneth cells  are cells in the small intestine  epithelium , alongside  goblet cells ,  enterocytes , and  enteroendocrine cells . [ 1 ]  Some can also be found in the  cecum  and  appendix . They are located below the intestinal stem cells in the  intestinal glands  (also called crypts of  Lieberk\u00fchn ) and the large  eosinophilic   refractile granules  that occupy most of their  cytoplasm ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2874", "text": "When exposed to  bacteria  or bacterial  antigens , Paneth cells secrete several anti-microbial compounds (notably  defensins  and  lysozyme ) that are known to be important in immunity and host-defense into the  lumen  of the intestinal gland, thereby contributing to maintenance of the gastrointestinal barrier by controlling the enteric bacteria. Therefore, Paneth cells play a role in the  innate immune system ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2875", "text": "Paneth cells are named after 19th-century pathologist  Joseph Paneth ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2876", "text": "Paneth cells are found throughout the  small intestine  and the appendix at the base of the  intestinal glands . [ 2 ]  There is an increase in Paneth cell numbers towards the end of the small intestine. [ 3 ]  Like the other epithelial cell lineages in the small intestine, Paneth cells originate at the stem cell region near the bottom of the gland. [ 4 ]  There are on average 5\u201312 Paneth cells in each small intestinal crypt. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2877", "text": "Unlike the other epithelial cell types, Paneth cells migrate downward from the stem cell region and settle just adjacent to it. [ 4 ]  This close relationship to the stem cell region suggests that Paneth cells are important in defending the gland stem cells from microbial damage, [ 4 ]  although their function is not entirely known. [ 2 ]  Furthermore, among the four aforementioned intestinal cell lineages, Paneth cells live the longest (approximately 57 days). [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2878", "text": "Paneth cells secrete antimicrobial peptides and proteins, which are \"key mediators of host-microbe interactions, including homeostatic balance with colonizing microbiota and innate immune protection from enteric pathogens.\" [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2879", "text": "Small intestinal crypts house  stem cells  that serve to constantly replenish  epithelial cells  that die and are lost from the  villi . [ 7 ]  Paneth cells support the physical barrier of the epithelium by providing essential niche signals to their neighboring  intestinal stem cells . Protection and stimulation of these  stem cells  is essential for long-term maintenance of the intestinal  epithelium , in which Paneth cells play a critical role. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2880", "text": "Paneth cells display  merocrine  secretion, that is, secretion via  exocytosis . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2881", "text": "Paneth cells are stimulated to secrete  defensins  when exposed to bacteria (both  Gram positive  and  Gram-negative  types), or such bacterial products as  lipopolysaccharide ,  lipoteichoic acid ,  muramyl dipeptide  and  lipid A . [ 10 ]  They are also stimulated by  cholinergic signaling  normally preceding the arrival of food which potentially may contain a new bacterial load. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2882", "text": "Paneth cells sense bacteria via  MyD88 -dependent  toll-like receptor  (TLR) activation which then triggers antimicrobial action. [ 11 ]  For example, research showed that in the secretory granules, murine and human Paneth cells express high levels of  TLR9 . TLR9 react to  CpG-ODN  and unmethylated oligonucleotides,  pathogen-associated molecular patterns (PAMPs)  typical for bacterial DNA. Internalizing these PAMPs and activating TLR9 leads to  degranulation  and release of antimicrobial peptides and other secretions. [ 12 ]  Surprisingly, murine Paneth cells do not express mRNA transcripts for  TLR4 . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2883", "text": "The principal defense molecules secreted by Paneth cells are  alpha-defensins , which are known as  cryptdins  in mice. [ 13 ]  These  peptides  have  hydrophobic  and positively charged domains that can interact with  phospholipids  in  cell membranes . This structure allows defensins to insert into membranes, where they interact with one another to form pores that disrupt membrane function, leading to cell lysis. Due to the higher concentration of negatively charged  phospholipids  in bacterial than vertebrate  cell membranes , defensins preferentially bind to and disrupt bacterial cells, sparing the cells they are functioning to protect. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2884", "text": "Human Paneth cells produce two \u03b1-defensins known as  human \u03b1-defensin HD-5 (DEFA5)  and  HD-6 (DEFA6) . [ 15 ]  HD-5 has a wide spectrum of killing activity against both Gram positive and Gram negative bacteria as well as fungi ( Listeria monocytogenes ,  Escherichia coli ,  Salmonella typhimurium , and C andida albicans ). [ 5 ]  The antimicrobial activity of HD-6 consists of self-assembling into extracellular nets that entrap bacteria in the intestine and thereby preventing their translocation across the epithelial barrier. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2885", "text": "Human Paneth cells also produce other AMPs including  lysozyme , secretory  phospholipase A2 , and  regenerating islet-derived protein IIIA . [ 17 ]  Lysozyme is an  antimicrobial  enzyme that dissolves the cell walls of many bacteria, and phospholipase A2 is an enzyme specialized in the lysis of bacterial  phospholipids  . [ 10 ]  This battery of secretory molecules gives Paneth cells a potent arsenal against a broad spectrum of agents, including bacteria,  fungi  and even some enveloped  viruses . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2886", "text": "During conventional protein secretion, proteins are transported through the  ER-Golgi complex  packaged in secretory granules and released to the extracellular space. Should invasive pathogens disrupt the  Golgi apparatus , causing an impairment in the Paneth cell secretion of antimicrobial proteins, an alternative secretion pathway exists: it has been shown that  lysozyme  can be rerouted through secretory  autophagy . In secretory autophagy, cargo is transported in an LC3+ vesicle and discharged at the  plasma membrane , thus bypassing the  ER-Golgi complex.  Not all bacteria prompts secretory autophagy: commensal bacteria, for example, does not cause Golgi breakdown and therefore does not trigger the secretory autophagy of  lysozyme . A dysfunction in secretory autophagy is thought to be a possible contriburing factor to Crohn's disease. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2887", "text": "Paneth cells maintain the health of the intestine by acting as  macrophages ; it has been shown that Paneth cells clear dying cells via apoptotic cell uptake. The phagocytic function of Paneth cells was discovered using a series of experiments, one of which made use of mice that were radiated with a low dose Cesium-137 (137Cs), mimicking chemotherapy undergone by cancer patients. [ 20 ]  These findings may be significant for addressing the side effects suffered by cancer patient whose intestinal health is damaged by chemotherapy: approximately 40% of all cancer therapy patients experience gastrointestinal (GI)  mucositis  during their treatment, with the number jumping to 80% in patients receiving abdominal or pelvic  irradiation . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2888", "text": "Paneth cells participate in the  Wnt signaling pathway  and  Notch signalling pathway , which regulate proliferation of intestinal stem cells and  enterocytes  necessary for epithelium cell renewal. They express the canonical Wnt ligands:  Wnt3a ,  Wnt9b , and  Wnt11 , which bind to  Frizzled  receptors on intestinal stem cells to drive  \u03b2-catenin / Tcf  signaling. Paneth cells are also a major source of Notch ligands  DLL1  and  DLL4 , binding to Notch receptors  Notch1  and  Notch2  on intestinal stem cells and  enterocyte  progenitors. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2889", "text": "Recently, however, it has been discovered that the regenerative potential of intestinal epithelial cells declines over time as a result of aged Paneth cells secreting the protein  Notum , which is an extracellular inhibitor of Wnt signaling. If Notum secretion is inhibited, the regenerative potential of the intestinal epithelium could increase. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2890", "text": "It has been established that  zinc  is essential for the function of Paneth cells. A defect in the Zn transporter (ZnT)2 impairs Paneth cell function by causing uncoordinated granule secretion. Mice lacking the (ZnT)2 transporter not only exhibit impaired granule secretion, they also suffer from increased inflammatory response to lipopolysaccharide and are less capable of bactericidal activity. [ 23 ]  Normally,  zinc  is stored in the secretory granules and, upon degranulation, is released in the lumen. It has been speculated that the storage of heavy metals contributes to direct antimicrobial toxicity, as Zn is released upon cholinergic PC stimulation. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2891", "text": "Zinc  deficiency is also implicated in alcohol\u2010induced Paneth cell \u03b1\u2010defensin dysfunction, which contributes to alcohol-related  steatohepatitis . Zinc can stabilize human \u03b1\u2010defensin 5 (HD5), which is responsible for microbiome homeostasis. In line with this, the administration of HD5 can effectively alter the microbiome (especially by increasing  Akkermansia muciniphila) , and reverse the damage inflicted on the microbiome by excessive alcohol consumption. Dietary zinc deficiency on the other hand exacerbates the deleterious effect of alcohol on the bactericidal activity of Paneth cells. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2892", "text": "Abnormal Paneth cells with reduced expression or secretion of defensins HD-5 and HD-6 (in human) and antimicrobial peptides are associated with  inflammatory bowel disease . [ 26 ] [ 17 ]  In addition to that, several of the  Crohn's disease -risk alleles are associated with Paneth cell dysfunction are involved in processes such as  autophagy , the  unfolded protein response , and the regulation of  mitochondrial  function. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2893", "text": "It is believed that the dysfunction of Paneth cells compromises antimicrobial peptides leading to a  microbiota  composition shift, and even dysbiosis. [ 27 ]   Crohn's disease  patients with a higher percentage of abnormal Paneth cells showed significantly reduced bacterial diversity compared with patients with a lower percentage of abnormal Paneth cells, reflecting a reduced abundance of anti-inflammatory microbes. [ 28 ]  Collectively, these findings support the theory that Paneth cell dysfunction may lead to a dysbiotic microbiota that, in turn, could predispose an individual to the development of Crohn's disease. [ 17 ]  However, it is yet to be established whether Paneth cell dysfunction is the cause of dysbiosis, or its concomitant effect. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2894", "text": "Paneth cells develop gradually during gestation and therefore preterm babies might not have them in sufficient numbers. This leaves preterm babies vulnerable to  necrotizing enterocolitis . About mid-way though the development of the small intestine,  cathelicidin  secretion is replaced by \u03b1-defensin secretion. [ 29 ]  The small intestine of the premature baby is at this transition stage when the baby is born, making preterm babies susceptible to intestinal injury and, subsequently, to  necrotizing enterocolitis . [ 18 ]  It should furthermore be noted that early Paneth cells do not possess fully functional, mature granules. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2895", "text": "The mechanism that links Paneth cells to  necrotizing enterocolitis  remains unclear, but it has been theorized that a bloom of  Proteobacteria  and, more specifically,  Enterobacteriaceae  species precedes the development of the condition. [ 31 ]  When an inflammation then subsequently occurs, nitrates can be fermented by  Enterobacteriaceae  sp. but not by obligate anaerobes, which cannot use nitrates as a growth substrate. Thus,  Proteobacteria  are able to use this selective pressure to out-compete the obligate anaerobic  Firmicutes  and  Bacteroidetes , resulting in their overgrowth and consequent dysbiosis. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2896", "text": "The process is thought to begin when the premature infant is exposed to foreign antigens via formula feeding. Inflammatory cytokines are subsequently released, creating a more aerobic state leading to a competitive advantage for  Proteobacteria . As the microbiome becomes more dysbiotic, anti-inflammatory mechanisms weaken, which contributes to a cycle of increasing intestinal inflammation. The inflammation leads to a further loss in Paneth cells density and function, resulting in the impairment of AMP secretion and the destruction of the stem cell niche. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2897", "text": "Whereas the role of Paneth cells in irritable bowel syndrome and Crohn's disease has received ample attention, [ 32 ] [ 17 ]  relatively little is known about the effect Panth cell impairment has on the pathogenesis of  non-alcoholic steato-hepatitis  or  non-alcoholic fatty liver disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2898", "text": "Murine models indicate that obesity may decrease the secretion of  \u03b1-defensin  from Paneth cells, leading to  dysbiosis . [ 33 ]  and at least one murine model suggests that when \u03b1-defensin levels in the intestinal lumen are restored by intravenous administration of  R-Spondin1  to induce Paneth cell regeneration, liver fibrosis is ameliorated as a result of the dysbiosis resolving. It is hypothesized that selective microbicidal activities, as well as increasing Muribaculaceae and decreasing  Harryflintia , contribute to amelioration in fibrogenesis. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2899", "text": "One study described the injection of  dithizone , which can disrupt cell granulates, into mice that were fed a high-fat diet in order to identify Paneth-cell-oriented microbial alterations. The application of  dithizone  improved high-fat diet glucose intolerance and insulin resistance and was associated with an alleviation in the severity of liver steatosis in HFD mice, possibly through gut microbiome modulation involving the increase in  Bacteroides.  It has therefore been suggested that microbiome-targeted therapies may have a role in the treatment of non-alcoholic fatty liver disease. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2900", "text": "Further research is needed to elucidate the connection between Paneth cells and the gut-liver-axis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2901", "text": "Pediatric gastroenterology  developed as a sub-specialty of  pediatrics  and  gastroenterology . It is concerned with treating the  gastrointestinal tract , liver and  pancreas  of children from infancy until age eighteen. The principal diseases it is concerned with are acute diarrhea, persistent vomiting,  gastritis , and problems with the development of the gastric tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2902", "text": "Pediatric gastroenterology has grown greatly in North America and Europe. It began with the speciality of pediatrics, which was developed along with children\u2019s hospitals in the 19th century. The concept of specialists concentrating on organ specific specialties started around the same time. A person who contributed to the development of the specialty was Dr.  Samuel Gee  in London with his focus on serious clinical conditions in children such as  celiac disease  and  cyclic vomiting syndrome . The first national gastrointestinal society was created in Germany in 1920 by  Ismar Isidor Boas . He was also the first physician devoted completely to only gastroenterology. Later the  American Gastroenterological Association  was founded in 1897 by Dr. D. Stewart. The combination to make a pediatric gastroenterological a specialty emerged in the 1960s, almost a century after the specialties of pediatrics and gastroenterology started out individually. All pediatric specialties started out with the concept that children with special needs were not receiving the adequate medical attention that they needed. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2903", "text": "Margot Shiner , who in 1956 invented a biopsy tube that could be used to diagnose intestinal disease in children, particularly celiac disease, has been credited with initiating the emergence of pediatric gastroenterology as a distinct clinical specialty. [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2904", "text": "Centers for gastrointestinal disorders in children began being established in the 1960s in Great Britain, Australia, and continental Europe. The first centers for pediatric gastroenterology were established by Dolf Weijers and the biochemist Van de Kamer. Pediatricians and biochemists were crucial to the development of such specialty since they created the ability to calculate the fat in the feces of celiac patients with or without gluten. A clinical and research program in pediatric gastroenterology and a gastroenterological research were established in the 1960s at the Royal Children\u2019s Hospital in Melbourne by  Charlotte Anderson . Later on an important center focused on nutrition and gut  pathophysiology  was established by Bertil Linquist in  Lund, Sweden . This was the first place in which  glucose-galactose malabsorption  was reported.  Pediatric gastroenterology centers in London contributed greatly to this field and  hepatology  by helping and recognizing multiple doctors with their investigations. An example is Tom Macdonald, who concentrated his immunological research on gastroenterological diseases in children and the use of a fetal intestinal organ culture model. Important pediatric gastroenterology centers were also established in  Helsinki  and  Tampere , Finland. These centers, led by Jamro Visakorpi, primarily focused on celiac disease,  gastroenteritis \u00b8 and food allergies. Other important centers were established in Switzerland, under the leadership of  Andrea Prader  making  Z\u00fcrich  one of the first main centers for pediatric gastroenterology. In that same center, David Shmerling started studying gluten elimination and celiac disease. Salvatore Auricchio along with Giorgio Semenza began comprehending and identifying sugar absorption disorders in children. Ettore Rossi in  Bern  founded centers in which Beat Hadorn and Michael Kentze, who later went on to establish German centers in  Munich  and  Bonn , which made great contributions in the research of absorption pathophysiology. After working in Zurich, Salvatore Auricchio went on to establish an important center in  Naples  which focused research on celiac disease, the physiology of absorption, and oral re hydration therapy. In a center located in  Brussels , led by E. Eggermont and Helmuth Loeb, Samy Cadranel started developing the concept of endoscopy in children. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2905", "text": "North America has also been a center for the development of pediatric gastroenterology. A pediatric gastroenterology program focusing on researching  inflammatory bowel disease ,  infectious diarrhea , and motility disorders associated with gastrointestinal complications such as constipation and gastro esophageal reflux was established by Murray Davidson at the Albert Einstein Medical School and the  Bronx-Lebanon Hospital Center  in New York. Harry Shwachman created the center of excellence for pediatric gastroenterology in Boston in the early 1960s.  This center, under the leadership of Richard Grand and Allan Walker, went on to become a major training program for pediatric gastroenterologists. In order to commemorate Dr. Shwaschman and his impact to the field, a Scwaschman Award is given annually since 1984 by the North American Society for Pediatric Gastroenterology and Nutrition to a person with important contributions to the field. In Canada, gastroenterology and hepatology surged independently from nutrition at the  Hospital for Sick Children  (HSC) in  Toronto .  Peter Durie combined the nutrition and gastroenterology research at the HSC in 1985. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2906", "text": "Many more centers have been developed in multiple places including Sydney, Adelaide, Brisbane, Jerusalem, S\u00e3o Paulo, Santiago, Taipei, and Tokyo. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2907", "text": "The specialty of pediatric gastroenterology requires four years of undergraduate courses at a college or university in order to obtain a BS, BA, or other bachelor's degree. During these four years a student studying pediatric gastroenterology can also take a pre-med course. Afterwards, the student needs four years of medical school in order to obtain an MD or DO degree and become a general doctor. Afterwards the student needs to take a specialty in pediatrics consisting in three more years of education called residency. Afterwards pediatrics sub-specialize in a more specific area such as pediatric gastroenterology. The time to sub-specialize is called post-residency training also known as a fellowship. It can take from one to three or more years consisting in a total of fourteen years or more. In the United States, the committees to certify pediatric gastroenterologist were created in the 1980s. This gave rise to sub-specialty boards in pediatric gastroenterology in 1990 under the leadership of American board of Pediatrics and its Pediatric Gastroenterology and Nutrition subspecialty sub-board, led by Bill Kish. A formal training program was created later in 1997 by the sub-specialty advisory committee for pediatric gastroenterology of the royal college of pediatrics and child health in Great Britain. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2908", "text": "The correct function of the gastric tract and the internal health is related to the nutrition that the child or its mother receives. From the prenatal period, correct nutrition can affect the developing of the system,  short bowel syndrome  (the most common one),  necrotizing enterocolitis ,  gastroschisis  or  omphalocele  to the postnatal period with diseases such as diarrhea. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2909", "text": "One of the principal problems of a newborn is an iron deficiency, which will generate  anemia . This is caused when the only food that the baby receives is maternal milk which does not fulfill the baby\u2019s nutrition. There is no treatment for this in this period because iron will reach normal levels with the weaning process. The weaning process consists in transitioning from feeding the baby low density food such as maternal milk to start feeding it more complex foods such as meat, fish, or chicken. (uniped) If the weaning process is not carried out correctly or if the child rejects the transition of food the iron deficiency will generate an anemia or even create allergies to certain food. In such cases gastric pediatricians, and not regular pediatricians, should be consulted to treat the anemia because they will now how to recover the correct iron levels without causing any secondary effects in the digestive system. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2910", "text": "The most common nutrition problems during the childhood are being overweight or underweight, both caused by an imbalance in the number of calories consumed versus the number burned. Both in children should be treated by a gastric pediatrician and a pediatric nutritionist at the same time to help the child recover his normal weight without secondary effects (hypertension, gastritis, etc.). The nutritionist will regulate the eating habits of the child, however, the pediatric gastroenterologist will be the one checking how the change in food habits affects the correct functionality of the digestive system. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2911", "text": "A pediatrician can provide treatment to many gastric diseases, but chronic diseases, related with the nutrition of the children, the pancreas or the liver needs to be treated by a specialist. The following are two of the most common ones. Acute diarrhea is one of the most common. Globally, each of the 140 million children born annually experience an average of 7-30 episodes of diarrhea in the first 5 years of life.  Some of the causes are infections, lower levels of zinc or problems with some gastric cells. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2912", "text": "Infant regurgitation is caused by a central nervous system reflex involving both autonomic and skeletal muscles in which gastric contents are forcefully expelled through the mouth because of coordinated movements of the small bowel, stomach, esophagus, and diaphragm.  Diagnosis requires that the child be between 1 and 12, the regurgitation must be two or more times per day for three or more weeks, and there is a strong involuntary effort to vomit,  hematemesis , aspiration,  apnea ,  failure to thrive , or abnormal posturing. This is transient problem, possibly cause to the immaturity of gastrointestinal motility. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2913", "text": "In  medicine , a  Phrygian cap  is the folded portion of some  gallbladders  that resembles the  Phrygian cap  (a soft conical cap with the top pulled forward, associated in antiquity with the inhabitants of  Phrygia , a region of central  Anatolia ). It is a normal  anatomical  variant seen in 1-6% of patients. [ 1 ]  It is caused by a fold in the gallbladder where the  gallbladder fundus  joins the gallbladder body. [ 2 ]  Apart from the chance of being mistaken for stones on a  sonogram , it has no other medical implications nor does it predispose one to other diseases. [ citation needed ] \nHowever, due to potential decrease in bile flow, it may warrant a preventive removal of the gallbladder.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2914", "text": "Phycomycosis  is an uncommon condition affecting the  gastrointestinal tract  and  skin , most commonly found in  dogs  and  horses .  The condition is caused by various  molds  (a type of  fungi ), with individual forms including  pythiosis ,  zygomycosis , and  lagenidiosis .  Pythiosis, the most common type, is caused by  Pythium , a type of  water mould .  Zygomycosis can be caused by two types of  zygomycetes :  Entomophthorales  (e.g.,  Basidiobolus  and  Conidiobolus ) and  Mucorales  (e.g.,  Mucor ,  Mortierella ,  Absidia ,  Rhizopus ,  Rhizomucor , and  Saksenaea ). [ 1 ]   The latter type of zygomycosis is also referred to as  mucormycosis . Lagenidiosis is caused by a  Lagenidium  species, which like  Pythium  is a water mould.  Since both pythiosis and lagenidiosis are caused by organisms from the  Oomycetes  and not the kingdom fungi, they are sometimes collectively referred to as  oomycosis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2915", "text": "Pythiosis is caused by  Pythium insidiosum  and occurs most commonly in dogs and  horses , but is also found in  cats ,  cattle , and humans.  In the United States, it is most commonly found in states bordering the Gulf of Mexico , especially  Louisiana , but has been found in the Midwest and Eastern states.  It is also found in  Southeast Asia , eastern  Australia ,  New Zealand , and  South America .  Pythiosis occurs in areas with mild winters due to the organism surviving in standing water that does not reach freezing temperatures. [ 2 ]   Pythium  occupies swamps in late summer and infects dogs who drink water containing it.  The disease is typically found in young, large breed dogs. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2916", "text": "It is suspected that pythiosis is caused by invasion of the organism into wounds, either in the skin or in the gastrointestinal tract. [ 2 ]   The disease grows slowly in the  stomach  and  small intestine , eventually forming large lumps of  granulation tissue .  It can also invade surrounding  lymph nodes .    Symptoms include vomiting, diarrhea, weight loss, a mass in the abdomen, and depression.  Pythiosis of the skin in dogs is very rare, and appears as  ulcerated  lumps.  Primary infection can also occur in the bones and lungs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2917", "text": "In horses,  subcutaneous  pythiosis is the most common form and infection occurs through a wound  while standing in water containing the pathogen. [ 3 ]   The disease is also known as  leeches ,  swamp cancer , and  bursatti .  Lesions are most commonly found on the lower limbs, abdomen, chest, and genitals.  They are  granulomatous  and itchy, and may be ulcerated or  fistulated .  The lesions often contain yellow, firm masses of dead tissue known as  kunkers . [ 4 ]   It is possible with chronic infection, the disease can spread to underlying bone. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2918", "text": "In cats, pythioisis is almost always confined to the skin as hairless and edematous lesions.  It is usually found on the limbs,  perineum , and at the base of the tail. [ 6 ]   Lesions may also develop in the  nasopharynx . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2919", "text": "In humans, it can cause  arteritis ,  keratitis , and  periorbital   cellulitis . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2920", "text": "Pythium insidiosum  is different from other members of the genus in that human and horse hair, skin, and decaying animal tissue are  chemoattractants  for its  zoospores , in addition to decaying plant tissue. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2921", "text": "Usually, zygomycosis is a disease of the skin, but can also occur in the sinuses or gastrointestinal tract. In humans, it is most prevalent in immunocompromised patients (human immunodeficiency virus/acquired immunodeficiency syndrome [ HIV/AIDS] , the  elderly , severe combined immunodeficiency [ SCID] , etc.) and patients with acidosis (i.e., diabetes, burns), particularly after barrier injury to the skin or mucous membranes.  Zygomycosis caused by  Mucorales  causes a rapidly progressing disease of sudden onset in sick or  immunocompromised  animals.   Entomophthorales  cause chronic, local infections in otherwise healthy animals.  The important species that causes  entomophthoromycosis  are  Conidiobolus coronatus ,  C. incongruous , and  Basidiobolus ranarum .   Conidiobolus  infections of the upper respiratory system have been reported in humans, sheep, horses, and dogs, and  Basidiobolus  has been reported less commonly in humans and dogs. [ 8 ]   Horses are one of the most common domestic animals to be affected by entomophthoromycosis.   C. coronatus  causes lesions in the nasal and oral  mucosa  of horses that may cause nasal discharge or difficulty breathing.   B. ranarum  causes large circular nodules on the upper body and neck of horses. [ 9 ]   Entomophthorales  is found in soil and decaying plant matter, and specifically,  Basidiobolus  can be contracted from insects and the feces of reptiles or amphibians. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2922", "text": "Zygomycosis of the sinuses can extend from the sinuses into the orbit and the cranial vault, leading to rhinocerebral mucormycosis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2923", "text": "The best known species of  Lagenidium  is  Lagenidium giganteum , a parasite of  mosquito  larvae used in the  biological control  of mosquitoes.  Two different species cause disease exclusively in dogs:  L. caninum  and  L. karlingii .   Lagenidium  is found in the Southeastern United States in lakes and ponds.  Lagenidiosis causes progressive skin and subcutaneous lesions in the legs, groin, trunk, and near the tail.  The lesions are firm nodules or ulcerated regions with  draining tracts .  Regional lymph nodes are usually swollen.  Spread of the disease to distant lymph nodes, large blood vessels, and the lungs may occur. [ 7 ]   An  aneurysm  of a  great vessel  can rupture and cause sudden death. [ 4 ]   L. caninum  is the more aggressive species and is more likely to spread to other organs than  L. karlingii . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2924", "text": "Diagnosis is through  biopsy  or  culture , although an enzyme-linked immunosorbent assay ( ELISA ) test has been developed for  Pythium insidiosum  in animals. [ 11 ]   Treatment is very difficult and includes  surgery  when possible.  Postoperative recurrence is common.   Antifungal drugs  show only limited effect on the disease, but  itraconazole  and  terbinafine hydrochloride  are often used for 2 to 3 months following surgery. [ 7 ]   Humans with  Basidiobolus  infections have been treated with  amphotericin B  and  potassium iodide . [ 8 ]   For pythiosis and lagenidiosis, a new drug targeting water moulds called  caspofungin  is available, but it is very expensive. [ 7 ]   Immunotherapy  has been used successfully in humans and horses with pythiosis. [ 11 ]   The  prognosis  for any type of phycomycosis is poor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2925", "text": "A  phytobezoar  is a type of  bezoar , or trapped mass in the gastrointestinal system, that consists of components of indigestible plant material, such as fibres, skins and seeds. While phytobezoars may be discovered incidentally on  barium x-ray  or  endoscopic  testing of the stomach, individuals with phytobezoars may develop symptoms: nausea, vomiting,  gastric outlet obstruction , perforation, abdominal pain, and  bleeding  have been reported. [ 1 ]  Conditions that lead to decreased motility in the stomach ( gastroparesis ) and surgeries on the stomach (such as  vagotomy  or  gastric bypass ) are associated with the development of phytobezoars. [ 2 ]   A specific type of phytobezoar, termed a  diospyrobezoar , is associated with ingestion of unripe  persimmons , which contain a soluble  tannin  called shibuol that  polymerizes  into a coagulative cellulose-protein compound in the acid environment of the stomach, to form the bezoar. [ 3 ]   In addition to their presence in human stomachs, phytobezoars have been documented in the stomachs of slaughtered plant-eating animals. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2926", "text": "Gastric phytobezoars are a form of  intestinal blockage  and are seen in those with poor gastric motility. The preferred treatment of bezoars includes different therapies and/or fragmentation to avoid surgery. Phytobezoars are most common and consist of undigested lignin, cellulose,  tannins, celery, pumpkin skin, grape skins, prunes, raisins, vegetables and fruits. [ 4 ]  Phytobezoars can form after eating persimmons and pineapples. These are more difficult to treat and are referred to as diospyrobezoars. [ 5 ]  Phytobezoars are more likely to form due to the ingestion of raw plant foods, even in persons without predisposing factors, as cooking softens them for easier digestion. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2927", "text": "Several treatments for phytobezoars have been described.  Endoscopy  involves using a fibre-optic flexible camera to identify the phytobezoar, that can be evacuated from the stomach using various assisted devices (such as  Roth baskets , snares, or Dormia baskets). [ 1 ] [ 3 ]  If the phytobezoar cannot be removed due to size, electrohydraulic  lithotripsy , mechanical  lithotripsy , snares, or  Nd:YAG laser  therapy may be used to fragment the mass. [ 3 ]   Papain  (meat tenderizer) and  cellulase  enzymes have been used to help reduce the size of phytobezoars. [ 3 ]   Carbonated soda  ingestion has also been found to be useful to decrease the size of diospyrobezoars. [ 3 ] [ 7 ]  A systematic review regarding initial treatment of phytobezoars with  Coca-Cola  found that Coca-Cola alone completely dissolved phytobezoars in half of cases, and that Coca-Cola combined with other endoscopic methods (particularly endoscopic fragmentation) was successful more than 90% of the time. [ 7 ]  The same review found that diospyrobezoars (which are considered more difficult to dissolve because of their hard consistency) were successfully treated with Coca-Cola alone in only 23% of cases, but that follow-up endoscopic fragmentation was successful in 84.6% of cases in the publications reviewed. [ 7 ]  When all other measures have failed, surgical  gastrotomy  is required to evacuate the bezoar. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2928", "text": "Generally, bezoars can be found in the stomach in less than 0.5% of patients having an  esophagogastroduodenoscopy . [ 4 ]  The formation of diospyrobezoars from persimmons is due to a chemical reaction between stomach acid and  phlobatannin  contained in the persimmon. [ 9 ]  Tannin and shibuol found in the skin of unripe persimmons reacts with gastric acid and  forms a coagulum. This structure then accumulates cellulose, hemicellulose and protein. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2929", "text": "In  medicine ,  pink lady  is a term used for a combination of medications used to treat  gastroesophageal reflux  or  gastritis . It usually consists of an  antacid  and the  anaesthetic   lidocaine .  Some variants contain an  anticholinergic .  The name of the preparation comes from its  colour  \u2013  pink ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2930", "text": "Pink ladies often relieve symptoms for  gastro-esophageal reflux disease  (GERD).  However, they are generally believed to be insufficient to  diagnose  GERD and rule-out other causes of  chest pain  and/or  abdominal pain  such as  myocardial infarction  (heart attack). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2931", "text": "The pink lady is the de facto term describing xylocaine viscous and a liquid antacid given  by mouth  to treat  emergency department  patients and help determine if the chest pains are either heart or digestive related.  If esophageal symptoms subside the treatment may indicate the symptoms are non-cardiac. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2932", "text": "Polyposis registries  exists for the purpose of understanding the  genetic disease   familial adenomatous polyposis . [ 1 ]  The registries provide a service to doctors for identification, surveillance and management of families and individuals with high  colorectal cancer  risk from  Familial Adenomatous Polyposis  (FAP) and  Hereditary Non-Polyposis Colorectal Cancer  (HNPCC). The  Centers for Disease Control and Prevention  of the United States provides,  royalty-free ,  Registry Plus  software for collecting and processing cancer registry data compliant with national standards established by  health professionals  and regulators to understand and address the burden of cancer more effectively."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2933", "text": "Polyposis  registries have been used in numerous  academic studies  to assess  morbidity  and  mortality  of  colorectal cancer  related to  FAP , and use of registry data has resulted in improved treatment and reduced mortality from polyposis-related colorectal cancer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2934", "text": "The  University of Texas M. D. Anderson Cancer Center  maintains an international  list of registries  related to  hereditary colon cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2935", "text": "Some of the registries include: -"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2936", "text": "Postpolypectomy coagulation syndrome  ( Postpolypectomy syndrome  or  PPCS ) is a condition that occurs following  colonoscopy  with  electrocautery   polypectomy , which results in a burn injury to the wall of the  gastrointestinal tract . The condition results in  abdominal pain ,  fever ,  elevated white blood cell count  and elevated serum  C-reactive protein ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2937", "text": "PPCS causes abdominal pain and fever. [ 3 ]  The condition usually onsets within 1\u20135 days after colonoscopy with polypectomy using electrocautery. [ 3 ]  Physical examination may show evidence of peritonitis. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2938", "text": "PPCS is caused by an electrocautery-induced injury to the wall of the colon that occurs during removal of colon polyps. [ 3 ]  PPCS occurs when the electric current extends beyond the mucosa, entering the muscularis propria and serosa, resulting in a full thickness (transmural) burn injury. [ 1 ]  The transmural burn results in localized inflammation of the peritoneum (peritonitis). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2939", "text": "PPCS may resemble perforation. Recognition of PPCS is important, since treatment usually does not require surgery, unlike gastrointestinal perforation. Laboratory studies may show elevated white blood cell count ( leukocytosis ) and elevated inflammatory markers such as  C-reactive protein . CT scan of the abdomen may show severe mural thickening, without air present outside the gastrointestinal tract. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2940", "text": "Treatment of PPCS consists of intravenous fluids, antibiotics, and avoiding any oral intake of food, water, etc. until symptoms improve. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2941", "text": "Some low quality evidence suggests that antibiotic prophylaxis may prevent PPCS. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2942", "text": "PPCS occurs about 1% of cases following polypectomy with electrocautery. [ 5 ] [ 1 ]  Risk factors for PPCS include right colon polypectomy, large polyp size (>2\u00a0cm), non-polypoid lesions (laterally spreading lesions), and hypertension. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2943", "text": "Proton-pump inhibitors  ( PPIs ) are a class of  medications  that cause a profound and prolonged reduction of  stomach acid  production. They do so by irreversibly inhibiting the stomach's  H + /K +  ATPase   proton pump . [ 1 ]  The body eventually synthesizes new proton pumps to replace the irreversibly inhibited ones, a process driven by normal cellular turnover, which gradually restores acid production. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2944", "text": "Proton-pump inhibitors have largely superseded the  H 2 -receptor antagonists , a group of medications with similar effects but a different mode of action, and heavy use of  antacids . [ 3 ]  A  potassium-competitive acid blocker  (PCAB)  revaprazan  was marketed in Korea as an alternative to a PPI. A newer PCAB  vonoprazan  with a faster and longer lasting action than revaprazan, and PPIs has been marketed in Japan (2013), Russia (2021), and the US (2023). [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2945", "text": "PPIs are among the most widely sold medications in the world. The class of proton-pump inhibitor medications is on the  World Health Organization's List of Essential Medicines . [ 7 ] [ 8 ]   Omeprazole  is the specific listed example. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2946", "text": "These medications are used in the treatment of many conditions, such as:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2947", "text": "Specialty professional organizations recommend that people take the lowest effective PPI dose to achieve the desired therapeutic result when used to treat gastroesophageal reflux disease long-term. [ 20 ] [ 21 ] [ 22 ]  In the United States, the  Food and Drug Administration  (FDA) has advised that over-the-counter PPIs, such as Prilosec OTC, should be used no more than three 14-day treatment courses over one year. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2948", "text": "Despite their extensive use, the quality of the evidence supporting their use in some of these conditions is variable. The effectiveness of PPIs has not been demonstrated for every case. For example, although they reduce the incidence of  esophageal adenocarcinoma  in Barrett's oesophagus, [ 16 ]  they do not change the length affected. [ 25 ]  In addition, research in the UK has suggested that PPIs are not effective at treating persistent throat symptoms. [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2949", "text": "PPIs are often used longer than necessary. In about half of people who are hospitalized or seen at a primary care clinic there is no documented reason for their long-term use of PPIs. [ 28 ]  Some researchers believe that, given the little evidence of long-term effectiveness, the cost of the medication and the potential for harm means that clinicians should consider stopping PPIs in many people. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2950", "text": "In general, proton pump inhibitors are well tolerated, and the incidence of short-term adverse effects is relatively low. The range and occurrence of  adverse effects  are similar for all of the PPIs, though they have been reported more frequently with  omeprazole . This may be due to its longer availability and, hence, clinical experience. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2951", "text": "Common adverse effects include  headache ,  nausea ,  diarrhea ,  abdominal pain ,  fatigue , and  dizziness . [ 30 ]  Infrequent adverse effects include  rash ,  itch ,  flatulence ,  constipation ,  anxiety , and  depression . Also infrequently, PPI use may be associated with occurrence of  myopathies , including the serious reaction  rhabdomyolysis . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2952", "text": "Long-term use of PPIs requires assessment of the balance of the  benefits and risks  of the therapy. [ 32 ] [ 33 ] [ 34 ] [ 35 ]  As of March 2017, various adverse outcomes have been associated with long-term PPI use in several primary reports, but reviews assess the overall quality of evidence in these studies as \"low\" or \"very low\". [ 34 ]   They describe inadequate evidence to establish  causal relationships  between PPI therapy and many of the proposed associations, due to study design and small estimates of effect size. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2953", "text": "As of March 2017, benefits outweighed risks when PPIs are used appropriately, but when used inappropriately, modest risks become important. [ 34 ] [ 36 ]  They recommend that PPIs should be used at the lowest effective dose in people with a proven indication, but discourage dose escalation and continued chronic therapy in people unresponsive to initial empiric therapy. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2954", "text": "With regard to iron and vitamin B 12 , the data is weak and several  confounding factors  have been identified. [ 33 ]   Low levels of magnesium  can be found in people on PPI therapy and these can be reversed when they are switched to  H 2 -receptor antagonist  medications. [ 33 ] [ 37 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2955", "text": "High dose or long-term use of PPIs carries an increased risk of  bone fractures  which was not found with short-term, low dose use; the FDA included a warning regarding this on PPI drug labels in 2010. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2956", "text": "In infants, acid suppression therapy is frequently prescribed to treat symptomatic gastroesophageal reflux in otherwise healthy infants (that is: without gastroesophageal reflux disease). A study from 2019 showed that  PPI use alone and together with histamine H2-receptor antagonists was associated with an increased bone fracture hazard, which was amplified by days of use and earlier initiation of therapy. [ 38 ]  The reason is not clear; increased bone break down by  osteoclasts  has been suggested. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2957", "text": "A recent 2024 study published in the  Journal of Clinical Endocrinology & Metabolism  found that chronic use of PPIs in men is linked to lower trabecular bone quality. [ 40 ]  Specifically, PPI use was associated with reduced lumbar spine trabecular bone score (TBS), as well as lower bone mineral density (BMD) T-scores in the lumbar spine, total hip, and femoral neck. [ 41 ]  These findings suggest that long-term PPI use may negatively affect bone health in men."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2958", "text": "Some studies have shown a correlation between use of PPIs and  Clostridioides difficile  infection . While the data are contradictory and controversial, the FDA had sufficient concern to include a warning about this adverse effect on the label of PPI medications. [ 33 ]  Concerns have also been raised about  spontaneous bacterial peritonitis  (SBP) in older people taking PPIs and in people with  irritable bowel syndrome  taking PPIs; both types of infections arise in these populations due to underlying conditions and it is not clear if this is a class effect of PPIs. [ 33 ]  PPIs may predispose an individual to developing   small intestinal bacterial overgrowth  or fungal overgrowth. [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2959", "text": "In  cirrhotic patients , large volume of ascites and reduced esophageal motility by varices can provoke  GERD . [ 44 ] [ 45 ] [ 46 ]  Acidic irritation, in return, may induce the rupture of varices. [ 47 ]  Therefore, PPIs are often routinely prescribed for cirrhotic patients to treat GERD and prevent variceal bleeding. However, it has been recently shown that long term use of PPIs in patients with  cirrhosis  increases the risk of SBP and is associated with the development of clinical decompensation and liver-related death during long-term follow-up. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2960", "text": "There is evidence that PPI use alters the composition of the bacterial populations inhabiting the  gut , the  gut microbiota . [ 49 ]  Although the mechanisms by which PPIs cause these changes are yet to be determined, they may have a role in the increased risk of bacterial infections with PPI use. [ 50 ]  These infections can include  Helicobacter pylori  due to this species not favouring an acid environment, leading to an increased risk of ulcers and gastric cancer risk in genetically susceptible patients. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2961", "text": "PPI use in people who have received attempted  H. pylori  eradication may also be associated with an increased risk of gastric cancer. [ 51 ]  The validity and robustness of this finding, with the lack of causality, have led to this association being questioned. [ 52 ]   It is recommended that long-term PPIs should be used judiciously after considering individual's risk\u2013benefit profile, particularly among those with history of  H. pylori  infection, and that further, well-designed, prospective studies are needed. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2962", "text": "Long-term use of PPIs is associated with the development of benign  polyps  from  fundic glands  (which is distinct from  fundic gland polyposis ); these polyps do not cause cancer and resolve when PPIs are discontinued. [ 33 ]  There is concern that use of PPIs may mask  gastric  cancers or other serious gastric problems. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2963", "text": "PPI use has also been associated with the development of  microscopic colitis . [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2964", "text": "Associations of PPI use and cardiovascular events have also been widely studied but clear conclusions have not been made as these relative risks are confounded by other factors. [ 55 ] [ 56 ]  PPIs are commonly used in people with cardiovascular disease for gastric protection when  aspirin  is given for its antiplatelet actions. [ 55 ] [ 57 ]  An interaction between PPIs and the metabolism of the platelet inhibitor  clopidogrel  is known and this drug is also often used in people with cardiac disease. [ 58 ] [ 59 ] [ 22 ]  There are associations with an increased risk of stroke, but this appears to be more likely to occur in people who already have an elevated risk. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2965", "text": "One suggested mechanism for cardiovascular effects is because PPIs bind and inhibit  dimethylargininase , the enzyme that degrades  asymmetric dimethylarginine  (ADMA), resulting in higher ADMA levels and a decrease in bioavailable  nitric oxide . [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2966", "text": "A 2022 umbrella review of 21 meta-analyses shows an association between proton-pump inhibitor use and an increased risk of four types of cancer. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2967", "text": "Associations have been shown between PPI use and an increased risk of pneumonia, particularly in the 30 days after starting therapy, where it was found to be 50% higher in community use. [ 63 ] [ 64 ]  Other very weak associations of PPI use have been found, such as with  chronic kidney disease , [ 65 ] [ 66 ] [ 67 ] [ 22 ] [ 68 ] [ 69 ]   dementia [ 70 ] [ 34 ] [ 71 ]  and  Hepatocellular carcinoma  (HCC). [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2968", "text": "As of 2016, results were derived from observational studies, it remained uncertain whether such associations were causal relationships. [ 34 ] [ 35 ] [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2969", "text": "Proton pump  inhibitors act by irreversibly blocking the  hydrogen / potassium   adenosine triphosphatase   enzyme  system (the  H + /K +  ATPase , or, more commonly, the gastric proton pump) of the gastric  parietal cells . [ 74 ]  The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H +  ions into the gastric lumen, making it an ideal target for inhibiting acid secretion. [ citation needed ]  Because the H,K-ATPase is the final step of acid secretion, an inhibitor of this enzyme is more effective than receptor antagonists in suppressing gastric acid secretion. [ 75 ]  All of these drugs inhibit the gastric H,K-ATPase by covalent binding, so the duration of their effect is longer than expected from their levels in the blood. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2970", "text": "Targeting the terminal step in acid production, as well as the  irreversible  nature of the inhibition, results in a class of medications that are significantly more effective than  H 2  antagonists  and reduce gastric acid secretion by up to 99%. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2971", "text": "Decreasing the acid in the stomach can aid the healing of  duodenal  ulcers and reduce the pain from indigestion and  heartburn . However,  stomach acids  are needed to digest proteins, vitamin B 12 , calcium, and other nutrients, and too little stomach acid causes the condition  hypochlorhydria . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2972", "text": "The PPIs are given in an inactive form, which is neutrally charged ( lipophilic ) and readily crosses  cell membranes  into intracellular compartments (like the parietal cell canaliculus) with acidic environments. In an acid environment, the inactive drug is protonated and rearranges into its active form. As described above, the active form will  covalently  and irreversibly bind to the gastric proton pump, deactivating it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2973", "text": "In  H. pylori  eradication , PPIs help by increasing the stomach pH, causing the bacterium to shift out of its coccoid form which is resistant to both acids and antibiotics. PPIs also show some weaker additional effects in eradication. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2974", "text": "The rate of omeprazole absorption is decreased by concomitant food intake. [ 79 ]  In addition, the absorption of lansoprazole and esomeprazole is decreased and delayed by food. It has been reported, however, that these  pharmacokinetic  effects have no significant impact on efficacy. [ 80 ] [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2975", "text": "In healthy humans, the half-life of PPIs is about 1 hour (9 hours for  tenatoprazole ), but the duration of acid inhibition is 48 hours because of irreversible binding to the H,K-ATPase. [ 82 ]  All the PPIs except tenatoprazole are rapidly metabolized in the liver by CYP enzymes (mostly by CYP2C19 and 3A4). [ 82 ]  Dissociation of the inhibitory  complex  is probably due to the effect of the  endogenous   antioxidant   glutathione  which leads to the release of omeprazole sulfide and reactivation of the enzyme. [ 83 ] [ 84 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2976", "text": "Medically used proton pump inhibitors: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2977", "text": "There is no clear evidence that one proton pump inhibitor works better than another. [ 1 ] [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2978", "text": "PPIs were developed in the 1980s, with omeprazole being launched in 1988. Most of these medications are  benzimidazole  derivatives, related to omeprazole, but  imidazopyridine  derivatives such as  tenatoprazole  have also been developed. [ 77 ]  Potassium-competitive inhibitors such as  revaprazan  reversibly block the potassium-binding site of the proton pump, acting more quickly, but are not available in most countries. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2979", "text": "In  British Columbia, Canada  the cost of the PPIs varies significantly from  CA$0.13  to  CA$2.38  per dose [ 91 ]  while all agents in the class appear more or less equally effective. [ 1 ] [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2980", "text": "A comparative table of  FDA -approved indications for PPIs is shown below."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2981", "text": "Gastric acid is important for breakdown of food and release of  micronutrients , and some studies have shown possibilities for interference with absorption of  iron ,  calcium ,  magnesium , and  vitamin B 12 .<ref name=\"pmid20882439\"> Ito T, Jensen RT (December 2010).  \"Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium\" .  Current Gastroenterology Reports .  12  (6):  448\u2013 57.  doi : 10.1007/s11894-010-0141-0 .  PMC \u00a0 2974811 .  PMID \u00a0 20882439 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2982", "text": "Pseudopolyps  are projecting masses of  scar tissue  that develop from  granulation tissue  during the  healing  phase in repeated cycle of  ulceration  (especially in  inflammatory bowel disease ).  Inflammatory   tissue  without  malignant  potential, [ 1 ]  pseudopolyps may represent either regenerating mucosal islands between areas of ulceration, edematous polypoid tags or granulation tissue covered by epithelium. [ 2 ]  There are reported cases when localized giant pseudopolyposis resulted in intestinal obstruction. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2983", "text": "Residual mucosal islands between ulcerated and denuded areas of mucosa may have a polypoid appearance and are referred to as pseudopolyps. [ 4 ]  Polyposis syndromes, such as  familial adenomatous polyposis , could give rise to a similar appearance on  imaging , although the  clinical presentation  would differ from that of inflammatory pseudopolyposis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2984", "text": "Numerous, confluent ulcerations with bulging of the edematous residual mucosa determine a  cobblestone  appearance at endoscopy. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2985", "text": "A  rectal  or  anal dilator  is a medical device similar to a  speculum  designed to open and relax the  internal / external anal sphincter  and  rectum  in order to facilitate  medical inspection  or relieve  constipation . [ 1 ]  One early version of a rectal dilator was  Dr. Young's Ideal Rectal Dilators , invented in 1892. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2986", "text": "Rectal dilators are also used as  sex toys . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2987", "text": "Rectal discharge  is intermittent or continuous expression of liquid from the anus ( per rectum ). Normal rectal mucus is needed for proper excretion of waste. Otherwise, this is closely related to types of  fecal incontinence  (e.g., fecal leakage) but the term rectal discharge does not necessarily imply degrees of incontinence. Types of fecal incontinence that produce a liquid leakage could be thought of as a type of rectal discharge."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2988", "text": "Different types of discharge are described. Generally \"rectal discharge\" refers to either a mucous or  purulent  discharge, but, depending upon what definition of rectal discharge is used, the following could be included:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2989", "text": "There are many different types of rectal discharge, but the most common presentation of a discharge is passage of mucus or pus wrapped around an otherwise normal bowel movement. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2990", "text": "Rectal discharge has many causes, and may present with other symptoms: [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2991", "text": "Pus  usually indicates  infection . Frequently medical sources do not differentiate between the two types of discharge, instead using the general term  mucopurulent discharge , which, strictly speaking, should only be used to refer to a discharge that contains both mucus and pus. Purulent discharges may be blood-streaked. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2992", "text": "Mucus  coats the walls of the  colon  in health, functioning as a protective barrier and also to aid  peristalsis  by  lubrication  of  stool . Mucous discharges can be thought of in three broad categories:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2993", "text": "A mucous rectal discharge may be blood-streaked. With some conditions, the blood can be homogenously mixed with the mucus, creating a pink goo. An example of this could be the so-called \"red currant jelly\" stools in  intussusception . This appearance refers to the mixture of sloughed  mucosa , mucus, and blood. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2994", "text": "Note : \"mucus\" is a noun, used to name the substance itself, and \"mucous\" is an adjective, used to describe a discharge. \"Mucoid\" is also an adjective and means mucus-like. \"Mucinous\" strictly speaking refers to something having a  mucin -like attribute, but it often is used interchangeably with the word \"mucous\" (as mucus usually contains a high percentage of mucin)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2995", "text": "The differential diagnosis of rectal discharge is extensive,  but the general  etiological  themes are  infection  and  inflammation . [ 11 ]   Some lesions can cause a discharge by mechanically interfering with, or preventing the complete closure of, the  anal canal . This type of lesion may not cause discharge intrinsically, but instead, allow transit of liquid stool components and mucus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2996", "text": "Perianal  Crohn's disease  is associated with fistulizing, fissuring and perianal abscess formation. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2997", "text": "After  colostomy , the distal section of bowel continues to produce mucus despite fecal diversion, often resulting in mucinous discharge. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2998", "text": "Occasionally,  intestinal parasitic  infection can present with discharge, for example  whipworm . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_2999", "text": "Several pathologies can present with perianal discharge. Although not exactly the same as rectal discharge, perianal discharge can be misinterpreted as such, given the anatomical proximity. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3000", "text": "Fistulae  draining into the perianal region, as well as  pilonidal diseases , are the main entities that fall within this category. Perianal tumours can also discharge when they fungate or otherwise become cystic or necrotic. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3001", "text": "Proctitis is inflammation of the lining of the rectum [ 21 ]  including the  distal  15\u00a0cm (6\u00a0in) of the rectum. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3002", "text": "Proctitis  has many causes. Common infection causes include: sexual intercourse with someone who has a sexually transmitted disease (STD), infection from a foodborne illness, and strep throat (in children). [ 22 ]   Proctitis may also be caused by some types of inflammatory bowel disease, radiation therapy, injury to the rectum or anus, or some types of antibiotic. [ 22 ] [ clarification needed ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3003", "text": "Tuberculosis  proctitis can create a mucous discharge. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3004", "text": "Anal warts are irregular, verrucous lesions caused by  human papilloma virus . Anal warts are usually transmitted by unprotected,  anoreceptive intercourse .  Anal warts may be asymptomatic, [ 24 ]  or may cause rectal discharge, anal wetness,  rectal bleeding , and  pruritus ani . [ 14 ]  Lesions can also occur within the anal canal, where they are more likely to create symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3005", "text": "The bacterium  Chlamydia trachomatis  can cause 2 conditions in humans; viz.  trachoma  and  lymphogranuloma venereum . Trachoma can cause an asymptomatic  proctitis , but the symptoms of lymphogranuloma venereum are usually more severe, including  pruritus ani , purulent rectal\ndischarge,  hematochezia   rectal pain  and  diarrhea  or  constipation . [ 14 ] [ 24 ]  Lymphogranuloma venereum can cause  fistulas ,  strictures  and  anorectal abscesses  if left untreated. Hence, it can be confused with Crohn's disease. [ 25 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3006", "text": "Rectal gonorrhea is caused by  Neisseria gonorrhoeae . [ 24 ]  The condition is usually asymptomatic, but symptoms can include rectal discharge (which can be creamy, purulent or bloody),  pruritus ani ,  tenesmus , and possibly  constipation . When symptomatic, these usually appear 5\u20137 days post-exposure. [ 14 ]  Discharge is the most common symptom, and it is usually a brownish mucopurulent consistency. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3007", "text": "Anorectal syphilis is caused by  Treponema pallidum  and is contracted through anoreceptive intercourse. Symptoms are usually minimal, but mucous discharge, bleeding, and  tenesmus  may be present. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3008", "text": "When the fecal stream is diverted as part of a  colostomy , a condition called  diversion colitis  may develop in the section of bowel that no longer is in contact with stool. The mucosal lining is nourished by short-chain fatty acids, which are produced as a result of bacterial fermentation in the gut. Long-term lack of exposure to these nutrients can cause inflammation of the colon (colitis). [ 28 ]  Symptoms include  rectal bleeding , mucous discharge,  tenesmus , and  abdominal pain . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3009", "text": "Anal carcinoma is much less common than  colorectal cancer . The most common form is  squamous cell carcinoma , followed by  adenocarcinoma  and  melanoma . [ 29 ]  SCC usually occurs in the anal canal, and more rarely on the anal margin. Anal margin SCC presents as a lesion with rolled, everted edges and central ulceration. [ 27 ]  Symptoms include a painful lump, bleeding,  pruritus ani ,  tenesmus , discharge or possibly  fecal incontinence . SSC in the anal canal most commonly causes bleeding, but may also cause anal pain, a lump,  pruritus ani , discharge,  tenesmus , change in bowel habits and  fecal incontinence . Because these symptoms are so unspecific, and because symptoms of anal carcinoma may not always be typical, this can lead to delays in diagnosis. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3010", "text": "Rare neoplasms at this site that can give rise to discharge include Paget's disease (which is possibly a type of adenocarcinoma) and verrucous carcinoma. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3011", "text": "Adenoma  is the most common colorectal  polyp . Adenomas are not malignant, but rarely  adenocarcinoma  can develop from them. Large adenomas can cause  rectal bleeding , mucus discharge,  tenesmus , and a sensation of urgency. Mucus production may be so great that it can cause  electrolyte  disturbances in the blood. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3012", "text": "Juvenile polyps  may cause rectal discharge."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3013", "text": "The  Rome process and Rome criteria  are an international effort to create scientific data to help in the  diagnosis  and treatment of  functional gastrointestinal disorders , such as  irritable bowel syndrome ,  functional dyspepsia  and  rumination syndrome . The Rome diagnostic criteria are set forth by  Rome Foundation , a  not for profit  501(c)(3) organization based in  Raleigh, North Carolina , United States."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3014", "text": "Several systematic approaches attempted to classify  functional gastrointestinal disorders  (FGIDs). As a result, there were several key events which ultimately led to the current Rome Classification. In 1962, Chaudhary and Truelove published their study of IBS patients in Oxford, England. This was the first attempt to classify the new field of functional gastrointestinal disorders. Much of what they reported has persisted to the present day. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3015", "text": "Subsequently, in 1978 came the \"Manning Criteria\" developed by  Kenneth Heaton  and colleagues in Bristol. This characterized IBS-D (IBS with predominant diarrhea), but importantly, a cluster of symptoms which were characteristic for this disorder. This ultimately became the basis for Rome's symptom-based criteria for IBS. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3016", "text": "From 1980 to 1994, there were several epidemiological and clinical studies evaluating symptom prevalence and frequency in healthy subjects and IBS patients. Thompson, Drossman, Talley, Whitehead, and Kruis. [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] \nIn 1989, the first consensus-based diagnostic criteria for IBS were established. [ 3 ] [ 10 ]  The following year, a classification system for FGIDs was established. [ 3 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3017", "text": "From 1991 to 1993, several working teams (esophagus, gastroduodenal, bowel, biliary, anorectal) published symptom-based criteria and clinical features of the functional GI disorders within these anatomic domains in  Gastroenterology International . [ 3 ] [ 12 ] [ 13 ] [ 14 ] [ 15 ] [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3018", "text": "In 1993, a validated questionnaire of all the diagnostic criteria was created and was then applied in a national survey, the US Householder Survey: the first national epidemiological database on the prevalence, demographic factors, and health care seeking features of people with FGIDs. [ 3 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3019", "text": "In 1994, FGIDs were categorized into anatomical domains and resulted in a book now recognized as Rome I \u2013  The Functional Gastrointestinal Disorders: Diagnosis, Pathophysiology and Treatment \u2013 A Multinational Consensus . [ 3 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3020", "text": "The Rome criteria have been evolving from the first set of criteria issued in 1989 (The Rome Guidelines for IBS) through the Rome Classification System for functional gastrointestinal disorders (1990), or Rome-1, the Rome I Criteria for IBS (1992) and the functional gastrointestinal disorders (1994), the Rome II Criteria for IBS (1999) and the functional gastrointestinal disorders (1999) to the Rome III Criteria (2006). \"Rome II\" and \"Rome III\" incorporated  pediatric  criteria to the consensus.\nThe Rome IV update was published 10 years later in May 2016. [ 20 ]   This covers epidemiology, pathophysiology, psychosocial and clinical features, and diagnostic evaluation and treatment recommendations for 33 adult and 17 pediatric functional gastrointestinal disorders. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3021", "text": "The Rome criteria are achieved and finally issued through a  consensual process , using the  Delphi method  (or Delphi technique). The Rome Foundation process is an international effort to create scientific data to help in the diagnosis and treatment of functional gastrointestinal disorders, also known as disorders of gut-brain interaction. [ 22 ]   The Rome Diagnostic criteria are set forth by the Rome Foundation, an independent, not for profit 501(c)(3) organization. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3022", "text": "The Rome Foundation, incorporated in 1996 and based in Raleigh, North Carolina, is an independent not for profit 501(c) 3 organization. The foundation provides support for activities which foster clinical research, data and educational information which aid in the diagnosis and treatment of functional gastrointestinal disorders. [ 22 ] [ 23 ] [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3023", "text": "Over the last 25 years, the Rome organization has sought to legitimize and update the knowledge of functional GI disorders. This has been accomplished by bringing together scientists and clinicians from around the world to classify and critically appraise the science of gastrointestinal function and dysfunction. This knowledge permits clinical scientists to make recommendations for diagnosis and treatment that can be applied in research and clinical practice. The mission is to improve the lives of people with these disorders. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3024", "text": "The goals of the Rome Foundation are to promote global recognition and legitimization of FGIDs, advance the scientific understanding of their pathophysiology, optimize clinical management for these patients and develop and provide educational resources to accomplish these goals. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3025", "text": "Using the Delphi method, the Rome Foundation and its board of directors, chairs and co-chairs of the ROME IV committees developed the current definition for disorders of gut-brain interaction. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3026", "text": "A group of disorders classified by GI symptoms related to any combination of: [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3027", "text": "In 1994, Rome I was published as The Functional Gastrointestinal Disorders:Diagnosis, Pathophysiology, and Treatment\u2014A Multinational Consensus. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3028", "text": "By the mid-1990s, the concept of FGID classification and the use of diagnostic criteria was promoted due to the US Food and Drug Administration (FDA) recommended the use of the IBS criteria for selection into pharmaceutical studies, and the pharmaceutical companies took interest in supporting the efforts of the Rome Foundation to improve the understanding, diagnosis, and treatment of FGIDs and to also apply the use of these criteria in their pharmaceutical studies. In Rome II, the pediatric population of FGIDs was added."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3029", "text": "After publication of Rome II, the number of studies published using the Rome criteria in clinical trials grew tremendously over the next 15 years. Rome III differed from Rome I and II by the use of more evidence-based rather than consensus-based data."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3030", "text": "After publication of Rome III in 2006, the Rome Foundation was well recognized as the authoritative body developing diagnostic criteria for research and also for providing education about the FGIDs. Rome IV tried to address the limitations of a symptom-based criteria in several ways:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3031", "text": "In Rome IV, the classification moved from a physiologically based classification to a symptom-based classification. The classifications were based upon organ regions (i.e. esophageal, gastroduodenal, bowel, biliary, anorectal)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3032", "text": "The original Rome classification was first published in 1990 and has since been modified with each iteration to develop the subsequent classifications with Rome II, III and IV. Beginning with the original publication in 1990 and leading to Rome I, the classification moved from a physiologically based classification to a symptom-based classification with additional classifications based upon organ regions (i.e. esophageal, gastroduodenal, bowel, biliary, anorectal). [ 22 ]  The current Rome IV classification [ 22 ]  is the culmination of the evolution of a series of iterations (Rome I, [ 19 ]  Rome II, [ 27 ]  and Rome III [ 28 ] ) with its inception as Rome I. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3033", "text": "The Rome criteria are a set of criteria used by clinicians to classify a diagnosis of a patient with an FGID (disorder of gut-brain interaction). These Rome criteria are updated every 6\u201310 years. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3034", "text": "The current Rome IV classification, published in 2016, is as follows: [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3035", "text": "A. Esophageal Disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3036", "text": "B. Gastroduodenal Disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3037", "text": "C. Bowel Disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3038", "text": "D. Centrally Mediated Disorders of Gastrointestinal Pain"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3039", "text": "E. Gallbladder and Sphincter of Oddi disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3040", "text": "F. Anorectal Disorders"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3041", "text": "G. Childhood Functional GI Disorders: Neonate/Toddler"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3042", "text": "H. Childhood Functional GI Disorders: Child/Adolescent"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3043", "text": "As a non-profit organization the Rome Foundation has a number of industry sponsors who provide financial support. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3044", "text": "Rotaviruses  are the most common cause of  diarrhoeal disease  among infants and young children. [ 1 ]  Nearly every child in the world is infected with a rotavirus at least once by the age of five. [ 2 ]   Immunity  develops with each infection, so subsequent infections are less severe. Adults are rarely affected. [ 3 ]   Rotavirus  is a  genus  of  double-stranded RNA viruses  in the  family   Reoviridae . There are nine  species  of the genus, referred to as A, B, C, D, F, G, H, I and J.  Rotavirus A  is the most common species, and these rotaviruses cause more than 90% of rotavirus infections in humans. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3045", "text": "The virus is transmitted by the  faecal\u2013oral route . It infects and damages the  cells  that line the  small intestine  and causes  gastroenteritis  (which is often called \"stomach flu\" despite having no relation to  influenza ). Although rotavirus was discovered in 1973 by  Ruth Bishop  and her colleagues by electron micrograph images [ 5 ]  and accounts for approximately one third of hospitalisations for severe diarrhoea in infants and children, [ 6 ]  its importance has historically been underestimated within the  public health  community, particularly in  developing countries . [ 7 ]  In addition to its impact on human health, rotavirus also infects other animals, and is a  pathogen  of livestock. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3046", "text": "Rotaviral enteritis is usually an easily managed disease of childhood, but among children under 5 years of age rotavirus caused an estimated 151,714 deaths from diarrhoea in 2019. [ 9 ]  In the United States, before initiation of the  rotavirus vaccination  programme in the 2000s, rotavirus caused about 2.7 \u00a0 million cases of severe gastroenteritis in children, almost 60,000 hospitalisations, and around 37 deaths each year. [ 10 ]  Following rotavirus vaccine introduction in the United States, hospitalisation rates have fallen significantly. [ 11 ] [ 12 ]  Public health campaigns to combat rotavirus focus on providing  oral rehydration therapy  for infected children and  vaccination  to prevent the disease. [ 13 ]  The incidence and severity of rotavirus infections has declined significantly in countries that have added rotavirus vaccine to their routine childhood  immunisation policies . [ 14 ] [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3047", "text": "There are nine species of rotavirus (sometimes informally called  groups ) referred to as A, B, C, D, F, G, H, I and J. [ 17 ] [ 18 ]  Humans are primarily infected by rotaviruses in the species  Rotavirus A . A\u2013I species cause disease in other animals, [ 19 ]  species H in pigs, D, F and G in birds, I in cats and J in bats. [ 20 ] [ 21 ] [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3048", "text": "Within group A  rotaviruses there are different strains, called  serotypes . [ 24 ]  As with  influenza  virus, a dual classification system is used based on two proteins on the surface of the virus. The  glycoprotein  VP7 defines the G serotypes and the  protease -sensitive protein VP4 defines P serotypes. [ 25 ]  Because the two genes that determine G-types and P-types can be passed on separately to progeny viruses, different combinations are found. [ 25 ]  A whole genome genotyping system has been established for group A rotaviruses, which has been used to determine the origin of atypical strains. [ 26 ]  The prevalence of the individual G-types and P-types varies between, and within, countries and years. [ 27 ]  There are at least 36 G types and 51 P types [ 28 ]  but in infections of humans only a few combinations of G and P types predominate. They are G1P[8], G2P[4], G3P[8], G4P[8], G9P[8] and G12P[8]. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3049", "text": "The  genome  of rotaviruses consists of 11 unique double helix molecules of  RNA  (dsRNA) which are 18,555 nucleotides in total. Each helix, or segment, is a  gene , numbered 1 to 11 by decreasing size. Each gene codes for one  protein , except genes 9, which codes for two. [ 30 ]  The RNA is surrounded by a three-layered  icosahedral  protein  capsid . Viral particles are up to 76.5 \u00a0 nm in diameter [ 31 ] [ 32 ]  and are not  enveloped . [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3050", "text": "There are six viral proteins (VPs) that form the virus particle ( virion ). These  structural  proteins are called VP1, VP2, VP3, VP4, VP6 and VP7. In addition to the VPs, there are six  nonstructural  proteins  (NSPs), that are only produced in cells infected by rotavirus. These are called  NSP1 ,  NSP2 ,  NSP3 ,  NSP4 ,  NSP5  and  NSP6 . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3051", "text": "At least six of the twelve proteins  encoded  by the rotavirus genome bind  RNA . [ 35 ]  The role of these proteins in rotavirus replication is not entirely understood; their functions are thought to be related to RNA synthesis and packaging in the virion, mRNA transport to the site of genome replication, and  mRNA  translation and regulation of gene expression. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3052", "text": "VP1 is located in the core of the virus particle and is an  RNA-dependent RNA polymerase   enzyme . [ 37 ]  In an infected cell this enzyme produces mRNA transcripts for the synthesis of viral proteins and produces copies of the rotavirus genome RNA segments for newly produced virus particles. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3053", "text": "VP2 forms the core layer of the virion and binds the RNA genome. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3054", "text": "VP3 is part of the inner core of the virion and is an enzyme called  guanylyl transferase . This is a  capping enzyme  that catalyses the formation of the  5' cap  in the  post-transcriptional modification  of mRNA. [ 40 ]  The cap stabilises viral mRNA by protecting it from  nucleic acid  degrading enzymes called  nucleases . [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3055", "text": "VP4 is on the surface of the virion that protrudes as a spike. [ 42 ]  It binds to molecules on the surface of cells called  receptors  and drives the entry of the virus into the cell. [ 43 ]  VP4 has to be modified by the  protease  enzyme  trypsin , which is found in the gut, into VP5* and VP8* before the virus is infectious. [ 44 ]  VP4 determines how  virulent  the virus is and it determines the P-type of the virus. [ 45 ]  In humans there is an association between the  blood group  ( Lewis antigen system ,  ABO blood group system  and  secretor status ) and susceptibility to infection. Non-secretors seem resistant to infection by types P[4] and P[8], indicating that blood group antigens are the receptors for these genotypes. [ 46 ]  This resistance is dependent on the rotavirus genotype. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3056", "text": "VP6 forms the bulk of the capsid. It is highly  antigenic  and can be used to identify rotavirus species. [ 48 ]  This protein is used in laboratory tests for rotavirus infections. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3057", "text": "VP7 is a  glycoprotein  that forms the outer surface of the virion. Apart from its structural functions, it determines the G-type of the strain and, along with VP4, is involved in  immunity  to infection. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3058", "text": "NSP1, the product of gene 5, is a  nonstructural  RNA-binding protein. [ 50 ]  NSP1 also blocks the  interferon  response, the part of the  innate immune system  that protects cells from viral infection. NSP1 causes the  proteosome  to degrade key signaling components required to stimulate production of interferon in an infected cell and to respond to interferon secreted by adjacent cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3059", "text": "Targets for degradation include several  IRF  transcription factors required for interferon gene transcription. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3060", "text": "NSP2 is an  RNA-binding protein  that accumulates in cytoplasmic inclusions ( viroplasms ) and is required for genome replication. [ 52 ] [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3061", "text": "NSP3 is bound to viral mRNAs in infected cells and it is responsible for the shutdown of cellular protein synthesis. [ 53 ]  NSP3 inactivates two translation initiation factors essential for synthesis of proteins from host mRNA."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3062", "text": "First, NSP3 ejects  poly(A)-binding protein  (PABP) from the translation initiation factor  eIF4F .  PABP is required for efficient translation of transcripts with a 3'  poly(A) tail , which is found on most host cell transcripts. Second, NSP3 inactivates  eIF2  by stimulating its phosphorylation. [ 54 ]  Efficient translation of rotavirus mRNA, which lacks the 3' poly(A) tail, does not require either of these factors. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3063", "text": "NSP4 is a viral  enterotoxin  that induces diarrhoea and was the first viral enterotoxin discovered. [ 56 ]  It is a  viroporin  that elevates cytosolic Ca 2+  in mammalian cells. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3064", "text": "NSP5 is encoded by genome segment 11 of rotavirus A. In virus-infected cells NSP5 accumulates in the viroplasm. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3065", "text": "NSP6 is a nucleic acid binding protein [ 59 ]  and is encoded by gene 11 from an out-of-phase  open reading frame . [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3066", "text": "This table is based on the  simian  rotavirus strain SA11. RNA-protein coding assignments differ in some strains."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3067", "text": "The attachment of the virus to the host cell is initiated by VP4, which attaches to molecules, called  glycans , on the surface of the cell. [ 33 ]  The virus enters cells by  receptor mediated endocytosis  and form a  vesicle  known as an  endosome . Proteins in the third layer (VP7 and the VP4 spike) disrupt the membrane of the endosome, creating a difference in the  calcium  concentration. This causes the breakdown of VP7  trimers  into single protein subunits, leaving the VP2 and VP6 protein coats around the viral dsRNA, forming a double-layered particle (DLP). [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3068", "text": "The eleven dsRNA strands remain within the protection of the two protein shells and the viral  RNA-dependent RNA polymerase  creates mRNA transcripts of the double-stranded viral genome. By remaining in the core, the viral RNA evades innate host immune responses including  RNA interference  that are triggered by the presence of double-stranded RNA. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3069", "text": "During the infection, rotaviruses produce mRNA for both  protein biosynthesis  and gene replication. Most of the rotavirus proteins accumulate in viroplasm, where the RNA is replicated and the DLPs are assembled. In the viroplasm the positive sense viral RNAs that are used as templates for the synthesis of viral genomic dsRNA are protected from  siRNA -induced RNase degradation. [ 64 ]  Viroplasm is formed around the cell nucleus as early as two hours after virus infection, and consists of viral factories thought to be made by two viral nonstructural proteins: NSP5 and NSP2. Inhibition of NSP5 by RNA interference  in vitro  results in a sharp decrease in rotavirus replication. The DLPs migrate to the  endoplasmic reticulum  where they obtain their third, outer layer (formed by VP7 and VP4). The  progeny  viruses are released from the cell by  lysis . [ 44 ] [ 65 ] [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3070", "text": "Rotaviruses are transmitted by the  faecal\u2013oral route , via contact with contaminated hands, surfaces and objects, [ 67 ]  and possibly by the respiratory route. [ 68 ]  Viral diarrhoea is highly contagious. The faeces of an infected person can contain more than 10 trillion infectious particles per gram; [ 48 ]  fewer than 100 of these are required to transmit infection to another person. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3071", "text": "Rotaviruses are stable in the environment and have been found in  estuary  samples at levels up to 1\u20135 infectious particles per US \u00a0 gallon. The viruses survive between 9 and 19 days. [ 69 ]  Sanitary measures adequate for eliminating  bacteria  and  parasites  seem to be ineffective in control of rotavirus, as the incidence of rotavirus infection in countries with high and low health standards is similar. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3072", "text": "Rotaviral enteritis is a mild to severe disease characterised by  nausea ,  vomiting , watery diarrhoea and low-grade  fever . Once a child is infected by the virus, there is an  incubation period  of about two days before symptoms appear. [ 70 ]  The period of illness is acute. Symptoms often start with vomiting followed by four to eight days of profuse diarrhoea.  Dehydration  is more common in rotavirus infection than in most of those caused by bacterial pathogens, and is the most common cause of death related to rotavirus infection. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3073", "text": "Rotavirus infections can occur throughout life: the first usually  produces symptoms , but subsequent infections are typically mild or  asymptomatic , [ 72 ] [ 48 ]  as the immune system provides some protection. [ 73 ]  Consequently, symptomatic infection rates are highest in children under two years of age and decrease progressively towards 45 years of age. [ 74 ]  The most severe symptoms tend to occur in children six months to two years of age, the elderly, and those with  immunodeficiency . Due to immunity acquired in childhood, most adults are not susceptible to rotavirus; gastroenteritis in adults usually has a cause other than rotavirus, but asymptomatic infections in adults may maintain the transmission of infection in the community. [ 75 ]  There is some evidence to suggest blood group can impact on the susceptibility to infection by rotaviruses. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3074", "text": "Rotaviruses replicate mainly in the  gut , [ 77 ]  and infect enterocytes of the  villi  of the  small intestine , leading to structural and functional changes of the  epithelium . [ 78 ]  There is evidence in humans, and particularly in animal models of extraintestinal dissemination of infectious virus to other organs and macrophages. [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3075", "text": "The diarrhoea is caused by multiple activities of the virus. [ 80 ]   Malabsorption  occurs because of the destruction of gut cells called  enterocytes . The  toxic  rotavirus protein  NSP4  induces age- and  calcium  ion-dependent  chloride  secretion, disrupts  SGLT1 (sodium/glucose cotransporter 2)   transporter -mediated reabsorption of water, apparently reduces activity of  brush-border membrane   disaccharidases , and activates the calcium ion-dependent  secretory   reflexes  of the  enteric nervous system . [ 56 ]  The elevated concentrations of calcium ions in the cytosol (which are required for the assembly of the progeny viruses) is achieved by NSP4 acting as a  viroporin . This increase in calcium ions leads to autophagy (self destruction) of the infected enterocytes. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3076", "text": "NSP4 is also secreted. This extracellular form, which is modified by  protease  enzymes in the gut, is an enterotoxin which acts on uninfected cells via  integrin  receptors, which in turn cause and increase in intracellular calcium ion concentrations, secretory diarrhoea and autophagy. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3077", "text": "The vomiting, which is a characteristic of rotaviral enteritis, is caused by the virus infecting the  enterochromaffin cells  on the lining of the digestive tract. The infection stimulates the production of 5' hydroxytryptamine ( serotonin ). This activates vagal afferent nerves, which in turn activates the cells of the brain stem that control the vomiting reflex. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3078", "text": "Healthy enterocytes secrete  lactase  into the small intestine; milk intolerance due to lactase deficiency is a symptom of rotavirus infection, [ 84 ]  which can persist for weeks. [ 85 ]  A recurrence of mild diarrhoea often follows the reintroduction of milk into the child's diet, due to bacterial fermentation of the  disaccharide   lactose  in the gut. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3079", "text": "Rotaviruses elicit both B and T cell immune responses. Antibodies to the rotavirus VP4 and VP7 proteins neutralise viral infectivity  in vitro  and  in vivo . [ 87 ]  Specific antibodies of the classes IgM, IgA and IgG are produced, which have been shown to protect against rotavirus infection by the passive transfer of the antibodies in other animals. [ 88 ]  Maternal trans-placental IgG might play a role in the protection neonates from rotavirus infections, but on the other hand might reduce vaccine efficacy. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3080", "text": "Following infection by rotaviruses there is a rapid innate immune response involving types I and III  interferons  and other  cytokines  (particularly Th1 and Th2) [ 90 ]  which inhibit the replication of the virus and recruit  macrophages  and  natural killer cells  to the rotavirus infected cells. [ 91 ]  The rotavirus dsRNA activates pattern recognition receptors such  toll-like receptors  that stimulate the production of interferons. [ 92 ]  The rotavirus protein NSP1 counteracts the effects of type 1 interferons by suppressing the activity of the interferon regulatory proteins IRF3, IRF5 and IRF7. [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3081", "text": "The levels of IgG and IgA in the blood and IgA in the gut correlate with protection from infection. [ 93 ]  Rotavirus specific serum IgG and IgA at high  titres  (e.g. >1:200) have been claimed to be protective and there is a significant correlation between IgA titres and rotavirus vaccine efficacy. [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3082", "text": "Diagnosis of infection with a rotavirus normally follows diagnosis of  gastroenteritis  as the cause of severe diarrhoea. Most children admitted to hospital with gastroenteritis are tested for rotavirus. [ 95 ] [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3083", "text": "Specific  diagnosis  of infection with rotavirus is made by finding the virus in the child's  stool  by  enzyme immunoassay . There are several licensed test kits on the market which are sensitive, specific and detect all serotypes of rotavirus. [ 97 ]  Other methods, such as  electron microscopy  and  PCR  (polymerase chain reaction), are used in research laboratories. [ 98 ]  Reverse transcription-polymerase chain reaction ( RT-PCR ) can detect and identify all species and serotypes of human rotaviruses. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3084", "text": "Treatment of acute rotavirus infection is nonspecific and involves management of symptoms and, most importantly,  management of dehydration . [ 13 ]  If untreated, children can die from the resulting severe dehydration. [ 100 ]  Depending on the severity of diarrhoea, treatment consists of  oral rehydration therapy , during which the child is given extra water to drink that contains specific amounts of salt and sugar. [ 101 ]  In 2004, the World Health Organisation (WHO) and UNICEF recommended the use of low-osmolarity  oral rehydration solution  and  zinc  supplementation as a two-pronged treatment of acute diarrhoea. [ 102 ]  Some infections are serious enough to warrant hospitalisation where fluids are given by  intravenous therapy  or  nasogastric intubation , and the child's  electrolytes  and  blood sugar  are monitored. [ 95 ]  Rotavirus infections rarely cause other complications and for a well managed child the prognosis is excellent. [ 103 ]   Probiotics  have been shown to reduce the duration of rotavirus diarrhoea, [ 104 ]  and according to the European Society for Pediatric Gastroenterology \"effective interventions include administration of specific probiotics such as  Lactobacillus rhamnosus  or  Saccharomyces boulardii ,  diosmectite  or  racecadotril .\" [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3085", "text": "Rotaviruses are highly contagious and cannot be treated with antibiotics or other drugs. Because improved  sanitation  does not decrease the prevalence of rotaviral disease, and the rate of hospitalisations remains high despite the use of oral rehydrating medicines, the primary public health intervention is vaccination. [ 2 ]  In 1998, a  rotavirus vaccine  was licensed for use in the United States.  Clinical trials  in the United States, Finland, and Venezuela had found it to be 80\u2013100% effective at preventing severe diarrhoea caused by  rotavirus A , and researchers had detected no  statistically significant  serious  adverse effects . [ 106 ] [ 107 ]  The manufacturer, however, withdrew it from the market in 1999, after it was discovered that the vaccine may have contributed to an increased risk for  intussusception , a type of  bowel obstruction , in one of every 12,000 vaccinated infants. [ 108 ]  The experience provoked intense debate about the relative risks and benefits of a rotavirus vaccine. [ 109 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3086", "text": "In 2006, two new vaccines against  rotavirus A  infection were shown to be safe and effective in children, [ 110 ]  and in 2009, the WHO recommended that rotavirus vaccine be included in all national immunisation programmes. [ 111 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3087", "text": "The incidence and severity of rotavirus infections has declined significantly in countries that have acted on this recommendation. [ 14 ] [ 15 ] [ 16 ]  A 2014 review of available clinical trial data from countries routinely using rotavirus vaccines in their national immunisation programs found that rotavirus vaccines have reduced rotavirus hospitalisations by 49\u201392% and all cause diarrhoea hospitalisations by 17\u201355%. [ 112 ]  In Mexico, which in 2006 was among the first countries in the world to introduce rotavirus vaccine, diarrhoeal disease death rates dropped during the 2009 rotavirus season by more than 65 percent among children age two and under. [ 113 ]  In Nicaragua, which in 2006 became the first developing country to introduce a rotavirus vaccine, severe rotavirus infections were reduced by 40 percent and emergency room visits by a half. [ 114 ]  In the United States, rotavirus vaccination since 2006 has led to drops in rotavirus-related hospitalisations by as much as 86 percent. [ 115 ]  The vaccines may also have prevented illness in non-vaccinated children by limiting the number of circulating infections. [ 115 ] [ 116 ]  In developing countries in Africa and Asia, where the majority of rotavirus deaths occur, a large number of safety and efficacy trials as well as recent post-introduction impact and effectiveness studies of Rotarix and RotaTeq have found that vaccines dramatically reduced severe disease among infants. [ 16 ] [ 117 ] [ 118 ] [ 119 ]  In September 2013, the vaccine was offered to all children in the UK, aged between two and three months. [ 120 ]  A 2022 study found that the number of rotavirus cases in infants in England under one year of age was reduced by 77\u201388%. In all age groups, the number of laboratory-confirmed rotavirus infections was reduced by 69\u201383%. [ 121 ]   In Europe, hospitalisation rates following infection by rotaviruses have decreased by 65% to 84% following the introduction of the vaccine. [ 122 ]  Globally, vaccination has reduced hospital admissions and emergency department visits by a median of 67%. [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3088", "text": "Rotavirus vaccines are licensed in over 100 countries, and more than 80 countries have introduced routine rotavirus vaccination, almost half with the support of the  GAVI  vaccine alliance. [ 124 ]  To make rotavirus vaccines available, accessible, and affordable in all countries\u2014particularly low- and middle-income countries in Africa and Asia where the majority of rotavirus deaths occur,  PATH  (formerly Program for Appropriate Technology in Health), the WHO, the U.S.  Centers for Disease Control and Prevention , and GAVI have partnered with research institutions and governments to generate and disseminate evidence, lower prices, and accelerate introduction. [ 125 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3089", "text": "The vaccine may prevent  type 1 diabetes . [ 126 ] [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3090", "text": "Rotavirus A , which accounts for more than 90% of rotavirus gastroenteritis in humans, [ 4 ]  is  endemic  worldwide. Each year rotaviruses cause millions of cases of diarrhoea in developing countries, almost 2 \u00a0 million of which result in hospitalisation. [ 7 ]  In 2019, an estimated 151,714 children younger than five died from rotavirus infections, 90 percent of whom were in developing countries. [ 9 ]  Almost every child has been infected with rotaviruses by age five. [ 2 ] [ 128 ]  Rotaviruses are the leading single cause of severe diarrhoea among infants and children, are responsible for about a third of the cases requiring hospitalisation, [ 11 ]  and cause 37% of deaths attributable to diarrhoea and 5% of all deaths in children younger than five. [ 129 ]  Boys are twice as likely as girls to be admitted to hospital for rotavirus infections. [ 130 ] [ 131 ]  In the pre-vaccination era, rotavirus infections occurred primarily during cool, dry seasons. [ 132 ] [ 133 ]  The number attributable to food contamination is unknown. [ 134 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3091", "text": "Outbreaks of  rotavirus A  diarrhoea are common among hospitalised infants, young children attending day care centres, and elderly people in nursing homes. [ 75 ] [ 135 ]  An outbreak caused by contaminated municipal water occurred in Colorado in 1981. [ 136 ]  During 2005, the largest recorded epidemic of diarrhoea occurred in Nicaragua. This unusually large and severe outbreak was associated with mutations in the  rotavirus A  genome, possibly helping the virus escape the prevalent immunity in the population. [ 137 ]  A similar large outbreak occurred in Brazil in 1977. [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3092", "text": "Rotavirus B , also called adult diarrhoea rotavirus or ADRV, has caused major epidemics of severe diarrhoea affecting thousands of people of all ages in China. These epidemics occurred as a result of sewage contamination of drinking water. [ 139 ] [ 140 ]   Rotavirus B  infections also occurred in India in 1998; the causative strain was named CAL. Unlike ADRV, the CAL strain is endemic. [ 141 ] [ 142 ]  To date, epidemics caused by  rotavirus B  have been confined to  mainland China , and surveys indicate a lack of immunity to this species in the United States. [ 143 ]   Rotavirus C  has been associated with rare and sporadic cases of diarrhoea in children, and small outbreaks have occurred in families. [ 144 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3093", "text": "Rotaviruses infect the young of many species of animals and they are a major cause of diarrhoea in wild and reared animals worldwide. [ 8 ]  As a pathogen of livestock, notably in young calves and piglets, rotaviruses cause  economic loss to farmers because of costs of treatment associated with high morbidity and mortality rates. [ 147 ]  These rotaviruses are a potential reservoir for genetic exchange with human rotaviruses. [ 147 ]  There is evidence that animal rotaviruses can infect humans, either by direct transmission of the virus or by contributing one or several RNA segments to  reassortants  with human strains. [ 148 ] [ 149 ] [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3094", "text": "In 1943, Jacob Light and Horace Hodes proved that a filterable agent in the faeces of children with infectious diarrhoea also caused scours (livestock diarrhoea) in cattle. [ 151 ]  Three decades later, preserved samples of the agent were shown to be rotavirus. [ 152 ]  In the intervening years, a virus in mice [ 153 ]  was shown to be related to the virus causing scours. [ 154 ]  In 1973,  Ruth Bishop  and colleagues described related viruses found in children with gastroenteritis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3095", "text": "In 1974,  Thomas Henry Flewett  suggested the name  rotavirus  after observing that, when viewed through an  electron microscope , a rotavirus particle looks like a wheel ( rota  in Latin) [ 155 ] [ 156 ]  the name was officially recognised by the  International Committee on Taxonomy of Viruses  four years later. [ 157 ]  In 1976, related viruses were described in several other species of animals. [ 154 ]  These viruses, all causing acute gastroenteritis, were recognised as a collective pathogen affecting humans and other animals worldwide. [ 155 ]  Rotavirus serotypes were first described in 1980, [ 158 ]  and in the following year, rotaviruses from humans were first grown in  cell cultures  derived from monkey kidneys, by adding  trypsin  (an enzyme found in the  duodenum  of  mammals  and now known to be essential for rotavirus to replicate) to the culture medium. [ 159 ]  The ability to grow rotaviruses in culture accelerated the pace of research, and by the mid-1980s the first candidate vaccines were being evaluated. [ 160 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3096", "text": "The  rotavirus vaccine  is a  vaccine  used to protect against  rotavirus  infections, which are the leading cause of severe  diarrhea  among young children. [ 6 ]  The vaccines prevent 15\u201334% of severe diarrhea in the  developing world  and 37\u201396% of the risk of death among young children due to severe diarrhea. [ 6 ]  Immunizing babies decreases rates of disease among older people and those who have not been immunized. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3097", "text": "The  World Health Organization  (WHO) recommends that rotavirus vaccine be included in national  routine vaccinations  programs, especially in areas where the disease is common. [ 6 ]  This should be done along with promoting  breastfeeding , handwashing, clean water, and good sanitation. [ 6 ]  It is given  by mouth  and requires two or three doses. [ 6 ]  The vaccines are safe. [ 6 ]  This includes their use in people with  HIV/AIDS . [ 6 ]  The vaccines are made from  weakened rotavirus . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3098", "text": "The vaccine first became available in the United States in 2006. [ 8 ]  It is on the  World Health Organization's List of Essential Medicines . [ 9 ]  The vaccine is available in many countries. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3099", "text": "Safety and efficacy trials in Africa and Asia found that the vaccines dramatically reduced severe disease among infants in developing countries, where a majority of rotavirus-related deaths occur. [ 10 ] [ 11 ]  A 2021  Cochrane  systematic review concluded that Rotavac, Rotateq, and Rotarix vaccines are safe and are effective at preventing diarrhea that is related to a rotavirus infection. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3100", "text": "Rotavirus vaccines are licensed in more than 100 countries, and more than 80 countries have introduced routine rotavirus vaccination. [ 13 ]  The incidence and severity of rotavirus infections has declined significantly in countries that have acted on the recommendation to introduce the rotavirus vaccine. [ 14 ]  In Mexico, which in 2006 was among the first countries in the world to introduce rotavirus vaccine, the diarrheal disease death rates from rotavirus dropped by more than 65% among children age two and under during the 2009 rotavirus season. [ 15 ]  In Nicaragua, which in 2006 became the first developing country to introduce the rotavirus vaccine, investigators recorded a substantial impact, with rotavirus vaccine preventing 60% of cases against severe rotavirus and cutting emergency room visits in half. [ 16 ]  In the United States, vaccination has reduced rotavirus-related hospitalizations by as much as 86% since 2006. In April 2016, the World Health Organization released statistics for the period of 2000\u20132013, which showed developing countries that have introduced rotavirus vaccines experienced significant decreases in deaths and hospitalizations from rotavirus diarrhea after introduction. [ 17 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3101", "text": "Additionally, the vaccines may also prevent illness in non-vaccinated children by limiting exposure through the number of circulating infections. [ 7 ]  A 2014 review of available clinical trial data from countries routinely using rotavirus vaccines in their national immunization programs found that rotavirus vaccines have reduced rotavirus hospitalizations by 49\u201392% and all-cause diarrhea hospitalizations by 17\u201355%. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3102", "text": "The World Health Organization recommends the first dose of vaccine be given right after six weeks of age. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3103", "text": "Rotarix is a  monovalent , human, live attenuated rotavirus vaccine containing one rotavirus strain of G1P[8] specificity.\nRotarix is indicated for the prevention of rotavirus gastroenteritis caused by G1 and non-G1 types (G3, G4, and G9) when administered as a 2-dose series in infants and children. [ 19 ]  It was approved in the European Union in 2006, and by the US FDA in April 2008. [ 20 ] [ 21 ]  It is taken  by mouth . [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3104", "text": "Rotateq is a live, oral  pentavalent vaccine  that contains five rotavirus strains produced by  reassortment . [ medical citation needed ]  The rotavirus \u00a0 A parent strains of the reassortants were isolated from human and bovine hosts. [ medical citation needed ]  Four reassortant rotaviruses express one of the outer capsid, VP7, proteins (serotypes G1, G2, G3, or G4) from the human rotavirus parent strain and the attachment protein VP4 (type P7) from the bovine rotavirus parent strain. [ medical citation needed ]  The fifth reassortant virus expresses the attachment protein VP4, (type P1A), from the human rotavirus parent strain and the outer capsid protein VP7 (serotype G6) from the bovine rotavirus parent strain. [ medical citation needed ]  In February 2006, the US  Food and Drug Administration  (FDA) approved Rotateq for use in the United States. [ 24 ] [ 25 ]  In August 2006,  Health Canada  approved Rotateq for use in Canada. [ 26 ]  Merck worked with a range of partners including governmental and non-governmental organisations to develop and implement mechanisms for providing access to this vaccine in the developing world, [ 27 ]  an effort which was slated to come to an end in 2020. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3105", "text": "Rotavac was licensed for use in India in 2014 and is manufactured by  Bharat Biotech International Limited . It is a live attenuated, monovalent vaccine containing a G9P[11] human strain isolated from an Indian child. [ 29 ]  It is given by mouth in a three-dose series, four weeks apart, beginning at six weeks of age up until eight months of age. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3106", "text": "Rotavin-M1 was licensed for use in Vietnam in 2007 and is manufactured by the Center for Research and Production of Vaccines. The vaccine contains a G1P[8] human rotavirus strain. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3107", "text": "The Lanzhou lamb rotavirus vaccine was licensed for use in China in 2000 and is manufactured by the Lanzhou Institute of Biological Products. It contains a G10P[12] lamb rotavirus strain. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3108", "text": "Rotasiil is a  lyophilized  pentavalent vaccine licensed for use in India in 2018. It contains human bovine reassortant strains of rotavirus serotypes G1, G2, G3, G4, and G9. This is the world's first thermostable vaccine which can be stored without refrigeration at or below 25\u00a0\u00b0C. Rotasiil is manufactured by the  Serum Institute of India . [ 32 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3109", "text": "In 1998, a rotavirus vaccine (RotaShield, by  Wyeth ) was licensed for use in the United States. Clinical trials in the United States,  Finland , and  Venezuela  had found it to be 80 to 100% effective at preventing severe diarrhea caused by rotavirus \u00a0 A, and researchers had detected no statistically significant serious adverse effects. However post-licensure studies conducted in the United States by  Trudy Murphy  and her colleagues at the Centers For Disease Control and Prevention (CDC) and Kramarz et al., found that Infants who received the vaccine were 30 times more likely to develop a severe form of bowel obstruction, called intussusception, during 3 to 7 days after the first dose than unvaccinated infants. [ 34 ] [ 35 ]  The excess risk was estimated between one case in 5,000 to 10,000 vaccinees. Based on these data, the Advisory Committee on Immunization Practices (ACIP) withdrew its recommendation to use the vaccine, [ 36 ]  and the manufacturer of the vaccine withdrew it from the market in 1999. There then followed eight years of delay until rival manufacturers were able to introduce new vaccines that were shown to be more safe and effective in children: Rotarix by  GlaxoSmithKline [ 19 ]  and Rotateq by  Merck . [ 37 ]  Both are taken orally and contain disabled live virus. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3110", "text": "The World Health Organization recommends that rotavirus vaccine be included in all national immunization schedules because the risk of intussusception following rotavirus vaccination remains very low compared with the benefits of preventing the impact of severe and deadly diarrhoea. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3111", "text": "A 2009 review estimated that vaccination against rotavirus would prevent about 45% of deaths due to rotavirus gastroenteritis, or about 228,000 deaths annually worldwide. At US$5 per dose, the estimated cost per life saved was $3,015, $9,951, and $11,296 in low-, lower-middle-, and upper-middle-income countries, respectively. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3112", "text": "More than 80 countries have introduced routine rotavirus vaccination, almost half with the support of  Gavi, the Vaccine Alliance . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3113", "text": "In March 2010, the detection of DNA from  porcine circovirus  types 1 and 2 within Rotateq and Rotarix prompted the FDA to suspend the use of rotavirus vaccines while conducting an investigation the finding of DNA from porcine circovirus-1 (PCV1) in the vaccine in collaboration with the 12 members of the Vaccines and Related Biological Products Advisory Committee (VRBPAC). [ 40 ]  On 6 May 2010, the FDA announced its decision to revoke the suspension, stating that porcine circovirus types 1 and 2 pose no safety risks in humans and concluded that health risks involved did not offset the benefits of the vaccination. [ 40 ]  In May 2010 the suspension of the Rotarix vaccine was lifted. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3114", "text": "Doctors Without Borders  (MSF) developed a heat-stable version named BRV-PV. Phase 3 of the clinical trials was completed in Niger on 31 December 2020. [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3115", "text": "The vaccine has been associated with lower rates of  type 1 diabetes . [ 44 ] [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3116", "text": "SeHCAT  ( 23-seleno-25-homotaurocholic acid ,  selenium homocholic acid taurine , or  tauroselcholic acid ) is a drug used in a clinical test to diagnose  bile acid malabsorption . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3117", "text": "SeHCAT is a taurine-conjugated  bile acid   analog  which was synthesized for use as a  radiopharmaceutical  to investigate  in vivo  the  enterohepatic circulation  of  bile salts . [ 2 ]  By incorporating the gamma-emitter  75 Se into the SeHCAT molecule, the retention in the body or the loss of this compound into the feces could be studied easily using a standard gamma camera, available in most clinical  nuclear medicine  departments. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3118", "text": "SeHCAT has been shown to be absorbed from the gut and excreted into the bile at the same rate as  cholic acid , one of the major natural bile acids in humans. It undergoes secretion into the biliary tree, gallbladder and intestine in response to food, and is reabsorbed efficiently in the ileum, with kinetics similar to natural bile acids. [ 2 ] [ 3 ]  It was soon shown to be the most convenient and accurate method available to assess and measure  bile acid  turnover in the intestine. [ 4 ]  SeHCAT testing was commercially developed by Amersham International Ltd ( Amersham plc  is now part of  GE Healthcare  Medical Diagnostics division) for clinical use to investigate  malabsorption  in patients with  diarrhea . This test has replaced  14 C-labeled glycocholic acid (or taurocholic acid) breath tests and fecal bile acid measurements, which now have no place in the routine clinical investigation of  malabsorption . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3119", "text": "A capsule containing radiolabelled  75 SeHCAT (with 370\u00a0kBq of Selenium-75 and less than 0.1\u00a0mg SeHCAT) is taken orally with water, to ensure passage of the capsule into the gastrointestinal tract. The physical half life of  75 Se is approximately 118 days; activity is adjusted to a standard reference date. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3120", "text": "Patients may be given instructions to fast prior to capsule administration; there is significant variation in clinical practice in this regard. [ 5 ]  The effective dose of radiation for an adult given 370\u00a0kBq of SeHCAT is 0.26\u00a0mSv. [ 6 ]  (For comparison, the radiation exposure from an abdominal  CT scan  is quoted at 5.3\u00a0mSv and annual background exposure in the UK 1-3\u00a0mSv. [ 7 ] ) Measurements were originally performed with a whole-body counter but are usually performed now with an uncollimated gamma camera.  The patient is scanned supine or prone with anterior and posterior acquisition from head to thigh 1 to 3 hours after taking the capsule. Scanning is repeated after 7 days. Background values are subtracted and care must be taken to avoid external sources of radiation in a nuclear medicine department."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3121", "text": "From these measurements, the percent retention of SeHCAT at 7 days is calculated.  A 7-day SeHCAT retention value greater than 15% is considered to be normal, with values less than 15% signifying excessive bile acid loss, as found in  bile acid malabsorption ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3122", "text": "With more frequent measurements, it is possible to calculate SeHCAT retention whole-body half-life; this is not routinely measured in a clinical setting. A half-life of greater than 2.8 days has been quoted as normal. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3123", "text": "The SeHCAT test is used to investigate patients with suspected  bile acid malabsorption , who usually experience  chronic diarrhea , often passing watery feces 5 to 10 times each day. When ileum has been removed following surgery, or is inflamed in  Crohn's disease , the 7-day SeHCAT retention usually is abnormal, and most of these patients will benefit from treatment with  bile acid sequestrants . [ 9 ] [ 10 ]  The  enterohepatic circulation  of bile acids is reduced in these patients with ileal abnormalities and, as the normal bile acid retention exceeds 95%, only a small degree of change is needed.  Bile acid malabsorption  can also be secondary to  cholecystectomy ,  vagotomy  and other disorders affecting intestinal motility or digestion such as radiation enteritis,  celiac disease , and  small intestinal bacterial overgrowth . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3124", "text": "A similar picture of  chronic diarrhea , an abnormal SeHCAT retention and a response to  bile acid sequestrants , in the absence of other disorders of the intestine, is characteristic of idiopathic  bile acid malabsorption  \u2013 also called  primary bile acid diarrhea . These patients are frequently misdiagnosed as having the  irritable bowel syndrome , as clinicians fail to recognize the condition, do not think of performing a SeHCAT test, or do not have it available. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3125", "text": "There have been at least 18 studies of the use of SeHCAT testing in diarrhea-predominant  irritable bowel syndrome  patients. When these data were combined, 32% of 1223 patients had a SeHCAT 7-day retention of less than 10%, and 80% of these reported a response to cholestyramine, a  bile acid sequestrant . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3126", "text": "A  self-expandable metallic stent  (or  SEMS ) is a metallic tube, or  stent  that holds open a structure in the  gastrointestinal tract  to allow the passage of food,  chyme ,  stool , or other secretions related to  digestion . Surgeons insert SEMS by  endoscopy , inserting a  fibre optic  camera\u2014either through the  mouth  or  colon \u2014to reach an area of narrowing. As such, it is termed an  endoprosthesis . SEMS can also be inserted using  fluoroscopy  where the surgeon uses an X-ray image to guide insertion, or as an adjunct to endoscopy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3127", "text": "The vast majority of SEMS are used to alleviate symptoms caused by  cancers  of the gastrointestinal tract that obstruct the interior of the tube-like (or luminal) structures of the bowel \u2014 namely the  esophagus ,  duodenum ,  common bile duct  and colon. SEMS are designed to be permanent and, as a result, are often used when the cancer is at an advanced stage and cannot be removed by surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3128", "text": "Self-expandable metallic stents are cylindrical in shape, and are devised in a number of diameters and lengths to suit the application in question. [ 1 ]  They typically consist of cross-hatched, braided or interconnecting rows of metal that are assembled into a tube-like structure. SEMS, when unexpanded, are small enough to fit through the channel of an  endoscope , which is meant for delivery of devices for therapeutic endoscopy. They expand through a deployment device placed at the end of the SEMS, and are held in place against the wall of the luminal surface by friction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3129", "text": "SEMS may be coated with chemicals designed to prevent tumour ingrowth; these are termed \"covered\" stents.  Nitinol [ 3 ]  (a  shape memory   nickel - titanium  alloy),  polyurethane , [ 4 ]  and  polyethylene [ 5 ]  are typically used as coatings for SEMS. Covered stents carry the advantage of preventing tumours from growing into the stent, although they run the risk of increased migration after deployment. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3130", "text": "A plastic self-expanding stent (Polyflex,  Boston Scientific ) has also been developed for similar applications. It confers an additional advantage as it is designed to be removable, and may have a less traumatic insertion than metal stents. The Polyflex stent has shown benefit in palliation of esophageal malignancies. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3131", "text": "The primary application of SEMS is in the  palliation  of tumours that obstruct the gastrointestinal tract. When they expand within the lumen, they are able to hold open the structure and allow passage of material, such as food, stool, or other secretions. The usual applications are for cancers of the  esophagus ,  pancreas ,  bile ducts  and  colon  that are not amenable to surgical therapy. SEMS are used to treat additional complications of cancer, such as  tracheoesophageal fistulas  from esophageal cancer, [ 8 ]  and  gastric outlet obstruction  from  stomach , duodenal, or pancreatic cancer. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3132", "text": "SEMS and self-expanding plastic stents have also been used for non-malignant conditions that cause narrowing or leaks of the esophagus or colon. These include  peptic strictures  caused by esophageal reflux [ 10 ]  and perforations of the esophagus. [ 11 ]  SEMS may also be placed in tandem fashion to treat ingrowth or overgrowth tumours, and fractures or migration of other SEMS. For the latter, the second SEMS in usually deployed within the lumen of the first. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3133", "text": "SEMS are also sometimes used in the  vascular system , usually in the  aorta  and  peripheral vascular system . In the past they have been used for  saphenous vein graft  and native  coronary artery   percutaneous coronary interventions . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3134", "text": "Self-expandable metallic stents are typically inserted at the time of  endoscopy , usually with assistance with  fluoroscopy  or  x-ray  images taken to guide placement. Prior to the development of SEMS small enough to pass through the channel of the endoscopy, SEMS were deployed using fluoroscopy alone. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3135", "text": "Esophageal SEMS are placed after a gastroscopy is performed to identify the area of narrowing. The area may need to be dilated to allow the gastroscope to pass. [ 14 ]  The tumour is usually better seen with the direct vision of endoscopy than on a fluoroscopic image. As a result, radio-opaque markers are usually placed on the surface of the patient to mark the area of narrowing on fluoroscopy. The SEMS is placed through the channel of the endoscope into the esophagus over a guidewire, marked on fluoroscopy, and mechanically deployed (using a device that sits outside of the endoscope) such that it expands when in position.  Hypaque  or other water-soluble dye may be placed through the passage to ensure patency of the stent on fluoroscopy. [ 15 ]  Enteric and colonic SEMS are inserted in a similar fashion, but in the duodenum and colon respectively. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3136", "text": "Biliary SEMS are used to palliatively treat tumours of the pancreas or bile duct that obstruct the  common bile duct . They are inserted at the time of  ERCP , a procedure that uses endoscopy and fluoroscopy to access the common bile duct. The bile duct is  cannulated  with the assistance of a guidewire and the  sphincter of Oddi  that is located at its base is typically cut. A wire is kept in the bile duct, and the SEMS is deployed over the wire in a similar fashion as  esophageal stents . The location of the SEMS is confirmed by fluoroscopy. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3137", "text": "The complications of SEMS are related to a number of factors. The first is that the endoscopic procedure used to insert a SEMS involves the use of  sedative  medications, which may lead to oversedation,  aspiration , or  drug reaction . SEMS also expand and can lead to  perforation  of the bowel or compression of structures adjacent to the bowel. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3138", "text": "Long-term complications of SEMS may be related to the underlying tumour being treated: the tumour may grow into the stent wall (tumour ingrowth) or over the end of the stent (tumour overgrowth), leading to obstruction. These complications may be limited by the use of coated stents. [ 6 ] [ 19 ]  Tumour ingrowth or overgrowth can be additionally palliated by the placement of a second stent through the lumen of the first, [ 6 ]  through  electrocautery  or  argon plasma coagulation  of the tumour tissue in the stent, [ 6 ]  or through the use of  photodynamic therapy . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3139", "text": "Over time, SEMS may also migrate to a different position that does not help with treatment of the obstructed area. [ 6 ]  This may be treated with placement of a second SEMS, or endoscopic attempts to reposition or remove the first. [ 21 ]  Rarely, SEMS may fracture [ 12 ]  or  intussescept  after endoscopic intervention. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3140", "text": "A  Sengstaken\u2013Blakemore tube  is a  medical device  inserted through the nose or mouth and used occasionally in the management of  upper gastrointestinal hemorrhage  due to  esophageal varices  (distended and fragile veins in the esophageal wall, usually a result of  cirrhosis ). The use of the tube was originally described in 1950, [ 1 ]  although similar approaches to bleeding varices were described by Westphal in 1930. [ 2 ]  With the advent of  modern endoscopic techniques  which can rapidly and definitively control variceal bleeding, Sengstaken\u2013Blakemore tubes are rarely used at present. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3141", "text": "The device consists of a flexible plastic tube containing several internal channels and two inflatable balloons. Apart from the balloons, the tube has an opening at the bottom (gastric tip) of the device. More modern models also have an opening near the upper esophagus; such devices are properly termed  Minnesota tubes . [ 3 ] [ 4 ]  The tube is passed down into the  esophagus  and the gastric balloon is inflated inside the stomach. A traction of 1\u00a0kg is applied to the tube so that the gastric balloon will compress the gastroesophageal junction and reduce the blood flow to esophageal varices. If the use of traction alone cannot stop the bleeding, the esophageal balloon is also inflated to help stop the bleeding. The esophageal balloon should not remain inflated for more than six hours, to avoid necrosis. The gastric lumen is used to aspirate stomach contents. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3142", "text": "Generally, Sengstaken\u2013Blakemore tubes and Minnesota tubes are used only in emergencies where bleeding from presumed varices is impossible to control with medication alone. The tube may be difficult to position, particularly in an unwell patient, and may inadvertently be inserted in the  trachea , hence endotracheal intubation before the procedure is strongly advised to secure the airway. The tube is often kept in the refrigerator in the hospital's emergency department, intensive care unit and gastroenterology ward. It is a temporary measure: ulceration and rupture of the esophagus and stomach are recognized complications. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3143", "text": "A related device with a larger gastric balloon capacity (about 500\u00a0ml), the  Linton\u2013Nachlas tube , is used for bleeding  gastric varices . It does not have an esophageal balloon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3144", "text": "It is named after Robert William Sengstaken Sr. (1923\u20131978), an American neurosurgeon, and Arthur Blakemore (1897\u20131970), an American vascular surgeon. They conceptualized and invented the tube in the early 1950s."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3145", "text": "A  sentinel loop  is a  sign  seen on a radiograph that indicates localized  ileus  from nearby inflammation. [ 1 ]  Simply put, it is the dilation of a segment of  small intestine  to be differentiated from  colonic cutoff sign  which is a dilation of a segment of large bowel. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3146", "text": "An isolated distended loop of bowel is seen near the site of injured viscus or inflamed organ. This loop is called a \"sentinel loop.\" It arises from the body's efforts to localize traumatic or inflammatory lesions. The local distention of that intestinal loop is due to local paralysis and accumulation of gas in the intestinal loop. In acute  pancreatitis , the sentinel loop is usually seen in the left  hypochondrium , while in acute  cholecystitis , it is seen in the right hypochondrium. In acute  appendicitis , the sentinel loop is seen in the  right lower quadrant . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3147", "text": "Sleisenger and Fordtran's Gastrointestinal and Liver Disease  is a textbook on  hepatology  and  gastroenterology  for medical students, internists, and surgeons. [ 1 ]  First published in 1978, it has undergone many revisions to reflect the rapid advances in internal medicine and is currently in its 11th edition. It has been described as \"a comprehensive and authoritative textbook of gastrointestinal diseases\", [ 2 ]  the \"standard bearer in gastrointestinal textbooks\", [ 3 ]  and \"the dominant textbook of gastroenterology\". [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3148", "text": "In  anatomy , a  stoma  ( pl. :  stomata   / \u02c8 s t o\u028a m \u0259 t \u0259 /  or  stomas ) is any opening in the body. For example, a  mouth , a  nose , and an  anus  are natural stomata. Any hollow  organ  can be manipulated into an artificial stoma as necessary.  This includes the  esophagus ,  stomach ,  duodenum ,  ileum ,  colon ,  pleural cavity ,  ureters ,  urinary bladder , and  renal pelvis . Such a stoma may be permanent or temporary. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3149", "text": "Surgical procedures that involve the creation of an artificial stoma have names that typically end with the suffix \"-ostomy\", and the same names are also often used to refer to the stoma thus created. For example, the word \" colostomy \" often refers either to an artificial anus or the procedure that creates one. Accordingly, it is not unusual for a stoma to be called an  ostomy  (plural  ostomies ), as is the norm in  wound, ostomy, and continence nursing ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3150", "text": "Stomata are created in particular in surgical procedures involving the  gastrointestinal tract  (GIT) or gastrointestinal system (GIS). The GIT begins at the mouth or oral cavity and continues until its termination, which is the anus. Examples of gastrointestinal stomata include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3151", "text": "One well-known form of an artificial stoma is a  colostomy , which is a surgically created opening in the  large intestine  that allows the removal of  feces  out of the body, bypassing the  rectum , to drain into a  pouch  or other collection device. This  surgical  procedure is invoked usually as a result of and solution to disease in the GIT. The procedure involves bisecting this tube, usually between the later stage of the small intestine ( ileum ) and the large intestine or  colon , hence colostomy, and exiting it from the body in the abdominal region. The point of exiting is what is known as the stoma."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3152", "text": "For greatest success and to minimize negative effects, it is preferable to perform this procedure as low down in the tract as possible, as this allows the maximal amount of natural  digestion  to occur before eliminating  fecal  matter from the body. The stoma is usually covered with a removable pouching system (adhesive or mechanical) that collects and contains the output for later disposal. Modern  pouching systems  enable most individuals to resume normal activities and lifestyles after surgery, often with no outward physical evidence of the stoma or its pouching system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3153", "text": "When planning the position of the stoma, a stoma nurse should bear in mind the height of the person's waist and beltline so that clothes can fit as before. Also a peri-stomal hernia belt worn from the start can help prevent the stoma from developing a serious hernia problem."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3154", "text": "The historical practice of  trepanation  was also a type of stoma."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3155", "text": "Stomachic  is a historic term for a medicine that serves to  tone  the  stomach , improving its function and increase appetite.  While many  herbal remedies  claim stomachic effects, modern  pharmacology  does not have an equivalent term for this type of action."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3156", "text": "Herbs with putative stomachic effects include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3157", "text": "The purported stomachic  mechanism of action  of these substances is to stimulate the appetite by increasing the gastric secretions of the stomach; however, the actual therapeutic value of some of these compounds is dubious.  Some other important agents used are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3158", "text": "In  fecal incontinence  (FI), surgery may be carried out if conservative measures alone are not sufficient to control symptoms. There are many surgical options described for FI, and they can be considered in 4 general groups. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3159", "text": "The relative effectiveness of surgical options for treating fecal incontinence is not known. [ 2 ]  A combination of different surgical and non-surgical therapies may be optimal. [ 2 ]  A surgical treatment algorithm has been proposed for FI, [ 3 ]  although this did not appear to include some surgical options. Isolated sphincter defects may be initially treated with sphincteroplasty and if this fails, the patient can be assessed for sacral nerve stimulation. Functional deficits of the external anal sphincter (EAS) and/or internal anal sphincter (IAS), i.e. where there is no structural defect, or only limited EAS structural defect, or with neurogenic incontinence, may be assessed for sacral nerve stimulation. If this fails, neosphincter with either dynamic graciloplasty or artificial anal sphincter may be indicated. Substantial muscular and/or neural defects may be treated with neosphincter initially."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3160", "text": "This operation aims to repair sphincter defects (which may be of unknown cause) or damage from trauma (usually caused by obstetric damage). Where the sphincter has separated from a tear, this procedure brings these ends back together. Primary sphincteroplasty is repair carried out soon after the trauma has occurred, whilst other repairs may be carried out years after the original trauma (secondary or delayed sphincter repair), usually because the trauma went unrecognised. Usually, sphincter defects are in the anterior position on the sphincter, when an anterior sphincteroplasty may be carried out. Where the sphincter defect is laterally or posteriorly placed, this carries a less successful outcome. [ 3 ] [ 4 ] [ 5 ]  Overlapping anterior sphincteroplasty is preceded by a bowel preparation and possibly antibiotics. Once the patient is under anesthesia, an incision is made in front of the anus (the anterior perineum). Scar tissue is removed and the mucosa of the anal canal separated from the damaged sphincter. The sphincter is cut and its ends overlapped and then stitched back together. The exact method of the procedure varies, e.g. the cut sphincter may be stitched back end to end, rather than overlapped, or the IAS and EAS may be repaired as separate stages. Sphincter repair may sometimes be combined with an anterior levatorplasty (an operation to tighten the pelvic floor). A surgical drain is left to prevent buildup of fluid. After the operation,  sitz baths  are recommended to maintain hygiene during healing, and laxatives prescribed to avoid hard stool. [ 5 ]  Overlapping anterior sphincteroplasty improves FI symptoms in the short term in most (50-80%) patients with sphincter defects. Thereafter, continence deteriorates. Most who undergo this operation are incontinent again after 5 years. Poor results with this procedure may be related to pelvic floor denervation (nerve damage). Primary sphincter repair is inadequate in most women with obstetric ruptures following vaginal delivery. Residual sphincter defects remain in most and around 50% remain incontinent. If there is a residual sphincter defect following the operation (as demonstrated by endoanal ultrasonography), then the procedure may be repeated. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3161", "text": "This procedure aims to improve FI by restoring the anorectal angle and lengthen the anal canal.  The main indication is denervation of the pelvic floor (e.g. descending perineum syndrome). After the patient is anesthetized, an incision is made posterior to (behind) the anus and a space between the EAS and IAS is opened up. This plane is followed, freeing the rectum from its attachment to the pelvic floor. Puborectalis and pubococcygeus are folded and held with stitches. These folds will lengthen the anal canal. It is safe and simple, but long term improvements in FI are poor (30-40%). Total pelvic floor repair refers to a procedure combining postanal and anterior anal repair. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3162", "text": "These procedures aim to inject  bio-compatible  material into the walls of the anal canal, aiming to bulk out these tissues. This may bring the walls of the anal canal into tighter contact, raising the resting pressure, creating more of a barrier to the loss of stool, and thereby reducing FI. Originally, this technique was described for urinary incontinence, but was first used for FI in 1993, [ 6 ]  especially passive soiling due to IAS dysfunction. The procedure can be carried out under  local anesthetic  on an  out patient  basis, or with  caudal epidural anesthesia , [ 7 ]  or with  intravenous sedation , or under  general anesthesia . [ 8 ]  This measure has many advantages over more invasive surgery, since there are rarely any serious complications. [ 8 ]  Many different materials have been used as perianal injectable bulking agents. [ 9 ]  Of the available materials, which one is the best is not known. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3163", "text": "In 2013 a  Cochrane  systematic review included 5 randomized trials, which in total was 382 patients. None of the included studies reported long term follow up after 3, 6 or 12 months post procedure. [ 9 ]  In another review of 889 patients across 23 studies, a pooled improvement rate in measures of incontinence was 39.5%. [ 8 ]  In some cases there is no improvement after the procedure, and the injections are repeated in up to 34% of cases. [ 8 ]  There can also be worsening of symptoms after an initial improvement period. [ 8 ]  In one randomized control trial, the placebo treatment gave over 30% improvement in symptoms, suggesting that patient psychology (i.e. the  placebo effect ) may be in part responsible for any positive results. [ 10 ]  One author criticized these procedures, stating that simply narrowing the anal canal was an instinctive and naive solution which does not consider the complex pathopysiological mechanisms of FI. [ 10 ]  Concerns have been raised about migration of the particles (in the case of Durasphere) away from the site of injection, or the total resorption of the material (in the case of hyaluronic acid and hydroxyl coaptite). [ 10 ]  Most research suggests that the positive effects of most of the bulking agents seem to reduce after 6 to 12 months. [ 7 ]  At 6 months the material has been reported as missing or migrated in 18.4% of cases, at 3 years or more in 20.2% of cases. [ 8 ]  One author drew attention to the fact that all existing research on these procedures was driven by the companies who also marketed the treatments, and therefore the studies are at high risk of bias. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3164", "text": "Mesenchymal stem cells  (MSC) and  muscle-derived stem cells  (MDSC) have been used in urology to treat urinary incontinence.  Fibroblasts  in a collagen carrier were injected into the submucosa of the urethra, and  myoblasts  were injected into the urethral sphincter. The procedure was reported as being successful in most cases. [ 11 ]  Injection of MSCs may lead to engrafting and forming multinucleated myotubes, which helps to regeneration after injury. [ 12 ]  In theory, use of stem cells removes the problems of reabsorption and migration of the bulking material. [ 11 ]  There is similar research which aims to regenerate muscles and repair tissues by  cell therapy  to treat injuries of the external anal sphincter. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3165", "text": "The \"Gatekeeper\" and \"SphinKeeper\" are self-expandable prostheses which are implanted into the intersphincteric space of the anal canal. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3166", "text": "Sacral nerve stimulation  was originally used in urinary incontinence. It was first used to treat FI in 1995. The procedure involves implantation of an electrical device (an implanted pulse generator, IPG) which applies a low amplitude electric current to a  sacral  nerve (usually  S3 ). This appears to modulate the nerves and muscles of the pelvic floor and rectum. A  Cochrane  review of the efficacy of sacral nerve stimulation concluded that more research was needed, but can be helpful in selected people with FI, and reduce symptoms in selected people with constipation. [ 13 ]  It is possible to simulate the effect of SNS without surgery. This is trial usually lasts around 2\u20133 weeks, where a temporary percutaneous peripheral nerve electrode is placed in the lower back, and then connected to an external stimulator. This trial may not always accurately predict a successful outcome. If there is an improvement, a permanent electrode can be implanted on the sacrum and connected to an stimulator which is in turn implanted in the lower abdominal wall or in the buttock. Implanted stimulators usually last 8 years. The patients who may benefit from SNS include those with intact anal sphincters and those with a history of unsuccessful anal repair. [ 5 ]  Complications of the surgery are rare, including pain and infection, which may require implant removal in 5% of cases. The effects of SNS may include increased resting and squeeze anal tone, and improved rectal sensitivity. There is reported reduction of involuntary loss of bowel contents and increased ability to postpone defecation. A substantial percentage of patients regain full continence. Patient quality of life has also been shown to be improved after the procedure. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3167", "text": "In the 1950s described an operation using the  gracilis muscle  from the inner thigh and wrapping it around the anus to function as a new anal sphincter (neosphincter). Non dynamic graciloplasty was not particularly successful because the gracilis is mostly composed of type II, fast-twitch, fatiguable muscle fibres, whereas the sphincter ideally needs to be able to automatically contract for long periods. A neurostimulation device with an impulse generator can be implanted to adapt the muscle to prolonged contraction (dynamic graciloplasty). Over time, the muscle becomes mostly composed of type I, slow twitch, fatigue resistant fibres. The patient uses an external magnetic programming device to deactivate the electrical stimulation, relaxing the muscular contraction and enabling defecation at a voluntary time. [ 3 ] [ 5 ]  Dynamic graciloplasty may be indicated for patients with a completely destroyed anal sphincter or a torn sphincter with a large gap between both ends that is not amenable to repair. The procedure involves detachment of the gracilis from the leg, preserving both its blood supply and innervation. The muscle is then moved to wrap around the anal canal completely, and also attached to the  periosteum  of the inferior ramus of the  pubic bone . Various arrangements are described, depending upon the length of the gracilis. The implanted stimulator electrode is placed intramuscularly (within the muscle), very close to the gracilis nerve, and the impulse generator is placed subcutaneously (under the skin). [ 3 ] [ 5 ]  The success rate of the operation is between 40 and 60%, and varies with surgeon experience. The complication rate is high, (infections 28%, device problems 15%, and\nleg pain 13%) but these are usually treatable without influence on the result. A second operation may be required for some complications. When dynamic graciloplasty is successful in curing FI, up to 50% of patients may develop signs and symptoms of  obstructed defecation . [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3168", "text": "This is also termed artificial anal sphincter or neosphincter. [ 14 ]  The usual surgical approach is through the  perineum  or alternatively via the vagina. The artificial bowel sphincter involves the implantation of 3 components: (i) A fluid filled silicone elastomer cuff placed around the anus, (ii) a liquid filled, pressure-regulating balloon positioned in the peritoneal fat, and (iii) a manual pump connecting these components (placed in either the  labia majora  or the  scrotum ). When the cuff is inflated, the anal canal sealed. The fluid is transferred to the balloon by the manual pump, resulting in deflation of the cuff, opening of the anal canal and allowing for defecation. [ 3 ] [ 4 ] [ 5 ]  This procedure improves FI scores and quality of life, and continence is excellent when the procedure works (successful outcome in 85% patients with a functioning device). The procedure is less technically demanding than the graciloplasty, but there is the disadvantage of using foreign material, which can erode through the anal canal. As with graciloplasty, obstructed defecation may develop with a working device, and may be treated with enemas. Complications include infection, which may warrant temporary removal of the device. [ 3 ] [ 4 ] [ 5 ]  Graciloplasty and artificial anal sphincter both significantly improve continence, with artificial anal sphincter being superior, [ 15 ]  however both methods have high rates of complications. [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3169", "text": "This was originally described as a surgical management for  rectal prolapse . This operation essentially involves encircling the anal canal with implanted foreign material. Various materials have been used, including nylon, silk, fascia strips, silver wire, and\nsilastic bands. Anal encirclement effectively supplements the anal sphincter, narrowing the anal canal and its barrier function to stool, without altering voluntary control. Since complications are common, and can be serious (fecal impaction, infection, erosion of encirclement through anal canal), modern surgeons prefer to perform colostomy. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3170", "text": "This refers to temperature-controlled radiofrequency energy being delivered to the anal canal, and is marketed as the SECCA procedure. This procedure aims to create a controlled scarring and  stricturing  of the anal canal. [ 1 ]  In theory, it is thought that radiofrequency induced IAS injury may cause collagen deposition and fibrosis (scarring), resulting in the affected area tightening. [ 17 ]  Specialized surgical instrument called a radiofrequency handpiece is used. It has 4 needles which enter the IAS and heat up to 85\u00a0\u00b0C. This causes the water molecules in the tissue to vibrate with subsequent frictional heating. The hand piece is cooled by water and monitors the temperature of the tissues it is applied to for safety. It is thought that the improvement in FI occurs over time as  collagen  is deposited and the tissues undergo remodeling. [ 18 ]  The procedure is carried out under  local anesthesia  (with or without  conscious sedation ) on an  outpatient  basis. [ 19 ]  There appear to be relatively few serious complications. [ 18 ] \nInitial studies of the SECCA procedure have shown promising improvements in quality of life and FI severity scores, however large  randomized control trials  and  systematic reviews  are currently lacking. [ 19 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3171", "text": "This procedure involves the surgical creation of a stoma (either an appendicostomy, cecostomy, or sigmoidostomy), which thereafter functions as an irrigation port. This antegrade colonic irrigation aims to introduce fluid to wash out the colon at regular intervals. The idea is to ensure regular emptying of the colon and rectum and hopefully, prevent involuntary loss of bowel content. [ 3 ]  The  Malone antegrade continence enema  (MACE) is where an appendicostomy is created, i.e. the  vermiform appendix  is stitched to the abdominal wall to form a stoma. ACE is often necessary in addition to others when FI is complicated by  neuropathy  and/or an incomplete IAS. Patients may have persistent leakage of fluid per rectum for several hours following the irrigation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3172", "text": "Diversion may be a temporary measure in the management of FI, e.g. to allow healing of another surgical procedure, or it may be a definitive procedure.  Stoma creation is considered to be the last resort treatment, [ 4 ]  when all other attempts to improve symptoms have been unsuccessful, although they are associated with many problems such as odor associated with leakage of stool and flatus from the stoma.  The  stoma  may be  colostomy  (where the colon is ended in a stoma) or  ileostomy  (where the  ileum  is ended in a stoma).  Both may involve the creation of an  internal waste-holding reservoir  in a procedure developed by Dr.  Nils Kock  in the late 1960s. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3173", "text": "Diversion colitis  is inflammation of the section of gut through which stool no longer passes. This condition arises because normally the lining of the gut obtains some of its nutrients from the fecal stream.  This condition may cause a foul-smelling, mucous  rectal discharge  from the distal, unused colon. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3174", "text": "Transanal irrigation  is medical procedure in which water is used to evacuate feces from the  rectum  and  descending colon  via the  anus . [ 5 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3175", "text": "Transanal irrigation uses a large volume water  enema  system. [ 2 ]  It is carried out every day (or every 2 days) by the patient or carer as a long term management for bowel dysfunction, including  fecal incontinence  and/or  constipation  (especially  obstructed defecation )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3176", "text": "Although the procedure and general goals may be similar, transanal irrigation is different from  colon cleansing  (colon hydrotherapy), which is a term used in alternative medicine. Transanal irrigation is used for medical conditions which affect defecation, such as  spinal cord injury  or  multiple sclerosis . Colon cleansing is used outside of mainstream medical supervision, and may be used in the belief that the procedure removes toxins from the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3177", "text": "The impact of transanal irrigation varies considerably. Some individuals experience complete control of incontinence, and other report little or no benefit. [ 5 ]  Evidence shows this treatment can be considered for children as well. [ 6 ] [ 7 ]  When diet and medication has proven ineffective, transanal irrigation may be used. [ 5 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3178", "text": "Transanal irrigation systems may use either a rectal balloon catheter or a cone-shaped colostomy tip. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3179", "text": "The catheter tip is inserted into the anal canal. Systems with balloon catheters require inflation of the balloon once the tip is in position. [ 9 ]  Cone shaped colostomy tip systems must be supported manually. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3180", "text": "Lukewarm tapwater (36-38\u00b0C) [ 4 ]  is used if it is drinkable. [ 9 ]   If tap water is not safe for drinking, a different source of clean water is needed. The irrigation bag is ideally placed or hung 1-1.5 m above the level of the toilet. The flow is switched on with a handheld valve. The flow rate of the water may be controlled by a manual pump or a battery pump. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3181", "text": "The volume of water used is normally about 1000 ml. [ 9 ]  Some sources recommend repeat irrigation with a higher volume up to 2300 ml. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3182", "text": "Transanal irrigation may be performed every day or every other day in order to simulate a normal defecation routine. [ 9 ]  Ideally, irrigation is performed at the same hour each day. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3183", "text": "The optimal volume and frequency may be determined by trail and error for each individual patient during the first few months of treatment. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3184", "text": "The time required for the procedure is in the range of 30\u2013120 min. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3185", "text": "Some individuals take oral constipating medications or oral laxative medications in addition to transanal irrigation. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3186", "text": "It is unclear whether the mechanism of action of irrigation is by simple mechanical washing out of the bowel, or by triggering of colonic mass movements, or both. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3187", "text": "Disadvantages of the treatment may include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3188", "text": "Specific conditions for which transanal irrigatio has been used include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3189", "text": "A Cochrane review found evidence that transanal irrigation was more effective compared to conservative management in the management of spinal cord injury. There were more positive benefits for constipation scores, neurogenic bowel dysfunction scores, and fecal incontinence scores. Patients spent less time in total on bowel care and were more satisfied with the treatment. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3190", "text": "The treatment is generally considered safe. However, adverse effects are reported, including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3191", "text": "Bowel perforation  is when the wall of the bowel ruptures. It is a potentially lethal complication [ 9 ]  which requires emergency surgery. 49 bowel perforations caused by transanal irrigation were reported between 2005 and 2013. [ 19 ]  This rate was used to calculate a risk of 2-6 perforations per 1 million procedures. [ 19 ]  This risk of perforation is significantly lower compared to other common medical procedures such as flexible sigmoidoscopy (1 perforation per 40000 procedures), colonoscopy (1 per 1000) and barium enema (1 per 10000). [ 10 ]  However, patients may need to conduct transanal irrigation daily or near-daily for many years, which increases their lifetime risk. [ 9 ]  Perforation is more likely in the first weeks after starting treatment. [ 19 ]  People who have had a surgical anastomosis (for example, after low anterior resection,  stapled transanal rectal resection ,  ventral mesh rectopexy , or other types of surgery for  rectal prolapse ) are more at risk of bowel perforation during transanal irrigation. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3192", "text": "One study reported before and after changes in anorectal physiology tests in patients with idiopathic faecal incontinence or chronic idiopathic constipation. The patients had all used transanal irrigation for at least 30 months. In the chronic idiopathic constipation group there was no reduction in anal sphincter function after long term use of transanal irrigation. In the idiopathic faecal incontinence group anal resting and squeeze pressures were lower after long term use of transanal irrigation. The researchers suggested that this was due to age related changes in sphincter function and the deterioration of the disease over time rather than due to the use of transanal irrigation. In both groups rectal urge volume increased after long term use of transanal irrigation. The researchers suggested that patients get accustomed to larger rectal volumes, and without the irrigation their everyday sensation of urge from the presence of stool in the rectum is decreased. This may encourage patients to continue using the irrigation. However, rectal compliance (how well the rectum can stretch and accommodate increasing volumes without triggering discomfort or pain) and biomechanical properties of the rectal wall were unchanged. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3193", "text": "Management of ulcerative colitis  involves first treating the  acute  symptoms of the disease, then maintaining  remission .  Ulcerative colitis  is a form of  colitis , a  disease  of the  intestine , specifically the large intestine or  colon , that includes characteristic  ulcers , or open sores, in the colon. The main symptom of active disease is usually  diarrhea  mixed with blood, of gradual onset which often leads to  anaemia . Ulcerative colitis is, however, a  systemic disease  that affects many parts of the body outside the intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3194", "text": "Standard treatment for ulcerative colitis depends on  extent of involvement  and disease  severity . The goal is to induce  remission  initially with medications, followed by the administration of maintenance medications to prevent a relapse of the disease. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing a remission which involves relief of symptoms and mucosal healing of the lining of the colon and then longer-term treatment to maintain the remission."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3195", "text": "Anaemia , caused by both chronic blood loss from the gastrointestinal tract and reduced absorption due to the up-regulation of  hepcidin  should also be treated, and this often requires the use of  parenteral iron . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3196", "text": "The following sections are sorted first by drug type and, second, by the type of ulcerative colitis:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3197", "text": "Aminosalicylates  are the main  anti-inflammatory  drugs used to treat ulcerative colitis. Sometimes remission can be achieved, or at least maintained, with these drugs alone. If not, they are usually used in combination with the drugs listed in the ensuing sections."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3198", "text": "The anti-inflammatory action in all these drugs is produced by 5-aminosalicylic acid (5-ASA), the active ingredient in Mesalazine. 5-ASA is produced from the other drugs in the intestine. The aminosalicylates used to treat ulcerative colitis include the following:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3199", "text": "5-ASA is poorly-absorbed by the intestines, and hence provides topical relief within the intestine. It is therefore a non-systemic drug. 5-ASA is related to the systemic  non-steroidal anti-inflammatory drugs  (NSAIDs), such as  Aspirin  and  Ibuprofen ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3200", "text": "The free radical induction theory, discussed below, proposes that 5-ASA is serving not just as an anti-inflammatory agent, but also as a free radical trap, destroying the hydroxyl and other radicals that may damage colonic epithelial barrier. [ 2 ]   5-ASA may also be an inhibitor of  TNF ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3201", "text": "Possible side effects of 5-ASA include, nausea and vomiting, reduced sperm count and damage to red or white blood cells, or to the liver, kidneys, pancreas, nerves or hearing. Allergic reactions to sulfasalazine characterized by dizziness, fever and skin rash have been reported in a small percentage of patients. In some cases, sulfasalazine can exacerbate ulcerative colitis resulting in diarrhea, abdominal cramps and discomfort."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3202", "text": "In the intestine sulfasalazine is converted to 5-ASA and sulfapyridine, which is responsible for some of its side-effects, and which should be monitored in patients taking sulfasalazine. Sulfapyridine levels above 50\u00a0\u03bcg/L are associated with the side-effects."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3203", "text": "Patients on high dose sulfasalazine require  folic supplementation  (1\u00a0mg/day) (1000\u00a0\u03bcg/day) to maintain normal cell division. This may, however, be counter-productive for patients who are also taking methotrexate, which is a folic acid inhibitor. Folic acid might also be counter-productive for patients taking 6-MP and related drugs that inhibit all cell division."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3204", "text": "It is often necessary to use  corticosteroids  in conjunction with 5-ASA drugs to bring about remission of ulcerative colitis. Thereafter it may be possible to maintain remission with 5-ASAs alone, though many patients require other, stronger immunosuppressive medications.  Corticosteroids should not be used for long-term therapy of UC, particularly without the concomitant use of an immunomodulator or anti-TNF. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3205", "text": "Corticosteroids reduce inflammation by blocking portions of the  leukocyte adhesion cascade  which results in inflammation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3206", "text": "Side effects of corticosteroids include  Cushing's syndrome , which most often exhibits itself as temporary facial puffiness, called \"moon face\". Cushing's syndrome can, however, involve  psychosis , including  manic  behavior. These drugs have been known to trigger  bipolar disorder . In prescribing these drugs it might be well to inquire as to any family history of bipolar disorder."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3207", "text": "Corticosteroids should not be confused with  anabolic steroids , the controversial performance-building \"steroids\" that are banned in certain sports."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3208", "text": "The following corticosteroids are used as immune system suppressants in treatment of ulcerative colitis:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3209", "text": "Immunosuppressive drugs  inhibit the immune system generally. These include the  cytostatic drugs  that inhibit cell division, including the  cloning  of  white blood cells  that is a part of the immune response. Immunosuppressive drugs used with ulcerative colitis include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3210", "text": "Mercaptopurine is a cytostatic drug that is an  antimetabolite . The mercaptopurine molecule mimics  purine , which is necessary for the synthesis of  DNA . With mercaptopurine present, cells are not able to make DNA, and cell division is inhibited."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3211", "text": "In administering mercaptopurine it is necessary to monitor the levels of mercaptopurine metabolites in the blood to establish the correct dosage for a patient. An initial concern is  hepatotoxicity ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3212", "text": "Mercaptopurine inhibits the production of  white blood cells  generally. Because this makes the body more susceptible to infection, patients need to watch for infections.  Vaccinations  are critically important, particularly the yearly flu shot and periodic pneumonia immunizations.  Vaccine response is best if given prior to initiation of immunosuppressive medications, and patients on immunosuppressives should use caution when receiving vaccines containing live virus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3213", "text": "Frequent  blood cell counts  are also recommended during administration of mercaptopurine. The drug may be toxic to  bone marrow , where many blood components are made. If there is an abnormally large drop in white blood cell count, or any blood cell count, administration of the drug should be halted at least temporarily."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3214", "text": "Methotrexate is another immunosuppressive drug. It works by inhibiting folic acid, which is necessary for DNA replication and, therefore, cell division."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3215", "text": "TNF  is a protein that is released by activated white blood cells, triggering more inflammation, an immune system response and more damage to the mucosa of the colon because of the immune activation. Certain drugs inhibit TNF, hence reducing inflammation and immune system involvement. Infliximab was approved by the FDA for treating ulcerative colitis in March 2005. It is usually given as an intravenous infusions at weeks 0,2 and 6 and then every eight weeks thereafter. It is very useful for inducing and maintaining a remission of ulcerative colitis. Infliximab works better when used in combination with immunmodulators such as 6-mercaptopurine or azathioprine, but a corresponding increase in adverse events means that the decision to use one drug or two must be based on an individualized discussion between the patient and their doctor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3216", "text": "Proctitis  is an  inflammation  of the  anus  and the lining of the  rectum , usually involving the distal, or lower, 10\u201315\u00a0cm (3.9\u20135.9\u00a0in) of the colon, including the  rectum . Approximately 30% of ulcerative colitis patients initially present with proctitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3217", "text": "Standard treatment for active disease includes Mesalazine suppositories and cortisone foam (Cortifoam). Mesalazine 1 g SUPP QHS or Cortifoam QHS/BID is continued until remission, with response seen usually within three weeks."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3218", "text": "Maintenance therapy is with Mesalazine 1g QHS or Q3HS. Those with anal irritation or discomfort from the suppositories may switch to oral medications, such as sulfasalazine, Mesalazine, or Colazol, although they are not as effective as suppositories for proctitis. Maintenance therapy is not recommended for those with a first episode that responded to the Mesalazine. Steroid foam is not shown to prevent relapse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3219", "text": "Systemic steroids such as prednisone are not used unless proctitis fails to respond to the above treatments. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3220", "text": "Proctosigmoiditis and left-sided colitis  involves the lower colon, from the rectum up the left side of the patient."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3221", "text": "Patients often respond to topical agents alone, such as Mesalazine, or hydrocortisone enemas. Again, the Mesalazine is preferred for maintenance therapy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3222", "text": "Oral anti-inflammatory drugs require four to six weeks to work."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3223", "text": "Once remission is induced, maintenance levels can be used: sulfasalazine 2\u00a0g/day, mesalamine 1.2-2.4\u00a0g/day, or olsalazine 1\u00a0g/day. Patients on high dose sulfasalazine require  folic supplementation  (1\u00a0mg/day) because it inhibits folate absorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3224", "text": "If oral Mesalazine is still not working, prednisone is often given, starting at 40\u201360\u00a0mg/day. Prednisone often takes effect within 10\u201314 days. The dose should then be tapered by about 5\u00a0mg/week until it can be stopped altogether."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3225", "text": "Extensive or pancolitis . Patients usually require a combination of oral Mesalazine or sulfasalazine along with topical Mesalazine or steroid enemas. Oral prednisone (40\u201360\u00a0mg/day) should be given only in severe cases or if oral Mesalazine fails. Once remission is induced, maintenance therapy is with standard oral Mesalazine doses. Supplemental iron ( ferrous sulfate  or  ferrous gluconate ) may be given due to chronic blood loss.  Loperamide  may be given for symptomatic relief of chronic diarrhea, but should not be given in suspected toxic megacolon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3226", "text": "Severe or fulminant colitis . Patients need to be hospitalized immediately with subsequent bowel rest, nutrition, and IV steroids. Typical starting choices are hydrocortisone 100\u00a0mg IV q8h, prednisolone 30\u00a0mg IV q12h, or methylprednisolone 16\u201320\u00a0mg IV q8h. The last two are preferred due to less sodium retention and potassium wasting. 24-hour continuous infusion is preferred than the stated dosing. If the patient has not had any corticosteroids within the last 30 days, IV ACTH 120 units/day as continuous infusion is superior than the IV steroids mentioned above. In either case, if symptoms persist after 2\u20133 days, Mesalazine or hydrocortisone enemas daily or bid can be given. The use of antibiotics in those with severe colitis is not clear. However, there are those patients who have sub-optimal response to corticosteroids and continue to run a low grade fever with bandemia. Typically they can be treated with IV ciprofloxacin and metronidazole. However, in those with fulminant colitis or megacolon, with high fever, leukocytosis with high bandemia, and peritoneal signs, broad spectrum antibiotics should be given (i.e.,  ceftazidime ,  cefepime ,  imipeneum ,  meropenem , etc.). Abdominal x-ray should also be ordered. If intestinal dilation is seen, patients should be decompressed with NG tube and or rectal tube."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3227", "text": "Refractory ulcerative colitis . Patients with toxic megacolon (colonic dilation > 6\u00a0cm and toxic appearing) who do not respond to steroid therapy within 72 hours should be consulted for colectomy. Those with less severe disease but do not respond to IV steroids within 7\u201310 days should be considered for colectomy or IV cyclosporine. IV cyclosporine at a rate of 2\u00a0mg/kg/day and if no response in 7\u201310 days, colectomy should be considered. If response is seen, oral cyclosporine at 8\u00a0mg/kg/day should be continued for 3\u20134 months while 6-MP or azathioprine is introduced. Those already on 6-MP or azathioprine should continue with these medications. A cholesterol level should be checked in patients taking cyclosporine as low cholesterol may predispose to seizures. Also, prophylaxis against PCP ( Pneumocystis carinii ) pneumonia is advised."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3228", "text": "Unlike Crohn's disease, which cannot be cured/eliminated by surgically removing the diseased portions of the intestine and reconnecting the healthy ends, ulcerative colitis can generally be cured by surgical removal of the large intestine.  Surgical removal of the large intestine will not get rid of extra-intestinal symptoms. This procedure is necessary in the event of  exsanguinating   hemorrhage , frank perforation, or documented or strongly suspected  carcinoma . Surgery is also indicated for patients with severe colitis or toxic megacolon. Patients with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life. Depending on the type of surgery performed, the patient may still require periodic lower endoscopies to assess the pouch for dysplasia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3229", "text": "Ulcerative colitis is a disease that affects many parts of the body outside the intestinal tract. In rare cases the extra-intestinal manifestations of the disease may require removal of the colon. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3230", "text": "A  Cochrane  review of  controlled trials  using various probiotics found low-certainty evidence that probiotic supplements may increase the probability of clinical remission.  [ 6 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects.  [ 6 ] Although there was no clear evidence of greater remission when probiotic supplements were compared with  5\u2010aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy. \u00a0 [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3231", "text": "It is currently unclear whether probiotics help to prevent future relapse in people with stable disease activity, either as a monotherapy or  combination therapy .  [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3232", "text": "There is no good evidence that dietary interventions have any impact on ulcerative colitis. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3233", "text": "The free radical induction theory suggests that the initial cause of ulcerative colitis may be a metabolic defect that allows a buildup of chemicals related to hydrogen peroxide beneath the membrane that protects the cells of the intestinal wall from the bacteria inside the intestine, resulting in destruction of the membrane. During remission the membrane is reestablished, but may be subject to new damage, resulting in a flare up of the disease. [ 2 ]  To the extent this may be true, it would be appropriate to take  antioxidants , dietary supplements that may support the body's defenses against oxidants like hydrogen peroxide. Antioxidants include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3234", "text": "Vitamin B6  and  iron  may be associated with increased hydrogen peroxide levels, and should not be taken in excess under this theory. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3235", "text": "Inflammatory bowel disease is less common in the developing world and it has been suggested that this may be because intestinal parasites are more common in underdeveloped countries. [ 15 ]  Some parasites are able to reduce the immune response of the intestine, an adaptation that helps the parasite colonize the intestine. A decrease in immune response could be helpful in inflammatory bowel disease. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3236", "text": "Helminthic therapy  using the  whipworm   Trichuris suis  was shown in a  randomized control trial  to produce benefit in patients with ulcerative colitis. This therapy tests the  hygiene hypothesis  which argues that the absence of  helminths  in the  colons  of patients in the western world may lead to  inflammation . Both  helminthic therapy  and  fecal bacteriotherapy  induce a characteristic  Th2  white cell response in the diseased areas, which is somewhat paradoxical given that ulcerative colitis immunology was thought to classically involve Th2 overproduction. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3237", "text": "In  medicine , the  urea-to-creatinine ratio  ( UCR [ 1 ] ), known in the United States as  BUN-to-creatinine ratio , is the  ratio  of the blood levels of  urea  ( BUN ) (mmol/L) and  creatinine  (Cr) (\u03bcmol/L). BUN only reflects the nitrogen content of urea (MW 28) and urea measurement reflects the whole of the molecule (MW 60), urea is just over twice BUN (60/28 = 2.14). In the United States, both quantities are given in mg/dL The ratio may be used to determine the cause of  acute kidney injury  or  dehydration ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3238", "text": "The principle behind this ratio is the fact that both urea (BUN) and creatinine are freely filtered by the  glomerulus ; however, urea reabsorbed by the  renal tubules  can be regulated (increased or decreased) whereas creatinine reabsorption remains the same (minimal reabsorption)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3239", "text": "Urea and creatinine are nitrogenous end products of metabolism. [ 2 ]  Urea is the primary metabolite derived from dietary protein and tissue protein turnover. Creatinine is the product of muscle creatine catabolism. Both are relatively small molecules (60 and 113 daltons, respectively) that distribute throughout total body water. In Europe, the whole urea molecule is assayed, whereas in the United States only the nitrogen component of urea (the blood or serum urea nitrogen, i.e., BUN or SUN) is measured. The BUN, then, is roughly one-half (7/15 or 0.466) of the blood urea. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3240", "text": "The normal range of urea nitrogen in blood or serum is 5 to 20\u00a0mg/dl, or 1.8 to 7.1\u00a0mmol urea per liter. The range is wide because of normal variations due to protein intake, endogenous protein catabolism, state of hydration, hepatic urea synthesis, and renal urea excretion. A BUN of 15\u00a0mg/dl would represent significantly impaired function for a woman in the thirtieth week of gestation. Her higher glomerular filtration rate (GFR), expanded extracellular fluid volume, and anabolism in the developing fetus contribute to her relatively low BUN of 5 to 7\u00a0mg/dl. In contrast, the rugged rancher who eats in excess of 125 g protein each day may have a normal BUN of 20\u00a0mg/dl."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3241", "text": "The normal serum creatinine (sCr) varies with the subject's body muscle mass and with the technique used to measure it. For the adult male, the normal range is 0.6 to 1.2\u00a0mg/dl, or 53 to 106 \u03bcmol/L by the kinetic or enzymatic method, and 0.8 to 1.5\u00a0mg/dl, or 70 to 133 \u03bcmol/L by the older manual Jaff\u00e9 reaction. For the adult female, with her generally lower muscle mass, the normal range is 0.5 to 1.1\u00a0mg/dl, or 44 to 97 \u03bcmol/L by the enzymatic method."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3242", "text": "Multiple methods for analysis of BUN and creatinine have evolved over the years. Most of those in current use are automated and give clinically reliable and reproducible results."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3243", "text": "There are two general methods for the measurement of urea nitrogen. The diacetyl, or Fearon, reaction develops a yellow chromogen with urea, and this is quantified by photometry. It has been modified for use in autoanalyzers and generally gives relatively accurate results. It still has limited specificity, however, as illustrated by spurious elevations with sulfonylurea compounds, and by colorimetric interference from hemoglobin when whole blood is used."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3244", "text": "In the more specific enzymatic methods, the enzyme urease converts urea to ammonia and carbonic acid. These products, which are proportional to the concentration of urea in the sample, are assayed in a variety of systems, some of which are automated. One system checks the decrease in absorbance at 340\u00a0nm when the ammonia reacts with alpha-ketoglutaric acid. The Astra system measures the rate of increase in conductivity of the solution in which urea is hydrolyzed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3245", "text": "Even though the test is now performed mostly on serum, the term BUN is still retained by convention. The specimen should not be collected in tubes containing sodium fluoride because the fluoride inhibits urease. Also chloral hydrate and guanethidine have been observed to increase BUN values."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3246", "text": "The 1886 Jaff\u00e9 reaction, in which creatinine is treated with an alkaline picrate solution to yield a red complex, is still the basis of most commonly used methods for measuring creatinine. This reaction is nonspecific and subject to interference from many noncreatinine chromogens, including acetone, acetoacetate, pyruvate, ascorbic acid, glucose, cephalosporins, barbiturates, and protein. It is also sensitive to pH and temperature changes. One or another of the many modifications designed to nullify these sources of error is used in most clinical laboratories today. For example, the recent kinetic-rate modification, which isolates the brief time interval during which only true creatinine contributes to total color formation, is the basis of the Astra modular system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3247", "text": "More specific, non-Jaff\u00e9 assays have also been developed. One of these, an automated dry-slide enzymatic method, measures ammonia generated when creatinine is hydrolyzed by creatinine iminohydrolase. Its simplicity, precision, and speed highly recommend it for routine use in the clinical laboratory. Only 5-fluorocytosine interferes significantly with the test."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3248", "text": "Creatinine must be determined in plasma or serum and not whole blood because erythrocytes contain considerable amounts of noncreatinine chromogens. To minimize the conversion of creatine to creatinine, specimens must be as fresh as possible and maintained at pH 7 during storage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3249", "text": "The amount of urea produced varies with substrate delivery to the liver and the adequacy of liver function. It is increased by a high-protein diet, by gastrointestinal bleeding (based on plasma protein level of 7.5 g/dl and a hemoglobin of 15 g/dl, 500 ml of whole blood is equivalent to 100 g protein), by catabolic processes such as fever or infection, and by antianabolic drugs such as tetracyclines (except doxycycline) or glucocorticoids. It is decreased by low-protein diet, malnutrition or starvation, and by impaired metabolic activity in the liver due to parenchymal liver disease or, rarely, to congenital deficiency of urea cycle enzymes. The normal subject on a 70 g protein diet produces about 12 g of urea each day."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3250", "text": "This newly synthesized urea distributes throughout total body water. Some of it is recycled through the enterohepatic circulation. Usually, a small amount (less than 0.5\u00a0g/day) is lost through the gastrointestinal tract, lungs, and skin; during exercise, a substantial fraction may be excreted in sweat. The bulk of the urea, about 10\u00a0g each day, is excreted by the kidney in a process that begins with glomerular filtration. At high urine flow rates (greater than 2\u00a0ml/min), 40% of the filtered load is reabsorbed, and at flow rates lower than 2\u00a0ml/min, reabsorption may increase to 60%. Low flow, as in urinary tract obstruction, allows more time for reabsorption and is often associated with increases in antidiuretic hormone (ADH), which increases the permeability of the terminal collecting tubule to urea. During ADH-induced antidiuresis, urea secretion contributes to the intratubular concentration of urea. The subsequent buildup of urea in the inner medulla is critical to the process of urinary concentration. Reabsorption is also increased by volume contraction, reduced renal plasma flow as in congestive heart failure, and decreased glomerular filtration."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3251", "text": "Creatinine formation begins with the transamidination from arginine to glycine to form glycocyamine or guanidoacetic acid (GAA). This reaction occurs primarily in the kidneys, but also in the mucosa of the small intestine and the pancreas. The GAA is transported to the liver where it is methylated by S-adenosyl methionine (SAM) to form creatine. Creatine enters the circulation, and 90% of it is taken up and stored by muscle tissue. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3252", "text": "Normal serum values"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3253", "text": "Serum ratios"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3254", "text": "The reference interval for normal BUN/creatinine serum ratio is 12\u00a0: 1 to 20\u00a0: 1. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3255", "text": "An elevated BUN:Cr due to a low or low-normal creatinine and a BUN within the reference range is unlikely to be of clinical significance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3256", "text": "The ratio is predictive of prerenal injury when BUN:Cr exceeds 20 [ 5 ]  or when urea:Cr exceeds 100. [ 6 ]   In prerenal injury, urea increases disproportionately to creatinine due to enhanced proximal tubular reabsorption that follows the enhanced transport of sodium and water."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3257", "text": "The ratio is useful for the diagnosis of  bleeding  from the  gastrointestinal (GI) tract  in patients who do not present with overt vomiting of blood. [ 7 ]  In children, a BUN:Cr ratio of 30 or greater has a sensitivity of 68.8% and a specificity of 98% for upper gastrointestinal bleeding. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3258", "text": "A common assumption is that the ratio is elevated because of amino acid digestion, since blood (excluding water) consists largely of the  protein   hemoglobin  and is broken down by  digestive enzymes  of the upper GI tract into amino acids, which are then reabsorbed in the GI tract and  broken down  into urea.  However, elevated BUN:Cr ratios are not observed when other high protein loads (e.g., steak) are consumed. [ citation needed ]  Renal hypoperfusion secondary to the blood lost from the GI  bleed has been postulated to explain the elevated BUN:Cr ratio. However, other research has found that renal hypoperfusion cannot fully explain the elevation. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3259", "text": "Because of decreased  muscle  mass, elderly patients may have an elevated BUN:Cr at baseline. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3260", "text": "Hypercatabolic states, high-dose glucocorticoids, and resorption of large hematomas have all been cited as causes of a disproportionate rise in BUN relative to the creatinine. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3261", "text": "Ventral rectopexy  is a surgical procedure for external  rectal prolapse , internal rectal prolapse (rectal intussusception), and sometimes other conditions such as  rectocele ,  obstructed defecation syndrome , or  solitary rectal ulcer syndrome . The  rectum  is fixed into the desired position, usually using a biological or synthetic  mesh  which is attached to the  sacral promontory . The effect of the procedure is correction of the abnormal descended position of the posterior compartment of the pelvis (i.e., the rectum), reinforcement of the anterior (front) surface of the rectum, and elevation of the  pelvic floor . [ 3 ]  In females, the rectal-vaginal septum is reinforced, and there is the opportunity to simultaneously correct any prolapse of the middle compartment (i.e., the  uterus ). [ 4 ]  In such cases, ventral rectopexy may be combined with  sacrocolpopexy . [ 5 ] [ 3 ]  The surgery is usually performed  laparoscopically  (via small openings made in the abdomen)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3262", "text": "There are over 300 different variations of surgical procedures described for rectal prolapse, and this area has seen rapid development. [ 3 ]  However, there is no clear consensus regarding the best method. [ 6 ]  Surgical treatment for rectal prolapse may be via the perineal or abdominal (transabdominal / peritoneal) approach. [ 5 ] [ 6 ]  Generally speaking, perineal procedures have less complications but higher rates of recurrence compared to abdominal procedures. [ 7 ]  Ventral rectopexy falls into the abdominal procedure category, and can be considered as a type of abdominal rectopexy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3263", "text": "Abdominal rectopexy encompasses several procedures which involve mobilization and fixation of the rectum, with or without resection, via abdominal approach. Some of types of abdominal rectopexy are now rarely or never performed. For example, the Ripstein rectopexy (anterior fixation of mesh below the sacral promontory) and the Wells procedure (involving detachment of the lateral ligaments of the rectum) have been abandoned. [ 8 ]  In general, abdominal rectopexy procedures have been associated with post-operative problems with defecation such as new or worsened constipation, obstructed defecation or fecal incontinence. [ 9 ] [ 2 ]  This does not seem to be a significant problem with ventral rectopexy, [ 2 ]  which represents the most recent development of abdominal rectopexy. In men, mobilization of the rectum may risk the development of  erectile dysfunction . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3264", "text": "Another way of categorizing surgery for prolapse of pelvic organs is suspensive or resective (involving removal of sections of the bowel wall). Ventral rectopexy alone is a syspensive type surgery, a category which also includes  colposacropexy . [ 10 ]  Resection rectopexy additionally involves removal of a section of the  sigmoid colon  ( sigmoidectomy ). It is thought to have decreased post operative problems of constipation, because the redundant colon is removed and therefore cannot \"kink\". However, there is no evidence that this improves the outcomes, and the necessary creation of an  anastomosis  (surgically created joining between two ends of bowel when a section of bowel is removed) increases the risk of severe complications. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3265", "text": "Ventral rectopexy with an  autologous graft  ( fascia lata ), [ 9 ]  and then with a synthetic mesh for external rectal prolapse was first reported in 1971. [ 11 ]  The Orr-Loygue procedure (lateral mesh rectopexy) was described in 1984. [ 12 ] [ 5 ]  The Orr-Loygue procedure involved anterior and posterior mobilization of the rectum to the level of the levator ani muscle and removal of the pouch of Douglas. Mesh was sutured to the lateral surfaces (sides) of the rectum. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3266", "text": "The Orr-Loygue procedure was modified by D'Hoore in 2004. [ 13 ]  In ventral rectopexy, there is no posterior dissection and mobilization of the rectum apart from to expose the sacral promontory. With no posterior (dorsal) or lateral dissection, damage to the autonomic nerves is minimized. As a result, there are less problems with post-operative constipation. There is no excision of the pouch of Douglas, and the mesh is placed directly onto the anterior (ventral) surface of the rectum. This procedure aims to suspend the middle and lower sections of the rectum. This modified procedure is now known as the anterior rectopexy or ventral rectopexy. [ 1 ]  D'Hoore also used a  laparoscopic  approach (laparoscopic ventral mesh rectopexy, LVMR). [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3267", "text": "After 2002, the minimally invasive trans-anal approach known as  Stapled Trans-Anal Rectal Resection  (STARR) became popular for treating  obstructed defecation syndrome . However, over time, there has been a general trend away from STARR towards abdominal rectopexy for surgical treatment of obstructed defecation syndrome. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3268", "text": "Ventral mesh rectopexy has become the one of the most popular options for rectal prolapse. [ 16 ] [ 7 ]  Ventral rectopexy also provides the opportunity to simultaneously correct any prolapse of the middle compartment of the pelvis, [ 4 ]  and is sometimes combined with  sacrocolpopexy . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3269", "text": "There has been some controversy connected with transvaginal placement of mesh in the treatment of  pelvic organ prolapse  and  stress urinary incontinence . This is because there is a risk of erosion (tissue breakdown around the mesh) and sepsis (infection). [ 4 ]  In 2008 and 2016 the  US Food and Drug Administration  published guidance about potential serious complications caused by such meshes and upgraded their risk classification of such meshes from Class II (moderate risk) to Class III (high risk). Procedures involving transvaginal mesh have since decreased by 40\u201360% in the USA. [ 14 ]  In 2011, manufacturers of permanent transvaginal meshes withdrew the products from the market. [ 17 ]  In Europe, the  Scientific Committee on Emerging and Newly Identified Health Risks  (SCENIHR) stated in 2015 that implantation of any mesh via the vaginal route should be done only in complicated cases where a primary repair has failed. [ 14 ]  A  Cochrane review  in 2016 stated that the risks were higher with such meshes compared to native tissue repair (using the patient's own tissues instead of mesh). [ 17 ]  Transvaginal meshes have higher risk of repeat surgery, injury to the bladder, and stress urinary incontinence which appears after the surgery. [ 17 ]  They concluded that transvaginal meshes have limited benefit in the primary surgical management of pelvic organ prolapse and stress urinary incontinence. [ 17 ] [ needs update ]  The review was updated in 2024 with the same conclusions but based on newly available evidence. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3270", "text": "In response to the controversy connected with transvaginal meshes, the Pelvic Floor Society on behalf of the Association of Coloproctology of Great Britain and Ireland issued a position statement regarding the use of mesh in ventral rectopexy in 2020. They stated that meshes in ventral rectopexy are not the same because the mesh is inserted between the rectum and the vagina and not directly into the vagina as with transvaginal meshes. [ 14 ]  They also stated that according to current evidence ventral mesh rectopexy is the best available treatment to restore normal rectal function, and that the estimated overall risk of complications is about 2.5% based on the worst-case scenario. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3271", "text": "The definitive indication for ventral rectopexy is:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3272", "text": "Relative indications are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3273", "text": "Absolute contraindications are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3274", "text": "Relative contraindications are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3275", "text": "There are 3 options for surgical approach: open abdominal surgery, laparoscopic approach or  robotic surgery . The laparoscopic approach is safer than open surgery, [ 4 ]  and there is less risk of complications after the procedure. [ 23 ]  There is also less blood loss, less pain after the procedure, shorter average length of stay in hospital and faster recovery. [ 8 ] [ 23 ]  Rarely, the procedure must be converted into an open abdominal surgery. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3276", "text": "The procedure is still almost always carried out via laparoscopic approach. [ 14 ]  However, increasingly some surgeons use robotic surgery to conduct the procedure. [ 5 ]  Some surgeons claim that the use of robotic surgery makes ventral rectopexy less technically demanding, because it requires careful dissection and suture placement in a tight, narrow space. [ 1 ]  This is especially true in patients with a narrow pelvis. [ 16 ]  Laparoscopic ventral rectopexy is also difficult in patients who are obese. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3277", "text": "Robotic approach has the benefit of three-dimensional visualization, precise dissection and the possibility of refined, articulated movements suitable for a narrow conical space such as the pelvis. [ 16 ]  There is less trauma to the tissues and less blood loss compared to conventional laparoscopy. [ 8 ]  In the case of ventral rectopexy, which is considered a difficult procedure requiring a lot of training (100 cases), robotic surgery is reported to speed up the learning curve for surgeons (20 cases). [ 8 ]  Longer operation times are usually reported with robotic surgery, but operation time is less With surgeons who are experienced in using the robotic technique. [ 8 ]  The laparoscopic approach is cheaper than robotic surgery, [ 16 ]  but when considering the reduced hospital stay, robotic surgery may be cheaper overall. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3278", "text": "The choice of synthetic material used to perform the rectopexy may also vary and can include nylon, Teflon, Marlex, Ivalon, Gore\u2010Tex, Vicryl or Dexon. There is debate regarding the best mesh material, and whether a biologic or synthetic mesh is superior. One systematic review found no significant difference between biologic or synthetic mesh with regards to the rates of mesh erosion or recurrence of prolapse. [ 21 ]  However, a later systematic review reported lower rate of mesh erosion for biologic mesh (0.22%) compared to synthetic mesh (1.87%). [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3279", "text": "Usually one strip of mesh is placed, but sometimes two are used. [ 7 ]  The meshes are 15, 17 or 20\u00a0cm long. [ 7 ]  Tackers (Protack), titanium screw tacks, or sutures (absorbably or non-absorbable) are used to fix the mesh to the sacral promontory. [ 7 ]  Absorbable or non-absorbable sutures (Ethibond, prolypropylene), or 4mm titanium staples are used to fix the mesh to anterior rectal wall. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3280", "text": "After the procedure, patients are advised to avoid sex and lifting heavy weights, and to use laxatives for 6 weeks. [ 5 ]  Continuing pelvic floor physical therapy may be beneficial in those cases where people had symptoms of obstructed defecation or incontinence before the procedure. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3281", "text": "According to one publication, risk of a complication occurring is 14%. [ 5 ]  Another systematic review reported an average complication rate of 4.8%. [ 7 ]  Complications involving the urinary tract are most common and mesh related complications are less common. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3282", "text": "Recurrence of the prolapse after ventral rectopexy is possible. Recurrence rates are reported as between 1.4 and 9.7% of cases. Recurrence occurs sooner and the overall rate is higher when ventral rectopexy is performed on a prolapse which has already recurred in the past (25% of cases after 5 years). Risk factors for recurrence after ventral rectopexy include old age, male gender, higher  body mass index , higher Cleveland Clinic incontinence score, prolonged  pudendal nerve terminal motor latency , weak pelvic floor, [ 5 ] [ 7 ]   benign joint hypermobility syndrome , [ 4 ]  and excessive perineal descent associated with chronic straining. [ 4 ]  Mesh of 20\u00a0cm length has lower risk of recurrence than mesh of 15\u201317\u00a0cm. [ 5 ]  Recurrence may occur as either full thickness prolapse or mucosal prolapse. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3283", "text": "Recurrence may occur if the mesh slips from the sacral promontory. This may happen because of inadequate fixation and adherence of the mesh to the anterior rectal wall or to the sacral promontory, or incorrectly placed staples to the upper sacrum. [ 5 ] [ 7 ]  Another technical reason for relapse is inadequate dissection on the anterior aspect of the rectum. [ 7 ]  Recurrence can be a challenging situation for surgeons, [ 7 ]  and in this case the patient is re-evaluated for 6 months to identify the reason for the recurrence. [ 5 ]  A further surgical procedure to re-fix the mesh may be required. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3284", "text": "Overall risk of complications associated with the mesh have been reported as 2.5%. [ 14 ]  Such complications include detachment and migration of the mesh. This complication is reported at a rate of 4.6% of cases. [ 5 ]  The mesh can erode into the vagina (1.3% of cases), or into the rectum.  The risk of mesh complications appears to be low regardless of what mesh material is used. [ 21 ]  However, biologic mesh may have a lower risk of complications compared to synthetic mesh. [ 23 ]  When suturing synthetic mesh to the rectum, the use of absorbable sutures leads to lower risk of complications compared to non-resorbable sutures. [ 5 ]   When mesh erosion into the vagina occurs, a further surgical procedure is required to remove the tissue from the mesh and to close the vaginal wall over the defect. [ 5 ]  Most mesh-related complications can be treated successfully. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3285", "text": "At the site where the mesh is attached (lumbosacral region), vertebral  discitis  may occur. This is a rare but serious complication. In one case, the discitis may have been caused by the use of titanium screws. Signs and symptoms of discitis include chronic back pain and infection. Discitis is treated with intravenous antibiotics and possible removal of the mesh. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3286", "text": "Urinary-related complications include  urinary tract infection ,  urinary retention , damage to structures like the  ureter ,  bladder  or  vas deferens . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3287", "text": "Other possible complications are infection or hernia at the port site,  ileus  and small bowel injury. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3288", "text": "The average improvement in fecal incontinence is reported as 62.5 [ 7 ]  to 79.3%, [ 5 ]  and the average improvement in constipation from 76.6% [ 7 ]  to 71%. [ 5 ]  However, these conditions may not fully resolve after the procedure. [ 5 ]  Ventral rectopexy may be more effective as an initial surgical repair of a prolapse rather than treatment for a recurrent prolapse which was previously operated upon. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3289", "text": "One systematic review comparing laparoscopic ventral mesh rectopexy and robotic ventral mesh rectopexy concluded that robotic approach resulted in a longer operation time. [ 16 ]  However, this may be related to lack of operator experience with the robotic platform, and it has been suggested that a surgeon who is experienced with the robotic approach can perform the operation as fast or faster than a surgeon who is experienced with the laparoscopic approach. The robotic approach resulted in a shorter stay in hospital for patients, which balanced the increased cost of the robotic surgery itself. This may be because robotic surgery is more precise and leads to less bleeding and pain after the procedure. One study showed lower scores for obstructed defecation after robotic approach. In general, both approaches showed improvement in function and quality of life, but some studies reported robotic approach as giving slightly more improvement in quality of life. Both approaches resulted in similar long term outcome and recurrence rates. The review authors concluded that robotic ventral mesh rectopexy is safe and results in at least the same outcomes as laparoscopic approach. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3290", "text": "The most commonly used material for synthetic mesh is polypropylene. This material has a lower risk of mesh exposure compared to polyester. [ 19 ]  The two most common biologic mesh products are Permacol, which is cross-linked collagen, and Biodesign, which is non-cross linked. It is not known if one type of biologic mesh is better. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3291", "text": "In 2020 another systematic review compared the use of synthetic mesh and biologic mesh in ventral mesh rectopexy for external rectal prolapse or symptomatic internal rectal prolapse. [ 19 ]  The review included 32 studies containing a total of 4001 cases where synthetic mesh was used and 762 where biologic mesh was used. The rate of mesh-related complications ranged from 0 to 2.4% for synthetic mesh, with a pooled incidence rate of 1%. The rate of mesh-related complications ranged from 0 and 0.7% for biologic mesh. The rate of recurrence ranged from 1.1 to 18.8% for synthetic mesh. The rate of recurrence ranged from 0 to 15.4% for biologic mesh. The reviewers stated that the risk of mesh related complications are low for both synthetic and biologic mesh, and there may a small reduction in mesh-related complications with biologic mesh. However, due to lack of sufficient high quality data for biologic mesh, they were unable to make definitive conclusions. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3292", "text": "One systematic review compared laparoscopic suture rectopexy with laparoscopic mesh rectopexy in the treatment of full-thickness rectal prolapse (external rectal prolapse, complete rectal prolapse). Compared to suture rectopexy, mesh rectopexy had lower rate of recurrence and longer operation time. There were no differences in degree of improvement of constipation, incontinence, bleeding during the surgery, length of stay in hospital, and overall rate of complications after the surgery. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3293", "text": "A  wale mark ,  red wale sign  or  wale sign  is an endoscopic sign suggestive of recent hemorrhage, or propensity to bleed, seen in individuals with  esophageal varices  at the time of  endoscopy .  The mark has the appearance of a longitudinal red streak located on an esophageal varix.  It derives its name from the visual similarity to patterns seen in the  textile   corduroy . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3294", "text": "Similar lesions that are suggestive of recent or impending bleeding from esophageal varices include the  cherry-red  spot, which is circular and red in colour.  Bleeding risk of esophageal varices can be ascertained at the time of endoscopy by evaluating for the presence of these markers. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3295", "text": "Aceglutamide  (brand name  Neuramina ), or  aceglutamide aluminium  (brand name  Glumal ), also known as  acetylglutamine , is a  psychostimulant ,  nootropic , and  antiulcer agent  that is marketed in  Spain  and  Japan . [ 1 ] [ 2 ] [ 3 ] [ 4 ]  It is an  acetylated  form of the  amino acid   L -glutamine , the  precursor  of  glutamate  in the body and  brain . [ 5 ]  Aceglutamide functions as a  prodrug  to glutamine with improved  potency  and  stability . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3296", "text": "Aceglutamide is used as a psychostimulant and nootropic, while aceglutamide aluminium is used in the treatment of ulcers. [ 6 ] [ 7 ] [ 8 ] [ 9 ]  Aceglutamide can also be used as a liquid-stable source of glutamine to prevent damage from protein energy malnutrition. [ 10 ] [ 11 ] [ 12 ]  The drug has shown  neuroprotective  effects in an  animal model  of  cerebral ischemia . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3297", "text": "Acetoxolone  (also known as acetylglycyrrhetic acid, acetylglycyrrhetinic acid, glycyrrhetinyl acetate and glycyrrhetic acid acetate) is a drug used for  peptic ulcer  and  gastroesophageal reflux disease . [ 1 ]   It is an  acetyl  derivative of  glycyrrhetinic acid . It is found in  Echinopora  lamellosa. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3298", "text": "Alicaforsen  (trade name  Camligo ) is an  antisense  oligonucleotide therapeutic that targets the  messenger RNA  for the production of human  ICAM-1  receptor [ 1 ]   and is being developed for the treatment of acute disease flares in moderate to severe  Inflammatory Bowel Disease  (IBD)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3299", "text": "Alicaforsen inhibits ICAM-1 production, which is an important adhesion molecule involved in leukocyte migration and trafficking to the site of inflammation. Hitherto, alicaforsen has been granted orphan drug designation and is prescribed as an unlicensed medicine in accordance with international regulation, for the treatment of  pouchitis  and left-sided  ulcerative colitis . Given the positive results from an open-label trial and one case series in patients with chronic refractory pouchitis,  US FDA  has agreed to a rolling submission for a license application for the treatment of pouchitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3300", "text": "It was discovered by  Ionis Pharmaceuticals  (formerly Isis Pharmaceuticals) and in 2017  Atlantic Healthcare plc took over the development for chronic antibiotic refractory  pouchitis  in an  enema  formulation. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3301", "text": "ICAM-1 promotes the  extravasation  and activation of  leukocytes  (white blood cells), which is part of the  inflammation  process. [ 3 ]   Alicaforsen inhibits the activity of  ICAM-1  protein by degrading  mRNA  coding for it via an  RNase-H  based mechanism. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3302", "text": "It appears to have better efficacy as a  topical medication  than via  systemic administration  which is typical of antisense drugs. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3303", "text": "In a Phase III randomised clinical trial with 299 patients with steroid dependent Crohn's disease, clinical response was correlated with drug exposure, with significant efficacy versus placebo being observed in the subgroup with greatest area under the curve, hence pharmacodynamic modelling suggests that alicaforsen (ISIS 2302) may be an effective therapy at adequate dose levels. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3304", "text": "In another placebo-controlled study with 331 subjects with active Crohn's Disease, alicaforsen failed to demonstrate efficacy in any of its primary outcome measures. However there was a suggestion of a therapeutic response in a sub-population with elevated serum CRP (C-reactive Protein) levels >2mg/dl. The differential response highlights the confounding symptoms of a large subset of subjects whose needs are apparently not being met by the current clinical trial design. There is a need for more specific biomarkers that clearly can identify disease severity and subtypes of Crohn's disease and can be used to monitor disease response objectively. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3305", "text": "Alicaforsen is a 20 unit phosphorothioate modified antisense  oligonucleotide . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3306", "text": "Alicaforsen was discovered and initially developed by Isis Pharmaceuticals, [ 7 ]  which changed its name to  Ionis Pharmaceuticals  in 2015."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3307", "text": "Isis partnered on development of alicaforsen with  Boehringer Ingelheim  starting in 1995; that deal ended in 1999, after each of IV and subcutaneously delivered alicaforsen failed in phase III trials for  Crohn's disease  and development of those formulations in that indication was terminated; development for  rheumatoid arthritis  was terminated the same year and development in kidney transplant apparently ceased as well at that time. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3308", "text": "The company reformulated alicaforsen as an  enema  and three small trials were published between 2004 and 2006, an open label trial in chronic  pouchitis  and two randomized trials in  ulcerative colitis  (UC); in the UC trials the drug missed its primary endpoint of improvements at 6 weeks, but showed a better effect in the longer term (between 18 and 30 weeks). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3309", "text": "A post hoc meta-analysis of individual data of 200 patients from four phase 2 studies evaluating nightly alicaforsen 240 mg enema for six weeks showed that alicaforsen is effective in patients with active, distal, moderate to severe UC. The efficacy of alicaforsen was durable in these sub-groups, with significantly improved duration of clinical response with no maintenance therapy, suggesting a disease-modifying effect. This analysis suggests that alicaforsen enema could offer an effective, potentially durable response in moderate/severe distal active UC. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3310", "text": "Alicaforsen was licensed to Atlantic Healthcare in 2007. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3311", "text": "The use of the enema formulation of alicaforsen to treat  pouchitis  was granted  orphan drug  status in the US in 2008 [ 10 ]  and received the same in Europe in 2009. [ 11 ]   The enema formulation of alicaforsen for  pouchitis  received  FDA Fast Track  designation. [ 12 ]  In a subsequent multicentre Phase 3 clinical trial in 138 subjects with Active, Chronic, Antibiotic Refractory Primary Idiopathic  Pouchitis , showed a clinically relevant 34% remission in stool frequency with 8% delta vs placebo. However the co-primary endpoints (an adaptation of the Mayo Score of improvement in endoscopic remission and bowel frequency) were not met, perhaps due to the high discontinuation rate of 35% that compromised the sample size available for statistical analysis. Disallowing background maintenance therapies contributed to this high dropout rate in this challenging, heterogenous patient group. Further the appropriateness of endoscopy as a primary end point is questionable."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3312", "text": "Atlantic Healthcare has supplied over 350 courses of alicaforsen enema treatment on a named patient / compassionate use programme. Clinical outcomes published in case series have confirmed durable disease remission in patients with Ulcerative Colitis with no treatment related SAEs. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3313", "text": "\u2022 \u00a0 \u00a0UC case series publications confirming prolonged duration of action:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3314", "text": "\u00d8  \u00a0 \u00a0Digestive Diseases Journal  (Nov 2017); 10/12 patients with left-sided UC/proctitis responded to treatment, with a median durable response of 18 weeks"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3315", "text": "\u00d8  \u00a0 \u00a0Gastrodagarna Congress, Sweden  (May 2016); all 7 distal UC patients that completed treatment responded, 57% remained in remission for 5-20 months"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3316", "text": "\u00d8  \u00a0 \u00a0Irish Society of Gastroenterology  (Nov 2014); reported remission achieved in 57% of patients with UC with a durable response  1"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3317", "text": "No drug-related SAEs have been reported in any usage of alicaforsen enema"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3318", "text": "Alka-Seltzer  is an  effervescent   antacid  and pain reliever owned by  Bayer  since 1978. First marketed by the  Dr. Miles Medicine Company  of  Elkhart, Indiana ,  United States , Alka-Seltzer contains three active ingredients:  aspirin  (acetylsalicylic acid or ASA),  sodium bicarbonate , and  anhydrous   citric acid . [ 1 ]  The aspirin is a pain reliever and  anti-inflammatory , the sodium bicarbonate is an antacid, and the citric acid reacts with the sodium bicarbonate and water to form  effervescence . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3319", "text": "It was developed by head chemist Maurice Treneer. [ 3 ] [ 4 ]  Alka-Seltzer is marketed for relief of minor aches, pains,  inflammation ,  fever ,  headache ,  heartburn ,  stomach ache ,  indigestion ,  acid reflux , and  hangovers  while  neutralizing  excess  stomach acid . [ 4 ]  It was launched in 1931. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3320", "text": "Its sister product, Alka-Seltzer Plus, treats cold and flu symptoms. A wide variety of formulae, many using  acetaminophen  (paracetamol) instead of aspirin, are available under the sister brand. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3321", "text": "Alka-Seltzer is a combination of  sodium bicarbonate ,  aspirin , and  anhydrous   citric acid  used for the relief of heartburn, acid indigestion, and stomach aches. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3322", "text": "Alka-Seltzer is sold in foil packets, each containing two tablets. Prior to 1984, it was also available stacked in cylindrical glass bottles. It is available in many different flavors."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3323", "text": "It was once marketed as a cure-all; at one time, its ads even suggested taking it for \"the blahs\". Subsequent promotion has taken into consideration that aspirin is a drug that is not tolerated by everyone, and the product is no longer advertised in this fashion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3324", "text": "Alka-Seltzer marketed as an antacid no longer contains aspirin (ASA).  [ 8 ]  The original effervescent formula has aspirin as its main active ingredient, and is marketed for pain relief."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3325", "text": "Though important to the overall effect of the medication, the aspirin ( acetylsalicylic acid ) is not required to produce the  effervescent  action of Alka-Seltzer; the effervescence is produced by the baking soda ( sodium bicarbonate ) and  citric acid  reacting to form sodium citrate and carbon dioxide gas. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3326", "text": "The product has been extensively advertised since its launch in the United States. It was originally marketed by Mikey Wiseman, a company scientist of Dr. Miles Medicine Company, who also helped direct its development."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3327", "text": "Print advertising was used immediately, and in 1932 the radio show  Alka-Seltzer Comedy Star of Hollywood  began, with  National Barn Dance  following in 1933, along with many more. The radio sponsorships continued into the 1950s, with the  Alka-Seltzer Time  show airing from 1949 to 1957."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3328", "text": "In his 1976 revival, American actor and radio performer  Richard Beals  proclaimed Alka-Seltzer's virtues and sang the \"Plop, plop, fizz, fizz, oh what a relief it is\" song in his iconic high, squeaky voice. In the early 1960s, a commercial showing two tablets dropping into a glass of water instead of the usual one caused sales to double. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3329", "text": "Alka-Seltzer TV ads from the 1960s and 1970s in the US were among the most popular of the 20th century, ranking number 13, according to  Advertising Age . To increase sales in a relatively flat business, Bayer  revived several of the vintage spots. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3330", "text": "During the race for space in the early 1960s before the Moon landing, there was a commercial with Speedy in a space suit and a jingle with the lyrics \"On Man's first trip through space, I only hope that I'm aboard, securely strapped in place. They'll track our ship with radar and telescopes and soon, imagine seeing Speedy Alka-Seltzer on the moon!\" [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3331", "text": "George Raft  starred in the 1969 Alka-Seltzer commercial \"The Unfinished Lunch\". It consisted of Raft incarcerated in a prison lunchroom. He takes a bite of the prison food and recoils. Suddenly he bangs his cup on the steel table. It ripples throughout the room. He starts intoning \"Alka-Seltzer, Alka-Seltzer...\" Soon, the other hundreds of inmates do the same. The commercial became so popular that several weeks later, Raft appeared as a guest on  The Tonight Show Starring Johnny Carson . Raft told Carson that it took more than 7 hours to tape the 30-second commercial. Raft was enraged by the end of the day, thus making his inmate portrayal that much more convincing for the final editing. The film crew gave Raft his crumpled tin cup, which he showed to Carson and the audience. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3332", "text": "An animated mid-1960s commercial, animated by  R. O. Blechman , shows a man and his own stomach sitting opposite each other in chairs, having an argument moderated by their therapist in a voiceover. The stomach (voiced by  Gene Wilder ) accuses the man of purposely trying to irritate it. The man accuses his stomach of complaining too much about the foods he likes. The therapist suggests Alka-Seltzer and that the two must take care of each other. The closing words are of the stomach saying to the man: \"Well, I'll try \u2014 if you will.\" [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3333", "text": "Alka-Seltzer had a series of commercials during the mid-1960s that used a song called \" No Matter What Shape (Your Stomach's In) \". A different version was recorded by  The T-Bones  and was released as a single, which became a hit in 1966. The ads featured only the midsections (no faces) of people of all shapes and sizes. A clip of the ad can be seen briefly in the 1988 motion picture  The In Crowd , immediately before the movie's first live broadcast of the fictitious \"Perry Parker's Dance Party.\""}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3334", "text": "In an Alka-Seltzer commercial from 1969, an actor named \"Jack\" (played by  Jack Somack ) in a commercial for the fictional product \"Magadini's Meatballs\" has to eat a meatball and then say \"Mamma mia, that's-a spicy meat-a ball-a!\" in an ersatz Italian accent. Take after take is ruined by some comedic trial or another (comedian  Ronny Graham  dropping the clapperboard). By the commercial's end, Jack has eaten so many meatballs that it's \"Alka-Seltzer to the rescue.\" With his stomach settled, Jack does a perfect take, except that the oven door falls off. The director (off-camera) sighs and says, \"OK, let's break for lunch.\" [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3335", "text": "A 1970 commercial shows a newlywed couple in the bedroom after the woman (played by  Alice Playten ) has finished serving her husband (played by  Terry Kiser ) a giant dumpling; the implication is that her cooking skills are severely lacking, despite her husband's lament, \"I can't believe I ate that whole thing!\", the commercial's  catchphrase . She lies on the bed in delusional triumph. She offers her beleaguered husband a heart-shaped meatloaf; he disappears to take some Alka-Seltzer. When she hears the fizzy noise coming from the bathroom, he quickly covers the glass of dissolving Alka-Seltzer as she wonders aloud if it is raining. Just when he has recovered his well-being, he hears her misreading recipes for dinner the next night: \"Marshmallowed meatballs,\" \"medium salad snails,\" and \"pouched (actually poached) oysters\". He returns to the bathroom for more Alka-Seltzer. [ 10 ]  The catchphrase, Howie Cohen told the  Los Angeles Times , was inspired when he ate too much of the food at a  London  commercial shoot because \"I am a nice Jewish kid from the Bronx, so I ate everything,\" and when he told his wife \"I can't believe I ate the whole thing\", she said, \"There's your next Alka-Seltzer commercial.\" [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3336", "text": "A 1971 commercial featured another catch-phrase from Cohen (along with Bob Pasqualina), \"Try it, you'll like it!\" It was remade with  Kathy Griffin  in 2006. [ 12 ]  In 1972, an actor (Milt Moss) spent the commercial moaning, \"I can't believe I ate that who-o-o-o-o-ole thing\" while his wife (Lynn Whinic) made sarcastic comments and finally advised him to take some Alka-Seltzer. [ 13 ]  In 2005, this ad was also remade, featuring  Peter Boyle  and  Doris Roberts  from the 1996\u20132005 TV sitcom  Everybody Loves Raymond . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3337", "text": "In 2009, the brand was featured in television commercials supporting the  United States Ski Team  that included alpine skier  Lindsey Vonn  and Nordic combined skier  Bill Demong . Miniature figures of the Speedy mascot were shown with each. Alka-Seltzer products are sold in nighttime [ 15 ]  and daytime, or nondrowsy, [ 16 ]  formulas. The non-drowsy claims have recently been questioned. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3338", "text": "In 1951, the \"Speedy\" character was introduced. The character was conceived by creative directors Bob Watkins and Chuck Tennant of the Wade Advertising agency and designed by illustrator  Wally Wood . Originally named Sparky, the name was changed to Speedy by sales manager Perry L. Shupert to align with that year's promotional theme, \"Speedy Relief\". Speedy appeared in over 200 TV commercials between 1954 and 1964. [ 18 ]  His body was one Alka-Seltzer tablet, while he wore another as a hat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3339", "text": "Buster Keaton  appeared along with the animated Speedy Alka-Seltzer figure in a series of 1950s commercials based on the product slogan, \"Relief is just a swallow away.\" Speedy Alka-Seltzer was voiced by  Dick Beals ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3340", "text": "Paul Margulies  (father of actress  Julianna Margulies ) created the famous \"Plop, plop, fizz, fizz\" ad campaign when he worked as a  Madison Avenue  ad executive. The ubiquitous jingle was composed by Tom Dawes, a former member of  The Cyrkle . The slogan was altered to \"Plink, plink, fizz\" in the United Kingdom. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3341", "text": "Speedy was revived for a \"Plop, plop, fizz, fizz\" song spot in 1976."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3342", "text": "Sammy Davis Jr. , recorded two versions of the \"Plop Plop Fizz Fizz\" jingle in 1978, one of which (the \"big band\" version) was featured on a television commercial. Both the big band and rock versions had additional lyrics (with at least one verse unique to each song) written by Tom Dawes, former lead singer of  The Cyrkle  who wrote the original jingle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3343", "text": "Speedy was again revived in 2008 when Alka-Seltzer began a series of new commercials featuring him (using a  CGI  character created by animation director  David Hulin  to recreate the stop-motion puppetry of the 1950s and 1960s); in these ads, he was voiced by  Debi Derryberry . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3344", "text": "Alverine  is a drug used for  functional gastrointestinal disorders . Alverine is a  smooth muscle  relaxant. Smooth muscle is a type of muscle that is not under voluntary control; it is the muscle present in places such as the  gut  and  uterus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3345", "text": "The side effects of Alverine include: [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3346", "text": "It was reported that alverine may induce toxic  hepatitis . [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3347", "text": "Alverine acts directly on the muscle in the gut, causing it to relax. Alverine is a 5HT1A antagonist, which reduces rectal hypersensitivity. [ 5 ]  This prevents the  muscle spasms  which occur in the gut in conditions such as  irritable bowel syndrome  and  diverticular disease . [ 6 ]  Diverticular disease is a condition in which small pouches form in the gut lining. These pouches can trap particles of food and become inflamed and painful. In irritable bowel syndrome, the normal activity of the gut muscle is lost. The muscle spasms result in symptoms such as  abdominal pain  and  bloating ,  constipation  or  diarrhoea . By relaxing the gut muscle, alverine citrate relieves the symptoms of this condition. Alverine also relaxes the smooth muscle in the womb (uterus). It is therefore also used to treat painful menstruation, which is caused by muscle spasms in the uterus ( dysmenorrhea )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3348", "text": "Alverine capsules [ 7 ]  are now available in the market. There are two strengths of capsule - 60\u00a0mg and 120\u00a0mg. The common dosage for adults and children over 12 years is 60\u2013120\u00a0mg taken one, two or three a day, either before or after meals. Alverine is not suitable for those aged under 12 years. Women who are pregnant or breast-feeding should follow the instruction of doctors for the drug."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3349", "text": "A combination of alverine citrate and  simeticone  (ACS) for irritable bowel syndrome therapy were compared with placebo in a phase IV  clinical trial . [ 8 ]  At week 4, the alverine citrate and simeticone group had lower VAS scores for abdominal pain/discomfort (median: 40\u00a0mm vs. 50\u00a0mm, P = 0.047) and higher responder rate (46.8% vs. 34.3%, OR = 1.3; P = 0.01) as compared with the  placebo  group. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3350", "text": "The drug was firstly authorized for marketing on 03/06/2014. The marketing authorisation holder is Dr. Reddy's Laboratories (UK) Ltd. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3351", "text": "An  aminosalicylate  is a class of medications that is often used to treat  ulcerative colitis [ 1 ]  and  Crohn's disease . The class includes among others: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3352", "text": "Side effects may include  abdominal pain ,  diarrhea ,  headaches , and nausea. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3353", "text": "Anticachexia  (AN-tee-kuh-KEK-see-uh)  is a drug or effect that works against  cachexia  (loss of body weight and muscle mass)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3354", "text": "This  pharmacology -related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3355", "text": "Antisialagogues  are  drugs  or substances that decrease the flow rate of  saliva  and their effect is opposite to that of  sialagogues . [ 1 ]  Their origin may be both natural and synthetic."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3356", "text": "Anticholinergics  generally have antisialagogue effects, and most produce some level of  sedation , both being advantageous in  surgical procedures . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3357", "text": "Classic antisialagogues [ 1 ]  include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3358", "text": "An  antispasmodic  (synonym:  spasmolytic ) is a  pharmaceutical drug  or other agent that suppresses muscle  spasms . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3359", "text": "One type of antispasmodics is used for  smooth muscle  relaxation, especially in tubular organs of the  gastrointestinal tract . The effect is to prevent spasms of the  stomach ,  intestine  or  urinary bladder .\nBoth  dicyclomine  and  hyoscyamine  are antispasmodic due to their  anticholinergic  action. [ medical citation needed ]  Both of these drugs have side effects common to anticholinergics and can worsen  gastroesophageal reflux disease  (GERD). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3360", "text": "Papaverine  is an  opium   alkaloid  used to treat  visceral  spasms, particularly those of the intestines. [ 3 ]   Mebeverine  is a papaverine analog and spasmolytic with a strong and selective action on the smooth muscles of the gastrointestinal tract, particularly of the colon. Despite being anticholinergic, it does not have the systemic anticholinergic side effects seen in other such drugs. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3361", "text": "Peppermint oil  has been traditionally used as an antispasmodic, and a review of studies on the topic found that it \"could be efficacious for symptom relief in  IBS \" [ 5 ]  (as an antispasmodic) although more carefully controlled studies are needed. A later study showed it is an effective antispasmodic when test-applied topically to the intestine during  endoscopy . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3362", "text": "Bamboo shoots have been used for gastrointestinal and antispasmodic symptoms. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3363", "text": "Anisotropine ,  atropine ,  clidinium bromide  are also the most commonly used modern antispasmodics. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3364", "text": "Pharmacotherapy may be used for  acute   musculoskeletal  conditions when  physical therapy  is unavailable or has not been fully successful. Another class of antispasmodics for such treatment includes  cyclobenzaprine ,  carisoprodol ,  diazepam ,  orphenadrine , and  tizanidine . [ 7 ]   Meprobamate  is another effective antispasmodic which was first introduced for clinical usage in 1955 mainly as an  anxiolytic  and soon afterward became a blockbuster psychotropic drug. While clinical usage of meprobamate has largely become obsolete since the development of  benzodiazepines  due to its liability for developing physical   dependence  and severe toxicity during instances of acute   overdose , it is still manufactured and available by prescription. Carisoprodol is similar to meprobamate as they both belong to the  carbamate   drug class  and meprobamate is a clinically significant  active metabolite  of carisoprodol, although carisoprodol itself possesses additional antispasmodic properties which are distinct from its metabolites. Effectiveness has not been clearly shown for  metaxalone ,  methocarbamol ,  chlorzoxazone ,  baclofen , or  dantrolene . [ 7 ]  Applicable conditions include acute back [ 8 ]  or neck pain, or pain after an injury. Long-term use of muscle relaxants in such cases is poorly supported. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3365", "text": "Spasm may also be seen in movement disorders featuring  spasticity  in neurologic conditions such as  cerebral palsy ,  multiple sclerosis , and  spinal cord disease . Medications are commonly used for spastic movement disorders, but research has not shown functional benefit for some drugs. [ 9 ] [ 10 ]  Some studies have shown that medications have been effective in decreasing spasticity, but that this has not been accompanied by functional benefits. [ 9 ]  Medications such as  baclofen ,  tizanidine , and  dantrolene  have been used. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3366", "text": "Aramchol  is an investigational drug being developed by  Galmed Pharmaceuticals  as a first-in-class, potentially disease modifying treatment for nonalcoholic  steatohepatitis , or NASH, a more advanced condition of  non-alcoholic fatty liver disease . [ 1 ] [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3367", "text": "Aramchol, a conjugate of  cholic acid  and  arachidic acid , is a member of a synthetic fatty-acid/bile-acid conjugate (FABAC). FABACs are composed of endogenous compounds, orally administrated with potentially good safety and tolerability parameters. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3368", "text": "Aramchol affects liver fat metabolism and has been shown in a Phase IIa clinical study to significantly reduce liver fat content as well as improve metabolic parameters associated with fatty liver disease. Furthermore, it has been shown to be safe for use, and with no severe adverse effects. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3369", "text": "Aramchol was initially intended to combine a cholesterol solubilizing moiety (a saturated fatty acid) with a bile acid (cholic acid) acting as a vehicle to enable secretion into bile and entry into the enterohepatic circulation to solubilise bile stones. [ 8 ]  However, early in the development, it was observed that Aramchol reduced liver fat infiltration in animals fed a high fat, lithogenic diet. [ 9 ]  This effect was confirmed in other animal models and the development plan was modified according to these findings, as fatty liver is an unmet need. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3370", "text": "Aramchol has been shown to work by two parallel pathways, leading to synergistic effects [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3371", "text": "Aramchol inhibits the activity of  stearoyl coenzyme A desaturase 1  (SCD1) in the liver. This is likely a direct effect since the mRNA of this and other lipogenic genes or the activities of nuclear receptors are not affected. The physiologic effects of SCD1 inhibition are: decreased synthesis of fatty acids, resulting in a decrease in storage triglycerides and other esters of fatty acids. This reduces liver fat (including triglycerides and free fatty acids), and results in an improvement in insulin resistance. [ 10 ]  Aramchol\u2019s mechanism of action, inhibition of the SCD1 enzyme, has been confirmed in human liver microsomes2 and in animal studies by showing a reduction of the SCD1 activity marker, the fatty acid ratio 16:1/16:0, following Aramchol treatment. These studies showed that the SCD1 inhibition effect of Aramchol is partial (can reach to 70 to 83%). Unlike other SCD1 inhibitors, it was shown that Aramchol\u2019s effects are non-atherogenic. [ 8 ]  There are at present no known inhibitors of SCD1 with the established safety and efficacy profile of Aramachol. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3372", "text": "Aramchol activates cholesterol efflux by stimulating (2 to 4-fold) the ABCA1 transporter, a universal cholesterol export pump present in all cells. [ 11 ] [ 12 ]  In animal models, this led to a significant reduction of blood and body cholesterol and an increase in fecal sterol output, mostly neutral sterols. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3373", "text": "Aramchol is the first small molecule that was shown to induce ABCA1-dependent cholesterol efflux without affecting transcriptional control. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3374", "text": "Axelopran  ( INN ,  USAN ) (developmental code name  TD-1211 ) is a  drug  which is under development by  Theravance Biopharma  and licensed to  Glycyx  for all indications. It acts as a  peripherally acting \u03bc-opioid receptor antagonist  and also acts on  \u03ba- , and  \u03b4-opioid receptors , with similar  affinity  for the \u03bc- and \u03ba-opioid receptors and about an order of magnitude lower affinity for the \u03b4-opioid receptor. Recent data suggests that \u03bc-opioid antagonists have a direct effect on  overall survival  in patients with advanced cancer. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3375", "text": "A \u03bc-opioid agonist (e.g., morphine) have been shown to have multiple pro-tumor effects in vivo and in vitro, which can be blocked with \u03bc-opioid antagonists including promoting  angiogenesis , [ 2 ] [ 3 ]  accelerating tumor cell proliferation, [ 4 ] [ 5 ]  and modifying the response to  chemotherapeutics .  An extensive body of literature has shown diverse and profound immunosuppressive effects of \u03bc-opioid activation in vivo and in vitro. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3376", "text": "Recent data for axelopran in three different pre-clinical models of cancer shows that a \u03bc-opioid antagonist isolates distinct effects of the endogenous opioid system on tumor growth and works in combination with  checkpoint inhibitors . The study of axelopran in  melanoma  in a  zebrafish  embryo model with an immature immune system and no  microbiome  tested axelopran direct effects on tumor growth and  metastasis . The study of  breast cancer  in chicken eggs with a functional immune system and no microbiome tested the direct effect of axelopran on tumor weight, tumor immune infiltration, metastasis and angiogenesis. The study of axelopran in MC-38 syngeneic  colorectal cancer  in mice in combination with murine  anti-PD-1  antibody tested the effect of a \u03bc-opioid blockade on tumor volume and survival in a full in vivo model with both fully functional immune system and mature gut function and enteric microbiome."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3377", "text": "All three pre-clinical studies showed a significant impact of axelopran on their respective endpoints, suggesting that \u03bc-opioid blockade is useful across different tumor types and has multiple mechanisms of action, including direct suppression of tumor cell proliferation, angiogenesis and metastasis, and immune surveillance. Furthermore, axelopran and murine anti-PD-1 antibody were synergistic in slowing tumor growth and increasing survival in the syngeneic mouse model."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3378", "text": "Axelopran has potent \u03bc-opioid receptor antagonist activity on the  gastrointestinal tract   in vivo , and thus it produces a dose-dependent inhibition of opioid-induced delaying in gastric emptying in mice and rats following  subcutaneous  or  oral  administration. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3379", "text": "Benexate  (BEX) is an anti-ulcer agent used in the treatment of acid-related disorders. It is unique in its inability to form salts that are both non-bitter and soluble. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3380", "text": "Benexate is approved from treatment of  gastric ulcer  in Japan. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3381", "text": "The  mechanism of action  of benexate involves promotion of  prostaglandin  synthesis,  protein secretion , and blood flow stimulation in the gastrointestinal tract. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3382", "text": "Bevenopran  ( INN ,  USAN ) (former developmental code names  CB-5945 ,  ADL-5945 ,  MK-2402 ,  OpRA III ) is a  peripherally acting \u03bc-opioid receptor antagonist  that also acts on  \u03b4-opioid receptors  and was under development by  Cubist Pharmaceuticals  for the treatment of chronic  opioid -induced  constipation . [ 1 ] [ 2 ] [ 3 ]  It reached  phase III   clinical trials  for this indication before being discontinued. [ 4 ] [ 5 ]"}
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{"_id": "WikiPedia_Gastroenterology$$$corpus_3385", "text": "Bismuth subgallate , with a chemical formula C 7 H 5 BiO 6 , is commonly used to treat malodor by deodorizing  flatulence  and  stools . In the United States, it (bismuth subgallate) is the active ingredient in  Devrom  (internal deodorant), an over-the-counter FDA-approved medicine.  Also, it has been used to treat  Helicobacter pylori  infection and is used in wound therapy.  As an internal deodorant, it is commonly used by individuals who have had  gastrointestinal stoma  surgery, bariatric surgery, fecal incontinence, and irritable bowel syndrome. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3386", "text": "Also, a double blind study in 1974 reported its effectiveness as a flatulence/stool deodorant in ileostomy patients. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3387", "text": "It can cause darkening of the tongue and stools, which is temporary. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3388", "text": "In 1974, a reversible  encephalopathy  was noted and examined in four colon cancer patients taking bismuth subgallate after  abdominoperineal resection . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3389", "text": "Bismuth subgallate is contraindicated in case of  hypersensitivity  to the substance, and should be used with caution in people with  liver disease  or  kidney disease . [ 3 ]  It is grouped in  pregnancy category C [ 3 ]  (risk not ruled out: Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks). During  lactation , very little bismuth subgallate passes over to the child. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3390", "text": "Crystal structure determination of bismuth subgallate revealed it is a  coordination polymer  with the formula [Bi(C 6 H 2 (O) 3 COOH)(H 2 O)] n 2nH 2 O. [ 5 ]  The phenolate oxygen atoms of the gallate ligand chelate to bismuth cations and form chains. The material is nanoporous and the open-channels can be filled with small gas molecules such as carbon dioxide. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3391", "text": "Bismuth subsalicylate , sold generically as  pink bismuth  and under brand names including  Pepto-Bismol ,  Pepti-Calm  and  BisBacter , is a medication used to treat temporary discomfort of the  stomach  and  gastrointestinal tract . This includes an  upset stomach ,  heartburn  or other similar symptoms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3392", "text": "Bismuth subsalicylate has the empirical chemical formula C 7 H 5 BiO 4 , [ 1 ]  and is a  colloidal  substance obtained by  hydrolysis  of  bismuth   salicylate  (Bi(C 6 H 4 (OH)CO 2 ) 3 )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3393", "text": "As a derivative of  salicylic acid , bismuth subsalicylate displays  anti-inflammatory [ 2 ]  and  bactericidal  action. [ 3 ]  It also acts as an  antacid ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3394", "text": "Bismuth subsalicylate is used as an antacid and  antidiarrheal , and to treat some other gastrointestinal symptoms, such as nausea. The means by which this occurs is still not well documented. It is thought to be some combination of the following: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3395", "text": "In vitro  and  in vivo  data have shown that bismuth subsalicylate hydrolyzes in the gut to  bismuth oxychloride  and  salicylic acid  and less commonly  bismuth hydroxide . In the stomach, this is likely an acid-catalyzed hydrolysis. The salicylic acid is absorbed and therapeutical concentrations of salicylic acid can be found in blood after bismuth subsalicylate administration. Bismuth oxychloride and bismuth hydroxide are both believed to have bactericidal effects, as is salicylic acid for  enterotoxigenic  E. coli , a common cause of \" traveler's diarrhea \". [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3396", "text": "Organobismuth compounds have historically been used in growth media for selective isolation of microorganisms. Such salts have been shown to inhibit proliferation of  Helicobacter pylori , other enteric bacteria, and some fungi. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3397", "text": "There are some  adverse effects . It can cause a  black tongue  and black  stools  in some users of the drug when it combines with trace amounts of  sulfur  in saliva and the colon to form  bismuth sulfide . [ 7 ]  Bismuth sulfide is a highly insoluble black salt, and the discoloration seen is temporary and harmless."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3398", "text": "Long-term use (more than six weeks) may lead to accumulation and toxicity. [ 8 ]  High daily intake over a period of months can possibly cause severe fatigue, weakness and neurological symptoms that reverse with discontinuation. [ 9 ]  Some of the risks of  salicylism  can apply to the use of bismuth subsalicylate. [ 10 ] [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3399", "text": "Children should not take medication with bismuth subsalicylate while recovering from  influenza  or  chicken pox , as epidemiologic evidence points to an association between the use of  salicylate -containing medications during certain viral infections and the onset of  Reye syndrome . [ 13 ]  For the same reason, it is typically recommended that nursing mothers not use medication containing bismuth subsalicylate because small amounts of the medication are excreted in human breast milk, and these pose a theoretical risk of Reye syndrome to nursing children. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3400", "text": "Salicylates are very toxic to cats, and thus bismuth subsalicylate should not be administered to cats. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3401", "text": "The  British National Formulary  does not recommend bismuth-containing antacids (unless  chelated ), cautioning that absorbed bismuth can be neurotoxic, causing encephalopathy, and that such antacids tend to be constipating. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3402", "text": "There is an increased risk of  bleeding  when using bismuth subsalicylate and anticoagulation therapy, like  Coumadin (Warfarin) . [ 17 ] [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3403", "text": "Bismuth salts were in use in Europe by the late 1700s. The combination of bismuth subsalicylate and zinc salts for astringency with  salol  (phenyl salicylate) appears to have begun in the US in the early 20th century as a remedy for life-threatening diarrhea in infants with  cholera . At first sold directly to physicians, it was first marketed as  Bismosal  in 1918. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3404", "text": "Pepto-Bismol was first sold in 1900 [ 20 ]  by a doctor in New York. It was originally sold as a remedy for infant diarrhea by  Norwich Pharmacal Company  under the name \"Bismosal: Mixture Cholera Infantum\". [ 20 ]  It was renamed Pepto-Bismol in 1919. Norwich Eaton Pharmaceuticals was acquired by Procter and Gamble in 1982. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3405", "text": "As of 1946 and 1959, Canadian advertisements placed by Norwich show the product as Pepto-Besmal both in graphic and text. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3406", "text": "Pepto-Bismol is an  over-the-counter drug  currently produced by the  Procter & Gamble  company in the United States, Canada and the United Kingdom. Pepto-Bismol is made in chewable tablets [ 24 ]  and swallowable caplets, [ 25 ]  but it is best known for its original formula, which is a thick liquid. This original formula is a medium pink in color, with a  teaberry  ( methyl salicylate ) flavor. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3407", "text": "Generic bismuth subsalicylate and other branded versions of the drug are widely available in pill and liquid form."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3408", "text": "Despite its common usage and commercial significance, the exact structure of the pharmaceutical long remained undetermined, but was revealed, through the use of advanced  electron crystallography  techniques, to be a layered coordination polymer with the formula BiO(C 7 H 5 O 3 ). [ 27 ]  In the structure, both the carboxylate and phenol groups of the salicylate coordinate towards the bismuth cations. The determination of bismuth subsalicylate had long been hindered due to the small particle size as well as defects within the structure, arising from variations in the stacking arrangement of the bismuth subsalicylate layers, which could be observed as part of the structural investigation. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3409", "text": "Bromo-Seltzer  is a brand of  antacid  formulated to  relieve pain  occurring together with  heartburn ,  upset stomach , or  acid indigestion . It originally contained  sodium bromide  and  acetanilide , both toxic substances which were eventually removed. Its current formulation contains the pain reliever  aspirin  and two reactive chemicals\u00a0\u2013  sodium bicarbonate  and  citric acid \u00a0\u2013 which creates effervescence when mixed with water. Sodium bicarbonate is an antacid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3410", "text": "Bromo-Seltzer was invented in 1888 by  Isaac E. Emerson  and produced by the Emerson Drug Company of  Baltimore, Maryland . It was sold in the United States in the form of  effervescent  granules that were mixed with water before  ingestion . [ 1 ]  The product took its name from a component of the original formula,  sodium bromide ; each dose contained 3.2  mEq /teaspoon of it.  Bromides  are a class of tranquilizers that were withdrawn from the U.S. market in 1975 due to their toxicity. Their  sedative  effect probably accounted for Bromo-Seltzer's popularity as a  hangover remedy . Early formulas also used  acetanilide  as the  analgesic  ingredient; it is now known to be toxic. [ 2 ]  Acetanilide was replaced with its metabolite  acetaminophen , and its current formulation uses  aspirin ,  sodium bicarbonate , and  citric acid , the latter two of which provide the  carbonation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3411", "text": "Bromo-Seltzer's main offices and factory were located in downtown Baltimore, Maryland, at the corner of West Lombard and South Eutaw streets. [ 3 ]  The factory's most notable feature was the  Emerson Bromo-Seltzer Tower , built in 1911, whose four clock faces are ringed by letters spelling out the product name. The tower was patterned on the  Palazzo Vecchio  in  Florence, Italy , and is listed on the  National Register of Historic Places . The tower originally held a 51-foot (16m) representation of a Bromo-Seltzer bottle at its top, glowing blue and rotating on a vertical axis. The sign weighed 20 tons (18.1 tonnes), included 314 incandescent light bulbs, and was topped with a crown. The sign was removed in 1936 because of structural concerns. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3412", "text": "Emerson, who traveled widely, said the fizz reminded him of the bubbling action of  Mount Bromo , a volcano in Java. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3413", "text": "Bromo-Seltzer is mentioned in several films and TV shows, including  The Crooked Circle  (1932),  Bed of Roses  (1933),  Topper  (1937),  Wonder Man  (1945),  Somewhere in the Night  (1946),   The Postman Always Rings Twice  (1981),  The Hudsucker Proxy  (1994), [ 5 ]  the 1998  The Simpsons  episode \" Bart Carny \", and in  Golden Girls  (Season 4, Episode 1)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3414", "text": "It is mentioned in  John Steinbeck 's 1939 novel  The Grapes of Wrath ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3415", "text": "Drugstore Bromo-Seltzer dispensers are mentioned in  Georges Simenon 's 1949 detective novel  Maigret chez le coroner  that takes place in Arizona."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3416", "text": "It was a sponsor of the old time radio program, \u201cThe Inner Sanctum\u201d."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3417", "text": "It is mentioned in several songs, including \" Bewitched, Bothered and Bewildered \" by  Rodgers and Hart , \" Adelaide's Lament \" in the musical  Guys and Dolls , and \" Pachuco Cadaver \" by  Captain Beefheart and his Magic Band . In  Spike Jones ' version of   Laura , the chorus chants \"Bromo-Seltzer, Bromo-Seltzer...\" to evoke the sound of a chugging train."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3418", "text": "Camicinal  was a  motilin   agonist  investigated for the treatment of  gastroparesis . [ 1 ] [ 2 ] [ 3 ]  It did not improve enteral feeding intolerance. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3419", "text": "Candoxatril  is the orally active  prodrug [ 1 ]  of candoxatrilat (UK-73967)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3420", "text": "Human neutral endopeptidase ( neprilysin ) as the neutral endopeptidase 24.11 [ 2 ]  complexed ( RB-101 ) with phosphoramidon degrades and inactivates [ 3 ]  a number of bioactive peptides. Two multiply connected folding domains [ 3 ]  of the neutral endopeptidase locus [ 3 ]  splicing of exons 1, 2a, or 2b to the common exon 3 composed of  24 exons of the human CALLA/NEP gene [ 2 ]  containing the active site, it is known as peptidase family M13 (neprilysin family, clan MA(E)) the gluzincins a faint but significant structural relationship of the metzincins [ 4 ] [ 5 ] [ 6 ] [ 7 ]   to the  thermolysin -like enzymes, [ 5 ]  Zincin is the simplest descriptor of biological space. [ 8 ]  The structure reveals two multiply connected folding domains which embrace a large central cavity containing the active site of the 5-indanyl ester prodrug candoxatril [ 9 ]  and differs from  phosphoramidon  [N-(N-(((6-Deoxy-\u03b1-L-mannopyranosyl)oxy)hydroxyphosphinyl)-L- leucyl)- L-tryptophan ] in several respects the structure of human  neutral endopeptidase  complexed with phosphoramidon is lost due to desolvation [ 9 ]  of the enzyme and ligand on formation of the complex candoxatril."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3421", "text": "Candoxatril is the first drug of its kind to be released for clinical trials regarding heart failure. [ medical citation needed ]   This is because candoxatril produces favorable haemodynamic effects in patients with chronic heart failure. It has been demonstrated that candoxatril is associated with a beneficial hemodynamic effect that is useful both in rest and exercise. In several different studies, candoxatril has been shown to improve performance in people with heart failure. In one study, 12 different patients were selected, all with moderately severe heart failure.  On day one of this study, the candoxatril had increased plasma ANP levels, suppressed aldosterone and decreased right atrial and pulmonary capillary wedge pressures. After treatment for 10 days, patients health had improved with an increase of basal ANP and a decrease of aldosterone, along with a reduced body weight that could be a reflection of chronic natriuretic, diuretic effects, or both.  It was decided that on day 10 of the study, the effects of candoxatril were similar to that on day one. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3422", "text": "In a separate study, patients were gathered throughout the United Kingdom from 16 different centers. Over a four-week bind, the patients were either given candoxatril or placebo for the 84 days and every 28 days, patients were reassessed.  Out of the 110 patients, 56 received candoxatril and 54 received the placebo.  Over the time of the study, the patients who were taking candoxatril had an overall improvement in exercise time compared to the patients taking the placebo. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3423", "text": "In a third study, there was only one patient who experienced worsening heart failure during this particular study.  However, the frequency was not statistically significantly different from another observed group that was on placebo. Together, the results of this study show the candoxatril offers a new, effective therapeutic  in the treatment of people with mild heart failure. The beneficial effects may begin to  improve the well-being of patients during everyday activities. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3424", "text": "Carbenoxolone  ( CBX ) is a  glycyrrhetinic acid  derivative with a steroid-like structure, similar to substances found in the root of the  licorice plant . Carbenoxolone is used for the treatment of peptic, esophageal and oral  ulceration  and inflammation. Electrolyte imbalance is a serious side effect of carbenoxolone when used systemically. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3425", "text": "Carbenoxolone reversibly inhibits the conversion of inactive  cortisone  to  cortisol  by blocking  11\u03b2-hydroxysteroid dehydrogenase  (11\u03b2-HSD). 11\u03b2-HSD also reversibly catalyzes the conversion of 7-ketocholesterol to 7-beta-hydroxycholesterol. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3426", "text": "Carbenoxolone is a modestly potent, reasonably effective, water-soluble blocker of  gap junctions . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3427", "text": "Carbenoxolone has also been used in topical creams such as Carbosan gel, marketed for treatment of lip sores and mouth ulcers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3428", "text": "Carbenoxolone has also been investigated for  nootropic  effects. [ 5 ]  This research started from an observation that long-term exposure to  glucocorticoids  may have negative effects on cognition. Carbenoxolone may decrease the amount of active glucocorticoid in the brain, because the drug inhibits 11\u03b2-HSD, an enzyme which regenerates  cortisol , an active glucocorticoid, from inactive  cortisone ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3429", "text": "In the research trial investigating this use of carbenoloxone, it was shown that the drug improved verbal fluency in elderly healthy men (aged 55\u201375). In type 2 diabetics aged 52\u201370, the drug improved verbal memory. However,  potassium-sparing diuretic   amiloride  was co-administered with carbenoxolone, since carbenoxolone used by itself may cause  hypertension  by increasing cortisol in the kidneys."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3430", "text": "A  carminative , known in Latin as  carminativum  ( plural   carminativa ), is a herb or preparation intended to combat  flatulence  either by preventing formation of gas in the gastrointestinal tract or facilitating its expulsion. [ clarify ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3431", "text": "The word  carminative  is a derivative of Latin  c\u0101rmen  \" card for wool \", according to Hensley Wedgewood, on the   humoral theory  that carminatives \"dilute and relax the gross humours from whence the wind arises, combing them out like the knots in wool\". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3432", "text": "Carminatives are often mixtures of  essential oils  and  spices  with a tradition in  folk medicine . [ citation needed ]  Some examples include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3433", "text": "Modern drugs used for the same purpose include  simethicone , [ citation needed ]  which simply lowers the  surface tension  of gas bubbles rather than having  physiological effects. [ clarify ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3434", "text": "The dictionary definition of  carminative  at Wiktionary"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3435", "text": "Cetraxate  ( INN ) is an oral  gastrointestinal   medication  which has a cytoprotective effect. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3436", "text": "Chlordiazepoxide/clidinium bromide  (marketed as  Librax ) is a  fixed-dose combination  medication used to treat  peptic ulcers ,  irritable bowel syndrome  (IBS), and  gastritis . [ 2 ]  It contains  chlordiazepoxide  and  clidinium bromide . It helps relieve stomach spasms, abdominal cramps, and anxiety related to gastric disorders. [ 3 ]  Librax is a fixed ratio of these two medications and, as such, is not typically prescribed with an accompanying dosage, but rather directions on how many capsules to take per day. It comes in a capsule taken by mouth, usually three or four times daily, before meals and at bedtime. [ 3 ]   Chlordiazepoxide is an anti-anxiety medication belonging to the  benzodiazepine  class. [ 4 ]   Its use in IBS is thought to be due to its calming ability for patients that have IBS symptoms that are worsened by anxiety.  Clidinium bromide is a synthetic quaternary ammonium  antimuscarinic , [ 5 ]  a sub-class of a family of drugs known as  anticholinergics . It treats IBS by decreasing gastrointestinal  motility ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3437", "text": "Chlordiazepoxide can be habit-forming. Tolerance may develop with long-term or excessive use, making this medication less effective. This medication must be taken regularly to be effective. Stopping the drug suddenly can worsen the condition and cause withdrawal symptoms (anxiousness, sleeplessness, and irritability). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3438", "text": "It was approved for medical use in the United States in 1966. [ 6 ] [ 7 ]  It is available as a generic medication. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3439", "text": "Chlordiazepoxide/clidinium bromide is indicated to control emotional and somatic factors in gastrointestinal disorders. [ 7 ]  It may also be used as adjunctive therapy in the treatment of peptic ulcer and in the treatment of the irritable bowel syndrome (irritable colon, spastic colon, mucous colitis) and acute enterocolitis. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3440", "text": "Dalby's Carminative  was one of the two most widely used  patent medicines  given to babies and children at the end of the 18th and beginning of the 19th centuries. Together with its rival,  Godfrey's Cordial , they were known as \"mother's friends\" and were used (often against a doctor's advice) for everything from colic and coughs to typhoid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3441", "text": "A  carminative  is a drug that relieves gas from the digestive tract, flatulence and   colic  in infants. The formula claimed to aid \u201cinfants afflicted with wind, watery gripes, fluxes and other disorders of the stomach and bowels\u201d. The main active ingredient in both formulas was opium. There are stories of nurses who overdosed the babies in their care to keep them quiet and no bother, [ 1 ]  and babies did die from time to time. [ 2 ]  Today, the medicine is mostly known by collectors of old glass bottles."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3442", "text": "The formula for Dalby's Carminative was created by Joseph Dalby, [ 3 ]  surgeon and apothecary of  London ,  England , in the 1770s. Born Joseph Dolby, Joseph changed the spelling of his name to \"Dalby\" when he married Anne Sparrow in 1739. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3443", "text": "In a 1773 Act of the Parliament of Great Britain, Dalby's Carminative is listed with other \"medicinal preparations\" as a product liable for  stamp duties , giving it official status."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3444", "text": "Joseph Dalby died in 1784. He left the recipe for the carminative to his daughter Frances (174\u2013-1845), who married Anthony Gell. Joseph's son James (1750\u20131815) kept the blue J. Dalby bottles and set up manufacturing himself, claiming to be the original creator. Frances and her husband then \"rebranded\" the product as Gell-Dalby, which was sold in brown bottles. Both children claimed to have the original recipe. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3445", "text": "The Will of Joseph Dalby, proved at London 27 July 1784 is often held up as one of the most eccentric Georgian wills. [ 6 ]  He is buried in  Westminster Abbey , South Cloister."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3446", "text": "By the 1770s, Dalby's Carminative and many other English medicines were also North American hits. Shipments of all sorts of medicines were sent from England to the colonies. The  American War of Independence  involved a blockade and ships carrying commodities from England were often sunk or captured. Many a bottle of medicine had to be smuggled to the new United States. It was not long before Americans found that they could wash out the distinctive Dalby's and other bottles and refill them with their own concoctions and the patent medicine business took off in America. Soon American glass companies were making knock-off bottles. Recipes were being traded around by apothecaries, and by the mid-1780s, Dalby's was actually no longer shipping overseas, although \"Dalby's Carminative\" was sold everywhere in the United States. Pirated versions were being manufactured and sold there until after 1900. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3447", "text": "As listed in  The Lancet , a recipe consists of:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3448", "text": "Drotaverine  ( INN , also known as  drotaverin ) is an  antispasmodic  drug, used to enhance  cervical dilation  during  childbirth  and to relieve  smooth muscle   spasms  in the  gastrointestinal tract ,  urinary system , and  gall bladder . [ 2 ] [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3449", "text": "It is structurally related to  papaverine , and is a selective  inhibitor of phosphodiesterase-4 , and has no  anticholinergic  effects. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3450", "text": "It is available in  Asia , [ specify ]   Central and Eastern Europe  (Poland, [ 7 ]  Hungary, [ 8 ]  Estonia, [ 9 ]  Latvia, [ 10 ]  Lithuania [ 11 ] ) under several brand names. [ 12 ]  A popular brand is  No-Spa,  owned by  Sanofi ). It is distributed by Sanofi as  \u041d\u043e-\u0428\u043f\u0430  (No-shpa) in Russia. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3451", "text": "Drotaverine hydrochloride has a  spasmolytic , myotropic,  vasodilation ,  hypotensive  action. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3452", "text": "Drotaverine decreases active ionized calcium supply binding to smooth muscle cells due to inhibition of  phosphodiesterase  and intracellular accumulation of  cAMP . It has an apparent and prolonged action on smooth muscles of internal organs and blood vessels and it moderately decreases  arterial blood pressure , increases  cardiac output  (minute volume of heart), and has some  antiarrhythmic  potential. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3453", "text": "Drotaverine decreases  vascular tone  of  cerebral blood vessels  and increases blood-filling. Practically, Drotaverine does not influence the  autonomic nervous system  and does not penetrate into the  central nervous system . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3454", "text": "Possible side effects include: heating sensation, dizziness, headache (rarely), insomnia. May be observed: arrhythmia (rarely), hypotension, tachycardia, sweating, nausea. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3455", "text": "Overdose of Drotaverine potentially can cause  atrioventricular (AV) block ,  cardiac arrest , paralysis of respiratory system. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3456", "text": "In  Israel  the product is known under the brand name \"No-Spa\" by the general public [ 14 ]  which did not receive a permit to be distributed by the  health ministry , [ 15 ]  however due to high demand local medical counterfeiters have managed to smuggle No-Spa tablets over the years. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3457", "text": "In 2008, the Israeli health organization warned consumers against counterfeit No-Spa pills after a smuggler had been arrested at the  Ben Gurion Airport  with several thousand pills. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3458", "text": "In 2011, the Israeli patent and trademark office declined the use of No-SPA. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3459", "text": "An article from 2013 described the effects from overdose (in a 19-year-old female) as including vomiting, seizures and fatal cardiac toxicity. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3460", "text": "In 2016, the young Russian chess player  Ivan Bukavshin  died of a massive overdose (or poisoning) of the drug, which was initially thought to be a stroke; the dose detected in his blood was 17 mg/kg. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3461", "text": "Ecadotril  is a  neutral endopeptidase  inhibitor ((NEP [ 1 ] ) EC 3.4.24.11 [ 2 ] ) and determined by the presence of peptidase family M13 as a neutral endopeptidase inhibited by  phosphoramidon . Ecadotril is the ( S )- enantiomer  of  racecadotril .  NEP-like enzymes include the  endothelin - converting enzymes . [ 3 ]   The peptidase M13 family  believed to activate or inactivate oligopeptide (pro)-hormones such as opioid peptides, [ 3 ]   neprilysin [ 3 ]  is another member of this group,  in the case of the metallopeptidases and aspartic, the nucleophiles clan or family for example MA, is an activated water molecule. [ 1 ]  The peptidase domain for members of this family also contains a bacterial member and resembles that of  thermolysin  the predicted active site residues for members of this family and thermolysin occur in the motif HEXXH. [ 4 ]  Thermolysin complexed with the inhibitor ( S )- thiorphan  are isomeric thiol-containing inhibitors of endopeptidase EC 24-11 [ 5 ]  (also called \" enkephalinase \")."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3462", "text": "Eupatilin  (5,7-Dihydroxy-3',4',6-trimethoxyflavone) is an  O-methylated flavone , a type of flavonoids. It can be found in  Artemisia asiatica  (Asteraceae). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3463", "text": "Ferrous tartrate  is a  chemical compound  and the  iron(II)   salt  of  tartaric acid . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3464", "text": "Ferrous tartrate has been used as a steel medicine. [ 2 ] [ 3 ]  It was generally prescribed during the 19th and early 20th centuries. It is usually prepared by  digesting  for 30 days, 2 ounces (880 grains)  tartarated  iron [ 4 ]  in a pint of  sherry . [ 5 ]  It can be difficult to prepare. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3465", "text": "Historically, it was used as a  stomachic  and tonic, at a dose of 2 tbsp. [ 5 ]   It was also used to treat  anemia , dose 1 to 2 fl. dr. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3466", "text": "Festal  is a brand name drug containing  pancreatin ,  hemicellulase , and certain  bile  components. [ 1 ]  It is indicated for use in people with gastrointestinal problems, in order to help actively digest food (especially fatty meals that require pancreatic  enzymes )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3467", "text": "Gefarnate  is a drug used for the treatment of  gastric ulcers . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3468", "text": "It also has been proposed for use in the treatment of  dry eye syndrome . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3469", "text": "This article about an  alkene  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3470", "text": "A  gastrointestinal cocktail , (also known as a  GI cocktail  or  gastric cocktail ), is a mixture of medications used to treat symptoms of  dyspepsia . [ 1 ]  The GI cocktail generally contains a mixture of viscous  lidocaine , an  antacid , and an  anticholinergic . [ 1 ] [ 2 ]  The GI cocktail is commonly prescribed in the hospital or emergency department, and has been used to help distinguish chest pain as either gastrointestinal or cardiac. [ 1 ]  While it has been widely used in the treatment of dyspepsia, studies have suggested that the GI cocktail is only as effective as antacids alone. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3471", "text": "The \"GI cocktail\" does not refer to a specific product. Rather, it refers to a mixture of viscous  lidocaine , an  antacid , and an  anticholinergic . [ 1 ] [ 2 ]  Viscous  lidocaine  works as an anesthetic to numb pain in the throat, esophagus, and stomach.  Antacids  work to neutralize stomach acid.  Anticholinergics  work to ease symptoms that accompany dyspepsia including nausea,  vomiting , and abdominal cramping."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3472", "text": "The GI cocktail is a mixture of a viscous anesthetic, an antacid, and an anticholinergic. [ 1 ] [ 2 ]  Common viscous anesthetics use are viscous lidocaine or  xylocaine . Common antacids used are  magnesium hydroxide ,  aluminum hydroxide , or  simethicone  (more commonly known as  Mylanta  or  Maalox ). [ 3 ]  Common anticholinergics used are  hyoscyamine sulfate ,  atropine sulfat e,  scopolamine hydrobromide , and  phenobarbital  (more commonly known as  Donnatal ). [ 3 ]  Typical dosing is 5ml of viscous anesthetic, 30ml of liquid antacid, and 10ml of anticholinergic. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3473", "text": "The GI cocktail is commonly prescribed in the hospital or emergency department to treat symptoms of  dyspepsia . [ 4 ]  These symptoms include: belching,  heartburn , chest pain, abdominal discomfort, abdominal bloating, nausea, loss of appetite, and flatulence. Dyspepsia itself is not an illness, rather it is an indicator of chronic underlying gastrointestinal issues such as  peptic ulcer disease ,  gastro-esophageal reflux disease ,  H. pylori  gastritis,  gastroparesis , or upper gastrointestinal cancers. [ 5 ] [ 6 ]  Dyspepsia can additionally be contributed to medications such as potassium supplements,  NSAIDs , digitalis, iron,  glucocorticoids , and  colchicine , as well as lifestyle factors such as diet, stress, and cigarette smoking. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3474", "text": "Some people experience side effects that are the result of the individual medications used to make the GI cocktail. They include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3475", "text": "Viscous lidocaine : [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3476", "text": "Antacid : [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3477", "text": "Anticholinergic : [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3478", "text": "Prior studies regarding the GI cocktail for management of dyspepsia in the emergency department have varied in quality of methodology and have demonstrated mixed results. A 1990 single-blind study performed by Welling and Watson [ 4 ]  compared 30 mL of antacid with or without the addition of 15 mL of viscous lidocaine and concluded that the addition of viscous lidocaine provided a significantly greater degree of immediate pain relief than antacids alone in patients with dyspepsia. A 2004 single-blind study performed by Vike and Davis, [ 7 ]  compared treatment with antacids plus either viscous lidocaine or benzocaine solution and did not find a statistically significant difference between the two treatment arms \u2013 however the study lacked an antacid monotherapy arm. A robust double-blind clinical trial performed in 2003 by Berman et al. [ 1 ]  compared 30 mL of antacid monotherapy, antacid with the addition of 10 ml of an anticholinergic, and an antacid with anticholinergic with the addition of 10 mL of 2% viscous lidocaine. That study demonstrated no statistically significant difference in pain relief between treatment arms and concluded that all treatments were clinically effective. The ultimately recommended antacid monotherapy alone in the treatment of dyspepsia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3479", "text": "Glucose-elevating agents  are medications used to treat  hypoglycemia  (low blood sugar) by raising  blood glucose . In diabetics, hypoglycemia can occur as a result of too much  insulin  or  antidiabetic medication , insufficient food intake, or sudden increase in physical activity or exercise. The most common glucose-elevating agents used to treat  diabetic hypoglycemia  are  glucose  (in the form of tablets or liquid) and  glucagon  injections when severe hypoglycemia occurs.  Diazoxide , which is used to counter hypoglycemia in disease states such as  insulinoma  (a tumor producing insulin) [ 1 ]  or  congenital hyperinsulinism , increases blood glucose and decreases  insulin  secretion and glucagon accelerates breakdown of  glycogen  in the liver ( glycogenolysis ) to release glucose into the bloodstream. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3480", "text": "Imiglucerase  is a medication used in the treatment of  Gaucher's disease . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3481", "text": "It is a  recombinant DNA -produced  analogue  of the human enzyme \u03b2- glucocerebrosidase .\n Cerezyme  is a  freeze-dried  medicine containing imiglucerase, manufactured by  Genzyme Corporation . It is given  intravenously  after reconstitution as a treatment for Type 1 and Type 3 [ 4 ]  Gaucher's disease. It is available in formulations containing 200 or 400 units per vial.  The specific activity of highly purified human enzyme is 890,000 units/mg, [ 5 ]  meanwhile the enzyme activity produced by recombinant DNA technology is approximately 40 units/mg. [ 6 ]  A typical dose is 2.5U/kg every two weeks, up to a maximum of 60 U/kg once every two weeks, and safety has been established from ages 2 and up. [ 7 ]   It is one of more expensive medications, with an annual cost of $200,000 per person in the United States. [ 8 ]  Imiglucerase has been granted  orphan drug  status in the United States, Australia, and Japan. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3482", "text": "Cerezyme was one of the drugs manufactured at  Genzyme's  Allston, Massachusetts plant, for which production was disrupted in 2009 after contamination with  Vesivirus  2017. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3483", "text": "The most common side effect is  hypersensitivity , which occurs in about 3% of patients. It is associated with symptoms such as cough,  shortness of breath ,  rashes , itching, and  angiooedema . Less common side effects include dizziness, headache, nausea, diarrhea, and reactions at the injection site; they are found in less than 1% of patients. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3484", "text": "No clinical interaction studies have been conducted. [ 4 ]   Miglustat  appears to increase the clearance of imiglucerase by 70%, resulting in decreased enzyme activity. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3485", "text": "Larazotide  ( INN ; also known as AT-1001; formulated as the  salt  with  acetic acid ,  larazotide acetate ) is a synthetic eight  amino acid   peptide  that functions as a  tight junction  regulator and reverses leaky junctions to their normally closed state. It has been studied in people with  coeliac disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3486", "text": "Larazotide is an octapeptide whose structure is derived from a protein (zonula occludens toxin) secreted by  Vibrio cholerae .  It has the amino acid sequence GGVLVQPG,  IUPAC  condensed descriptor of H-Gly-Gly-Val-Leu-Val-Gln-Pro-Gly-OH, and the systematic name glycylglycyl- L -valyl- L -leucyl- L -valyl- L -glutaminyl- L -prolyl-glycine. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3487", "text": "Larazotide is an inhibitor of paracellular permeability.  In  celiac disease , one pathway that allows fragments of  gliadin  protein to get past the intestinal epithelium and subsequently trigger an  immune response  begins with binding of indigestible gliadin fragments to the  chemokine  CXC motif receptor 3 ( CXCR3 ) on the  luminal  side of the intestinal epithelium (see  this page ). This leads to the induction of myeloid differentiation factor 88 ( MYD88 ) and the release of zonulin into the lumen. Zonulin then binds to  epidermal growth factor receptor (EGFR)  and  protease-activated receptor 2 (PAR2)  in the intestinal epithelium. This complex then initiates a signalling pathway that eventually results in tight junction disassembly and increased intestinal permeability. Larazotide acetate intervenes in the middle of this pathway by blocking zonulin receptors, thereby preventing tight junction disassembly and associated increase in intestinal permeability. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3488", "text": "Larazotide acetate is a  synthetic peptide  based on a  Vibrio cholerae   enterotoxin  called zonula occludens toxin that decreases  intestinal permeability . An investigation was carried out to discover which specific part of this toxin was responsible for this activity. Several mutants were constructed, and tested for their biological activity and their ability to bind to intestinal epithelial cells in  culture . The responsible region was located near the  carboxyl terminus  of the toxin protein. This region coincided with a peptide product generated by  Vibrio cholerae . The eight amino acid sequence in this region was shared with  zonulin , an endogenous protein involved in tight junction modulation. This sequence was later designated larazotide acetate. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3489", "text": "It has been used in experiments related to coeliac disease and  rheumatoid arthritis . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3490", "text": "9 Meters Biopharma was conducting clinical trials for larazotide for Celiac Disease, but announced in 2022 that it would discontinue their Phase 3 clinical trial.  [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3491", "text": "Linaclotide , (sold under the brand name  Linzess  in the US and Mexico, and as  Constella  elsewhere) [ 6 ]  is a drug used to treat  irritable bowel syndrome  with  constipation  and  chronic constipation with no known cause . [ 4 ] [ 3 ]  It has a  black box warning  about the risk of serious  dehydration  in children in the US; the most common adverse effects in others include diarrhea. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3492", "text": "It is an  oligopeptide   agonist  of  guanylate cyclase 2C  and remains in the  GI tract  after it is taken  by mouth . It was approved in the US and the European Union in 2012. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3493", "text": "It is marketed by  Abbvie  (formerly   Allergan ) in the United states and by  Astellas  in Asia; [ citation needed ]   Ironwood Pharmaceuticals  was the originator. [ 8 ] [ failed verification ]  In 2022, it was the 189th most commonly prescribed medication in the United States, with more than 2 \u00a0 million prescriptions. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3494", "text": "Linaclotide is  indicated  to treat  irritable bowel syndrome  with constipation and chronic constipation with no known cause. [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3495", "text": "In June 2023, the indication was expanded in the US to include the treatment of  functional constipation . [ 4 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3496", "text": "The US label has a black box warning to not use linaclotide in children less than six years old and to avoid in people from 6 to 18 years old, due to the risk of serious dehydration. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3497", "text": "More than 10% of people taking linaclotide have diarrhea. Between 1% and 10% of people have decreased appetite, dehydration, low potassium,  dizziness when standing up too quickly , nausea, vomiting, urgent need to defecate, fecal incontinence, and bleeding in the colon, rectum, and anus. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3498", "text": "It has not been tested in pregnant women and it is unknown if it is excreted in breast milk. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3499", "text": "Systemic absorption of the globular tetradecapeptide is minimal. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3500", "text": "Linaclotide, like the  endogenous   guanylin  and  uroguanylin  it mimics, is an  agonist  that activates the  cell surface receptor  of  guanylate cyclase 2C  (GC-C). [ 12 ] [ 4 ] [ 14 ]  The medication binds to the surface of the  intestinal   epithelial  cells. [ 4 ]  Linaclotide is minimally absorbed and it is undetectable in the systemic circulation at therapeutic doses. [ 12 ]  Activation of GC-C increases  cyclic guanosine monophosphate  (cGMP). [ 4 ]  Elevated cGMP stimulates secretion of chloride and bicarbonate and water into the intestinal lumen, mainly by way of  cystic fibrosis transmembrane conductance regulator  (CFTR)  ion channel  activation. [ 4 ] [ 15 ]  This results in increased intestinal fluid and accelerated transit. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3501", "text": "Linaclotide is a hybrid  peptide  design of the  E.coli  heat-stable  enterotoxin  (STa) and the endogenous peptide hormones  endogenous   guanylin  and  uroguanylin . [ 16 ] [ 12 ] [ 14 ]  It is a  synthetic  tetradecapeptide (14  amino acid  peptide) with the sequence CCEYCCNPACTGCY by one-letter abbreviation, [ citation needed ]  or by three-letter abbreviation: [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3502", "text": "H\u2013 Cys 1 \u2013Cys 2 \u2013 Glu 3 \u2013 Tyr 4 \u2013Cys 5 \u2013Cys 6 \u2013 Asn 7 \u2013 Pro 8 \u2013 Ala 9 \u2013Cys 10 \u2013 Thr 11 \u2013 Gly 12 \u2013Cys 13 \u2013Tyr 14 \u2013OH"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3503", "text": "However, the actual structure of linaclotide is not fully specified without the three  disulfide  (R-S-S-R) bonds it contains, which are between Cys 1  and Cys 6 , between Cys 2  and Cys 10 , and between Cys 5  and Cys 13 ; [ 17 ]  these are shown in exaggerated fashion in the line-angle graphic showing the chemical bonds within and between each amino acid (and their stereochemistries, see the infobox, above right), and are represented using a one-letter abbreviations in the following additional schematic: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3504", "text": "A study in discovery synthesis reported that 2 of 14 strategies available to synthesize linaclotide were successful\u2014the successful ones involving  trityl   protection  of all cysteines, or trityl protection of all cysteines except Cys 1  and Cys 6 , which were protected with  tert -butylsulphenyl groups . The study also reported that solution-phase oxidation (disulfide formation) was advisable over solid-supported synthesis for linaclotide, and that the Cys 1 \u2013Cys 6  disulfide bridge was the most favored energetically. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3505", "text": "The drug was discovered at  Microbia, Inc , which had been spun out of the  Whitehead Institute  in 1998 by postdocs from the lab of  Gerald Fink  to commercialize the lab's know-how and inventions related to microbial pathogens and biology. [ 18 ] [ 19 ]  In 2002 the company hired Mark Currie who had worked at the  Searle  division of  Monsanto  and then had gone to  Sepracor . [ 18 ]  Currie directed the efforts that led to the discovery of linaclotide, which was based on an  enterotoxin  produced by some strains of  Escherichia coli  that cause  traveler's diarrhea . [ 20 ] [ 21 ]  The company started Phase I trials in 2004. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3506", "text": "Under a partnership agreement announced in 2007, between  Forest Laboratories  and Microbia, Forest would pay $70 million in licensing fees towards the development of linaclotide, with profits shared between the two companies in the US; Forest obtained exclusive rights to market in Canada and Mexico. [ 22 ]  By 2010, Microbia had changed its name to Ironwood Pharmaceuticals and had licensed rights to distribute the drug in Europe to  Almirall  and had licensed Asian rights to  Astellas Pharma . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3507", "text": "It was approved in the United States and in the European Union in 2012. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3508", "text": "Forest was acquired in 2014 and eventually became part of  Allergan . [ 24 ]  Allergan acquired rights from Almirall in 2015, [ 25 ]  and in 2017, acquired remaining rights in most of the rest of the world, excluding North America, Japan, and China. [ 26 ]   Allergan has since been acquired by AbbVie in 2020. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3509", "text": "In 2014, Ironwood and Forest then Allergan began running  direct-to-consumer advertising  which raised sales by 21%; campaigns in 2015 and 2016 raised sales by 27% and 30%. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3510", "text": "In 2017, the list price for linaclotide in the US was  US$378  for 30 pills; Allergan and Ironwood increased the price of linaclotide to around $414 in 2018. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3511", "text": "Lubiprostone , sold under the brand name  Amitiza  among others, is a  medication  used in the management of  chronic idiopathic constipation , predominantly  irritable bowel syndrome -associated constipation in women and  opioid-induced constipation . The drug is owned by  Mallinckrodt  and is marketed by  Takeda Pharmaceutical Company ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3512", "text": "The drug was developed by  Sucampo Pharmaceuticals  and approved by the  Food and Drug Administration  (FDA) in 2006. [ 2 ] [ 3 ] [ 4 ]  It was recommended for use in the UK by the  National Institute for Health and Care Excellence  (NICE) in July 2014. [ 5 ]   Health Canada  approved the drug in 2015. [ 6 ]  Lubiprostone received approval from the Food and Drug Administration in 2008, to treat irritable bowel syndrome with  constipation  (IBS-C), [ 7 ]  and in 2013, for the treatment of  opioid-induced constipation in adults with chronic noncancer pain. [ 4 ]  It is available as a  generic medication . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3513", "text": "Lubiprostone is a laxative used for the treatment of constipation, specifically: [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3514", "text": "Lubiprostone has not been studied in children. [ 10 ] [ 12 ]  There is current research under way to determine the safety and efficacy in postoperative bowel dysfunction."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3515", "text": "It comes in a liquid filled capsule and is available only with a doctor's prescription. [ 10 ]  If one misses a dose it should be taken as soon as possible unless it is almost time for the next dose, in which case it should be skipped and the user should return to their regular dosing schedule. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3516", "text": "In clinical trials, the most common adverse event was  nausea  (31%). Other adverse events (\u22655% of patients) included  diarrhea  (13%),  headache  (13%),  abdominal distension  (5%),  abdominal pain  (5%),  flatulence  (6%),  sinusitis  (5%),  vomiting  (5%), and  fecal incontinence  (1%)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3517", "text": "The FDA lists the following: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3518", "text": "For subjects with chronic idiopathic constipation taking Amitiza:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3519", "text": "For opioid-induced constipation:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3520", "text": "For subjects with irritable bowel syndrome with constipation:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3521", "text": "A 2018 pooled analysis from three  phase III , randomized, double-blind, placebo-controlled studies on usage for Opioid-Induced Constipation, found that the numbers of patients reporting adverse effects were similar in both the lubiprostone and placebo treatment groups for all opioid classes (P\u2009\u2265\u20090.125); however, gastrointestinal adverse effects were reported more frequently by those receiving lubiprostone than 2 of the 3 opioid groups. The most commonly reported TEAEs in the lubiprostone treatment groups were nausea (13.4%\u201318.1%), diarrhea (1.2%\u201313.9%), and abdominal pain (4.7%\u20135.6%). In the population overall, the greatest likelihood of experiencing the first episode of any of these three TEAEs was greatest in the first week of treatment and decreased thereafter. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3522", "text": "According to Medscape, the most common (>10%) were: Nausea, Diarrhea (7-12%), Headache (2-11%). Less common side effects (1-10%) included: Abdominal pain (4-8%), Abdominal distension (3-6%), Flatulence (4-6%), Vomiting (3%), Loose stools (3%), Edema (1-3%), Abdominal discomfort (1-3%), Dizziness (3%), Chest discomfort/pain (2%), Dyspnea (2%), Dyspepsia (2%), Fatigue (2%), Dry mouth (1%). [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3523", "text": "The effects on pregnancy have not been studied in humans, but testing in  guinea pigs  resulted in fetal loss. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3524", "text": "Lubiprostone is contraindicated in people exhibiting chronic  diarrhea ,  bowel obstruction , or diarrhea-predominant  irritable bowel syndrome . [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3525", "text": "Lubiprostone is a bicyclic  fatty acid [ 15 ]  derived from  prostaglandin E1  that acts by specifically activating  ClC-2 chloride channels  on the apical aspect of gastrointestinal  epithelial  cells, producing a chloride-rich fluid secretion. These secretions soften the stool, increase motility, and promote spontaneous bowel movements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3526", "text": "Unlike many  laxative  products, lubiprostone does not show signs of  drug tolerance ,  chemical dependency , or altered serum  electrolyte  concentration. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3527", "text": "Minimal distribution of the drug occurs beyond the immediate gastrointestinal tissues. [ medical citation needed ]  Lubiprostone is rapidly metabolized by  reduction / oxidation , mediated by carbonyl reductase. [ medical citation needed ]  There is no metabolic involvement of the hepatic  cytochrome P450  system. [ medical citation needed ]  The measurable metabolite, M3, exists in very low levels in plasma and makes up less than 10% of the total administered dose. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3528", "text": "Data indicate that metabolism occurs locally in the  stomach  and  jejunum . [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3529", "text": "The cost to the  NHS  was \u00a329.68 per 24\u00a0mcg 28-cap pack as of April 2017."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3530", "text": "Lubiprostone is available in the United States, Japan, Switzerland, India, Bangladesh, the United Kingdom, and Canada. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3531", "text": "In  Bangladesh  and  India , lubiprostone is sold under the brand name Lubigut by  Ziska Pharmaceuticals , Lubilax by  Beacon Pharmaceuticals , and under the brand name Lubowel by  Sun Pharmaceutical . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3532", "text": "Maalox  was a brand of  antacid  owned by  Sanofi . Their main product is a flavored liquid containing a suspension of  aluminum hydroxide  and  magnesium hydroxide , which act to neutralize or reduce  stomach acid , for the purpose of relieving the symptoms of  indigestion ,  heartburn ,   gastroesophageal reflux disease , and also  stomach  or  duodenal  ulcers. It also contains  simethicone , an anti-foaming agent which helps eliminate bloating from gas. In large doses, the medicine can act as a  laxative . The trademark is owned by  Novartis International AG , and was first produced commercially in 1949."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3533", "text": "The acronym \u2018MAALOX\u2019 refers to the solution\u2019s compositional elements:  MA gnesium and  AL uminum as  OX ides. The oxides and hydroxides react with the  hydrochloric acid  in the stomach, neutralizing it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3534", "text": "Some may find certain Maalox medications, such as Maalox Multi-Action, to be a successful anti- diarrhea  treatment due to the aluminum hydroxide content, which in normal situations has a tendency to result in constipation. Maalox may also be used to treat nausea and stomach cramps associated with dyspepsia, diarrhea, or constipation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3535", "text": "Maalox was developed in a collaboration between  William H. Rorer, Inc. , and a medical doctor and researcher specializing in gastrointestinal issues, Alison Howe Price from  Philadelphia . [ 1 ]  The collaboration occurred after  World War II  when Claude Newhart, a salesman and  pharmacist  for the company, had an idea that he thought might change the company's fortunes. According to the Rorer family, he suggested that instead of selling pain relievers manufactured by others, they should create their own products. Gerald Rorer, then President of Rorer, told Newhart to \"go and find something.\" Newhart took up the challenge and contacted an old acquaintance from his student days working at a Philadelphia drugstore, Martin H. Rehfuss, who happened to be chief of medicine at Thomas Jefferson Hospital. It was Rehfuss who introduced Newhart to Price. Soon thereafter, Newhart convinced Price to become a consultant for the  Fort Washington, Pennsylvania  based Willam H. Rorer, Inc. In the end, Maalox became the first product the partnership produced. [ 2 ] [ 3 ]  Maalox eventually became the world's best selling antacid and forever changed the company's fortunes. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3536", "text": "Liquid Maalox contains  aluminum hydroxide ,  magnesium hydroxide , and  simethicone ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3537", "text": "Maalox Regular Strength chewable tablets contain 600 mg of calcium carbonate. Maalox Extra Strength + Anti-Gas tablets contain 1000 mg of calcium carbonate and 60 mg of simethicone."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3538", "text": "Maalox is used to treat moderate  dyspepsia , which includes symptoms of a burning sensation in the stomach or chest area, bloating, and/or gas pain, especially occurring after meals. It is used in combination with  oxycodone  to treat esophageal pain in cancer therapy patients. It is also a common component of a  GI cocktail  used in emergency rooms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3539", "text": "Maalox is used in scientific research to simulate for silt/mud/soil in water, along with other dissolved particulates. The particulate size exceeds 11 micrometres. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3540", "text": "Maalox can be used as a standalone antacid treatment or in conjunction with prescription strength medication such as  proton pump inhibitors  and H2 blockers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3541", "text": "Activists  in the United States, the Czech Republic, Venezuela, and Turkey have reported using Maalox or other antacid solutions diluted with water as a  home remedy  for  tear gas  attacks. [ 6 ] [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3542", "text": "Maalox generally doesn\u2019t produce serious side effects in individuals who use it for less than two weeks, but some mild side effects may appear. Possible side effects of Maalox include  nausea ,  diarrhea , constipation, and  headaches . These symptoms generally go away without further treatment. It may be necessary to contact a doctor if these symptoms become severe or persist for long periods of time. Maalox has been linked to phosphate deficiencies in some individuals as a result of the aluminum binding to phosphate in the stomach. This causes the body to flush out this important chemical which can lead to a deficiency.  [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3543", "text": "Women who are  pregnant  can, with the permission of a health care provider, use this product as the aluminum content is deemed safe for the developing or nursing child. Individuals who suffer from kidney issues, however, should not take this product unless advised to do so by a doctor. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3544", "text": "In February 2012, Novartis Consumer Health announced that they were temporarily, voluntarily suspending operations at the Novartis Consumer Health Lincoln facility that produces Maalox as well as suspending shipments. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3545", "text": "The shutdown was a result of inspections in 2011. \"Two FDA inspections that year, about five months apart, noted numerous instances of the company not addressing consumer complaints and, in some cases, ignoring them.\" [ 10 ]  At that time, Novartis decided to stop manufacturing Maalox at their Lincoln plant and to have third parties produce it. [ 10 ]  The problems at the Lincoln plant included the possibility of chipped particles from one medication being mixed into the bottles of other medications as well as 1,300 other consumer complaints. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3546", "text": "In August 2013, there was a recall of Maalox products. [ 12 ]  \"The recall encompasses 9 different types of its Maalox chewable tablets, including more than 3.4 million bottles of Maalox Advanced Maximum Strength Antacid & Antigas.\" [ 13 ]  They planned to restart production on a line-by-line basis, but the Maalox line had not by then been restarted. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3547", "text": "As of 2014, Novartis's Maalox brand was to be merged, along with other consumer brands, with the consumer brands of  GlaxoSmithKline  (GSK). This was part of a $20 billion exchange of business units between the two companies. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3548", "text": "Malotilate  ( INN ) is a drug that has been used in studies for the treatment of  liver disease . It has been shown to facilitate  liver  regeneration in rats. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3549", "text": "Maralixibat chloride , sold under the brand name  Livmarli , is a  medication  used to treat  cholestatic pruritus  in people with  Alagille syndrome . [ 5 ] [ 6 ]  Maralixibat chloride is an  ileal bile acid transporter  (IBAT) inhibitor. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3550", "text": "The most common side effects include diarrhea and abdominal pain (belly ache). [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3551", "text": "Maralixibat chloride was approved for medical use in the United States in September 2021, [ 5 ] [ 7 ] [ 8 ] [ 9 ]  and in the European Union in December 2022. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3552", "text": "Maralixibat chloride is  indicated  for the treatment of cholestatic pruritus in patients with Alagille syndrome. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3553", "text": "The U.S.  Food and Drug Administration  (FDA) granted the application for maralixibat chloride  orphan drug  designations in 2013, [ 10 ] [ 11 ]  and in 2020. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3554", "text": "In October 2022, the  Committee for Medicinal Products for Human Use  (CHMP) of the  European Medicines Agency  (EMA) adopted a positive opinion, recommending the granting of a marketing authorization under exceptional circumstances for the medicinal product Livmarli, intended for the treatment of cholestatic pruritus in patients with Alagille syndrome (ALGS). [ 14 ]  The applicant for this medicinal product is Mirum Pharmaceuticals International B.V. [ 14 ]  Maralixibat chloride was approved for medical use in the European Union in December 2022. [ 6 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3555", "text": "Maralixibat chloride is the  international nonproprietary name  (INN). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3556", "text": "Obeticholic acid  ( OCA ), sold under the brand name  Ocaliva , is a  semi-synthetic   bile acid  analogue which has the chemical structure  6\u03b1-ethyl-chenodeoxycholic acid .  It is used as a  medication  used to treat  primary biliary cholangitis .  Intercept Pharmaceuticals  Inc. hold the worldwide rights to develop OCA outside Japan and China, where it is licensed to  Dainippon Sumitomo Pharma . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3557", "text": "The natural bile acid  chenodeoxycholic acid  was identified in 1999 as the most active physiological  ligand  for the  farnesoid X receptor  (FXR), which is involved in many physiological and pathological processes.  A series of alkylated bile acid analogues were designed, studied and patented by Roberto Pellicciari and colleagues at the  University of Perugia , with 6\u03b1-ethyl-chenodeoxycholic acid emerging as the most highly potent FXR agonist. [ 6 ]   FXR-dependent processes in liver and intestine were proposed as therapeutic targets in human diseases. [ 7 ]   Obeticholic acid is the first FXR agonist to be used in human drug studies. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3558", "text": "The  FDA  has flagged cases of serious liver injury associated with the use of obeticholic acid. [ 8 ]  The agency stated that  Intercept Pharmaceuticals \u2019 liver disease medication, Ocaliva (obeticholic acid), is under scrutiny for causing liver damage in patients without advanced scarring. [ 9 ]  This follows the FDA\u2019s 2021 decision to restrict the drug\u2019s use in patients with advanced  cirrhosis . On Thursday, the FDA revealed its findings of severe liver injury in individuals treated for  primary biliary cholangitis  based on post-market clinical trial data. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3559", "text": "Obeticholic acid is undergoing [ when? ]  development in phase II and III studies for specific liver and gastrointestinal conditions. [ 11 ]  The U.S.  Food and Drug Administration  (FDA) approved obeticholic acid on 27 May 2016, for the treatment of primary biliary cholangitis. It was approved as an  orphan drug  based on its reduction in the level of the biomarker  alkaline phosphatase  as a surrogate endpoint for clinical benefit. [ 12 ]  It is indicated for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid in adults with an inadequate response to UDCA, or as monotherapy in adults unable to tolerate UDCA. [ 13 ]  Additional studies are being required to prove its clinical benefit. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3560", "text": "Primary biliary cholangitis  (PBC), also known as primary biliary cirrhosis, is an auto-immune, inflammatory liver disease which produces  bile duct  injury,  fibrosis ,  cholestasis  and eventual  cirrhosis . [ 15 ]  It is much more common in women than men and can cause  jaundice , itching ( pruritus ) and fatigue.  Ursodeoxycholic acid  therapy is beneficial, but the disease often progresses and may require  liver transplantation . [ 16 ]  Animal studies suggested that treatment with FXR agonists should be beneficial in cholestatic diseases such as PBC. [ 17 ]  OCA at doses between 10\u00a0mg and 50\u00a0mg was shown to provide significant biochemical benefit, but pruritus was more frequent with higher doses. [ 18 ] [ 19 ]   The results of a randomized, double-blind phase III study of OCA, 5\u00a0mg or 10\u00a0mg, compared to placebo (POISE) were presented in April 2014, and showed that the drug met the trial's primary endpoint of a significant reduction in serum  alkaline phosphatase , a  biomarker  predictive of disease progression, liver transplantation or death. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3561", "text": "Non-alcoholic steatohepatitis  is a common cause of abnormal liver function with  histological  features of  fatty liver ,   inflammation  and  fibrosis . It may progress to  cirrhosis  and is becoming an increasing indication for  liver transplantation . It is increasing in prevalence. OCA is proposed to treat NASH. [ 21 ]  A phase II trial published in 2013, showed that administration of OCA at 25\u00a0mg or 50\u00a0mg daily for six weeks reduced markers of liver inflammation and fibrosis and increased insulin sensitivity. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3562", "text": "The Farnesoid X Receptor Ligand Obeticholic Acid in Nonalcoholic Steatohepatitis Treatment (FLINT) trial, sponsored by  NIDDK , was halted early in January 2014, after about half of the 283 subjects had completed the study, when a planned interim analysis showed that a) the primary endpoint had been met and b) lipid abnormalities were detected and arose safety concerns. Treatment with OCA (25\u00a0mg/day for 72 weeks) resulted in a highly statistically significant improvement in the primary histological endpoint, defined as a decrease in the NAFLD Activity Score of at least two points, with no worsening of fibrosis. 45% (50 of 110) of the treated group had this improvement compared with 21% (23 of 109) of the placebo-treated controls. [ 23 ]  However concerns about longterm safety issues such as increased cholesterol and adverse cardiovascular events may warrant the concomitant use of statins in OCA-treated patients. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3563", "text": "In 2023, a FDA panel voted against approval of obeticholic acid for NASH, citing a lack of evidence that the benefits of the drug outweighed the risks. [ 25 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3564", "text": "Animal studies suggest that OCA improves intrahepatic vascular resistance and so may be of therapeutic benefit in  portal hypertension . [ 27 ]  An open label phase IIa clinical study is under way. [ when? ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3565", "text": "Bile acid diarrhea  (also called  bile acid malabsorption ) can be secondary to  Crohn's disease  or be a primary condition.  Reduced median levels of  FGF19 , an  ileal  hormone that regulates increased hepatic bile acid synthesis, have been found in this condition. [ 28 ]  FGF19 is potently stimulated by bile acids and especially by OCA. [ 29 ]  A proof of concept study of OCA (25\u00a0mg/d) has shown clinical and biochemical benefit. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3566", "text": "In June 2024, the  Committee for Medicinal Products for Human Use  of the  European Medicines Agency  concluded its review of the medicine Ocaliva (obeticholic acid) and recommended that the medicine's marketing authorization be revoked, because its benefits are no longer considered to outweigh its risks. [ 3 ] [ 31 ] [ 32 ]  Ocaliva is used to treat adults with primary biliary cholangitis, an autoimmune condition that causes gradual destruction of the bile ducts in the liver, which can lead to liver failure and increase the risk of liver cancer. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3567", "text": "A systematic review and meta-analysis of obeticholic acid, published in 2024, found that its effects on lipid parameters and its other adverse effects warrant further investigation. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3568", "text": "Pegunigalsidase alfa , sold under the brand name  Elfabrio , is an  enzyme replacement therapy  for the treatment of  Fabry disease . [ 2 ] [ 4 ]  It is a recombinant human  \u03b1-galactosidase-A . [ 4 ]  It is a hydrolytic lysosomal neutral glycosphingolipid-specific enzyme. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3569", "text": "The most common side effects are infusion-related reactions, hypersensitivity and asthenia. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3570", "text": "Pegunigalsidase alfa was approved for medical use in both the European Union and the United States in May 2023. [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3571", "text": "Pegunigalsidase alfa is  indicated  for long-term enzyme replacement therapy in aduls with a confirmed diagnosis of Fabry disease (deficiency of alpha-galactosidase). [ 2 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3572", "text": "On 23 February 2023, the  Committee for Medicinal Products for Human Use  (CHMP) of the  European Medicines Agency  (EMA) adopted a positive opinion, recommending the granting of a marketing authorization for the medicinal product Elfabrio, intended for the treatment of Fabry disease. [ 4 ]  The applicant for this medicinal product is Chiesi Farmaceutici S.p.A. [ 5 ] [ 6 ]  Elfabrio was approved for medical use in the European Union in May 2023. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3573", "text": "Pegvaliase , sold under the brand name  Palynziq , is a medication used for the treatment of the genetic disease  phenylketonuria  (PKU). [ 5 ] [ 9 ] [ 10 ]  It is a phenylalanine (Phe)\u2011metabolizing enzyme. [ 5 ]  Chemically, it is a  pegylated   derivative  of the enzyme  phenylalanine ammonia-lyase  that metabolizes  phenylalanine  to reduce its blood levels. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3574", "text": "The most common adverse events include injection site reactions, joint pain, hypersensitivity reactions, headache, generalized skin reactions lasting at least 14 days, pruritus (itchy skin), nausea, dizziness, abdominal pain, throat pain, fatigue, vomiting, cough and, diarrhea. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3575", "text": "It was approved by the US  Food and Drug Administration  (FDA) for use in the United States in 2018. [ 9 ]  The FDA considers it to be a  first-in-class medication . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3576", "text": "Pegvaliase is  indicated  to reduce blood Phe concentrations in adults with phenylketonuria who have uncontrolled blood Phe concentrations greater than 600 micromol/L on existing management. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3577", "text": "The FDA label for pegvaliase includes a  boxed warning  for anaphylaxis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3578", "text": "The safety and efficacy of pegvaliase were studied in two clinical trials in adult participants with PKU with blood phenylalanine concentrations greater than 600 \u03bcmol/L on existing management. [ 9 ]  Most PKU participants in the pegvaliase trials were on an unrestricted diet prior to and during the trials. [ 9 ]  The first trial was a randomized, open-label trial in participants treated with increasing doses of pegvaliase administered as a subcutaneous injection up to a target dose of either 20 mg once daily or 40 mg once daily. [ 9 ]  The second trial was an 8-week, placebo-controlled, randomized withdrawal trial in participants who were previously treated with pegvaliase. [ 9 ]  Participants treated with pegvaliase achieved statistically significant reductions in blood phenylalanine concentrations from their pre-treatment baseline blood Phe concentrations. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3579", "text": "The FDA granted approval of Palynziq to BioMarin Pharmaceutical. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3580", "text": "Plaunotol  ( 18-hydroxygeranylgeraniol ) is a chemical compound with the molecular formula C 20 H 34 O 2 .  It is a  diterpene  that was first isolated from  Croton sublyratus . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3581", "text": "Plaunotol has been identified as present in  Croton sublyratus [ 1 ]  and  Croton stellatopilosus . [ 2 ]   In plants, the compound is  biosynthesized  by  hydroxylation  of  geranylgeraniol , a reaction which is catalyzed by the enzyme  geranylgeraniol 18-hydroxylase . [ 3 ]   A laboratory synthesis of plaunotol has been reported. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3582", "text": "Plaunotol has antibacterial activity against  Helicobacter pylori , the bacteria that causes  gastric ulcers . [ 5 ]   In Japan, plauntool is used as a pharmaceutical drug under the trade name Kelnac for the treatment of  gastritis  and gastric ulcers. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3583", "text": "Plecanatide , sold under the brand name  Trulance , is a  medication  for the treatment of  chronic idiopathic constipation  (CIC) [ 4 ]  and  irritable bowel syndrome  with constipation. [ 5 ]   It is available in India under the brand name  Plectide  (OQM Div, MSN Laboratories, India). Plecanatide is an  agonist  of  guanylate cyclase-C . Plecanatide increases intestinal transit and fluid through a buildup of  cGMP . [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3584", "text": "As of January 2017, plecanatide is approved in the United States for the treatment of  chronic idiopathic constipation  in adults. [ 4 ]  later it was also approved for irritable bowel syndrome with constipation (IBS-C). [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3585", "text": "The presence of this condition is determined using the  Rome  III diagnostic criteria for chronic constipation which requires that the patient meet stool frequency, stool consistency, incomplete evacuation, and straining requirements in addition to not being a likely candidate for irritable bowel syndrome. [ 5 ] [ 9 ]  The symptoms should also have been present for at least three of the last six months to establish the chronic nature of the condition before treatment with plecanatide is indicated. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3586", "text": "Plecanatide has been shown to be safe and effective. It has shown to be at least equally as effective as its main competitor,  linaclotide  (brand name Linzess), but has been shown to have a lower rate of diarrhea as an adverse drug reaction. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3587", "text": "The recommended dosage of plecanatide is 3\u00a0mg taken by mouth once daily. [ 8 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3588", "text": "A plecanatide tablet can be taken with or without food and should be swallowed whole. For adults with swallowing difficulties, plecanatide tablets can be crushed and administered orally either in apple sauce or with water or administered with water via a nasogastric or gastric feeding tube. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3589", "text": "Plecanatide has not been shown to be safe or effective in persons 6 years to 18 years of age. [ 12 ]  Use of plecanatide by persons under the age of 6 poses a serious dehydration risk and studies have demonstrated plecanatide can cause death in juvenile mice due to this dehydrating effect. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3590", "text": "Use of plecanatide is also contraindicated in persons who are suspected of having a mechanical gastrointestinal obstruction. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3591", "text": "Plecanatide is a 16 amino acid peptide with the amino acid sequence:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3592", "text": "(one-letter sequence: NDECELCVNVACTGCL). Plecanatide is nearly structurally identical to human  uroguanylin , apart from the substitution of Asp 3  with Glu 3 . [ 13 ]   Disulfide bonds  exist between Cys 4  and Cys 12 , as well as Cys 7  and Cys 15 . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3593", "text": "Plecanatide has two important motifs. The first being the acidic residues Asp 2  and Glu 3  which modulate the affinity for its receptor in response to environmental pH. [ 12 ] [ 13 ] [ 15 ]  Simulations predict the optimal activity of Plecanatide to occur at pH 5,  making it suitable for targeting cells within the proximal intestine, which has a pH of between 5 and 6. [ 12 ]  The second is the ACTGC motif (residues Ala 11  to Cys 15 ) which is the region responsible for its binding to the receptor, guanylate cyclase-C. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3594", "text": "Plecanatide works as a laxative by drawing water in to the gastrointestinal tract thereby softening stool and encouraging its natural passage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3595", "text": "Similar to its endogenous counterpart, plecanatide activates guanylate cyclase-C on endothelial cells within the gastrointestinal tract. [ 13 ]   The activation of guanylate cyclase-C catalyses the production of the second messenger guanosine 3\u2019,5\u2019-cyclic monophosphate (cGMP) which leads to the protein kinase A (PKA) and protein kinase G II (PKGII)-mediated phosphorylation of the  cystic fibrosis transmembrane conductance regulator  (CFTR) protein. [ 17 ] [ 18 ]  CFTR is an anion channel and upon activation it will secrete negatively charged ions, particularly chloride (Cl \u2212 ) and bicarbonate (HCO 3 \u2212 ) in to the GI tract lumen. [ 19 ] [ 20 ]  This disruption to the electrochemical gradient is in part rectified by the passive secretion of positively charged sodium ions in to the lumen and water follows by osmosis. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3596", "text": "Plecanatide is also known to have an anti-nociceptive effect in animal models, however the exact mechanism of action is not yet fully elucidated. [ 12 ]  It has been suggested that this may be in part to the anti-inflammatory action of guanylate cyclase-C by its inhibition of pro-inflammatory cytokines, or through the inhibition of associated sensory neurons. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3597", "text": "As plecanatide acts on receptors present on the apical side of endothelial cells lining the gastrointestinal tract it is able to impart its effect without ever entering circulation. [ 13 ]  As with most orally ingested peptides, plecanatide is degraded by intestinal enzymes, and so very little of the active drug enters systemic circulation. [ 12 ]  Minimal amounts of the drug are expected to be transported in to the body, and concentrations of plecanatide and its metabolites are undetectable in plasma following the recommended dosage of 3\u00a0mg. [ 12 ] [ 13 ]  It has also been shown that dosages up to 48.6\u00a0mg produced no detectable concentration of plecanatide in human plasma at any time point after ingestion. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3598", "text": "Polymethylsiloxane polyhydrate  ( PMSPH ), or methylsilicic acid hydrogel (brand name \u2014  Enterosgel ), is an enterosorbent [ 1 ]  used for binding and removing various toxic substances, infectious agents and metabolites from the gastrointestinal tract. It is available in the form of a homogeneous pasty mass of white or almost white colour, odorless and tasteless."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3599", "text": "This product was synthesized in the late 1970s - early 1980s in the  USSR  by I. B. Slinyakova and I. \u041c. Samodumova of L. B. Pisarzhevskiy Institute of Physical Chemistry [ 2 ]  ( Kyiv ), where the theoretical foundations for the formation of the porous structure of organosilicon adsorbents with an adjustable porous structure and a pre-defined chemical nature of the surface were established; there were also efforts to synthesize organosilicon adsorbents, namely porous polymers polyorganosiloxanes. Industrial production of the preparation began in early 1991. [ 3 ]  In 1994, a medicinal drug with methylsilicic acid hydrogel as the active ingredient, marketed under the brand name Enterosgel, was registered in Ukraine and Russia, and active sales of the new product began."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3600", "text": "Currently, the product is already available in 40 countries."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3601", "text": "The study of the use of the preparation was conducted in cooperation with the Medical Service of Krasnoznamennyi Kiev Military District (Medical Service Colonel Professor F. G. Novikov, Medical Service Colonel N. P. Bezlyuda). [ 4 ]  Since, many clinical trials investigating the preparation have been conducted by Ukrainian and Russian companies in the CIS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3602", "text": "A large-scale study of its effect was conducted in the United Kingdom between 2019 and 2022. It established a proven base of effectiveness of the preparation in the treatment of irritable bowel syndrome with diarrhea, help in relieving bloating, abdominal pain and urgency. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3603", "text": "The preparation is registered in Russia and the CIS countries as a medicinal drug, [ 5 ]  and in the countries of the European Union, Serbia, New Zealand, Africa as a medical device, since the product is not absorbed into the bloodstream and acts as an adsorbent only in the gastrointestinal tract, it fits the relevant definition according to the Classification of the European Commission."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3604", "text": "The medical device Enterosgel is produced in a modern high-tech factory in Jesen\u00edk, Czech Republic, from where it is exported to all countries of the world, except Russia and the CIS countries. This region supplies production in Russia, where a factory is situated in the city of Dankov."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3605", "text": "Enterosgel (PMSPH) or methylsilicic acid hydrogel is a polymeric gelatinous organosilicon compound. The gel is dispersed in water to a particle size of no more than 300 microns. The preparation is a  suspension  which is taken orally"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3606", "text": "Electron microscopic studies have shown that its gel-forming matrix has a globular structure and consists of an ensemble of fused globules. These globules, bound together by siloxane bonds, form pores. The pores are the spaces between the globules. They are filled with water. Pore size is restricted. [ 6 ] :\u200a38\u200a  The presence of methyl groups on the surface ensures its hydrophobic properties. [ 6 ] :\u200a27\u200a  Enterosgel particles (PMSPH) tend to form a continuous network in a suspension to reduce the interaction of hydrophobic SiCH 3  with water. These particles can be viewed as two-dimensional sheets rather than three-dimensional solid particles. Aqueous suspensions of polymethylsiloxane polyhydrate are characterized by high viscosity. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3607", "text": "The physical and chemical characteristics of Enterosgel define its absorptive and protective properties:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3608", "text": "It absorbs toxic substances produced in the gastrointestinal tract, as well as toxic substances entering the gastrointestinal tract from the environment (e.g., ethyl alcohol). [ 11 ]  It also prevents reabsorption of toxic substances and metabolites excreted into the intestinal lumen from the blood, as well as getting into the intestine with bile."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3609", "text": "In an  in vitro  experiment, it reduced the production of staphylococcal enterotoxin and inhibited the growth of  Staphylococcus aureus . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3610", "text": "It reduced malonic dialdehyde formation and increased integral antiradical activity in toxic liver damage  in vivo . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3611", "text": "Due to adsorption in the gastrointestinal tract, it helps reduce blood sugar and  glycated hemoglobin  levels, eliminate lipid distress syndrome, including diabetic dyslipidemia, improves energy processes in liver tissues in experimental diabetes. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3612", "text": "Enterosgel (PMSPH) firmly binds and excretes pathogenic bacteria [ 15 ]  and  rotaviruses . [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3613", "text": "Highly viscous PMSPH particles cover mucosal areas and protect them from the damaging effects of bacterial toxins and various active chemical compounds (e.g., deconjugated bile salts that damage the mucosa of the gastrointestinal tract)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3614", "text": "Enterosgel has a pronounced ability to absorb lipopolysaccharide molecules. Large molecules of lipopolysaccharide are co-precipitated in the gel and excreted from the body. [ 9 ]  A daily dose of PMSPH (Enterosgel paste) binds 410\u00a0mg of LPS. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3615", "text": "Lipopolysaccharide  (LPS), which has extremely high biological activity, can be found in the outer wall of all  Gram-negative bacteria  and is released only when the bacterium is destroyed, and is also known as  endotoxin  (the prefix endo- means inside, inside the bacterium). The distal section of the intestine is the main reservoir of Gram-negative microflora and lipopolysaccharides. Normally, only a small amount of endotoxin enters the bloodstream because the intestinal wall works as a barrier and limits the inflow of endotoxin into the bloodstream. Most (94%) of the endotoxin entering the bloodstream undergoes detoxification in the liver. However, a small amount of endotoxin bypasses the liver and enters the systemic bloodstream, maintaining physiological concentration of endotoxin in the blood (physiological endotoxinemia)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3616", "text": "The process of endotoxin entering the bloodstream can be intensified by various lesions of the intestinal mucosa and by dysbacteriosis, which is accompanied by translocation of bacteria and products of their life activity into the small intestine [ 19 ]  and as a result of antibiotic-induced death of Gram-negative microflora and the release of large amounts of endotoxin. [ 20 ]  It should be particularly emphasized that various stressful situations (severe seizures, burns, trauma, etc.) cause damage to the mucous membrane of the gastrointestinal tract. This damage occurs due to redistribution of energy and structural resources of the body, i.e. transfer from systems not involved in adaptation to the stress factor to systems providing adaptation. [ 21 ]  An increase in the concentration of endotoxin in the blood exceeding the physiological norm leads to a pathological condition known as endotoxin aggression. Endotoxin aggression is a universal factor in the pathogenesis of human diseases, the development of which is caused by an excess of endotoxin entering the general bloodstream and a lack of endotoxin-binding systems. [ 22 ] [ 23 ] [ 24 ] [ 25 ] [ 26 ] [ 27 ]  Excess endotoxin causes endothelial damage [ 28 ]  in the microcirculatory vessels of the intestinal mucosa and leads to the development of mucosal ischemia. This, in turn, causes further damage to the mucosa and a weakening of the intestinal barrier."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3617", "text": "Reduction of endotoxin back to physiological levels in the blood prevents damage to the vascular wall and restores impaired blood supply to the intestinal mucosa and eliminates mucosal ischemia. The latter, in turn, contributes to its regeneration and restoration of the barrier function of the intestinal mucosa. The positive effect of using Enterosgel (PMSPH) is primarily aimed at preserving/restoring the intestinal barrier, restoring the physiological level of endotoxin and breaking the vicious circle caused by damage to the mucous membrane. This inhibits the development of endotoxin aggression."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3618", "text": "From the left:  As a result of intestinal barrier insufficiency, there is an increase in the concentration of LPS in the mucosal bloodstream, which leads to impaired microcirculation and ischemia of the mucosa, its damage and further development of intestinal barrier insufficiency. Endotoxin aggression develops."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3619", "text": "From the right:  The use of Enterosgel ( PMSPH ) reverses the course of events: the level of LPS is reduced, microcirculation processes in the intestinal mucosa are restored, the intestinal mucosa is restored, and the function of the intestinal barrier is restored (more details) ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3620", "text": "Notes"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3621", "text": "Figure 1:  As a result of insufficiency of the intestinal barrier, the concentration of LPS in the blood flow of the mucous membrane increases, which leads to disruption of microcirculation and ischemia of the mucous membrane, its damage and further development of intestinal barrier insufficiency. Endotoxin aggression develops."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3622", "text": "Figure 2:  The use of Enterosgel (PMS PH) reverses the course of events: the level of LPS decreases, microcirculation processes in the intestinal mucosa are restored, and so are the intestinal mucosa and the functions of the intestinal barrier (more) ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3623", "text": "PMSPH is not absorbed in the gastrointestinal tract and is excreted in an unchanged form within 12 hours."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3624", "text": "It binds and removes endogenous and exogenous toxic substances of various nature, including bacteria and bacterial toxins, antigens, food allergens, drugs and poisons, salts of heavy metals, alcohol, from the lumen of the gastrointestinal tract. It also sorbs some metabolic products of metabolism, including excess bilirubin, urea, cholesterol, and lipid complexes, as well as metabolites responsible for the development of endogenous  intoxication . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3625", "text": "Indications for use [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3626", "text": "Enterosgel (PMSPH) is used in adults and children for the treatment and prevention of acute and chronic intoxications of various etiology (e.g. alcohol intoxication, [ 30 ]  botulism, [ 31 ]  mushroom poisoning [ 32 ] ) including  viral  and bacterial ones."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3627", "text": "The efficacy and safety of the drug for registered indications is continuously monitored as part of routine pharmacovigilance according to Eurasian Union and European Union (GVP) requirements. [ 33 ] [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3628", "text": "The results of randomized clinical trials, including double-blind placebo-controlled trials, in Russia, the CIS, Europe, etc., are evaluated."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3629", "text": "In the 2022 RELIEVE IBS-D randomized double blinded placebo controlled study was published in the GUT journal. The study confirmed safety and efficacy in treatment of Irritable bowel syndrome with diarrhea. Enterosgel was effective in relieving the abdominal pain, diarrhoea, bloating and urgency. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3630", "text": "Enterosgel is included in the clinical guidelines of state and non-state medical organizations of healthcare professionals in the CIS countries. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3631", "text": "For example in a study in Croatia, it was used as concomitant therapy in women receiving radiotherapy and chemotherapy for pelvic cancer, and the results showed that it had an effect on the reduction of intoxication symptoms (nausea, vomiting, etc.). [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3632", "text": "It has been successfully used for hyperbilirubinemia (viral hepatitis, [ 37 ] ) [ 38 ] [ 39 ] [ 40 ]  including for hemolytic disease in newborns. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3633", "text": "Also in chronic renal insufficiency (hyperazotemia). [ 41 ]  It has proved itself in the treatment of allergic diseases such as atopic dermatitis. [ 42 ] [ 43 ]  When indicated, it is used to treat gastroenterological disorders. [ 44 ]  Thus, it is recommended for the treatment of acute [ 45 ] [ 46 ]  and chronic  diarrhea , [ 47 ] [ 48 ]  dysbiosis [ 49 ] [ 50 ]  including diarrhea of non-infectious origin, [ 51 ] [ 4 ]  including for the treatment of  irritable bowel syndrome  with diarrhea. [ 4 ]  In acute and chronic infectious and inflammatory diseases, it is used in obstetrics [ 52 ]  and gynecology, since it is approved for use in pregnant women and children from birth. [ 53 ] [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3634", "text": "Proctosedyl  is the brand name for a family of two products with identical  active ingredients  designed to treat a variety of  proctological  disorders. One is a  topical   ointment , the other a  rectal   suppository . In the  United Kingdom  both products are contract manufactured by  Patheon Limited  on behalf of the  Sanofi-Aventis  group. [ 1 ] [ 2 ]  Manufacture and distribution is provided by Sanofi Aventis subsidiaries [ 3 ]   Hoechst and Hoechst Marion Roussel  in other territories worldwide. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3635", "text": "Both the yellowish-white, translucent, greasy ointment [ 1 ]  and the smooth, off-white suppositories [ 2 ]  are formulated for the relief of chronic  pruritus ani  (otherwise known anal itching or anusitis) [ 1 ] [ 2 ] [ 5 ]  and the treatment of pain, irritation, discharge and itching associated with  haemorrhoids  (otherwise known as piles). [ 1 ] [ 2 ] [ 5 ]  However both products are also used to provide pain relief in the treatment of  anal fissure , [ 6 ] [ 7 ] [ 8 ]  for patients undergoing  haemorrhoidectomy , (pre and post-operative), [ 8 ]  in the relief of  post-partum  (otherwise known as post-natal) haemorrhoidal conditions, [ 8 ] [ 9 ]  and in the treatment of non-infective  proctitis . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3636", "text": "Both preparations contain:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3637", "text": "Preparations in some territories may also contain:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3638", "text": "Prostaglandin analogues  are a  class of drugs  that bind to a  prostaglandin receptor . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3639", "text": "Wider use of prostaglandin analogues is limited by unwanted side effects and their  abortive  potential. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3640", "text": "Prostaglandin analogues such as  misoprostol  are used in treatment of  duodenal  and  gastric ulcers . [ 2 ]  Misoprostol and other prostaglandin analogues protect the lining of the gastrointestinal tract from harmful stomach acid and are especially indicated for the  elderly  on continuous doses of  NSAIDs ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3641", "text": "In the field of  ophthalmology , drugs of this class are used to lower  intraocular pressure  (IOP) in people with  glaucoma .  Up until the late 1970s prostaglandins were thought to raise IOP, but a paper published in 1977 showed that  prostaglandin F2\u03b1  lowered it, and subsequent studies found that this was due to increasing the outflow of  aqueous humor , mainly by relaxing the  ciliary muscle , and possibly also due to changes in  extracellular matrix  and to widening of spaces within the  trabecular meshwork . [ 1 ]   This work led to the development of  prodrugs  of PGF2\u03b1, including  latanoprost , an isopropyl analogue of PGF2\u03b1, approved by the FDA in 1996,  bimatoprost  and  travoprost , both approved in 2001, and  tafluprost , approved in 2012. [ 1 ]    However, there are notable side effects associated with usage, including increased eyelash growth, pigmentation of the iris, and darkening of the skin around the eye. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3642", "text": "This  drug  article relating to the  blood  and  blood forming organs  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3643", "text": "This  drug  article relating to the  genito-urinary system  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3644", "text": "A  reflux suppressant  is any one of a number of  drugs  used to combat  oesophageal reflux . [ 1 ] [ 2 ]  Commonly, following ingestion a 'raft' of  alginic acid  is created, floating on the stomach contents by carbon dioxide released by the drug. This forms a mechanical barrier to further reflux. Some preparations also contain  antacids  to protect the  oesophagus . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3645", "text": "Reflux can also be coincidentally reduced by the  motility stimulants  and  antidopaminergics . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3646", "text": "Relamorelin  ( INN ,  USAN ) (developmental code names  RM-131 ,  BIM-28131 ,  BIM-28163 ) is a  synthetic   peptide ,  centrally penetrant , selective  agonist  of the  ghrelin/growth hormone secretagogue receptor  (GHSR) which is under development by  Allergan pharmaceuticals  for the treatment of  diabetic gastroparesis ,  chronic idiopathic constipation , and  anorexia nervosa . [ 1 ] [ 2 ] [ 3 ]  It is a  pentapeptide  and an  analogue  of  ghrelin  with improved  potency  and  pharmacokinetics . [ 1 ] [ 2 ]  In humans, relamorelin produces increases in  plasma   growth hormone ,  prolactin , and  cortisol  levels, [ 2 ] [ 4 ]  and, like other GHSR agonists, increases  appetite . [ 3 ]  As of June 2015, relamorelin is in  phase II   clinical trials  for diabetic gastroparesis and constipation. [ 5 ]  The United States  Food and Drug Administration  (FDA) has granted  Fast Track  designation to relamorelin for diabetic gastroparesis. [ 6 ]  The development of the drug is uncertain as the most recent mention of it was in a 2019 SEC filing from the drug manufacturer lists the drug's expected launch year as 2024, but not in subsequent filings or press releases. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3647", "text": "This  hormonal preparation  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3648", "text": "Rolaids  is an American brand of calcium and magnesium-based  antacid  produced by  Procter & Gamble .  It was invented by  American   chemist   Irvine W. Grote  in the late 1920s, and originated with manufacturing in  Chattanooga, Tennessee , under one of Chattem's forerunner companies, which manufactured the brand for  Warner-Lambert ; Warner-Lambert merged with Pfizer in 2000."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3649", "text": "In 2006,  McNeil Consumer Healthcare , a subsidiary of  Johnson & Johnson , acquired the brand from  Pfizer  Consumer Healthcare. In 2013, McNeil sold the brand to Sanofi, [ 1 ]  following a two-year period where the brand was pulled off the market due to  product recalls  resulting from  quality control  and manufacturing issues that also kept former fellow antacid brand  Pepcid AC 's \"chewables\" product and other fellow McNeil products like some varieties of  Tylenol  off store shelves for the same period. [ 2 ]  Rolaids returned to the market at the beginning of September 2013 under Chattem ownership with new packaging,  trade dress , and a new liquid variety. On March 27, 2024, the brand was acquired by  Procter & Gamble . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3650", "text": "Rolaids tablets come in many different flavors, including original peppermint, cherry, freshmint, fruit, tropical, punch, cool mint, berry, and apple."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3651", "text": "McNeil Consumer Healthcare voluntarily recalled Rolaids products in the Americas, the United Arab Emirates (UAE), and Fiji on January 15, 2010, in consultation with the FDA. The company initiated the recall following an investigation of consumer reports of an unusual moldy, musty, or mildewlike odor that, in a small number of cases, was associated with temporary and nonserious gastrointestinal events. These events included nausea, stomach pain, vomiting, and diarrhea. At that time, the Rolaids website carried the following statement regarding product availability: \"You may have noticed that ROLAIDS\u00ae products are not available at your local retailers. We are changing some of our manufacturing facilities where our products are made, a process that will take time to complete. We apologize for the inconvenience this may be causing you. Your health and comfort are important to us, and we assure you we are working hard to get ROLAIDS\u00ae product back on store shelves.\" [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3652", "text": "Another recall was issued around December 9, 2010, as a result of foreign objects that contained metal and wood particles. [ 5 ]  The foreign materials were caused by a third-party manufacturer during the production process. [ 5 ]  Several people complained when they took the product; they also had vomiting, strange taste, and tooth and gum injury. [ 5 ]  After this recall, beyond the small \"candy aisle\" rolls and chewable lines, the Rolaids line of products was drastically reduced and disappeared from most American retailers until Chattem returned the product to the market in the fall of 2013."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3653", "text": "Rolaids' best-known commercial from the 1970s featured the famous tag line:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3654", "text": "In connection with the famous slogan, Rolaids sponsored the  Major League Baseball  award for top  relief pitchers  called the  Rolaids Relief Man of the Year Award . The award was given yearly from 1976 through 2012."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3655", "text": "Pfizer  released a new version of Rolaids on April 6, 2006, [ 6 ]  branded  Extra Strength Rolaids Plus Gas Relief Softchews . The product was produced as an alternative for people averse to the chalky consistency of regular Rolaids. They were widely advertised in multiple media formats."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3656", "text": "Rolaids Softchews were originally developed and test marketed in Oklahoma City under the brand name Remegel by Warner Lambert in 1984."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3657", "text": "The  active ingredients  are  calcium carbonate  (550\u00a0mg) and  magnesium hydroxide  (110\u00a0mg). The inactive ingredients are  dextrose ,  flavoring ,  magnesium stearate ,  polyethylene glycol ,  pregelatinized starch , sucralose and  sucrose . The new Chattem varieties have increased the amount of the active ingredients in the product, up to 1000\u00a0mg of calcium carbonate and 200\u00a0mg of magnesium hydroxide for the \"ultra strength\" varieties."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3658", "text": "Minor side effects may include constipation or stomach cramps. Serious side effects include loss of appetite, vomiting, dizziness, and headache. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3659", "text": "Seidlitz powders  is the generic name under which a commonly known  laxative  and digestion regulator was  marketed  and sold by numerous manufacturers under names such as \"Rexall Seidlitz Powders\", particularly in the late 19th and early 20th centuries. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3660", "text": "The three ingredients of Seidlitz powders ( tartaric acid ,  potassium sodium tartrate  and  sodium bicarbonate ) were manufactured by chemical factories from the mid-19th century onwards. The name 'Seidlitz powders' ultimately derives from the village of  Sedlec  in the  Czech Republic .  See also  \u00a7 Etymology  below ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3661", "text": "The municipality of Sedlec (somewhat confusingly) is also the source of 'Sedlitz bitter water'  ( see also  \u00a7 Sedlitz water  below ), a naturally occurring  spa  mineral water which has an entirely different chemical composition and side-effects from Seidlitz powders: there is apparently no connection between the two products except the name. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3662", "text": "The powders were often packaged in a small envelope containing two coloured paper wraps, one white and one blue. The white packets contained  tartaric acid , and the blue packets contained a mixture of 75%  w/w  Rochelle salt ( potassium sodium tartrate ) and 25% baking soda ( sodium bicarbonate ). The powdery contents of both packets were stirred or dissolved separately in water and then mixed, giving off carbon dioxide with a characteristic fizzing sound. [ 3 ]  The drink was described as \"a cooling, agreeable draught\". [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3663", "text": "After ingestion, the powder combines with gastric juices to develop  cathartic  intestinal gases which can be somewhat helpful in evacuating the users' bowels. However, their use can also lead to unpleasant side effects, [ 5 ]  and can even be fatal [ 6 ]  in subjects with conditions such as  hernia ,  bowel obstruction  or other ailments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3664", "text": "Seidlitz powders, manufactured by numerous chemical factories from the early 19th century onwards, take their name from the village of  Sedlec  near  Most ,  Czech Republic  (previously in  Bohemia ). The village seems to have received its Germanic name (Seidlitz) some time after 1526, when the  Battle of Moh\u00e1cs  brought about the collapse of  Medieval Hungary . The  Lands of the Bohemian Crown  fell under the control of the  Habsburgs , the German-speaking rulers of Austria (later the  Austro-Hungarian Empire )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3665", "text": "Although Seidlitz powders have a  digestive  effect, they should not be confused with 'Sedlitz water' (also named for Sedlec), a well-known bitter mineral water which has been used since the 16th century as a digestion regulator and  laxative . Sedlec (Seidlitz) was described in an 1867 guide to European  spa towns  as \"a wretched-looking place, hardly meriting the name of a village, and the wells - whence the water should be derived - are a few shallow, circular pits, whose contents very seldom find their way to this country [ie England].\" The Sedlitz water has a chemical analysis similar to sources in nearby towns such as  Zaje\u010dick\u00e1 ho\u0159k\u00e1  from Zajecice (NB German name 'Seidschitz' bitter water'),  Korozluky  (Ger: Kollosoruk) and  B\u00edlina  (Bylany or P\u00fcllna). The water itself was characterized as \"a yellowish, somewhat oily-looking fluid, with a nauseous, intensely bitter taste.\" [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3666", "text": "These and similar products - with somewhat interchangeable terminology - appear to have no connection with Seidlitz powders. Likewise, the powders have little connection (apart from the digestive effect) with these types of mineral-rich water which were evaporated and the residue formed into pills such as  Bilina  digestive  pastilles , not unlike  Vichy pastilles ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3667", "text": "Though rarely used today, the term \"Seidlitz powder\" lives on as a lyric from the  popular song  \" A Fine Romance \" by  Jerome Kern  and  Dorothy Fields . Written for the 1936 musical film,  Swing Time , with  Fred Astaire  and  Ginger Rogers , it was released on a 1956 jazz album by  Ella Fitzgerald  and  Louis Armstrong ,  Ella and Louis Again , with the lines \"We two should be like clams in a dish of chowder / But we just fizz like parts of a Seidlitz powder.\""}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3668", "text": "\"Sounds like a seidlitz powder\" is in a  O. Henry  story, \"The Foreign Policy of Company 99\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3669", "text": "One of the four clerks of Dodson and Fogg is mixing a \"Seidlitz Powder,\" perhaps to treat a hangover, in chapter 20 of  Charles Dickens '  Pickwick Papers ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3670", "text": "No\u00ebl Coward  would tease the US theatre critic  Alexander Woollcott  \u201cby recalling that one of [the latter\u2019s] critical colleagues had called him \u2018the Seidlitz Powder of Times Square\u2019.\u201d [Barry Day (2021), No\u00ebl Coward On & In Theatre, Alfred Knopf: New York, p.279]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3671", "text": "Sofalcone  ( INN ) is an oral  gastrointestinal   medication  used in Japan. [ 1 ]   It is a synthetic  analog  of  sophoradin , [ 2 ]  a type of natural phenol found in  Sophora tonkinensis , an herb used in  traditional Chinese medicine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3672", "text": "Sucralfate , sold under various brand names, is a  medication  used to treat  stomach ulcers ,  gastroesophageal reflux disease  (GERD),  radiation proctitis , and  stomach inflammation  and to prevent  stress ulcers . [ 3 ] [ 4 ] [ 5 ]  Its usefulness in people infected by  H. pylori  is limited. [ 3 ]  It is used by mouth (for upper GIT ulcers) and rectally (for radiation proctitis). [ 3 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3673", "text": "Common side effects include  constipation . [ 3 ]  Serious side effects may include  bezoar  formation and  encephalopathy . [ 6 ]  Use appears to be safe in  pregnancy  and  breastfeeding . [ 6 ]  How it works is unclear but is believed to involve binding to the ulcer and protecting it from further damage. [ 3 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3674", "text": "Sucralfate was approved for medical use in the United States in 1981. [ 3 ]  It is available as a  generic medication . [ 6 ] [ 7 ]  In 2022, it was the 214th most commonly prescribed medication in the United States, with more than 1 \u00a0 million prescriptions. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3675", "text": "Sucralfate is used for the treatment of active  duodenal ulcers  not related to the use of  nonsteroidal anti-inflammatory drugs  (NSAIDs), as the  mechanism  behind these ulcers is due to acid oversecretion. [ 1 ]  It is not FDA approved for  gastric ulcers , but is widely used because of evidence of efficacy. [ 10 ]  The use for sucralfate in  peptic ulcer disease  has diminished recently, but it is still the preferred agent for  stress ulcer  prevention. [ 11 ] [ 12 ] [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3676", "text": "Sucralfate has also been used for the following conditions:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3677", "text": "The most common  side effect  seen is  constipation  (2\u20133%). Less commonly reported side effects (<0.5%) include  flatulence ,  headache ,  hypophosphatemia ,  xerostomia  (dry mouth), and  bezoar  formation. [ 24 ] [ 25 ] [ 26 ] \nUse of this drug is not recommended for people with  chronic kidney failure , as it might cause aluminium accumulation and  toxicity .\nA few well-controlled studies have been carried out investigating the safety and efficacy of sucralfate in children and pregnant women ( Pregnancy Category  B). [ 1 ] [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3678", "text": "Sucralfate is a locally acting  substance  that in an acidic environment (pH < 4) reacts with  hydrochloric acid  in the  stomach  to form a cross-linking,  viscous , paste-like material capable of acting as an  acid buffer  for as long as 6 to 8 hours after a single  dose . [ 29 ]  It also attaches to  proteins  on the surface of ulcers, such as  albumin  and  fibrinogen , to form stable  insoluble  complexes. These complexes serve as protective barriers at the ulcer surface, preventing further damage from  acid ,  pepsin , and  bile . [ 29 ]  In addition, sucralfate prevents back  diffusion  of  hydrogen ions , and absorbs both pepsin and  bile acids ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3679", "text": "It has been thought that sucralfate also stimulates the production of  prostaglandin  E 2 ,  epidermal growth factors  (EGF),  bFGF , and  gastric mucus . [ 1 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3680", "text": "Brand names include Carafate in the US, Sucramal in Italy, Sucrafil, Sufrate, Sucralpro, Sucralcoat, Pepsigard, Sucral, Hapifate, Sucralpro tablets and Sucralpro cream in India, Sutra or Musin in parts of South-East Asia, Sulcrate in Canada, Discral (sucralfato) in M\u00e9xico, Ulsanic in South Africa and Israel, Andapsin in Sweden, Antepsin in Turkey, Sucracell in India, and Ulsidex in Indonesia"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3681", "text": "Sulfasalazine , sold under the brand name  Azulfidine  among others, is a  medication  used to treat  rheumatoid arthritis ,  ulcerative colitis , and  Crohn's disease . [ 5 ]  It is considered by some to be a first-line treatment in rheumatoid arthritis. [ 6 ]  It is taken  by mouth  or can be administered rectally. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3682", "text": "Significant side effects occur in about 25% of people. [ 6 ]  Commonly these include loss of appetite, nausea, headache, and rash. [ 5 ]  Severe side effects include  bone marrow suppression ,  liver problems ,  Stevens\u2013Johnson syndrome , and  kidney problems . [ 6 ] [ 7 ] [ 4 ]  It should not be used in people allergic to  aspirin  or  sulfonamide . [ 6 ]  Use during  pregnancy  appears to be safe for the baby. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3683", "text": "Sulfasalazine is in the  disease-modifying antirheumatic drugs  (DMARDs) family of medications. [ 5 ]  It is unclear exactly how it works. [ 5 ]  One proposed mechanism is the inhibition of  prostaglandins , resulting in local  anti-inflammatory  effects in the colon. [ 4 ]  The medication is broken down by  intestinal bacteria  into  sulfapyridine  and  5-aminosalicylic acid . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3684", "text": "Sulfasalazine was approved for medical use in the United States in 1950. [ 5 ]  It is on the  World Health Organization's List of Essential Medicines . [ 8 ]  Sulfasalazine is available as a  generic medication . [ 5 ]  In 2020, it was the 284th most commonly prescribed medication in the United States, with more than 1 \u00a0 million prescriptions. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3685", "text": "Sulfasalazine is used in the treatment of  inflammatory bowel disease , including  ulcerative colitis  and  Crohn's disease . It is also indicated for use in  rheumatoid arthritis  and used in other types of inflammatory arthritis (e.g.  psoriatic arthritis  and  reactive arthritis ). [ 11 ] [ 3 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3686", "text": "It is usually not given to children under two years of age. [ 3 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3687", "text": "Use of sulfasalazine is contraindicated in people with  sulfa allergies  and in those with  urinary tract obstructions ,  intestinal obstructions , and severe  liver  or  kidney problems . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3688", "text": "Sulfasalazine metabolizes to sulfapyridine. Serum levels should be monitored every three months, and more frequently at the outset. Serum levels above 50 \u03bcg/L are associated with side effects. In rare cases, sulfasalazine can cause severe  depression  in young males. It can also cause oligospermia and temporary  infertility . Immune  thrombocytopenia  has been reported. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3689", "text": "Sulfasalazine inhibits  dihydropteroate synthase , and can cause  folate deficiency  and  megaloblastic anemia . [ 13 ] [ 14 ] [ 15 ]  and various other undesirable effects. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3690", "text": "Sulfasalazine can cause  hemolytic anemia  in people with  G6PD deficiency . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3691", "text": "Sulfasalazine can cause kidney stones. [ 18 ] \nSulfasalazine may cause stomach upset,  nausea , vomiting, loss of  appetite , headache,  dizziness , or unusual tiredness. [ 5 ]  Skin and urine can become orange, with occasional allergic reactions. [ 19 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3692", "text": "Sulfasalazine may cause  sulfhemoglobinemia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3693", "text": "Around 90% of a dose of sulfasalazine reaches the colon, where most of it is metabolized by bacteria into  sulfapyridine  and  mesalazine  (also known as 5-aminosalicylic acid or 5-ASA). Both metabolites are active; most of the sulfapyridine is absorbed and then further metabolized, but most mesalazine is not, and remains in the colon. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3694", "text": "A mix of unchanged, hydroxylated, and glucuronidated sulfapyridine is eliminated in urine, as is acetylated mesalazine and unmetabolized sulfasalazine. [ 3 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3695", "text": "The mechanism of action is not clear, but it appears that sulfasalazine and its metabolites have  immunosuppressive , antibacterial, and anti-inflammatory effects. [ 11 ] [ 3 ]   It also appears to inhibit the  cystine - glutamate   antiporter , [ 20 ]  as well as  sepiapterin reductase . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3696", "text": "It is a  codrug  which is a combination of  sulfapyridine  and  5-aminosalicylic acid  coupled with an azo linkage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3697", "text": "In people with rheumatoid arthritis, the  cost-effectiveness  of sulfasalazine is improved by combining it with other drugs. [ 22 ]   It is commonly used in treating  inflammatory bowel disease  in part due to its cost effectiveness. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3698", "text": "Sulfasalazine has been studied in  cirrhosis , [ 24 ]   psoriasis , [ 25 ]  idiopathic  urticaria , [ 26 ]  and  amyloidosis . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3699", "text": "Sulglicotide  (or  sulglycotide ) is a  drug  used for  peptic ulcer  and  gastro-oesophageal reflux disease . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3700", "text": "A  suppository  is a  dosage form  used to deliver  medications  by insertion into a  body orifice  (any opening in the body), where it dissolves or melts to exert local or systemic effects. There are three types of suppositories, each to insert into a different sections: rectal suppositories into the  rectum , vaginal suppositories into the  vagina , and urethral suppositories into the  urethra of a male ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3701", "text": "Suppositories are ideal for infants, elderly individuals and post-operative patients, who are unable to swallow oral medications, and for individuals experiencing severe nausea and/or vomiting. [ 1 ] [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3702", "text": "Several different ingredients can be used to form the base of a suppository:  cocoa butter  or a similar substitute,  polyethylene glycol ,  hydrogels , and glycerinated  gelatin . The type of material used depends on the type of suppository, the type of drug, and the conditions in which the suppository will be stored. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3703", "text": "In 1991, a study on suppository insertion in  The Lancet  found that the \"torpedo\" shape helps the device to travel internally, increasing its efficacy. [ 5 ]  The findings of this single study have been challenged as there is insufficient evidence on which to base clinical practice. [ 6 ]  Rectal suppositories are intended for localized or systemic action to relieve pain, constipation, irritation, inflammation, nausea and vomiting, fever, migraines, allergies, and sedation. [ 7 ] [ 8 ]  If they cause inflammation, chronic use of suppositories may cause  rectal stricture , [ 9 ]  but overall this is a safe method of drug delivery. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3704", "text": "Alprostadil  pellets are urethral suppositories used for the treatment of severe  erectile dysfunction (impotence) . They are marketed under the name  Muse  in the United States. [ 11 ]  Its use has diminished since the development of oral impotence medications."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3705", "text": "Teduglutide , sold under the brand names  Revestive  (EU) and  Gattex  (US), is a 33-membered poly peptide  and  glucagon-like peptide-2  (GLP-2) analog that is used for the treatment of  short bowel syndrome . It works by promoting  mucosal  growth and possibly restoring  gastric emptying  and secretion. [ 7 ]  It was approved in both the European Union [ 5 ]  and the United States in 2012. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3706", "text": "Up to a certain point, the gut can adapt to partial  resections  that result in short bowel syndrome. Still,  parenteral  substitution of water, minerals and vitamins (depending on which part of the gut has been removed) is often necessary. Teduglutide may reduce or shorten the necessity of such infusions by improving the  intestinal mucosa  and possibly by other mechanisms. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3707", "text": "Common adverse effects in clinical studies included abdominal discomfort (49% of patients),  respiratory infections  (28%), nausea (27%) and vomiting (14%), local reactions at the injection site (21%), and headache (17%). [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3708", "text": "Teduglutide differs from natural GLP-2 by a single  amino acid : an  alanine  is replaced with a  glycine . This blocks breaking down of the molecule by  dipeptidyl peptidase  and increases its half-life from seven minutes (GLP-2) to about two hours, while retaining its biological actions. These include maintenance of the intestinal mucosa, increasing intestinal blood flow, reducing  gastrointestinal motility  and  secretion  of gastric acid. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3709", "text": "It was approved in both the European Union (brand name Revestive) [ 5 ] [ 6 ]  and the United States (brand name Gattex) in 2012. [ 4 ]  It was granted  orphan drug  designation by the  European Medicines Agency  (EMA). [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3710", "text": "Tenapanor , sold under the brand name  Ibsrela  among others, is a  medication  used for the treatment of adults with a disease of the gut called  irritable bowel syndrome  with  constipation  commonly referred to as IBS-C. [ 3 ] [ 5 ]  It is used in form of tenapanor hydrochloride. [ 3 ]  It is also used in the treatment of hyperphosphatemia associated with  chronic kidney disease . [ 4 ]  Tenapanor is a sodium hydrogen exchanger 3 (NHE3) inhibitor. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3711", "text": "Tenapanor is a drug developed by Ardelyx, which acts as an inhibitor of the  sodium-proton exchanger NHE3 . This  antiporter  protein is found in the kidney and intestines, and normally acts to regulate the levels of  sodium  absorbed and secreted by the body. When administered orally, tenapanor selectively inhibits sodium uptake in the intestines, limiting the amount absorbed from food, and thereby reduces levels of sodium in the body. [ 6 ]  This may make it useful in the treatment of chronic kidney disease and  hypertension , both of which are exacerbated by excess sodium in the diet. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3712", "text": "It was approved for medical use in the United States in September 2019. [ 3 ] [ 8 ] [ 5 ] [ 9 ]  The U.S.  Food and Drug Administration  (FDA) considers it to be a  first-in-class medication . [ 10 ]  In October 2023, tenapanor was approved by the FDA for the treatment of  hyperphosphatemia . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3713", "text": "Teprenone  (or  geranylgeranylacetone ), sold under the brand name  Selbex , [ 1 ]  is a  medication  used for the treatment of  gastric ulcers . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3714", "text": "Testosterone  is a  medication  and naturally occurring  steroid hormone . [ 9 ]  It is used to treat  male hypogonadism ,  gender dysphoria , and certain types of  breast cancer . [ 9 ] [ 10 ]  It may also be used to increase  athletic ability  in the form of  doping . [ 9 ]  It is unclear if the use of testosterone for  low levels due to aging  is beneficial or harmful. [ 11 ]  Testosterone can be administered through several different routes, including  topical   gels  or  patches ,  nasal sprays,  subdermal implants, or  tablets dissolved inside the mouth . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3715", "text": "Common  side effects  of testosterone include  acne ,  swelling , and  breast enlargement in men . [ 9 ]  Serious side effects may include  liver toxicity ,  heart disease , and behavioral changes. [ 9 ]  Women and children who are exposed may develop  masculinization . [ 9 ]  It is recommended that individuals with  prostate cancer  should not use the medication. [ 9 ]  It can cause harm to the baby if used during  pregnancy  or  breastfeeding . [ 9 ]  Testosterone is in the  androgen  family of medications. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3716", "text": "Testosterone was first isolated in 1935, and approved for medical use in 1939. [ 12 ] [ 13 ]  Rates of use have increased three times in the United States between 2001 and 2011. [ 14 ]  It is on the  World Health Organization's List of Essential Medicines . [ 15 ]  It is available as a  generic medication . [ 9 ]  In 2022, it was the 118th most commonly prescribed medication in the United States, with more than 5 \u00a0 million prescriptions. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3717", "text": "The primary use of testosterone is the treatment of males with too little or no natural testosterone production, also termed  male hypogonadism  or  hypoandrogenism  (androgen deficiency). [ 18 ]  This treatment is referred to as  hormone replacement therapy  (HRT), or alternatively, and more specifically, as testosterone replacement therapy (TRT) or  androgen replacement therapy  (ART). It is used to maintain serum testosterone levels in the normal male range. Decline of testosterone production with age has led to interest in testosterone supplementation. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3718", "text": "A 2020 guideline from the  American College of Physicians  supports the discussion of testosterone in adult men with age-related  low levels of testosterone  who have  sexual dysfunction . They recommend yearly evaluation regarding possible improvement and, if none, to discontinue testosterone; physicians should consider intramuscular treatments, rather than transdermal treatments, due to costs and since the effectiveness and harm of either method is similar. Testosterone treatment for reasons other than possible improvement of sexual dysfunction may not be recommended. [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3719", "text": "Testosterone deficiency (also termed hypotestosteronism or hypotestosteronemia) is an abnormally low testosterone production. It may occur because of testicular dysfunction ( primary hypogonadism ) or hypothalamic\u2013pituitary dysfunction ( secondary hypogonadism ) and may be  congenital  or acquired. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3720", "text": "Testosterone levels may decline gradually with age. [ 23 ] [ 24 ]  The United States  Food and Drug Administration  (FDA) stated in 2015 that neither the benefits nor the safety of testosterone supplement have been established for low testosterone levels due to aging. [ 11 ]  The FDA has required that labels on testosterone include warnings about increased risk of heart attacks and stroke. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3721", "text": "To take advantage of its  virilizing  effects, testosterone is administered to  transgender men  and other  transmasculine individuals  as part of  masculinizing hormone therapy , [ 25 ]  titrated to clinical effect with a \"target level\" of the average male's testosterone level. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3722", "text": "Testosterone therapy is effective in the short-term for the treatment of  hypoactive sexual desire disorder  (HSDD) in women. [ 37 ]  However, its long-term  safety  is unclear. [ 37 ]  Because of a lack data to support its efficacy and safety, the  Endocrine Society  recommends against the routine use of testosterone in women to treat  low androgen levels  due to  hypopituitarism ,  adrenal insufficiency ,  surgical removal of the ovaries , high-dose  corticosteroid  therapy, or other causes. [ 37 ]  Similarly, because of a lack of data to support its efficacy and safety, the Endocrine Society recommends against the use of testosterone in women to improve general  well-being , to treat  infertility ,  sexual dysfunction  due to causes other than HSDD, or to improve  cognitive ,  cardiovascular ,  metabolic , and/or  bone  health. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3723", "text": "A 2014 systematic review and meta-analysis of 35 studies consisting of over 5,000  postmenopausal  women with normal  adrenal gland  function found that testosterone therapy was associated with significant improvement in a variety of domains of sexual function. [ 38 ]  These domains included frequency of  sexual activity ,  orgasm ,  arousal , and sexual satisfaction, among others. [ 38 ]  Women who were menopausal due to  ovariectomy  showed significantly greater improvement in sexual function with testosterone relative to those who had normal menopause. [ 38 ]  In addition to beneficial effects on sexual function, testosterone was associated with unfavorable changes in  blood lipids . [ 38 ]  These included decreased levels of total  cholesterol ,  triglycerides , and  high-density lipoprotein  (HDL) cholesterol, and increased levels of  low-density lipoprotein  (LDL) cholesterol. [ 38 ]  However, the changes were small in magnitude, and the long-term significance in relation to  cardiovascular  outcomes is uncertain. [ 38 ]  The changes were more pronounced with oral  testosterone undecanoate  than with  parenteral  routes, such as  transdermal  testosterone. [ 38 ]  Testosterone showed no significant effect on  depressed   mood   anxiety ,  bone mineral density  (BMD), or  anthropomorphic measures  like  body weight  or  body mass index . [ 38 ]  Conversely, it was associated with a significant incidence of androgenic side effects, including  acne  and  hirsutism  (excessive facial/body hair growth). [ 38 ]  Other androgenic side effects, such as  weight gain ,  pattern hair loss , and  voice deepening , were also reported in some trials, but were excluded from analyses due to insufficient data. [ 38 ]  The overall quality of the evidence was rated as low and was considered to be inconclusive in certain areas, for instance on long-term safety. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3724", "text": "A subsequent 2017 systematic review and meta-analysis of studies including over 3,000 postmenopausal women with HSDD similarly found that short-term transdermal testosterone therapy was effective in improving multiple domains of sexual function. [ 39 ]  Androgenic adverse effects such as acne and hirsutism were significantly greater in incidence with testosterone therapy, whereas no significant differences in \"increase in facial hair, alopecia, voice deepening, urinary symptoms, breast pain, headache, site reaction to the patch, total adverse events, serious adverse events, reasons for withdrawal from the study, and the number of women who completed the study\" were seen relative to controls. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3725", "text": "Although testosterone has been found to be effective at improving sexual function in postmenopausal women, the doses employed have been supraphysiological. [ 40 ] [ 41 ]  In contrast to these high doses, there is little support for the notion that testosterone is a critical hormone for sexual desire and function in women under normal physiological circumstances. [ 40 ] [ 41 ]  Low doses of testosterone resulting in physiological levels of testosterone (<50\u00a0ng/dL) have not been found to significantly increase sexual desire or function in women in most studies. [ 40 ]  Similarly, there appears to be little or no relationship between total or free testosterone levels in the normal physiological range and sexual desire in premenopausal women. [ 41 ] [ 40 ]  Only high doses of testosterone resulting in supraphysiological levels of testosterone (>50\u00a0ng/dL) significantly increase sexual desire in women, with levels of testosterone of 80 to 150\u00a0ng/dL \"slightly\" increasing sex drive. [ 40 ] [ 41 ]  In accordance, men experience  sexual dysfunction  at testosterone levels of below 300\u00a0ng/dL, and men that have levels of testosterone of approximately 200\u00a0ng/dL frequently experience such problems. [ 41 ]  The high doses of testosterone required to increase sexual desire in women may have a significant risk of masculinization with long-term therapy. [ 41 ] [ 40 ]  For this reason, and due to the unknown health effects and safety of testosterone therapy, its use may be inappropriate. [ 41 ] [ 40 ]  In 2003, the FDA rejected Intrinsa, a 300\u00a0\u03bcg/day  testosterone patch  for the treatment of sexual dysfunction in postmenopausal women. [ 40 ] [ 41 ]  The reasons cited were limited efficacy (about one additional sexually satisfying event per month), concerns about safety and potential adverse effects with long-term therapy, and concerns about inappropriate  off-label use . [ 40 ] [ 41 ]  It appears that in women, rather than testosterone,  estradiol  may be the most important hormone involved in sexual desire, although data on the clinical use of  estradiol  to increase sexual desire in women is limited. [ 40 ] [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3726", "text": "There are no testosterone products approved for use in women in the United States and many other countries. [ 44 ]  There are approved testosterone products for women in Australia, where it is considered a drug of dependence, medicines that are subject to misuse and trafficking,  [ 45 ]  and some European countries. [ 44 ]  Testosterone pellet implants are approved for use in postmenopausal women in the United Kingdom. [ 46 ] [ 47 ]  Testosterone products for men can be used  off-label  in women in the United States. [ 44 ]  Alternatively, testosterone products for women are available from  compounding pharmacies  in the United States, although such products are unregulated and manufacturing quality is not ensured. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3727", "text": "Testosterone has been marketed for use by  oral ,  sublingual ,  buccal ,  intranasal ,  transdermal  ( patches ),  topical  ( gels ),  intramuscular  ( injection ), and  subcutaneous  ( implant )  administration . [ 49 ] [ 50 ] [ 51 ] [ 52 ]  It is provided unmodified and as a  testosterone ester  such as  testosterone cypionate ,  testosterone enanthate ,  testosterone propionate , or  testosterone undecanoate , which act as  prodrugs  of testosterone. [ 49 ] [ 50 ] [ 51 ]  The most common  route of administration  for testosterone is by intramuscular injection. [ 49 ]  However, it has been reported that AndroGel, a transdermal gel formulation of testosterone, has become the most popular form of testosterone in androgen replacement therapy for hypogonadism in the United States. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3728", "text": "Testosterone is used as a form of  doping  among  athletes  in order to improve performance. [ 65 ]  Testosterone is classified as an  anabolic  agent and is on the  World Anti-Doping Agency  (WADA) List of Prohibited Substances and Methods. [ 65 ]  Hormone supplements cause the endocrine system to adjust its production and lower the natural production of the hormone, so when supplements are discontinued, natural hormone production is lower than it was originally. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3729", "text": "Anabolic\u2013androgenic steroids  (AAS), including testosterone and its esters, have also been taken to enhance muscle development, strength, or endurance. They do so directly by increasing the muscles' protein synthesis. As a result, muscle fibers become larger and repair faster than the average person's. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3730", "text": "After a series of scandals and publicity in the 1980s (such as  Ben Johnson's  improved performance at the  1988 Summer Olympics ),  prohibitions  of AAS use were renewed or strengthened by many sports organizations. Testosterone and other AAS were designated a \" controlled substance \" by the  United States Congress  in 1990, with the  Anabolic Steroid Control Act . [ 66 ]  Their use is seen as an issue in modern sport, particularly given the lengths to which athletes and professional laboratories go to in trying to conceal such use from sports regulators. Steroid use once again came into the spotlight as a result of Canadian  professional wrestler   Chris Benoit 's double murder-suicide in 2007; however, there is no evidence implicating steroid use as a factor in the incident. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3731", "text": "Some female athletes may have naturally higher levels of testosterone than others, and may be asked to consent to  sex verification  and either surgery or drugs to decrease testosterone levels. [ 67 ]  This has proven contentious, with the  Court of Arbitration for Sport  suspending the IAAF policy due to insufficient evidence of a link between high androgen levels and improved athletic performance. [ 68 ] [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3732", "text": "A number of methods for detecting testosterone use by athletes have been employed, most based on a  urine test . These include the testosterone/ epitestosterone  ratio (normally less than 6), the testosterone/luteinizing hormone ratio and the  carbon-13 / carbon-12  ratio (pharmaceutical testosterone contains less carbon-13 than endogenous testosterone). In some testing programs, an individual's own historical results may serve as a reference interval for interpretation of a suspicious finding. Another approach being investigated is the detection of the administered form of testosterone, usually an ester, in hair. [ 70 ] [ 71 ] [ 72 ] [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3733", "text": "Absolute  contraindications  of testosterone include  prostate cancer ,  elevated hematocrit  (>54%), uncontrolled  congestive heart failure , various other  cardiovascular diseases , and uncontrolled  obstructive sleep apnea . [ 74 ]   Breast cancer  is said by some sources to be an absolute contraindication of testosterone therapy, [ 74 ]  but androgens including testosterone have also actually been used to treat breast cancer. [ 75 ]  Relative contraindications of testosterone include elevated  prostate-specific antigen  (PSA) in men with a high risk of prostate cancer due to  ethnicity  or family history, severe  lower urinary tract symptoms , and elevated hematocrit (>50%). [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3734", "text": "Adverse effects may also include minor side effects such as oily skin, acne, and seborrhea, as well as loss of scalp hair, which may be prevented or reduced with  5\u03b1-reductase inhibitors . In women, testosterone can produce  hirsutism  (excessive facial/body hair growth),  deepening of the voice , and other signs of  virilization . Exogenous testosterone may cause suppression of  spermatogenesis  in men, leading to, in some cases, reversible  infertility . [ 76 ]   Gynecomastia  and  breast tenderness  may occur with high dosages of testosterone due to peripheral conversion of testosterone by  aromatase  into excessive amounts of the  estrogen   estradiol . [ 77 ]  Testosterone treatment, particularly in high dosages, can also be associated with  mood changes , increased  aggression , increased  sex drive ,  spontaneous erections , and  nocturnal emissions . [ 78 ] [ 79 ] [ 80 ] [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3735", "text": "Other side effects include increased  hematocrit , which can require  venipuncture  in order to treat, and exacerbation of  sleep apnea . [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3736", "text": "The FDA stated in 2015 that neither the benefits nor the safety of testosterone have been established for low testosterone levels due to aging. [ 11 ]  The FDA has required that testosterone pharmaceutical labels include warning information about the possibility of an increased risk of heart attacks and stroke. [ 11 ]  They have also required the label include concerns about abuse and dependence. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3737", "text": "Injectable forms of testosterone can cause a lung problem called pulmonary oil microembolism (POME).  Symptoms of POME include cough, shortness of breath, tightening of the throat, chest pain, sweating, dizziness, and fainting. [ 84 ] [ 85 ]  A postmarketing analysis by the manufacturer of Aveed (testosterone undeconate injection) found that POME occurred at a rate of less than 1% per injection per year for Aveed. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3738", "text": "Adverse effects of testosterone supplementation may include increased cardiovascular events (including  strokes  and  heart attacks ) and  deaths  based on three peer-reviewed studies involving men taking testosterone replacement. [ 87 ]  In addition, an increase of 30% in deaths and heart attacks in older men has been reported. [ 88 ]  Due to an increased incidence of adverse cardiovascular events compared to a  placebo group , a Testosterone in Older Men with Mobility Limitations (TOM) trial (a  National Institute of Aging  randomized trial) was halted early by the  Data Safety and Monitoring Committee . [ 89 ]  On January 31, 2014, reports of  strokes ,  heart attacks , and  deaths  in men taking FDA-approved testosterone-replacement led the FDA to announce that it would be investigating the issue. [ 90 ]  Later, in September 2014, the FDA announced, as a result of the \"potential for adverse cardiovascular outcomes\", a review of the appropriateness and safety of Testosterone Replacement Therapy (TRT). [ 91 ] [ 92 ] [ 93 ]  The FDA now requires warnings in the drug labeling of all approved testosterone products regarding  deep vein thrombosis  and  pulmonary embolism . [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3739", "text": "Up to the year 2010, studies had not shown any effect on the risk of death,  prostate cancer  or  cardiovascular disease ; [ 95 ] [ 96 ]  more recent [ when? ]  studies, however, do raise concerns. [ 97 ]  A 2013 study, published in the Journal of the American Medical Association, reported \"the use of testosterone therapy was significantly associated with increased risk of adverse outcomes.\" The study began after a previous, randomized, clinical trial of testosterone therapy in men was stopped prematurely \"due to adverse cardiovascular events raising concerns about testosterone therapy safety.\" [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3740", "text": "However, when given to men with hypogonadism in the short- and medium-term, testosterone replacement therapy does not increase the risk of cardiovascular events (including strokes and heart attacks and other heart diseases). The long-term safety of the therapy is not known yet. [ 98 ] [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3741", "text": "Testosterone therapy for patients with late-onset hypogonadism, in addition to increasing risk of cardiovascular disease and prostate cancer, may exacerbate the risk factors associated with  benign prostatic hyperplasia , a condition that involves the noncancerous enlargement of the prostate gland, which can lead to urinary symptoms. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3742", "text": "Testosterone in the presence of a slow-growing prostate cancer is assumed to increase its growth rate. However, the association between testosterone supplementation and the development of prostate cancer is unproven. [ 101 ]  Nevertheless, physicians are cautioned about the cancer risk associated with testosterone supplementation. [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3743", "text": "Testosterone may accelerate pre-existing  prostate cancer  growth in individuals who have undergone androgen deprivation. [ 82 ]  It is recommended that physicians screen for prostate cancer with a digital rectal exam and  prostate-specific antigen  (PSA) level before starting therapy, and monitor PSA and hematocrit levels closely during therapy. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3744", "text": "Ethnic groups have different rates of prostate cancer. [ 103 ]  Differences in sex hormones, including testosterone, have been suggested as an explanation for these differences. [ 103 ]  This apparent paradox can be resolved by noting that prostate cancer is very common. In autopsies, 80% of 80-year-old men have prostate cancer. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3745", "text": "Testosterone is  contraindicated  in  pregnancy  and not recommended during  breastfeeding . [ 105 ]  Androgens like testosterone are  teratogens  and are known to cause  fetal  harm, such as producing  virilization  and  ambiguous genitalia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3746", "text": "5\u03b1-Reductase inhibitors  like  finasteride  and  dutasteride  can slightly increase circulating levels of testosterone by inhibiting its  metabolism . [ 106 ]  However, these drugs do this via prevention of the conversion of testosterone into its more potent  metabolite   dihydrotestosterone  (DHT), and this results in dramatically reduced circulating levels of DHT (which circulates at much lower relative concentrations). [ 106 ] [ 107 ]  In addition, local levels of DHT in so-called androgenic (5\u03b1-reductase-expressing) tissues are also markedly reduced, [ 106 ] [ 107 ]  and this can have a strong impact on certain effects of testosterone. [ 51 ] [ 108 ]  For instance, growth of body and facial hair and  penile growth  induced by testosterone may be inhibited by 5\u03b1-reductase inhibitors, and this could be considered undesirable in the context of, for instance,  puberty induction . [ 108 ] [ 109 ]  On the other hand, 5\u03b1-reductase inhibitors may prevent or reduce adverse androgenic side effects of testosterone like  scalp hair loss ,  oily skin ,  acne , and  seborrhea . [ 51 ]  In addition to the prevention of testosterone conversion into DHT, 5\u03b1-reductase inhibitors also prevent the formation of  neurosteroids  like  3\u03b1-androstanediol  from testosterone, and this may have neuropsychiatric consequences in some men. [ 110 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3747", "text": "Aromatase inhibitors  like  anastrozole  prevent the conversion of testosterone into  estradiol  by  aromatase . [ 51 ]  As only a very small fraction of testosterone is converted into estradiol, this does not affect testosterone levels, but it can prevent  estrogenic  side effects like gynecomastia that can occur when testosterone is administered at relatively high dosages. [ 51 ]  However, estradiol exerts  negative feedback  on the  hypothalamic\u2013pituitary\u2013gonadal axis  and, for this reason, prevention of its formation can reduce this feedback and disinhibit gonadal production of testosterone, which in turn can increase levels of endogenous testosterone. [ 111 ]  Testosterone therapy is sometimes combined with an aromatase inhibitor for men with secondary hypogonadism who wish to conceive children with their partners. [ 112 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3748", "text": "Inhibitors  and  inducers  of  cytochrome P450   enzymes  like  CYP3A4  have been associated with little or no effect on circulating testosterone levels. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3749", "text": "Antiandrogens  like  cyproterone acetate ,  spironolactone , and  bicalutamide  can block the androgenic and anabolic effects of testosterone. [ 113 ] [ 59 ]   Estrogens  can reduce the effects of testosterone by increasing the hepatic production and in turn circulating levels of  sex hormone-binding globulin  (SHBG), a  carrier protein  that binds to and occupies androgens like testosterone and DHT, and thereby reducing free concentrations of these androgens. [ 59 ] [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3750", "text": "Testosterone is a high  affinity   ligand  for and  agonist  of the  nuclear   androgen receptor  (AR). In addition, testosterone binds to and activates  membrane androgen receptors  (mARs) such as  GPRC6A  and  ZIP9 . Testosterone is also potentiated via  transformation  by  5\u03b1-reductase  into the more  potent  androgen DHT in so-called androgenic  tissues  such as the  prostate gland ,  seminal vesicles ,  skin , and  hair follicles . In contrast to the case of testosterone, such potentiation occurs to a reduced extent or not at all with most  synthetic  AAS (as well as with DHT), and this is primarily responsible for the dissociation of  anabolic  and androgenic effects with these agents. [ 115 ]  In addition to DHT, testosterone is converted at a rate of approximately 0.3% into the  estrogen   estradiol  via  aromatase . [ 116 ]  This occurs in many tissues, especially  adipose tissue , the  liver , and the  brain , but primarily in adipose tissue. [ 116 ]  Testosterone, after conversion into DHT, is also metabolized into 3\u03b1-androstanediol, a  neurosteroid  and potent  positive allosteric modulator  of the  GABA A  receptor , and  3\u03b2-androstanediol , a potent and preferential agonist of the  ER\u03b2 . [ 117 ]  These metabolites, along with estradiol, may be involved in a number of the effects of testosterone in the brain, including its  antidepressant ,  anxiolytic ,  stress -relieving,  rewarding , and  pro-sexual  effects. [ 117 ]  Whereas testosterone produced both anabolic and androgenic effects, despite the lack of clear boundaries between these effects, as there is a great deal of mutual overlap between them, [ 118 ]  the relative potency of these effects exerted by testosterone can depend on various factors and is a topic of ongoing research. [ 119 ] [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3751", "text": "The ARs are expressed widely throughout the body, including in the  penis ,  testicles ,  epididymides ,  prostate gland ,  seminal vesicles ,  fat ,  skin ,  bone ,  bone marrow ,  muscle ,  larynx ,  heart ,  liver ,  kidneys ,  pituitary gland ,  hypothalamus , and elsewhere throughout the  brain . [ 121 ] [ 122 ]  Through activation of the ARs (as well as the mARs), testosterone has many effects, including the following: [ 121 ] [ 49 ] [ additional citation(s) needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3752", "text": "Testosterone can be taken by a variety of different  routes of administration . [ 123 ]  These include  oral ,  buccal ,  sublingual ,  intranasal ,  transdermal  ( gels ,  creams ,  patches ),  rectal   suppositories ), by  intramuscular  or  subcutaneous   injection  (in  oil  or  aqueous ), and as a  subcutaneous implant . [ 123 ]  The  pharmacokinetics  of testosterone, including its  bioavailability , circulating testosterone levels,  metabolism ,  biological half-life , and other parameters, differ by route of administration. [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3753", "text": "Testosterone is a  naturally occurring   androstane   steroid  and is also known by the chemical name androst-4-en-17\u03b2-ol-3-one. [ 124 ]  It has a  double bond  between the C4 and C5 positions (making it an  androstene ), a  ketone   group  at the C3 position, and a  hydroxyl  ( alcohol ) group at the C17\u03b2 position. [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3754", "text": "Testosterone esters are  substituted  at the C17\u03b2 position with a  lipophilic   fatty acid   ester   moiety  of varying  chain  length. [ 125 ]  Major testosterone esters include  testosterone cypionate ,  testosterone enanthate ,  testosterone propionate , and  testosterone undecanoate . [ 59 ] [ 124 ] [ 126 ]  A C17\u03b2  ether   prodrug  of testosterone,  cloxotestosterone acetate , has also been marketed, although it is little known and is used very rarely or no longer. [ 124 ]  Another C17\u03b2 ether prodrug of testosterone,  silandrone , also exists but was never marketed, and is notable in that it is orally active. [ 124 ]  In addition to ester and ether prodrugs,  androgen prohormones  or  precursors  of testosterone, such as  dehydroepiandrosterone  (DHEA),  androstenediol , and  androstenedione , exist as well, and convert into testosterone to variable extents upon oral ingestion. [ 127 ]  Unlike testosterone ester and ether prodrugs however, these prohormones are only weakly androgenic/anabolic. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3755", "text": "All synthetic AAS are  derivatives  of testosterone. [ 127 ]  Prominent examples include  nandrolone  (19-nortestosterone),  metandienone  (17\u03b1-methyl-\u03b4 1 -testosterone), and  stanozolol  (a 17\u03b1-alkylated derivative of DHT). Unlike testosterone, AAS that are  17\u03b1-alkylated , like metandienone and stanozolol, are orally active. This is due to  steric hindrance  of C17\u03b2-position metabolism during the first-pass through the liver. In contrast, most AAS that are not 17\u03b1-alkylated, like nandrolone, are not active orally, and must instead be administered via intramuscular injection. This is almost always in ester form; for instance, in the case of nandrolone, as  nandrolone decanoate  or  nandrolone phenylpropionate ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3756", "text": "Testosterone was first isolated and  synthesized  in 1935. [ 128 ]  Shortly thereafter, in 1937, testosterone first became commercially available as a  pharmaceutical drug  in the form of  pellets  and then in ester form for intramuscular injection as the relatively short-acting testosterone propionate. [ 51 ] [ 49 ] [ 129 ]   Methyltestosterone , one of the first synthetic AAS and orally active androgens, was introduced in 1935, but was associated with hepatotoxicity and eventually became largely medically obsolete. [ 129 ]  In the mid-1950s, the longer-acting testosterone esters  testosterone enanthate  and  testosterone cypionate  were introduced. [ 129 ]  They largely superseded testosterone propionate and became the major testosterone esters used medically for over half a century. [ 129 ]  In the 1970s,  testosterone undecanoate  was introduced for oral use in Europe, [ 129 ]  although intramuscular testosterone undecanoate had already been in use in China for several years. [ 130 ]  Intramuscular testosterone undecanoate was not introduced in Europe and the United States until much later (in the early to mid 2000s and 2014, respectively). [ 8 ] [ 131 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3757", "text": "The history of testosterone as a medication has been reviewed. [ 132 ] [ 133 ] [ 134 ] [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3758", "text": "In the US in the 2000s, companies and figures in the popular media have heavily marketed notions of \"andropause\" as something parallel to  menopause ; these notions have been rejected by the medical community. [ 136 ] [ 137 ]  Additionally, advertising from drug companies selling testosterone and human growth hormone, as well as  dietary supplement  companies selling all kinds of \"boosters\" for aging men, have emphasized the \"need\" of middle-aged or ageing men for testosterone. [ 138 ]  There is a medical condition called  late-onset hypogonadism ; according to Thomas Perls and David J. Handelsman, writing in a 2015 editorial in the  Journal of the American Geriatrics Society , it appears that this condition is  overdiagnosed  and  overtreated . [ 138 ]  Perls and Handelsman note that in the US, \"sales of testosterone increased from $324 million in 2002 to $2 billion in 2012, and the number of testosterone doses prescribed climbed from 100 million in 2007 to half a billion in 2012, not including the additional contributions from compounding pharmacies, Internet, and direct-to-patient clinic sales.\" [ 138 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3759", "text": "Testosterone  is the  generic name  of testosterone in English and Italian and the  INN Tooltip International Nonproprietary Name ,  USAN Tooltip United States Adopted Name ,  USP Tooltip United States Pharmacopeia ,  BAN Tooltip BAN , and  DCIT Tooltip Denominazione Comune Italiana  of the drug, while  testost\u00e9rone  is its French name and the  DCF Tooltip D\u00e9nomination Commune Fran\u00e7aise . [ 124 ] [ 139 ] [ 140 ]  It is also referred to in  Latin  as  testosteronum , in Spanish and Portuguese as  testosterona , and in German,  Dutch , and Russian and other  Slavic languages  as  testosteron . [ 139 ] [ 140 ]  The  Cyrillic script  of testosterone is  \u0442\u0435\u0441\u0442\u043e\u0441\u0442\u0435\u0440\u043e\u043d . [ 141 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3760", "text": "Testosterone is marketed under a large number of brand names throughout the world. [ 139 ]  Major brand names of testosterone and/or its esters include Andriol, Androderm, AndroGel, Axiron, Delatestryl, Depo-Testosterone,  Intrinsa , Nebido,  Omnadren , Primoteston,  Sustanon , Testim, TestoGel, TestoPatch, Testoviron, and Tostran. [ 59 ] [ 115 ] [ 139 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3761", "text": "As of November\u00a02016 [update] , unmodified (non-esterified) testosterone is available in the United States in the following formulations: [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3762", "text": "And the following ester prodrugs of testosterone are available in the United States in oil solutions for intramuscular injection: [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3763", "text": "Unmodified testosterone was also formerly available for intramuscular injection but was discontinued. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3764", "text": "Testosterone cypionate and testosterone enanthate were formerly available in combination with  estradiol cypionate  and  estradiol valerate , respectively, under the brand names Depo-Testadiol and Ditate-DS, respectively, as oil solutions for intramuscular injection, but these formulations have been discontinued. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3765", "text": "Unlike in Europe, Canada, and much of the rest of the world, oral testosterone undecanoate is not available in the United States. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3766", "text": "[ 142 ] [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3767", "text": "As of November\u00a02016 [update] , testosterone is available in Canada in the form of topical gels (AndroGel, Testim), topical solutions (Axiron), transdermal patches (Androderm), and intranasal gels (Natesto). [ 144 ]  Testosterone cypionate (Depo-Testosterone, Testosterone Cypionate (generic)), testosterone enanthate (Delatestryl, PMS-Testosterone Enanthate), and testosterone propionate (Testosterone Propionate (generic)) are available as oil solutions for intramuscular injection and testosterone undecanoate (Andriol, PMS-Testosterone, Taro-Testosterone) is available in the form of oral capsules. [ 144 ]  Testosterone buccal tablets and pellet implants do not appear to be available in Canada. [ 144 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3768", "text": "Testosterone and/or its esters are widely available in countries throughout the world in a variety of formulations. [ 139 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3769", "text": "Testosterone and its esters, along with other AAS, are  prescription-only   controlled substances  in many countries throughout the world. In the United States, they are  Schedule III  drugs under the  Controlled Substances Act , in Canada, they are  Schedule IV  drugs under the  Controlled Drugs and Substances Act , and in the United Kingdom, they are  Class C  drugs under the  Misuse of Drugs Act . [ 145 ] [ 146 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3770", "text": "As of 2014 [update] , a number of lawsuits are underway against manufacturers of testosterone, alleging a significantly increased rate of stroke and heart attack in elderly men who use testosterone supplementation. [ 147 ] [ needs update ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3771", "text": "There are many known cases of  doping in sports  with testosterone and its esters by  professional   athletes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3772", "text": "Testosterone has been used to treat depression in men who are of middle age with low testosterone. However, a 2014 review showed no benefit on the mood of the men with normal levels of testosterone or on the mood of the older men with low testosterone. [ 148 ]  Conversely, a 2009 review found that testosterone had an antidepressant effect in men with depression, especially those with hypogonadism, HIV/AIDS, and in the elderly. [ 149 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3773", "text": "Testosterone replacement can significantly improve  exercise capacity ,  muscle strength  and reduce  QT intervals  in men with  chronic heart failure  (CHF). Over the 3 to 6-month course of the studies reviewed, testosterone therapy appeared safe and generally effective, and (ruling out prostate cancer) the authors found no justification to absolutely restrict its use in men with CHF. [ 150 ]  A similar 2012 review also found increased exercise capacity and reasoned the benefits generlizable to women. [ 151 ]  However, both reviews advocate larger, longer term,  randomized controlled trials . [ 150 ] [ 151 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3774", "text": "Testosterone, as esters such as testosterone undecanoate or testosterone buciclate, has been studied and promoted as a  male contraceptive  analogous to  estrogen-based contraceptives  in women. Otherwise considered an adverse effect of testosterone, reduced spermatogenesis can be further suppressed with the addition of a  progestin  such as  norethisterone enanthate  or  levonorgestrel butanoate , improving the contraceptive effect. [ 152 ] [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3775", "text": "Testosterone is under development in a low-dose intranasal formulation for the treatment of  anorgasmia  in women. [ 154 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3776", "text": "Testosterone therapy may improve the management of  type 2 diabetes . [ 155 ]  Low testosterone has been associated with the development of  Alzheimer's disease . [ 156 ] [ 157 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3777", "text": "Topical androgens like testosterone have been used and studied in the treatment of  cellulite  in women. [ 158 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3778", "text": "Tidiacic  is a  hepatoprotective  drug.  It is a component of  tidiacic arginine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3779", "text": "Tidiacic arginine (trade name  Tiadilon ) is a 1:1 combination of the  amino acid   arginine  and tidiacic (thiazolidine-2,4-dicarboxylic acid), which acts as a sulfur donor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3780", "text": "In France, its indications and use have been described as \"identical to those of  silymarin \". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3781", "text": "Tiropramide  is the  International nonproprietary name  of an  antispasmodic  drug. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3782", "text": "The  acylation  of  racemic   tyrosine  (1) with  benzoyl chloride  gives N,O-dibenzoyl-tyrosine (2).  Amide  formation with  dipropylamine  (3) using the  mixed anhydride  method gives the intermediate (4).  Hydrolysis  of the  phenolic ester  with  sodium hydroxide  forms (5), which is  alkylated  with  ClCH 2 CH 2 N(CH 2 CH 3 ) 2  to produce the  ether  tiropramide. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3783", "text": "Ulimorelin  ( INN ,  USAN ) (developmental code name  TZP-101 ) is a  drug  with a modified  cyclic   peptide   structure  which acts as a selective  agonist  of the  ghrelin/growth hormone secretagogue receptor  (GHSR-1a). [ 1 ]  Unlike many related drugs, ulimorelin has little or no effect on  growth hormone  (GH)  release  in rats. [ 2 ]   However, like ghrelin and other ghrelin agonists, ulimorelin does stimulate GH release with concomitant increases in insulin-like growth factor 1 (IGF-1) in humans. [ 3 ]  It has been researched for enhancing  gastrointestinal motility , especially in  gastroparesis [ 4 ]  and in aiding recovery of bowel function following  gastrointestinal surgery , where  opioid   analgesic  drugs used for post-operative pain relief may worsen existing  constipation . [ 5 ] [ 6 ] [ 7 ] [ 8 ]  While ulimorelin has been shown to increase both upper and lower gastrointestinal motility in rats, [ 8 ]  and showed promising results initially in humans, [ 4 ] [ 6 ]  it failed in pivotal clinical trials in post operative  ileus . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3784", "text": "A common  side effect  of ghrelin is  reduced blood pressure . Ulimorelin has been shown to inhibit  vasoconstriction  of rat arteries in vitro elicited by the   \u03b1 1 -adrenoceptors  agonists  phenylephrine  and  methoxamine , and to increase artery tension at high concentrations. [ 9 ]  Effects on blood pressure, however, were not observed in human clinical trials. [ 4 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3785", "text": "Ursodeoxycholic acid  ( UDCA ), also known as  ursodiol , is a secondary  bile acid , produced in humans and most other species from metabolism by intestinal bacteria. It is synthesized in the liver in some species, and was first identified in  bile of bears  of genus  Ursus , from which its name derived. [ 8 ]  In purified form, it has been used to treat or prevent several diseases of the  liver  or  bile ducts ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3786", "text": "It is available as a  generic medication . [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3787", "text": "UDCA has been used as medical therapy in  gallstone  disease (cholelithiasis) and for  biliary sludge . [ 11 ] [ 12 ]   UDCA helps reduce the  cholesterol  saturation of bile and leads to gradual dissolution of cholesterol-rich gallstones. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3788", "text": "UDCA may be given after bariatric surgery to prevent cholelithiasis, which commonly occurs due to the rapid weight loss producing biliary cholesterol oversaturation and also biliary dyskinesia secondary to hormonal changes. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3789", "text": "UDCA is used as therapy in  primary biliary cholangitis  (PBC; previously known as primary biliary cirrhosis) where it can produce an improvement in biomarkers. [ 14 ]  Meta-analyses have borne out conflicting results on the mortality benefit. [ 15 ]   However analyses that exclude trials of short duration (i.e. < 2 years) have demonstrated a survival benefit and are generally considered more clinically relevant. [ 16 ]  A Cochrane systematic review in 2012 found no significant benefit in reducing mortality, the rate of liver transplantation,  pruritus  or fatigue. [ 17 ]  Ursodiol and  obeticholic acid  are FDA-approved for the treatment of primary biliary cholangitis. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3790", "text": "UDCA use is associated with improved serum liver tests that do not always correlate with improved liver disease status. [ 19 ]  WHO Drug Information advises against its use in primary sclerosing cholangitis in unapproved doses beyond 13\u201315\u00a0mg/kg/day. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3791", "text": "UDCA in a dose of 28\u201330 mg/kg/day increases risk of death and need for liver transplant by 2.3-fold among those with primary sclerosing cholangitis, despite decrease in liver enzymes. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3792", "text": "UDCA has been used for  intrahepatic cholestasis of pregnancy . UDCA lessens itching in the mother and may reduce the number of preterm births. Effects on fetal distress and other adverse outcomes are unlikely to be great. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3793", "text": "UDCA use is not licensed in children, as its safety and effectiveness have not been established. Evidence is accumulating that ursodeoxycholic acid is ineffective, unsafe and its use is associated with significant risk of morbidity and mortality in neonatal hepatitis and neonatal cholestasis. [ 24 ] [ 25 ] [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3794", "text": "UDCA has been suggested to be an adequate treatment of bile reflux  gastritis . [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3795", "text": "In  cystic fibrosis  there is insufficient evidence to justify routine use of UDCA, especially as there is a lack of available data for long-term outcomes such as death or need for liver transplantation. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3796", "text": "UDCA has also been in effective in  non-alcoholic fatty liver disease , in liver bile duct-paucity syndromes. It is contraindicated in obstruction of biliary tracts such as  biliary atresia . It is not effective in liver allograft rejection, and in  Graft-versus-host disease  involving the liver. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3797", "text": "Diarrhea was the most frequent adverse event seen in trial of UDCA in gallstone dissolution, occurring in 2 to 9%, which is less frequent than with  chenodeoxycholic acid  therapy. Bacterial conversion of UDCA to chenodeoxycholic acid may be the mechanism for this side effect. Right upper quadrant abdominal pain and exacerbation of pruritus was occasionally reported in trials in patients with PBC. [ 30 ]   Additional symptoms may include bloating, weight gain, and occasionally, thinning of hair. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3798", "text": "Primary bile acids are produced by the  liver  and stored in the  gall bladder . When secreted into the intestine, primary bile acids can be metabolized into secondary bile acids by intestinal bacteria. Primary and secondary bile acids help the body  digest   fats . Ursodeoxycholic acid helps regulate  cholesterol  by reducing the rate at which the  intestine  absorbs cholesterol molecules while breaking up  micelles  containing cholesterol. The drug reduces cholesterol absorption and is used to dissolve (cholesterol)  gallstones  in  patients  who want an alternative to  surgery . [ 32 ]  There are multiple mechanisms involved in cholestatic liver diseases. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3799", "text": "Ursodeoxycholic acid has also been shown experimentally to suppress  immune response  such as immune cell  phagocytosis . Prolonged exposure and/or increased quantities of systemic (throughout the body, not just in the digestive system) ursodeoxycholic acid can be toxic. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3800", "text": "Ursodeoxycholic acid has been shown to exert anti-inflammatory and protective effects in human epithelial cells of the  gastrointestinal tract . It has been linked to regulation of immunoregulatory responses by regulation of  cytokines , [ 35 ]  antimicrobial peptides  defensins , [ 36 ]  and take an active part in increased restitution of wound in the colon. [ 37 ]  Moreover, UDCA's effects has been shown to have exert actions outside the epithelial cells. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3801", "text": "While some bile acids are known to be colon tumor promoters ( e.g.   deoxycholic acid ), others such as ursodeoxycholic acid are thought to be  chemopreventive , perhaps by inducing cellular differentiation and/or cellular senescence in colon epithelial cells. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3802", "text": "Ursodeoxycholic acid is an  epimer  of  chenodeoxycholic acid , which has similar choleretic effects and a wider species distribution. However, CDCA is not as well-tolerated in humans and it does not show immunomodulating or chemoprotective effects. Both are 7-hydroxyl derivatives of deoxycholic acid, but UDCA has the group in the beta instead of the alpha orientation. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3803", "text": "Among mammals, only bears ( Ursidae ; excluding  giant pandas ) produce UDCA at useful amounts [ 40 ]  (>30%). It is produced in the bear liver, but the pathway remains unknown. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3804", "text": "Other vertebrates produce UDCA in much smaller amounts by gut bacteria. CDCA is oxidized into 7-oxo-CDCA then reduced into UDCA. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3805", "text": "UDCA is most commonly produced from  cholic acid  (CA) derived from bovine bile, a by-product of the beef industry. The current yield of this  semisynthesis  is about 30%. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3806", "text": "The term is from the Latin noun  ursus  meaning bear, as  bear bile  contains the substance. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3807", "text": "Ursodeoxycholic acid can be chemically synthesized and is marketed under multiple trade names, including Ursetor, Udikast, Actibile, Actigall, Biliver, Deursil, Egyurso, Heptiza 300/150, Stener, Udcasid, Udiliv, Udinorm, Udoxyl, Urso, Urso Forte, Ursocol, Ursoliv, Ursofalk, [ 44 ]  Ursosan, Ursoserinox, Udimarin, and Ursonova. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3808", "text": "Bear bile, a natural source of UDCA, is used in  traditional Chinese medicine  since the seventh century. Japanese scientists successfully synthesized UDCA chemically in 1955. [ 40 ]  The earliest reference to UDCA in  PubMed  dates to 1957 under an alternative spelling \"ursodesoxycholic acid\", in a small-scale clinical trial. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3809", "text": "Ursodeoxycholic acid (application filed by  Allergan ) was approved for use in the United States in December 1987, [ 46 ]  and was designated an  orphan drug . [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3810", "text": "Volixibat  ( INN ; [ 1 ]  development code  SHP626 ) is a  medication  under  development  as a possible treatment for nonalcoholic steatohepatitis (NASH), the most severe form of  non-alcoholic fatty liver disease  (NAFLD). No other  pharmacotherapy  yet exists for NASH, so there is interest in whether volixibat can prove to be both safe and effective. To encourage development and testing, the U.S.  Food and Drug Administration  (FDA) has issued  fast track  status. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3811", "text": "Volixibat is an IBAT inhibitor, meaning that it blocks the function of the IBAT protein (ileal bile acid transporter), which is also called  SLC10A2  (solute carrier family 10 member 2) or ASBT (apical sodium\u2013bile acid transporter). IBAT is  most highly expressed in the  ileum , where it is found on the  brush border  membrane of  enterocytes .  It is responsible for the initial uptake of  bile acids , particularly conjugated bile acids, from the intestine as part of their  enterohepatic circulation . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3812", "text": "Vonoprazan , sold under the brand name  Voquezna  among others, is a  first-in-class   potassium-competitive acid blocker  medication. [ 2 ] [ 1 ]  Vonoprazan is used in form of the  fumarate  for the treatment of  gastroduodenal ulcer  (including some drug-induced peptic ulcers) and reflux  esophagitis , and can be combined with antibiotics for the eradication of  Helicobacter pylori . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3813", "text": "It was approved in Japan in February 2015, [ 3 ] [ 4 ]  and in Russia in April 2021. [ 5 ]  Vonoprazan was approved for medical use in the United States in November 2023. [ 1 ] [ 6 ]  Co-packaged combinations of  vonoprazan with amoxicillin  and  vonoprazan with amoxicillin and clarithromycin  are available. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3814", "text": "Vonoprazan  is  indicated  for healing of all grades of erosive esophagitis and relief of heartburn associated with erosive esophagitis in adults; to maintain healing of all grades of erosive esophagitis and relief of heartburn associated with erosive esophagitis in adults; in combination with amoxicillin and clarithromycin for the treatment of Helicobacter pylori (H. pylori) infection in adults; in combination with amoxicillin for the treatment of H. pylori infection in adults. [ 1 ] [ 7 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3815", "text": "In July 2024, the indication was expanded in the US to include non-erosive gastroesophageal reflux disease. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3816", "text": "The most common side effects are constipation, diarrhea,  enlarged feeling of abdomen , nausea, rash, and  edema . [ 1 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3817", "text": "Long-term use may lead to  vitamin B12 deficiency ,  hypomagnesemia , and  fundic gland polyps . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3818", "text": "Vonoprazan is the  international nonproprietary name  (INN). [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3819", "text": "Vonoprazan/amoxicillin , sold under the brand name  Voquezna Dual Pak  among others, is a co-packaged medication used for the treatment of  Helicobacter pylori  ( H. pylori ) infection. [ 1 ]  It contains  vonoprazan  (as the fumarate), a  potassium-competitive acid blocker  and  amoxicillin , a  beta-lactam antibiotic . [ 1 ]  It is taken  by mouth . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3820", "text": "The co-packaged medication was approved for medical use in the United States in May 2022. [ 1 ] [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3821", "text": "Vonoprazan/amoxicillin is  indicated  for the treatment of  H. pylori  infection in adults. [ 1 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3822", "text": "The dual therapy of using vonoprazan with amoxicillin has been investigated for the treatment of  H. pylori  infection [ 6 ]  and also compared with the  triple therapy  of using vonoprazan,  amoxicillin , and  clarithromycin  for the eradication of  H. pylori  infection. [ 7 ]  Both treatments have been found to be effective. [ 6 ] [ 7 ]  As of 2024, [update]  evidence indicates that vonoprazan/amoxicillin therapy has similar efficacy to  bismuth-containing quadruple therapies  in eliminating  H. pylori . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3823", "text": "Vonoprazan/amoxicillin/clarithromycin , sold under the brand name  Vonosap  among others, is a co-packaged medication used for the treatment of  Helicobacter pylori  ( H. pylori ) infection. [ 1 ] [ 4 ]  It contains  vonoprazan  (as the fumarate), a  potassium-competitive acid blocker ;  amoxicillin , a  beta-lactam antibiotic ; and  clarithromycin , a  macrolide antibiotic . [ 1 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3824", "text": "It was approved for medical use in Japan in 2016, [ 3 ]  and in the United States in May 2022. [ 1 ] [ 2 ] [ 5 ] [ 6 ]  The US  Food and Drug Administration  (FDA) considers it to be a  first-in-class medication . [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3825", "text": "Zastaprazan  (trade name  Jaqbo ) is a pharmaceutical drug for gastrointestinal disorders.  It is classified as a  potassium-competitive acid blocker . [ 1 ] [ 2 ]  In April 2024, it was approved for use in South Korea for the treatment of erosive  gastroesophageal reflux disease  (GERD). [ 3 ]   In addition, it is in Phase III clinical trials for  gastric ulcer  and  peptic ulcer . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3826", "text": "An  abdominal examination  is a portion of the  physical examination  which a physician or nurse uses to clinically observe the abdomen of a patient for signs of disease. The abdominal examination is conventionally split into four different stages: first,  inspection  of the patient and the visible characteristics of their abdomen.  Auscultation  (listening)  of the abdomen with a  stethoscope .  Palpation  of the patient's abdomen. Finally,  percussion  (tapping) of the patient's abdomen and abdominal organs. [ 1 ]  Depending on the need to test for specific diseases such as  ascites ,  special tests  may be performed as a part of the physical examination. [ 2 ]  An abdominal examination may be performed because the physician suspects a disease of the organs inside the  abdominal cavity  (including the liver, spleen, large or small intestines), or simply as a part of a complete physical examination for other conditions. In a complete physical examination, the abdominal exam classically follows the respiratory examination and cardiovascular examination. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3827", "text": "A suggested position is for the patient to be  supine  (on their back), with their arms to their sides. The patient should be placed in an environment with good lighting, and should be draped with towels or sheets to preserve privacy and warmth. [ 2 ]  The patient's hips and knees should be flexed (in a bent position) so that their abdominal muscles remain relaxed during the examination. [ 4 ]  Asking the patient to indicate areas that may be tender or painful is recommended to avoid exacerbating the pain during inspection and to increase the patient's comfort.  [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3828", "text": "Although physicians have had concern that giving patients pain medications during acute abdominal pain may hinder diagnosis and treatment, separate  systematic reviews  by the  Cochrane Collaboration [ 5 ]  and the Rational Clinical Examination [ 6 ]  refute this."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3829", "text": "The doctor will look at the movement of the abdomen checking specifically for waves or odd flexing. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3830", "text": "Auscultation refers to the use of a  stethoscope  by the examiner to listen to sounds from the abdomen.  [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3831", "text": "Unlike other physical exams, auscultation is performed prior to percussion or palpation, as both of these could alter the regularity of bowel sounds. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3832", "text": "Some controversy exists as to the length of time required to confirm or exclude bowel sounds, with suggested durations up to seven minutes.  Bowel obstruction  may present with grumbling bowel sounds or high-pitched noises. Healthy persons can have no bowel sounds for several minutes  [ 9 ]  and intestinal contractions can be silent. [ 10 ]  Hyperactive bowel sounds may be caused by partial or complete bowel obstruction as the intestines initially try to clear the obstruction. [ 11 ]  Absence of sounds may be caused by peritonitis, paralytic ileus, late-stage bowel obstruction, intestinal ischemia or other causes. [ 12 ]  Some authors suggest that listening at a single location is enough as sounds can be transmitted throughout the abdomen. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3833", "text": "A prospective study published in 2014 where 41 physicians listened to the bowel sounds of 177 volunteers (19 of which had bowel obstructions and 15 with an ileus) found that \"Auscultation of bowel sounds is not a useful clinical practice when differentiating patients with normal versus pathologic bowel sounds. The listener frequently arrives at an incorrect diagnosis. Agreement between raters was also low (54%).\". [ 14 ]  This article suggests focusing on other indicators (flatus, pain, nausea) instead. There is no research evidence that reliably corroborates the assumed association between bowel sounds and gastro-intestinal motility status. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3834", "text": "The examiner also typically listens to the two  renal arteries  for abnormal blood flow  sounds  (bruits) by listening in each upper quadrant, adjacent to and above the  umbilicus . Bruits heard in the  epigastrium  that are confined to systole are considered normal. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3835", "text": "The examiner should first talk to the patient and explain what this part of the examination will involve. [ 4 ]  He or she will typically  palpate  all nine areas of the patient's abdomen, and being mindful of areas of discomfort, begin by palpating areas of no pain. This is typically performed twice, first with light pressure and then with deeper pressure to better exam the abdominal organs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3836", "text": "On light palpation, the examiner tests for any palpable mass, rigidity, or pain on the surface."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3837", "text": "On deep palpation, the examiner is testing for any  organomegaly  (enlarged organs.) Typically, the clinician is looking for enlargement of the liver and spleen or abnormal masses in the intestines. Sometimes the physician looks for the kidney and uterus as well. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3838", "text": "Reactions that may indicate pathology include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3839", "text": "Percussion  can be performed in all four quadrants of the abdomen and may reveal a painful response by the patient. During the abdominal examination, percussion may allow the estimation of location and quantity of gas, hard or soft masses, and sizes of certain organs, such as the liver and the spleen. Abnormal findings may include  splenomegaly ,  hepatomegaly  and  urinary retention . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3840", "text": "Organomegaly of the liver and the spleen can be appreciated by percussing in a particular manner:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3841", "text": "Examination of the spleen may reveal  Castell's sign  or alternatively  Traube's space ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3842", "text": "Dull sounds on the abdomen could suggest pregnancy, an  ovarian tumor , a distended bladder, hepatomegaly or splenomegaly. Dullness on either side of the abdomen could suggest  ascites . Some other areas of the abdomen may sound dull suggesting that there may be some fluid or  feces . The dullness of the liver can be appreciated by percussing at the edge of the lower chest right above the  costal margins . The resonant sounds of gastric air bubbles can be appreciated at the left side. In rare cases, when organs are reversed as is the case in  situs inversus , resonant (hollow) sounds would be expected on the right side and liver dullness on the left.  [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3843", "text": "Special maneuvers may also be performed, to elicit signs of specific diseases. [ 16 ] [ 17 ]  These include"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3844", "text": "The  Alvarado score  is a clinical scoring system used in the diagnosis of  appendicitis . [ 1 ]   Alvarado scoring has largely been superseded as a clinical prediction tool by the  Appendicitis Inflammatory Response score . [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3845", "text": "Also known by the  mnemonic  MANTRELS, the scale has 6 clinical items (3  signs  and 3  symptoms ) and 2 laboratory measurements, each given an additive point score, with a maximum of 10 points possible. [ 5 ]   It was introduced in 1986 by Dr. Alfredo Alvarado and although meant for pregnant females, it has been extensively validated in the non-pregnant population.  A known limitation of the score is that only 20% of elderly patients present with classic findings on which the score focuses. [ 5 ]  A modified Alvarado score is at present in use. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3846", "text": "Elements from the person's  history , the  physical examination  and from laboratory tests: [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3847", "text": "The two most important factors, tenderness in the right lower quadrant and leukocytosis, are assigned two points, and the six other factors are assigned one point each, for a possible total score of ten points. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3848", "text": "A score of 5 or 6 is compatible with the diagnosis of acute appendicitis. A score of 7 or 8 indicates probable appendicitis, and a score of 9 or 10 indicates very probable acute appendicitis. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3849", "text": "The original Alvarado score describes a possible total of 10 points, but those medical facilities that are unable to perform a differential white blood cell count, are using a Modified Alvarado Score with a total of 9 points which could be not as accurate as the original score. The high diagnostic value of the score has been confirmed in a number of studies across the world. The consensus is that the Alvarado score is a noninvasive, safe, diagnostic method, which is simple, reliable, repeatable, and able to guide the clinician in the management of the case. However, a recent study demonstrated a sensitivity of only 72% of the Modified Alvarado Score for detection of appendicitis which has led to criticism of the usefulness of the score. Scores of less than five in children were useful for eliminating appendicitis from the differential diagnosis. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3850", "text": "It carries high significance in the diagnosis of acute appendicitis. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3851", "text": "Online calculator of the Alvarado Score"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3852", "text": "The  Appendicitis Inflammatory Response  ( AIR )  score  is a  diagnostic  scoring system used to assist with the identification of  appendicitis  in children and adults."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3853", "text": "The scoring system was developed in 2008. [ 1 ]  The AIR score was developed to overcome some of the drawbacks of the  Alvarado score , another diagnostic scoring system for identifying appendicitis. [ 2 ]  The AIR score is one of the two scores (the other being the  Adult Appendicitis Score , AAS) recommended by the 2020 World Society of Emergency Surgery clinical practice guidelines for the diagnosis and treatment of acute appendicitis. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3854", "text": "The AIR score is calculated by tallying \"points\" ascribed to meeting its criteria, which are: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3855", "text": "A 2017 review found that the AIR score has a sensitivity of 92% and specificity of 63% if a score of 5 is used as a cut off for indicating a positive test, whereas the sensitivity is 20% and the specificity is 97% if a score of 8 is used. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3856", "text": "While the AIR score has better predictive power than certain other diagnostic tools for appendicitis (e.g. the  Alvarado score ), it has only been validated in a small number of studies as of 2017 [update] . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3857", "text": "Boas' point  is an area of tenderness to  palpation  to the left of the  12th thoracic vertebra  found in some patients with  gastric ulcer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3858", "text": "This  medical sign  is named after  Ismar Isidor Boas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3859", "text": "Boas' point  at  Who Named It?"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3860", "text": "The  bow and arrow sign  is an  endoscopic   sign  for determining the location of the  ileocecal valve  during  colonoscopy .  Identifying the ileocecal valve in a colonoscopy is important, as it indicates that the entire  colon  has been visualized."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3861", "text": "The identifiable landmarks in the  cecum  are the  appendiceal orifice \u2014which is a curvilinear indent indicating the location of the appendix from the lumen of the bowel\u2014and the ileocecal valve, which appears as a puckering in the most distal fold of the cecum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3862", "text": "The bow and arrow sign uses the curve of the appendiceal orifice to point toward the direction of the ileocecal valve, as if it were a  bow  guiding an  arrow . The  colonoscope  can be passed in this direction in order to enter the  terminal ileum . [ 1 ]   This is used as one of two identifiable landmarks of the colon (the other being the  anus ), and signifies that the entire colon has been visualized."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3863", "text": "The  Bristol stool scale  is a diagnostic  medical  tool designed to classify the form of  human faeces  into seven categories. [ 4 ]  It is used in both clinical and  experimental  fields. [ 5 ] [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3864", "text": "It was developed at the  Bristol Royal Infirmary  as a clinical assessment tool in 1997, by Stephen Lewis and Ken Heaton [ 8 ]  and is widely used as a research tool to evaluate the effectiveness of treatments for various diseases of the bowel, as well as a clinical communication aid; [ 9 ] [ 10 ]  including being part of the diagnostic triad for  irritable bowel syndrome . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3865", "text": "The seven types of stool are: [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3866", "text": "Types 1 and 2 indicate  constipation , with 3 and 4 being the ideal stools as they are easy to  defecate  while not containing excess liquid, and 6 and 7 indicate diarrhea. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3867", "text": "In the initial study, in the population examined in this scale, the type 1 and 2 stools were more prevalent in females, while the type 5 and 6 stools were more prevalent in males; furthermore, 80% of subjects who reported  rectal tenesmus  (sensation of incomplete defecation) had type 7. These and other data have allowed the scale to be validated. [ 12 ]  The initial research did not include a pictorial chart with this being developed at a later point. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3868", "text": "The Bristol stool scale is also very sensitive to changes in intestinal transit time caused by medications, such as  antidiarrhoeal   loperamide ,  senna , or  anthraquinone  with  laxative  effect. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3869", "text": "People with irritable bowel syndrome (IBS) typically report that they suffer with abdominal  cramps  and  constipation .\nIn some patients, chronic constipation is interspersed with brief episodes of  diarrhoea ; while a minority of patients with IBS have only diarrhoea.\nThe presentation of symptoms is usually months or years and commonly patients consult different doctors, without great success, and doing various specialized investigations.\nIt notices a strong correlation of the reported symptoms with  stress ; indeed diarrhoeal discharges are associated with  emotional phenomena .\nIBS blood is present only if the disease is associated with  haemorrhoids . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3870", "text": "Research conducted on irritable bowel syndrome in the 2000s, [ 16 ] [ 17 ]   faecal incontinence [ 18 ] [ 19 ] [ 20 ] [ 21 ]  and the gastrointestinal complications of  HIV [ 22 ]  have used the Bristol scale as a diagnostic tool easy to use, even in research which lasted for 77 months. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3871", "text": "Historically, this scale of assessment of the faeces has been recommended by the  consensus group  of  Kaiser Permanente  Medical Care Program ( San Diego , California, US) for the collection of data on functional bowel disease (FBD). [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3872", "text": "More recently, according to the latest revision of the  Rome III Criteria , six clinical manifestations of IBS can be identified: [ 24 ] [ 25 ] [ 26 ] [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3873", "text": "These four identified subtypes correlate with the consistency of the stool, which can be determined by the Bristol stool scale. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3874", "text": "In 2007, the  Mayo Clinic College of Medicine  in  Rochester, Minnesota , United States, reported a piece of  epidemiological research  conducted on a population of 4,196 people living in  Olmsted County   Minnesota , in which participants were asked to complete a questionnaire based on the  Bristol stool scale . [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3875", "text": "The research results (see table) indicate that about 1 in 5 people have a slow transit (type 1 and 2 stools), while 1 in 12 has an accelerated transit (type 5 and 6 stools). Moreover, the nature of the stool is affected by age, sex,  body mass index , whether or not they had  cholecystectomy  and possible  psychosomatic  components ( somatisation ); there were no effects from factors such as  smoking ,  alcohol , the level of education, a history of  appendectomy  or familiarity with gastrointestinal diseases, civil state, or the use of  oral contraceptives ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3876", "text": "Several investigations correlate the Bristol stool scale in response to medications or therapies, in fact, in one study was also used to titrate the dose more finely than one drug ( colestyramine ) in subjects with  diarrhoea  and faecal incontinence. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3877", "text": "In a  randomised controlled study , [ 32 ]  the scale is used to study the response to two laxatives:  Macrogol  ( polyethylene glycol ) and  psyllium  ( Plantago psyllium  and other  species  of the same  genus ) of 126 male and female patients for a period of 2 weeks of treatment; failing to show the most rapid response and increased efficiency of the former over the latter. In the study, they were measured as primary  outcomes : the number weekly bowel movements, stool consistency according to the types of the  Bristol stool scale , time to defecation, the overall effectiveness, the difficulty in defecating and stool consistency. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3878", "text": "From 2010, several studies have used the scale as a diagnostic tool validated for recognition and evaluation of response to various treatments, such as  probiotics , [ 33 ] [ 34 ]   moxicombustion , [ 35 ]  laxatives in the elderly, [ 36 ]  preparing  Ayurvedic  poly-phytotherapy filed TLPL/AY, [ 37 ]  psyllium, [ 38 ]   mesalazine , [ 39 ]   methylnaltrexone , [ 40 ]  and  oxycodone / naloxone , [ 41 ]  or to assess the response to physical activity in athletes. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3879", "text": "Developed and proposed for the first time in  England  by Stephen Lewis and  Ken Heaton  at the University Department of Medicine,  Bristol Royal Infirmary , it was suggested by the authors as a clinical assessment tool in 1997 in the  Scandinavian Journal of Gastroenterology [ 14 ]  after a previous  prospective study , conducted in 1992 on a  sample  of the population (838 men and 1,059 women), had shown an unexpected  prevalence  of  defecation  disorders related to the shape and type of stool. [ 43 ]  The authors of the former paper concluded that the form of the stool is a useful surrogate measure of  colon  transit time. That conclusion has since been challenged as having limited validity for Types 1 and 2; [ 44 ]  however, it remains in use as a research tool to evaluate the effectiveness of treatments for various diseases of the bowel, as well as a clinical communication aid. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3880", "text": "The same scale has been validated in  Spanish , [ 45 ] [ 20 ]   Brazilian Portuguese , [ 46 ]  and  Polish  versions. [ 47 ]  A version has also been designed and validated for children. [ 48 ] [ 49 ]  More recently, in September 2011, a modified version of the scale was validated using a criterion of self-assessment for ages six\u2013eight years of age. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3881", "text": "A version of the scale was developed into a chart suitable for use on US television by Gary Kahan of  NewYork\u2013Presbyterian Hospital . [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3882", "text": "Capsule endoscopy  is a medical procedure used to record internal images of the  gastrointestinal tract  for use in  disease diagnosis . Newer developments are also able to take  biopsies  and release medication at specific locations of the entire gastrointestinal tract. [ 1 ]  Unlike the more widely used  endoscope , capsule endoscopy provides the ability to see the middle portion of the  small intestine . It can be applied to the detection of various  gastrointestinal cancers ,  digestive diseases , ulcers, unexplained bleedings, and general abdominal pains. After a patient swallows the capsule, it passes along the gastrointestinal tract, taking a number of images per second which are transmitted wirelessly to an array of receivers connected to a portable recording device carried by the patient. General advantages of capsule endoscopy over standard  endoscopy  include the minimally invasive procedure setup, ability to visualize more of the gastrointestinal tract, and lower cost of the procedure. [ 2 ] [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3883", "text": "Capsule endoscopy was first conceptualized by Israeli engineer  Gavrial Iddan  and Israeli gastroenterologist Eitan Scapa in Boston, Massachusetts in the early 1980s. The two partners first developed a CCD ( charged coupled device ) camera-based imaging system using a fiber-optic tether. This initial design suffered from high power consumption and slow transmission times of image data of at best 10 minutes. In 1993 Iddan had the idea to split the system into three components, the camera and transmitter, the recorder attached to a  sensor array  on the patient's abdomen, and a software package that processes the stored data at leisure by a physician at a later time. This new setup was made possible by the replacement of the CCD camera with a CMOS ( complementary metal\u2013oxide\u2013semiconductor ) camera. These cameras consume just one percent of the energy of their CCD counterparts. The more efficient power system allowed for the removal of the fiber optic cable for a stand-alone imaging system. This three-component imaging system remains popular today. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3884", "text": "In 2001 the FDA ( Food and Drug Administration ) approved the first capsule endoscope developed by  Given Imaging  for use in patients. Many new models such as the PillCam SB and DBE for obscure gastrointestinal bleeding, the Olympus CE for the small bowel, the PillCam ESO for investigation of esophageal diseases, and the PillCam COLON for detection of colonic neoplasias have been created. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3885", "text": "As research into capsule endoscopy has increased and technology has advanced better wireless and more energy-efficient systems have allowed for the creation of more compact capsules and image processing systems, with many in development today."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3886", "text": "Capsule endoscopy uses a small vitamin-sized wireless camera to capture images of a patient's digestive tract. The capsule is generally composed of a camera, antenna, and light array. [ 5 ]  Due to the small nature of the device images can not be stored within it. As a result, a sensor array with a storage unit is placed on the abdomen of the patient for the imaging period. This storage unit can then be connected to a computer at a later time so that a medical professional can analyze the images. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3887", "text": "Newer models of the capsule endoscope have looked to add camera systems on both ends of the pill or even store images within the pill itself to minimize the amount of medical equipment carried while using the device. [ 6 ]  For systems that store images directly within the pill, the pill must be collected after excretion for extraction of the images by a secondary device. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3888", "text": "The main shortcoming of capsule endoscopy is the  field of view . Depending on the placement of the camera system within the device images may become obstructed by folds in the digestive tract. Due to the passive nature of image capture and lack of control in maneuvering the device through the digestive tract novel solutions are being developed by various companies and research labs. For systems that utilize the setup with the camera system at the end of the capsule, the field of view ranges from 140 to 170 degrees. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3889", "text": "There are several advantages to choosing to use capsule endoscopy over standard  endoscopy . Standard endoscopy can be more uncomfortable for a patient, can be more prone to puncturing the digestive tract walls, and is not able to access the middle portion of the small intestine. Endoscopes must enter either through the mouth/nasal cavities or the rectum. Due to restrictions in length, extremely important regions for diagnosis in the small intestine are not able to be accessed. Currently, [ when? ]  within the United States, capsule endoscopy can not be used as a primary imaging method over standard endoscopy first. [ citation needed ]  As a result, many patients must first undergo standard endoscopy to then be referred for capsule endoscopy. Further innovation will be required to make capsule endoscopy comparable to the current standard of care, but extensive work is being performed to achieve this. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3890", "text": "Esophagogastroduodenoscopy  (EGD), employs a camera attached to a long flexible tube to view the upper portion of the gastrointestinal tract, namely the  esophagus , the  stomach , and the beginning of the first part of the  small intestine  called the  duodenum . A  colonoscope , inserted through the  rectum , can view the  colon  and the distal portion of the small intestine, the terminal  ileum . These two types of endoscopy however cannot visualize the majority of the middle portion of the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3891", "text": "Capsule endoscopy is therefore used to examine parts of the gastrointestinal tract that cannot be seen by standard endoscopy. It is useful when the disease is suspected in the small intestine, and can sometimes be used to find the site of  gastrointestinal bleeding  or the cause of unexplained abdominal pain, such as  Crohn's disease . However, unlike EGD or colonoscopy, it cannot be used to treat pathology that may be discovered. Common reasons for using capsule endoscopy include diagnosis of unexplained bleeding, iron deficiency, or abdominal pain, searching for polyps, ulcers, and tumors of the small intestine, and diagnosis of  inflammatory bowel disease . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3892", "text": "The images collected by the miniature camera during a session are transferred wirelessly to an external receiver worn by the patient, using any one of a band of appropriate frequencies. The collected images are then transferred to a computer for display, review, and diagnosis. [ 11 ]  A transmitted radio-frequency signal emitted by some capsules can be used to accurately estimate the location of the capsule and to track it in real-time inside the body and gastrointestinal tract. [ 12 ]  Capsule endoscopy can still not yet replace standard endoscopy for various diseases, as is the case for those with  cirrhosis . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3893", "text": "As of 2014, research was targeting additional sensing mechanisms and localization and motion control systems to enable new applications for the technology, for example, drug delivery. Wireless energy transmission was also being investigated as a way of providing a continuous energy source for the capsule. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3894", "text": "Capsule endoscopy requires a number of different preparatory procedures to ensure clear images are taken of a patient's gastrointestinal tract for an accurate diagnosis of disease. [ 15 ]  There are various types of capsule endoscopes, but for a generalized description, one can assume the most common setup requires the capsule, sensor array, storage unit, and computer system being used. First, a patient will need to have the sensor array placed on their abdomen with a recording unit worn as a belt. The patient may be asked to stay at the hospital or return home depending on the start time. Next, the pill must be swallowed by the patient. After approximately 8 hours the sensor array can be removed and returned to a physician. The capsule will be excreted through regular bowel movements. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3895", "text": "During the procedure, there are a number of different policies to follow. A patient should only drink clear liquids for the first two hours after swallowing the pill and may eat after 4 hours. MRI studies, ham radios, metal detectors, and strenuous physical activity should all be avoided. Additionally, all external equipment must be kept dry. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3896", "text": "As of 2022, there are a number of manufacturers who produce capsule endoscopes. [ 17 ]  The technology was originally developed by Israeli scientists,  Gavriel Iddan  and Eitan Scapa, with the first pill swallowed in 1997; [ 18 ]  Iddan founded  Given Imaging  in Israel which received FDA approval in 2001. [ 18 ]   Medtronic  today (2024) produces one of the more widely used capsule endoscope systems called the PillCam having sold over 4 million units. [ 19 ]  Medtronic purchased the PillCam system from Given Imaging in 2014. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3897", "text": "Capsule endoscopy is considered to be a very safe method for gastrointestinal tract examination. The capsule is usually excreted with a patient's  feces  within 24\u201348 hours after ingestion. There has been a single report of retention of the capsule lasting almost four and a half years although the patient was asymptomatic. However, the risk of bowel obstruction may be countered by an abdominal X-ray to locate the device for removal by endoscopy or surgery. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3898", "text": "In a review of 22,840 cases, the capsule was retained 1.4% of the time, with  Crohn's disease  a common cause; most were surgically removed. [ 22 ]  The rate of capsule retention varies by the indication for the procedure, with the highest rate seen with known Crohn's disease (5-13%), followed by obscure gastrointestinal bleeding (1.5%), suspected Crohn's disease (1.4%), and healthy volunteers (0%). [ 23 ]  Risk factors for capsule retention include Crohn's disease, NSAID use, and abdominal radiation. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3899", "text": "Charcot's cholangitis triad  is the combination of  jaundice ;  fever , usually with  rigors ; and  right upper quadrant   abdominal pain . It occurs as a result of  ascending cholangitis  (an infection of the  bile duct  in the liver). When the presentation also includes  low blood pressure  and  mental status changes , it is known as  Reynolds' pentad . [ 1 ]  It is named after  Jean-Martin Charcot . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3900", "text": "In  medicine , specifically  gastroenterology , the  Child\u2013Pugh score  (or the  Child\u2013Turcotte\u2013Pugh  ( CTP )  score  or  Child Criteria ) is used to assess the prognosis of chronic liver disease, mainly  cirrhosis . Although it was originally used to predict mortality during surgery, it is now used to determine the prognosis, as well as the required strength of treatment and the necessity of  liver transplantation . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3901", "text": "The score employs five clinical measures of liver disease. Each measure is scored 1\u20133, with 3 indicating most severe derangement. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3902", "text": "Either the prothrombin time or INR should be used to calculate the Child\u2013Pugh score, not both."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3903", "text": "In  primary sclerosing cholangitis  (PSC) and  primary biliary cholangitis  (PBC), some use a modified Child\u2013Pugh score where the bilirubin references are changed to reflect the fact that these diseases feature high  conjugated bilirubin  levels. The upper limit for 1 point is 68 \u03bcmol/L (4\u00a0mg/dL) and the upper limit for 2 points is 170 \u03bcmol/L (10\u00a0mg/dL). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3904", "text": "Chronic liver disease is classified into Child\u2013Pugh class A to C, employing the added score from above. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3905", "text": "The surgeon and portal hypertension expert Charles Gardner Child (1908\u20131991) (with Turcotte) of the  University of Michigan  first proposed the scoring system in 1964 in a textbook on liver disease. [ 3 ]  It was modified by Pugh et al. in 1972 in a report on surgical treatment of bleeding from  esophageal varices . [ 4 ]  They replaced Child's criterion of nutritional status with the  prothrombin time  or INR, and assigned scores of 1\u20133 to each variable. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3906", "text": "Colonoscopy  ( / \u02cc k \u0252 l \u0259 \u02c8 n \u0252 s k \u0259 p i / ) or  coloscopy  ( / k \u0259 \u02c8 l \u0252 s k \u0259 p i / ) [ 1 ]  is a medical procedure involving the  endoscopic  examination of the  large bowel  (colon) and the  distal  portion of the small bowel. This examination is performed using either a  CCD camera  or a  fiber optic camera , which is mounted on a flexible tube and passed through the anus. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3907", "text": "The purpose of a colonoscopy is to provide a visual diagnosis via inspection of the internal lining of the colon wall, which may include identifying issues such as ulceration or  precancerous  polyps, and to enable the opportunity for  biopsy  or the removal of suspected  colorectal cancer  lesions. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3908", "text": "Colonoscopy is similar in principle to  sigmoidoscopy , with the primary distinction being the specific parts of the colon that each procedure can examine. The same instrument used for sigmoidoscopy performs the colonoscopy. A colonoscopy permits a comprehensive examination of the entire colon, which is typically around 1,200 to 1,500 millimeters in length. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3909", "text": "In contrast, a sigmoidoscopy allows for the examination of only the distal portion of the colon, which spans approximately 600 millimeters. [ 7 ]  This distinction is medically significant because the benefits of colonoscopy in terms of improving cancer survival have primarily been associated with the detection of lesions in the distal portion of the colon. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3910", "text": "Routine use of colonoscopy screening varies globally. In the US, colonoscopy is a commonly recommended and widely utilized screening method for colorectal cancer, often beginning at age 45 or 50, depending on risk factors and guidelines from organizations like the American Cancer Society. [ 9 ]  However, screening practices differ worldwide. For example, in the European Union, several countries primarily employ fecal occult blood testing (FOBT) or sigmoidoscopy for population-based screening. [ 10 ]  These variations stem from differences in healthcare systems, policies, and cultural factors. Recent studies [ 11 ]  have stressed the need for screening strategies and awareness campaigns to combat colorectal cancer - on a global scale. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3911", "text": "Conditions that call for colonoscopies include  gastrointestinal hemorrhage , unexplained changes in bowel habit and suspicion of  malignancy . [ 14 ]  Colonoscopies are often used to diagnose  colon polyp  and  colon cancer , [ 15 ]  but are also frequently used to diagnose  inflammatory bowel disease . [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3912", "text": "Another common indication for colonoscopy is the investigation of iron deficiency with or without  anaemia . The examination of the colon, to rule out a lesion contributing to blood loss, along with an upper gastrointestinal endoscopy (gastroscopy) to rule out oesophageal, stomach, and proximal duodenal sources of blood loss."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3913", "text": "Fecal occult blood  is a quick test which can be done to test for microscopic traces of blood in the stool. A positive test is almost always an indication to do a colonoscopy. In most cases the positive result is just due to  hemorrhoids ; however, it can also be due to  diverticulosis , inflammatory bowel disease ( Crohn's disease ,  ulcerative colitis ), colon cancer, or  polyps .  Colonic polypectomy  has become a routine part of colonoscopy, allowing quick and simple removal of polyps during the procedure, without invasive surgery. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3914", "text": "With regard to blood in the stool either visible or occult, it is worthy of note, that occasional rectal bleeding may have multiple non-serious potential causes. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3915", "text": "Colonoscopy is one of the colorectal cancer screening tests available to people in the US who are 45 years of age and older. The other screening tests include  flexible sigmoidoscopy ,  double-contrast barium enema ,  computed tomographic (CT) colonography  (virtual colonoscopy),  guaiac-based fecal occult blood test  (gFOBT),  fecal immunochemical test  (FIT), and  multitarget stool DNA screening test  (Cologuard). [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3916", "text": "Subsequent rescreenings are then scheduled based on the initial results found, with a five- or ten-year recall being common for colonoscopies that produce normal results. [ 21 ] [ 22 ]  People with a family history of colon cancer are often first screened during their teenage years.\nAmong people who have had an initial colonoscopy that found no polyps, the risk of developing colorectal cancer within five years is extremely low. Therefore, there is no need for those people to have another colonoscopy sooner than five years after the first screening. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3917", "text": "Some medical societies in the US recommend a screening colonoscopy every 10 years beginning at age 50 for adults without increased risk for colorectal cancer. [ 25 ]  Research shows that the risk of cancer is low for 10 years if a high-quality colonoscopy does not detect cancer, so tests for this purpose are indicated every ten years. [ 25 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3918", "text": "Colonoscopy screening is associated with approximately two-thirds fewer deaths due to colorectal cancers on the left side of the colon, and is not associated with a significant reduction in deaths from right-sided disease. It is speculated that colonoscopy might reduce rates of death from colon cancer by detecting some colon polyps and cancers on the left side of the colon early enough that they may be treated, and a smaller number on the right side. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3919", "text": "Since polyps often take 10 to 15 years to transform into cancer in someone at average risk of colorectal cancer, guidelines recommend 10 years after a normal screening colonoscopy before the next colonoscopy. (This interval does not apply to people at high risk of colorectal cancer or those who experience symptoms of the disease.) [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3920", "text": "The large  randomized   pragmatic clinical trial  NordICC was the first published trial on the use of colonoscopy as a screening test to prevent colorectal cancer, related death, and death from any cause. It included 84,585 healthy men and women aged 55 to 64 years in Poland, Norway, and Sweden, who were randomized to either receive an invitation to undergo a single screening colonoscopy (invited group) or to receive no invitation or screening (usual-care group). Of the 28,220 people in the invited group, 11,843 (42.0%) underwent screening. A total of 15 people who underwent colonoscopy (0.13%) had major bleeding after polyp removal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3921", "text": "None of the participants experienced a  colon perforation  due to colonoscopy. After 10 years, an  intention-to-screen analysis  showed a significant  relative risk reduction  of 18% in the risk of colorectal cancer (0.98% in the invited group vs. 1.20% in the usual-care group). The analysis showed no significant change in the risk of death from colorectal cancer (0.28% vs. 0.31%) or in the risk of death from any cause (11.03% vs. 11.04%). To prevent one case of colorectal cancer, 455 invitations to colonoscopy were required. [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3922", "text": "As of 2023, the CONFIRM trial, a randomized trial evaluating colonoscopy vs. FIT is currently ongoing. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3923", "text": "In 2021, the US spent $43 billion on cancer screening to prevent five cancers, with colonoscopies accounting for 55% of the total. [ 33 ]  The death rate from colon cancer has been on a linear decline for 40 years, falling by nearly 50 percent from the 1980s (when few were screened) to 2024; however, the increase in screening did not accelerate the decline. [ 34 ]  Therefore, resources devoted to cancer screening would be better directed toward ensuring widespread access to effective cancer treatment. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3924", "text": "The  American Cancer Society  issues recommendations on colorectal cancer screening guidelines. These guidelines often change and are updated as new studies and technologies have become available [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3925", "text": "Many other national organizations also issue such guidance, such as the UK's  NHS [ 36 ]  and various European agencies, [ 37 ]  guidance can vary between such agencies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3926", "text": "In the United States,  Medicare  insurance covers a number of colorectal-cancer screening tests. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3927", "text": "The American Society for Gastrointestinal Endoscopy estimates around three in 1,000 colonoscopies lead to serious complications. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3928", "text": "The most serious complication is generally  gastrointestinal perforation , which is life-threatening and requires immediate surgical intervention. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3929", "text": "The key to managing a colonoscopic perforation is diagnosis at the time. Typically, the reasons are that the bowel prep done to facilitate the examination acts to reduce the potential for contamination, resulting in a higher likelihood of conservative management. In addition, detection at the time allows the physician to deploy strategies to seal the colon, or mark it should the patient require surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3930", "text": "As with any procedure involving  anaesthesia , complications can occur, such as: [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3931", "text": "Electrolyte imbalance caused by bowel preparation solutions is possible, but current bowel cleansing laxatives are formulated to account for electrolyte balance, making this a very rare event. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3932", "text": "During colonoscopies, when a  polyp  is removed (a polypectomy), the risk of complication increases. [ 44 ] [ 45 ]  One of the most serious complications is  postpolypectomy coagulation syndrome , occurring in 1 in  1000  procedures. [ 46 ]  It results from a burn injury to the wall of the colon causing abdominal pain, fever, elevated white blood cell count and elevated serum  C-reactive protein . Treatment consists of intravenous fluids, antibiotics, and avoiding oral intake of food, water, etc. until symptoms improve. Risk factors include right colon polypectomy, large polyp size (>2\u00a0cm), non-polypoid lesions (laterally spreading lesions), and hypertension. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3933", "text": "Although rare, infections of the colon are a potential colonoscopy risk. The colon is not a  sterile  environment, and infections can occur during biopsies from what is essentially a 'small shallow cut', enabling bacterial intrusion into lower parts of the colon wall. In cases where the lining of the colon is perforated, bacteria can infiltrate the  abdominal cavity . [ 48 ]   Infection may also be introduced if the endoscope is not cleaned and sterilized appropriately between procedures."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3934", "text": "Minor colonoscopy risks may include  nausea ,  vomiting  or  allergies  to the  sedatives  that may have been used. If medication is given intravenously, the  vein  may become irritated, or mild  phlebitis  may occur. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3935", "text": "The colon must be free of solid matter for the test to be performed properly. [ 50 ]  For one to three days, the patient is required to follow a  low fiber  or clear-liquid-only diet. Examples of clear fluids are  apple juice , chicken and/or beef broth or  bouillon ,  lemon-lime   soda , lemonade,  sports drink , and  water . It is important that the patient remains hydrated. Sports drinks contain  electrolytes  which are depleted during the purging of the bowel. Drinks containing fiber such as  prune  and  orange juice   should not be consumed, nor should liquids  dyed  red, purple, orange, or sometimes brown; however, cola is allowed. In most cases,  tea  or  coffee  taken without milk are allowed. [ 51 ] [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3936", "text": "The day before the colonoscopy (or  colorectal surgery ), the patient is either given a  laxative  preparation (such as  bisacodyl ,  phospho soda ,  sodium picosulfate , or  sodium phosphate  and/or  magnesium citrate ) and large quantities of fluid, or  whole bowel irrigation  is performed using a solution of  polyethylene glycol  and  electrolytes . [ 53 ] [ 54 ]  The procedure may involve both a pill-form laxative and a bowel irrigation preparation with the polyethylene glycol powder dissolved into any clear liquid, such as a sports drink that contains electrolytes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3937", "text": "The patient may be asked not to take aspirin or similar products such as  salicylate ,  ibuprofen , etc. for up to ten days before the procedure to avoid the risk of bleeding if a polypectomy is performed during the procedure. A blood test may be performed before the procedure. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3938", "text": "During the procedure, the patient is often given  sedation  intravenously, employing agents such as  fentanyl  or  midazolam . Although meperidine (Demerol) may be used as an alternative to fentanyl, the concern of seizures has relegated this agent to second choice for sedation behind the combination of fentanyl and midazolam. The average person will receive a combination of these two drugs, usually between 25 and 100 \u00a0 \u03bcg IV fentanyl and 1\u20134 \u00a0 mg IV midazolam. Sedation practices vary between practitioners and nations; in some clinics in Norway, sedation is rarely administered. [ 56 ] [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3939", "text": "The first step is usually a  digital rectal examination  (DRE), to examine the tone of the anal  sphincter  and to determine if preparation has been adequate. A DRE is also useful in detecting anal  neoplasms  and the clinician may note issues with the prostate gland in men undergoing this procedure. [ 58 ]  The  endoscope  is then passed through the  anus  up the  rectum , the  colon  (sigmoid, descending, transverse and ascending colon, the cecum), and ultimately the  terminal ileum . The endoscope has a movable tip and multiple channels for instrumentation, air, suction and light. The bowel is occasionally insufflated with air to maximize visibility (a procedure that gives the patient the false sensation of needing to take a  bowel movement ). Biopsies are frequently taken for  histology . Additionally in a procedure known as  chromoendoscopy , a contrast-dye (such as  indigo carmine ) may be sprayed through the endoscope onto the bowel wall to help visualize any abnormalities in the mucosal morphology. A  Cochrane review  updated in 2016 found strong evidence that chromoscopy enhances the detection of cancerous tumors in the colon and rectum. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3940", "text": "In most experienced hands, the endoscope is advanced to the junction of where the colon and small bowel join up ( cecum ) in under 10 minutes in 95% of cases. Due to tight turns and redundancy in areas of the colon that are not \"fixed\", loops may form in which advancement of the endoscope creates a \"bowing\" effect that causes the tip to actually retract. These loops often result in discomfort due to stretching of the colon and its associated  mesentery . Manoeuvres to \"reduce\" or remove the loop include pulling the endoscope backwards while twisting it. Alternatively, body position changes and abdominal support from external hand pressure can often \"straighten\" the endoscope to allow the scope to move forward. In a minority of patients, looping is often cited as a cause for an incomplete examination. Usage of alternative instruments leading to completion of the examination has been investigated, including use of pediatric colonoscope, push enteroscope and upper GI endoscope variants. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3941", "text": "Lawsuits over missed cancerous lesions have recently prompted some institutions to better document endoscope examination times, as rapid examination times may be a source of potential medical legal liability. [ 61 ]  This is often a real concern in clinical settings where high caseloads could provide financial incentive to complete colonoscopies as quickly as possible."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3942", "text": "The pain associated with the procedure is not caused by the insertion of the scope but rather by the inflation of the colon in order to do the inspection. The scope itself is essentially a long, flexible tube about a centimeter in diameter \u2014 that is, as big around as the little finger, which is less than the diameter of an average stool. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3943", "text": "The colon is wrinkled and corrugated, somewhat like an accordion or a clothes-dryer exhaust tube, which gives it the large surface area needed for nutrition and water absorption. In order to inspect this surface thoroughly, the physician blows it up like a balloon, using air from a compressor or  carbon dioxide  from a gas bottle (CO 2  is absorbed into the bloodstream through the mucosal lining of the colon much faster than air and then exhaled through the lungs which is associated with less post procedural pain), in order to get the creases out."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3944", "text": "The colon has sensors that can tell when there is unexpected gas pushing the colon walls out\u2014which may cause mild discomfort. Usually, total anesthesia or a partial  twilight sedative  are used to reduce the patient's awareness of pain or discomfort, or just the unusual sensations of the procedure. Once the colon has been inflated, the doctor inspects it with the scope as it is slowly pulled backward. If any polyps are found they are then cut out for later biopsy. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3945", "text": "Colonoscopy can be carried out without any sedation and a number of studies have been performed evaluating colonoscopy outcomes without sedation. [ 64 ]  Though in the US and EU the procedure is usually carried out with some form of sedation. [1]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3946", "text": "Researchers have found that older patients with three or more significant health problems (i.e., dementia or heart failure) had higher rates of repeat colonoscopies without medical indications. These patients are less likely to live long enough to develop colon cancer. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3947", "text": "In the 1960s, Niwa and Yamagata at Tokyo University developed the  fibre-optic endoscopy device. [ 66 ]  After 1968, William Wolff and Hiromi Shinya pioneered the development of the colonoscope. [ 67 ]  Their invention, in 1969 in Japan, was a significant advance over the barium enema and the flexible sigmoidoscope because it allowed for the visualization and removal of polyps from the entire colon. Wolff and Shinya advocated for their invention and published much of the early evidence needed to overcome skepticism about the device's safety and efficacy. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3948", "text": "Some of the leading medical device companies in the colonoscopy market as of 2023 include:  Fujifilm ,  Karl Storz SE , Pro Scope Systems,  Olympus Corporation ,  Medtronic Plc ,  Steris  and  Pentax  Medical. [ 69 ] [ better\u00a0source\u00a0needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3949", "text": "The terms  colonoscopy [ 70 ] [ 71 ] [ 72 ]  or  coloscopy [ 71 ]  are derived from [ 71 ]  the ancient Greek noun \u03ba\u03cc\u03bb\u03bf\u03bd, same as English  colon , [ 73 ]  and the verb \u03c3\u03ba\u03bf\u03c0\u03b5\u1fd6\u03bd,  look (in)to ,  examine . [ 73 ]  The term  colonoscopy  is however ill-constructed, [ 74 ]  as this form supposes that the first part of the compound consists of a possible root \u03ba\u03bf\u03bb\u03c9\u03bd- or \u03ba\u03bf\u03bb\u03bf\u03bd-, with the connecting vowel -o, instead of the root \u03ba\u03cc\u03bb- of \u03ba\u03cc\u03bb\u03bf\u03bd. [ 74 ]  A compound such as \u03ba\u03bf\u03bb\u03c9\u03bd\u03bf\u03b5\u03b9\u03b4\u03ae\u03c2,  like a hill , [ 73 ]  (with the additional -on-) is derived from the ancient Greek word \u03ba\u03bf\u03bb\u03ce\u03bd\u03b7 or \u03ba\u03bf\u03bb\u03c9\u03bd\u03cc\u03c2,  hill . [ 73 ]  Similarly, colonoscopy (with the additional -on-) can literally be translated as  examination of the hill , [ 74 ]  instead of the  examination of the colon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3950", "text": "In English, multiple words exist that are derived from \u03ba\u03cc\u03bb\u03bf\u03bd, such as  colectomy , [ 71 ] [ 75 ]   colocentesis , [ 71 ]   colopathy , [ 71 ]  and  colostomy [ 71 ]  among many others, that actually lack the incorrect additional -on-. A few compound words such as  colonopathy  have doublets with -on- inserted. [ 71 ] [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3951", "text": "The procedure of colonoscopy gained national attention in the  United States  in 1985 when  President   Ronald Reagan  underwent a life-saving colonoscopy. [ 76 ] [ 77 ] [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3952", "text": "A survey on colonoscopy shows a poor understanding of its protective value and widespread misconceptions. The public has perceptual gaps around the purpose of colonoscopies, the subjective experience of the colonoscopy procedure, and the quantity of bowel preparation needed. [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3953", "text": "Actors  Ryan Reynolds  and  Rob McElhenney  have used their social media platform to raise awareness about the importance of colonoscopy as a procedure for  colon cancer screening . They filmed their own colonoscopies as part of a campaign called \"Lead From Behind\", [ 80 ] [ 81 ]  demonstrating that the procedure can be both easy and lifesaving. [ 82 ] [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3954", "text": "Courvoisier's principle  (known as  Courvoisier's sign  or  Courvoisier\u2013Terrier's sign , or  Courvoisier syndrome ) states that a painless palpably enlarged  gallbladder   accompanied with mild  jaundice  is unlikely to be caused by  gallstones . Usually, the term is used to describe the physical examination finding of the  right-upper quadrant of the abdomen . This sign implicates possible  malignancy of the gallbladder  or  pancreas  and the swelling is unlikely due to  gallstones . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3955", "text": "This observation is best explained as a matter of the gradual increase in gallbladder distention that occurs secondary to chronic processes versus the abrupt increase in gallbladder pressure observed in acute processes. Courvoisier's sign occurs due to the gradual (chronic) nature of the obstruction caused by cancer (e.g. pancreatic, often located in pancreatic head, cholangiocarcinoma, etc.), which gradually causes biliary back-pressure and gradually distends the gallbladder over time, without causing acute damage, thus without causing pain. Conversely, gallstones cause obstruction of the biliary tree in a more abrupt (acute) nature when the gallstone becomes suddenly lodged somewhere along the biliary tree, blocking the passage of bile. This process causes the gallbladder to distend as it contracts against an abruptly blocked/higher pressure biliary tree, resulting in acute inflammation of the gallbladder (acute cholecystitis) and right upper quadrant abdominal pain (i.e., not Courvoisier's sign). Fibrosis of the gallbladder is another chronic process that occurs due to repeated acute inflammation (i.e., chronic cholecystitis), resulting in a shrunken, fibrotic (therefore hard), and calcified gallbladder (\"porcelain gallbladder\"), which typically will not present with Courvoisier's sign and is diagnosed with imaging."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3956", "text": "Ludwig Georg Courvoisier 's [ 3 ]  original observations, published in Germany in 1890, were not originally cited as a 'law', and no mention of malignancy or pain (tenderness) was made. These points are commonly misquoted or confused in the medical literature. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3957", "text": "Exceptions to Courvoisier's law imply that a stone is responsible for jaundice and a non-tender, palpable gall bladder. Typically gall bladder stones form slowly which allow time for the gall bladder to become tender. The exceptions to the law are stones that dislodge and acutely block the duct distally to the hepatic/cystic duct junction:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3958", "text": "Cholangiocarcinoma ,  Klatskin tumors , ascariasis, or recurrent pyogenic cholangitis are not exceptions to the law because they all fall under it. For example, in the case of  recurrent pyogenic cholangitis  complicated by calcium bilirubinate stone dislodging to the common bile duct causing a distended gallbladder by back pressure. (Where formation of stones are not strictly in gallbladder, hence not fibrotic, but in the  intrahepatic bile ducts ). To reiterate, the law simply says that jaundice and non-tender, palpable gall bladders are caused by other things than chronic bile gallstone formation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3959", "text": "The law does not say that these symptoms automatically mean pancreatic cancer. It just happens that pancreatic cancer is the most common cause that falls under Courvoisier's law. [ 4 ]  Other cause includes malignancy of the  CBD  (i.e.  cholangiocarcinoma ), head of  pancreas  and  ampulla of Vater ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3960", "text": "A palpable  tender  gallbladder (hence the law cannot be applied) may be seen in acute acalculous  cholecystitis , which commonly follows trauma or  ischemia  and causes acute inflammation of the gallbladder in the absence of gallstones. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3961", "text": "A palpable gallbladder without mild jaundice (hence the law cannot be applied) can also be seen in  Mirizzi's syndrome ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3962", "text": "The following case is an illustration of using the rationale underlying the Courvoisier Law clinically. In a patient with a history of lung cancer presenting with jaundice and a non-palpable gallbladder it is likely that it is caused by a double cancer affected the common hepatic ducts and not from metastasis to the lymph node causing obstructive jaundice. This is because in the latter case, location of the lymph node has got to be in the CBD (simply by anatomical location) and one would expect a palpable gallbladder. All these speculations assume that the patient did not have gallstone disease previously (where the gallbladder would be fibrotic and not palpable) and that the patient does not have a history of other liver diseases (such as recurrent pyogenic cholangitis)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3963", "text": "Double-balloon enteroscopy , also known as  push-and-pull  enteroscopy , is an  endoscopic  technique for visualization of the  small bowel .  It was developed by  Hironori Yamamoto  in 2001. [ 1 ]   It is novel in the field of diagnostic  gastroenterology  as it is the first endoscopic technique that allows for the entire  gastrointestinal tract  to be visualized in real time. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3964", "text": "The technique involves the use of a  balloon  at the end of a special  enteroscope  camera and an overtube, which is a tube that fits over the endoscope, and which is also fitted with a balloon. [ 2 ]   The procedure is usually done under general  anesthesia , but may be done with the use of  conscious sedation . [ 3 ]   The enteroscope and overtube are inserted through the  mouth  and passed in conventional fashion (that is, as with  gastroscopy ) into the  small bowel . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3965", "text": "Following this, the endoscope is advanced a small distance in front of the overtube and the balloon at the end is inflated.  Using the assistance of friction at the interface of the enteroscope and intestinal wall, the small bowel is accordioned back to the overtube.  The overtube balloon is then deployed, and the enteroscope balloon is deflated.  The process is then continued until the entire small bowel is visualized. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3966", "text": "The double-balloon enteroscope can also be passed in retrograde fashion, through the  colon  and into the  ileum  to visualize the end of the small bowel. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3967", "text": "Double-balloon enteroscopy has found a niche application in the following settings:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3968", "text": "Double-balloon enteroscopy offers a number of advantages to other small bowel image techniques, including  barium  imaging,  wireless capsule endoscopy  and push enteroscopy:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3969", "text": "The key disadvantage of double-balloon enteroscopy is the time required to visualize the small bowel; this can exceed three hours, and may require that patients be admitted to hospital for the procedure. [ 11 ]   There have also been case reports of  acute pancreatitis  (at a rate of 0.3%\u20130.4%, when the oral route is used) [ 12 ] [ 13 ]  and intestinal necrosis [ 14 ]  associated with the technique."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3970", "text": "A 2015 study in the  World Journal of Gastrointestinal Endoscopy  reported that: \"Due to prolonged procedure and air  insufflation ,  abdominal pain  can be observed in up to 20% patients.\" [ 12 ]  Depending on whether the oral or rectal approach was used, a patient may experience a sore throat (following use of the oral route), upset stomach, vomiting, and painful  bloating , cramping, or abdominal discomfort in reaction to the gas in the intestines. [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3971", "text": "An  electrogastrogram  ( EGG ) is a computer generated graphic produced by  electrogastrography , which detects, analyzes and records the myoelectrical signal generated by the movement of the smooth muscle of the stomach, intestines and other smooth muscle containing organs.  An  electrogastroenterogram  or electroviscerogram (or  gastroenterogram ) is a similar display of the recording of myoelectrical activity of gastrointestinal or other organs which are able to  generate myoelectrical activity."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3972", "text": "These names are made of different parts:  electro , because it is related to electrical activity,  gastro ,  Greek  for stomach,  entero or viscero , Greek for intestines,  gram , a Greek root meaning \"to write\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3973", "text": "An electrogastrogram (EGG), electroviscerogram (EVG) or a gastroenterogram are similar in principle to an  electrocardiogram  (ECG) in that sensors on the skin detect electrical signals indicative of muscular activity within. Where the electrocardiogram detects muscular activity in various regions of the heart, the electrogastrogram or electroviscerogram  detects the myoelectrical activity of the wave-like contractions of the stomach, intestines or other organs ( peristalsis )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3974", "text": "Walter C. Alvarez  discovered the EGG signal and pioneered early studies of electrogastrography in 1921\u201322. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3975", "text": "Motility  of  gastrointestinal tract  (GI tract) results from coordinated contractions of  smooth muscle , which in turn derive from two basic patterns of electrical activity across the  membranes  of smooth muscle cells\u2014 slow waves  and  action potentials . [ 2 ]  Slow waves are initiated by pacemakers\u2014the  interstitial cells of Cajal  (ICC). Slow wave frequency varies in the different organs of the GI tract and is characteristic for that organ. They set the maximum frequency at which the muscle can contract:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3976", "text": "The electrical activity or more properly termed myoelectrical activity of the GI tract can be subdivided into two categories: electrical control activity (ECA) and electrical response activity (ERA). ECA is characterized by regularly recurring electrical potentials, originating in the gastric pacemaker located in the  body of stomach .\nThe slow waves are not a direct reason of peristalsis of a GI tract, but a correlation between deviations of slow waves from norm and motility abnormalities however is proved. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3977", "text": "Recording of the Electrogastrogram can be made from either the gastrointestinal surface  mucosa ,  serosa , or the external skin surface. The cutaneous electrogastrography provides an indirect representation of the electrical activity, that has been demonstrated in numerous studies to exactly correspond to simultaneous recordings of the mucosa or serosa. Since it is much easier to perform, the cutaneous electrogastrography has been used most frequently. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3978", "text": "Several EGG signals may be recorded from various standardized positions on the abdominal wall, However, for maximal accuracy and analysis it is important to select the one channel with the highest amplitude. Each channel usually consists of three  Ag-AgCl  electrodes. [ 6 ]   Recordings are made both fasting (usually 10\u201330 minutes) and after a stimulation meal (usually 30\u201360 minutes) with the patient lying quietly. The stimulation meal may vary but the most commonly used medium is room temperature water. Deviations from the normal frequency may be referred to as alterations in the gastric myoelectrical activity (GMA) or intestinal myoelectrical activity(IMA), These include: 1) bradygastria GMA, 2) tachygastria GMA, or 3) 3 cycle per minute hypernormal GMA or hyponormal GMA ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3979", "text": "In normal individuals the power of the electrical signals increases after the meal. In patients with abnormalities of stomach and/or gastrointestinal motility, the rhythm often is irregular or there is no post-stimulation meal increase in electrical power."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3980", "text": "Terms bradygastria and tachygastria are used at the description of deviations of frequency of an electric signal from slow waves are initiated by pacemaker in the stomach from normal frequency of 3 cycles per minute. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3981", "text": "A  bradygastria  is defined, as decreased rate of myoelectrical activity in the stomach, as less than 2.5 cycles per minute for at least 1 minute."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3982", "text": "A  tachygastria  is defined, as increased rate of myoelectrical activity in the stomach, as more than 3.75 cycles per minute for at least 1 minute."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3983", "text": "A bradygastria and tachygastria may be associated with  nausea ,  gastroparesis ,  irritable bowel syndrome , and  functional dyspepsia . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3984", "text": "There are following  Current Procedural Terminology  (CPT) and  Healthcare Common Procedure Coding System  (HCPCS) codes (maintained by the  American Medical Association ) for cutaneous electrogastrography: [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3985", "text": "An electrogastroenterography (EGEG) is based that different organs of a GI tract give different frequency slow wave."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3986", "text": "EGEG electrodes are as much as possible removed from a stomach and an intestines\u2014usually three electrodes are placed on the extremities. It allows to receive stabler and comparable results."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3987", "text": "An electrogastroenterography analysis program calculate [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3988", "text": "where  S(n) \u00a0\u2013 spectral components in the rank from st i  to fin i  (defined by received investigated range of this organ of GI tract) by  Discrete Fourier transform  of the electric signal from GI tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3989", "text": "EGEG parameters for normal patients: [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3990", "text": "Psychologists have performed psychophysiological studies to see what happens in the body during affective experiences.  Electrogastrograms have recently been used to test physiological  arousal , which was already determined by measures such as  heart rate ,  electrodermal skin responses , and changes in hormone levels in  saliva . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3991", "text": "Currently, a pattern of interest to psychologists is an increase in bradygastria, which is when electrical activity in the stomach drops to below 2 cpm resulting in a slower stomach rhythm, when exposed to  disgusting  stimuli, which may be a precursor to nausea and vomiting, both physiological responses to disgust. [ 11 ]  In this study, the presence of bradygastria was able to predict trait and state disgust, which no other physiological measure used in the study was able to detect. [ 11 ]  This abnormal myoelectrical activity is usually combined with other precursors to nausea and vomiting, such as increased salivary production, which further supports the idea that these rhythms show early signs of nausea and vomiting. These reactions are viewed as a way in which the body rejects unhealthy foods, [ 11 ]  which is linked with the view that disgust is an  evolutionary  adaptation to help humans avoid consuming toxic substances. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3992", "text": "During  sham feeding  sessions of both appetizing and unappetizing foods, 3 cycles per minute (cpm) power was measured. During the sham feeding of appetizing foods, 3cpm power increased. This increase was not reported in the sham feeding of unappetizing foods. [ 12 ]  The researchers concluded that the presence of this pattern seems to mark the beginning of the body preparing for  digestion , and the absence of this pattern in the disgust condition could indicate that the body is readying to reject the food. [ 12 ]  The increase of 3cpm power is also linked with increased saliva and digestive juice production, all of which support the idea that this reflex, called the  cephalic-vagal reflex , [ 12 ]  is the precursor of digestion. The differential response to appetizing and unappetizing foods suggest that the body uses disgust as a cue to whether a food is good to eat and responds accordingly."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3993", "text": "Another emotion with a bodily effect that can be measured by EGG is that of  stress .  When the body is stressed and engages in the  fight-or-flight response , blood flow is directed to the muscles in the arms and legs and away from the digestive system. This loss of blood flow slows the digestive system, and this slowing can be seen on the EGG. [ 13 ]  However, this response can vary from person to person and situation to situation. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3994", "text": "All of these examples are part of a larger theory of a  brain\u2013gut connection . This theory states that the  vagus nerve  provides a direct link between the brain and the gut so that emotions can affect stomach rhythms and vice versa. [ 12 ] [ 13 ]  This idea originated in the mid-1800s when  Alexis St. Martin , a man with a gunshot-induced  fistula  in his abdomen, experienced lower secretions of digestive juices and a slower stomach emptying when he was upset. [ 13 ]  In this case, the emotions St. Martin was feeling affected his physiological reaction, but the reverse can also be true. In a study with  Crohn's disease  patients where patients and unaffected controls watched happy, frightening, disgusting, and saddening films, patients with active Crohn's disease had more responsive EGG (a greater physiological response) and reported feeling more aroused when feeling the negative emotions of disgust or sadness. [ 14 ]  This leads researchers to believe that increased physiological activation can influence increased experience of emotions. [ 14 ]   Another study published in 1943 that studied the fistulated man Tom discovered that if \"Tom was fearful or depressed his gastic activity decreased but when he was angry or hostile his gastric activity increased\". [ 13 ]  This finding is contrasted by an EGG study by Ercolani et al. who had subjects perform either difficult or easy mental arithmetic or puzzles. They found that new tasks slowed down the myoelectrical activity of the stomach, suggesting that  stress  tends to impede gastric activity and that this can be picked up on an EGG. [ 15 ]  While there is still much research to be done on the brain-gut connection, research thus far has indeed shown that your stomach does indeed churn differently when you are emotionally aroused, [ 16 ]  and this could be the basis of the gut feeling that many people describe experiencing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3995", "text": "In recent years, some research has been done about  gender differences  in the perception and experience of disgust.  One such study, upon presenting both male and female subjects with video clips designed to trigger disgust and found that although women reported feeling more disgust than men at these stimuli, the physiological responses did not show much difference. [ 10 ]  This could mean that, psychologically, women are more sensitive to disgust than men; however this assertion cannot be supported with physiological data. [ 10 ]  More research has to be done in this area to see if there are gender differences in the psychophysiological experience of disgust."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3996", "text": "There are some limitations to the use of electrogastroenterography: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3997", "text": "Electrogastrography or gastroenterography is used when a patient is suspected of having a motility disorder, which can be indicated by recurrent nausea and vomiting, signs that the stomach is not emptying food normally. The clinical use of electrogastrography has been most widely evaluated in patients with gastroparesis and functional dyspepsia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3998", "text": "An  endoscopy  is a procedure used in  medicine  to look inside the body. [ 1 ]  The endoscopy procedure uses an  endoscope  to examine the interior of a hollow organ or cavity of the body. Unlike many other  medical imaging  techniques, endoscopes are inserted directly into the organ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_3999", "text": "There are many types of endoscopies. Depending on the site in the body and type of procedure, an endoscopy may be performed by either a doctor or a  surgeon . A patient may be fully conscious or  anaesthetised  during the procedure. Most often, the term  endoscopy  is used to refer to an examination of the upper part of the  gastrointestinal tract , known as an  esophagogastroduodenoscopy . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4000", "text": "For nonmedical use, similar instruments are called  borescopes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4001", "text": "Adolf Kussmaul  was fascinated by  sword swallowers  who would insert a sword down their throat without gagging. This drew inspiration to insert a hollow tube for observation; the next problem to solve was how to shine light through the tube, as they were still relying on candles and oil lamps as light sources. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4002", "text": "The term  endoscope  was first used on February 7, 1855, by engineer-optician Charles Chevalier, in reference to the  ur\u00e9throscope  of  D\u00e9sormeaux , who himself began using the former term a month later. [ 4 ]  The self-illuminated endoscope was developed at  Glasgow Royal Infirmary  in  Scotland  (one of the first hospitals to have mains electricity) in 1894/5 by  John Macintyre  as part of his specialization in the investigation of the larynx. [ 5 ] [ failed verification ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4003", "text": "Endoscopy may be used to investigate symptoms in the  digestive system  including  nausea ,  vomiting ,  abdominal pain ,  difficulty swallowing , and  gastrointestinal bleeding . [ 6 ]  It is also used in diagnosis, most commonly by performing a biopsy to check for conditions such as  anemia , bleeding,  inflammation , and  cancers of the digestive system . [ 6 ]  The procedure may also be used for treatment such as  cauterization  of a bleeding vessel, widening a narrow esophagus, clipping off a polyp or removing a foreign object. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4004", "text": "Specialty   professional organizations  that specialize in digestive problems advise that many patients with  Barrett's esophagus  receive endoscopies too frequently. [ 7 ]  Such societies recommend that patients with Barrett's esophagus and no cancer symptoms after two biopsies receive biopsies as indicated and no more often than the recommended rate. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4005", "text": "Health care providers can use endoscopy to review any of the following body parts:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4006", "text": "Endoscopy is used for many procedures:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4007", "text": "An endoscopy is a simple procedure that allows a doctor to look inside human bodies using an instrument called an endoscope.  A cutting tool can be attached to the end of the endoscope, and the apparatus can then be used to perform minor procedures such as tissue biopsies, banding of oesophageal varices or removal of polyps."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4008", "text": "The main risks are infection, over-sedation, perforation, or a tear of the stomach or esophagus lining and bleeding. [ 10 ]  Although perforation generally requires surgery, certain cases may be treated with antibiotics and intravenous fluids. Bleeding may occur at the site of a biopsy or polyp removal. Such typically minor bleeding may simply stop on its own or be controlled by cauterisation. Seldom does surgery become necessary. Perforation and bleeding are rare during gastroscopy. Other minor risks include drug reactions and complications related to other diseases the patient may have. Consequently, patients should inform their doctor of all allergic tendencies and medical problems. Occasionally, the site of the  sedative  injection may become inflamed and tender for a short time. This is usually not serious and warm compresses for a few days are usually helpful. While any of these complications may possibly occur, each of them occurs quite infrequently. A doctor can further discuss risks with the patient with regard to the particular need for gastroscopy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4009", "text": "After the procedure, the patient will be observed and monitored by a qualified individual in the endoscopy room, or a recovery area, until a significant portion of the medication has worn off. Occasionally the patient is left with a mild sore throat, which may respond to saline gargles, or chamomile tea. It may last for weeks or not happen at all. The patient may have a feeling of distention from the insufflated air that was used during the procedure. Both problems are mild and fleeting. When fully recovered, the patient will be instructed when to resume their usual diet (probably within a few hours) and will be allowed to be taken home. Where sedation has been used, most facilities mandate that the patient be taken home by another person and that they not drive or handle machinery for the remainder of the day. Patients who have had an endoscopy without sedation are able to leave unassisted."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4010", "text": "An  esophageal motility study  ( EMS ) or  esophageal manometry  is a test to assess  motor function  of the  upper esophageal sphincter  (UES), esophageal body and  lower esophageal sphincter  (LES). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4011", "text": "An EMS is typically done to evaluate suspected disorders of  motility  or  peristalsis  of the  esophagus . These include  achalasia ,  diffuse esophageal spasm ,  nutcracker esophagus  and  hypertensive lower esophageal sphincter . These disorders typically present with  dysphagia , or difficulty swallowing, usually to both solids and liquids even initially. Other patients with  spasm  disorders may have the test done to diagnose  chest pain  thought not to be of  cardiac  cause."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4012", "text": "The test is not useful for anatomical disorders of the esophagus (that is, disorders that distort the anatomy of the esophagus), such as  peptic strictures  and  esophageal cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4013", "text": "A technician places a  catheter  into the nose and then guides it into the stomach. Once placed in the stomach lining, the catheter is slowly withdrawn, allowing it to detect pressure changes and to record information for later review. The patient will be asked at times to take a deep breath or to take some swallows of water. The degree of discomfort varies among patients. Patients are not  sedated  because sedatives would alter the functioning of the esophageal muscles. Overall the procedure takes about 45 minutes. After the procedure is complete, patients can usually resume their normal daily activities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4014", "text": "Upper gastrointestinal series  and their  fluoroscopic  counterparts use  x-rays  to image the swallowing motions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4015", "text": "Recently, [ when? ]   high resolution manometry  (HRM) has been developed that significantly reduces the procedure time (10 minutes versus 45 minutes with conventional manometry) and provides enhanced patient comfort. Newer catheters incorporate concurrent impedance with HRM."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4016", "text": "In  gastroenterology ,  esophageal pH monitoring  is the current  gold standard  for diagnosis of  gastroesophageal reflux disease  (GERD). It provides direct physiologic measurement of acid in the  esophagus  and is the most objective method to document reflux disease, assess the severity of the disease and monitor the response of the disease to medical or surgical treatment. It can also be used in diagnosing  laryngopharyngeal reflux ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4017", "text": "The importance of refluxed gastric contents in the  pathogenesis  of  GERD  was emphasized by Winkelstein who introduced the term \" peptic   esophagitis \" and by Bernstein and Baker who reported the symptom of  heartburn  following instillation of  hydrochloric acid  in the distal  esophagus  in what then became known as the  acid perfusion test . Formal measurement of  acid  in the  esophagus  was first described in 1960 by Tuttle. He used a glass  pH  probe to map the gastroesophageal pH gradient, and demonstrated a sharp gradient in normal subjects and a gradual, sloping gradient in patients with esophagitis. Four years later, Miller used an indwelling esophageal pH electrode to continuously measure esophageal and gastric pH for a period up to 12 hours. This technique required that the patient keep their hands immersed in saline to serve as a reference. Prolonged monitoring became feasible in 1974 when Johnson and  DeMeester  developed a dependable external reference electrode. [ 1 ]  Using this technique to monitor esophageal acid exposure patients for periods up to 24 hours, DeMeester and Johnson were able to identify the most important parameters of esophageal acid exposure, and they developed a composite pH score to quantify gastroesophageal reflux. The initial 24-hour pH studies required hospitalization until the introduction of  microcircuits  in the 1980s that allowed portable esophageal pH monitoring in an outpatient setting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4018", "text": "Gastroesophageal reflux disease  (GERD) is a common disease in western countries. In the  United States , 7% of the population experiences  heartburn  daily and 44% at least once a month. [ 2 ]   Heartburn  occurs when esophageal mucosa is exposed to the acidic gastric content, but the complaint of  heartburn  is not always a reliable guide to the presence of acid reflux in the esophagus. [ 3 ]  Further, only half of the patients with increased esophageal acid exposure will have  esophagitis . [ 4 ]   Therefore, the diagnosis of  gastroesophageal reflux disease  (GERD) on the basis of symptoms or endoscopic findings is problematic. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4019", "text": "Although there remains no gold standard for the diagnosis of GERD, ambulatory esophageal  pH  monitoring can provide data to guide further evaluation and treatment of patients with GERD-associated symptoms. In the past, an indwelling nasoesophageal  catheter  was the only way to measure esophageal acid exposure. Because this method is associated with  nasal  and  pharyngeal  discomfort and  rhinorrhea , patients may have limited their activity and become more sedentary during the monitored period. [ 5 ]  This may have resulted in less acid reflux and a false negative test. A catheter-free radio  telemetric  system allows a longer period of monitoring and may be better tolerated. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4020", "text": "Esophageal pH monitoring is currently performed using one of the following three techniques:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4021", "text": "The duration of the test is 24 hours in the first and second techniques and 48 hours for the Bravo capsule or more (96 hours) for OMOM capsule."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4022", "text": "In assessment of distal esophageal pH, the sensor is placed 5\u00a0cm above the upper border of the  lower esophageal sphincter  (LES) determined by  esophageal manometry . To measure  proximal  esophageal acid exposure, the second sensor is placed 1-5 below the lower border of the  upper esophageal sphincter  (UES). The Bravo pH capsule is placed either transnasally based on manometric measurements, or following  endoscopy . In transnasal placement, the capsule is placed 5\u00a0cm above the upper border of the LES, and in endoscopic placement 6\u00a0cm above  the gastroesophageal junction . The same applies to OMOM pH monitoring capsule."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4023", "text": "A reflux episode is defined as esophageal pH drops below four. Esophageal pH monitoring is performed for 24 or 48 hours and at the end of recording, a patient's tracing is analyzed and the results are expressed using six standard components. Of these 6 parameters, a pH score called  Composite pH Score  or  DeMeester Score  has been calculated, which is a global measure of esophageal acid exposure. A Demeester score > 14.72 indicates reflux. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4024", "text": "The widespread prescription of  proton pump inhibitors  (PPI) by primary care physicians has resulted in a change in pattern of GERD in patients who use these medications. Quite often gastroenterologist and foregut surgeons receive consultations to assess patients with persistent reflux symptoms despite the fact that patients is on acid suppression medications. This is due to the fact that symptoms of these patients are the results of weak acid or non-acid reflux.\nIn 1991  Silny  was the first investigator who described Multichannel Intraluminal Impedance (MII), a technique which detects intraesophageal bolus transport. This method is based on measuring the resistance to alternating current (i.e., impedance) of the content of the esophageal lumen. MII- pH monitoring was then developed by several clinical investigators. [ 8 ]  The clinical application of this technique is mainly in GERD patients who have persistent symptoms despite medical therapy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4025", "text": "Retrograde flow of gastric contents to the upper aerodigestive tract causes a variety of symptoms such as  cough ,  asthma  and  hoarseness . These respiratory manifestations of the reflux disease are commonly called  laryngopharyngeal reflux  (LPR) or extraesophegeal reflux disease (EERD). Distal esophageal pH monitoring has been used as an objective test to establish reflux as the cause of the atypical reflux symptoms, but its role in causally associating patients' symptoms to GERD is controversial. In an effort to improve diagnostic accuracy of testing, a catheter with two pH sensors has been used to measure the degree of esophageal acid exposure in both distal and proximal esophagus. The ideal location for pH measurement to confirm the diagnosis of the laryngopharyngeal reflux is the  pharynx  and new studies have focused on the development of a new pH sensor which can function in the challenging environment of the oropharynx. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4026", "text": "Esophagogastroduodenoscopy  ( EGD ) or  oesophagogastroduodenoscopy  ( OGD ), also called by  various other names , is a  diagnostic   endoscopic  procedure that visualizes the upper part of the  gastrointestinal tract  down to the  duodenum . It is considered a  minimally invasive procedure  since it does not require an  incision  into one of the major body cavities and does not require any significant recovery after the procedure (unless  sedation  or  anesthesia  has been used). However, a  sore throat  is common. [ 1 ] [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4027", "text": "The words  esophagogastroduodenoscopy  (EGD;  American English ) and  oesophagogastroduodenoscopy  (OGD;  British English ; see  spelling differences ) are pronounced  / \u026a \u02cc s \u0252 f \u0259 \u0261 o\u028a \u02cc \u0261 \u00e6 s t r o\u028a \u02cc d ( j ) u\u02d0 o\u028a d \u026a \u02c8 n \u0252 s k \u0259 p i / . It is also called  panendoscopy  (PES) and  upper GI endoscopy . It is also often called just  upper endoscopy ,  upper GI , or even just  endoscopy ; because EGD is the most commonly performed type of endoscopy, the ambiguous term  endoscopy  is sometimes informally used to refer to EGD by default. The term  gastroscopy  literally focuses on the stomach alone, but in practice, the usage overlaps."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4028", "text": "The complication rate is about 1 in 1000. [ 4 ]  They include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4029", "text": "When used in  infants , the esophagogastroduodenoscope may compress the  trachealis muscle , which narrows the  trachea . [ 5 ]  This can result in reduced airflow to the  lungs . [ 5 ]  Infants may be  intubated  to make sure that the trachea is fixed open. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4030", "text": "Problems of gastrointestinal  function  are usually not well diagnosed by endoscopy since  motion  or  secretion  of the gastrointestinal tract is not easily inspected by EGD. Nonetheless, findings such as excess fluid or poor motion of the gut during endoscopy can be suggestive of disorders of function.  Irritable bowel syndrome  and  functional dyspepsia  are not diagnosed with EGD, but EGD may be helpful in excluding other diseases that mimic these common disorders. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4031", "text": "The tip of the endoscope should be lubricated and checked for critical functions including tip angulations, air and water suction, and image quality."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4032", "text": "The patient is kept  NPO (nil per os) or NBM (nothing by mouth)  for at least 4 hours before the procedure. Most patients tolerate the procedure with only  topical anesthesia  of the  oropharynx  using  lidocaine  spray. However, some patients may need sedation and the very anxious/agitated patient may even need a general anesthetic.  Informed consent  is obtained before the procedure. The main risks are bleeding and perforation. The risk is increased when a biopsy or other intervention is performed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4033", "text": "The patient lies on their left side with the head resting comfortably on a pillow. A mouth-guard is placed between the teeth to prevent the patient from biting on the endoscope. The endoscope is then passed over the tongue and into the oropharynx. This is the most uncomfortable stage for the patient. Quick and gentle manipulation under vision guides the endoscope into the esophagus. The endoscope is gradually advanced down the esophagus making note of any pathology. Excessive  insufflation  of the stomach is avoided at this stage. The endoscope is quickly passed through the stomach and through the  pylorus  to examine the first and second parts of the  duodenum . Once this has been completed, the endoscope is withdrawn into the stomach and a more thorough examination is performed including a J-maneuver. This involves retroflexing the tip of the scope so it resembles a 'J' shape in order to examine the  fundus  and gastroesophageal junction. Any additional procedures are performed at this stage. The air in the stomach is aspirated before removing the endoscope. Still  photographs  can be made during the procedure and later shown to the patient to help explain any findings."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4034", "text": "In its most basic use, the endoscope is used to inspect the internal anatomy of the digestive tract. Often inspection alone is sufficient, but  biopsy  is a valuable adjunct to endoscopy. Small biopsies can be made with a pincer (biopsy  forceps ) which is passed through the scope and allows sampling of 1 to 3\u00a0mm pieces of tissue under direct vision. The intestinal mucosa heals quickly from such biopsies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4035", "text": "Clinical practice varies with respect to routine biopsy for histological analysis of the examined upper gastrointestinal system. A rapid urease test is quick, easy, and cost-effective screening for Helicobacter pylori infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4036", "text": "Faecal calprotectin  ( or   fecal calprotectin ) is a  biochemical measurement  of the protein  calprotectin  in the  stool . Elevated faecal calprotectin indicates the migration of  neutrophils  to the intestinal  mucosa , which occurs during intestinal inflammation, including inflammation caused by  inflammatory bowel disease .  Under a specific clinical scenario, the test may eliminate the need for invasive  colonoscopy  or radio-labelled  white cell  scanning."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4037", "text": "Calprotectin is a 24\u00a0kDa  dimer  of  calcium  binding proteins  S100A8  and  S100A9 . [ 1 ]   The complex accounts for up to 60% of the soluble protein content of the  neutrophil   cytosol . [ 2 ] [ 3 ]   In vitro  studies show that calprotectin has  bacteriostatic  and  fungistatic  properties, that arise from its ability to sequester  manganese  and  zinc . [ 1 ]   Calprotectin has two  transition metal  binding sites that form at the interface of the S100A8 and S100A9 monomers, and metal sequestration by calprotectin has been shown to be calcium dependent. [ 1 ]  The complex is resistant to  enzymatic  degradation, and can be easily measured in  faeces . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4038", "text": "The main diseases that cause an increased excretion of faecal calprotectin are   inflammatory bowel diseases  (IBD),  coeliac disease ,  infectious colitis ,  necrotizing enterocolitis  in infants, intestinal  cystic fibrosis  and  colorectal cancer . [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4039", "text": "Although a relatively new test, faecal calprotectin is regularly used as indicator for IBD during treatment and as a diagnostic marker. [ 6 ]   IBD are a group of conditions that cause a  pathological   inflammation  of the  bowel  wall.  Crohn's disease  and  ulcerative colitis  are the principal types of inflammatory bowel disease. Inflammatory processes result in an influx of neutrophils into the bowel  lumen . [ 8 ]  Since calprotectin comprises as much as 60% of the soluble protein content of the cytosol of neutrophils, it can serve as a marker for the level of intestinal inflammation. [ 9 ]  Measurement of faecal calprotectin has been shown to be strongly correlated with 111- indium -labelled  leucocytes  \u2013 considered the gold standard measurement of  intestinal  inflammation. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4040", "text": "Levels of faecal calprotectin are usually normal in patients with  irritable bowel syndrome  (IBS). [ 11 ] [ better\u00a0source\u00a0needed ]  In untreated coeliac disease, concentration levels of faecal calprotectin correlate with the degree of  intestinal mucosal lesion  and normalize with a  gluten-free diet . [ 6 ] \nHigh fecal calprotectin is a common finding among hospitalized coronavirus disease 2019 ( COVID-19 ) patients, especially those with  SARS-CoV-2  fecal shedding. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4041", "text": "Faecal calprotectin is measured using  immunochemical  techniques such as  ELISA  or  immunochromatographic  assays. The  antibodies  used in these assays target specific  epitopes  of the calprotectin molecule. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4042", "text": "Increased faecal calprotectin may be indicative of intestinal tuberculosis or pulmonary tuberculosis. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4043", "text": "Although faecal calprotectin correlates significantly with disease activity in people with confirmed IBD, faecal calprotectin can be false-positive if the laboratory uses low calprotectin cut-off levels. [ 11 ]  Most importantly, intake of  non-steroidal anti-inflammatory drugs  (aspirin included) increases calprotectin values, possibly due to the associated induced  enteropathy . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4044", "text": "Fecal occult blood  ( FOB ) refers to  blood  in the  feces  that is not visibly apparent (unlike other types of  blood in stool  such as  melena  or  hematochezia ). A fecal occult blood test (FOBT) checks for hidden (occult) blood in the stool (feces). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4045", "text": "The American College of Gastroenterology has recommended the abandoning of gFOBT testing as a colorectal cancer screening tool, in favor of the  fecal immunochemical test  (FIT). [ 2 ]   The newer and recommended tests look for  globin ,  DNA , or other blood factors including  transferrin , while conventional  stool guaiac tests  look for  heme ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4046", "text": "Fecal occult blood testing (FOBT), as its name implies, aims to detect subtle blood loss in the  gastrointestinal tract , anywhere from the  mouth  to the  colon . Positive tests (\"positive stool\") may result from either  upper gastrointestinal bleeding  or  lower gastrointestinal bleeding  and warrant further investigation for  peptic ulcers  or a  malignancy  (such as  colorectal cancer  or  gastric cancer ). The test does not directly detect  colon cancer  but is often used in clinical  screening  for that disease. It can also be used to look for active occult blood loss in  anemia [ 3 ]  or when there are gastrointestinal symptoms. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4047", "text": "An estimated 1\u20135% of large tested populations have a positive fecal occult blood test. [ citation needed ]  Of those, about 2\u201310% have cancer, while 20\u201330% have  adenomas .  Screening  methods for colon cancer depend on detecting either precancerous changes such as certain kinds of polyps or on finding early and thus more treatable cancer. The extent to which screening procedures reduce the risk of gastrointestinal cancer or deaths depends on the rate of precancerous and cancerous disease in that population. gFOBT (guaiac fecal occult blood test) and flexible sigmoidoscopy screening have each shown benefit. Other colon cancer screening tools such as iFOBT (immunochemical fecal occult blood test) or colonoscopy are also included in guidelines. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4048", "text": "In 2009, the  American College of Gastroenterology  (ACG) suggested that colon cancer screening modalities that are also directly preventive by removing precursor lesions should be given precedence, and prefer a  colonoscopy  every ten years in average-risk individuals, beginning at age 50. [ 2 ]  The ACG suggests that cancer detection tests such as any type of FOB are an alternative that is less preferred, and if a colonoscopy is declined, the FIT (fecal immunochemical test, or iFOBT) should be offered instead. The 2017 US Multi-Society Task Force (MSTF)'s recommended first-tier tests are a colonoscopy every 10 years or annual FIT test. [ 6 ]  If FIT is utilized, proper steps must be taken to ensure appropriate use and follow-up of abnormal FIT results. [ 7 ]  FIT tests however are not that useful in picking up adenomas, even when advanced. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4049", "text": "The  United States Preventive Services Task Force  (USPSTF)'s 2016 recommendation, instead of emphasizing specific screening approaches, has instead chosen to highlight that there is convincing evidence that colorectal cancer screening substantially reduces deaths from the disease among adults aged 50 to 75 years and that not enough adults are using this effective preventive intervention. [ 9 ]  The ACG and MSTF also included CT colonography every five years, and fecal DNA testing as considerations. All three recommendation panels recommended replacing any older low-sensitivity, guaiac-based fecal occult blood testing (gFOBT) with either newer high-sensitivity guaiac-based fecal occult blood testing (hs gFOBT) or fecal immunochemical testing (FIT). MSTF looked at six studies that compared high-sensitivity gFOBT (Hemoccult SENSA) to FIT, and concluded that there was no clear difference in overall performance between these methods."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4050", "text": "The English  National Health Service  (NHS) introduced a Bowel Cancer Screening Program in 2006. [ 10 ]  It is now offered to patients aged 60\u201374 years. In 2019 FIT was introduced as the primary screening test in England and Wales, replacing gFOBt.  [ 11 ] [ 12 ]  However, research carried out in the UK has suggested that the FIT threshold for further investigation is set at a point that may miss more than half of bowel cancer cases and only identifies one in four high-risk polyps. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4051", "text": "The American College of Gastroenterology has recommended the abandoning of gFOBT testing as a colorectal cancer screening tool, in favor of the fecal immunochemical test. [ 2 ]  Though the FIT test is preferred, even the guaiac FOB testing of average risk populations may have been sufficient to reduce the mortality associated with  colon cancer  by about 25%. [ 15 ]  With this lower efficacy, it was not always cost-effective to screen a large population with gFOBT. [ 16 ] [ 17 ] [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4052", "text": "If colon cancer is suspected in an individual (such as in someone with an unexplained  anemia ), fecal occult blood tests may not be clinically helpful. If a doctor suspects colon cancer, more rigorous investigation is necessary, whether or not the test is positive. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4053", "text": "In 2006, the Australian Government introduced the National Bowel Cancer Program which has been updated several times since; targeted screening will be done of all Australians aged from 50 to 74 by 2020. Cancer Council Australia recommended that FOBT should be done every two years. People over 50 not yet eligible for the national program can arrange with their doctor for an FOBT. [ 20 ] \nThe  Canadian Cancer Society  recommends that men and women aged 50 and over have an FOBT at least every two years. [ 21 ] \nIn colon cancer screening, using only one sample of feces collected by a doctor performing a  digital rectal examination  is discouraged. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4054", "text": "The use of the  M2-PK Test  is encouraged over gFOBT for routine screening, as it may pick up tumors whether or not they are bleeding. [ 23 ]  It is able to detect 80 percent of colorectal cancers and 44 percent for adenoma > 1 centimeter, while gFOBT picks up 13 to 50 percent of colorectal cancers. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4055", "text": "Gastrointestinal bleeding  has many potential sources, and positive results usually result in further testing for the bleeding site, usually looking for  lower gastrointestinal bleeding  before  upper gastrointestinal bleeding  causes unless there are other clues. [ 24 ]  Colonoscopy is usually preferred to computerized tomographic colonography. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4056", "text": "A positive test can result from  upper gastrointestinal bleeding  or  lower gastrointestinal bleeding . The common causes are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4057", "text": "In the event of a positive fecal occult blood test, the next step in the workup is a form of visualization of the gastrointestinal tract by one of several means:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4058", "text": "The use of an FOBT for bleeding from the mouth, nose, esophagus, lungs, stomach and the initial portion of the small intestine, while the same as fecal testing, is discouraged, due to technical considerations including poorly characterized test performance characteristics such as sensitivity, specificity, and analytical interference. [ 29 ]  However, chemical confirmation that coloration is due to blood rather than coffee, beets, medications, or food additives can be of significant clinical assistance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4059", "text": "Gastrointestinal (GI) complaints and low-intensity GI bleeding frequently occur in marathon runners. [ 30 ]  Strenuous exercise, particularly in elite athlete runners and less frequently in other exercise activities, can cause acute incapacitating gastrointestinal symptoms including heartburn, nausea, vomiting, abdominal pain, diarrhea and gastrointestinal bleeding. [ 31 ]  Approximately one third of endurance runners experience transient but exercise-limiting symptoms, and repetitive gastrointestinal bleeding occasionally causes iron deficiency and anaemia. [ 32 ] [ 33 ]  Runners can sometimes experience significant symptoms including  hematemesis . [ 34 ]  Exercise is associated with extensive changes in gastrointestinal (GI) tract physiology, including diversion of blood flow from the GI tract to muscles and lungs, decreased GI absorption and small intestinal motility, increased colonic transit, neuroimmunoendocrine changes in hormones and peptides such as  vasoactive intestinal peptide ,  secretin  and peptide-histidine-methionine. [ 35 ]  Substantial changes occur in stress hormones including cortisol, in circulating concentrations and metabolic behavior of various  leucocytes , and in  immunoglobulin  levels and  major histocompatibility complex  expression. [ 36 ]  Symptoms can be exacerbated by dehydration or by pre-exercise ingestion of certain foods and  hypertonic  liquids, and lessened by adequate training. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4060", "text": "Ingestion of 800 \u00a0 mg of  cimetidine  two hours before running a marathon did not significantly affect the frequency of gastrointestinal symptoms or occult gastrointestinal bleeding. [ 37 ]  Conversely, 800 \u00a0 mg of cimetidine 1 hr before the start and again at 50 miles of a 100-mile running race substantially decreased GI symptoms and post-race guaiac test positivity but did not affect race performance. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4061", "text": "There are four methods in clinical use to test for occult blood in feces. These look at different properties, such as  antibodies ,  heme ,  globin , or  porphyrins  in blood, or at  DNA  from cellular material such as from lesions of the intestinal mucosa."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4062", "text": "Additional methods of looking for occult blood are being explored, including  transferrin  dipstick [ 48 ]  and stool  cytology . [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4063", "text": "The estimates for test performance characteristics are based on comparison with a variety of  reference methods  including 51-chromium studies, [ citation needed ]  analytical recovery studies in spiked stool samples, analytical recovery after ingestion of autologous blood, rarer studies of carefully quantified blood instilled at bowel surgery  [ citation needed ] , as well as other research approaches. [ citation needed ]  Additionally, clinical studies look at a variety of additional factors."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4064", "text": "In healthy people about 0.5 to 1.5 \u00a0 ml of blood escapes blood vessels into the stool each day. [ 50 ] [ 51 ] [ 52 ]  Significant amounts of blood can be lost without producing visible blood in the stool, estimated as 200 \u00a0 ml in the stomach, [ 53 ]  100 \u00a0 ml in the duodenum, and lesser amounts in the lower intestine. Tests for occult blood identify lesser blood loss."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4065", "text": "Fecal immunochemical testing (FIT) can identify as little as 0.3 \u00a0 ml of daily blood in the stool; yet this test threshold does not cause undue false positives from normal upper intestinal blood leakage because it does not detect occult blood from the stomach and upper small intestine. Thus, the FIT test is much more specific for bleeding from the colon or lower gastrointestinal tract than alternatives. [ 54 ]  The detection rate of the test decreases if the time from sample collection to laboratory processing is delayed; processing the sample in under five days from collection is recommended. [ 55 ]  It does not appear to be affected by aspirin, anticoagulants, or nonsteroidal anti-inflammatory drugs. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4066", "text": "Stool guaiac test  for fecal occult blood (gFOBT) sensitivity varies depending on the site of bleeding. Moderately sensitive gFOBT can pick up a daily blood loss of about 10 \u00a0 ml (about two teaspoonfuls), and higher sensitivity gFOBT can pick up lesser amounts, requires at least 2 \u00a0 ml to become positive. The sensitivity of a single-stool guaiac test to pick up bleeding has been quoted at 10 to 30%, but if a standard three tests are done as recommended the sensitivity rises to 92%. [ 57 ]  Reduced patient compliance with the collection of three samples hampers the usefulness of this test. Further discussion of sensitivity and specificity issues that relate particularly to the guaiac method is found in the  stool guaiac test  article."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4067", "text": "Fecal  porphyrin  quantification by HemoQuant can yield a  false positive  result due to exogenous blood and various porphyrins. HemoQuant is the most sensitive test for upper gastrointestinal bleeding and therefore may be most appropriate fecal occult blood test to use in the evaluation of iron deficiency. [ 58 ]  It is advisable to stop ingesting red meat and aspirin for three days prior to specimen collection. [ 59 ]  False positives can occur with myoglobin, catalase, or protohemes [ 60 ]  and in certain types of porphyria. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4068", "text": "Fecal DNA tests as of 2008 had not been studied enough to support widespread use. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4069", "text": "Safety regulations from US accreditor  the Joint Commission  may have unintentionally decreased digital rectal examination and FOBT in hospital settings such as Emergency Departments. [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4070", "text": "In  medicine , the  fluid wave test  or  fluid thrill test  is a test for  ascites  (free fluid in the peritoneal cavity). It is performed by having the patient (or a colleague) push their hands down on the midline of the abdomen. The examiner then taps one flank, while feeling on the other flank for the tap. The pressure on the midline prevents vibrations through the abdominal wall while the fluid allows the tap to be felt on the other side.\nThe result is considered positive if tap can be felt on the other side. However, even with the midline pressure, transmission through the skin must be excluded.\nA positive fluid wave test indicates that there is a free fluid (ascites) in the abdomen. When one side of the abdomen is pressed, the other side may also be painful due to the transfer of the fluid in it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4071", "text": "Forrest classification  is a classification of  upper gastrointestinal hemorrhage  used for purposes of comparison and in selecting patients for  endoscopic treatment . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4072", "text": "Acute hemorrhage"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4073", "text": "Signs of recent hemorrhage"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4074", "text": "Lesions without active bleeding"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4075", "text": "Forrest's classification is instrumental when stratifying patients with upper gastrointestinal hemorrhage into high and low risk categories for  mortality . It is also a significant method of prediction of the risk of rebleeding and very often is used for evaluation of the\nendoscopic intervention modalities. [ 3 ]  A prospective  controlled study  revealed that \"Forrest criteria are essential for proper planning of endoscopic therapy and urgent surgery in bleeding peptic ulcers\". [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4076", "text": "The classification was first published by J.A. Forrest,  et al.  in the  Lancet  in 1974. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4077", "text": "Functional Lumen Imaging Probe  ( FLIP ) is a test used to evaluate the function of the  esophagus , by measuring the dimensions of the esophageal lumen using  impedance   planimetry . Typically performed with sedation during  upper endoscopy , FLIP is used to evaluate for  esophageal motility disorders , such as  achalasia ,  diffuse esophageal spasm , etc. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4078", "text": "FLIP is most often performed immediately following upper endoscopy (EGD). [ 1 ]  EGD helps to rule out a mechanical obstruction as a cause for symptoms, and also provides an estimation on the distance from the incisors to the EGJ. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4079", "text": "FLIP uses impedance planimetry to measure the cross sectional area of the esophageal lumen. [ 1 ]  The FLIP device consists of a balloon that encases a catheter with multiple pairs of impedance electrodes. Two catheter configurations are available, which are 8\u00a0cm and 16\u00a0cm in length. The 8\u00a0cm catheter includes 16 sensors spaced 0.5\u00a0cm apart, and is used to evaluate esophagogastric junction (EGJ) distensibility and CSA. [ 1 ]  Alternatively, the 16\u00a0cm catheter has 16 sensors spaced 1\u00a0cm apart, and may be used to evaluate contractility via secondary peristalsis patterns, in addition to evaluating the esophagogastric junction (EGJ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4080", "text": "Following upper endoscopy, the balloon is inserted into the esophagus and the balloon is distended with a fluid with known properties (e.g. conductivity and volume). [ 1 ]  Each electrode then measures impedance, and a single pressure sensor at the end of the device measures pressure within the balloon. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4081", "text": "The distensibility index (DI) is the most studied and most helpful result obtained with FLIP testing. [ 1 ]  The normal DI ranges from 3.1 to 9.0 mm2 per mmHg. [ 1 ]  As the balloon is distended, the results of secondary esophageal secondary contractions may be seen via FLIP panometry. [ 1 ]  Possible results may include: repetitive anterograde contractions (a normal finding), repetitive retrograde contractions (abnormal), absent contractility, and other abnormalities. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4082", "text": "FLIP may be used for several indications to evaluate esophageal symptoms, such as dysphagia, chest pain, or regurgitation, or to assess response to treatment. FLIP is used to evaluate for esophageal motility disorders, such as  achalasia ,  diffuse esophageal spasm , etc. [ 1 ]  FLIP may be used as a complementary or alternative to esophageal manometry for evaluating esophageal outflow obstructive disorders, including achalasia. FLIP may be used as a complementary test for barium esophagram for evaluating esophageal outflow obstructive disorders. FLIP may be used to assess the effect of treatment for achalasia. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4083", "text": "FLIP is recommended to further evaluate suspected  esophagogastric junction outflow obstruction  (EGJOO) where the manometry is normal or borderline. [ 2 ]  FLIP measurements may be used to guide intraoperative reflux surgery, or to assess the degree of fibrostenotic disease from eosinophilic esophagitis. [ 1 ] [ 3 ]  FLIP may be used to guide endoscopic dilation of esophageal strictures. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4084", "text": "While recommendations exist for its use, the evidence supporting the use of FLIP is of very low quality and further research would be useful in more clearly defining its role. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4085", "text": "Early development of impedance planimetry for evaluating the gastrointestinal tract began in the 1980s. [ 6 ]  FLIP was first developed with a short balloon catheter, which measures distension across the esophagogastric junction. [ 7 ]  A second generation device was later released, which measures secondary peristalsis proximal to the EGJ. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4086", "text": "Given Imaging Ltd.  ( Hebrew : \u05d2\u05d9\u05d5\u05d5\u05df \u05d0\u05d9\u05de\u05d2'\u05d9\u05e0\u05d2) is an Israeli  medical technology  company that manufactures and markets diagnostic products for the visualization and detection of disorders of the  gastrointestinal tract . Until March 2014, it was  dual-listed  on both the  NASDAQ  and the  Tel Aviv Stock Exchange , where it was a component of the  TA-100 Index  and the  TA BlueTech Index . In March 2014 it was acquired by  Covidien  and became a private company. In 2015  Covidien  was purchased by  Medtronic ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4087", "text": "Given Imaging pioneered the  capsule endoscopy  technology and has also developed capsule-based pH monitoring. [ 1 ]  Through Sierra Scientific Instruments, a subsidiary, Given Imaging also provides an array of diagnostic modalities including high-resolution manometry and ambulatory reflux monitoring. Given Imaging's technology is currently marketed in over 60 countries."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4088", "text": "Given Imaging was founded in 1998 by Gavriel Meron and  Rafael Development Corporation  (RDC) Ltd. based on the purchase of an early patent from Rafael Advanced Defense Systems Ltd. Initial funding for the company was provided by  Elron Electronic Industries , Israel's leading technology holding company, in cooperation with Rafael. Today,  Elron  still holds 28% Given Imaging's shares. [ 2 ]  The idea for the solution was developed by Dr. Iddan, while working in the missile division of Rafael, where he envisioned that missile technology could be miniaturized to create a medical product. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4089", "text": "The company's first  capsule endoscopy  products was named M2A capsule and received it  CE marking  in May 2001 and in August 2001 was cleared\nby the  US Food and Drug Administration  (FDA) for visualization of abnormalities of the small intestine [ 4 ]  The capsule uses a radio developed for Given by Zarlink Semiconductor's medical team in San Diego and Jarfalla, Sweden."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4090", "text": "In October 2001, Given Imaging had an  Initial public offering  on  NASDAQ  under ticker GIVN.) [ 5 ]  In September 2004, M2A capsule re-branded PillCam SB(R)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4091", "text": "In March 2004, Given Imaging became a member of the  Tel Aviv Stock Exchange [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4092", "text": "In November 2004, US FDA clears PillCam(R) ESO for the esophagus"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4093", "text": "In May 2006, US FDA clears Agile Patency System [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4094", "text": "In October 2006, PillCam COLON was cleared for marketing in the European Union (CE Mark) [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4095", "text": "In December 2008, Given Imaging acquired Bravo pH Monitoring System(R)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4096", "text": "In May 2009, 1 millionth PillCam capsule was sold [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4097", "text": "In September 2009, PillCam COLON 2 receives CE Mark [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4098", "text": "In July 2012, Given Imaging's  capsule endoscopy  featured in a live broadcast on the  BBC , when the reporter Michael Mosley spent the day as an exhibit at  the Science Museum  in London, after swallowing a PillCam which transmitted live pictures to a public screen. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4099", "text": "In February 2014, 100% of Given Imaging's shares were purchased by  Covidien , making it a  Private Company  fully owned by Covidien. As a result, its shares are no longer traded neither in NASDAQ nor in TASE [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4100", "text": "In 2015  Covidien  was purchased by  Medtronic"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4101", "text": "PillCam SB is a tool for visualization of the entire small bowel and detection of small bowel abnormalities.  No sedation is needed, however bowel prep is needed. A liquid bowel prep is consumed before the procedure emptying the bowel completely, this allows clear photos to be taken. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4102", "text": "PillCam ESO provides a method for visualization of the esophagus. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4103", "text": "PillCam COLON 2 is complementary to traditional colonoscopy and is used for patients who have received incomplete colonoscopy, are contraindicated for colonoscopy or are unwilling to undergo traditional colonoscopy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4104", "text": "The PillCam CROHN\u2019S system offers direct visualization of the entire small bowel and colonic mucosa with a noninvasive procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4105", "text": "In May 2010, Given Imaging released a new manually guided GI scope based on PillCam swallowable devices. In cases where patient anatomy does not allow for natural passage of large tablets the size of traditional PillCams, the PillCam Express can be delivered through the stomach and into the small intestine with help of an endoscope and a proprietary balloon deployment mechanism. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4106", "text": "The Bravo pH Monitoring System is a catheter-free ambulatory pH test. [ 16 ]   Ambulatory pH testing is considered the gold standard for pH measurement and monitoring of gastric reflux, helping clinicians manage gastroesophageal reflux disease (GERD).  Featuring data collection for up to 96 hours, Bravo allows patients to maintain their regular diets and activities, accurately reflecting normal physiologic conditions. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4107", "text": "In April 2010, Given Imaging acquired Sierra Scientific Instruments. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4108", "text": "The company's corporate headquarters, research and development laboratories, and manufacturing facilities are located in  Yokneam , Israel. [ 18 ] [ 19 ]  It maintains offices in  Duluth, Georgia  and  Heerlen ,  Netherlands . Additional sales and marketing offices are located in  France ,  Japan ,  Australia , and  Singapore . The company also has a plant in  Ireland . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4109", "text": "Given Imaging's wholly owned subsidiary, Sierra Scientific Instruments, is located in  Los Angeles , California, with manufacturing operations in Vietnam. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4110", "text": "The  Glasgow-Blatchford bleeding score  ( GBS ) is a  screening tool  to assess the likelihood that a person with an acute  upper gastrointestinal bleeding  (UGIB) will need to have medical intervention such as a  blood transfusion  or  endoscopic  intervention. [ 1 ]  The tool may be able to identify people who do not need to be admitted to hospital after a UGIB. Advantages of the GBS over the  Rockall score , which assesses the risk of death in UGIB, include a lack of  subjective  variables such as the severity of systemic diseases and the lack of a need for  oesophagogastroduodenoscopy  (OGD) to complete the score, a feature unique to the GBS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4111", "text": "It was developed in 2000 by Oliver Blatchford (born 24 August 1954) at the  Glasgow Royal Infirmary ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4112", "text": "In a controlled study, 16% of people presenting with UGIB had a GBS score of \"0\", considered low. Among this group there were no deaths or interventions needed and people were able to be effectively treated in an outpatient setting. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4113", "text": "The score is calculated using the table below:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4114", "text": "In the validation group, scores of 6 or more were associated\nwith a greater than 50% risk of needing an intervention."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4115", "text": "Score is equal to \"0\" if the following are all present: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4116", "text": "Klemm's sign , also known as  air cushion sign , [ 1 ]  is a sign of chronic appendicitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4117", "text": "A  lower gastrointestinal series  is a medical procedure used to examine and diagnose problems with the human  colon  of the  large intestine .  Radiographs  ( X-ray  pictures) are taken while  barium sulfate , a  radiocontrast agent , fills the colon via an  enema  through the  rectum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4118", "text": "The term  barium enema  usually refers to a lower gastrointestinal series, although enteroclysis (an  upper gastrointestinal series ) is often called a small bowel barium enema."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4119", "text": "For any suspected large bowel disease,  colonoscopy  is the investigation of choice because tissue sample can be taken for investigation.  Virtual colonoscopy  (also known as CT colonography) is another preferred investigation, provided that facilities and expertise are available. Virtual colonoscopy also avoids the risk of total blockage of any stricture in the large bowel due to barium impaction. [ 1 ]  Some conditions are absolutely contraindicated for barium enema namely:  toxic megacolon ,  pseudomembranous colitis , and recent history rigid endoscopy of the large bowel in the past five days and recent history of flexible endoscopy in the past 24 hours. This is because, rigid endoscopy tends to use larger biopsy forceps to take tissue samples from the bowel wall while flexible endoscopy uses small biopsy forceps to take superficial samples. [ 1 ]  For those with incomplete bowel preparation, the subject can return the next day or the day after next to repeat the procedure. If barium meal was performed recently, then it is advised to wait for another seven to ten days before repeating the procedure. Some frail subject may not be suitable for barium meal. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4120", "text": "Barium enemas are most commonly used to check bowel health; they can help diagnose and evaluate the extent of inflammatory bowel diseases such as  ulcerative colitis  and  Crohn's disease .   Polyps  can be seen, though not removed during the exam like with a  colonoscopy \u2014they may be cancerous. Other problems such as  diverticulosis  (small pouches formed on the colon wall that can become inflamed) and  intussusception  can be found (and in certain cases the test itself can treat intussusception).  An acute  appendicitis  or twisted loop of the bowel may also be seen. If the picture is normal a functional cause such as  irritable bowel syndrome  (IBS) may be considered."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4121", "text": "In a healthy colon, barium should fill the colon uniformly and show normal bowel contour, patency (should be freely open), and position."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4122", "text": "Additional conditions under which the test may be performed:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4123", "text": "Barium enema can be done in two ways, namely  double contrast  and single contrast methods. Double contrast (where air is inflated into the bowel after excess barium are drained through anus) is useful in visualising mucosal pattern. For single contrast study (whole bowel is filled up with barium without inflating any air), it is used to visualise any obstruction in the large bowel, and it is used in children where visualisation of mucosal pattern is not needed. Barium enema is also used to reduce an  intussusception  where this disorder is more commonly found in children. [ 1 ]  500 ml of Polibar 150% ( barium sulfate suspension ) is used to perform this study. Subject should be fasted and Picolax ( sodium picosulfate ) is taken orally to empty the bowels before barium enema procedure. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4124", "text": "This test may be done in a hospital or clinic. The individual lies on the X-ray table and a preliminary X-ray is taken. The individual is then asked to lie on their side while a well lubricated  enema  tube is inserted into the  rectum . As the enema enters the body, the individual might have the sensation that they need to have a bowel movement. The barium sulfate, a  radiodense  (shows as white on X-ray)  contrast medium , flows through the rectum into the  colon . A large balloon at the tip of the enema tube may be inflated to help keep the barium sulfate inside. The flow of the barium sulfate is monitored by the health care provider on an X-ray  fluoroscope  screen (like a TV monitor). Air may be puffed into the colon to distend it and provide better images (often called a \"double-contrast\" exam). If air is used, the enema tube will be reinserted if it had been removed and a small amount of air will be introduced into the colon, and more X-ray pictures are taken."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4125", "text": "The individual is usually asked to move to different positions and the table is slightly tipped to get different views."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4126", "text": "If there is a suspected  bowel perforation , a water-soluble  contrast agent  (such as  diatrizoate ) is used instead of barium.  The procedure is otherwise very similar, although the images will be of poorer quality. If a perforation exists, the contrast will leak from the bowel to the  peritoneal cavity ; water-soluble material is less obscuring compared to barium should  an abdominal incision  to remove the contrast be necessary."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4127", "text": "Assume that the x-ray tube is moving above the table and the x-ray film is moving below the table (overcouch): [ 1 ] \nThe subject lying supine to give AP (anteroposterior) view of all the bowels. [ 1 ] \nLeft lateral view of rectum is to view the rectum from lateral position. [ 1 ] \nRight anterior oblique (RAO) position is to view the caecum, ascending colon, right hepatic flexure and sigmoid colon without overlapping of other bowels. [ 1 ] \nLeft anterior oblique (LAO) position is to view the splenic flexure without overlapping of other bowels. [ 1 ] \nLeft posterior oblique (LPO) position is to view the sigmoid colon without overlapping of other bowels. [ 1 ] \nHampton's view (prone caudal view) of rectosigmoid colon is taken when the subject is in prone position with the X-ray tube tilted towards the feet at 30 degrees. This is to separate out the loops of sigmoid colon. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4128", "text": "Other views include right and left decubitus views [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4129", "text": "X-rays are monitored and regulated to provide the minimum amount of radiation exposure needed to produce the image. Most experts feel that the risk is low compared with the benefits. Pregnant women and children are more sensitive to the risks of ionizing radiation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4130", "text": "A more serious risk is a bowel perforation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4131", "text": "CT scans  and  ultrasounds  are now the tests of choice for the initial evaluation of abdominal masses, and colonoscopies are becoming the standard for routine colon screening for those over age 50 or with a familial history of polyps or colon cancer, although it is not uncommon for a barium enema to be done after a colonoscopy for further evaluation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4132", "text": "Narrow-band imaging  is an imaging technique for  endoscopic  diagnostic medical tests, where light of specific blue and green  wavelengths  is used to enhance the detail of certain aspects of the surface of the  mucosa . A special filter is electronically activated by a switch in the  endoscope  leading to the use of ambient light of wavelengths of 415\u00a0nm (blue) and 540\u00a0nm (green). [ 1 ] [ 2 ]  Because the peak light absorption of hemoglobin occurs at these wavelengths, blood vessels will appear very dark, allowing for their improved visibility and in the improved identification of other surface structures. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4133", "text": "In  gastrointestinal  endoscopy, narrow-band imaging has found use in the identification of  Barrett's esophagus , [ 3 ]  in the identification of pit patterns to classify colorectal  polyps  and  tumours , [ 4 ]  and in the identification of atypical  dysplastic  cells in the colon of patients with  ulcerative colitis . [ 5 ]  Also, in  cystoscopy , which is the examination of the  urinary bladder  with an  endoscope , narrow-band imaging is useful in differentiating between benign and malignant cells. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4134", "text": "Alternative methods to improve visualization of the mucosa in endoscopy include  chromoendoscopy ,  confocal microscopy  and  optical coherence tomography . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4135", "text": "The  non-lifting sign  is a finding on  endoscopic  examination that provides information on the suitability of large flat or sessile colorectal polyps for  polypectomy  by  endoscopic mucosal resection  (EMR). When fluid is injected under a polyp in preparation for endoscopic mucosal resection, some polyps do not \"lift\", indicating that the polyp is not separating from the  submucosa . This makes polypectomy more technically difficult, and increases the risk of  intestinal perforation  if polypectomy is then attempted. It is also thought to be indicative of an early colorectal cancer that has invaded the submucosa significantly (sm3 \u2013 invasion down to the lower one-third of the submucosa), which would make surgical removal of the tumour preferable to allow complete removal of the cancer. Consequently, the non-lifting sign is generally considered to be a  contraindication  to performing endoscopic mucosal resection. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4136", "text": "The non-lifting sign was first described in 1994 by Yoshiharu Uno and Akihiro Munakata of the Hirosaki University School of Medicine, Japan. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4137", "text": "In 1999 the same team showed that the presence of a non-lifting sign correlated with the depth of invasion of the submucosa by early colorectal cancers that were being considered for endoscopic resection. [ 3 ]  The tumours which did lift when fluid was injected were found to be less invasive than those that did not (sm1 or sm2 - invasion confined to the upper two-thirds of the submucosa, with at least 1mm of uninvolved submucosa underneath). It is thought that the non-lifting sign is due to fibrosis around the tumour causing tethering of the tumour to the  muscularis mucosae ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4138", "text": "Subsequent research suggested that the non-lifting sign is less accurate in determining depth of tumour invasion than the assessment of tumours by the endoscopist, but still suggests that the presence of the sign makes endoscopic resection technically difficult. [ 4 ]  However, more recently it has been found that fibrosis may be caused when a tumour is biopsied before endoscopic mucosal resection is attempted, which leads to a false positive non-lifting sign and therefore reduces the apparent accuracy of the sign. [ 1 ]  The authors, therefore, recommended avoidance of biopsy of the lesions if EMR is to be attempted, and if biopsies have been taken the time before EMR is attempted should be minimised."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4139", "text": "The Ottawa Bowel Preparation Scale  is used to assess a patient's bowel preparation for  colonoscopies . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4140", "text": "The scale assesses three components of the large intestine: (1) the  rectosigmoid colon , (2) the mid colon and (3) the right colon. A maximum score of 4 is used for each section of the  large intestine . A score of 0 is given if the bowel preparation is excellent, meaning the mucosal detail is visible, there is no fluid and almost no stool. A score of 1 is given if the bowel preparation is good, meaning there is turbid fluid/stool but the  mucosa  is visible and wash/suction is not needed. A score of 2 is given if the bowel preparation is fair, meaning there is fluid/stool obscuring the mucosa, suction is needed but wash is not needed. A score of 3 is given if the bowel preparation is poor, meaning that stool obscures the mucosa and suctioning/washing only provides an OK mucosa view. A score of 4 is given if the bowel preparation is inadequate, meaning that stool obscures the mucosa despite major washing/suctioning. The total score is calculated by adding up all 3 scores. The scale has a range from 0 (perfect) to 14 (solid stool in each section and lots of fluid, i.e., a completely unprepared colon). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4141", "text": "Other validated preparation scales are the Aronchick Scale and the Boston Bowel Preparation Scale. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4142", "text": "In medicine, the  poppy seed test  is a  diagnostic test  used before surgery to predict if surgery will find a  vesicointestinal fistula  or  colovesical fistula  (an abnormal direct pathway between the  colon  and  urinary bladder ) or other type of  vesicointestinal fistula ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4143", "text": "The test is very simple. The patient is fed 1.25 ounces of  poppy seeds  with 12 ounces of fluid or 6 ounces of yogurt. The patient's  urine  is then collected for the next 48 hours and examined for poppy seeds. If a poppy seed is found in the urine, the patient has a colovesical or related fistula. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4144", "text": "The test is very accurate.  In a series of 49 patients who underwent surgery for colovesical fistula due to  sigmoid diverticulitis , the poppy seed test gave a correct diagnosis more often than abdominopelvic computerized tomography, magnetic resonance tomography of the abdomen, cystogram, retrograde colonic enema, urethrocystoscopy, and colonoscopy. [ 2 ]   In a series of 20 patients in the  United States , the poppy seed test was significantly more accurate than  computed tomography . [ 3 ]   In these two series, respectively,  sensitivity  of the test was 94.6% and 100%.  Because of the physical nature of the test,   specificity  of the test is necessarily 100%. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4145", "text": "The test is very inexpensive.  In the United States it has been reported to cost under 6 dollars and two  orders of magnitude  less than computed tomography. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4146", "text": "The test was first described in the  English  medical literature in 2001, by a group of  urologists  in  Germany .  From 1994 to 1999, they gave 250 grams (8.8\u00a0oz) of poppy seeds to a series of 17 patients, then examined the patients' urine for two days.  The test results were correct for all patients:  11 patients with fistulas did pass poppy seeds in their urine and 6 patients without fistulas did not pass poppy seeds. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4147", "text": "Pouchoscopy  is a minimally invasive  endoscopic  procedure to examine an  ileo-anal pouch , a replacement for the  colon  /  rectum  which is surgically created from the  small intestine  (ileum) as treatment for  ulcerative colitis , a preventive measure in certain genetic illnesses such as  FAP  or  HNPCC  or as a procedure in the treatment of  colon cancer . Typically, a  fiber optic camera  on a flexible tube is passed through the  anus . Pouchoscopy is the first line test to evaluate pouch dysfunction, and is used for surveillance in individuals with genetic cancer syndromes (FAP). [ 1 ]  While pouchoscopy may help assess the integrity of the  J-pouch  (hence the name pouchoscopy), this evaluation is more commonly completed using a pouchogram (a necessary step in preparing for reversal of the temporary  ileostomy , or takedown surgery). A pouchoscopy is normally part of a routine follow up and is used to confirm the diagnosis of  pouchitis  and  cuffitis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4148", "text": "The  Ranson criteria  form a  clinical prediction rule  for predicting the prognosis and mortality risk of  acute pancreatitis . They were introduced in 1974 by the  English - American   pancreatic  expert and  surgeon  Dr. John Ranson (1938\u20131995). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4149", "text": "A score of 3 or more indicates severe acute pancreatitis. This can cause  organ failure ,  necrosis , infected necrosis,  pseudocyst , and  abscess . If diagnosed with severe acute pancreatitis, people will need to be admitted to a  high-dependency unit  or  intensive care unit ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4150", "text": "At admission:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4151", "text": "Within 48 hours:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4152", "text": "Alternatively, pancreatitis severity can be assessed by any of the following: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4153", "text": "Or"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4154", "text": "Digital rectal examination  (DRE), also known as a  prostate exam  ( Latin :  palpatio per anum (PPA) ,  lit. \u2009 'palpation through the anus'), is an internal examination of the  rectum  performed by a  healthcare provider ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4155", "text": "Prior to a 2018 report from the  United States Preventive Services Task Force , a digital exam was a common component of  annual exams  for older men, as it was thought to be a reliable  screening test  for  prostate cancer . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4156", "text": "This examination may be used:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4157", "text": "The digital rectal examination is a relatively simple medical procedure. The patient undresses and is then placed in a position where the  anus  is accessible (lying on the side,  squatting  on the examination table, bent over it, or lying down with feet in stirrups). If the patient is lying on their side, the physician will usually have them bring one or both legs up to their chest. If the patient bends over the examination table or the back of a chair, the physician will have them place their elbows on the table and squat down slightly. If the patient uses the supine position, the physician will ask the patient to slide down to the end of the examination table until their buttocks are positioned just beyond the end and then place their feet in the stirrups. The physician spreads the buttocks apart and will usually examine the external area (anus and perineum) for any abnormalities such as  hemorrhoids , lumps, or rashes. Then, as the patient relaxes and bears down (as if having a bowel movement), the physician slips a lubricated finger into the rectum through the anus and palpates the insides for a short time. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4158", "text": "Due to the taboos surrounding the anus and the potential for discomfort and embarrassment, the rectal exam is a common  comedic device , including in episodes of  Saturday Night Live , [ 30 ]   Impractical Jokers ,  Futurama ,  Family Guy ,  South Park ,  Letterkenny , and the movie  Fletch , with  M. Emmet Walsh  as the general practitioner and  Chevy Chase  as the patient being examined. Similar activities to the rectal exam are attributed to extraterrestrials in video games such as  Saints Row IV ,  Gaia Online  and  Destroy All Humans! . [ 31 ]  The practice of rectal exams without prior consent by medical students has been an area of concern. [ 32 ]  In 2024, the US  Department of Health and Human Services  banned  rectal examination (and pelvic and breast exams) without written informed consent, when such exams are done by medical students, nurse practitioners, or physician assistants for  \u201ceducational and training purposes\u201d. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4159", "text": "In  veterinary medicine  rectal examination is useful in  dogs  for analysis of the  prostate  (as in men), pelvic  urethra , sublumbar  lymph nodes , and  anal glands . In  horses  it is a vital component of the clinical examination for  colic , to determine the presence or absence of bowel torsion,  impaction , or displacement. When horses undergo a rectal examination there is a small risk of a  rectal  tear occurring, which can be a life-threatening event, rapidly leading to  peritonitis  and  septic shock . It is also a common procedure in cattle, and is one method of diagnosing pregnancy in both the horse and the cow. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4160", "text": "The procedure in dogs and cats is similar to humans. For the horse, the patient stands in a  stock  and may be sedated. The examiner puts on a  long glove  that extends to the shoulder. The examiner inserts the hand and arm into the rectum as far as necessary. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4161", "text": "Reynolds' pentad  is a collection of signs and symptoms consistent with obstructive  ascending cholangitis , a serious infection of the  biliary tract . It is a combination of  Charcot's triad  ( right upper quadrant  pain,  jaundice , and  fever ) with  shock  ( low blood pressure ,  tachycardia ) and an  altered mental status . [ 1 ]  Sometimes the two additional signs are listed simply as  low blood pressure  and  confusion . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4162", "text": "It was named after surgeon  Benedict Reynolds , who described it (along with Everett Dargan) in 1959. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4163", "text": "Rockall risk scoring system   attempts to identify patients at risk of adverse outcome following acute  upper gastrointestinal bleeding . Rockall  et al.  identified independent risk factors [ 1 ]  in 1996 which were later shown to predict mortality accurately. The scoring system uses clinical criteria (increasing age, co-morbidity, shock) as well as endoscopic finding (diagnosis, stigmata of acute bleeding). It is named for Professor Tim Rockall, who was the main investigator and first author of the studies that led to its formulation. A convenient mnemonic is ABCDE - i.e. Age, Blood pressure fall (shock), Co-morbidity, Diagnosis and Evidence of bleeding. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4164", "text": "Total score is calculated by simple addition. A score less than 3 carries good prognosis but total score more than 8 carries high risk of mortality. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4165", "text": "The  Schilling test  was a medical investigation used for patients with  vitamin B 12  (cobalamin) deficiency. [ 1 ]  The purpose of the test was to determine how well a patient is able to absorb B12 from their intestinal tract.  The test is now considered obsolete and is rarely performed, and is no longer available at many medical centers.  It is named for  Robert F. Schilling . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4166", "text": "The Schilling test has multiple stages. [ 3 ]  As noted below, it can be done at any time after vitamin B 12  supplementation and body store replacement, and some clinicians recommend that in severe deficiency cases, at least several weeks of vitamin repletion be done before the test (more than one B 12  shot, and also oral folic acid), in order to ensure that impaired absorption of B 12  (with or without intrinsic factor) is not occurring due to damage to the intestinal mucosa from the B 12  and folate deficiency themselves."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4167", "text": "In the first part of the test, the patient is given  radiolabeled  vitamin B 12  to drink or eat. The most commonly used radiolabels are  57 Co and  58 Co . An  intramuscular  injection of unlabeled vitamin B 12  is given an hour later. This is not enough to replete [ clarification needed ]  or saturate body stores of B 12 . The purpose of the single injection is to temporarily saturate B 12  receptors in the liver with enough normal vitamin B 12  to prevent radioactive vitamin B 12  binding in body tissues (especially in the liver), so that if absorbed from the G.I. tract, it will pass into the urine. The patient's urine is then collected over the next 24 hours to assess the absorption."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4168", "text": "Normally, the ingested radiolabeled vitamin B 12  will be absorbed into the body. Since the body already has liver receptors for  transcobalamin /vitamin B 12  saturated by the injection, much of the ingested vitamin B 12  will be  excreted  in the urine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4169", "text": "The normal test will result in a higher amount of the radiolabeled cobalamin in the urine because it would have been absorbed by the intestinal epithelium, but passed into the urine because all hepatic B12 receptors were occupied. An abnormal result is caused by less of the labeled cobalamin to appear in the urine because it will remain in the intestine and be passed into the feces."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4170", "text": "If an abnormality is found, i.e. the B12 in the urine is only present in low levels, the test is repeated, this time with additional oral  intrinsic factor ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4171", "text": "This stage is useful for identifying patients with  bacterial overgrowth syndrome . The physician will provide a course of 2 weeks of antibiotics to eliminate any possible bacterial overgrowth and repeat the test to check whether radio-labeled Vitamin B12 would be found in urine or not."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4172", "text": "This stage, in which  pancreatic enzymes  are administered, can be useful in identifying patients with  pancreatic insufficiency . The physician will give 3 days of pancreatic enzymes followed by repeating the test to check if radio-labeled Vitamin B12 would be detected in urine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4173", "text": "In some versions of the Schilling test, B 12  can be given both with and without intrinsic factor at the same time, using different cobalt radioisotopes  57 Co and  58 Co, which have different radiation signatures, in order to differentiate the two forms of B 12 . This is performed with the 'Dicopac' kitset. This allows for only a single radioactive urine collection. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4174", "text": "Note that the B 12  shot which begins the Schilling test is enough to go a considerable way toward treating B 12  deficiency, so the test is also a partial  treatment  for B 12  deficiency. Also, the classic Schilling test can be performed at any time, even after full B 12  repletion and correction of the anemia, and it will still show if the cause of the B 12  deficiency was intrinsic-factor related. In fact, some clinicians have suggested that folate and B 12  replacement for several weeks be normally performed  before  a Schilling test is done, since folate and B 12  deficiencies are both known to interfere with intestinal cell function, and thus cause malabsorption of B 12  on their own, even if intrinsic factor is being made. This state would then tend to cause a false-positive test for both simple B 12  and intrinsic factor-related B 12  malabsorption. Several weeks of vitamin replacement are necessary, before epithelial damage to the G.I. tract from B 12  deficiency is corrected."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4175", "text": "Many labs have stopped performing the Schilling test, [ 5 ]  due to lack of production of the cobalt radioisotopes and labeled-B 12  test substances. Also, injection replacement of B 12  has become relatively inexpensive, and can be self-administered by patients, as well as megadose oral B 12 . Since these are the same treatments which would be administered for most causes of B 12  malabsorption even if the exact cause were identified, the diagnostic test may be omitted without damage to the patient (so long as follow-up treatment and occasional serum B 12  testing is not allowed to lapse)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4176", "text": "It is possible for use of other radiopharmaceuticals to interfere with interpretation of the test. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4177", "text": "Sigmoidoscopy  (\"sigma\", the Greek term for letter \" s/\u03c2 \" + \"eidos\" + \"scopy\": namely, to look inside an \"s\"/\"\u03c2\"-like object) is the  minimally invasive   medical  examination of the large  intestine  from the  rectum  through to the nearest part of the  colon , the  sigmoid colon . There are two types of sigmoidoscopy:  flexible sigmoidoscopy , which uses a flexible  endoscope , and  rigid sigmoidoscopy , which uses a rigid device. Flexible sigmoidoscopy is generally the preferred procedure. A sigmoidoscopy is similar to, but not the same as, a  colonoscopy . A sigmoidoscopy only examines up to the  sigmoid , the most distal part of the colon, while colonoscopy examines the whole large bowel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4178", "text": "Flexible sigmoidoscopy enables the  physician  to look at the inside of the large intestine from the rectum to the left side of the colon, called the sigmoid. Physicians may use the procedure to find the cause of  diarrhea ,  abdominal pain , or  constipation . They also use it to look for benign and malignant  polyps , as well as early signs of  cancer  in the descending colon and rectum. [ 1 ]  With flexible sigmoidoscopy, the physician can see  intestinal bleeding ,  inflammation , abnormal growths, and  ulcers  in the descending colon and rectum. Flexible sigmoidoscopy is not sufficient to detect polyps or cancer in the ascending or transverse colon (two-thirds of the colon). However, although in absolute terms only a relatively small section of the large intestine can be examined using sigmoidoscopy, the sites which can be observed represent areas which are most frequently affected by diseases such as  colorectal cancer , for example the  rectum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4179", "text": "For the procedure, the patient must lie on their side on the examining table. The physician inserts a short, flexible, lit tube into the rectum and slowly guides it into the colon. The tube is called a sigmoidoscope. The scope transmits an image of the inside of the rectum and colon, so the physician can carefully examine the lining of these organs. The scope also blows air into these organs, which inflates them in order to help the physician see better."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4180", "text": "If anything unusual is in the rectum or colon, like a polyp or inflamed tissue, the physician can remove a piece of it using instruments inserted into the scope. The physician will send that piece of tissue ( biopsy ) to the lab for testing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4181", "text": "Bleeding and puncture of the colon are possible complications of sigmoidoscopy. However, such complications are uncommon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4182", "text": "Flexible sigmoidoscopy takes 10 to 20 minutes. During the procedure, the patient might feel pressure and slight cramping in the lower abdomen, but the patient will feel better afterward when the air leaves the colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4183", "text": "The colon and rectum must be completely empty for flexible sigmoidoscopy to be thorough and safe, thus the patient must drink only clear liquids for 12 to 24 hours beforehand. This includes bouillon or  broth ,  gelatin , strained fruit  juice , water, plain  coffee , plain  tea , or diet  soft drinks ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4184", "text": "The night before or right before the procedure, the patient receives a  laxative  (e.g.  macrogol ,  lactulose  etc.) and/or an  enema , which is a liquid solution that washes out the intestines. \nNo sedation is required during this procedure as long as the examination does not exceed the level of the  splenic flexure ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4185", "text": "Rigid sigmoidoscopy may be useful in ano-rectal diseases such as bleeding per rectum or inflammatory rectal disease, particularly in the general practice and pediatrics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4186", "text": "For performing the examination, the patient must lie on the left side, in the so-called  Sims' position . The bowels are previously emptied with a  suppository , and a  digital rectal examination  is first performed. The sigmoidoscope is lubricated and inserted with  obturator  in general direction of the  navel . The direction is then changed and the obturator is removed so that the physician may penetrate further with direct vision. A  bellows  is used to insufflate air to distend the rectum. Lateral movements of the sigmoidoscope's tip negotiate the  Houston valve  and the  recto-sigmoid junction ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4187", "text": "Several studies have shown the potential benefits of sigmoidoscopy in detecting colorectal cancer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4188", "text": "In a 2009 Norwegian study, results were somewhat inconclusive at seven years. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4189", "text": "We found a trend towards reduced mortality from colorectal cancer for both total colorectal cancer mortality (27% reduction) and rectosigmoidal cancer mortality (37%), but this was not statistically significant in intention to screen analysis. Corresponding reductions in mortality among attenders (that is, the people actually screened, instead of just the ones in the group to be screened\u2014this data set may include selection bias) were 59% and 76%, both statistically significant compared with the control group[.] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4190", "text": "The study saw no detectable difference in all-cause mortality."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4191", "text": "A 2010 British study [ 3 ]  showed sigmoidoscopy reduced \"overall colorectal cancer incidence and mortality by 31 percent\", and \"incidence of cancer in just the lower part of the colon (or distal colon) was reduced by approximately 50 percent for those who underwent screening compared with those in the control group.\" [ 4 ] \nOverall colon-cancer mortality was reduced by 43% (thus preventing one cancer per 200 screenings, and one cancer death per 500 screenings).  The study also showed that the effect was persistent\u2014a single sigmoidoscopy reduced cancer rates for the length of the 11-year study."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4192", "text": "Although generally considered quite safe, sigmoidoscopy does carry the very rare possibility of tearing of the intestinal wall by the instrument, which could require immediate surgery to repair the tear; in addition, removal of a polyp may sometimes lead to localized bleeding which is resistant to cauterization by the instrument and must be stopped by surgical intervention. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4193", "text": "The  Sims position , or left lateral Sims position, named after the gynaecologist  J. Marion Sims , is usually used for  rectal examination , treatments,  enemas , and examining patients for  vaginal wall prolapse . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4194", "text": "The Sims Position is described as in the person lying on the left side, left hip and lower extremity straight, and right hip and knee bent. It is also called lateral recumbent position. [ 3 ]  Sims' position is also described as the person lying on the left side with both legs bent. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4195", "text": "The position is described as follows:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4196", "text": "Common uses:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4197", "text": "Steatocrit  or acid steatocrit is a simple, rapid  gravimetric  method to determine  steatorrhea . The test is simple, rapid, inexpensive, and reliable. It is a  qualitative test that can be used when other methods are impractical."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4198", "text": "An elevated steatocrit is indicative of fat malabsorption resulting in  steatorrhea . This generally results from pancreatic exocrine insufficiency but can also occur with severe small bowel disease i.e.  celiac disease , liver diseases such as  Primary Biliary Cirrhosis  or medications that inhibit fat absorption such as  orlistat ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4199", "text": "The  stool guaiac test  or  guaiac fecal occult blood test  ( gFOBT ) is one of several methods that detects the presence of  fecal occult blood [ 1 ]  ( blood  invisible in the  feces ). [ 2 ]  The test involves placing a fecal sample on  guaiac  paper (containing a phenolic compound, alpha-guaiaconic acid, extracted from the wood  resin  of  Guaiacum  trees) and applying hydrogen peroxide which, in the presence of blood, yields a blue reaction product within seconds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4200", "text": "The American College of Gastroenterology has recommended the abandoning of gFOBT testing as a colorectal cancer screening tool, in favor of the fecal immunochemical test (FIT). [ 3 ]   Though the FIT is preferred, even the guaiac FOB testing of average risk populations may have been sufficient to reduce the mortality associated with  colon cancer  by about 25%. [ 4 ]   With this lower efficacy, it was not always cost effective to screen a large population with gFOBT. [ 5 ] [ 6 ] [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4201", "text": "The stool guaiac test involves fasting from iron supplements, red meat (the blood it contains can turn the test positive), certain vegetables (which contain a chemical with peroxidase properties that can turn the test positive), and vitamin C and citrus fruits (which can turn the test falsely negative) for a period of time before the test. It has been suggested that cucumber, cauliflower and horseradish, and often other vegetables, should be avoided for three days before the test. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4202", "text": "In testing,  feces  are applied to a thick piece of paper attached to a thin film coated with guaiac.  Either the patient or medical professional smears a small fecal sample on to the film.  The fecal sample is obtained by catching the stool and transferring a sample with an applicator.  Digital rectal examination specimens are also used but this method is discouraged for colorectal cancer screening due to very poor performance characteristics. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4203", "text": "Both sides of the test card can be peeled open, to access the inner guaiac paper.  One side of the card is marked for application of the stool and the other is for the developer fluid. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4204", "text": "After applying the feces, one or two drops of  hydrogen peroxide  are then dripped on to the other side of the film, and it is observed for a rapid blue color change. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4205", "text": "When the hydrogen peroxide is dripped on to the guaiac paper, it oxidizes the alpha-guaiaconic acid to a blue colored  quinone . [ 11 ] [ 12 ]  Normally, when no blood and no peroxidases or catalases from vegetables are present, this oxidation occurs very slowly.  Heme, a component of hemoglobin found in blood, catalyzes this reaction, giving a result in about two seconds.  Therefore, a positive test result is one where there is a quick and intense blue color change of the film."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4206", "text": "The guaiac test can often be  false-positive  which is a positive test result when there is in fact no source of bleeding. This is particularly common if the recommended dietary preparation is not followed, as the heme in red meat or the peroxidase or catalase activity in vegetables, especially if uncooked, can cause analytical false positives."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4207", "text": "Vitamin C  can cause analytical  false negatives  due to its anti-oxidant properties inhibiting the color reaction. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4208", "text": "If the card has not been promptly developed, the water content of the feces decreases, and this can reduce the detection of blood. [ 15 ]  Although rehydration of stored samples can reverse this effect [ 16 ]  this is not recommended because the test becomes unduly analytically sensitive and thus much less specific. [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4209", "text": "Some stool specimens have a high bile content that causes a green color to show after applying the developer drops. If entirely green, such samples are negative, but if questionably green to blue, such samples are designated positive. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4210", "text": "The package insert guidelines from the manufacturers, for example Hemoccult SENSA, [ 20 ]  recommend that nonsteroidal anti-inflammatory drugs ( NSAID ), such as ibuprofen and aspirin, and iron supplements be discontinued for at least several days before the tests.  There is a concern that these agents may irritate the body and cause biologically positive tests even in the absence of a more substantial illness, [ 21 ] [ 22 ]  but there is some doubt about how frequently this occurs with NSAID medication. [ 23 ] [ 24 ] [ 25 ]  Although both iron and bismuth containing products such as antacids and antidiarrheals can cause dark stools that are occasionally confused as containing blood, actual bleeding from iron is unusual. [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4211", "text": "There is no consensus on whether to stop warfarin before a guaiac test. [ 28 ]  Even when using anticoagulants a high proportion of positive guaiac tests were found to be due to diagnosable lesions, suggesting anticoagulants may not cause bleeding unless there is an abnormality. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4212", "text": "The article  fecal occult blood  (FOB) provides an expanded consideration of the clinical application of FOB tests generally, including other clinical methods, and the comments here are those that relate specifically to the guaiac gFOBT method."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4213", "text": "One major use of stool testing for blood is detection of  colorectal cancer . However, other possible positive results include: gastroesophageal cancer, GI bleeds,  diverticulae ,  hemorrhoids ,  anal fissures ,  colon polyps ,  ulcerative colitis ,  Crohn's disease ,  celiac disease ,  GERD ,  esophagitis ,  peptic ulcers ,  gastritis ,  inflammatory bowel disease ,  vascular ectasias ,  portal hypertensive gastropathy ,  aortoenteric fistulas ,  hemobilia ,  endometriosis , and  trauma ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4214", "text": "The stool guaiac test was originally the principal colon cancer screening technology available, but modern tests which look for  globin  or DNA are now also available.  Several recent colon cancer screening guidelines have recommended replacing any older low-sensitivity, guaiac-based fecal occult blood testing (gFOBT) with either newer high-sensitivity guaiac-based fecal occult blood testing (gFOBT) or fecal immunochemical testing (FIT), which tests for  globin  rather than the  heme  detected by the guaiac method. The US Multisociety Task Force (MSTF) looked at 6 studies that compared high sensitivity gFOBT (Hemoccult SENSA) to FIT, and  concluded that there were no clear difference in overall performance between these methods, [ 31 ]  and a similar recommendation was made by the National Guideline Clearinghouse (NGC). [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4215", "text": "Results of a single fecal sample should be interpreted cautiously, as there is a high rate of false negativity associated with the test. [ 33 ] [ 10 ]  Using three cards, each on a different day, is recommended to improve sensitivity. [ 34 ]  The Centers for Disease Control and Prevention (CDC) in a 2006\u20132007 survey found extensive inappropriate use of low sensitivity gFOBT and of single specimens; it is unclear if these widespread suboptimal approaches have since declined. [ 35 ]   The Current Procedural Terminology (CPT) coding was changed in January 2006 to include CPT code 82270, which indicates that consecutive collection of three stool samples has occurred, either as three single cards or a single triple card. Since January 2007, the US Medicare program reimburses for colorectal cancer screening with gFOBT only when this code is used. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4216", "text": "The stool guaiac test method may be preferable to fecal immunochemical testing (FIT) if there is a clinical concern about possible gastric or proximal upper intestinal bleeding. [ 37 ]  However, although  heme  breakdown is less than  globin  during intestinal transit, false negative results can be seen with the stool guaiac tests due to degradation of the peroxidase-activity. This can cause false negative results in upper gastrointestinal bleeding sources, or in right colon adenomas and cancers that have comparable blood losses to positively testing left colon lesions. [ 38 ]  A positive gFOBT with subsequent negative colonoscopy may lead to an upper endoscopy. [ 39 ]  It is unclear whether this is an effective intervention if there is a positive gFOBT but no anemia. [ 40 ] [ 41 ] [ 42 ]  Endoscopy when there is a positive gFOBT along with iron deficiency anemia, or iron deficiency anemia on its own, has a higher rate of finding problems. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4217", "text": "String sign , or  gastrointestinal string sign  (also called string sign of Kantour), is a medical term for a radiographic finding on an  upper GI series , in which the patient is given a  radio-opaque  material, such as barium, to drink.    X-rays  are then taken of the patient's stomach and intestines."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4218", "text": "The gastrointestinal string sign represents a severe narrowing of loop of bowel, in which a thin stripe of contrast within the lumen looks like a string."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4219", "text": "It may be seen in  Crohn's disease ,  hypertrophic pyloric stenosis ,  carcinoid  tumor and  colon cancer . In people with Crohn's Disease, the string sign is caused by incomplete filling of the intestinal lumen, which results from irritability and spasm associated with severe ulceration. In such cases, the string sign is most frequently seen at the terminal ileum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4220", "text": "In infants with hypertrophic pyloric stenosis, the pylorus is narrowed and the radio-opaque material will take on the appearance of a thin string as it passes through this narrowed channel.  Often, there are several of these strings seen (called the \"railroad track sign\"). The use of the upper GI series for the diagnosis of HPS, which was the primary diagnostic tool for this condition in the 1980s and 1990s, has been largely replaced by the use of  ultrasound , which is less invasive and can visualize the thickened pylorus, giving actual measurements of this thickening."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4221", "text": "An  upper gastrointestinal series , also called a  barium swallow ,  barium study , or  barium meal , is a series of  radiographs  used to examine the  gastrointestinal tract  for abnormalities. A  contrast medium , usually a  radiocontrast agent  such as  barium sulfate  mixed with water, is ingested or instilled into the gastrointestinal tract, and  X-rays  are used to create radiographs of the regions of interest. The barium enhances the visibility of the relevant parts of the gastrointestinal tract by coating the inside wall of the tract and appearing white on the film. This in combination with other plain radiographs allows for the imaging of parts of the upper gastrointestinal tract such as the  pharynx ,  larynx ,  esophagus ,  stomach , and  small intestine  such that the inside wall lining, size, shape, contour, and patency are visible to the examiner. With  fluoroscopy , it is also possible to visualize the functional movement of examined organs such as  swallowing ,  peristalsis , or  sphincter  closure. Depending on the organs to be examined, barium radiographs can be classified into \"barium swallow\", \"barium meal\", \"barium follow-through\", and \"enteroclysis\" (\"small bowel enema\"). To further enhance the quality of images, air or gas is sometimes introduced into the gastrointestinal tract in addition to barium, and this procedure is called double-contrast imaging. In this case the gas is referred to as the negative contrast medium. Traditionally the images produced with barium contrast are made with plain-film radiography, but  computed tomography  is also used in combination with barium contrast, in which case the procedure is called \" CT enterography \". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4222", "text": "Various types of barium X-ray examinations are used to examine different parts of the gastrointestinal tract. These include barium swallow, barium meal, barium follow-through, and  barium enema . [ 2 ]  The barium swallow, barium meal, and barium follow-through are together also called an upper gastrointestinal series (or study), whereas the barium enema is called a  lower gastrointestinal series  (or study). [ 3 ]  In upper gastrointestinal series examinations, the barium sulfate is mixed with water and swallowed orally, whereas in the lower gastrointestinal series (barium enema), the barium  contrast agent  is administered as an  enema  through a small tube inserted into the  rectum . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4223", "text": "Barium X-ray examinations are useful tools for the study of appearance and function of the parts of the gastrointestinal tract. They are used to diagnose and monitor  esophageal reflux ,  dysphagia ,  hiatus hernia ,  strictures ,  diverticula ,  pyloric stenosis ,  gastritis ,  enteritis ,  volvulus ,  varices ,  ulcers ,  tumors , and gastrointestinal dysmotility, as well as to detect  foreign bodies . [ 3 ] [ 6 ]  Although barium X-ray examinations are increasingly being replaced by more modern techniques, such as  computer tomography ,  magnetic resonance imaging ,  ultrasound imaging ,  endoscopy  and  capsule endoscopy , [ 7 ]  barium contrast imaging remains in common use because it offers the advantages of greater affordability, wider availability, [ 1 ] [ 5 ]  and better resolution in assessing superficial mucosal lesions. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4224", "text": "Barium sulfate is swallowed and is a  radio opaque  substance that does not allow the passage of X-rays. As a result, areas coated by barium sulfate will appear white on an X-ray film. The passage of barium sulfate through the gastrointestinal tract is observed by a radiologist using a  fluoroscope  attached to a TV monitor. The radiologist takes a series of individual X-ray images at timed intervals depending on the areas to be studied. Sometimes medication which produces gas in the gastrointestinal tract is administered together with the Barium sulfate. This gas distends the gastrointestinal lumen, providing better imaging conditions and in this case the procedure is called double-contrast imaging. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4225", "text": "Clinical status and relevant medical history are reviewed prior to the studies. [ 10 ]   Patient consent  is required. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4226", "text": "A barium swallow study is also known as a  barium  esophagram  and needs little if any preparations for the study of the larynx, pharynx, and esophagus when studied alone. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4227", "text": "Amongst the uses of barium swallow are: persistent  dysphagia  and  odynophagia  despite negative  esophagogastroduodenoscopy  (OGDS) findings, failed OGDS,  esophageal motility disorder ,  globus pharyngis , assessment of  tracheoesophageal fistula , and timed barium swallow to monitor the progress of  esophageal achalasia  therapy. [ 13 ]   Barium sulfate suspension  such as 100 ml or more of E-Z HD 200 to 250% concentration and Baritop 100% can be used. Water-soluble contrast agent such as Gastrografin ( diatrizoate ) and Conray ( Iotalamic acid ) is used instead of barium if oesophageal perforation is suspected. Low osmolar contrast medium with concentration of 300\u00a0mg/ml is used instead of gastrografin if there is risk of  aspiration  or there is tracheoesophageal fistula. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4228", "text": "A thick barium mixture is swallowed in supine position and fluoroscopic images of the swallowing process are made. Then several swallows of a thin barium mixture are taken and the passage is recorded by fluoroscopy and standard radiographs. The procedure is repeated several times with the examination table tilted at various angles. A total of 350\u2013450\u00a0mL of barium is swallowed during the process. [ 14 ] [ 15 ]  Normally, 90% of ingested fluid should have passed into the stomach after 15 seconds. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4229", "text": "Right anterior oblique (RAO) view is to see the oesophagus clearly, away from overlapping spine. [ 13 ]  AP (anterior-posterior) view is also done to visualise the  gastroesophageal junction . [ 13 ]  AP and lateral views are also done to visualise the  hypopharynx  during swallowing at a frame rate of 3\u20134 per second. Left posterior oblique (LPO) position is used to identify hernias, mucosal rings, and varices. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4230", "text": "Intravenous injection of Buscopan ( Hyoscine butylbromide ) 20\u00a0mg or  glucagon  0.3\u00a0mg is used to distend the stomach and slow down the emptying of the contrast into the duodenum. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4231", "text": "Right anterior oblique (RAO) view is used to demonstrate antrum and greater curve of stomach. Supine position is to demonstrate antrum and body of stomach. Left anterior oblique (LAO) view is used to see the lesser curve of stomach en face. This position is also used to check for gastroesophageal reflux when patient is asked to cough or swallow (water siphon test). Left lateral tilted with head up 45 degrees is used to demonstrate the fundus of the stomach. [ 13 ]  To demonstrate the duodenal loop, the subject can lie down in prone position on a compression pad to prevent excessive barium flowing into the duodenal loop. Anterior view of duodenal loop can be seen at RAO position. [ 13 ]  Duodenal cap can be visualised by taking images when subject lie down in prone position, RAO, supine, and then LAO positions or it can be seen on erect position with RAO and steep LAO views. [ 13 ]  Total mucosal coating of the stomach is done by asking the subject to roll to the right side into a complete circle until RAO position. Arae gastriae in the antrum (fine reticular network of grooves) is visible if good coating is achieved. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4232", "text": "Indications to do this procedure are: unexplained chronic abdominal pain with weight loss, unexplained diarrhea, anemia which is caused by gastrointestinal bleeding or dependent on  blood transfusion  where the cause cannot be explained despite OGDS or colonoscopy investigations, partial obstruction of bowel/small bowel adhesive obstruction suspected, and unexplained  malabsorption  of nutrients. [ 13 ]  For barium follow-through examinations, a 6-hour period of fasting is observed prior to the study. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4233", "text": "Barium is administered orally, sometimes mixed with  diatrizoic acid  (gastrografin) to reduce transit time in the bowel. Intravenous  metoclopramide  is sometimes also added to the mixture to enhance gastric emptying. [ 17 ]  600 ml of 0.5% methylcellulose can be given orally, after barium meal is given, to improve the images of small bowel follow-through by reducing the time taken for barium to pass through the small intestines, and increase the transparency of the contrast-filled small bowels. [ 18 ]  Other methods to reduce transit time are to add ice cold normal saline after the administration of barium saline mixture [ 19 ]  or to give a dry meal. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4234", "text": "X-ray images are then taken in a supine position at intervals of 20\u201330 minutes. Real-time fluoroscopy is used to assess bowel motility. The radiologist may press or palpate the abdomen during images to separate intestinal loops. The total time necessary for the test depends on the speed of bowel motility or transit time and may vary between 1 and 3 hours. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4235", "text": "Enteroclysis is also known as small bowel enema. [ 21 ]  It has been largely replaced by  magnetic resonance enterography/enteroclysis [ 13 ]  and  computed tomography enterography/enteroclysis . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4236", "text": "In addition to fasting for 8 hours prior to examination, a  laxative  may also be necessary for bowel preparation and cleansing. [ 12 ]  The main aim of this study is to distend the proximal bowel through infusion of large amount of barium suspension. Otherwise, the distension of distal small bowel is generally similar with small bowel follow-through. Therefore, there is a need to pass a tube through the nose into the  jejunum  (nasojejunal tube) to administer large amount of contrast. This can be unpleasant to the subject, requires more staff, longer procedural time, and higher radiation dose when compared to small bowel follow-through. The indications for enteroclysis are generally similar to small bowel follow-through. Barium suspensions such as diluted E-Z Paque 70% and Baritop 100% can be used. After that, 600 ml of 0.5% methylcellulose is administered after 500 ml of 70% barium suspension is given. Bilbao-Dotter tube and Silk tube can be used to administer barium suspension. The subject should be fasted overnight, any  antispasmodic  drugs should be stopped one day before the examination, and  Tetracaine  lozenges can be used 30 minutes before the procedure to numb the throat for nasojejunal tube insertion. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4237", "text": "The filling of the small intestines can be viewed continuously using  fluoroscopy , or viewed as standard radiographs taken at frequent intervals. The technique is a double-contrast procedure that allows detailed imaging of the entire small intestine. However, the procedure may take 6 hours or longer to complete and is quite uncomfortable to undergo. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4238", "text": "Complete  gastrointestinal obstruction  is a contraindication for barium studies. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4239", "text": "Barium sulfate as a contrast medium was evolved from the prior use of bismuth preparations which were too toxic. The use of bismuth preparations had been described as early as 1898. Barium sulfate as a contrast medium in medical practice was introduced largely as a result of the works of Krause a director of the Bonn Polyclinic, now the medical faculty of the  University of Bonn  and his colleagues Bachem and Gunther. In a paper read in 1910 at the radiological congress they advocated for the use of barium sulfate as an opaque contrast medium in medicine. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4240", "text": "D-xylose absorption test  is a medical test performed to diagnose conditions that present with  malabsorption  of the proximal  small intestine [ 1 ]  due to defects in the integrity of the gastrointestinal mucosa. [ 2 ]   D-xylose  is a  monosaccharide , or simple sugar, that does not require enzymes for digestion prior to absorption. Its absorption requires an intact mucosa only. In contrast,  polysaccharides  require enzymes, such as  amylase , to break them down so that they can eventually be absorbed as monosaccharides. This test was previously in use but has been made redundant by  antibody tests . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4241", "text": "In normal individuals, a 25\u00a0g oral dose of D-xylose will be absorbed and excreted in the urine at approximately 4.5\u00a0g in 5 hours. A decreased urinary excretion of D-xylose is seen in conditions involving the gastrointestinal mucosa, such as  small intestinal bacterial overgrowth  and  Whipple's disease . In cases of bacterial overgrowth, the values of D-xylose absorption return to normal after treatment with  antibiotics . In contrast, if the D-xylose urinary excretion is not normal after a course of antibiotics, then the problem must be due to a non-infectious cause of malabsorption (i.e.,  celiac disease ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4242", "text": "The  human digestive system  consists of the  gastrointestinal tract  plus the accessory organs of digestion (the  tongue ,  salivary glands ,  pancreas ,  liver , and  gallbladder ).  Digestion  involves the breakdown of food into smaller and smaller components, until they can be absorbed and assimilated into the body. The process of digestion has three stages: the  cephalic phase , the  gastric phase , and the  intestinal phase ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4243", "text": "The first stage, the cephalic phase of digestion, begins with secretions from  gastric glands  in response to the sight and smell of food. This stage includes the mechanical breakdown of food by  chewing , and the chemical breakdown by  digestive enzymes , that takes place in the  mouth .  Saliva  contains the digestive enzymes  amylase , and  lingual lipase , secreted by the salivary and  serous glands  on the tongue. Chewing, in which the food is mixed with saliva, begins the mechanical process of digestion. This produces a  bolus  which is swallowed down the  esophagus  to enter the  stomach ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4244", "text": "The second stage, the gastric phase, happens in the stomach. Here, the food is further broken down by mixing with  gastric acid  until it passes into the  duodenum , the first part of the  small intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4245", "text": "The third stage, the intestinal phase, begins in the duodenum. Here, the partially digested food is mixed with a number of  enzymes  produced by the pancreas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4246", "text": "Digestion is helped by the chewing of food carried out by the  muscles of mastication , the tongue, and the  teeth , and also by the  contractions  of  peristalsis , and  segmentation . Gastric acid, and the production of  mucus  in the stomach, are essential for the continuation of digestion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4247", "text": "Peristalsis is the rhythmic contraction of  muscles  that begins in the esophagus and continues along the wall of the stomach and the rest of the gastrointestinal tract. This initially results in the production of  chyme  which when fully broken down in the small intestine is absorbed as  chyle  into the  lymphatic system . Most of the digestion of food takes place in the small intestine. Water and some  minerals  are reabsorbed back into the blood in the colon of the  large intestine . The waste products of digestion ( feces ) are  defecated  from the  rectum  via the  anus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4248", "text": "There are several organs and other components involved in the digestion of food. The organs known as the  accessory digestive organs  are the  liver ,  gall bladder  and  pancreas . Other components include the  mouth ,  salivary glands ,  tongue ,  teeth  and  epiglottis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4249", "text": "The largest structure of the digestive  system  is the  gastrointestinal tract  (GI tract). This starts at the mouth and ends at the  anus , covering a distance of about nine metres (30\u00a0ft). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4250", "text": "A major digestive organ is the  stomach . Within its  mucosa  are millions of embedded  gastric glands . Their secretions are vital to the functioning of the organ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4251", "text": "Most of the digestion of food takes place in the  small intestine  which is the longest part of the GI tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4252", "text": "The largest part of the GI tract is the colon or  large intestine . Water is absorbed here and the remaining waste matter is stored prior to  defecation . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4253", "text": "There are many specialised  cells  of the GI tract. These include the various cells of the gastric glands,  taste cells ,  pancreatic duct cells ,  enterocytes  and  microfold cells ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4254", "text": "Some parts of the digestive system are also part of the  excretory system , including the large intestine. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4255", "text": "The  mouth  is the first part of the  upper gastrointestinal tract  and is equipped with several structures that begin the first processes of digestion. [ 3 ]  These include salivary glands, teeth and the tongue. The mouth consists of two regions; the vestibule and the oral cavity proper. The vestibule is the area between the teeth, lips and cheeks, [ 4 ]  and the rest is the oral cavity proper. Most of the oral cavity is lined with  oral mucosa , a  mucous membrane  that produces a lubricating  mucus , of which only a small amount is needed. Mucous membranes vary in structure in the different regions of the body but they all produce a lubricating mucus, which is either secreted by surface cells or more usually by underlying glands. The mucous membrane in the mouth continues as the thin mucosa which lines the bases of the teeth. The main component of mucus is a  glycoprotein  called  mucin  and the type secreted varies according to the region involved. Mucin is  viscous, clear, and clinging. Underlying the mucous membrane in the mouth is a thin layer of  smooth muscle tissue  and the loose connection to the membrane gives it its great elasticity. [ 5 ]  It covers the cheeks, inner surfaces of the  lips , and floor of the mouth, and the mucin produced is highly protective against  tooth decay . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4256", "text": "The roof of the mouth is termed the  palate  and it separates the oral cavity from the nasal cavity. The palate is hard at the front of the mouth since the overlying mucosa is covering a plate of  bone ; it is softer and more pliable at the back being made of muscle and connective tissue, and  it can move to swallow food and liquids. The  soft palate  ends at the  uvula . [ 7 ]  The surface of the  hard palate  allows for the pressure needed in eating food, to leave the nasal passage clear. [ 8 ]  The opening between the lips is termed the oral fissure, and the opening into the throat is called the  fauces . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4257", "text": "At either side of the soft palate are the  palatoglossus muscles  which also reach into regions of the tongue. These muscles raise the back of the tongue and also close both sides of the fauces to enable food to be swallowed. [ 10 ] :\u200a1208\u200a  Mucus helps in the mastication of food in its ability to soften and collect the food in the formation of the bolus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4258", "text": "There are three pairs of main  salivary glands  and between 800 and 1,000 minor salivary glands, all of which mainly serve the digestive process, and also play an important role in the maintenance of dental health and general mouth lubrication, without which speech would be impossible. [ 11 ]  The main glands are all  exocrine glands , secreting via ducts. All of these glands terminate in the mouth. The largest of these are the  parotid glands \u2014their secretion is mainly  serous . The next pair are underneath the jaw, the  submandibular glands , these produce both serous fluid and mucus. The serous fluid is produced by  serous glands  in these salivary glands which also produce  lingual lipase . They produce about 70% of the oral cavity saliva. The third pair are the  sublingual glands  located underneath the tongue and their secretion is mainly mucous with a small percentage of saliva."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4259", "text": "Within the oral mucosa, and also on the tongue, palates, and floor of the mouth, are the minor salivary glands; their secretions are mainly mucous and they are innervated by the  facial nerve  ( CN7 ). [ 12 ]  The glands also secrete  amylase  a first stage in the breakdown of food acting on the carbohydrate in the food to transform the starch content into maltose. There are other serous glands on the surface of the tongue that encircle  taste buds  on the back part of the tongue and these also produce lingual  lipase . Lipase is a  digestive enzyme  that catalyses the  hydrolysis  of  lipids  (fats). These glands are termed  Von Ebner's glands  which have also been shown to have another function in the secretion of  histatins  which offer an early defense (outside of the immune system) against microbes in food, when it makes contact with these glands on the tongue tissue. [ 11 ] [ 13 ]  Sensory information can stimulate the secretion of saliva providing the necessary fluid for the tongue to work with and also to ease swallowing of the food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4260", "text": "Saliva  moistens and softens food, and along with the chewing action of the teeth, transforms the food into a smooth  bolus . The bolus is further helped by the lubrication provided by the saliva in its passage from the mouth into the esophagus. Also of importance is the presence in saliva of the digestive enzymes amylase and lipase. Amylase starts to work on the  starch  in  carbohydrates , breaking it down into the simple  sugars  of  maltose  and  dextrose  that can be further broken down in the small intestine. Saliva in the mouth can account for 30% of this initial starch digestion. Lipase starts to work on breaking down  fats . Lipase is further produced in the pancreas where it is released to continue this digestion of fats. The presence of salivary lipase is of prime importance in young babies whose pancreatic lipase has yet to be developed. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4261", "text": "As well as its role in supplying digestive enzymes, saliva has a cleansing action for the teeth and mouth. [ 15 ]  It also has an  immunological  role in supplying antibodies to the system, such as  immunoglobulin A . [ 16 ]  This is seen to be key in preventing  infections  of the salivary glands, importantly that of  parotitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4262", "text": "Saliva also contains a glycoprotein called  haptocorrin  which is a binding protein to vitamin B 12 . [ 17 ]  It binds with the vitamin in order to carry it safely through the acidic content of the stomach. When it reaches the duodenum, pancreatic enzymes break down the glycoprotein and free the vitamin which then binds with  intrinsic factor ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4263", "text": "Food enters the mouth where the first stage in the digestive process takes place, with the action of the  tongue  and the secretion of saliva. The tongue is a fleshy and  muscular   sensory organ , and the first sensory information is received via the taste buds in the  papillae  on its surface. If the taste is agreeable, the tongue will go into action, manipulating the food in the mouth which stimulates the secretion of saliva from the salivary glands. The liquid quality of the saliva will help in the softening of the food and its enzyme content will start to break down the food whilst it is still in the mouth. The first part of the food to be broken down is the starch of carbohydrates (by the enzyme amylase in the saliva)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4264", "text": "The tongue is attached to the floor of the mouth by a ligamentous band called the  frenum [ 5 ]  and this gives it great mobility for the manipulation of food (and  speech ); the range of manipulation is optimally controlled by the action of several muscles and limited in its external range by the stretch of the frenum. The tongue's two sets of muscles, are four  intrinsic muscles  that originate in the tongue and are involved with its shaping, and four  extrinsic muscles  originating in bone that are involved with its movement."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4265", "text": "Taste  is a form of  chemoreception  that takes place in the specialised  taste receptors , contained in structures called  taste buds  in the mouth. Taste buds are mainly on the upper surface (dorsum) of the tongue. The function of taste perception is vital to help prevent harmful or rotten foods from being consumed. There are also taste buds on the  epiglottis  and upper part of the  esophagus . The taste buds are innervated by a branch of the facial nerve the  chorda tympani , and the  glossopharyngeal nerve . Taste messages are sent via these  cranial nerves  to the  brain . The brain can distinguish between the chemical qualities of the food. The five  basic tastes  are referred to as those of  saltiness ,  sourness ,  bitterness ,  sweetness , and   umami . The detection of saltiness and sourness enables the control of salt and acid balance. The detection of bitterness warns of poisons\u2014many of a plant's defences are of poisonous compounds that are bitter. Sweetness guides to those foods that will supply energy; the initial breakdown of the energy-giving carbohydrates by salivary amylase creates the taste of sweetness since simple sugars are the first result. The taste of umami is thought to signal protein-rich food. Sour tastes are acidic which is often found in bad food. The brain has to decide very quickly whether the food should be eaten or not. It was the findings in 1991, describing the first  olfactory  receptors that helped to prompt the research into taste. The olfactory receptors are located on cell surfaces in the  nose  which bind to chemicals enabling the detection of smells. It is assumed that signals from taste receptors work together with those from the nose, to form an idea of complex food flavours. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4266", "text": "Teeth  are complex structures made of materials specific to them. They are made of a bone-like material called  dentin , which is covered by the hardest tissue in the body\u2014 enamel . [ 8 ]  Teeth have different shapes to deal with different aspects of  mastication  employed in tearing and chewing pieces of food into smaller and smaller pieces. This results in a much larger surface area for the action of digestive enzymes.\nThe teeth are named after their particular roles in the process of mastication\u2014 incisors  are used for cutting or biting off pieces of food;  canines , are used for tearing,  premolars  and  molars  are used for chewing and grinding. Mastication of the food with the help of saliva and mucus results in the formation of a soft bolus which can then be  swallowed  to make its way down the  upper gastrointestinal tract  to the stomach. [ 19 ]  \nThe digestive enzymes in saliva also help in keeping the teeth clean by breaking down any lodged food particles. [ 20 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4267", "text": "The  epiglottis  is a flap of  elastic cartilage  attached to the entrance of the  larynx . It is covered with a mucous membrane and there are taste buds on its lingual surface which faces into the mouth. [ 21 ]  Its laryngeal surface faces into the larynx. The epiglottis functions to guard the entrance of the  glottis , the opening between the  vocal folds . It is normally pointed upward during breathing with its underside functioning as part of the pharynx, but during swallowing, the epiglottis folds down to a more horizontal position, with its upper side functioning as part of the pharynx. In this manner it prevents food from going into the trachea and instead directs it to the esophagus, which is behind. During swallowing, the backward motion of the tongue forces the epiglottis over the glottis' opening to prevent any food that is being swallowed from entering the larynx which leads to the lungs; the larynx is also pulled upwards to assist this process. Stimulation of the larynx by ingested matter produces a strong  cough reflex  in order to protect the lungs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4268", "text": "The  pharynx  is a part of the  conducting zone  of the  respiratory system  and also a part of the digestive system. It is the part of the throat immediately behind the  nasal cavity  at the back of the mouth and above the esophagus and  larynx . The pharynx is made up of three parts. The lower two parts\u2014the  oropharynx  and the  laryngopharynx  are involved in the digestive system. The laryngopharynx connects to the esophagus and it serves as a passageway for both air and food. Air enters the larynx anteriorly but anything swallowed has priority and the passage of air is temporarily blocked. The pharynx is innervated by the  pharyngeal plexus of the vagus nerve . [ 10 ] :\u200a1465\u200a   Muscles in the pharynx  push the food into the esophagus. The pharynx joins the esophagus at the oesophageal inlet which is located behind the  cricoid cartilage ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4269", "text": "The  esophagus , commonly known as the foodpipe or gullet, consists of a muscular tube through which food passes from the pharynx to the stomach. The esophagus is continuous with the laryngopharynx. It passes through the posterior  mediastinum  in the  thorax  and enters the  stomach  through a hole in the  thoracic diaphragm \u2014the  esophageal hiatus , at the level of the tenth  thoracic vertebra  (T10). Its length averages 25\u00a0cm, varying with an individual's height. It is divided into cervical,  thoracic  and  abdominal  parts. The pharynx joins the esophagus at the esophageal inlet which is behind the  cricoid cartilage ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4270", "text": "At rest the esophagus is closed at both ends, by the  upper and lower esophageal sphincters . The opening of the upper sphincter is triggered by the  swallowing reflex  so that food is allowed through. The sphincter also serves to prevent back flow from the esophagus into the pharynx. The esophagus has a mucous membrane and the epithelium which has a protective function is continuously replaced due to the volume of food that passes inside the esophagus. During swallowing, food passes from the mouth through the pharynx into the esophagus. The epiglottis folds down to a more horizontal position to direct the food into the esophagus, and away from the  trachea ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4271", "text": "Once in the esophagus, the bolus travels down to the stomach via rhythmic contraction and relaxation of muscles known as  peristalsis . The lower esophageal sphincter is a muscular sphincter surrounding the lower part of the esophagus. The  gastroesophageal junction  between the esophagus and the stomach is controlled by the lower esophageal sphincter, which remains constricted at all times other than during swallowing and vomiting to prevent the contents of the stomach from entering the esophagus. As the esophagus does not have the same protection from acid as the stomach, any failure of this sphincter can lead to heartburn."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4272", "text": "The  diaphragm  is an important part of the body's digestive system. The muscular diaphragm separates the  thoracic cavity  from the  abdominal cavity  where most of the digestive organs are located. The  suspensory muscle  attaches the ascending duodenum to the diaphragm. This muscle is thought to be of help in the digestive system in that its attachment offers a wider angle to the  duodenojejunal flexure  for the easier passage of digesting material. The diaphragm also attaches to, and anchors the liver at its  bare area . The esophagus enters the abdomen through a  hole in the diaphragm  at the level of  T10 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4273", "text": "The  stomach  is a major organ of the gastrointestinal tract and digestive system. It is a consistently J-shaped organ joined to the esophagus at its upper end and to the duodenum at its lower end.\n Gastric acid  (informally  gastric juice ), produced in the stomach plays a vital role in the digestive process, and mainly contains  hydrochloric acid  and  sodium chloride . A  peptide hormone ,  gastrin ,  produced by  G cells  in the  gastric glands , stimulates the production of gastric juice which activates the digestive enzymes.  Pepsinogen  is a precursor enzyme ( zymogen ) produced by the  gastric chief cells , and gastric acid activates this to the enzyme  pepsin  which begins the digestion of  proteins . As these two chemicals would damage the stomach wall, mucus is secreted by innumerable gastric glands in the stomach, to provide a slimy protective layer against the damaging effects of the chemicals on the inner layers of the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4274", "text": "At the same time that protein is being digested, mechanical churning occurs through the action of peristalsis, waves of muscular contractions that move along the stomach wall. This allows the mass of food to further mix with the digestive enzymes.  Gastric lipase  secreted by the chief cells in the fundic glands in the gastric mucosa of the stomach, is an acidic lipase, in contrast with the alkaline pancreatic lipase. This breaks down fats to some degree though is not as efficient as the pancreatic lipase."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4275", "text": "The  pylorus , the lowest section of the stomach which attaches to the  duodenum  via the  pyloric canal , contains countless glands which secrete digestive enzymes including gastrin. After an hour or two, a thick semi-liquid called  chyme  is produced. When the  pyloric sphincter , or valve opens, chyme enters the duodenum where it mixes further with digestive enzymes from the pancreas, and then passes through the small intestine, where digestion continues."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4276", "text": "The  parietal cells  in the fundus of the stomach, produce a glycoprotein called intrinsic factor which is essential for the absorption of  vitamin B12 . Vitamin B12 (cobalamin), is carried to, and through the stomach, bound to a glycoprotein secreted by the salivary glands \u2013  transcobalamin I  also called haptocorrin, which protects the acid-sensitive vitamin from the acidic stomach contents. Once in the more neutral duodenum, pancreatic enzymes break down the protective glycoprotein. The freed vitamin B12 then binds to intrinsic factor which is then absorbed by the enterocytes in the ileum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4277", "text": "The stomach is a distensible organ and can normally expand to hold about one litre of food. [ 22 ]  This expansion is enabled by a series of  gastric folds  in the inner walls of the stomach. The stomach of a newborn baby will only be able to expand to retain about 30 ml."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4278", "text": "The  spleen  is the largest lymphoid organ in the body but has other functions. [ 23 ]  It breaks down both red and white  blood cells  that are  spent . This is why it is sometimes known as the 'graveyard of red blood cells'. [ 23 ]  A product of this  digestion  is the pigment  bilirubin , which is sent to the  liver  and secreted in the  bile . Another product is  iron , which is used in the formation of new blood cells in the  bone marrow . [ 5 ]   Medicine  treats the spleen solely as belonging to the  lymphatic system , though it is acknowledged that the full range of its important functions is not yet understood. [ 10 ] :\u200a1751"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4279", "text": "The  liver  is the second largest organ (after the  skin ) and is an accessory digestive gland which plays a role in the body's  metabolism . The liver has many functions some of which are important to digestion. The liver can detoxify various  metabolites ; synthesise proteins and produce  biochemicals  needed for digestion. It regulates the storage of  glycogen  which it can form from  glucose  ( glycogenesis ). The liver can also synthesise glucose from certain  amino acids . Its digestive functions are largely involved with the breaking down of carbohydrates. It also maintains protein metabolism in its synthesis and degradation. In lipid metabolism it synthesises  cholesterol . Fats are also produced in the process of  lipogenesis . The liver synthesises the bulk of lipoproteins. The liver is located in the upper right quadrant of the abdomen and below the diaphragm to which it is attached at one part, the bare area of the liver. This is to the right of the stomach and it overlies the gall bladder. The liver synthesises  bile acids  and  lecithin  to promote the digestion of fat. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4280", "text": "Bile  produced by the liver is made up of water (97%),  bile salts , mucus and  pigments , 1% fats and inorganic salts. [ 25 ]   Bilirubin  is its major pigment. Bile acts partly as a  surfactant  which lowers the surface tension between either two liquids or a solid and a liquid and helps to  emulsify  the fats in the chyme. Food fat is dispersed by the action of bile into smaller units called  micelles . The breaking down into micelles creates a much larger surface area for the pancreatic enzyme, lipase to work on. Lipase digests the  triglycerides  which are broken down into two  fatty acids  and a  monoglyceride . These are then absorbed by  villi  on the intestinal wall. If fats are not absorbed in this way in the small intestine problems can arise later in the large intestine which is not equipped to absorb fats. Bile also helps in the absorption of  vitamin K  from the diet.\nBile is collected and delivered through the  common hepatic duct . This duct joins with the  cystic duct  to connect in a  common bile duct  with the gallbladder.\nBile is stored in the gallbladder for release when food is discharged into the duodenum and also after a few hours. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4281", "text": "The  gallbladder  is a hollow part of the  biliary tract  that sits just beneath the liver, with the gallbladder body resting in a small depression. [ 26 ]  It is a small organ where the bile produced by the liver is stored, before being released into the small intestine. Bile flows from the liver through the  bile ducts  and into the gall bladder for storage. The bile is released in response to  cholecystokinin  (CCK), a peptide hormone released from the duodenum. The production of CCK (by endocrine cells of the duodenum) is stimulated by the presence of fat in the duodenum. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4282", "text": "It is divided into three sections, a fundus, body and neck. The neck tapers and connects to the biliary tract via the  cystic duct , which then joins the common hepatic duct to form the common bile duct. At this junction is a mucosal fold called  Hartmann's pouch , where  gallstones  commonly get stuck. The  muscular layer  of the body is of smooth muscle tissue that helps the gallbladder contract, so that it can discharge its bile into the bile duct. The gallbladder needs to store bile in a natural, semi-liquid form at all times.  Hydrogen ions  secreted from the inner lining of the gallbladder keep the bile acidic enough to prevent hardening. To dilute the bile, water and  electrolytes  from the digestion system are added. Also, salts attach themselves to cholesterol molecules in the bile to keep them from  crystallising . If there is too much cholesterol or bilirubin in the bile, or if the gallbladder does not empty properly the systems can fail. This is how gallstones form when a small piece of calcium gets coated with either cholesterol or bilirubin and the bile crystallises and forms a gallstone. The main purpose of the gallbladder is to store and release bile, or  gall . Bile is released into the small intestine in order to help in the digestion of fats by breaking down larger molecules into smaller ones. After the fat is absorbed, the bile is also absorbed and transported back to the liver for reuse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4283", "text": "The  pancreas  is a major organ functioning as an accessory digestive gland in the digestive system. It is both an  endocrine gland  and an  exocrine gland . [ 28 ]  The endocrine part secretes  insulin  when the  blood sugar  becomes high; insulin moves glucose from the blood into the muscles and other tissues for use as energy. The endocrine part releases  glucagon  when the blood sugar is low; glucagon allows stored sugar to be broken down into glucose by the liver in order to re-balance the sugar levels. The pancreas produces and releases important digestive enzymes in the  pancreatic juice  that it delivers to the duodenum. [ 24 ]  The pancreas lies below and at the back of the stomach. It connects to the duodenum via the  pancreatic duct  which it joins near to the bile duct's connection where both the bile and pancreatic juice can act on the chyme that is released from the stomach into the duodenum. Aqueous pancreatic secretions from  pancreatic duct cells  contain  bicarbonate  ions which are alkaline and help with the bile to neutralise the acidic chyme that is churned out by the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4284", "text": "The pancreas is also the main source of enzymes for the digestion of fats and proteins. Some of these are released in response to the production of cholecystokinin in the duodenum. (The enzymes that digest polysaccharides, by contrast, are primarily produced by the walls of the intestines.) The cells are filled with secretory granules containing the precursor digestive enzymes. The major  proteases , the pancreatic enzymes which work on proteins, are  trypsinogen  and  chymotrypsinogen .  Elastase  is also produced. Smaller amounts of lipase and amylase are secreted. The pancreas also secretes  phospholipase A2 ,  lysophospholipase , and cholesterol  esterase . The precursor  zymogens , are inactive variants of the enzymes; which avoids the onset of  pancreatitis  caused by autodegradation. Once released in the intestine, the enzyme  enteropeptidase  present in the intestinal mucosa activates trypsinogen by cleaving it to form trypsin; further cleavage results in chymotripsin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4285", "text": "The lower gastrointestinal tract (GI), includes the  small intestine  and all of the  large intestine . [ 29 ]  The intestine is also called the bowel or the gut. The lower GI starts at the pyloric sphincter of the stomach and finishes at the anus. The small intestine is subdivided into the  duodenum , the  jejunum  and the  ileum . The cecum marks the division between the small and large intestine. The large intestine includes the rectum and  anal canal . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4286", "text": "Partially digested food starts to arrive in the  small intestine  as semi-liquid  chyme , one hour after it is eaten. [ citation needed ]  The stomach is half empty after an average of 1.2 hours. [ 30 ]  After four or five hours the stomach has emptied. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4287", "text": "In the small intestine, the  pH  becomes crucial; it needs to be finely balanced in order to activate digestive enzymes. The chyme is very acidic, with a low pH, having been released from the stomach and needs to be made much more alkaline. This is achieved in the  duodenum  by the addition of bile from the gall bladder combined with the  bicarbonate  secretions from the pancreatic duct and also from secretions of bicarbonate-rich mucus from duodenal glands known as  Brunner's glands . The chyme arrives in the intestines having been released from the stomach through the opening of the  pyloric sphincter . The resulting alkaline fluid mix neutralises the gastric acid which would damage the lining of the intestine. The mucus component lubricates the walls of the intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4288", "text": "When the digested food particles are reduced enough in size and composition, they can be absorbed by the intestinal wall and carried to the bloodstream. The first receptacle for this chyme is the  duodenal bulb . From here it passes into the first of the three sections of the small intestine, the duodenum (the next section is the  jejunum  and the third is the  ileum ). The duodenum is the first and shortest section of the small intestine. It is a hollow, jointed C-shaped tube connecting the stomach to the jejunum. It starts at the duodenal bulb and ends at the  suspensory muscle of duodenum . The attachment of the suspensory muscle to the diaphragm is thought to help the passage of food by making a wider angle at its attachment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4289", "text": "Most food digestion takes place in the small intestine.  Segmentation contractions  act to mix and move the chyme more slowly in the small intestine allowing more time for absorption (and these continue in the large intestine). In the duodenum, pancreatic lipase is secreted together with a  co-enzyme ,  colipase  to further digest the fat content of the chyme. From this breakdown, smaller particles of emulsified fats called  chylomicrons  are produced. There are also digestive cells called  enterocytes  lining the intestines (the majority being in the small intestine). They are unusual cells in that they have  villi  on their surface which in turn have innumerable  microvilli  on their surface. All these villi make for a greater surface area, not only for the absorption of chyme but also for its further digestion by large numbers of digestive enzymes present on the microvilli."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4290", "text": "The chylomicrons are small enough to pass through the enterocyte villi and into their  lymph  capillaries called  lacteals . A milky fluid called  chyle , consisting mainly of the emulsified fats of the chylomicrons, results from the absorbed mix with the lymph in the lacteals. [ clarification needed ]  Chyle is then transported through the  lymphatic system  to the rest of the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4291", "text": "The suspensory muscle marks the end of the duodenum and the division between the upper gastrointestinal tract and the lower GI tract. The digestive tract continues as the jejunum which continues as the ileum. The jejunum, the midsection of the small intestine contains  circular folds , flaps of doubled mucosal membrane which partially encircle and sometimes completely encircle the  lumen  of the intestine. These folds together with villi serve to increase the surface area of the jejunum enabling an increased absorption of digested sugars, amino acids and fatty acids into the bloodstream. The circular folds also slow the passage of food giving more time for nutrients to be absorbed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4292", "text": "The last part of the small intestine is the ileum. This also contains villi and  vitamin B12 ; bile acids and any residue nutrients are absorbed here. When the chyme is exhausted of its nutrients the remaining waste material changes into the semi-solids called  feces , which pass to the large intestine, where bacteria in the  gut flora  further break down residual proteins and starches. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4293", "text": "Transit time through the small intestine is an average of 4 hours. Half of the food residues of a meal have emptied from the small intestine by an average of 5.4 hours after ingestion. Emptying of the small intestine is complete after an average of 8.6 hours. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4294", "text": "The  cecum  is a pouch marking the division between the small intestine and the large intestine. It lies below the  ileocecal valve  in the  lower right quadrant  of the abdomen. [ 33 ]  The cecum receives chyme from the last part of the small intestine, the  ileum , and connects to the  ascending colon  of the large intestine. At this junction there is a sphincter or valve, the ileocecal valve which slows the passage of chyme from the ileum, allowing further digestion. It is also the site of the  appendix  attachment. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4295", "text": "In the  large intestine , [ 2 ]  the passage of the digesting food in the  colon  is a lot slower, taking from 30 to 40 hours until it is removed by  defecation . [ 31 ]  The colon mainly serves as a site for the fermentation of digestible matter by the  gut flora . The time taken varies considerably between individuals. The remaining semi-solid waste is termed  feces  and is removed by the coordinated contractions of the intestinal walls, termed  peristalsis , which propels the  excreta  forward to reach the  rectum  and exit through the  anus  via defecation. The wall has an outer layer of longitudinal muscles, the  taeniae coli , and an inner layer of circular muscles. The circular muscle keeps the material moving forward and also prevents any back flow of waste. Also of help in the action of peristalsis is the  basal electrical rhythm  that determines the frequency of contractions. [ 34 ]  The taeniae coli can be seen and are responsible for the bulges ( haustra ) present in the colon. Most parts of the GI tract are covered with  serous membranes  and have a  mesentery . Other more muscular parts are lined with  adventitia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4296", "text": "The digestive system is supplied by the  celiac artery . The celiac artery is the first major branch from the  abdominal aorta , and is the only major artery that nourishes the digestive organs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4297", "text": "There are three main divisions \u2013 the  left gastric artery , the  common hepatic artery  and the  splenic artery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4298", "text": "The celiac artery supplies the liver, stomach, spleen and the upper 1/3 of the duodenum (to the  sphincter of Oddi ) and the pancreas with oxygenated blood. Most of the blood is returned to the liver via the  portal venous system  for further processing and detoxification before returning to the  systemic circulation  via the  hepatic veins ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4299", "text": "The next branch from the abdominal aorta is the  superior mesenteric artery , which supplies the regions of the digestive tract derived from the midgut, which includes the distal 2/3 of the duodenum, jejunum, ileum, cecum, appendix, ascending colon, and the proximal 2/3 of the transverse colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4300", "text": "The final branch which is important for the digestive system is the  inferior mesenteric artery , which supplies the regions of the digestive tract derived from the hindgut, which includes the distal 1/3 of the transverse colon, descending colon, sigmoid colon, rectum, and the anus above the  pectinate line ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4301", "text": "Blood flow to the digestive tract reaches its maximum 20\u201340 minutes after a meal and lasts for 1.5\u20132 hours. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4302", "text": "The  enteric nervous system  consists of some one hundred million  neurons [ 36 ]  that are embedded in the  peritoneum , the lining of the  gastrointestinal tract  extending from the esophagus to the anus. [ 37 ]  These neurons are collected into two  plexuses  \u2013 the  myenteric (or Auerbach's) plexus  that lies between the longitudinal and the smooth muscle layers, and the  submucosal (or Meissner's) plexus  that lies between the circular smooth muscle layer and the mucosa. [ 38 ] [ 39 ] [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4303", "text": "Parasympathetic innervation  to the  ascending colon  is supplied by the  vagus nerve .  Sympathetic innervation  is supplied by the  splanchnic nerves  that join the  celiac ganglia . Most of the digestive tract is innervated by the two large celiac ganglia, with the upper part of each ganglion joined by the  greater splanchnic nerve  and the lower parts joined by the  lesser splanchnic nerve . It is from these ganglia that many of the  gastric plexuses  arise."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4304", "text": "Early in  embryonic development , the  embryo  has three  germ layers  and abuts a  yolk sac . During the second week of development, the embryo grows and begins to surround and envelop portions of this sac. The enveloped portions form the basis for the adult gastrointestinal tract. Sections of this  foregut  begin to differentiate into the organs of the gastrointestinal tract, such as the esophagus, stomach, and intestines. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4305", "text": "During the fourth week of development, the stomach rotates. The stomach, originally lying in the midline of the embryo, rotates so that its body is on the left. This rotation also affects the part of the gastrointestinal tube immediately below the stomach, which will go on to become the duodenum. By the end of the fourth week, the developing duodenum begins to spout a small outpouching on its right side, the  hepatic diverticulum , which will go on to become the  biliary tree . Just below this is a second outpouching, known as the  cystic diverticulum , that will eventually develop into the gallbladder. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4306", "text": "Each part of the digestive system is subject to a wide range of disorders many of which can be  congenital .  Mouth diseases  can also be caused by  pathogenic   bacteria ,  viruses ,  fungi  and as a side effect of some  medications . Mouth diseases include  tongue diseases  and  salivary gland diseases . A common  gum  disease in the mouth is  gingivitis  which is caused by bacteria in  plaque . The most common viral infection of the mouth is  gingivostomatitis  caused by  herpes simplex . A common  fungal  infection is  candidiasis  commonly known as  thrush  which affects the  mucous membranes  of the mouth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4307", "text": "There are a number of  esophageal diseases  such as the development of  Schatzki rings  that can restrict the passageway, causing difficulties in swallowing. They can also completely block the esophagus. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4308", "text": "Stomach diseases  are often chronic conditions and include  gastroparesis ,  gastritis , and  peptic ulcers ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4309", "text": "A number of problems including  malnutrition  and  anemia  can arise from  malabsorption , the abnormal absorption of nutrients in the GI tract. Malabsorption can have many causes ranging from  infection , to enzyme deficiencies such as  exocrine pancreatic insufficiency . It can also arise as a result of other gastrointestinal diseases such as  coeliac disease . Coeliac disease is an  autoimmune  disorder of the small intestine. This can cause  vitamin deficiencies  due to the improper absorption of nutrients in the small intestine. The  small intestine can also be  obstructed  by a  volvulus , a loop of intestine that becomes twisted enclosing its attached  mesentery . This can cause  mesenteric ischemia  if severe enough."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4310", "text": "A common disorder of the bowel is  diverticulitis .  Diverticula  are small pouches that can form inside the bowel wall, which can become inflamed to give diverticulitis. This disease can have complications if an inflamed diverticulum bursts and infection sets in. Any infection can spread further to the lining of the abdomen ( peritoneum ) and cause potentially fatal  peritonitis . [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4311", "text": "Crohn's disease  is a common chronic  inflammatory bowel disease  (IBD), which can affect any part of the GI tract, [ 44 ]  but it mostly starts in the  terminal ileum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4312", "text": "Ulcerative colitis , an ulcerative form of  colitis , is the other major inflammatory bowel disease which is restricted to the colon and rectum. Both of these IBDs can give an increased risk of the development of  colorectal cancer . Ulcerative colitis is the most common of the IBDs [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4313", "text": "Irritable bowel syndrome  (IBS) is the most common of the  functional gastrointestinal disorders . These are  idiopathic  disorders that the  Rome process  has helped to define. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4314", "text": "Giardiasis  is a disease of the small intestine caused by a  protist   parasite   Giardia lamblia . This does not spread but remains confined to the lumen of the small intestine. [ 47 ]  It can often be  asymptomatic , but as often can be indicated by a variety of symptoms. Giardiasis is the most common  pathogenic   parasitic infection  in humans. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4315", "text": "There are diagnostic tools mostly involving the ingestion of  barium sulphate  to investigate disorders of the GI tract. [ 49 ]  These are known as  upper gastrointestinal series  that enable  imaging  of the pharynx, larynx, oesophagus, stomach and small intestine [ 50 ]  and  lower gastrointestinal series  for imaging of the colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4316", "text": "Gestation  can predispose for certain digestive disorders.  Gestational diabetes  can develop in the mother as a result of  pregnancy  and while this often presents with few symptoms it can lead to  pre-eclampsia . [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4317", "text": "In the early 11th century, the Islamic medical philosopher  Avicenna  wrote extensively on many subjects including medicine. Forty of these treatises on medicine survive, and in the most famous one titled the  Canon of Medicine  he discusses \"rising gas\". Avicenna believed that digestive system dysfunction was responsible for the overproduction of gas in the gastrointestinal tract. He suggested lifestyle changes and a compound of herbal drugs for its treatment. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4318", "text": "In 1497,  Alessandro Benedetti  viewed the stomach as an unclean organ separated off by the diaphragm. This view of the stomach and intestines as being base organs was generally held until the mid-17th century. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4319", "text": "In the Renaissance of the 16th century,  Leonardo da Vinci  produced some early drawings of the stomach and intestines. He thought that the digestive system aided the respiratory system. [ 53 ]   Andreas Vesalius  provided some early anatomical drawings of the abdominal organs in the 16th century."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4320", "text": "In the middle of the 17th century, a Flemish physician  Jan Baptist van Helmont  offered the first  chemical account of digestion  which was later described as being very close to the later conceptualised enzyme. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4321", "text": "In 1653,  William Harvey  described the intestines in terms of their length, their blood supply, the mesenteries, and fat (adenylyl cyclase). [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4322", "text": "In 1823,  William Prout  discovered  hydrochloric acid  in the gastric juice. [ 54 ]  In 1895,  Ivan Pavlov  described its secretion as being stimulated by a neurologic reflex with the  vagus nerve  having a crucial role. Black in the 19th century suggested an association of histamine with this secretion. In 1916, Popielski described histamine as a gastric secretagogue of hydrochloric acid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4323", "text": "William Beaumont  was an army surgeon who in 1825, was able to observe digestion as it took place in the stomach. [ 55 ]  This was made possible by experiments on a man with a stomach wound that did not fully heal leaving an opening into the stomach. The churning motion of the stomach was described among other findings. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4324", "text": "In the 19th century, it was accepted that chemical processes were involved in the process of digestion.  Physiological research  into secretion and the gastrointestinal tract was pursued with experiments undertaken by Claude Bernard, Rudolph Heidenhain and Ivan Pavlov."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4325", "text": "The rest of the 20th century was dominated by research into enzymes. The first to be discovered was  secretin  by  Ernest Starling  in 1902, with ensuing results from John Edkins in 1905 who first suggested  gastrin  with its structure being determined in 1964. [ 54 ]  Andre Latarjet and Lester Dragstedt found a role for  acetylcholine  in the digestive system. [ 54 ]  In 1972,  H2 receptor agonists  were described by J. Black, that block the action of histamine and decrease the production of hydrochloric acid. In 1980,  proton pump inhibitors  were described by Sachs. In 1983, the role of  Helicobacter pylori  in the formation of ulcers was described by  Barry Marshall , and  Robin Warren . [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4326", "text": "Art historians have often noted that  banqueters  on iconographic records of ancient Mediterranean societies almost always appear to be lying down on their left sides. One possible explanation could lie in the anatomy of the stomach and in the digestive mechanism. When lying on the left, the food has room to expand because the curvature of the stomach is enhanced in that position. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4327", "text": "The  abomasum , also known as the  maw , [ 1 ]   rennet-bag , [ 1 ]  or  reed tripe , [ 1 ]  is the fourth and final  stomach  compartment in  ruminants . It secretes  rennet , which is used in  cheese  creation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4328", "text": "The word  abomasum  ( ab-  \"away from\" +  omasum  \" intestine  of an  ox \") is from  Neo-Latin  and it was first used in  English  in 1706. It is possibly from the  Gaulish language ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4329", "text": "The abomasum's normal anatomical location is along the ventral midline. It is a  secretory  stomach similar in  anatomy  and function to the  monogastric  stomach. It serves primarily in the  acid   hydrolysis  of  microbial  and dietary  protein , preparing these protein sources for further  digestion  and  absorption  in the  small intestine . The abomasum is lined with glands to release  hydrochloric acid  and digestive enzymes needed to break down food. It is very similar to the nonruminant stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4330", "text": "Dairy cattle on high production diets are susceptible to a number of pathologies, most commonly after calving. A gas-filled abomasum can move into an abnormal location and become  displaced . If the abomasum displaces to the right, it is at risk of torsion. A displaced abomasum will cause cows to present all or some of the following signs: loss of appetite, decrease rumen contractions, decrease cud-chewing, and drop in milk production. While a displaced abomasum is not immediately life-threatening, veterinary care is required for surgical correction. Milder cases can be corrected by rolling the cow over or forcing her to run up a steep hill. [ 2 ]   Abomasitis  is a relatively rare, but serious, disease of the abomasum whose causes are currently unknown."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4331", "text": "The abomasum is used to make the  lampredotto , a typical dish of  Florence . It is also fried and eaten with onions as part of the Korean dish  Makchang gui . Another dish made with the abomasum is the Persian  Sirabi-Shirdan  (borrowed in Turkey as  \u015e\u0131rdan ). Chusta (literally abomasum) is a famous dish in Bihar, India. In Japan, it is grilled and served as  horumonyaki , this particular type of horumon is known as Akasen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4332", "text": "Accessory pancreas  is a rare condition in which small groups of pancreatic cells are separate from the  pancreas . They may occur in the  mesentery  of the  small intestine , the wall of the  duodenum , the upper part of the  jejunum , or more rarely, in the wall of the  stomach ,  ileum ,  gallbladder  or  spleen . The condition was first described by Klob in 1859. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4333", "text": "Accessory pancreas is a small cluster of pancreas cells detached from the pancreas and sometimes found in the wall of the stomach or intestines."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4334", "text": "Pancreatic disorders are often accompanied by weakness and fatigue. The past Medical history may reveal previous disorders of the  biliary tract  or  duodenum , abdominal trauma or surgery, and metabolic disorders such as  diabetes mellitus . The medication history should be detailed and specifically include the use of  thiazides ,  furosemide ,  estrogens ,  corticosteroids , sulfonamides, and opiates. Note a family history of pancreatic disorders. In the review of systems, obtain a complete description of any pain in the upper abdomen or  epigastric  area. Symptoms that may be important in relation to pancreatic disorders are  pruritus , abdominal pain,  dyspnea , nausea, and vomiting. The functional assessment includes data about the patient's dietary habits and use of alcohol."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4335", "text": "Note any restlessness, flushing, or  diaphoresis  during the examination. Vital signs may disclose low-grade fever,  tachypnea ,  tachycardia , and hypotension. Inspect the skin for jaundice. Assess the abdomen for distention, tenderness, discoloration, and diminished bowel sounds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4336", "text": "Tests and procedures used to diagnose pancreatic disorders include laboratory analyses of blood, urine, stool, and pancreatic fluid, and imaging studies. Specific blood studies used to assess pancreatic function include measurements of serum amylase, lipase, glucose, calcium, and  triglyceride levels . Urine amylase and renal amylase clearance tests may also be ordered. Stool specimens may be analyzed for fat content. The secretin stimulation test measures the bicarbonate concentration of pancreatic fluid after secretin is given intravenously to stimulate the production of pancreatic fluid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4337", "text": "Treatment of accessory pancreas depends on the location and extent of the injured tissue. Surgery may be an option, or some physicians order  prophylactic antibiotics ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4338", "text": "Alkaline mucus  is a thick fluid produced by animals which confers tissue protection in an  acidic  environment, such as in the  stomach . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4339", "text": "Mucus  that serves a protective function against acidic environments generally has a high  viscosity , though the thickness and viscosity of the mucus layer can vary due to several factors. For example, alkaline mucus in the stomach increases in thickness when the stomach is distended. [ 2 ]  The  pH  level of the mucus also plays a role in its viscosity, as higher pH levels tend to alter the thickness of the mucus, making it less viscous. [ 1 ]  Because of this, invading agents such as  Helicobacter pylori , a bacterium that causes stomach ulcers, can alter the pH of the mucus to make the mucus pliable enough to move through. [ 3 ]  Exposure to atmospheric air also tends to increase the pH level of alkaline mucus. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4340", "text": "In humans, alkaline mucus is present in several organs and provides protection by way of its alkalinity and high  viscosity . Alkaline mucus exists in the human  eye ,  stomach ,  saliva , and  cervix . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4341", "text": "In the stomach, alkaline mucus is secreted by gastric glands in the  gastric mucosa  of the stomach wall. [ 6 ]  Secretion of alkaline mucus is necessary to protect the  mucous membrane  of the stomach from acids released during digestion. [ 6 ]  Ulcers can develop as a result of damage caused to the  gastric mucosal barrier . [ 7 ]  Duodenal ulcers have been shown to develop in sites that are in direct contact with pepsin and acids. [ 8 ]  To prevent damage and protect the mucus epithelium, alkaline mucus secretions increase in the digestive system when food is being eaten. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4342", "text": "In the cervix, alkaline mucus has been shown to possess  bactericidal  properties to protect the cervix, uterus, peritoneal cavity, and vagina from microbes. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4343", "text": "Alkaline tide (mal del puerco)  refers to a condition, normally encountered after eating a meal, where during the production of  hydrochloric acid  by the  parietal cells  in the stomach, the parietal cells secrete  bicarbonate ions  across their basolateral membranes and into the  blood , causing a temporary increase in blood pH. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4344", "text": "During hydrochloric acid secretion in the stomach, the gastric  parietal cells  extract chloride anions, carbon dioxide, water and sodium cations from the blood plasma and in turn release bicarbonate back into the plasma after forming it from carbon dioxide and water constituents. This is to maintain the plasma's electrical balance, as the chloride anions have been extracted. The bicarbonate content causes the venous blood leaving the stomach to be more alkaline than the arterial blood delivered to it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4345", "text": "The alkaline tide is neutralised by a secretion of H +  into the blood during HCO 3 \u2212  secretion in the pancreas. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4346", "text": "Postprandial  (i.e., after a meal) alkaline tide lasts until the acids in food absorbed in the small intestine reunite with the bicarbonate that was produced when the food was in the stomach. Thus, alkaline tide is self-limited and normally lasts less than two hours."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4347", "text": "Postprandial alkaline tide has also been shown to be a causative agent of  calcium oxalate   urinary stones  in cats, [ 3 ]  and potentially in other species. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4348", "text": "A more pronounced alkaline tide results from  vomiting , which stimulates hyperactivity of gastric  parietal cells  to replace lost stomach acid. [ verification needed ]  Thus, protracted vomiting can result in  metabolic alkalosis . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4349", "text": "This  cardiovascular system  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4350", "text": "The  anal canal  is the part that connects the  rectum  to the  anus , located below the level of the  pelvic diaphragm . [ 1 ]  It is located within the  anal triangle  of the  perineum , between the right and left  ischioanal fossa . As the final functional segment of the  bowel , it functions to regulate release of  excrement  by two muscular  sphincter  complexes. The anus is the aperture at the terminal portion of the anal canal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4351", "text": "In humans, the anal canal is approximately 2.5 to 4\u00a0cm (0.98 to 1.57\u00a0in) long, from the anorectal junction to the  anus . [ 2 ] [ 3 ] [ 4 ]  It is directed downwards and backwards. It is surrounded by inner involuntary and outer voluntary sphincters which keep the  lumen  closed in the form of an anteroposterior slit."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4352", "text": "The canal is differentiated from the rectum by a transition along the internal surface from  endodermal  to skin-like   ectodermal  tissue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4353", "text": "The anal canal is traditionally divided into two segments, upper and lower, separated by the  pectinate line  (also known as the dentate line):"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4354", "text": "The  anal verge  refers to the  distal  end of the anal canal, a transitional zone between the  epithelium  of the anal canal and the  perianal skin . It should not be confused with the pectinate line between the upper and lower zones within the anal canal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4355", "text": "The  anal gland  secretes lymphal discharge and built-up  fecal matter  from the  colon  lining. In some animals this gland expungement can be done routinely every 24\u201336 months to prevent infection and  fistula  formation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4356", "text": "The  external anal sphincter  muscle is the voluntary muscle that surrounds and adheres to the anus at the lower margin of the anal canal. This muscle is in a state of  tonic contraction , but during  defecation , it relaxes to allow the release of  feces ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4357", "text": "Movement of the feces is also controlled by the involuntarily controlled internal anal sphincter, which is an extension of the circular muscle surrounding the anal canal. It relaxes to expel feces from the rectum and anal canal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4358", "text": "Anal columns  ( Columns of Morgagni  or less commonly  Morgagni's columns ) are a number of vertical folds, produced by an infolding of the  mucous membrane  and some of the muscular tissue in the upper half of the  lumen  of the  anal canal . They are named after  Giovanni Battista Morgagni , who has several other  eponyms named after him ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4359", "text": "This article incorporates text in the  public domain  from  page 1185  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4360", "text": "An  anal sinus  ( rectal sinus ) is a furrow formed between any two adjacent  anal columns  of the  anal canal . An anal sinus is limited inferiorly by an  anal valve  (which unites the inferior ends of a pair of adjacent anal columns). The  anal glands  open into the anal sinuses. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4361", "text": "An  anal valve  is a small horizontal fold uniting the inferior ends of any two adjacent  anal columns  of the  anal canal . An anal valve forms the inferior boundary of an  anal sinus . The anal valves demarcate the level of the  pectinate line . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4362", "text": "An  anastomosis  ( / \u0259 \u02cc n \u00e6 s t \u0259 \u02c8 m o\u028a s \u026a s / ,  pl. :  anastomoses ) is a connection or opening between two things (especially cavities or passages) that are normally diverging or branching, such as between  blood vessels ,  leaf veins , or  streams . Such a connection may be normal (such as the  foramen ovale in a fetus' heart ) or abnormal (such as the  patent foramen ovale  in an adult's heart); it may be acquired (such as an  arteriovenous fistula ) or innate (such as the arteriovenous shunt of a  metarteriole ); and it may be natural (such as the aforementioned examples) or artificial (such as a  surgical anastomosis ). The reestablishment of an anastomosis that had become blocked is called a reanastomosis. Anastomoses that are abnormal, whether  congenital  or acquired, are often called  fistulas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4363", "text": "The term is used in  medicine , [ 1 ]   biology ,  mycology ,  geology , and  geography ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4364", "text": "Anastomosis: medical or Modern Latin, from Greek \u1f00\u03bd\u03b1\u03c3\u03c4\u03cc\u03bc\u03c9\u03c3\u03b9\u03c2, anastomosis, \"outlet, opening\", Greek ana- \"up, on, upon\", stoma \"mouth\", \"to furnish with a mouth\". [ 2 ]  Thus the  -stom-  syllable is cognate with that of  stoma  in botany  or  stoma  in medicine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4365", "text": "An anastomosis is the connection of two normally divergent structures. [ 3 ]  It refers to connections between  blood vessels  or between other tubular structures such as loops of  intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4366", "text": "In  circulatory anastomoses , many arteries naturally anastomose with each other; for example, the  inferior epigastric artery  and  superior epigastric artery , or the anterior and/or posterior communicating arteries in the  Circle of Willis  in the brain. The circulatory anastomosis is further divided into arterial and venous anastomosis. Arterial anastomosis includes actual arterial anastomosis (e.g.,  palmar arch ,  plantar arch ) and potential arterial anastomosis (e.g.  coronary arteries  and cortical branch of  cerebral arteries ). Anastomoses also form alternative routes around  capillary  beds in areas that do not need a large blood supply, thus helping regulate  systemic blood flow . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4367", "text": "Surgical anastomosis  occurs when segments of  intestine , blood vessel, or any other structure are connected together surgically (anastomosed). Examples include arterial anastomosis in  bypass surgery , intestinal anastomosis after a piece of intestine has been resected,  Roux-en-Y anastomosis  and  ureteroureterostomy .  Surgical anastomosis techniques include linear stapled anastomosis, [ 4 ]  hand sewn anastomosis, [ 4 ]  end-to-end anastomosis (EEA). [ 5 ]  Anastomosis can be performed by hand or with an anastomosis assist device. [ 6 ]  Studies have been performed comparing various anastomosis approaches taking into account surgical \"time and cost, postoperative anastomotic bleeding, leakage, and stricture\". [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4368", "text": "Pathological  anastomosis results from  trauma  or  disease  and may involve  veins ,  arteries , or  intestines . These are usually referred to as  fistulas . In the cases of veins or arteries, traumatic fistulas usually occur between artery and vein. Traumatic intestinal fistulas usually occur between two loops of intestine (entero-enteric fistula) or intestine and  skin  (enterocutaneous fistula).  Portacaval anastomosis , by contrast, is an anastomosis between a vein of the  portal circulation  and a vein of the  systemic circulation , which allows blood to bypass the  liver  in patients with  portal hypertension , often resulting in  hemorrhoids ,  esophageal varices , or  caput medusae . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4369", "text": "In  evolution , anastomosis is a recombination of evolutionary lineage. Conventional accounts of evolutionary lineage present themselves as the branching out of species into novel forms.  Under anastomosis, species might recombine after initial branching out, such as in the case of recent research that shows that ancestral populations along human and chimpanzee lineages may have interbred after an initial branching event. [ 8 ]  The concept of anastomosis also applies to the theory of  symbiogenesis , in which new  species  emerge from the formation of novel symbiotic relationships. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4370", "text": "In  mycology , anastomosis is the fusion between branches of the same or different  hyphae . [ 9 ]  Hence the bifurcating fungal hyphae can form true reticulating networks. By sharing materials in the form of dissolved  ions ,  hormones , and  nucleotides , the fungus maintains bidirectional communication with itself. The fungal network might begin from several origins; several spores (i.e. by means of  conidial anastomosis tubes ), several points of penetration, each a spreading circumference of absorption and assimilation. Once encountering the tip of another expanding, exploring self, the tips press against each other in  pheromonal  recognition or by an unknown recognition system, fusing to form a genetic singular clonal colony that can cover hectares called a  genet  or just microscopical areas. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4371", "text": "For fungi, anastomosis is also a component of reproduction. In some fungi, two different  haploid  mating types \u2013 if compatible \u2013 merge.  Somatically , they form a morphologically similar mycelial wave front that continues to grow and explore. The significant difference is that each  septated  unit is binucleate, containing two unfused  nuclei , i.e. one from each parent that eventually undergoes  karyogamy  and meiosis to complete the sexual cycle. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4372", "text": "Also the term \"anastomosing\" is used for mushroom gills which interlink and separate to form a network. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4373", "text": "The growth of a  strangler fig  around a host tree, with tendrils fusing together to form a mesh, is called anastomosing. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4374", "text": "In  geology ,  veins  of  quartz  (or other) minerals can display anastomosis. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4375", "text": "Ductile  shear zones  frequently show anastomosing geometries of highly- strained  rocks around lozenges of less-deformed material. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4376", "text": "Molten  lava flows  sometimes flow in anastomosed  lava channels [ 15 ]  or  lava tubes . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4377", "text": "In cave systems, anastomosis is the splitting of cave passages that later reconnect. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4378", "text": "Anastomosing rivers ,  anastomosing streams  consist of multiple channels that divide and reconnect and are separated by semi-permanent banks formed of cohesive material, such that they are unlikely to migrate from one channel position to another. They can be confused with  braided rivers  based on their planforms alone, but braided rivers are much shallower and more dynamic than anastomosing rivers. Some definitions require that an anastomosing river be made up of interconnected channels that enclose floodbasins, [ 18 ]  again in contrast with braided rivers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4379", "text": "Rivers with anastomosed  reaches  include the  Magdalena River  in  Colombia , [ 19 ]  the upper  Columbia River  in  British Columbia , Canada, [ 20 ]  the  Drumheller Channels  of the  Channeled Scablands  of the state of Washington, US, and the upper  Narew River  in  Poland . [ 21 ]  The term  anabranch  has been used for segments of anastomosing rivers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4380", "text": "Braided streams  show anastomosing channels around  channel bars  of  alluvium . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4381", "text": "The  angle of His , also known as the  esophagogastric angle , is the acute angle created between the  cardia  at the entrance to the  stomach , and the  esophagus . It helps to prevent acid reflux of stomach acid into the esophagus. It is commonly undeveloped in  infants , making acid reflux more common."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4382", "text": "The angle of His is the  acute angle  between the  stomach  and the  esophagus . [ 1 ]  It is created by the collar sling fibres and the circular muscles around this gastroesophageal junction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4383", "text": "The angle of His is normally undeveloped in  infants , with the esophagus making a vertical junction with the stomach. [ 3 ]  As a result, reflux of stomach contents is common. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4384", "text": "The angle of His forms an anatomical sphincter. This prevents the reflux of  stomach acid ,  digestive enzymes , and duodenal  bile  from entering the esophagus. [ 4 ] [ 5 ]  This is important in preventing  gastroesophageal reflux disease  and  inflammation  of the esophagus. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4385", "text": "The angle of His is also known as the esophagogastric angle. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4386", "text": "The  angular incisure  (or  angular notch ) is a small notch on the  stomach . It is located on the  lesser curvature of the stomach  near the  pyloric  end. Its location varies depending on how distended the stomach is. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4387", "text": "The angular incisure is used as a separation point between the right and left portions of the stomach, the body and the pylorus. [ 2 ]  An imaginary line drawn perpendicular to the lesser curvature of the stomach through the angular incisure makes up the boundary between the  body of the stomach  and pylorus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4388", "text": "The  anocutaneous line , also called the  Hilton white line  or  intersphincteric groove , is a boundary in the  anal canal . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4389", "text": "Below the anocutaneous line, lymphatic drainage is to the  superficial inguinal nodes . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4390", "text": "The anocutaneous line is slightly below the  pectinate line  and a landmark for the intermuscular border between  internal  and  external anal sphincter  muscles."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4391", "text": "The anocutaneous line represents the transition point from non-keratinized  stratified squamous epithelium  of the anal canal to  keratinized  stratified squamous epithelium of the  anus  and  perianal skin . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4392", "text": "In live persons, the color of the line is white, hence the alternative name. It is named for  John Hilton . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4393", "text": "In  mammals ,  invertebrates  and most  fish , [ 1 ] [ 2 ]  the  anus  ( pl. :  anuses  or  ani ; from  Latin , 'ring' or 'circle') is the external  body orifice  at the  exit  end of the  digestive tract  ( bowel ), i.e. the opposite end from the  mouth . Its function is to facilitate the  expulsion  of wastes that remain after  digestion ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4394", "text": "Bowel contents that pass through the anus include the gaseous  flatus  and the semi-solid  feces , which (depending on the type of animal) include: indigestible matter such as  bones ,  hair   pellets ,  endozoochorous   seeds  and  digestive rocks ; [ 3 ]  residual  food  material after the digestible  nutrients  have been extracted, for example  cellulose  or  lignin ; ingested matter which would be toxic if it remained in the digestive tract;  excreted   metabolites  like  bilirubin -containing  bile ; and dead  mucosal   epithelia  or excess  gut bacteria  and other  endosymbionts . Passage of feces through the anus is typically controlled by  muscular   sphincters , and failure to stop unwanted passages results in  fecal incontinence ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4395", "text": "Amphibians ,  reptiles  and  birds  use a similar orifice (known as the  cloaca ) for excreting liquid and solid wastes, for  copulation  and  egg-laying .  Monotreme  mammals also have a cloaca, which is thought to be a feature inherited from the earliest  amniotes .  Marsupials  have a single orifice for excreting both solids and liquids and, in females, a separate  vagina  for reproduction. Female  placental  mammals have completely separate orifices for  defecation ,  urination , and reproduction; males have one opening for defecation and  another for both urination and reproduction , although the channels flowing to that orifice are almost completely separate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4396", "text": "The development of the anus was an important stage in the evolution of multicellular animals. It appears to have happened at least twice, following different paths in  protostomes  and  deuterostomes . This accompanied or facilitated other important evolutionary developments: the  bilaterian body plan , the  coelom , and  metamerism , in which the body was built of repeated \"modules\" which could later specialize, such as the heads of most  arthropods , which are composed of fused, specialized segments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4397", "text": "In  comb jellies , there are species with one and sometimes two permanent anuses, species like the  warty comb jelly  grows an anus, which then disappear when it is no longer needed. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4398", "text": "In animals at least as complex as an  earthworm , the  embryo  forms a dent on one side, the  blastopore , which deepens to become the  archenteron , the first phase in the growth of the  gut . In deuterostomes, the original dent becomes the anus while the gut eventually tunnels through to make another opening, which forms the mouth. The protostomes were so named because it was thought that in their embryos the dent formed the mouth first ( proto\u2013  meaning \"first\") and the anus was formed later at the opening made by the other end of the gut. Research from 2001 shows the edges of the dent close up in the middles of protosomes, leaving openings at the ends which become the mouths and anuses. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4399", "text": "In the  anatomy  of humans and homologous primates, the  ascending colon  is the part of the  colon  located between the  cecum  and the  transverse colon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4400", "text": "The ascending colon is smaller in calibre than the cecum from where it starts. It passes upward, opposite the  colic valve , to the under surface of the  right lobe of the liver , on the right of the  gall-bladder , where it is lodged in a shallow depression, the  colic impression ; here it bends abruptly forward and to the left, forming the  right colic flexure  (hepatic) where it becomes the transverse colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4401", "text": "It is retained in contact with the posterior wall of the abdomen by the peritoneum, which covers its anterior surface and sides, its posterior surface being connected by  loose areolar tissue  with the  iliacus ,  quadratus lumborum ,  aponeurotic  origin of  transversus abdominis , and with the front of the lower and lateral part of the right kidney."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4402", "text": "Sometimes the  peritoneum  completely invests it and forms a distinct but narrow  mesocolon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4403", "text": "It is in relation, in front, with the convolutions of the  ileum  and the abdominal walls."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4404", "text": "Parasympathetic innervation  to the ascending colon is supplied by the  vagus nerve .  Sympathetic innervation  is supplied by the thoracic  splanchnic nerves ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4405", "text": "The ascending colon is on the right side of the body (barring any malformations). The term  right colon  is  hypernymous  to  ascending colon  in precise use; many casual mentions of the right colon chiefly concern the ascending colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4406", "text": "This article incorporates text in the  public domain  from  page 1180  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4407", "text": "The  myenteric plexus  (or  Auerbach 's plexus ) provides motor innervation to both layers of the  muscular layer  of the gut, having both parasympathetic and sympathetic input (although present ganglion cell bodies belong to  parasympathetic  innervation, fibers from sympathetic innervation also reach the plexus), whereas the  submucous plexus  provides  secretomotor  innervation to the  mucosa  nearest the  lumen  of the gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4408", "text": "It arises from cells in the  vagal trigone  also known as the nucleus ala cinerea, the parasympathetic nucleus of origin for the tenth cranial nerve ( vagus nerve ), located in the  medulla oblongata . The fibers are carried by both the anterior and posterior vagal nerves. The myenteric plexus is the major nerve supply to the  gastrointestinal  tract and controls GI tract  motility . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4409", "text": "According to preclinical studies, 30% of myenteric plexus' neurons are  enteric sensory neurons , thus Auerbach's plexus has also a sensory component. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4410", "text": "A part of the  enteric nervous system , the myenteric plexus exists between the longitudinal and circular layers of muscularis externa in the gastrointestinal tract.  It is found in the muscles of the esophagus, stomach, and intestine. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4411", "text": "The ganglia have properties similar to the  central nervous system  (CNS). These properties include presence of glia, interneurons, a small extracellular space, dense synaptic neuropil, isolation from blood vessels, multiple synaptic mechanisms and multiple neurotransmitters."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4412", "text": "The myenteric plexus originates in the  medulla oblongata  as a collection of neurons from the ventral part of the brain stem. The vagus nerve then carries the axons to their destination in the gastrointestinal tract. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4413", "text": "They contain  Dogiel cells . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4414", "text": "The myenteric plexus functions as a part of the enteric nervous system (digestive system). The enteric nervous system can and does function autonomously, but normal digestive function requires communication links between this intrinsic system and the central nervous system. The ENS contains sensory receptors, primary afferent neurons, interneurons, and motor neurons. The events that are controlled, at least in part, by the ENS are multiple and include motor activity, secretion, absorption, blood flow, and interaction with other organs such as the gallbladder or pancreas. These links take the form of parasympathetic and sympathetic fibers that connect either the central and enteric nervous systems or connect the central nervous system directly with the digestive tract. Through these cross connections, the gut can provide sensory information to the CNS, and the CNS can affect gastrointestinal function. Connection to the central nervous system also means that signals from outside of the digestive system can be relayed to the digestive system: for instance, the sight of appealing food stimulates secretion in the stomach. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4415", "text": "The enteric nervous system makes use of over 30 different neurotransmitters, most similar to those of the CNS such as  acetylcholine ,  dopamine , and  serotonin . More than 90% of the body's serotonin lies in the gut; as well as about 50% of the body's dopamine, which is currently being studied to further our understanding of its utility in the brain. [ 7 ] \nThe heavily studied  neuropeptide  known as  substance P  is present in significant levels and may help facilitate the production of saliva, smooth muscle contractions, and other tissue responses."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4416", "text": "Since many of the same neurotransmitters are found in the ENS as the brain, it follows that myenteric neurons can express receptors for both peptide and non-peptide (amines, amino acids, purines) neurotransmitters. Generally, expression of a receptor is limited to a subset of myenteric neurons, with probably the only exception being expression of nicotinic cholinergic receptors on all myenteric neurons. One receptor that has been targeted for therapeutic reasons has been the  5-hydroxytryptamine (5-HT 4 ) receptor . Activating this pre-synaptic receptor enhances cholinergic neurotransmission and can stimulate gastrointestinal motility. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4417", "text": "The enteric nervous system exhibits taste receptors similar to the ones in the tongue. The taste receptor  TAS1R3  and the taste G protein  gustducin  are two of the most common. These receptors sense \"sweetness\" on the tongue and sense glucose in the enteric nervous system. These receptors help regulate the secretion of insulin and other hormones that are responsible for controlling blood sugar levels. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4418", "text": "Hirschsprung's disease  is a congenital disorder of the colon in which nerve cells of the myenteric plexus in its walls, also known as ganglion cells, are absent. Hirschsprung's disease is a form of functional low bowel obstruction due to failure of caudal migration of  neuroblasts  within developing bowel \u2013 this results in an absence of parasympathetic intrinsic ganglion cells in both Auerbach's and Meissner's plexuses. The distal large\nbowel from the point of neuronal arrest to the anus is continuously aganglionic. It is a rare disorder (1:5000), with prevalence among males being four times that of females. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4419", "text": "Achalasia  is a motor disorder of the esophagus characterized by decrease in ganglion cell density in the myenteric plexus. The cause of the lesion is unknown. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4420", "text": "Myenteric plexi destruction has been found to be secondary to Chagas disease (T. cruzi infection sequelae). Destruction occurs in the esophagus, intestines, and ureters. This denervation can lead to secondary achalasia (lower esophageal sphincter will not open; loss of inhibitory neurons), megacolon, and megaureter, respectively."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4421", "text": "Because the ENS is known as the \"brain of the gut\", due to its similarities with the CNS, researchers have been using colonic biopsies of Parkinson's patients to help better understand and manage  Parkinson's disease . [ 12 ]  PD patients are known to experience severe constipation due to GI tract dysfunction years before the onset of motor movement complications, which characterises Parkinson's disease. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4422", "text": "Leopold Auerbach , a neuropathologist, was one of the first to further research the nervous system using histological staining methods. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4423", "text": "The  basal  or  basic electrical rhythm  ( BER ) or  electrical control activity  ( ECA ) is the spontaneous depolarization and repolarization of pacemaker cells known as  interstitial cells of Cajal  (ICCs) in the  smooth muscle  of the stomach, small intestine, and large intestine. This electrical rhythm is spread through  gap junctions  in the smooth muscle of the  GI tract . [ 1 ]  These pacemaker cells, also called the ICCs, control the frequency of contractions in the gastrointestinal tract. The cells can be located in either the circular or longitudinal layer of the smooth muscle in the GI tract; circular for the small and large intestine, longitudinal for the stomach. [ 2 ]  The frequency of contraction differs at each location in the GI tract beginning with 3 per minute in the  stomach , then 12 per minute in the  duodenum , 9 per minute in the  ileum , and a normally low one contraction per 30 minutes in the  large intestines  that increases 3 to 4 times a day due to a phenomenon called  mass movement . [ 2 ]  The basal electrical rhythm controls the frequency of contraction but additional neuronal and hormonal controls regulate the strength of each contraction."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4424", "text": "Smooth muscle  within the GI tract causes the involuntary  peristaltic  motion that moves consumed food down the  esophagus  and towards the  rectum . [ 1 ]   The smooth muscle throughout most of the GI tract is divided into two layers: an outer longitudinal layer and an inner circular layer. [ 1 ]   Both layers of muscle are located within the  muscularis externa .  The stomach has a third layer: an innermost oblique layer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4425", "text": "The physical contractions of the smooth muscle cells can be caused by  action potentials  in  efferent   motor neurons  of the  enteric nervous system , or by receptor mediated calcium influx. [ 1 ]  These efferent motor neurons of the enteric nervous system are cholinergic and adrenergic neurons. [ 2 ]  The inner circular layer is innervated by both excitatory and inhibitory motor neurons, while the outer longitudinal layer is innervated by mainly excitatory neurons.  These action potentials cause the smooth muscle cells to contract or relax, depending on the particular stimulation the cells receive.  Longitudinal muscle fibers depend on calcium influx into the cell for  excitation-contraction coupling , while circular muscle fibers rely on intracellular calcium release.  Contraction of the smooth muscle can occur when the BER reaches its plateau (an absolute value less than -45mV) [ citation needed ]  while a simultaneous stimulatory action potential occurs.  A contraction will not occur unless an action potential occurs.  Generally, BER waves stimulate action potentials and action potentials stimulate contractions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4426", "text": "The  interstitial cells of Cajal  are specialized pacemaker cells  [ 3 ]  located in the wall of the stomach, small intestine, and large intestine. [ 1 ]   These cells are connected to the smooth muscle via  gap junctions  and the  myenteric plexus .  The cell membranes of the pacemaker cells undergo a rhythmic  depolarization  and repolarization from -65 mV  to -45mV. [ citation needed ]   This rhythm of depolarization-repolarization of the cell membrane creates a slow wave known as a BER, and it is transmitted to the smooth muscle cells.  The frequency of these depolarizations in a region of the GI tract determines the possible frequency of contractions.  In order for a contraction to occur, a  hormone  or  neurocrine  signal must induce the smooth muscle cell to have an action potential.  The basal electrical rhythm allows the smooth muscle cell to depolarize and contract rhythmically when exposed to hormonal signals.  This action potential is transmitted to other smooth muscle cells via gap junctions, creating a peristaltic wave."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4427", "text": "The specific mechanism for the contraction of smooth muscle in the GI tract depends upon  IP3R calcium release  channels in the muscle. [ 4 ]   Calcium  release from IP3 sensitive calcium stores activates calcium dependent  chloride channels . [ 4 ]  These chloride channels trigger spontaneous transient inward current which couples the calcium oscillations to electrical activity. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4428", "text": "The number of action potentials during the plateau of a particular BER slow wave can vary.  This variation in action potential generation does not impact the frequency of waves through the GI tract, only the strength of those contractile waves. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4429", "text": "The cells that respond to and secrete these substances include  I cells  and  K cells  in the proximal small intestine, whose stimulation is dependent on nutrient exposure and entry into the duodenum, and  L cells  in the distal small intestine and colon which are stimulated by unabsorbed nutrients and gastric emptying. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4430", "text": "The frequency of the BER, and thus the contractions, changes throughout the GI tract.  The  frequency  in the stomach is 3 per minute, while the  duodenum  is 11 to 12 per minute and the  ileum  is 9 per minute. [ 1 ]   The colon can have a BER frequency between 2 and 13 per minute. The electrical activity is oscillatory, so that the BER has peaks and valleys when graphed over time."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4431", "text": "B. a. animalis B. a. lactis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4432", "text": "Bifidobacterium animalis  is a  gram-positive , anaerobic, rod-shaped bacterium of the  Bifidobacterium  genus which can be found in the  large intestines  of most  mammals , including humans."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4433", "text": "Bifidobacterium animalis  and  Bifidobacterium lactis  were previously described as two distinct species. Presently, both are considered  B. animalis  with the subspecies  Bifidobacterium animalis  subsp.  animalis  and  Bifidobacterium animalis  subsp.  lactis . [ 1 ] [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4434", "text": "Both old names  B. animalis  and  B. lactis  are still used on product labels, as this species is frequently used as a  probiotic . In most cases, which subspecies is used in the product is not clear."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4435", "text": "Several companies have attempted [ clarification needed ]  to trademark particular strains, and as a marketing technique, have invented scientific-sounding names for the strains."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4436", "text": "Danone  (Dannon in the United States) markets the subspecies strain  DN 173 010  as Bifidus Digestivum (UK), Bifidus Regularis (US and Mexico), Bifidobacterium Lactis or B.L. Regularis (Canada), DanRegularis (Brazil), Bifidus Actiregularis (Argentina, Austria, Belgium, Bulgaria, Chile, Czech Republic, France, Germany, Greece, Hungary, Israel, Italy, Kazakhstan, Netherlands, Portugal, Romania, Russia, South Africa, Spain and the UK), and Bifidus Essensis in the Middle East (and formerly in Hungary, Bulgaria, Romania and The Netherlands) through  Activia  from Safi Danone KSA. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4437", "text": "Chr. Hansen A/S  from Denmark has a similar claim on a strain of  Bifidobacterium animalis  subsp.  lactis , marketed under the trademark BB-12. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4438", "text": "Lidl  lists \"Bifidobacterium BB-12\" in its \"Proviact\" yogurt."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4439", "text": "Bifidobacterium lactis  Bl-04 and Bi-07 are strains from  DuPont 's  Danisco  FloraFIT range. They are used in many dietary probiotic supplements."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4440", "text": "Theralac contains the strains  Bifidobacterium lactis  BI-07 and  Bifidobacterium lactis  BL-34 [ 5 ]  (also called BI-04) in its probiotic capsule."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4441", "text": "Bifidobacterium animalis lactis  HN019 (DR10) is a strain from  Fonterra  licensed to DuPont, which markets it as HOWARU Bifido. It is sold in a variety of commercial probiotics, among them  Tropicana Products  Essentials Probiotics, [ 6 ]  Attune Wellness Bars [ 7 ]  and NOW Foods Clinical GI Probiotic. [ 8 ]  Fonterra has a yogurt that is sold in New Zealand called Symbio Probalance, where the strain is labelled as DR10."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4442", "text": "Bifidobacterium animalis  subspecies lactis BB-12 administered in combination with other probiotics has showed \"a trend toward increased remission\" in a study of 32 patients with  ulcerative colitis . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4443", "text": "Research on  Bifidobacterium animalis  supplementation in preterm infants, as detailed in the systematic review by Szajewska et al., a meta-analysis of four randomized controlled trials (RCTs) involving a total of 324 infants, has shown promising results. These include increased fecal bifidobacteria counts, reduced Enterobacteriaceae and Clostridium spp counts, as well as improvements in stool pH, fecal calprotectin concentrations, fecal immunoglobulin A levels, and short-chain fatty acid concentrations. However, the analysis did not find significant effects on the risk of necrotizing enterocolitis stage \u22652, risk of sepsis, or use of antibiotics compared to controls. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4444", "text": "B. animalis  is present in many food products and dietary supplements. The  probiotic  is mostly found in dairy products. [ 11 ]   Bifidobacterium animalis  subsp.  lactis  BB-12 is a bacterial subspecies within the  animalis  strain that exhibits rod-shaped structure and lacks catalase activity. The subspecies was initially identified as  Bifidobacterium bifidum , however advancements in molecular classification later reclassified it as  Bifidobacterium animalis , and subsequently as  Bifidobacterium animalis  subsp.  lactis.  It was first preserved in Chr. Hansen's cell culture bank in 1983 as part of the dairy culture collection. It exhibits suitability for producing probiotic dairy products and has found application in infant formula, dietary supplements, and fermented milk products. This is due to a variety of favorable technological characteristics such as its fermentation activity, high tolerance to air, stability, and resilience to acidic and bile environments, even in freeze-dried products. Moreover,  Bifidobacterium animalis  subsp.  lactis BB-12 does not alter the taste, appearance, or texture of food products and maintains viability in probiotic foods until consumption. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4445", "text": "The manipulation of the  gut flora  is complex and may cause bacteria-host interactions. [ 13 ]  Although  probiotics , in general, are considered safe, there are concerns about their use in certain cases. [ 13 ] [ 14 ]  Some people, such as those with  compromised immune systems ,  short bowel syndrome ,  central venous catheters ,  heart valve disease  and  premature infants , may be at higher risk for adverse events. [ 15 ]  Rarely, consumption of probiotics may cause  bacteremia , and  sepsis , potentially fatal infections in children with lowered immune systems or who are already critically ill. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4446", "text": "Bile  (from Latin  bilis ), or  gall , is a yellow-green/misty green fluid produced by the  liver  of most  vertebrates  that aids the  digestion  of  lipids  in the  small intestine . In humans, bile is primarily composed of  water , is produced continuously by the liver, and is stored and concentrated in the  gallbladder . After a human eats, this stored bile is discharged into  the first section of the small intestine . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4447", "text": "In the human  liver , bile is composed of 97\u201398%  water , 0.7%  bile salts , 0.2%  bilirubin , 0.51% fats ( cholesterol ,  fatty acids , and  lecithin ), and 200 meq/L inorganic salts. [ 2 ] [ 3 ]  The two main pigments of bile are  bilirubin , which is orange-yellow, and its oxidised form  biliverdin , which is green. When mixed, they are responsible for the brown color of  feces . [ 4 ]  About 400 to 800 milliliters (14 to 27 U.S. fluid ounces) of bile is produced per day in adult human beings. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4448", "text": "Bile or gall acts to some extent as a  surfactant , helping to  emulsify  the lipids in food. Bile salt  anions  are  hydrophilic  on one side and  hydrophobic  on the other side; consequently, they tend to aggregate around droplets of lipids ( triglycerides  and  phospholipids ) to form  micelles , with the hydrophobic sides towards the fat and hydrophilic sides facing outwards. [ 6 ]  The hydrophilic sides are negatively charged, and this charge prevents fat droplets coated with bile from re-aggregating into larger fat particles. Ordinarily, the micelles in the  duodenum  have a diameter around 1\u201350\u00a0 \u03bcm  in humans. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4449", "text": "The dispersion of food fat into micelles provides a greatly increased surface area for the action of the enzyme  pancreatic lipase , which digests the triglycerides, and is able to reach the fatty core through gaps between the bile salts. [ 8 ]  A triglyceride is broken down into two fatty acids and a  monoglyceride , which are absorbed by the  villi  on the intestine walls. After being transferred across the intestinal membrane, the fatty acids reform into triglycerides ( re-esterified ), before being absorbed into the lymphatic system through  lacteals . Without bile salts, most of the lipids in food would be excreted in feces, undigested. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4450", "text": "Since bile increases the absorption of fats, it is an important part of the absorption of the fat-soluble substances, [ 10 ]  such as the  vitamins   A ,  D ,  E , and  K . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4451", "text": "Besides its digestive function, bile serves also as the route of excretion for bilirubin, a byproduct of  red blood cells  recycled by the liver. Bilirubin derives from  hemoglobin  by  glucuronidation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4452", "text": "Bile tends to be  alkaline  on average. The  pH  of common duct bile (7.50 to 8.05) is higher than that of the corresponding gallbladder bile (6.80 to 7.65). Bile in the gallbladder becomes more  acidic  the longer a person goes without eating, though resting slows this fall in pH. [ 12 ]  As an alkali, it also has the function of neutralizing excess  stomach acid  before it enters the duodenum, the first section of the  small intestine .  Bile salts  also act as  bactericides , destroying many of the microbes that may be present in the food. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4453", "text": "In the absence of bile, fats become indigestible and are instead excreted in  feces , a condition called  steatorrhea . Feces lack their characteristic brown color and instead are white or gray, and greasy. [ 14 ]  Steatorrhea can lead to deficiencies in  essential fatty acids  and  fat-soluble vitamins . [ 15 ]  In addition, past the small intestine (which is normally responsible for absorbing fat from food) the  gastrointestinal tract  and  gut flora  are not adapted to processing fats, leading to problems in the large intestine. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4454", "text": "The  cholesterol  contained in bile will occasionally accrete into lumps in the gallbladder, forming  gallstones . Cholesterol gallstones are generally treated through surgical removal of the gallbladder. However, they can sometimes be dissolved by increasing the concentration of certain naturally occurring bile acids, such as  chenodeoxycholic acid  and  ursodeoxycholic acid . [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4455", "text": "On an empty stomach \u2013 after repeated  vomiting , for example \u2013 a person's vomit may be green or dark yellow, and very bitter. The bitter and greenish component may be bile or normal digestive juices originating in the stomach. [ 19 ]  Bile may be forced into the stomach secondary due to a weakened valve ( pylorus ), the presence of certain drugs including  alcohol , or powerful muscular contractions and duodenal spasms. This is known as  biliary reflux . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4456", "text": "Biliary obstruction refers to a condition when  bile ducts  which deliver bile from the gallbladder or liver to the duodenum become obstructed. The blockage of bile might cause a buildup of  bilirubin  in the  bloodstream  which can result in  jaundice . There are several potential causes for biliary obstruction including gallstones, cancer, [ 21 ]  trauma,  choledochal cysts , or other benign causes of bile duct narrowing. [ 22 ]  The most common cause of bile duct obstruction is when gallstone(s) are dislodged from the gallbladder into the cystic duct or common bile duct resulting in a blockage. A blockage of the gallbladder or  cystic duct  may cause  cholecystitis . If the blockage is beyond the confluence of the pancreatic duct, this may cause gallstone  pancreatitis . In some instances of biliary obstruction, the bile may become infected by bacteria resulting in  ascending cholangitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4457", "text": "In medical theories prevalent in the West from  classical antiquity  to the  Middle Ages , the body's health depended on the equilibrium of  four \"humors\" , or vital fluids, two of which related to bile: blood,  phlegm , \"yellow bile\" (choler), and \"black bile\". These \"humors\" are believed to have their roots in the appearance of a blood sedimentation test made in open air, which exhibits a dark clot at the bottom (\"black bile\"), a layer of unclotted erythrocytes (\"blood\"), a layer of white blood cells (\"phlegm\") and a layer of clear yellow serum (\"yellow bile\"). [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4458", "text": "Excesses of black bile and yellow bile were thought to produce depression and aggression, respectively, and the Greek names for them gave rise to the English words  cholera  (from Greek \u03c7\u03bf\u03bb\u03ae  khol\u0113 , \"bile\") and  melancholia . In the former of those senses, the same theories explain the derivation of the English word bilious from  bile , the meaning of gall in English as \"exasperation\" or \"impudence\", and the Latin word  cholera , derived from the Greek  khol\u00e9 , which was passed along into some Romance languages as words connoting anger, such as  col\u00e8re  (French) and  c\u00f3lera  (Spanish). [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4459", "text": "Soap can be mixed with bile from mammals, such as  ox gall . This mixture, called bile soap [ 25 ]  or gall soap, can be applied to textiles a few hours before washing as a traditional and effective method for removing various kinds of tough stains. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4460", "text": "Pinapaitan  is a dish in  Philippine cuisine  that uses bile as flavoring. [ 27 ]  Other areas where bile is commonly used as a cooking ingredient include  Laos  and northern parts of  Thailand ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4461", "text": "During the  Boshin War ,  Satsuma  soldiers of the early  Imperial Japanese Army  reportedly  ate human livers  boiled in bile. [ 28 ]  The practice of eating a slain enemy's liver, known as  hiemondori  ( \u51b7\u3048\u7269\u53d6\u308a ) , was a tradition of the Satsuma people."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4462", "text": "In regions where bile products are a popular ingredient in  traditional medicine , the  use of bears  in bile-farming has been widespread. This practice has been condemned by activists, and some pharmaceutical companies have developed synthetic (non-ursine) alternatives. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4463", "text": "A  bile duct  is any of a number of long tube-like structures that carry  bile , and is present in most  vertebrates . The bile duct is separated into three main parts: the fundus (superior), the body (middle), and the neck (inferior)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4464", "text": "Bile is required for the  digestion  of food and is secreted by the  liver  into passages that carry bile toward the  hepatic duct . It joins the  cystic duct  (carrying bile to and from the  gallbladder ) to form the  common bile duct  which then opens into the  intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4465", "text": "The top half of the common bile duct is associated with the liver, while the bottom half of the common bile duct is associated with the  pancreas , through which it passes on its way to the intestine. It opens into the part of the intestine called the duodenum via the  ampulla of Vater ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4466", "text": "The  biliary tree  (see below) is the whole network of various sized ducts branching through the liver."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4467", "text": "The path is as follows:  bile canaliculi   \u2192   canals of Hering   \u2192   interlobular bile ducts   \u2192   intrahepatic bile ducts   \u2192  left and right  hepatic ducts   merge to form   \u2192   common hepatic duct   exits liver and joins   \u2192   cystic duct  (from  gall bladder )  forming   \u2192   common bile duct   \u2192   joins with   pancreatic duct   \u2192   forming   ampulla of Vater   \u2192   enters   duodenum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4468", "text": "Inflation of a balloon in the bile duct causes, through the  vagus nerve , activation of the  brain stem  and the  insular cortex ,  prefrontal cortex , and  somatosensory cortex . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4469", "text": "Blockage or obstruction of the bile duct by  gallstones , scarring from injury, or cancer prevents the bile from being transported to the intestine and the active ingredient in the bile ( bilirubin ) instead accumulates in the blood. This condition results in  jaundice , where the skin and eyes become yellow from the bilirubin in the blood. This condition also causes severe itchiness from the bilirubin deposited in the tissues. In certain types of  jaundice , the urine will be noticeably darker, and the stools will be much paler than usual. This is caused by the bilirubin all going to the bloodstream and being filtered into the urine by the kidneys, instead of some being lost in the stools through the  ampulla of Vater ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4470", "text": "Jaundice is commonly caused by conditions such as  pancreatic cancer , which causes blockage of the bile duct passing through the cancerous portion of the pancreas;  cholangiocarcinoma , cancer of the bile ducts; blockage by a stone in patients with gallstones; and from scarring after injury to the bile duct during gallbladder removal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4471", "text": "Biliary drainage is performed with a tube or catheter (called a  biliary drain ,  biliary  stent  or  biliary catheter ) by a surgeon or, commonly, an  interventional radiologist . [ 3 ]  It can be used to relieve a blockage in the bile duct, either permanently or as a temporary solution before definite treatment such as surgery. The drain can be placed  percutaneously  through the liver, with the procedure then being called  percutaneous transhepatic biliary drainage  (PTBD). [ 4 ]  This can additionally be performed as part of a  percutaneous transhepatic cholangiography , then a form of interventional radiology. A biliary drain can also be used to take bile samples for diagnostic workup or disease monitoring, as well as providing a  route of administration  for medical substances."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4472", "text": "A surgically created passage between the common bile duct and the  jejunum  in a procedure called a  choledochojejunostomy , can be carried out to relieve the symptoms of biliary obstruction as well as allows the bile duct to drain. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4473", "text": "In infants with  biliary atresia ,  hepatoportoenterostomy  is an alternative method of providing bile drainage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4474", "text": "Cholangiocarcinoma  or bile duct cancer is a form of cancer that is composed of mutated  epithelial  cells (or cells showing characteristics of epithelial differentiation) that originate in the bile ducts. Cholangiocarcinoma is considered to be an incurable and rapidly lethal cancer unless both the primary tumor and any  metastases  can be fully removed by surgery. No potentially curative treatment exists except surgery, but most people have advanced stage disease at presentation and are inoperable at the time of diagnosis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4475", "text": "In  cholecystectomy  there is a slight risk (0.3\u20130.5%) of injury of the bile ducts, most commonly of the  common bile duct . [ 6 ]  This complication can range from mild forms, which are easy to address during the operation, to more severe forms. [ 6 ]  If not addressed such injury can be debilitating and lead to considerable morbidity. [ 6 ]  Such injury can be prevented by routinely using X-ray investigation of the bile ducts (intraoperative  cholangiography ). [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4476", "text": "BioGaia  is a Swedish biotechnology company that develops, markets and sells a range of   probiotic  products. [ 1 ] [ 2 ] [ 3 ]  It has patented the use of several  Lactobacillus reuteri  strains and offers gut and immune health products containing  L. reuteri  Protectis ( DSM  17938). Their oral health products contain  L. reuteri  Prodentis,  a blend of the  L. reuteri  strains DSM 17938 and  ATCC  PTA 5289. [ citation needed ]  Products containing  L. reuteri  have been proven to be both effective and safe in several applications: [ dubious  \u2013  discuss ]  infant colic, [ 4 ] [ 5 ]  diarrhea prevention and mitigation in children, [ 6 ] [ 7 ]  eradication of  H. pylori  infection and reduction of side effects from standard  H. pylori  treatment, [ 8 ] [ 9 ] [ 10 ]  amelioration of  gingivitis , [ 11 ] [ 12 ]  and general illness prevention in children [ 13 ]  and adults. [ 14 ]  BioGaia was ranked 9th in the Top 30 Global Probiotic Food Ingredient Companies list by FoodTalks in 2021. [ 15 ]  The BioGaia -B share is listed on the  NASDAQ OMX Nordic Exchange . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4477", "text": "BioGaia was founded in 1990 to develop and commercialize a new strain of  L. reuteri . The company's research director Dr. Ivan Casas believed that newborn chickens consumed their mothers' feces, allowing the transfer of beneficial microorganisms from the mother to the sterile newborn bird. He believed that the same was true for humans. [ 16 ]  It is generally accepted that newborn babies are sterile at birth and are very sensitive to pathogenic bacteria before they establish a microbial flora of their own. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4478", "text": "This flora should preferably come from their mother. Ivan believed that  Lactobacillus reuteri  is one of the bacteria that a mother should transfer to her offspring, whether a chicken, a human baby or any other mammal. He wanted to create probiotic products that would confirm this \"Circle of Life\u201d. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4479", "text": "The first step involved analysis of breast milk from mothers in the United States,  Sweden ,  Israel ,  South Africa ,  Denmark ,  Japan , Peru and South Korea. Approximately 14-15% of the samples contained  L. reuteri . [ 18 ]  In a separate study, Casas found that samples of breast milk collected from women in Andean villages in Peru also contained numerous strains of  L. reuteri , which were subsequently isolated. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4480", "text": "One of these strains is still used in BioGaia\u2019s probiotic products. [ 20 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4481", "text": "In  digestion , a  bolus  (from  Latin   bolus , \"ball\") is a ball-like mixture of food and  saliva  that forms in the mouth during the process of  chewing  (which is largely an adaptation for  plant-eating   mammals ). [ 1 ]  It has the same color as the food being eaten, and the saliva gives it an  alkaline   pH ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4482", "text": "Under normal circumstances, the bolus is  swallowed , and travels down the  esophagus  to the  stomach  for digestion. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4483", "text": "Brunner's glands  (or  duodenal glands ) are compound tubuloalveolar  submucosal   glands  found in that portion of the  duodenum  proximal to the  hepatopancreatic sphincter  (i.e  sphincter of Oddi ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4484", "text": "For decades, it was believed that the main function of the glands is to  secrete alkaline ( bicarbonate -containing) mucus in order to: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4485", "text": "However, more recent studies have demonstrated that Brunner\u2019s glands actually act as major modulators of the gut microbiome and systemic immunity."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4486", "text": "They are the distinguishing feature of the duodenum, and are named for the  Swiss  physician who first described them,  Johann Conrad Brunner . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4487", "text": "Duodenal glands are situated within the mucosa and submucosa of the duodenum. They are most abundant near the pylorus, growing shorter and more sparse distally towards the terminal portion of the duodenum. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4488", "text": "The duodenum can be distinguished from the  jejunum  and  ileum  by the presence of Brunner's glands in the submucosa. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4489", "text": "Their excretory cannals are tortuous, opening at the bases of the villi. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4490", "text": "Two forms of duodenal glands are distinguished: the external group (which are more voluminous and extend into the duodenal submucosa), and the internal group (which are smaller and are situated within the duodenal mucosa). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4491", "text": "They also secrete  epidermal growth factor , which inhibits  parietal  and  chief cells  of the stomach from secreting acid and their digestive enzymes. [ 2 ] [ citation needed ]  This is another form of protection for the duodenum. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4492", "text": "The Brunner glands, which empty into the  intestinal glands , secrete an alkaline fluid composed of  mucin , which exerts a physiologic anti-acid function by coating the duodenal epithelium, therefore protecting it from the acid chyme of the stomach. Furthermore, in response to the presence of acid in the duodenum, these glands secrete  pepsinogen  and  urogastrone , which inhibit gastric acid secretion. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4493", "text": "More recent studies have demonstrated that Brunner\u2019s glands are major modulators of the gut microbiome and systemic immunity. Studies conducted by  Ivan De Araujo \u2019s laboratory revealed that Brunner\u2019s gland secretions promote the proliferation of probiotics and protect the host against foreign pathogens. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4494", "text": "Hyperplasia of Brunner glands with a lesion greater than 1\u00a0cm was initially described as a Brunner gland adenoma. Several features of these lesions favor their designation as  hamartomas , including the lack of encapsulation; the mixture of acini, smooth muscles, adipose tissue, Paneth cells, and mucosal glands; and the lack of any cell atypia. These hamartomas are rare, with approximately 150 cases described in the literature. It is estimated that they represent approximately 5\u201310% of benign duodenal tumors. They are variable in size, typically 1\u20133\u00a0cm, with only a few reported cases of lesions larger than 5\u00a0cm. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4495", "text": "Most patients with Brunner gland hamartomas are asymptomatic or have nonspecific complaints such as nausea, bloating, or vague abdominal pain. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4496", "text": "Most reports in the literature describe local surgical resection of Brunner gland hamartoma via duodenotomy. Increasingly, successful endoscopic resection has been reported and is primarily used for  pedunculated  Brunner gland hamartomas. The endoscopic approach in selective cases appears to be safe, less invasive, and less costly. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4497", "text": "Consistent with the more recent idea that Brunner\u2019s glands influence systemic immunity via the microbiome, patients who had the duodenal bulb removed (where the glands are mostly located) showed greater alterations in immune factors compared to patients having\u00a0\u00a0more distal parts of the duodenum removed. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4498", "text": "Catastalsis  is the rhythmic contraction and relaxation of the  muscle  of the  intestines . It resembles ordinary  peristalsis  but is not preceded by a  wave of inhibition . [ 1 ] [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4499", "text": "The  cecum  or  caecum  is a pouch within the  peritoneum  that is considered to be the beginning of the  large intestine . [ 1 ]  It is typically located on the right side of the body (the same side of the body as the  appendix , to which it is joined). The word cecum ( / \u02c8 s i\u02d0 k \u0259m / , plural  ceca   / \u02c8 s i\u02d0 k \u0259 / ) stems from the  Latin   caecus  meaning  blind ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4500", "text": "It receives  chyme  from the  ileum , and connects to the  ascending colon  of the  large intestine . It is separated from the ileum by the  ileocecal valve  (ICV), also called Bauhin's valve. It is also separated from the  colon  by the cecocolic junction. While the cecum is usually intraperitoneal, the ascending colon is  retroperitoneal . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4501", "text": "In  herbivores , the cecum stores food material where bacteria are able to break down the  cellulose . In humans, the cecum is involved in absorption of  salts  and  electrolytes  and lubricates the solid waste that passes into the large intestine. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4502", "text": "The cecum and appendix are derived from the bud of cecum that forms during week six in the midgut next to the apex of the umbilical herniation. [ 5 ]  Specifically, the cecum and appendix are formed by the enlargement of the postarterial segment of the midgut loop.  The proximal part of the bud grows rapidly to form the cecum. The lateral wall of the cecum grows much more rapidly than the medial wall, with the result that the point of attachment of the  appendix  comes to lie on the medial side. [ citation needed ]  The cecum's position changes after the midgut rotates and the ascending colon elongates, and the accumulation of meconium inside the cecum may result in the latter's increased diameter. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4503", "text": "The term  cecum  comes from Latin  (intestinum) caecum , literally 'blind intestine', in the sense 'blind gut' or ' cul de sac '. [ 6 ]  It is a direct translation from Ancient Greek  \u03c4\u03c5\u03c6\u03bb\u1f78\u03bd  ( \u1f14\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd )  typhl\u00f2n  ( \u00e9nteron ). Thus the inflammation of the cecum is called typhlitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4504", "text": "In  dissections  by the  Greek   philosophers , the connection between the  ileum  of the  small intestine  and the cecum was not fully understood. Most of the studies of the  digestive tract  were done on animals and the results were compared to human  structures . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4505", "text": "The junction between the small intestine and the colon, called the  ileocecal valve , is so small in some animals that it was not considered to be a connection between the small and large intestines. During a dissection, the colon could be traced from the  rectum , to the  sigmoid colon , through the  descending ,  transverse , and  ascending  sections. The cecum is an end point for the colon with a dead-end portion terminating with the  appendix . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4506", "text": "The connection between the end of the small intestine (ileum) and the start (as viewed from the perspective of food being processed) of the colon (cecum) is now clearly understood, and is called the ileocecal orifice. The connection between the end of the cecum and the beginning of the ascending colon is called the cecocolic orifice."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4507", "text": "A cecal carcinoid tumor is a  carcinoid tumor  of the cecum. An  appendiceal carcinoid tumor  (a carcinoid tumor of the appendix) is sometimes found next to a cecal carcinoid. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4508", "text": "Neutropenic enterocolitis  (typhlitis) is the condition of inflammation of the cecum, primarily caused by bacterial infections."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4509", "text": "Over 99% of the bacteria in the gut are  anaerobes , [ 10 ] [ 11 ] [ 12 ] [ 13 ] [ 14 ]  but in the cecum,  aerobic bacteria  reach high densities. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4510", "text": "A cecum is present in most  amniote  species, and also in  lungfish , but not in any living species of  amphibian . In  reptiles , it is usually a single median structure, arising from the dorsal side of the large intestine.  Birds  typically have two paired ceca, as do, unlike other mammals,  hyraxes . [ 16 ]  Parrots do not have ceca. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4511", "text": "Most mammalian  herbivores  have a relatively large cecum.  In many species, it is considerably wider than the colon. For some herbivores such as  lagomorphs  (rabbits, hares, pikas), easily digestible food is processed in the gastrointestinal tract and expelled as regular feces.  But in order to get nutrients out of hard to digest fiber, lagomorphs ferment fiber in the cecum and then expel the contents as  cecotropes , which are reingested (cecotrophy).  The cecotropes are then absorbed in the small intestine to utilize the nutrients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4512", "text": "In contrast, obligate  carnivores , whose diets contain little or no plant matter, have a reduced cecum, which is often partially or wholly replaced by the  appendix . [ 16 ]  Mammalian species which do not develop a cecum include  raccoons , [ 18 ]   bears , [ 19 ]  and the  red panda . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4513", "text": "Many fish have a number of small outpockets, called  pyloric ceca , along their intestine; despite the name, they are not  homologous  with the cecum of amniotes \u2013 their purpose is to increase the overall area of the digestive epithelium. [ 16 ]  Some invertebrates, such as squid, [ 21 ]  may also have structures with the same name, but these have no relationship with those of vertebrates."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4514", "text": "Centroacinar cells  are spindle-shaped cells in the exocrine  pancreas . They are small and have  microvilli  on the  apical  surface. They work with organs such as the kidney, lungs, stomach, brain, intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4515", "text": "The exocrine pancreas is one of two compartments that include digestive-acting acinar cells and duct cells.They represent an extension of the  intercalated duct  into each pancreatic  acinus . [ 1 ]  These cells are commonly known as  duct cells , and secrete an aqueous  bicarbonate  solution under stimulation by the hormone  secretin . They also secrete  mucin . As well as direct the pathway of the enzyme into the gut, which helps the endocrine pancreas in secreting the hormone into the circulation. This is important in glucose metabolism, insulin-producing B cells, glucagon-producing A cells and somatostatin producing \u03b4 cells"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4516", "text": "The intercalated ducts take the bicarbonate to  intralobular ducts  which become lobular ducts. These lobular ducts finally converge to form the main pancreatic duct. [ 2 ]  These intercalated ducts take the bicarbonate to intralobular ducts which become lobular ducts. These lobular ducts finally converge to form the main pancreatic duct. [ 1 ]  These pancreatic ducts can act as a response mechanism when injury occurs and to avoid disruptions in the pancreatic lumen. [ 3 ]  This keeps the ionic content in check while keeping it open for flow to occur. Mutations that can occur because of blockage/ accumulation in the pancreatic duct are disorders such as cystic fibrosis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4517", "text": "This article incorporates text in the  public domain  from  page 1204  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4518", "text": "This  cell biology  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4519", "text": "Chewing  or  mastication  is the process by which  food  is  crushed and ground  by the  teeth . It is the first step in the process of  digestion , allowing a greater surface area for  digestive enzymes  to break down the foods."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4520", "text": "During the mastication process, the food is positioned by the  cheek  and  tongue  between the teeth for grinding. The  muscles of mastication  move the  jaws  to bring the teeth into intermittent contact, repeatedly  occluding  and opening. As chewing continues, the food is made softer and warmer, and the enzymes in saliva begin to break down  carbohydrates  in the food. After chewing, the food (now called a  bolus ) is swallowed. It enters the  esophagus  and via  peristalsis  continues on to the stomach, where the next step of digestion occurs. [ 1 ]  Increasing the number of chews per bite increases relevant gut hormones. [ 2 ]  Studies suggest that chewing may decrease self-reported hunger and food intake. [ 2 ]   Chewing gum  has been around for many centuries; there is evidence that northern Europeans chewed  birch bark tar  9,000 years ago."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4521", "text": "Chewing, needing specialized teeth, is mostly a mammalian adaptation that appeared in early  Synapsids , though some later herbivorous dinosaurs, since extinct, had developed chewing too. Nowadays, only mammals chew in the strict sense of the word, though some fishes have a somewhat similar behavior. Neither birds, nor amphibians or any living reptiles chew."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4522", "text": "Premastication  is sometimes performed by human parents for infants who are unable to do so for themselves. The food is masticated in the mouth of the parent into a bolus and then transferred to the infant for consumption [ 3 ]  (some other animals also premasticate)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4523", "text": "Cattle  and some other animals, called  ruminants , chew food more than once to extract more nutrients. After the first round of chewing, this food is called  cud ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4524", "text": "Chewing is primarily an unconscious ( semi-autonomic ) act, but can be mediated by higher conscious input. The motor program for mastication is a hypothesized central nervous system function by which the complex patterns governing mastication are created and controlled."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4525", "text": "It is thought that feedback from  proprioceptive  nerves in teeth and the  temporomandibular  joints govern the creation of neural pathways, which in turn determine duration and force of individual muscle activation (and in some cases muscle fiber groups as in the masseter and temporalis)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4526", "text": "This motor program continuously adapts to changes in food type or occlusion. [ 4 ]  This adaptation is a learned skill that may sometimes require relearning to adapt to loss of teeth or to dental appliances such as  dentures ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4527", "text": "It is thought that conscious mediation is important in the limitation of  parafunctional habits  as most commonly, the motor program can be excessively engaged during periods of sleep and times of stress. It is also theorized that excessive input to the motor program from myofascial pain or occlusal imbalance can contribute to  parafunctional habits ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4528", "text": "Chewing stimulates  saliva  production and increases sensory perception of the food being eaten, controlling when the food is swallowed. [ 5 ]  Evidence from one study suggests that chewing almonds 25-40 times kept people fuller while also allowing them to get more nutrients out of the almonds. The researchers also suggest that this is likely to be the case in other foods. [ 6 ]  A 2015  systemic review  found evidence that chewing can decrease self-reported hunger and therefore food intake. [ 7 ]  Eating food which does not require chewing, by choice or for medical reasons as  tooth loss , is known as a  soft diet . Such a diet may lead to inadequate nutrition due to a reduction in fruit and vegetable intake. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4529", "text": "Chewing also stimulates the  hippocampus  and is necessary to maintain its normal function. [ 9 ]  Chewing stimulates hippocampal  neurogenesis  in both humans and mice. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4530", "text": "Chewing is largely an adaptation for  mammalian   herbivory .  Carnivores  generally chew very little or swallow their food whole or in chunks. [ 11 ]  This act of gulping food (or medicine pills) without chewing has inspired the English  idiom  \"wolfing it down\". [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4531", "text": "Other animals such as cows chew their food for long periods to allow for proper digestion in a process known as rumination. Rumination in cows has been shown by researchers to intensify during the night. They concluded that cows chewed more intently in the night time compared to the morning. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4532", "text": "Ornithopods , a group of  dinosaurs  including the  Hadrosaurids  (\"duck-bills\"), developed teeth analogous to mammalian  molars  and  incisors  during the  Cretaceous  period; this advanced, cow-like dentition allowed the creatures to obtain more nutrients from the tough plant life. This may have given them the advantage needed to compete with the formidable  sauropods , who depended on their massive gastrointestinal tracts to digest food without grinding it. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4533", "text": "The process of chewing has, by analogy, been applied to machinery. The  U.S. Forest Service  uses a machine called a  masticator  (also called a  forestry mulching machine ) to \"chew\" through brush and timber in order to clear  firelines  in advance of a wildfire. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4534", "text": "Cholangiocytes  are the  epithelial cells  of the  bile duct . [ 1 ]  They are  cuboidal epithelium  in the small interlobular bile ducts, but become  columnar  and  carbonate -secreting in larger bile ducts approaching the  porta hepatis  and the extrahepatic ducts. They contribute to  hepatocyte  survival by transporting  bile acids ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4535", "text": "In the healthy liver, cholangiocytes contribute to  bile  secretion via release of  bicarbonate  and water. Several hormones and locally acting mediators are known to contribute to cholangiocyte fluid/electrolyte secretion. These include  secretin ,  acetylcholine ,  ATP , and  bombesin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4536", "text": "Cholangiocytes act through bile-acid independent bile flow, which is driven by the active transport of electrolytes. In contrast,  hepatocytes  secrete bile through bile-acid dependent bile flow, which is coupled to canalicular secretion of bile acids via ATP-driven transporters. This results in passive transcellular and paracellular secretion of fluid and electrolytes through an osmotic effect."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4537", "text": "Disordered functioning of cholangiocytes is at the center of a variety of pathological conditions known as \"cholangiopathies.\" These diseases include  primary biliary cirrhosis ,  primary sclerosing cholangitis , AIDS cholangiopathy, disappearing bile duct syndromes,  Alagille's syndrome ,  cystic fibrosis , and  biliary atresia . Often either the best or the only curative treatment option for cholangiopathies is  liver transplantation , and as a group, cholangiopathies account for a substantial percentage of both adult and pediatric liver transplants. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4538", "text": "Active scientific investigation of cholangiocytes focuses on such diverse processes as mechanisms of fluid/electrolyte secretion, regulation of cholangiocyte proliferation, roles of cholangiocytes in the pathogenesis of liver fibrosis and cirrhosis, and cholangiocyte apoptosis. Specific investigation of individual cholangiopathies is also pursued actively. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4539", "text": "Chyle  (from  Greek     \u03c7\u03c5\u03bb\u03cc\u03c2  (chylos) \u00a0'juice' [ 1 ] ) is a milky  bodily fluid  consisting of  lymph  and emulsified  fats , or free  fatty acids  (FFAs). It is formed in the  small intestine  during digestion of fatty foods, and taken up by  lymph vessels  specifically known as  lacteals . The lipids in the chyle are  colloidally  suspended in  chylomicrons ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4540", "text": "A chyle  fistula  occurs when defect(s) of lymphatic vessel(s) result in leakage of lymphatic fluid, typically accumulating in the thoracic (pleural) or abdominal (peritoneal) cavities, [ 2 ]  leading to a chylous pleural effusion ( chylothorax ) or  chylous ascites , respectively."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4541", "text": "Diagnosis of a chyle fistula may be accomplished by analysis of pleural/peritoneal fluid. Identifying the source (localizing the lymphatic defect) is often challenging, but may be accomplished with lymphangiography, which is occasionally associated with a serendipitous therapeutic effect (resolution of the leak), thought to be secondary to a sclerosant effect of the lymphangiography contrast."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4542", "text": "Due to the extreme  friability  of the lymphatic vessels, direct repair of defects is impractical. Therefore, treatment of chyle fistulae relies upon either decreased production of lymphatic fluid to allow for healing of lymphatic defect(s) or permanent diversion of lymphatic fluid away from lymphatic defect(s). Decreased production of lymphatic fluid may be accomplished by dietary restriction (or complete replacement of oral intake with  total parenteral nutrition ), as well as by the medications  octreotide  (a synthetic analogue of the hormone  somatostatin ) [ 3 ]  and  orlistat  (a lipase inhibitor that decreases absorption of dietary fats). Permanent diversion of lymphatic fluid may be accomplished by   thoracic duct  embolization (a needle-based procedure to occlude the duct by depositing glue/embolic material into it) or by thoracic duct ligation (an open surgical procedure to occlude the duct by suturing tightly around it)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4543", "text": "Chyme  or  chymus  ( / k a\u026a m / ; from  Greek  \u03c7\u03c5\u03bc\u03cc\u03c2  khymos , \"juice\" [ 1 ] [ 2 ] ) is the semi-fluid mass of partly digested food that is expelled by the  stomach , through the  pyloric valve , into the  duodenum [ 3 ]  (the beginning of the  small intestine )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4544", "text": "Chyme results from the mechanical and chemical breakdown of a  bolus  and consists of partially digested food, water,  hydrochloric acid , and various  digestive enzymes . Chyme slowly passes through the pyloric  sphincter  and into the duodenum, where the extraction of  nutrients  begins. Depending on the quantity and contents of the meal, the stomach will digest the food into chyme in some time from 40 minutes to 3 hours. [ 4 ]  \nWith a  pH  of approximately 2, chyme emerging from the stomach is very acidic. The duodenum secretes a  hormone ,  cholecystokinin  (CCK), which causes the  gall bladder  to contract, releasing alkaline  bile  into the duodenum. CCK also causes the release of digestive enzymes from the  pancreas . The duodenum is a short section of the small intestine located between the stomach and the rest of the small intestine. The duodenum also produces the hormone  secretin  to stimulate the pancreatic secretion of large amounts of  sodium bicarbonate , which then raises pH of the chyme to 7. The chyme moves through the  jejunum  and the  ileum , where digestion progresses, and the non-useful portion continues onward into the  large intestine . The duodenum is protected by a thick layer of  mucus  and the neutralizing actions of the sodium bicarbonate and bile."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4545", "text": "At a pH of 7, the enzymes that were present from the stomach are no longer active. The breakdown of any nutrients still present is by  anaerobic bacteria , which at the same time help to package the remains. These bacteria also help synthesize  vitamin B  and  vitamin K , which will be absorbed along with other nutrients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4546", "text": "Chyme has a low pH that is countered by the production of  bile , which helps the further digestion of food. Chyme is part liquid and part solid: a thick semifluid mass of partially digested food and digestive secretions that is formed in the  stomach  and small intestine during digestion. Chyme also contains cells from the mouth and esophagus that slough off from the mechanical action of chewing and swallowing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4547", "text": "After hours of mechanical and chemical digestion, food has been reduced into chyme. As particles of food become small enough, they are passed out of the stomach at regular intervals into the small intestine, which stimulates the  pancreas  to release fluid containing a high concentration of  bicarbonate . This fluid neutralizes the gastric juices, which can damage the lining of the intestine and result in  duodenal ulcer . Other secretions from the pancreas,  gallbladder ,  liver , and  glands  in the intestinal wall help in digestion, as these secretions contain a variety of  digestive enzymes  and chemicals that assist in the breakdown of complex compounds into those that can be absorbed and used by the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4548", "text": "When food particles are sufficiently reduced in size and composition, they are absorbed by the intestinal wall and transported to the bloodstream. Some food material is passed from the small intestine to the  large intestine . In the large intestine, bacteria break down any proteins and starches in chyme that were not digested fully in the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4549", "text": "When all of the nutrients have been absorbed from chyme, the remaining waste material changes into semisolids that are called  feces . The feces pass to the  rectum , to be stored until ready to be discharged from the body during  defecation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4550", "text": "The chyme of an  unweaned  calf is the defining ingredient of  pajata , a traditional  Roman recipe ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4551", "text": "Chyme is sometimes used in  Pinapaitan , a bitter  Ilocano  stew."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4552", "text": "The  circular folds  (also known as  valves of Kerckring ,  valves of Kerchkring ,  plicae circulares ,  plicae circulae , and  valvulae conniventes ) are large  valvular  flaps projecting into the  lumen  of the  small intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4553", "text": "The entire  small intestine  has circular folds of  mucous membrane . [ 1 ]  The majority extend transversely around the  cylinder  of the small intestine, [ 2 ]  for about one-half or two-thirds of its  circumference . Some form complete  circles . Others have a spiral direction. The latter usually extend a little more than once around the bowel, but occasionally two or three times. While the larger folds are about 1\u00a0cm in depth at their broadest part, most folds are smaller. There tends to be an alternating pattern between larger and smaller folds. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4554", "text": "They are not found at the commencement of the  duodenum , but begin to appear about 2.5 or 5\u00a0cm beyond the  pylorus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4555", "text": "In the lower part of the descending portion, below the point where the  bile  and  pancreatic ducts  enter the small intestine, they are very large and closely approximated."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4556", "text": "In the horizontal and ascending portions of the duodenum and upper half of the  jejunum , they are large and numerous. [ 3 ]  From this point, down to the middle of the ileum, they diminish considerably in size."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4557", "text": "In the lower part of the  ileum , they almost entirely disappear; [ 4 ]  hence the comparative thinness of this portion of the intestine, as compared with the duodenum and jejunum. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4558", "text": "Unlike the  gastric folds  in the  stomach , they are permanent, and are not obliterated when the  intestine  is distended."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4559", "text": "The spaces between circular folds are smaller than the  haustra  of the  colon , and, in contrast to haustra, circular folds reach around the whole circumference of the intestine. These differences can assist in distinguishing the small intestine from the colon on an  abdominal x-ray ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4560", "text": "The circular folds slow the passage of the partly digested  food  along the intestines, and afford an increased surface for  absorption . [ 5 ]  They are covered with small finger-like projections called  villi  (singular, villus). Each villus, in turn, is covered with  microvilli . The microvilli absorb fats and nutrients from the  chyme ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4561", "text": "The circular folds are also called the valves of Kerckring, [ 3 ]  valves of Kerchkring, [ 6 ]  plicae circulares, [ 3 ] [ 5 ]   plicae circulae , [ 6 ]  and  valvulae conniventes . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4562", "text": "This article incorporates text in the  public domain  from  page 1173  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4563", "text": "A  cloaca  ( / k l o\u028a \u02c8 e\u026a k \u0259 /   \u24d8   kloh- AY -k\u0259 ),  pl. :  cloacae  ( / k l o\u028a \u02c8 e\u026a s i /   kloh- AY -see  or  / k l o\u028a \u02c8 e\u026a k i /   kloh- AY -kee ), or  vent , is the rear  orifice  that serves as the only opening for the  digestive  ( rectum ),  reproductive , and  urinary tracts  (if present) of many  vertebrate  animals. All  amphibians ,  reptiles ,  birds , and a few mammals ( monotremes ,  afrosoricids , and  marsupial moles , etc.) have this orifice, from which they excrete both  urine  and  feces ; this is in contrast to most  placental mammals , which have separate orifices for evacuation and reproduction.  Excretory  openings with analogous purpose in some  invertebrates  are also sometimes called cloacae. Mating through the cloaca is called cloacal  copulation  and cloacal kissing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4564", "text": "The cloacal region is also often associated with a secretory organ, the cloacal gland, which has been implicated in the scent-marking behavior of some reptiles, [ 1 ]  marsupials, [ 2 ]  amphibians, and  monotremes . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4565", "text": "The word is from the  Latin  verb  cluo , \"(I) cleanse\", thus the noun  cloaca , \" sewer , drain\". [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4566", "text": "Birds reproduce using their cloaca; this occurs during a cloacal kiss in most birds. [ 7 ]  Birds that mate using this method touch their cloacae together, in some species for only a few seconds, sufficient time for  sperm  to be transferred from the male to the female. [ 8 ]  For  palaeognaths  and  waterfowl , the males do not use the cloaca for reproduction, but have a  phallus . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4567", "text": "One study [ 10 ]  has looked into birds that use their cloaca for cooling. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4568", "text": "Among  falconers , the word vent is also a verb meaning \"to defecate\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4569", "text": "Among fish, a true cloaca is present only in  elasmobranchs  (sharks and rays) and  lobe-finned fishes . In  lampreys  and in some  ray-finned fishes , part of the cloaca remains in the adult to receive the urinary and reproductive ducts, although the anus always opens separately. In  chimaeras  and most  teleosts , however, all three openings are entirely separated. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4570", "text": "With a few exceptions noted below, mammals have no cloaca. Even in the marsupials that have one, the cloaca is partially subdivided into separate regions for the  anus  and  urethra ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4571", "text": "The  monotremes  (egg-laying mammals) possess a true cloaca. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4572", "text": "In  marsupials , the genital tract is separate from the anus, but a trace of the original cloaca does remain externally. [ 12 ]  This is one of the features of marsupials (and monotremes) that suggest their basal nature, as the  amniotes  from which mammals evolved had a cloaca, and probably so did the earliest  mammals ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4573", "text": "Unlike other marsupials,  marsupial moles  have a true cloaca. [ 15 ]  This fact has been used to argue that they are not marsupials. [ 16 ] [ 17 ] [ unreliable source? ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4574", "text": "Most adult  placentals  have no cloaca. In the embryo, the  embryonic cloaca  divides into a posterior region that becomes part of the  anus , and an anterior region that develops depending on sex: in males, it forms the  penile urethra , while in females, it develops into the  vestibule  or  urogenital sinus  that receives the urethra and vagina. [ 12 ] [ 18 ]  However, some placentals retain a cloaca as adults: those are members of the order   Afrosoricida  (small mammals native to Africa) as well as  pikas ,  beavers , and some  shrews . [ 19 ] [ 20 ] [ 21 ] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4575", "text": "Being placental animals, humans have an embryonic cloaca which divides into separate tracts during the  development of the urinary and reproductive organs . However, a few human  congenital disorders  result in persons being born with a cloaca, including  persistent cloaca  and  sirenomelia  (mermaid syndrome)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4576", "text": "In reptiles, the cloaca consists of the  urodeum ,  proctodeum , and  coprodeum . [ 23 ] [ 24 ]  Some species have modified cloacae for increased gas exchange (see  reptile respiration  and  reptile reproduction ). This is where reproductive activity occurs. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4577", "text": "Some  turtles , especially those specialized in diving, are highly reliant on cloacal  respiration  during dives. [ 26 ]  They accomplish this by having a pair of accessory air bladders connected to the cloaca, which can absorb oxygen from the water. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4578", "text": "Sea cucumbers  use cloacal respiration. The constant flow of water through it has allowed various  fish ,  polychaete  worms and even  crabs  to specialize to take advantage of it while living protected inside the cucumber. At night, many of these species emerge through the anus of the sea cucumber in search of food. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4579", "text": "Colonization resistance  is the mechanism whereby the  microbiome  protects itself against incursion by new and often harmful  microorganisms . [ 1 ] [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4580", "text": "Colonization resistance was first identified in 1967, and it was initially referred to as  antibiotic -associated susceptibility. It was observed that animals being treated with the antibiotic  streptomycin  were susceptible to  Salmonella enterica  at doses 10,000 fold lower than the standard minimal infectious dose. [ 4 ]  This led to investigations about the mechanisms utilized by endogenous microbial populations that conferred protection against exogenous pathogens attempting to  colonize  the  gut flora ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4581", "text": "It has been observed that colonization resistance can occur within the host in a 'direct' or 'indirect' manner. [ 5 ]  The former refers to particular components of the microbiota directly competing with exogenous pathogens for nutritional niches (e.g.  E. coli  directly competes with  Citrobacter rodentium  for  carbohydrates  in the  intestinal lumen [ 6 ] ) or by producing growth inhibitors (e.g.  Bacteroides thuringiensis  can secrete  bacteriocin  that directly targets spore-forming  Clostridioides difficile , thus inhibiting its growth through an unknown mechanism), [ 7 ]  that directly inhibit the colonizing pathogen. Indirect colonization resistance is thought to be mediated through the induction of  immune  responses in the host that concomitantly inhibit the colonizing pathogen. An example of this has been observed with  B. thetaiotaomicron , which can induce the host to produce antimicrobial C-type lectins  REGIII\u03b3  and  REGIII\u03b2 , both anti-microbial peptides that target  gram-positive  bacteria. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4582", "text": "Scientists found that gut infections increase its microbiota's resistance to subsequent infections, that  taurine  is used in as a nutrient to nourish and train the microbiota for this by potentiating its production of sulfide and that the exogenous supply of taurine can induce this microbiota alteration. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4583", "text": "The  bile duct [ 1 ] [ 4 ]  (formerly known as the  common bile duct [ 4 ] ) is a part of the  biliary tract . [ 4 ]  It is formed by the union of the  common hepatic duct  and  cystic duct . It ends by uniting with the  pancreatic duct  to form the  hepatopancreatic ampulla . It possesses its  sphincter  to enable the regulation of bile flow."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4584", "text": "The bile duct is some 6\u20138\u00a0cm long, and normally up to 8\u00a0mm in diameter. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4585", "text": "Its proximal supraduodenal part is situated within the free edge of the  lesser omentum . Its middle retroduodenal part is oriented inferiorly and right-ward, and is situated posterior to the first part of the duodenum, and anterior to the inferior vena cava. Its distal paraduodenal part is oriented still more right-ward, is accommodated by a groove upon (sometimes a channel within) the posterior aspect of the head of the pancreas, and is situated anterior to the right  renal vein . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4586", "text": "The bile duct terminates by uniting with the  pancreatic duct  (at an angle of about 60\u00b0) to form the  hepatopancreatic ampulla . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4587", "text": "The distal extremity of the bile duct invariably features its own  sphincteric muscle  (the pancreatic duct and the hepatopancreatic ampulla usually possess sphincters of their own to allow the flow of pancreatic juice to be regulated independently, however, these two can be absent). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4588", "text": "Several problems can arise within the common bile duct, usually related to its obstruction. Opinions vary slightly on the maximum calibre of a normal CBD, but 6 mm is one accepted upper limit of normal  [ 5 ]  with a further 1mm diameter allowed for each decade over 60 years."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4589", "text": "It normally gets slightly dilated after  cholecystectomy , with upper limit (95%  prediction interval ) being about 10\u00a0mm after a few months. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4590", "text": "On  abdominal ultrasonography , the common bile duct is most readily seen in the  porta hepatis  (where the CBD lies anterior to the  portal vein  and  hepatic artery ). The absence of  Doppler  signal distinguishes it from the  portal vein  and  hepatic artery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4591", "text": "Tumours in the head of the pancreas  may come to  obstruct the distal bile duct. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4592", "text": "If obstructed by a  gallstone , a condition called  choledocholithiasis  can result. [ 7 ]  In this obstructed state, the duct is especially vulnerable to an infection called  ascending cholangitis . One form of treatment is a  cholecystenterostomy . Rare deformities of the common bile duct are cystic dilations (4\u00a0cm), choledochoceles (cystic dilation of the ampula of Vater (3\u20138\u00a0cm)), and  biliary atresia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4593", "text": "Obstruction of the common bile duct and related  jaundice  has been documented since at least since the time of  Erasistratus . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4594", "text": "The  common hepatic duct  is the first part of the  biliary tract . It joins the  cystic duct  coming from the  gallbladder  to form the  common bile duct ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4595", "text": "The common hepatic duct is the first part of the biliary tract. [ 2 ]  It is formed by the union of the right hepatic duct (which drains bile from the right functional lobe of the liver) and the left hepatic duct (which drains bile from the left functional lobe of the liver). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4596", "text": "The duct is about 3\u00a0cm long. [ 4 ]  The common hepatic duct is about 6\u00a0mm in diameter in adults, with some variation. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4597", "text": "The common hepatic duct typically unites with the cystic duct some 1\u20132\u00a0cm superior to the duodenum and anterior to the right hepatic artery, with the cystic duct approaching the common hepatic duct from the right. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4598", "text": "The right branch of the  hepatic artery proper  usually passes posterior to the duct, but may rarely pass anterior to it instead. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4599", "text": "The inner surface is covered in a  simple columnar epithelium . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4600", "text": "Accessory hepatic ducts"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4601", "text": "Around 1.7% [ 6 ]  of people have additional accessory hepatic ducts that opens into the common hepatic duct. [ 6 ]  Accessory hepatic ducts may also instead open into the cystic duct or gallbladder. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4602", "text": "Termination"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4603", "text": "Occasionally, the cystic duct may first run along the right side of the common bile duct for some distance before joining it, or may pass posteriorly around to the common hepatic duct to unite with it from the left side. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4604", "text": "Rarely, the common hepatic duct and gallbladder join directly (with the cystic duct being absent), [ 6 ] [ 4 ]  leading to illness. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4605", "text": "The hepatic duct is part of the  biliary tract  that transports secretions from the liver into the  intestines ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4606", "text": "The common hepatic ducts carries a higher volume of bile in people who have had their gallbladder removed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4607", "text": "The common hepatic duct is an important anatomic landmark during surgeries such as  cholecystectomy . It forms one edge of  Calot's triangle , along with the cystic duct and the  cystic artery . All constituents of this triangle must be identified to avoid cutting or clipping the wrong structure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4608", "text": "A diameter of more than 8\u00a0mm is regarded as abnormal dilatation, and is a sign of  cholestasis . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4609", "text": "Mirizzi's syndrome  occurs when the common hepatic duct is blocked by  gallstones . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4610", "text": "Cud  is a portion of food that returns from a  ruminant 's stomach to the mouth to be chewed for the second time. More precisely, it is a  bolus  of semi-degraded food  regurgitated  from the  reticulorumen  of a  ruminant . Cud is produced during the physical digestive process of rumination. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4611", "text": "The  alimentary canal  of ruminants, such as  cattle ,  giraffes ,  goats ,  sheep ,  alpacas , and  antelope , are unable to produce the  enzymes  required to break down the  cellulose  and  hemicellulose  of plant matter. [ 2 ]  Accordingly, these animals rely on a  symbiotic  relationship with a wide range of  microbes , which largely reside in the  reticulorumen , and which are able to synthesize the requisite enzymes. The reticulorumen thus hosts a microbial fermentation which yields products (mainly  volatile fatty acids  and microbial protein), which the ruminant is able to digest and absorb. This allows the animals to extract nutritional value from cellulose which is usually undigested."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4612", "text": "The process of rumination is stimulated by the presence of  roughage  in the upper part of the  reticulorumen . The chest cavity is stretched, forming a vacuum in the gullet that sucks the semi-liquid stomach content into the  esophagus . From the esophagus it is taken back to the mouth with retro  peristaltic  movements. When the stomach content, or the cud, arrives in the mouth of the ruminant, it is pushed against the palate with the tongue to remove excess liquid, the latter is swallowed and the solid material is chewed thoroughly so the cattle can extract the minerals present in the cud brought to the surface during rumination. The function of rumination is that food is physically refined to expose more surface area for bacteria working in the reticulorumen, as well as stimulation of  saliva  secretion to  buffer  the rumen  pH ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4613", "text": "When food has been degraded sufficiently it passes from the reticulorumen through the reticulomasal orifice to the  omasum  followed by the  abomasum  to continue the digestion process in the lower parts of the alimentary canal. No enzymes are secreted in the rumen. Enzymes and  hydrochloric acid  are only secreted from the  abomasum  (fourth stomach) onwards, and ruminants function from that point onwards much like monogastric animals, such as  pigs  and humans."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4614", "text": "The reticulorumen has an optimum pH of 6.5 for the microbe population to thrive. Consumption by ruminants of an insufficiently fibrous diet leads to little cud formation and therefore lowered amounts of saliva production. This in turn is associated with rumen  acidosis , where the rumen pH can fall to 5 or lower. Rumen acidosis is associated with a lowered appetite which leads to still lower rates of saliva secretion. Eventually, a collapse of the microbial  ecosystem  in the rumen will occur because of the low pH. Acute rumen acidosis can lead to death of the animal, and will occur if the animal is allowed to eat a diet with no roughage but high levels of highly  digestible  starchy concentrate. Some dairy cows in intensive systems of milk production may have sub-acute acidosis because of the high rates of cereals in their diets relative to an insufficient amount of forage. However, most producers provide adequate  fodder  in the form of  hay  to prevent this. [ 3 ] [ additional citation(s) needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4615", "text": "Jewish dietary laws  state that an animal that chews the cud and has a  cloven hoof  is acceptable for consumption. Any animal that doesn't chew the cud and have a  cloven hoof  is unclean."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4616", "text": "Goat cud is sometimes an ingredient in  Pinapaitan ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4617", "text": "The  cystic duct  is the  duct  that (typically) joins the  gallbladder  and the  common hepatic duct ; the union of the cystic duct and common hepatic duct forms  the bile duct  (formerly known as the common bile duct). Its length varies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4618", "text": "The cystic duct typically [ 2 ]  measures (sources differ) 2\u20134\u00a0cm [ 3 ] [ 4 ] /2\u20133\u00a0cm [ 2 ]  in length (though its length has been known to range from 0.5\u00a0cm to 9\u00a0cm [ 3 ] ), and 2\u20133\u00a0mm in diameter. [ 2 ] [ 4 ]  It is often tortuous. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4619", "text": "It is the distal continuation of the neck of the gallbladder, from where it is directed inferoposteriorly and to the left [ 2 ] /medially [ 4 ]  (this occurs in half of individuals [ 3 ] ). It typically [ 2 ]  terminates by uniting with the  common hepatic duct  to form the  bile duct  (usually anterior to the right hepatic artery). [ 2 ]  It usually joins the common bile duct from the right lateral side (forming an oblique angle between the two), [ 4 ]  and at such a distance that the bile duct is twice as long as the common hepatic duct. [ 3 ] [ 4 ]  It often fuses with the common hepatic duct before actually opening into it after a variable distance [ 4 ] [ 3 ]  (this arrangement may have the purpose of directing bile flow distally instead of back towards the liver [ 3 ] )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4620", "text": "The inner surface of the cystic duct features spiral, crescentic mucosal folds - the  spiral folds of cystic duct . [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4621", "text": "The inner surface of the proximal cystic duct exhibits a network of submicroscopic convoluted folds (rugae), whereas that of the distal cystic duct exhibits submicroscopic parallel longitudinal folds. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4622", "text": "The epithelial lining of the inner surface of the duct is similar to that of the gallbladder and consists mostly of  columnar epithelial cells  with short  microvilli  upon their apical surfaces. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4623", "text": "The subepithelial layer consists of  elastic connective tissue  and is highly vascular; vessels that are adjacent to the epithelial  basement membrane  are  fenestrated , possibly to facilitate ion and fluid exchange with the bile as is the case in the gallbladder itself. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4624", "text": "The outer fibromuscular layer contains  smooth muscle  continuous with that of the gallbladder; some of the smooth muscle extends into the spiral valves. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4625", "text": "It usually lies next to the  cystic artery . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4626", "text": "The cystic duct may rarely be doubled. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4627", "text": "An accessory hepatic duct may join the cystic duct. [ 2 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4628", "text": "A pathological diverticulum known as the  Hartmann\u2019s pouch  may be present at the junction of the neck of bladder and the cystic duct. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4629", "text": "Length"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4630", "text": "The duct may sometimes be extremely short (making cholecystectomy risky) [ 2 ]  or may rarely be altogether absent (so that the gallbladder is directly attached to the bile duct). [ 2 ] [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4631", "text": "Shape"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4632", "text": "While most often tortuous, it may occasionally be curved, straight, or S-shaped. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4633", "text": "The cystic duct may unite with the common hepatic duct so that the common hepatic duct is either very short or very long (and the bile duct in turn very long or very short, respectively), [ 4 ]  or it may instead unite with the a hepatic duct. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4634", "text": "Occasionally, the cystic duct may first run alongside the common hepatic duct for some distance [ 2 ] [ 4 ]  within the  hepatoduodenal ligament [ 4 ]  before joining it. [ 2 ] [ 4 ]  It sometimes join the common hepatic duct at its anterior, posterior, or medial side [ 4 ] [ 3 ]  (in the latter case by passing posteriorly around the common bile duct to join it from the other side). [ 2 ]   It may spiral around the common hepatic duct before joining it. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4635", "text": "Very rarely, the cystic duct opens into the  duodenum . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4636", "text": "Bile can flow in either direction between the gallbladder, and the common bile duct and  hepatic duct . [ 3 ]  In this way, bile is stored in the gallbladder in between meal times. The hormone  cholecystokinin , when stimulated by a fatty meal, promotes bile secretion by increased production of hepatic bile, contraction of the gall bladder, and relaxation of the  Sphincter of Oddi ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4637", "text": "The bile duct was once thought to possess a  sphincteric  function, however, it is now known that bile flow through the cystic duct proceeds unimpeded and is instead regulated by other mechanisms at other points of the biliary system. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4638", "text": "Gallstones  can enter and obstruct the cystic duct, preventing the flow of bile. The increased pressure in the gallbladder leads to swelling and pain. This pain, known as  biliary colic , is sometimes referred to as a gallbladder \"attack\" because of its sudden onset."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4639", "text": "During a  cholecystectomy , the cystic duct is clipped two or three times and a cut is made between the clips, freeing the gallbladder to be taken out."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4640", "text": "Defecation  (or  defaecation ) follows  digestion , and is a necessary process by which organisms eliminate a solid, semisolid, or liquid  waste  material known as  feces  from the  digestive tract  via the  anus  or  cloaca . The act has a variety of names ranging from the common, like  pooping  or  crapping , to the technical, e.g.  bowel movement , to the obscene ( shitting ), to the  euphemistic  (\"doing a number two\", \"dropping a deuce\" or \"taking a dump\"), to the juvenile (\"making doo-doo\"). The topic, usually avoided in polite company, can become the basis for some  potty humor ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4641", "text": "Humans  expel  feces  with a frequency varying from a few times daily to a few times weekly. [ 1 ]  Waves of  muscular contraction  (known as  peristalsis ) in the walls of the  colon  move fecal matter through the digestive tract towards the  rectum . Undigested food may also be expelled within the feces, in a process called  egestion . When  birds  defecate, they also expel  urine  and  urates  in the same mass, whereas other animals may also  urinate  at the same time, but spatially separated. Defecation may also accompany  childbirth  and  death . Babies defecate a unique substance called  meconium  prior to eating external foods."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4642", "text": "There are a number of medical conditions associated with defecation, such as  diarrhea  and  constipation , some of which can be serious. The feces expelled can carry diseases, most often through the contamination of food.  E. coli  is a particular concern."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4643", "text": "Before  toilet training , human feces are most often collected into a  diaper . Thereafter, in many societies people commonly defecate into a  toilet . However,  open defecation , the practice of defecating outside without using a toilet of any kind, is still widespread in some  developing countries . [ 2 ]  Some people defecate into  the ocean . First world countries use  sewage treatment plants  and/or  on-site treatment ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4644", "text": "The  rectum ampulla  stores fecal waste (also called stool) before it is excreted. As the waste fills the rectum and expands the rectal walls, stretch receptors in the rectal walls stimulate the desire to defecate. This urge to defecate arises from the reflex contraction of rectal muscles, relaxation of the  internal anal sphincter , and an initial contraction of the skeletal muscle of the  external anal sphincter . If the urge is not acted upon, the material in the rectum is often returned to the colon by  reverse peristalsis , where more water is absorbed and the feces are stored until the next mass peristaltic movement of the transverse and descending colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4645", "text": "When the rectum is full, an increase in pressure within the rectum forces apart the walls of the  anal canal , allowing the fecal matter to enter the canal. The rectum shortens as material is forced into the anal canal and peristaltic waves push the feces out of the rectum. The internal and external anal sphincters along with the  puborectalis muscle  allow the feces to be passed by muscles pulling the anus up over the exiting feces. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4646", "text": "The  external anal sphincter  is under voluntary control whereas the  internal anal sphincter  is involuntary. In  infants , the defecation occurs by  reflex action  without the voluntary control of the external anal sphincter. Defecation is voluntary in adults. Young children learn voluntary control through the process of  toilet training . Once trained, loss of control, called  fecal incontinence , may be caused by physical injury, nerve injury, prior surgeries (such as an  episiotomy ),  constipation ,  diarrhea , loss of storage capacity in the  rectum , intense fright,  inflammatory bowel disease ,  psychological  or  neurological  factors,  childbirth , or  death . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4647", "text": "Sometimes, due to the inability to control one's bowel movement or due to excessive fear, defecation (usually accompanied by urination) occurs involuntarily, soiling a person's undergarments. This may cause significant embarrassment to the person if this occurs in the presence of other people or a public place."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4648", "text": "The positions and modalities of defecation are  culture-dependent .  Squat toilets  are used by the vast majority of the world, including most of Africa, Asia, and the Middle East. [ 5 ]  The use of sit-down  toilets  in the  Western world  is a relatively recent development, beginning in the 19th century with the advent of indoor plumbing. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4649", "text": "Regular bowel movements determine the functionality and the health of the alimentary tracts in human body. Defecation is the most common regular bowel movement which eliminates waste from the human body. The frequency of defecation is hard to identify, which can vary from daily to weekly depending on individual bowel habits, the impact from the environment and genetic. [ 7 ]  If defecation is delayed for a prolonged period the fecal matter may harden, resulting in  constipation . If defecation occurs too fast, before excess liquid is absorbed,  diarrhea  may occur. [ 8 ]  Other associated symptoms can include abdominal bloating, abdominal pain, and abdominal distention. [ 9 ]  Disorders of the bowel can seriously impact quality of life and daily activities. The causes of functional bowel disorder are multifactorial, and dietary habits such as food intolerance and low fiber diet are considered to be the primary factors. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4650", "text": "Constipation, also known as defecatory dysfunction, is difficulty experienced when passing stools. It is one of the most notable alimentary disorders that affects different age groups in the population. Common constipation is associated with abdominal distention, pain or bloating. [ 11 ]  Research has revealed that chronic constipation complied with higher risk of cardiovascular events such as coronary heart disease and ischemic stroke, while associating with an increasing risk of mortality. [ 12 ]  Besides dietary factors, psychological traumas and 'pelvic floor disorders' can also cause chronic constipation and defecatory disorder respectively. [ 11 ]  Multiple interventions, including physical activities, 'high-fibre diet', probiotics [ 13 ]  and drug therapies can be widely and efficiently used to treat constipation and defecatory disorder."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4651", "text": "Inflammatory disease is characterized as long-lasting, chronic inflammation throughout the gastrointestinal tract.  Crohn's disease  (CD) and  ulcerative colitis  (UC) are two universal types of inflammatory bowel disease that have been studied over a century. They are closely related to different environmental risk factors, family genetics, and lifestyle choices such as smoking. [ 14 ]  Crohn's disease has been found to be related to immune disorders particularly. [ 15 ]  Different levels of cumulative intestinal injuries can cause different complications, such as fistulae, damage of bowel function, symptom recurrence, disability, etc. [ 16 ]  Patients can be children or adults. Recent research shows that immunodeficiency and monogenic disorders are the causes in young patients with inflammatory bowel diseases. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4652", "text": "Common symptoms of inflammatory bowel diseases differ by the infection level, but may include severe abdominal pain, diarrhea, fatigue, and unexpected weight loss.  Crohn's disease  can lead to infection of any part of the digestive tract, including ileum to anus. [ 18 ]  Internal manifestations include diarrhea, abdomen pain, fever, chronic anaemia, etc. External manifestations include impact on skin, joints, eyes, and liver. Significantly reduced microbiota diversity inside the gastrointestinal tract can also be observed. Ulcerative colitis mainly affects the function of the large bowel, and its incidence rate is three times greater than that of Crohn's disease. [ 19 ]  In terms of clinical features, over 90 percent of patients exhibit constant diarrhea, rectal bleeding, softer stool, mucus in the stool, tenesmus, and abdominal pain. [ 19 ]  The symptoms may continue for around 6 weeks or even longer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4653", "text": "The inflammatory bowel diseases could be effectively treated by 'pharmacotherapies' to relieve and maintain the symptoms, which showed in 'mucosal healing' and symptoms elimination. [ 20 ]  However, an optimal therapy for curing both inflammatory diseases are still under research due to the heterogeneity in clinical feature. [ 20 ]  Although both UC and CD are sharing similar symptoms, the medical treatment of them are distinctively different. [ 20 ]  Dietary treatment can benefit for curing CD by increase the dietary zinc and fish intake, which is related to mucosal healing of the bowel. [ 15 ]  Treatments vary from drug treatment to surgery based on the active level of the CD. UC can also be relieved by using immunosuppressive therapy for mild to moderate disease level and application of biological agents for severe cases. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4654", "text": "Irritable bowel syndrome is diagnosed as an intestinal disorder with chronic abdominal pain and inconsistency in form of stool, and is a common bowel disease that can be easily diagnosed in modern society. [ 21 ]  The variation in incident rate can be explained by different diagnostic criteria in different countries, with the 18\u201334 age group being recognized as the high frequency incident group. [ 21 ]  The definite cause of irritable bowel syndrome remains a mystery; however, it has been found to relate to multiple factors, such as 'alternation of mood and pressure, sleep disorders, food triggers, changing of dysbiosis and even sexual dysfunction'. [ 21 ]  One third of irritable bowel syndrome patients has family history with the disease suggesting that genetic predisposition could be a significant cause for irritable bowel syndrome. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4655", "text": "Patients with irritable bowel syndrome commonly experience abdominal pain, changes to stool form, recurrent abdominal bloating and gas, [ 22 ]  co-morbid disorders and alternation in bowel habits that caused diarrhea or constipation. [ 21 ]  However, anxiety and tension can also be detected, although patients with irritable bowel disease seem healthy. Apart from these typical symptoms, rectal bleeding, unexpected weight loss and increased inflammatory markers require further medical examination and investigation. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4656", "text": "Treatment for irritable bowel disease is multimodal. Dietary intervention and pharmacotherapies can both relieve the symptoms to a certain degree. Avoiding allergic food groups can be beneficial by reducing fermentation in the digestive tract and gas production, hence effectively alleviating abdominal pain and bloating. [ 21 ]  Drug interventions, such as laxatives, loperamide, [ 21 ]  and lubiprostone [ 22 ]  are applied to relieve intense symptoms including diarrhea, abdominal pain and constipation. Psychological treatment, dietary supplements [ 21 ]  and gut-focused hypnotherapy [ 22 ]  are recommended for targeting depression, mood disorders and sleep disturbance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4657", "text": "Bowel obstruction is a bowel condition which is a blockage that can be found in both the small intestines and large intestines. Increase of contractions can relieve blockages; however, continuous contractions with decreasing functionality may lead to terminated mobility of the small intestines, which then forms the obstruction. At the same time, the lack of contractility encourages liquid and gas accumulation. [ 23 ]  and \"electrolyte disturbances\". [ 24 ]  Small bowel obstruction can result in severe renal damage and hypovolemia. [ 24 ]  while evolving into \"mucosal ischemia and perforation\". [ 23 ]  Patients with small bowel obstruction were found to experience constipation, strangulation and abdominal pain and vomiting. [ 23 ]  Surgical intervention is primarily used to cure severe small bowel obstruction condition. Nonoperative therapy included nasogastric tube decompression, water-soluble-contrast medium process or symptomatic management can be applied to treat less severe symptoms [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4658", "text": "According to research, large bowel obstruction is less common than small bowel obstruction, but is still associated with a high mortality rate. [ 25 ]  Large bowel obstruction, also known as colonic obstruction, includes acute colonic obstruction, where a blockage is formed in the colon. Colonic obstructions frequently occur within the elder population, often accompanied by significant 'comorbidities'. [ 26 ]  Although colonic malignancy is revealed as the major cause of the colonic obstruction, volvulus has also been founded as a secondary common cause around the world. [ 25 ]  In addition, lower mobility, unhealthy mentality and restricted living environment are also listed as risk factors. Surgery and colonic stent placements are widely applied for curing colonic obstructions. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4659", "text": "Attempting forced expiration of breath against a closed airway (the  Valsalva maneuver ) is sometimes practiced to induce defecation while on a  toilet . This contraction of expiratory  chest  muscles,  diaphragm , abdominal wall muscles, and  pelvic  diaphragm exerts pressure on the digestive tract.  Ventilation  at this point temporarily ceases as the lungs push the chest diaphragm down to exert the pressure.  Cardiac arrest [ 28 ]  and other cardiovascular complications [ 29 ]  can in rare cases occur due to attempting to defecate using the Valsalva maneuver.  Valsalva retinopathy  is another pathological syndrome associated with the Valsalva maneuver. [ 30 ] [ 31 ]  Thoracic  blood pressure  rises and as a reflex response the amount of blood pumped by the heart decreases. Death has been known to occur in cases where defecation causes the blood pressure to rise enough to cause the rupture of an  aneurysm  or to dislodge blood clots (see  thrombosis ). Also, in releasing the Valsalva maneuver blood pressure falls; this, coupled with standing up quickly to leave the toilet, can result in a blackout. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4660", "text": "Open defecation  is the human practice of defecating outside (in the open environment) rather than into a  toilet . People may choose fields, bushes, forests, ditches, streets, canals or other open space for defecation. They do so because either they do not have a toilet readily accessible or due to traditional cultural practices. [ 32 ]  The practice is common where  sanitation  infrastructure and services are not available. Even if toilets are available,  behavior change  efforts may still be needed to promote the use of toilets."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4661", "text": "Open defecation can pollute the environment and cause health problems. High levels of open defecation are linked to high  child mortality , poor  nutrition ,  poverty , and large disparities between rich and poor. [ 33 ] :\u200a11"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4662", "text": "Ending open defecation is an indicator being used to measure progress towards the  Sustainable Development Goal Number 6 .  Extreme poverty  and lack of sanitation are statistically linked. Therefore, eliminating open defecation is thought to be an important part of the effort to eliminate poverty. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4663", "text": "The  anus  and  buttocks  may be  cleansed  after defecation with  toilet paper , similar paper products, or other absorbent material. In many cultures, such as Hindu and Muslim, water is used for anal cleansing after defecation, either in addition to using toilet paper or exclusively. When water is used for anal cleansing after defecation, toilet paper may be used for drying the area afterwards. Some doctors and people who work in the science and  hygiene  fields have stated that switching to using a  bidet  as a form of anal cleansing after defecation is both more hygienic and more environmentally friendly. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4664", "text": "Some peoples have culturally significant stories in which defecation plays a role. For example:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4665", "text": "Some aspects of  psychology  surround the act of defecation. There is an inherent desire for privacy among humans.  Freud  stipulated a second stage of development, the  Anal Stage , which centers around the release of waste from the bladder and bowels. He categorized two types:  anal retentive  and  anal expulsive ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4666", "text": "Digestion  is the breakdown of large insoluble  food  compounds into small water-soluble components so that they can be absorbed into the  blood plasma . In certain organisms, these smaller substances are absorbed through the  small intestine  into the  blood stream . Digestion is a form of  catabolism  that is often divided into two processes based on how food is broken down: mechanical and chemical digestion. The term  mechanical digestion  refers to the physical breakdown of large pieces of food into smaller pieces which can subsequently be accessed by  digestive enzymes . Mechanical digestion takes place in the  mouth  through  mastication  and in the small intestine through  segmentation contractions . In  chemical digestion ,  enzymes  break down food into the small compounds that the body can use."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4667", "text": "In the  human digestive system , food enters the mouth and mechanical digestion of the food starts by the action of mastication (chewing), a form of mechanical digestion, and the wetting contact of  saliva . Saliva, a liquid secreted by the  salivary glands , contains  salivary amylase , an enzyme which starts the digestion of  starch  in the food. [ 1 ]  The saliva also contains  mucus , which lubricates the food; the  electrolyte  hydrogencarbonate ( HCO \u2212 3 ), which provides the ideal conditions of pH for amylase to work; and other electrolytes ( Na + ,  K + ,  Cl \u2212 ). [ 2 ]  About 30% of starch is  hydrolyzed  into  disaccharide  in the oral cavity (mouth). After undergoing mastication and starch digestion, the food will be in the form of a small, round slurry mass called a  bolus . It will then travel down the  esophagus  and into the  stomach  by the action of  peristalsis .  Gastric juice  in the stomach starts  protein digestion . Gastric juice mainly contains  hydrochloric acid  and  pepsin . In  infants  and  toddlers , gastric juice also contains  rennin  to digest milk proteins. As the first two chemicals may damage the stomach wall, mucus and bicarbonates are secreted by the stomach. They provide a slimy layer that acts as a shield against the damaging effects of chemicals like concentrated hydrochloric acid while also aiding lubrication. [ 3 ]  Hydrochloric acid provides acidic pH for pepsin. At the same time protein digestion is occurring, mechanical mixing occurs by peristalsis, which is waves of muscular contractions that move along the stomach wall. This allows the mass of food to further mix with the digestive enzymes. Pepsin breaks down proteins into  peptides  or  proteoses , which is further broken down into dipeptides and  amino acids  by enzymes in the small intestine. Studies suggest that increasing the number of chews per bite increases relevant gut hormones and may decrease self-reported hunger and food intake. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4668", "text": "When the  pyloric sphincter valve  opens, partially digested food ( chyme ) enters the  duodenum  where it mixes with digestive enzymes from the  pancreas  and bile juice from the  liver  and then passes through the small intestine, in which digestion continues. When the chyme is fully digested, it is absorbed into the blood. 95% of nutrient absorption occurs in the small intestine. Water and minerals are reabsorbed back into the blood in the  colon  (large intestine) where the pH is slightly acidic (about 5.6 ~ 6.9). Some vitamins, such as  biotin  and  vitamin K  (K 2 MK7) produced by bacteria in the colon are also absorbed into the blood in the colon. Absorption of water, simple sugar and alcohol also takes place in stomach. Waste material ( feces ) is eliminated from the  rectum  during  defecation . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4669", "text": "Digestive systems take many forms. There is a fundamental distinction between internal and external digestion. External digestion developed earlier in evolutionary history, and most  fungi  still rely on it. [ 6 ]  In this process,  enzymes  are  secreted  into the environment surrounding the organism, where they break down an organic material, and some of the products  diffuse  back to the organism.  Animals  have a tube ( gastrointestinal tract ) in which internal digestion occurs, which is more efficient because more of the broken down products can be captured, and the internal chemical environment can be more efficiently controlled. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4670", "text": "Some organisms, including nearly all  spiders , secrete biotoxins and digestive chemicals (e.g., enzymes) into the extracellular environment prior to ingestion of the consequent \"soup\". In others, once potential nutrients or food is inside the  organism , digestion can be conducted to a  vesicle  or a sac-like structure, through a tube, or through several specialized organs aimed at making the absorption of nutrients more efficient."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4671", "text": "Bacteria  use several systems to obtain nutrients from other organisms in the environments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4672", "text": "In a channel transport system, several proteins form a contiguous channel traversing the inner and outer membranes of the bacteria. It is a simple system, which consists of only three protein subunits: the  ABC protein ,  membrane fusion protein  (MFP), and  outer membrane protein . [ specify ]  This secretion system transports various chemical species, from ions, drugs, to proteins of various sizes (20\u2013900 kDa). The chemical species secreted vary in size from the small  Escherichia coli  peptide colicin V, (10 kDa) to the  Pseudomonas fluorescens  cell adhesion protein LapA of 900 kDa. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4673", "text": "A  type III secretion system  means that a molecular syringe is used through which a bacterium (e.g. certain types of  Salmonella ,  Shigella ,  Yersinia ) can inject nutrients into protist cells. One such mechanism was first discovered in  Y. pestis  and showed that toxins could be injected directly from the bacterial cytoplasm into the cytoplasm of its host's cells rather than be secreted into the extracellular medium. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4674", "text": "The  conjugation  machinery of some bacteria (and archaeal flagella) is capable of transporting both DNA and proteins. It was discovered in  Agrobacterium tumefaciens , which uses this system to introduce the Ti plasmid and proteins into the host, which develops the crown gall (tumor). [ 10 ]  The VirB complex of  Agrobacterium tumefaciens  is the prototypic system. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4675", "text": "In the  nitrogen-fixing   Rhizobia , conjugative elements naturally engage in inter- kingdom  conjugation. Such elements as the  Agrobacterium  Ti or Ri plasmids contain elements that can transfer to plant cells. Transferred genes enter the plant cell nucleus and effectively transform the plant cells into factories for the production of  opines , which the bacteria use as carbon and energy sources. Infected plant cells form  crown gall  or  root tumors . The Ti and Ri plasmids are thus  endosymbionts  of the bacteria, which are in turn endosymbionts (or parasites) of the infected plant."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4676", "text": "The Ti and Ri plasmids are themselves conjugative. Ti and Ri transfer between bacteria uses an independent system (the  tra , or transfer, operon) from that for inter-kingdom transfer (the  vir , or  virulence , operon). Such transfer creates virulent strains from previously avirulent  Agrobacteria ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4677", "text": "In addition to the use of the multiprotein complexes listed above,  gram-negative bacteria  possess another method for release of material: the formation of  outer membrane vesicles . [ 12 ] [ 13 ]   Portions of the outer membrane pinch off, forming spherical structures made of a lipid bilayer enclosing periplasmic materials.  Vesicles from a number of bacterial species have been found to contain virulence factors, some have immunomodulatory effects, and some can directly adhere to and intoxicate host cells.  While release of vesicles has been demonstrated as a general response to stress conditions, the process of loading cargo proteins seems to be selective. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4678", "text": "The  gastrovascular cavity  functions as a stomach in both digestion and the distribution of nutrients to all parts of the body.  Extracellular digestion takes place within this central cavity, which is lined with the gastrodermis, the internal layer of  epithelium . This cavity has only one opening to the outside that functions as both a  mouth  and an  anus : waste and undigested matter is excreted through the mouth/anus, which can be described as an incomplete  gut ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4679", "text": "In a plant such as the  Venus flytrap  that can make its own food through photosynthesis, it does not eat and digest its prey for the traditional objectives of harvesting energy and carbon, but mines prey primarily for essential nutrients (nitrogen and phosphorus in particular) that are in short supply in its boggy, acidic habitat. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4680", "text": "A  phagosome  is a  vacuole  formed around a particle absorbed by  phagocytosis .  The vacuole is formed by the fusion of the  cell membrane  around the particle. A phagosome is a  cellular compartment  in which  pathogenic  microorganisms can be killed and digested. Phagosomes fuse with  lysosomes  in their maturation process, forming  phagolysosomes . In humans,  Entamoeba histolytica  can phagocytose  red blood cells . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4681", "text": "To aid in the digestion of their food, animals evolved organs such as beaks,  tongues ,  radulae , teeth, crops, gizzards, and others."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4682", "text": "Birds  have bony  beaks  that are specialised according to the bird's  ecological niche . For example,  macaws  primarily eat seeds, nuts, and fruit, using their beaks to open even the toughest seed. First they scratch a thin line with the sharp point of the beak, then they shear the seed open with the sides of the beak."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4683", "text": "The mouth of the  squid  is equipped with a sharp horny beak mainly made of cross-linked  proteins . It is used to kill and tear prey into manageable pieces. The beak is very robust, but does not contain any minerals, unlike the teeth and jaws of many other organisms, including marine species. [ 17 ]  The beak is the only indigestible part of the squid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4684", "text": "The  tongue  is skeletal muscle on the floor of the  mouth  of most vertebrates, that manipulates  food  for chewing ( mastication ) and  swallowing  (deglutition). It is sensitive and kept moist by  saliva . The underside of the tongue is covered with a smooth  mucous membrane . The tongue also has a touch sense for locating and positioning food particles that require further chewing. The tongue is used to roll food particles into a  bolus  before being transported down the  esophagus  through  peristalsis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4685", "text": "The  sublingual  region underneath the front of the tongue is a location where the  oral mucosa  is very thin, and underlain by a plexus of veins. This is an ideal location for introducing certain medications to the body. The sublingual route takes advantage of the highly  vascular  quality of the oral cavity, and allows for the speedy application of medication into the cardiovascular system, bypassing the gastrointestinal tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4686", "text": "Teeth (singular tooth) are small whitish structures found in the jaws (or mouths) of many vertebrates that are used to tear, scrape, milk and chew food. Teeth are not made of bone, but rather of tissues of varying density and hardness, such as enamel, dentine and cementum. Human teeth have a blood and nerve supply which enables proprioception. This is the ability of sensation when chewing, for example if we were to bite into something too hard for our teeth, such as a chipped plate mixed in food, our teeth send a message to our brain and we realise that it cannot be chewed, so we stop trying."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4687", "text": "The shapes, sizes and numbers of types of animals' teeth are related to their diets. For example, herbivores have a number of molars which are used to grind plant matter, which is difficult to digest.  Carnivores  have  canine teeth  which are used to kill and tear meat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4688", "text": "A  crop , or croup, is a thin-walled expanded portion of the  alimentary tract  used for the storage of food prior to digestion. In some birds it is an expanded, muscular pouch near the  gullet  or throat. In adult doves and pigeons, the crop can produce  crop milk  to feed newly hatched birds. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4689", "text": "Certain insects may have a crop or enlarged  esophagus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4690", "text": "Herbivores  have evolved  cecums  (or an  abomasum  in the case of  ruminants ). Ruminants have a fore-stomach with four chambers. These are the  rumen ,  reticulum ,  omasum , and abomasum. In the first two chambers, the rumen and the reticulum, the food is mixed with saliva and separates into layers of solid and liquid material.  Solids clump together to form the cud (or  bolus ). The cud is then regurgitated, chewed slowly to completely mix it with saliva and to break down the particle size."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4691", "text": "Fibre, especially  cellulose  and  hemi-cellulose , is primarily broken down into the  volatile fatty acids ,  acetic acid ,  propionic acid  and  butyric acid  in these chambers (the reticulo-rumen) by microbes: ( bacteria ,  protozoa , and fungi). In the omasum, water and many of the inorganic mineral elements are absorbed into the blood stream."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4692", "text": "The abomasum is the fourth and final stomach compartment in ruminants. It is a close equivalent of a monogastric stomach (e.g., those in humans or pigs), and digesta is processed here in much the same way. It serves primarily as a site for acid hydrolysis of microbial and dietary protein, preparing these protein sources for further digestion and absorption in the small intestine.  Digesta is finally moved into the small intestine, where the digestion and absorption of nutrients occurs. Microbes produced in the reticulo-rumen are also digested in the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4693", "text": "Regurgitation  has been mentioned above under abomasum and crop, referring to crop milk, a secretion from the lining of the crop of  pigeons and doves  with which the parents feed their young by regurgitation. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4694", "text": "Many  sharks  have the ability to turn their stomachs inside out and evert it out of their mouths in order to get rid of unwanted contents (perhaps developed as a way to reduce exposure to toxins)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4695", "text": "Other animals, such as  rabbits  and  rodents , practise  coprophagia  behaviours \u2013 eating specialised faeces in order to re-digest food, especially in the case of roughage. Capybara, rabbits, hamsters and other related species do not have a complex digestive system as do, for example, ruminants. Instead they extract more  nutrition  from grass by giving their food a second pass through the  gut . Soft faecal pellets of partially digested food are excreted and generally consumed immediately. They also produce normal droppings, which are not eaten."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4696", "text": "Young elephants, pandas, koalas, and hippos eat the faeces of their mother, probably to obtain the bacteria required to properly digest vegetation. When they are born, their intestines do not contain these bacteria (they are completely sterile). Without them, they would be unable to get any nutritional value from many plant components."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4697", "text": "An  earthworm 's digestive system consists of a mouth,  pharynx ,  esophagus , crop,  gizzard , and  intestine . The mouth is surrounded by strong lips, which act like a hand to grab pieces of dead grass, leaves, and weeds, with bits of soil to help chew. The lips break the food down into smaller pieces. In the pharynx, the food is lubricated by mucus secretions for easier passage. The esophagus adds calcium carbonate to neutralize the acids formed by food matter decay. Temporary storage occurs in the crop where food and calcium carbonate are mixed. The powerful muscles of the gizzard churn and mix the mass of food and dirt. When the churning is complete, the glands in the walls of the gizzard add enzymes to the thick paste, which helps chemically breakdown the organic matter. By  peristalsis , the mixture is sent to the intestine where friendly bacteria continue chemical breakdown. This releases carbohydrates, protein, fat, and various vitamins and minerals for absorption into the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4698", "text": "In most  vertebrates , digestion is a multistage process in the digestive system, starting from ingestion of raw materials, most often other organisms. Ingestion usually involves some type of mechanical and chemical processing. Digestion is separated into four steps:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4699", "text": "Underlying the process is muscle movement throughout the system through swallowing and  peristalsis . Each step in digestion requires energy, and thus imposes an \"overhead charge\" on the energy made available from absorbed substances. Differences in that overhead cost are important influences on lifestyle, behavior, and even physical structures. Examples may be seen in humans, who differ considerably from other hominids (lack of hair, smaller jaws and musculature, different dentition, length of intestines, cooking, etc.)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4700", "text": "The major part of digestion takes place in the small intestine. The large intestine primarily serves as a site for fermentation of indigestible matter by  gut  bacteria and for resorption of water from digests before excretion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4701", "text": "In  mammals , preparation for digestion begins with the  cephalic phase  in which saliva is produced in the mouth and  digestive enzymes  are produced in the  stomach .  Mechanical and chemical digestion begin in the mouth where food is  chewed , and mixed with saliva to begin enzymatic processing of  starches .  The stomach continues to break food down mechanically and chemically through churning and mixing with both acids and enzymes.  Absorption  occurs in the stomach and  gastrointestinal tract , and the process finishes with defecation. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4702", "text": "The  human gastrointestinal tract  is around 9 metres (30 feet) long. Food digestion physiology varies between individuals and upon other factors such as the characteristics of the food and size of the meal, and the process of digestion normally takes between 24 and 72 hours. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4703", "text": "Digestion begins in the  mouth  with the secretion of saliva and its digestive enzymes. Food is formed into a  bolus  by the mechanical  mastication  and swallowed into the  esophagus  from where it enters the stomach through the action of  peristalsis .  Gastric juice  contains  hydrochloric acid  and  pepsin  which could damage the stomach lining, but  mucus  and bicarbonates are secreted for protection. In the stomach further release of enzymes break down the food further and this is combined with the churning action of the stomach. Mainly proteins are digested in stomach. The partially digested food enters the  duodenum  as a thick semi-liquid  chyme . In the small intestine, the larger part of digestion takes place and this is helped by the secretions of  bile ,  pancreatic juice  and  intestinal juice .  The intestinal walls are lined with  villi , and their  epithelial cells  are covered with numerous  microvilli  to improve the absorption of nutrients by increasing the  surface area  of the intestine. Bile helps in emulsification of fats and also activates lipases."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4704", "text": "In the large intestine, the passage of food is slower to enable fermentation by the  gut flora  to take place. Here, water is absorbed and waste material stored as  feces  to be removed by defecation via the  anal canal  and  anus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4705", "text": "Different  phases of digestion  take place including: the  cephalic phase ,  gastric phase , and  intestinal phase ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4706", "text": "The cephalic phase occurs at the sight, thought and smell of food, which stimulate the  cerebral cortex . Taste and smell stimuli are sent to the  hypothalamus  and  medulla oblongata . After this it is routed through the  vagus nerve  and release of acetylcholine. Gastric secretion at this phase rises to 40% of maximum rate. Acidity in the stomach is not buffered by food at this point and thus acts to inhibit parietal (secretes acid) and  G cell  (secretes gastrin) activity via  D cell  secretion of  somatostatin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4707", "text": "The gastric phase takes 3 to 4 hours. It is stimulated by  distension  of the stomach, presence of food in stomach and decrease in  pH . Distention activates long and myenteric reflexes. This activates the release of  acetylcholine , which stimulates the release of more gastric juices. As protein enters the stomach, it binds to  hydrogen  ions, which raises the pH of the stomach. Inhibition of gastrin and  gastric acid  secretion is lifted. This triggers G cells to release  gastrin , which in turn stimulates  parietal cells  to secrete gastric acid.  Gastric acid is about 0.5%  hydrochloric acid , which lowers the pH to the desired pH of 1\u20133.  Acid release is also triggered by  acetylcholine  and  histamine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4708", "text": "The intestinal phase has two parts, the excitatory and the inhibitory. Partially digested food fills the  duodenum . This triggers intestinal gastrin to be released. Enterogastric reflex inhibits vagal nuclei, activating  sympathetic fibers  causing the  pyloric sphincter  to tighten to prevent more food from entering, and inhibits local reflexes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4709", "text": "Protein digestion occurs in the stomach and  duodenum  in which 3 main enzymes, pepsin secreted by the stomach and  trypsin  and  chymotrypsin  secreted by the pancreas, break down food proteins into  polypeptides  that are then broken down by various  exopeptidases  and  dipeptidases  into  amino acids .  The digestive enzymes however are mostly secreted as their inactive precursors, the  zymogens .  For example, trypsin is secreted by pancreas in the form of  trypsinogen , which is activated in the duodenum by  enterokinase  to form trypsin.  Trypsin then cleaves  proteins  to smaller polypeptides."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4710", "text": "Digestion of some fats can begin in the mouth where  lingual lipase  breaks down some short chain lipids into  diglycerides . However fats are mainly digested in the small intestine. [ 21 ]   The presence of fat in the small intestine produces hormones that stimulate the release of  pancreatic lipase  from the pancreas and  bile  from the liver which helps in the emulsification of fats for absorption of  fatty acids . [ 21 ]   Complete digestion of one molecule of fat (a  triglyceride ) results a mixture of fatty acids, mono- and di-glycerides, but no  glycerol . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4711", "text": "In humans, dietary starches are composed of  glucose  units arranged in long chains called amylose, a  polysaccharide . During digestion, bonds between glucose molecules are broken by salivary and pancreatic  amylase , resulting in progressively smaller chains of glucose.  This results in simple sugars glucose and  maltose  (2 glucose molecules) that can be absorbed by the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4712", "text": "Lactase  is an enzyme that breaks down the  disaccharide   lactose  to its component parts, glucose and  galactose .  Glucose and galactose can be absorbed by the small intestine.  Approximately 65 percent of the adult population produce only small amounts of lactase and are unable to eat  unfermented  milk-based foods.  This is commonly known as  lactose intolerance .  Lactose intolerance varies widely by genetic heritage;  more than 90 percent of peoples of east Asian descent are lactose intolerant, in contrast to about 5 percent of people of northern European descent. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4713", "text": "Sucrase  is an enzyme that breaks down the disaccharide  sucrose , commonly known as table sugar, cane sugar, or beet sugar. Sucrose digestion yields the sugars  fructose  and glucose which are readily absorbed by the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4714", "text": "DNA and RNA are broken down into  mononucleotides  by the  nucleases   deoxyribonuclease  and  ribonuclease  (DNase and RNase) from the pancreas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4715", "text": "Some nutrients are complex molecules (for example  vitamin B 12 ) which would be destroyed if they were broken down into their  functional groups .  To digest vitamin B 12  non-destructively,  haptocorrin  in saliva strongly binds and protects the B 12  molecules from stomach acid as they enter the stomach and are cleaved from their protein complexes. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4716", "text": "After the B 12 -haptocorrin complexes pass from the stomach via the pylorus to the duodenum, pancreatic proteases cleave haptocorrin from the B 12  molecules which rebind to  intrinsic factor  (IF).  These B 12 -IF complexes travel to the ileum portion of the small intestine where  cubilin  receptors enable  assimilation  and circulation of B 12 -IF complexes in the blood. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4717", "text": "There are at least five hormones that aid and regulate the digestive system in mammals. There are variations across the vertebrates, as for instance in birds. Arrangements are complex and additional details are regularly discovered. Connections to metabolic control (largely the glucose-insulin system) have been uncovered."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4718", "text": "Digestion is a complex process controlled by several factors. pH plays a crucial role in a normally functioning digestive tract. In the mouth, pharynx and esophagus, pH is typically about 6.8, very weakly acidic. Saliva controls pH in this region of the digestive tract.  Salivary amylase  is contained in saliva and starts the breakdown of carbohydrates into  monosaccharides . Most digestive enzymes are sensitive to pH and will denature in a high or low pH environment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4719", "text": "The stomach's high acidity inhibits the breakdown of  carbohydrates  within it. This acidity confers two benefits: it  denatures  proteins for further digestion in the small intestines, and provides  non-specific immunity , damaging or eliminating various  pathogens . [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4720", "text": "In the small intestines, the duodenum provides critical pH balancing to activate digestive enzymes. The liver secretes bile into the duodenum to neutralize the acidic conditions from the stomach, and the  pancreatic duct  empties into the duodenum, adding  bicarbonate  to neutralize the acidic chyme, thus creating a neutral environment. The mucosal tissue of the small intestines is alkaline with a pH of about 8.5. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4721", "text": "The  digestive system of gastropods  has evolved to suit almost every kind of diet and feeding behavior.  Gastropods  ( snails  and  slugs ) as the largest taxonomic class of the  mollusca  are very diverse: the group includes  carnivores ,  herbivores ,  scavengers ,  filter feeders , and even  parasites ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4722", "text": "In particular, the  radula  is often highly adapted to the specific diet of the various group of gastropods. Another distinctive feature of the digestive tract is that, along with the rest of the  visceral  mass, it has undergone  torsion , twisting around through 180 degrees during the larval stage, so that the  anus  of the animal is located above its head. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4723", "text": "A number of species have developed special adaptations to feeding, such as the \"drill\" of some  limpets , or the harpoon of the  neogastropod  genus  Conus . Filter feeders use the  gills , mantle lining, or nets of mucus to trap their prey, which they then pull into the mouth with the radula. The highly modified parasitic genus  Enteroxenos  has no digestive tract at all, and simply absorbs the blood of its host through the body wall. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4724", "text": "The digestive system usually has the following parts:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4725", "text": "The buccal mass is the first part of the digestive system, and consists of the mouth and pharynx. The mouth includes a  radula , and in most cases, also a pair of jaws. The pharynx can be very large, especially in carnivorous species."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4726", "text": "Many carnivorous species have developed a  proboscis , containing the oral cavity, radula, and part of the oesophagus. At rest, the proboscis is enclosed within a sac-like sheath, with an opening at the front of the animal that resembles a true mouth. When the animal feeds, it pumps blood into the proboscis, inflating it and pushing it out through the opening to grasp the gastropod's prey. A set of retractor muscles help pull the proboscis back inside the sheath once feeding is completed. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4727", "text": "The  radula  is a  chitinous  ribbon used for scraping or cutting food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4728", "text": "Several herbivorous species, as well as carnivores that prey on  sessile  animals, have also developed simple jaws, which help to hold the food steady while the radula works on it. The jaw is opposite to the  radula  and reinforces part of the  foregut . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4729", "text": "The more purely carnivorous the diet, the more the jaw is reduced. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4730", "text": "There are often pieces of food in the gut corresponding to the shape of the jaw. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4731", "text": "The jaw structure can be ribbed or smooth:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4732", "text": "Some species have no jaw."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4733", "text": "Salivary glands  plays primary role in the anatomical and physiological adaptations of the digestive system of predatory gastropods. [ 3 ]  Ducts from large salivary glands lead into the buccal cavity, and the oesophagus also supplies the digestive enzymes that help to break down the food. [ 1 ]  Salivary secretions lubricate the food and they also contain  bioactive compounds . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4734", "text": "The mouth of gastropods opens into an  oesophagus , which connects to the  stomach . Because of torsion, the oesophagus usually passes around the stomach, and opens into its posterior portion, furthest from the mouth. In species that have undergone de-torsion, however, the oesophagus may open into the anterior of the stomach, which is therefore reversed from the usual gastropod arrangement. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4735", "text": "In  Tarebia granifera , the  brood pouch  is above the oesophagus. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4736", "text": "There is available an extensive  rostrum  on the anterior part of the oesophagus in all carnivorous gastropods. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4737", "text": "Some basal gastropod clades have  oesophageal gland ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4738", "text": "In most species, the stomach itself is a relatively simple sac, and is the main site of digestion. In many herbivores, however, the hind part of the oesophagus is enlarged to form a  crop , which, in terrestrial  pulmonates , may even replace the stomach entirely. In many aquatic herbivores, however, the stomach is adapted into a  gizzard  that helps to grind up the food. The gizzard may have a tough  cuticle , or may be filled with abrasive sand grains. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4739", "text": "In the most primitive gastropods, however, the stomach is a more complex structure. In these species, the hind part of the stomach, where the oesophagus enters, is  chitinous , and includes a sorting region lined with  cilia . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4740", "text": "In all gastropods, the portion of the stomach furthest from the oesophagus, called the \"style sac\", is lined with cilia. These beat in a rotary motion, pulling the food forward in a steady stream from the mouth. Usually, the food is embedded in a string of mucus produced in the mouth, creating a coiled conical mass in the style sac. This action, rather than muscular  peristalsis , is responsible for the movement of food through the gastropod digestive tract. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4741", "text": "Two diverticular glands open into the stomach, and secrete enzymes that help to break down the food. In the more primitive species, these glands may also absorb the food particles directly and digest them intracellularly. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4742", "text": "The hepatopancreas is the largest organ in  stylommatophoran  gastropods. [ 7 ]  It produces enzymes, and absorbs and stores nutrients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4743", "text": "The anterior portion of the stomach opens into a coiled  intestine , which helps to resorb water from the food, producing  faecal pellets . The anus opens above the head. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4744", "text": "Diosmectite  (brand names  Smecta ,  Smecdral ) is a natural  silicate  of  aluminium  and  magnesium  used as an  intestinal   adsorbent  in the treatment of several  gastrointestinal diseases , including infectious and non-infectious acute and chronic  diarrhoea , including  irritable bowel syndrome  diarrhea subtype. Other uses include: chronic diarrhea caused by radiation-induced, chemotherapy-induced, and  HIV/AIDS -associated chronic diarrhea. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4745", "text": "It is  insoluble  in water. It is usually taken orally as a suspension in warm water. In the field of geology, it is more commonly known as  montmorillonite . Diosmectite is a contraction of \" dioctahedral   smectite \"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4746", "text": "Its effectiveness in improving stool consistency is the result of its alleged ability to absorb bacteria, viruses and toxins as well as strengthening the intestinal mucus barrier to reduce  luminal   antigens  passing through the mucus barrier which in turn helps to reduce inflammation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4747", "text": "Diosmectite may be a useful additive in the treatment of acute childhood diarrhoea. As evidence is of \u2018low quality\u2019, future research is needed with higher quality designs before any firm recommendations can be made.  [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4748", "text": "The  duodenal bulb  (also  ampulla of duodenum ,  duodenal ampulla , or  duodenal cap ) is the initial, dilated portion of (the superior part of) the  duodenum [ 1 ]  just distal to the  stomach ; it begins at the  pylorus  and ends at the neck of the  gallbladder . It is normally about 5 centimeters long. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4749", "text": "It is located posterior to the liver and the gallbladder and superior to the  pancreatic head . [ citation needed ]  The  gastroduodenal artery , [ 3 ]   portal vein , and  common bile duct  are situated posterior to the duodenal bulb. The distal part of the bulb is located retroperitoneally. It is located immediately distal to the  pyloric sphincter . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4750", "text": "The duodenal bulb is the site of duodenal ulcer occurrence. Duodenal ulcers are more common than gastric ulcers and - unlike gastric ulcers - are caused by increased gastric acid secretion. Duodenal ulcers are commonly located anteriorly, and rarely posteriorly. Anterior ulcers can be complicated by perforation, while the posterior ones bleed. The reason for that is explained by their location. The peritoneal or abdominal cavity is located anterior to the duodenum. Therefore, if the ulcer grows deep enough, it will perforate, whereas if a posterior ulcer grows deep enough, it will penetrate the  gastroduodenal artery  and bleed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4751", "text": "The  duodenojejunal flexure  or  duodenojejunal junction , also known as the  angle of Treitz , [ 1 ] [ 2 ]  is the border between the  duodenum  and the  jejunum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4752", "text": "The ascending portion of the  duodenum  ascends on the left side of the  aorta , as far as the level of the upper border of the second  lumbar vertebra . At this point, it turns abruptly forward to merge with the  jejunum , forming the duodenojejunal flexure. This forms the beginning of the jejunum. [ 3 ]  The duodenojejunal flexure is surrounded by the  suspensory muscle of the duodenum . [ 4 ] :\u200a274\u200a  It is  retroperitoneal , so is less mobile than the jejunum that comes after it, helping to stabilise the jejunum. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4753", "text": "The duodenojejunal flexure lies in front of the left  psoas major muscle , the  left renal artery , and the  left renal vein . It is covered in front, and partly at the sides, by  peritoneum  continuous with the left portion of the  mesentery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4754", "text": "The  ligament of Treitz , a peritoneal fold, from the  right crus of diaphragm , is an identification point for the duodenojejunal flexure during  abdominal surgery . [ 6 ] :\u200a85"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4755", "text": "This article incorporates text in the  public domain  from  page 1170  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4756", "text": "The  duodenum  is the first section of the  small intestine [ 3 ]  in most  higher vertebrates , including  mammals ,  reptiles , and  birds . In mammals, it may be the principal site for  iron  absorption.\nThe duodenum precedes the  jejunum  and  ileum  and is the shortest part of the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4757", "text": "In human beings, the duodenum is a hollow jointed tube about 25\u201338 centimetres (10\u201315 inches) long connecting the  stomach  to the  middle part of the small intestine . [ 4 ] [ 5 ]  It begins with the  duodenal bulb  and ends at the  suspensory muscle of duodenum . [ 6 ]  The duodenum can be divided into four parts: the first (superior), the second (descending), the third (transverse) and the fourth (ascending) parts. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4758", "text": "The duodenum is the first section of the  small intestine  in most  higher vertebrates , including  mammals ,  reptiles , and  birds . In  fish , the divisions of the small intestine are not as clear, and the terms  anterior intestine  or  proximal intestine  may be used instead of duodenum. [ 7 ]  In mammals the duodenum may be the principal site for  iron  absorption. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4759", "text": "In humans, the duodenum is a C-shaped hollow jointed tube, 25\u201338 centimetres (10\u201315 inches) in length, lying adjacent to the  stomach  (and connecting it to the small intestine). It is divided anatomically into four sections. The first part lies within the  peritoneum  but its other parts are  retroperitoneal . [ 9 ] :\u200a273"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4760", "text": "The  first part , or  superior part , of the duodenum is a continuation from the  pylorus  to the transpyloric plane. It is superior (above) to the rest of the segments, at the  vertebral  level of  L1 . The  duodenal bulb , about  2\u00a0cm ( 3 \u2044 4 \u00a0in) long, is the first part of the duodenum and is slightly dilated. The duodenal bulb is a remnant of the mesoduodenum, a  mesentery  that suspends the organ from the posterior abdominal wall in fetal life. [ 10 ]  The first part of the duodenum is mobile, and connected to the liver by the  hepatoduodenal ligament  of the  lesser omentum . The first part of the duodenum ends at the corner, the  superior duodenal flexure . [ 9 ] :\u200a273"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4761", "text": "Relations: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4762", "text": "The  second part , or  descending part , of the duodenum begins at the superior duodenal flexure. It goes  inferior  to the lower border of vertebral body L3, before making a sharp turn  medially  into the  inferior duodenal flexure , the end of the descending part. [ 9 ] :\u200a274"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4763", "text": "The  pancreatic duct  and  common bile duct  enter the descending duodenum, through the  major duodenal papilla . The second part of the duodenum also contains the minor duodenal papilla, the entrance for the  accessory pancreatic duct . The junction between the embryological  foregut  and  midgut  lies just below the major duodenal papilla. [ 9 ] :\u200a274"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4764", "text": "The  third part , or  horizontal part  or  inferior part  of the duodenum is 10~12\u00a0cm in length. It begins at the  inferior duodenal flexure  and passes transversely to the left, passing in front of the  inferior vena cava ,  abdominal aorta  and the  vertebral column . The  superior mesenteric artery  and  vein  are  anterior  to the third part of the duodenum. [ 9 ] :\u200a274\u200a  This part may be compressed between the aorta and SMA causing  superior mesenteric artery syndrome ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4765", "text": "The  fourth part , or  ascending part , of the duodenum passes upward, joining with the  jejunum  at the  duodenojejunal flexure . The fourth part of the duodenum is at the vertebral level L3, and may pass directly on top, or slightly to the left, of the  aorta . [ 9 ] :\u200a274"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4766", "text": "The duodenum receives arterial blood from two different sources. The transition between these sources is important as it demarcates the foregut from the midgut. Proximal to the 2nd part of the duodenum (approximately at the major duodenal papilla \u2013 where the bile duct enters) the arterial supply is from the  gastroduodenal artery  and its branch the  superior pancreaticoduodenal artery . Distal to this point (the midgut) the arterial supply is from the  superior mesenteric artery  (SMA), and its branch the  inferior pancreaticoduodenal artery  supplies the 3rd and 4th sections.\nThe  superior  and  inferior pancreaticoduodenal  arteries (from the gastroduodenal artery and SMA respectively) form an  anastomotic  loop between the  celiac trunk  and the SMA; so there is potential for collateral circulation here."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4767", "text": "The venous drainage of the duodenum follows the arteries. Ultimately these veins drain into the  portal system , either directly or indirectly through the  splenic  or  superior mesenteric vein  and then to the portal vein."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4768", "text": "The  lymphatic vessels  follow the arteries in a retrograde fashion. The anterior lymphatic vessels drain into the pancreatoduodenal  lymph nodes  located along the superior and inferior pancreatoduodenal arteries and then into the pyloric lymph nodes (along the gastroduodenal artery). The posterior lymphatic vessels pass posterior to the head of the pancreas and drain into the superior mesenteric lymph nodes. Efferent lymphatic vessels from the duodenal lymph nodes ultimately pass into the celiac lymph nodes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4769", "text": "Under  microscopy , the duodenum has a  villous   mucosa . This is distinct from the mucosa of the  pylorus , which directly joins the duodenum. Like other structures of the  gastrointestinal tract , the duodenum has a  mucosa ,  submucosa ,  muscularis externa , and  adventitia . Glands line the duodenum, known as  Brunner's glands , which secrete  mucus  and  bicarbonate  in order to neutralise stomach acids. These are distinct glands not found in the ileum or jejunum, the other parts of the small intestine. [ 11 ] :\u200a274\u2013275"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4770", "text": "The duodenum's close anatomical association with the pancreas creates differences in function based on the position and orientation of the organs. The congenital abnormality, annular pancreas, causes a portion of the pancreas to encircle the duodenum. In an extramural annular pancreas, the pancreatic duct encircles the duodenum which results in gastrointestinal obstruction. An intramural annular pancreas is characterized by pancreatic tissue that is fused with the duodenal wall, causing duodenal ulceration. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4771", "text": "About 20,000 protein coding genes are expressed in human cells and 70% of these genes are expressed in the normal duodenum. [ 13 ] [ 14 ]  Some 300 of these genes are more specifically expressed in the duodenum with very few genes expressed only in the duodenum. The corresponding specific proteins are expressed in the duodenal mucosa, and many of these are also expressed in the small intestine, such as  alanine aminopeptidase , a digestive enzyme,  angiotensin-converting enzyme , involved in controlling  blood pressure , and  RBP2 , a protein involved in the uptake of  vitamin A . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4772", "text": "The duodenum is largely responsible for the breakdown of food in the small intestine, using  enzymes . The duodenum also regulates the rate of emptying of the stomach via hormonal pathways.  Secretin  and  cholecystokinin  are released from cells in the duodenal  epithelium  in response to acidic and fatty stimuli present there when the  pylorus  opens and emits gastric  chyme  into the duodenum for further digestion. These cause the  liver  and  gallbladder  to release  bile , and the  pancreas  to release bicarbonate and digestive enzymes such as  trypsin ,  lipase  and  amylase  into the duodenum as they are needed. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4773", "text": "The duodenum is a critical contributor to the regulation of food intake [ 17 ]  and glycemic control. [ 18 ]  As the first part of the small intestine, the duodenum is the initial site of nutrient absorption in the gastrointestinal tract. The duodenum senses nutrient intake and composition, and signals to the liver, pancreas, adipose tissue and brain [ 19 ]  through the direct and indirect [ 20 ]  release of several key hormones and signaling molecules, including the  incretin  peptides  Glucose-dependent insulinotropic polypeptide  (GIP) and  Glucagon-like peptide-1  (GLP-1), [ 20 ]  as well as  Cholecystokinin  (CCK) and  Secretin .\u00a0 The duodenum also signals to the brain directly via vagal afferents enabling neural control over food intake and glycemia. [ 21 ] \u00a0 Intestinal secretion of GIP and GLP-1 stimulates glucose-dependent insulin secretion from pancreatic beta-cells, known as the incretin effect. [ 22 ]  Incretin peptides, principally GLP-1 and GIP, regulate islet hormone secretion, glucose concentrations, lipid metabolism, gut motility, appetite and body weight, and immune function. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4774", "text": "The villi of the duodenum have a leafy-looking appearance, which is a histologically identifiable structure.  Brunner's glands , which secrete  mucus , are only found in the duodenum. The duodenum wall consists of a very thin layer of cells that form the  muscularis mucosae ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4775", "text": "Ulcers of the duodenum commonly occur because of infection by the bacteria  Helicobacter pylori . These bacteria, through a number of mechanisms, erode the protective mucosa of the duodenum, predisposing it to damage from gastric acids. The first part of the duodenum is the most common location of ulcers since it is where the acidic chyme meets the duodenal mucosa before mixing with the alkaline secretions of the duodenum. [ 24 ]  Duodenal ulcers may cause recurrent abdominal pain and  dyspepsia , and are often investigated using a  urea breath test  to test for the bacteria, and  endoscopy  to confirm ulceration and take a  biopsy . If managed, these are often managed through  antibiotics  that aim to eradicate the bacteria, and  proton-pump inhibitors  and  antacids  to reduce the gastric acidity. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4776", "text": "The  British Society of Gastroenterology  guidelines specify that a duodenal biopsy is required for the diagnosis of adult  celiac disease . The biopsy is ideally performed at a moment when the patient is on a gluten-containing diet. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4777", "text": "Duodenal cancer is a cancer in the first section of the small intestine. Cancer of the duodenum is relatively rare compared to  stomach cancer  and  colorectal cancer ; malignant tumors in the duodenum constitute only around 0.3% of all the gastrointestinal tract tumors but around half of cancerous tissues that develop in the small intestine. [ 27 ]  Its histology is often observed to be  adenocarcinoma , meaning that the cancerous tissue arises from glandular cells in the  epithelial tissue  lining the duodenum. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4778", "text": "A  western diet  induces duodenal mucosal hyperplasia and dysfunction that underlie insulin resistance, type 2 diabetes and obesity. [ 29 ] [ 30 ]  Diet-induced duodenal mucosal hyperplasia consists of increased mucosal mass, [ 31 ]  increased villus length, [ 29 ] [ 32 ] [ 33 ] [ 34 ]  decreased crypt density, [ 29 ]  proliferation of enteroendocrine cells, [ 35 ]  increased enterocyte mass, [ 36 ]  and an accumulation of lipid droplets in the mucosa. [ 37 ] [ 38 ]  Diet induced duodenal dysfunction  includes increased duodenal nutrient absorption, [ 32 ] [ 39 ] [ 40 ] [ 41 ]  altered duodenal hormone secretion, [ 29 ] [ 35 ]  and altered intestinal vagal afferent neuronal function. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4779", "text": "Inflammation of the duodenum is referred to as  duodenitis . There are multiple known causes. [ 43 ]  Celiac disease and inflammatory bowel disease are two of the known causes. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4780", "text": "The name  duodenum  is  Medieval Latin , short for  intest\u012bnum duod\u0113num digit\u014drum , meaning intestine of twelve finger-widths (in length), genitive pl. of duod\u0113n\u012b, twelve each, from Latin duodeni \"twelve each\" (from duodecim \"twelve\"). Coined by Gerard of Cremona (d. 1187) in his Latin translation of \"Canon Avicennae,\" \"\u0627\u062b\u0646\u0627 \u0639\u0634\u0631\" itself a loan-translation of Greek dodekadaktylon, literally \"twelve fingers long.\" The intestine part was so called by the Greek physician  Herophilus  (c. 335\u2013280 BCE) for its length, about equal to the breadth of 12 fingers. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4781", "text": "Many languages retain a similar etymology for this word. For example,  German   Zw\u00f6lffingerdarm ,  Dutch   Twaalfvingerige darm  and  Turkish   Oniki parmak ba\u011f\u0131rsa\u011f\u0131 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4782", "text": "In  pharmacology , the  elimination  or  excretion  of a drug is understood to be any one of a number of processes by which a drug is eliminated (that is,  cleared  and  excreted ) from an organism either in an unaltered form (unbound molecules) or modified as a metabolite. The  kidney  is the main excretory organ although others exist such as the  liver , the  skin , the  lungs  or  glandular  structures, such as the  salivary glands  and the  lacrimal glands . These organs or structures use specific routes to expel a drug from the body, these are termed  elimination pathways :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4783", "text": "Drugs are excreted from the kidney by  glomerular filtration  and by active  tubular secretion  following the same steps and mechanisms as the products of intermediate metabolism. Therefore, drugs that are filtered by the  glomerulus  are also subject to the process of passive  tubular reabsorption .  Glomerular filtration will only remove those drugs or metabolites that are not bound to proteins present in blood plasma (free fraction) and many other types of drugs (such as the organic acids) are actively secreted.  In the  proximal  and   distal convoluted tubules , non-ionised acids and weak bases are reabsorbed both actively and passively. Weak acids are excreted when the tubular fluid becomes too alkaline and this reduces passive reabsorption. The opposite occurs with weak bases. Poisoning treatments use this effect to increase elimination, by alkalizing the urine causing  forced diuresis  which promotes excretion of a weak acid, rather than it getting reabsorbed. As the acid is  ionised , it cannot pass through the  plasma membrane  back into the blood stream and instead gets excreted with the urine. Acidifying the urine has the same effect for weakly basic drugs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4784", "text": "On other occasions drugs combine with bile juices and enter the intestines. In the intestines the drug will join with the unabsorbed fraction of the administered dose and be eliminated with the faeces or it may undergo a new process of absorption to eventually be eliminated by the kidney."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4785", "text": "The other elimination pathways are less important in the elimination of drugs, except in very specific cases, such as the respiratory tract for alcohol or anaesthetic gases. The case of mother's milk is of special importance. The liver and kidneys of newly born  infants  are relatively undeveloped and they are highly sensitive to a drug's  toxic effects . For this reason it is important to know if a drug is likely to be eliminated from a woman's body if she is breast feeding in order to avoid this situation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4786", "text": "Pharmacokinetics studies the manner and speed with which drugs and their metabolites are eliminated by the various excretory organs. This elimination will be proportional to the drug's plasmatic concentrations. In order to model these processes a working definition is required for some of the concepts related to excretion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4787", "text": "The plasma half-life or  half life of elimination  is the time required to eliminate 50% of the absorbed dose of a drug from an organism. Or put another way, the time that it takes for the plasma concentration to fall by half from its maximum levels."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4788", "text": "The difference in a drug's concentration in arterial blood (before it has circulated around the body) and venous blood (after it has passed through the body's organs) represents the amount of the drug that the body has eliminated or  cleared . Although clearance may also involve other organs than the kidney, it is almost synonymous with  renal clearance  or  renal plasma clearance .  Clearance is therefore expressed as the plasma volume totally free of the drug per unit of time, and it is measured in units of volume per units of time.\nClearance can be determined on an overall, organism level (\u00absystemic clearance\u00bb) or at an organ level (hepatic clearance, renal clearance etc.). The equation that describes this concept is:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4789", "text": "Where:  \n \n \n \n C \n \n L \n \n o \n \n \n \n \n {\\displaystyle CL_{o}} \n \n  is the organ's clearance rate,  \n \n \n \n \n C \n \n A \n \n \n \n \n {\\displaystyle C_{A}} \n \n  is the drug's plasma concentration in arterial blood,  \n \n \n \n \n C \n \n V \n \n \n \n \n {\\displaystyle C_{V}} \n \n  is the drug's plasma concentration in venous blood and  \n \n \n \n Q \n \n \n {\\displaystyle Q} \n \n  an organ's blood flow."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4790", "text": "Each organ will have its own specific clearance conditions, which will relate to its mode of action. The \u00abrenal clearance\u00bb rate will be determined by factors such as the degree of  plasma protein binding  as the drug will only be filtered out if it is in the unbound free form, the degree of  saturation  of the transporters (active secretion depends on transporter proteins that can become saturated) or the number of functioning  nephrons  (hence the importance of factors such as  kidney failure )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4791", "text": "As \u00abhepatic clearance\u00bb is an active process it is therefore determined by factors that alter an organism's metabolism such as the number of functioning  hepatocytes , this is the reason that  liver failure  has such clinical importance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4792", "text": "The steady state or  stable concentration  is reached when the drug's supply to the blood plasma is the same as the rate of elimination from the plasma. It is necessary to calculate this concentration in order to decide the period between doses and the amount of drug supplied with each dose in prolonged treatments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4793", "text": "Other parameters of interest include a drug's  bioavailability  and the  apparent volume of distribution ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4794", "text": "For elimination via bile please see: Estimation of Biliary Excretion of Foreign Compounds Using Properties of Molecular Structure. 2014. Sharifi M., Ghafourian T. AAPS J. 16(1) 65\u201378."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4795", "text": "The  embryological origin of the mouth and anus  is an important characteristic, and forms the morphological basis for separating  bilaterian  animals into two  natural groupings : the  protostomes  and  deuterostomes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4796", "text": "In animals at least as complex as an  earthworm , a dent forms in one side of the early,  spheroidal   embryo . This dent, the  blastopore , deepens to become the  archenteron , the first phase in the growth of the  gut . In  deuterostomes , the original dent becomes the anus, while the gut eventually tunnels through the embryo until it reaches the other side, forming an opening that becomes the mouth. [ 1 ]  It was originally thought that the blastopore of the  protostomes  formed the mouth, and the anus formed second when the gut tunneled through the embryo. More recent research has shown that our understanding of protostome mouth formation is somewhat less secure than we had thought. [ 2 ]   Acoelomorpha , which form a sister group to the rest of the bilaterian animals, have a single mouth that leads into a blind gut (with no anus). The genes employed in the embryonic construction of the flatworm mouth are the same as those expressed for the protostome and deuterostome mouth, which suggests that the structures are equivalent  homologous , and that the older ideas [ which? ]  about  protostome  mouth formation were correct. [ 1 ]  An alternative way to develop two openings from the blastopore during  gastrulation , called amphistomy, appears to exist in some animals, such as  nematodes . [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4797", "text": "In humans, the perforation of the mouth and anus happen at four weeks and eight weeks respectively. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4798", "text": "Xenacoelomorpha"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4799", "text": "Protostomia"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4800", "text": "Deuterostomia"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4801", "text": "Bilaterians likely evolved from an ancestor that was radially symmetrical. There have been suggestions that the blastopore started out as the digestive surface on a radial organism that became elongated (and thus bilaterally symmetrical) before its sides closed over to leave a mouth at the front and an anus at the rear. [ 1 ]  This matches with the \"flaps-folding-over\" model of gut formation, but an alternative view is that the original blastopore migrated forwards to one end of the ancestral organism before deepening to become a blind gut. [ 1 ]  This is consistent with living  Xenacoelomorpha , which are the sister taxon to protostomes and deuterostomes. [ 6 ] [ 7 ]  The story is a little more complex, because the blastopore itself does not directly give rise to the mouth of these worms. [ 1 ]  This suggests that the  last common ancestor of bilaterians  had a similar gut configuration, and that the anus evolved after the mouth. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4802", "text": "Exactly how a through gut formed from this blind gut is somewhat harder to tell. The genetic mechanisms responsible for anus formation are quite variable, which might suggest that the anus evolved several times in different groups. Scientists are currently looking into this matter to generate a more complete picture. [ 1 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4803", "text": "In humans (a deuterostome), the development proceeds differently. The  buccopharyngeal membrane  is created in the  foregut  and is perforated during the fourth week of human development, creating the primitive mouth, whereas the  cloacal membrane  is created in the  hindgut  and is perforated during the eighth week of human development, creating the primitive anus after the mouth opening has already been created. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4804", "text": "Enteral respiration , also referred to as  cloacal respiration  or  intestinal respiration , [ 1 ]  is a form of  respiration  in which  gas exchange  occurs across the  epithelia  of the  enteral system , usually in the caudal cavity ( cloaca ). This is used in various species as an alternative respiration mechanism in hypoxic environments as a means to supplement  blood oxygen ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4805", "text": "Some  turtles , especially those specialized in diving, are highly reliant on  cloacal   respiration  during dives. [ 2 ]  They accomplish this by having a pair of accessory air bladders connected to the cloaca which can absorb oxygen from the water. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4806", "text": "Various  fish , as well as  polychaete  worms and even  crabs , are specialized to take advantage of the constant flow of water through the cloacal respiratory tree of  sea cucumbers  while simultaneously gaining the protection of living within the sea cucumber itself. At night, many of these species emerge from the anus of the sea cucumber in search of food. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4807", "text": "The  pond loach  is able to respond to the periodic drying in their native habitats by burrowing into the mud and exchanging gas through the posterior end of their alimentary canal. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4808", "text": "Studies have shown that mammals are capable of performing intestinal respiration to a limited degree in a laboratory setting. [ 1 ]  Mice were subjected to hypoxic conditions and supplied oxygen through their intestines survived an average of 18 minutes compared to 11 minutes in the control group. In 2024  Ig Nobel Prize  an award in physiology has been given to a study proving that pigs are capable of this as well. [ 7 ]  When the intestinal lining was abraded before oxygen was introduced, most of the animals survived for at least 50 minutes. Investigations are planned regarding the effectiveness of the strategy, the safety of this application of  perfluorocarbons , and the feasibility of application to humans. [ 8 ]  It has potential application to people with a  respiratory disease  or lung damage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4809", "text": "Enterochromaffin-like cells  or  ECL cells  are a type of  neuroendocrine cell  found in the gastric glands of the  gastric mucosa  beneath the  epithelium , in particular in the vicinity of  parietal cells , that aid in the production of  gastric acid  via the release of  histamine . They are also considered a type of  enteroendocrine cell . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4810", "text": "ECL cells synthesize and secrete  histamine .  These cells are stimulated by the hormones  gastrin  (not depicted in the adjacent diagram) and  pituitary adenylyl cyclase-activating peptide .  G cells are stimulated by  vagal  stimulation through the neurotransmitter  gastrin-releasing peptide ; this causes the G cells to secrete gastrin, which in turn stimulates ECL cells to release histamine.  Note that this circuit is not activated by acetylcholine (ACh), which is of particular importance because the administration of  atropine  will not block the vagal stimulation of the G cells, as ACh is not the neurotransmitter for these cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4811", "text": "However, ECL cells are activated directly by ACh on M1 receptors from direct vagal innervation leading to histamine release. This pathway will be inhibited by atropine. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4812", "text": "Gastrin is transferred from a specific type of  G cell  in the gastric epithelium to the ECL cells by  blood . Histamine and gastrin act synergistically as the most important stimulators of  hydrochloric acid  secretion from parietal cells and stimulators of secretion of pepsinogen from  chief cells .  The most important inhibitor of the ECL cell is somatostatin from oxyntic  D cells ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4813", "text": "Enterochromaffin-like cells also produce  pancreastatin  and probably other  peptide hormones  and  growth factors ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4814", "text": "A prolonged stimulation of these cells causes their  hyperplasia . This is especially important in  gastrinoma  (the  tumors  in which there is an excessive secretion of gastrin), as this is one of the factors contributing to  Zollinger\u2013Ellison's syndrome . It was once believed that tumors of ECL origin form after a prolonged inhibition of gastric acid secretion, however there is no data to support this conclusion and proton pump inhibitors are not thought to contribute to gastric cancer. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4815", "text": "The name is derived from their location in the enteric system and their  chromaffin -like staining pattern in  histologic sections , which is characterized by  silver staining ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4816", "text": "Enterocytes , or  intestinal absorptive cells , are  simple columnar   epithelial cells  which line the inner surface of the  small  and  large intestines . A  glycocalyx  surface coat contains  digestive enzymes .  Microvilli  on the apical surface increase its surface area. This facilitates transport of numerous small molecules into the enterocyte from the intestinal  lumen . These include broken down  proteins ,  fats , and  sugars , as well as water,  electrolytes ,  vitamins , and  bile salts . Enterocytes also have an  endocrine  role, secreting hormones such as  leptin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4817", "text": "The major functions of enterocytes include: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4818", "text": "Intestinal stem cell  aging has been studied in  Drosophila  as a model for understanding the biology of stem cell/niche aging. [ 4 ]   Using knockdown mutants defective in various genes that function in the  DNA damage  response in enterocytes, it was shown that deficiency in the DNA damage response accelerates intestinal stem cell aging, thus providing a better understanding of the molecular mechanisms of this aging process. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4819", "text": "An  enterogastrone  is any  hormone  secreted by the  mucosa  of the  duodenum  in the lower  gastrointestinal tract  in response to dietary  lipids  that inhibits the caudal (or \"forward, analward\") motion of the contents of  chyme . The function of enterogastrone is almost the same as gastric inhibitor peptide, it inhibits gastric secretion and motility of the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4820", "text": "Examples include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4821", "text": "Enterohepatic circulation  is the circulation of  biliary acids ,  bilirubin , drugs or other substances from the  liver  to the  bile , followed by entry into the  small intestine , absorption by the  enterocyte  and transport back to the liver. Enterohepatic circulation is an especially important concept in the field of  toxicology  as many  lipophilic   xenobiotics  undergo this process causing repeated liver damage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4822", "text": "Hepatocytes   metabolize   cholesterol  to  cholic acid  and  chenodeoxycholic acid . These  lipid - soluble   bile acids  are conjugated (reversibly attached) mainly to  glycine  or  taurine  molecules to form  water   soluble  primary conjugated bile acids, sometimes called \"bile salts\".  These bile acids travel to the gall bladder during the interdigestive phase for storage and to the descending part of the  duodenum  via the  common bile duct  through the major duodenal\npapilla during digestion.  95% of the bile acids which are delivered to the duodenum will be recycled by the enterohepatic circulation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4823", "text": "Due to the pH of the small intestine, most of the bile acids are ionized and mostly occur as their sodium salts which are then called \u201cprimary conjugated bile salts.\u201d  In the lower small intestine and  colon , bacteria dehydroxylate some of the primary bile salts to form secondary conjugated bile salts (which are still water-soluble). Along the proximal and distal  ileum , these conjugated primary bile salts are reabsorbed actively into hepatic portal circulation. Bacteria deconjugate some of the primary and secondary conjugated bile salts back to lipid-soluble bile acids, which are passively absorbed into hepatic portal circulation. Finally, the conjugated bile acids which remained un-ionized conjugated bile acids are passively absorbed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4824", "text": "Venous blood from the ileum goes straight into the portal vein and then into the  liver sinusoids .  There, hepatocytes extract bile acids very efficiently, and little escapes the healthy liver into systemic circulation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4825", "text": "The net effect of enterohepatic recirculation is that each bile salt molecule is reused about 20 times, often multiple times during a single digestive phase."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4826", "text": "The presence of biliary acids in the intestines helps in  absorption  of fats and other substances. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4827", "text": "Bilirubin  is conjugated with  glucuronic acid  in the liver by the enzyme  glucuronyltransferase , making it soluble in water. Much of it goes into the bile and thus out into the small intestine. Although 20% of the secreted bilirubinoid bile is reabsorbed by the small intestine, [ 2 ]  conjugated bilirubin is not reabsorbed in small intestine. All conjugated bilirubin in the large intestine is metabolised by colonic bacteria to  urobilinogen , which is then further oxidized to  urobilin  and  stercobilin . Urobilin, stercobilin and their degradation products give feces its brown color.   [ 3 ]   However, just like bile, some of the urobilinogen  reabsorbed is resecreted in the bile which is also part of enterohepatic circulation. The rest of the reabsorbed urobilinogen is excreted in the urine where it is converted to an oxidized form,  urobilin , which gives urine its characteristic yellow color."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4828", "text": "Chloramphenicol ,  aspirin ,  paracetamol ,  diazepam ,  lorazepam ,  morphine ,  metronidazole . Not only drugs but also endogenous substrates like bilirubin,  steroidal hormones  and  thyroxine  utilize this pathway."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4829", "text": "Enterohepatic circulation of drugs describes the process by which drugs are conjugated to glucuronic acid in the liver, excreted into bile, metabolized back into the free drug by intestinal bacteria, and the drug is then reabsorbed into plasma. For many drugs that undergo this process, lower doses of drugs can be therapeutically effective because elimination is reduced by the 'recycling' of the drug. But for a small number of drugs that are very toxic to the intestine (e.g.  irinotecan ), these molecules which would not otherwise be very toxic can become so because of this process, and therefore inhibition of this step can be protective. For the majority of drugs which undergo enterohepatic circulation that are not toxic to the intestine, inhibition of this process leads to a reduction of the levels of drug and reduced therapeutic effect. For example, antibiotics that kill gut bacteria often reduce enterohepatic drug circulation and this requires a temporary increase of the drug's dose until the antibiotic use is discontinued and the gut repopulates with bacteria. This effect of antibiotics on enterohepatic circulation of other drugs is one of several types of drug interactions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4830", "text": "Pharmacokinetic  models of the enterohepatic circulation process has been summarized in a recent article. [ 4 ] [ further explanation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4831", "text": "Enterostatin  is a  pentapeptide [ 1 ]  derived from a  proenzyme  in the  gastrointestinal tract  called  procolipase . It reduces food intake, in particular fat intake, [ 2 ]  when given peripherally or into the brain. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4832", "text": "Enterostatin has the sequence Val-Pro-Asp-Pro-Arg in most mammals, but Val-Pro-Gly-Pro-Arg or Val-Pro-Asp-Pro-Arg in rodents and Ala-Pro-Gly-Pro-Arg in humans. [ 4 ]  The sequence that it necessary for its anorexic effects is X-pro-Y-pro-arg and conserved among several vertebrate species. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4833", "text": "Enterostatin has been detected in gut endocrine cells. [ 7 ]  It is created in the intestine by pancreatic procolipase, the other colipase serving as an obligatory cofactor for  pancreatic lipase  during fat digestion. Enterostatin can be created in the gastric mucosa and the mucosal epithelia in the small intestine. A high fat diet will cause the procolipase gene transcription and enterostatin to release into the gastrointestinal lumen. Enterostatin appears in the lymph and circulation after a meal. Enterostatin has been shown to selectively reduce fat intake during a normal meal. The testing has been successful with different species. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4834", "text": "The signaling pathway of the peripheral mechanism uses afferent vagal to hypothalamic centers. The central responses are mediated through a pathway including serotonergic and opioidergic components. [ 9 ]  Enterostatin cuts fat intake, bodyweight, and body fat. This reaction may involve multiple metabolic effects of enterostatin, which include a decrease of insulin secretion, [ 10 ]  a growth in sympathetic drive to brown adipose tissue, and the stimulation of adrenal corticosteroid secretion. It has been demonstrated that enterostatin stimulates neurons in the amygdala, the arcuate nucleus, the lateral and the ventromedial hypothalamus that have anatomic and functional projections to the paraventricular nucleus (PVN) of the hypothalamus. [ 11 ]  Additionally, enterostatin regulates the expression of  Agouti-related peptide  (AgRP) in a complex manner. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4835", "text": "A possible pathophysiological role is indicated by studies that have associated low enterostatin output and/or responsiveness to breeds of rat that become obese and prefer dietary fat. Humans with obesity also exhibit a lower secretion from pancreatic procolipase after a test meal, compared with persons of normal weight. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4836", "text": "Its effects include a reduction of  insulin  secretion, an increase in sympathetic drive to  brown adipose tissue , and the stimulation of adrenal  corticosteroid  secretion. At the end level, it initiates a sensation of fullness of  stomach  which could be the reason for its role in regulation of fat intake and reduction of  body weight . For enterostatin to be utilized it needs the presence of CCK A receptors. Studies based on rats who lack these receptors have found them to be un-responsive to enterostatin. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4837", "text": "When rats have been injected with high doses of enterostatin into the brain the rats ate progressively less food as the dose was increased. [ 14 ] :\u200a969\u200a \nIn rats, examination of experiments involving the effects of peripheral or intracerebroventricular administration of enterostatin show this selectively slows down fat consumption. [ 15 ] :\u200a8"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4838", "text": "Although enterostatin-like immunoreactivities exist in blood, brain, and gut, and exogenous enterostatins decrease fat appetite and insulin secretion in rats, the roles of these peptides in human obesity remain to be examined. [ 16 ]  It has been hypothesized that resistance to enterostatin impairs its effects in obesity. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4839", "text": "In  biochemistry ,  enzymatic hydrolysis  is a process in which  enzymes  facilitate the  cleavage of bonds  in  molecules  with the addition of the elements of  water  (i.e.  hydrolysis ). It plays an important role in the  digestion  of food. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4840", "text": "It may be used to help provide  renewable energy , as with  cellulosic ethanol . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4841", "text": "This  molecular  or  cell biology  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4842", "text": "This  enzyme -related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4843", "text": "The  epiglottis  ( pl. :  epiglottises  or  epiglottides ) is a leaf-shaped flap in the  throat  that prevents food and water from entering the trachea and the lungs. It stays open during breathing, allowing air into the larynx. During  swallowing , it closes to prevent  aspiration  of food into the lungs, forcing the swallowed liquids or food to go along the  esophagus  toward the stomach instead. It is thus the valve that diverts passage to either the  trachea  or the esophagus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4844", "text": "The epiglottis is made of  elastic cartilage  covered with a  mucous membrane , attached to the entrance of the  larynx . It projects upwards and backwards behind the  tongue  and the  hyoid bone ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4845", "text": "The epiglottis may be inflamed in a condition called  epiglottitis , which is most commonly due to the vaccine-preventable bacterium  Haemophilus influenzae . Dysfunction may cause the inhalation of food, called aspiration, which may lead to  pneumonia  or  airway obstruction . The epiglottis is also an important landmark for  intubation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4846", "text": "The epiglottis has been identified as early as Aristotle, and gets its name from being above the  glottis  ( epi-  +  glottis )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4847", "text": "The epiglottis sits at the entrance of the  larynx . It is shaped like a leaf of  purslane  and has a free upper part that rests behind the tongue, and a lower stalk ( Latin :  petiolus ). [ 2 ]  The stalk originates from the back surface of the  thyroid cartilage , connected by a  thyroepiglottic ligament . At the sides, the stalk is connected to the  arytenoid cartilages  at the walls of the larynx by  folds . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4848", "text": "The epiglottis originates at the entrance of the  larynx , and is attached to the hyoid bone. From there, it projects upwards and backwards behind the  tongue . [ 3 ]  The space between the epiglottis and the tongue is called the  vallecula . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4849", "text": "The epiglottis has two surfaces; a forward-facing  anterior  surface, and a  posterior  surface facing the larynx. [ 2 ]  The forward-facing surface is covered with several layers of thin cells ( stratified squamous epithelium ), and is  not covered with keratin , the same surface as the back of the tongue. [ 2 ]  The back surface is covered in a layer of  column-shaped cells  with  cilia , similar to the rest of the  respiratory tract . It also has  mucus -secreting  goblet cells . [ 2 ]  There is an intermediate zone between these surfaces that contains cells that transition in shape. [ 4 ]  The body of the epiglottis consists of  elastic cartilage . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4850", "text": "The epiglottis arises from the fourth  pharyngeal arch . It can be seen as a distinct structure later than the other cartilage of the pharynx, visible around the fifth month of development. [ 1 ]  The position of the epiglottis also changes with ageing. In infants, it touches the  soft palate , whereas in adults, its position is lower. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4851", "text": "A high-rising epiglottis is a normal anatomical variation, visible during an examination of the mouth. It does not cause any serious problem apart from maybe a mild sensation of a foreign body in the throat. It is seen more often in children than adults and does not need any medical or surgical intervention. [ 5 ]  The front surface of the epiglottis is occasionally notched. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4852", "text": "The epiglottis is normally pointed upward during  breathing  with its underside functioning as part of the  pharynx . [ 2 ]  There are  taste buds  on the epiglottis. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4853", "text": "During  swallowing , the epiglottis bends backwards, folding over the entrance to the trachea, and preventing food from going into it. [ 2 ]  The folding backwards is a complex movement the causes of which are not completely understood. [ 2 ]  It is likely that during swallowing the  hyoid bone  and the  larynx  move upwards and forwards, which increases passive pressure from the back of the tongue; the  aryepiglottic muscles  contract; the passive weight of the food pushes down; and the laryngeal and thyroarytenoid muscles contract. [ 2 ]  The consequence of this is that during swallowing the bent epiglottis blocks off the  trachea , preventing food from going into it; food instead travels down the  esophagus , which is behind it. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4854", "text": "In many languages, the epiglottis is not essential for producing sounds. [ 2 ]  In some languages, the epiglottis is used to produce  epiglottal consonant  speech sounds, though this sound-type is rather rare. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4855", "text": "Inflammation of the epiglottis is known as epiglottitis. Epiglottitis is mainly caused by  Haemophilus influenzae . A person with epiglottitis may have a fever, sore throat, difficulty swallowing, and difficulty breathing. For this reason, acute epiglottitis is considered a  medical emergency , because of the risk of obstruction of the pharynx. Epiglottitis is often managed with  antibiotics , inhaled aerosolised  epinephrine  to act as a  bronchodilator , and may require  tracheal intubation  or a  tracheostomy  if breathing is difficult. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4856", "text": "The incidence of epiglottitis has decreased significantly in countries where  vaccination  against  Haemophilus influenzae  is administered. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4857", "text": "When food or other objects travel down the respiratory tract rather than down the esophagus to the stomach, this is called  aspiration . This can lead to  the obstruction of airways ,  inflammation of lung tissue , and  aspiration pneumonia ; and in the long term,  atelectasis  and  bronchiectasis . [ 3 ]  One reason aspiration can occur is because of failure of the epiglottis to close completely. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4858", "text": "If food or liquid enters the airway due to the epiglottis failing to close properly, throat-clearing or a cough reflex may occur to protect the respiratory system and expel material from the airway. [ 3 ] [ 11 ]  Where there is impairment in laryngeal vestibule sensation, silent aspiration (entry of material to the airway that does not result in a cough reflex) may occur. [ 3 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4859", "text": "The epiglottis and vallecula are important anatomical landmarks in intubation. [ 13 ]  Abnormal positioning of the epiglottis is a rare cause of  obstructive sleep apnoea . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4860", "text": "The epiglottis is present in  mammals , [ 15 ]  including land mammals and  cetaceans , [ 16 ]  also as a cartilaginous structure. [ 17 ]  Like in humans, it functions to prevent entry of food into the trachea during swallowing. [ 17 ]  The position of the larynx is flat in mice and other rodents, as well as rabbits. [ 4 ]  For this reason, because the epiglottis is located behind the soft palate in rabbits, they are obligate nose breathers, [ 18 ] [ 19 ]  as are mice and other rodents. [ 4 ]  In rodents and mice, there is a unique pouch in front of the epiglottis, and the epiglottis is commonly injured by inhaled substances, particularly at the transition zone between the flattened and cuboidal epithelium. [ 20 ] [ 4 ]  It is also common to see taste buds on the epiglottis in these species. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4861", "text": "The epiglottis was noted by  Aristotle , [ 15 ]  although the epiglottis' function was first defined by  Vesalius  in 1543. [ 21 ]  The word has Greek roots. [ 22 ]  The epiglottis gets its name from being above ( Ancient Greek :  \u1f10\u03c0\u03af ,  romanized :\u00a0 epi- ) the  glottis  ( Ancient Greek :  \u03b3\u03bb\u03c9\u03c4\u03c4\u03af\u03c2 ,  romanized :\u00a0 glottis ,  lit. \u2009 'tongue'). [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4862", "text": "The  esophageal glands  are glands that are part of the digestive system of various animals, including humans."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4863", "text": "In humans the glands are known as the  esophageal submucosal glands  and are a part of the  human digestive system . [ 1 ]  They are a small compound  racemose   exocrine glands  of the  mucous  type. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4864", "text": "There are two types:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4865", "text": "Each opens upon the surface by a long excretory  duct . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4866", "text": "The esophageal gland is enlarged in large  monoplacophoran  species. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4867", "text": "The esophageal gland or  oesophageal pouch  is a part of the  digestive system of some gastropods . The esophageal gland or pouch is a common feature in so-called basal gastropod clades, including  Patelloidea ,  Vetigastropoda ,  Cocculiniformia ,  Neritimorpha  and  Neomphalina . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4868", "text": "The size of the esophageal gland of the  scaly-foot gastropod   Chrysomallon squamiferum  (family  Peltospiridae  within Neomphalina) is about two orders of magnitude over the usual size. [ 4 ]  The scaly-foot gastropod houses endosymbiotic bacteria in the esophageal gland. [ 4 ]   Chrysomallon squamiferum  was thought to be the only species of Peltospiridae, that has an enlarged esophageal gland, but later it was shown that both species  Gigantopelta  the gland also enlarged. [ 5 ]  In other peltospirids, the posterior portion of the oesophagus forms a pair of blind mid-oesophageal pouches or gutters extending only to the anterior end of the foot ( Rhynchopelta ,  Peltospira ,  Nodopelta ,  Echinopelta ,  Pachydermia ). [ 4 ]  The same situation is in  Melanodrymia  within the family  Melanodrymiidae . [ 4 ]   Bathyphytophilidae  and  Lepetellidae  are also known to have enlarged esophageal pouches, however, though not to the extent of  Chrysomallon . [ 4 ]  Both are known to house endosymbiotic bacteria, in the case of bathyphytophilids most likely also in the esophageal glands but in the lepetellids the endosymbionts are spread in the  hemocoel . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4869", "text": "This article incorporates text in the  public domain  from  page 1146  of\u00a0the 20th edition of   Gray's Anatomy   (1918) . \nThis article incorporates Creative Commons (CC-BY-4.0) text from the reference [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4870", "text": "Esophageal spasm  is a disorder of  motility  of the  esophagus . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4871", "text": "There are two types of esophageal spasm: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4872", "text": "Both conditions are linked to  gastroesophageal reflux disease  (GERD). [ 2 ]  DES and nutcracker esophagus present similarly and can may require  esophageal manometry  for differentiation. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4873", "text": "When the coordinated  muscle contraction  are irregular or uncoordinated, this condition may be called diffuse esophageal spasm. These spasms can prevent food from reaching the stomach where food gets stuck in the esophagus. At other times the coordinated muscle contraction is very powerful, which is called nutcracker esophagus. These contractions move food through the esophagus but can cause severe pain. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4874", "text": "The symptoms may include  trouble swallowing ,  regurgitation ,  chest pain , [ 5 ]   heartburn , [ 6 ]   globus pharyngis  (which is a feeling that something is stuck in the  throat ) or a dry  cough . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4875", "text": "It is not clear what causes esophageal spasms. [ 1 ] [ 7 ]  Sometimes esophageal spasms start when someone eats hot or cold foods or drinks. However, they can also occur without eating or drinking. [ 7 ]  The increased release of  acetylcholine  may also be a factor, but the triggering event is not known. [ 6 ]  Spasms may also be the result of a food intolerance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4876", "text": "The diagnosis is generally confirmed by  esophageal manometry . [ 2 ]  DES is present when more than a fifth of swallows results in distal esophageal contractions. [ 2 ]  NE is present if the average strength of the contractions of the distal esophagus is greater than 180 mmHg but the contraction of the esophagus is otherwise normal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4877", "text": "Often, symptoms that may suggest esophageal spasm are the result of another condition such as food intolerance,  gastroesophageal reflux disease  (GERD) or  achalasia . [ 4 ]  The symptoms can commonly be mistaken as heart palpitations."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4878", "text": "Since esophageal spasms are often associated with other disorders, management in these cases involve attempts to correct the underlying problem. Medications may include use of  calcium channel blockers  (CCBs) and nitrates.  Tricyclic antidepressants  (TCA) and  sildenafil  can be used as alternative treatment options. If caused by food allergy, an elimination diet may be necessary."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4879", "text": "There have been reports of treatment of distal esophageal spasm in 8 patients using low amounts of  peppermint oil  (five drops of peppermint oil in 10ml of water), [ 8 ]  and a report of treatment of an elderly patient with the same diagnosis. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4880", "text": "If medical therapy fails either  botulinum toxin  injection or surgical  myotomy  may be tried in distal esophageal spasms. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4881", "text": "Distal esophageal spasm is rare. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4882", "text": "The  esophagus  ( American English ),  oesophagus  ( British English ), or \u0153sophagus ( archaic spelling ) ( see spelling difference ) all  / i\u02d0 \u02c8 s \u0252 f \u0259 \u0261 \u0259 s ,   \u026a -/ ; [ 1 ]   pl. :  ((o)e)(\u0153)sophagi  or ( (o)e)(\u0153)sophaguses ), colloquially known also as the  food pipe ,  food tube , or  gullet , is an  organ  in  vertebrates  through which  food  passes, aided by  peristaltic contractions , from the  pharynx  to the  stomach . The esophagus is a  fibromuscular  tube, about 25\u00a0cm (10\u00a0in) long in adults, that travels behind the  trachea  and  heart , passes through the  diaphragm , and empties into the uppermost region of the  stomach . During swallowing, the  epiglottis  tilts backwards to prevent food from going down the  larynx  and lungs. The word  oesophagus  is from Ancient Greek \u03bf\u1f30\u03c3\u03bf\u03c6\u03ac\u03b3\u03bf\u03c2 (oisoph\u00e1gos), from \u03bf\u1f34\u03c3\u03c9 (o\u00eds\u014d), future form of \u03c6\u03ad\u03c1\u03c9 (ph\u00e9r\u014d, \"I carry\") + \u1f14\u03c6\u03b1\u03b3\u03bf\u03bd (\u00e9phagon, \"I ate\")."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4883", "text": "The wall of the esophagus from the  lumen  outwards consists of  mucosa ,  submucosa  (connective tissue),  layers of muscle fibers  between layers of  fibrous tissue , and an outer layer of connective tissue. The mucosa is a  stratified squamous epithelium  of around three layers of squamous cells, which contrasts to the  single layer of columnar cells  of the stomach. The transition between these two types of epithelium is visible as a zig-zag line. Most of the muscle is  smooth muscle  although  striated muscle  predominates in its upper third. It has two muscular rings or  sphincters  in its wall, one at the top and one at the bottom. The lower sphincter helps to prevent reflux of acidic stomach content. The esophagus has a rich blood supply and venous drainage. Its smooth muscle is innervated by involuntary nerves ( sympathetic nerves  via the  sympathetic trunk  and  parasympathetic nerves  via the  vagus nerve ) and in addition voluntary nerves ( lower motor neurons ) which are carried in the vagus nerve to innervate its striated muscle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4884", "text": "The esophagus passes through the thoracic cavity into the  diaphragm  into the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4885", "text": "The esophagus may be affected by  gastric reflux ,  cancer , prominent dilated blood vessels called  varices  that can bleed heavily,  tears , constrictions, and disorders of motility. Diseases may cause difficulty swallowing ( dysphagia ), painful swallowing ( odynophagia ),  chest pain , or cause no symptoms at all. Clinical investigations include  X-rays  when swallowing  barium sulfate ,  endoscopy , and  CT scans . Surgically, \nthe esophagus is difficult to access in part due to its position between critical organs and directly between the sternum and spinal column. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4886", "text": "The esophagus is one of the upper parts of the  digestive system . There are  taste buds  on its upper part. [ 3 ]  It begins at the back of the mouth, passing downward through the rear part of the  mediastinum , through the  diaphragm , and into the stomach. In humans, the esophagus generally starts around the level of the sixth  cervical vertebra  behind the  cricoid cartilage  of the  trachea , enters the diaphragm at about the level of the  tenth thoracic vertebra , and ends at the  cardia  of the stomach, at the level of the  eleventh thoracic vertebra . [ 4 ]  The esophagus is usually about 25\u00a0cm (10\u00a0in) in length. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4887", "text": "Many  blood vessels  serve the esophagus, with blood supply varying along its course. The upper parts of the esophagus and the upper esophageal sphincter receive blood from the  inferior thyroid artery , the parts of the esophagus in the thorax from the  bronchial arteries  and branches directly from the  thoracic aorta , and the lower parts of the esophagus and the lower esophageal sphincter receive blood from the  left gastric artery  and the left  inferior phrenic artery . [ 6 ] [ 7 ]  The venous drainage also differs along the course of the esophagus. The upper and middle parts of the esophagus drain into the  azygos  and  hemiazygos veins , and blood from the lower part drains into the  left gastric vein . All these veins drain into the  superior vena cava , with the exception of the left gastric vein, which is a branch of the  portal vein . [ 6 ]  Lymphatically, the upper third of the esophagus drains into the  deep cervical lymph nodes , the middle into the superior and posterior mediastinal lymph nodes, and the lower esophagus into the  gastric  and  celiac lymph nodes . This is similar to the lymphatic drainage of the abdominal structures that arise from the  foregut , which all drain into the celiac nodes. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4888", "text": "The upper esophagus lies at the back of the mediastinum behind the  trachea , adjoining along the  tracheoesophageal stripe , and in front of the  erector spinae muscles  and the  vertebral column . The lower esophagus lies behind the  heart  and curves in front of the  thoracic aorta . From the  bifurcation of the trachea  downwards, the esophagus passes behind the right  pulmonary artery ,  left main bronchus , and  left atrium . At this point, it passes through the diaphragm. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4889", "text": "The  thoracic duct , which drains the majority of the body's  lymph , passes behind the esophagus, curving from lying behind the esophagus on the right in the lower part of the esophagus, to lying behind the esophagus on the left in the upper esophagus. The esophagus also lies in front of parts of the  hemiazygos veins  and the  intercostal veins  on the right side. The  vagus nerve  divides and covers the esophagus in a  plexus . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4890", "text": "The esophagus has four points of constriction. When a corrosive substance, or a solid object is swallowed, it is most likely to lodge and damage one of these four points. These constrictions arise from particular structures that compress the esophagus. These constrictions are: [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4891", "text": "The esophagus is surrounded at the top and bottom by two muscular rings, known respectively as the upper esophageal sphincter and the lower esophageal sphincter. [ 4 ]  These  sphincters  act to close the esophagus when food is not being swallowed. The upper esophageal sphincter is an anatomical sphincter, which is formed by the lower portion of the inferior pharyngeal constrictor, also known as the cricopharyngeal sphincter due to its relation with  cricoid cartilage  of the  larynx  anteriorly. However, the lower esophageal sphincter is not an anatomical but rather a functional sphincter, meaning that it acts as a sphincter but does not have a distinct thickening like other sphincters."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4892", "text": "The upper esophageal sphincter surrounds the upper part of the esophagus. It consists of  skeletal muscle  but is not under  voluntary control . Opening of the upper esophageal sphincter is triggered by the  swallowing reflex . The primary muscle of the upper esophageal sphincter is the  cricopharyngeal part  of the  inferior pharyngeal constrictor . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4893", "text": "The lower esophageal sphincter, or gastroesophageal sphincter, surrounds the lower part of the esophagus at the junction between the esophagus and the stomach. [ 10 ]  It is also called the cardiac sphincter or cardioesophageal sphincter, named from the adjacent part of the stomach, the  cardia . Dysfunction of the gastroesophageal sphincter causes gastroesophageal  reflux , which causes  heartburn , and, if it happens often enough, can lead to  gastroesophageal reflux disease , with damage of the esophageal mucosa. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4894", "text": "The esophagus is innervated by the vagus nerve and the cervical and thoracic  sympathetic trunk . [ 6 ]  The vagus nerve has a  parasympathetic  function, supplying the muscles of the esophagus and stimulating glandular contraction. Two sets of nerve fibers travel in the vagus nerve to supply the muscles. The upper striated muscle, and upper esophageal sphincter, are supplied by neurons with bodies in the  nucleus ambiguus , whereas fibers that supply the smooth muscle and lower esophageal sphincter have bodies situated in the  dorsal motor nucleus . [ 6 ]  The vagus nerve plays the primary role in initiating  peristalsis . [ 12 ]  The sympathetic trunk has a  sympathetic  function. It may enhance the function of the vagus nerve, increasing peristalsis and glandular activity, and causing sphincter contraction. In addition, sympathetic activation may relax the muscle wall and cause blood vessel constriction. [ 6 ]  Sensation along the esophagus is supplied by both nerves, with gross sensation being passed in the vagus nerve and pain passed up the sympathetic trunk. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4895", "text": "The gastroesophageal junction (also known as the esophagogastric junction) is the junction between the esophagus and the stomach, at the lower end of the esophagus. [ 13 ]  The pink color of the esophageal mucosa contrasts to the deeper red of the gastric mucosa, [ 6 ] [ 14 ]  and the mucosal transition can be seen as an irregular zig-zag line, which is often called the z-line. [ 15 ]  Histological examination reveals abrupt transition between the  stratified squamous epithelium  of the esophagus and the  simple columnar epithelium  of the  stomach . [ 16 ]  Normally, the  cardia  of the stomach is immediately distal to the z-line [ 17 ]  and the z-line coincides with the upper limit of the gastric folds of the cardia; however, when the anatomy of the mucosa is distorted in  Barrett's esophagus  the true gastroesophageal junction can be identified by the upper limit of the gastric folds rather than the mucosal transition. [ 18 ]  The functional location of the lower oesophageal sphincter is generally situated about  3\u00a0cm ( 1 + 1 \u2044 4 \u00a0in) below the z-line. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4896", "text": "The human esophagus has a  mucous membrane  consisting of a tough  stratified squamous epithelium  without  keratin , a smooth  lamina propria , and a  muscularis mucosae . [ 6 ]  The epithelium of the esophagus has a relatively rapid turnover and serves a protective function against the abrasive effects of food. In many animals, the epithelium contains a layer of keratin, representing a coarser diet. [ 19 ]  There are two types of glands, with mucus-secreting  esophageal glands  being found in the  submucosa  and esophageal cardiac glands, similar to  cardiac glands  of the stomach, located in the lamina propria and most frequent in the terminal part of the organ. [ 19 ] [ 20 ]  The  mucus  from the glands gives a good protection to the lining. [ 21 ]  The submucosa also contains the  submucosal plexus , a network of  nerve cells  that is part of the  enteric nervous system . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4897", "text": "The  muscular layer  of the esophagus has two types of muscle. The upper third of the esophagus contains  striated muscle , the lower third contains  smooth muscle , and the middle third contains a mixture of both. [ 6 ]  Muscle is arranged in two layers: one in which the muscle fibers run longitudinal to the esophagus, and the other in which the fibers encircle the esophagus. These are separated by the  myenteric plexus , a tangled network of nerve fibers involved in the secretion of mucus and in peristalsis of the smooth muscle of the esophagus. The outermost layer of the esophagus is the  adventitia  in most of its length, with the abdominal part being covered in  serosa . This makes it distinct from many other structures in the gastrointestinal tract that only have a serosa. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4898", "text": "In early  embryogenesis , the esophagus develops from the  endodermal   primitive gut tube . The ventral part of the embryo abuts the  yolk sac . During the second week of embryological development, as the embryo grows, it begins to surround parts of the sac. The enveloped portions form the basis for the adult gastrointestinal tract. [ 22 ]  The sac is surrounded by a network of  vitelline arteries . Over time, these arteries consolidate into the three main arteries that supply the developing gastrointestinal tract: the  celiac artery ,  superior mesenteric artery , and  inferior mesenteric artery . The areas supplied by these arteries are used to define the  midgut ,  hindgut  and  foregut . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4899", "text": "The surrounded sac becomes the primitive gut. Sections of this gut begin to differentiate into the organs of the gastrointestinal tract, such as the esophagus,  stomach , and  intestines . [ 22 ]  The esophagus develops as part of the foregut tube. [ 22 ]  The innervation of the esophagus develops from the  pharyngeal arches . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4900", "text": "Food is  ingested  through the  mouth  and when  swallowed  passes first into the  pharynx  and then into the esophagus. The esophagus is thus one of the first components of the  digestive system  and the  gastrointestinal tract . After food passes through the esophagus, it enters the stomach. [ 10 ]  When food is being swallowed, the  epiglottis  moves backward to cover the  larynx , preventing food from entering the  trachea . At the same time, the upper esophageal sphincter relaxes, allowing a  bolus  of  food  to enter.  Peristaltic  contractions of the esophageal muscle push the food down the esophagus. These rhythmic contractions occur both as a reflex response to food that is in the mouth, and also as a response to the sensation of food within the esophagus itself. Along with peristalsis, the lower esophageal sphincter relaxes. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4901", "text": "The stomach produces  gastric acid , a strongly  acidic  mixture consisting of  hydrochloric acid  (HCl) and  potassium  and  sodium  salts to enable food  digestion . Constriction of the upper and lower esophageal sphincters helps to prevent reflux (backflow) of gastric contents and acid into the esophagus, protecting the esophageal mucosa. The acute  angle of His  and the lower  crura of the diaphragm  also help this sphincteric action. [ 10 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4902", "text": "About 20,000 protein-coding genes are expressed in human cells and nearly 70% of these genes are expressed in the normal esophagus. [ 24 ] [ 25 ]  Some 250 of these genes are more specifically expressed in the esophagus with less than 50 genes being highly specific. The corresponding esophagus-specific proteins are mainly involved in squamous differentiation such as  keratins   KRT13 ,  KRT4  and  KRT6C . Other specific proteins that help lubricate the inner surface of esophagus are  mucins  such as  MUC21  and MUC22. Many genes with elevated expression are also shared with skin and other organs that are composed of  squamous epithelia . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4903", "text": "The main conditions affecting the esophagus are described here. For a more complete list, see  esophageal disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4904", "text": "Inflammation of the esophagus is known as  esophagitis .  Reflux  of  gastric acids  from the stomach, infection, substances ingested (for example,  corrosives ), some  medications  (such as  bisphosphonates ), and  food allergies  can all lead to esophagitis.  Esophageal candidiasis  is an infection of the yeast  Candida albicans  that may occur when a person is  immunocompromised . As of 2021 [update]  the causes of some forms of esophagitis, such as  eosinophilic esophagitis , are not well-characterized, but may include  Th2 -mediated  atopies  or genetic factors. There appear to be correlations between eosinophilic esophagitis,  asthma  (itself with an  eosinophilic  component),  eczema , and  allergic rhinitis , though it is not clear whether these conditions contribute to eosinophilic esophagitis or vice versa, or if they are symptoms of mutual underlying factors. [ 27 ]  Esophagitis can cause  painful swallowing  and is usually treated by managing the cause of the esophagitis - such as managing reflux or treating infection. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4905", "text": "Prolonged esophagitis, particularly from gastric reflux, is one factor thought to play a role in the development of  Barrett's esophagus . In this condition, there is  metaplasia  of the lining of the lower esophagus, which changes from  stratified squamous epithelia  to  simple columnar epithelia . Barrett's esophagus is thought to be one of the main contributors to the development of  esophageal cancer . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4906", "text": "There are two main types of  cancer of the esophagus .  Squamous cell carcinoma  is a  carcinoma  that can occur in the squamous cells lining the esophagus. This type is much more common in  China  and  Iran . The other main type is an  adenocarcinoma  that occurs in the glands or columnar tissue of the esophagus. This is most common in  developed countries  in those with Barrett's esophagus, and occurs in the cuboidal cells. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4907", "text": "In its early stages, esophageal cancer may not have any symptoms at all. When severe, esophageal cancer may eventually cause obstruction of the esophagus, making swallowing of any solid foods very difficult and causing weight loss. The progress of the cancer is  staged using a system  that measures how far into the esophageal wall the cancer has invaded, how many  lymph nodes  are affected, and whether there are any  metastases  in different parts of the body. Esophageal cancer is often managed with radiotherapy, chemotherapy, and may also be managed by  partial surgical removal of the esophagus . Inserting a  stent  into the esophagus, or inserting a  nasogastric tube , may also be used to ensure that a person is able to digest enough food and water. As of 2014 [update] , the prognosis for esophageal cancer is still poor, so  palliative therapy  may also be a focus of treatment. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4908", "text": "Esophageal varices  are swollen twisted branches of the  azygous vein  in the lower third of the esophagus. These blood vessels  anastomose  (join up) with those of the  portal vein  when  portal hypertension  develops. [ 28 ]  These blood vessels are engorged more than normal, and in the worst cases may partially obstruct the esophagus. These blood vessels develop as part of a collateral circulation that occurs to drain blood from the  abdomen  as a result of  portal hypertension , usually as a result of  liver diseases  such as  cirrhosis . [ 5 ] :\u200a941\u201342\u200a  This collateral circulation occurs because the lower part of the esophagus drains into the left gastric vein, which is a branch of the portal vein. Because of the extensive venous plexus that exists between this vein and other veins, if portal hypertension occurs, the direction of blood drainage in this vein may reverse, with blood draining from the portal venous system, through the plexus. Veins in the plexus may engorge and lead to varices. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4909", "text": "Esophageal varices often do not have symptoms until they rupture. A ruptured varix is considered a medical emergency because varices can bleed a lot. A bleeding varix may cause a person  to vomit blood , or suffer  shock . To deal with a ruptured varix, a band may be placed around the bleeding blood vessel, or a small amount of a clotting agent may be injected near the bleed. A surgeon may also try to use a small inflatable balloon to apply pressure to stop the wound.  IV fluids  and  blood products  may be given in order to prevent  hypovolemia  from excess blood loss. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4910", "text": "Several disorders affect the motility of food as it travels down the esophagus. This can cause difficult swallowing, called  dysphagia , or painful swallowing, called  odynophagia .  Achalasia  refers to a failure of the lower esophageal sphincter to relax properly, and generally develops later in life. This leads to progressive enlargement of the esophagus, and possibly eventual  megaesophagus . A  nutcracker esophagus  refers to swallowing that can be extremely painful.  Diffuse esophageal spasm  is a spasm of the esophagus that can be one cause of chest pain. Such  referred pain  to the wall of the upper chest is quite common in esophageal conditions. [ 29 ]  Sclerosis of the esophagus, such as with  systemic sclerosis  or in  CREST syndrome  may cause hardening of the walls of the esophagus and interfere with peristalsis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4911", "text": "Esophageal strictures  are usually benign and typically develop after a person has had  reflux  for many years. Other strictures may include  esophageal webs  (which can also be congenital) and damage to the esophagus by radiotherapy, corrosive ingestion, or eosinophilic esophagitis. A  Schatzki ring  is fibrosis at the gastroesophageal junction. Strictures may also develop in chronic  anemia , and  Plummer-Vinson  syndrome. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4912", "text": "Two of the most common  congenital  malformations affecting the esophagus are an  esophageal atresia  where the esophagus ends in a blind sac instead of connecting to the stomach; and an  esophageal fistula  \u2013 an abnormal connection between the esophagus and the trachea. [ 30 ]  Both of these conditions usually occur together. [ 30 ]  These are found in about 1 in 3500 births. [ 31 ]  Half of these cases may be part of a  syndrome  where other abnormalities are also present, particularly of the  heart  or  limbs . The other cases occur singly. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4913", "text": "An  X-ray  of  swallowed barium  may be used to reveal the size and shape of the esophagus, and the presence of any masses. The esophagus may also be  imaged  using a flexible camera inserted into the esophagus, in a procedure called an  endoscopy . If an endoscopy is used on the stomach, the camera will also have to pass through the esophagus. During an endoscopy, a  biopsy  may be taken. If cancer of the esophagus is being investigated, other methods, including a  CT scan , may also be used. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4914", "text": "The word  esophagus  ( British English :  oesophagus ), comes from the  Greek :  \u03bf\u1f30\u03c3\u03bf\u03c6\u03ac\u03b3\u03bf\u03c2  ( oisophagos ) meaning  gullet . It derives from  two roots   (eosin)  to carry and ( phagos ) to eat. [ 33 ]  The use of the word oesophagus, has been documented in anatomical literature since at least the time of  Hippocrates , who noted that \"the oesophagus\u00a0... receives the greatest amount of what we consume.\" [ 34 ]  Its existence in other animals and its relationship with the  stomach  was documented by the  Roman   naturalist   Pliny the Elder  (AD23\u2013AD79), [ 35 ]  and the  peristaltic  contractions of the esophagus have been documented since at least the time of  Galen . [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4915", "text": "The first attempt at surgery on the esophagus focused in the neck, and was conducted in dogs by  Theodore Billroth  in 1871. In 1877  Czerny  carried out surgery in people. By 1908, an operation had been performed by Voeckler to remove the esophagus, and in 1933 the first surgical removal of parts of the lower esophagus, (to control  esophageal cancer ), had been conducted. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4916", "text": "The  Nissen fundoplication , in which the stomach is wrapped around the lower  esophageal sphincter  to stimulate its function and control  reflux , was first conducted by  Rudolph Nissen  in 1955. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4917", "text": "In  tetrapods , the pharynx is much shorter, and the esophagus correspondingly longer, than in fish. In the majority of vertebrates, the esophagus is simply a connecting tube, but in some  birds , which regurgitate components to feed their young, it is extended towards the lower end to form a  crop  for storing food before it enters the true stomach. [ 39 ] [ 40 ]  In  ruminants , animals with four chambered stomachs, a groove called the  sulcus reticuli  is often found in the esophagus, allowing milk to drain directly into the hind stomach, the  abomasum . [ 41 ]  In the  horse  the esophagus is about 1.2 to 1.5\u00a0m (4 to 5\u00a0ft) in length, and carries food to the stomach. A muscular ring, called the cardiac sphincter, connects the stomach to the esophagus. This sphincter is very well developed in horses. This and the oblique angle at which the esophagus connects to the stomach explains why horses cannot  vomit . [ 42 ]  The esophagus is also the area of the digestive tract where horses may have the condition known as  choke ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4918", "text": "The esophagus of  snakes  is remarkable for the distension it undergoes when swallowing prey. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4919", "text": "In most fish, the esophagus is extremely short, primarily due to the length of the pharynx (which is associated with the  gills ). However, some fish, including  lampreys ,  chimaeras , and  lungfish , have no true stomach, so that the esophagus effectively runs from the pharynx directly to the  intestine , and is therefore somewhat longer. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4920", "text": "In many vertebrates, the esophagus is lined by  stratified squamous epithelium  without glands. In fish, the esophagus is often lined with  columnar epithelium , [ 40 ]  and in  amphibians ,  sharks  and  rays , the esophageal epithelium is  ciliated , helping to wash food along, in addition to the action of muscular peristalsis. [ 39 ]  In addition, in the  bat   Plecotus auritus , fish and some amphibians, glands secreting  pepsinogen  or  hydrochloric acid  have been found. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4921", "text": "The muscle of the esophagus in many mammals is initially striated but then becomes smooth muscle in the caudal third or so. In  canines  and  ruminants , however, it is entirely striated to allow regurgitation to feed young (canines) or regurgitation to chew cud (ruminants). It is entirely smooth muscle in amphibians, reptiles and birds. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4922", "text": "Contrary to popular belief, [ 44 ]  an adult  human body  would not be able to pass through the esophagus of a  whale , which generally measures less than 10\u00a0cm (4\u00a0in) in diameter, although in larger  baleen whales  it may be up to 25\u00a0cm (10\u00a0in) when fully distended. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4923", "text": "A structure with the same name is often found in invertebrates, including  molluscs  and  arthropods , connecting the oral cavity with the stomach. [ 46 ]  In terms of the  digestive system of snails and slugs , the mouth opens into an esophagus, which connects to the stomach. Because of  torsion , which is the rotation of the main body of the animal during larval development, the esophagus usually passes around the stomach, and opens into its back, furthest from the mouth. In species that have undergone de-torsion, however, the esophagus may open into the anterior of the stomach, which is the reverse of the usual gastropod arrangement. [ 47 ]  There is an extensive  rostrum  at the front of the esophagus in all carnivorous snails and slugs. [ 48 ]  In the freshwater snail species  Tarebia granifera , the brood pouch is above the esophagus. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4924", "text": "In the  cephalopods , the brain often surrounds the esophagus. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4925", "text": "Excretion  is elimination of  metabolic waste , which is an essential process in all  organisms . In  vertebrates , this is primarily carried out by the  lungs ,  kidneys , and  skin . [ 1 ]  This is in contrast with  secretion , where the substance may have specific tasks after leaving the  cell . For example,  placental mammals  expel  urine  from the  bladder  through the  urethra , [ 2 ]  which is part of the  excretory system .  Unicellular organisms  discharge waste products directly through the surface of the cell."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4926", "text": "During life activities such as  cellular respiration , several chemical reactions take place in the body. These are known as  metabolism . These chemical reactions produce waste products such as  carbon dioxide , water,  salts ,  urea  and  uric acid . Accumulation of these wastes beyond a level inside the body is harmful to the body. The excretory organs remove these wastes. This process of removal of metabolic waste from the body is known as excretion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4927", "text": "Green  plants  excrete carbon dioxide and water as respiratory products. In green plants, the  carbon dioxide  released during respiration gets used during photosynthesis.  Oxygen  is a byproduct generated during  photosynthesis , and exits through  stomata , root cell walls, and other routes. Plants can get rid of excess water by transpiration and  guttation . It has been shown that the leaf acts as an 'excretophore' and, in addition to being a primary organ of photosynthesis, is also used as a method of excreting toxic wastes via diffusion. Other waste materials that are exuded by some plants\u00a0\u2014  resin , saps,  latex , etc. are forced from the interior of the plant by hydrostatic pressures inside the plant and by absorptive forces of plant cells. These latter processes do not need added energy, they act passively. However, during the pre-abscission phase, the metabolic levels of a leaf are high. [ 3 ] [ 4 ]  Plants also excrete some waste substances into the soil around them. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4928", "text": "In animals, the main excretory products are  carbon dioxide ,  ammonia  (in  ammoniotelics ),  urea  (in  ureotelics ),  uric acid  (in  uricotelics ),  guanine  (in  Arachnida ), and  creatine . The liver and kidneys  clear  many substances from the  blood  (for example, in  renal excretion ), and the cleared substances are then excreted from the body in the  urine  and  feces . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4929", "text": "Aquatic animals  usually excrete  ammonia  directly into the external environment, as this compound has high  solubility  and there is ample water available for dilution. In  terrestrial animals , ammonia-like compounds are converted into other nitrogenous materials, i.e.  urea , that are less harmful as there is less water in the environment and ammonia itself is  toxic . This process is called detoxification. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4930", "text": "Birds  excrete their nitrogenous wastes as  uric acid  in the form of a paste. Although this process is metabolically more expensive, it allows more efficient  water  retention and it can be stored more easily in the  egg . Many avian species, especially  seabirds , can also excrete salt via specialized nasal salt glands, the saline solution leaving through nostrils in the  beak ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4931", "text": "In  insects , a system involving  Malpighian tubules  is used to excrete  metabolic waste . Metabolic waste diffuses or is actively transported into the tubule, which transports the wastes to the intestines. The metabolic waste is then released from the body along with fecal matter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4932", "text": "The excreted material may be called  ejecta . [ 8 ]  In  pathology  the word ejecta is more commonly used. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4933", "text": "Fart  is a word in the  English language  most commonly used in reference to  flatulence  that can be used as a  noun  or a  verb . [ 1 ]  The immediate roots are in the Middle English words  ferten ,  feortan  and  farten , kin of the Old High German word  ferzan .  Cognates are found in  Old Norse , Slavic and also Greek and Sanskrit. The word  fart  has been incorporated into the  colloquial  and  technical speech  of a number of occupations, including computing. It is often considered unsuitable in formal situations as it may be considered vulgar or offensive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4934", "text": "The English word  fart  is one of the oldest words in the English lexicon.  Its  Indo-European  origins are confirmed by the many  cognate  words in some other  Indo-European languages :  It is cognate with  Greek  verb \u03c0\u03ad\u03c1\u03b4\u03bf\u03bc\u03b1\u03b9 (perdomai), [ 2 ]  as well as the  Latin   p\u0113d\u0115re ,  Sanskrit   pardate ,  Ashkun   pidi\u1e45 , [ 3 ]   Avestan   p\u0259r\u0259\u03b4aiti ,  Italian   fare un peto ,  French  \"p\u00e9ter\",  Russian  \u043f\u0435\u0440\u0434\u0435\u0442\u044c (perdet') and  Polish  \" pierd \" <<  PIE  * perd  [break wind loudly] or * pezd  [the same, softly], all of which mean the same thing.  Like most Indo-European roots in the  Germanic languages , it was altered under  Grimm's law , so that Indo-European  /p/  >  /f/ , and  /d/  >  /t/ , as the  German  cognate  furzen  also manifests. [ 4 ] [ 5 ] [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4935", "text": "In certain circles the word is considered merely a common  profanity  with an often  humorous   connotation . For example, a person may be referred to as a 'fart', or an 'old fart', not necessarily depending on the person's age.  This may convey the sense that a person is boring or unduly fussy and be intended as an insult, mainly when used in the second or third person.  For example, '\"he's a boring old fart!\"  However the word may be used as a colloquial term of  endearment  or in an attempt at humorous self-deprecation (e.g., in such phrases as \"I know I'm just an old fart\" or \"you do like to fart about!\").  'Fart' is often only used as a term of endearment when the subject is personally well known to the user."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4936", "text": "In both cases though, it tends to refer to personal habits or traits that the user considers to be a negative feature of the subject, even when it is a self-reference.  For example, when concerned that a person is being overly methodical they might say 'I know I'm being an old fart', potentially to forestall negative thoughts and opinions in others. When used in an attempt to be offensive, the word is still considered vulgar, but it remains a mild example of such an insult. This usage dates back to the Medieval period, where the phrase 'not worth a fart' would be applied to an item held to be worthless. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4937", "text": "The word  fart  in  Middle English  occurs in \" Sumer Is Icumen In \", where one sign of summer is \"bucke uerte\u00fe\" (the  buck  farts). It appears in several of  Geoffrey Chaucer 's  Canterbury Tales . In \" The Miller's Tale \", Absolon has already been tricked into kissing Alison's buttocks when he is expecting to kiss her face. Her boyfriend Nicholas hangs his  buttocks  out of a window, hoping to trick Absolon into kissing his buttocks in turn and then farts in the face of his rival. In \" The Summoner's Tale \", the friars in the story are to receive the smell of a fart through a twelve-spoked wheel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4938", "text": "In the early modern period, the word  fart  was not considered especially vulgar; it even surfaced in literary works. For example,  Samuel Johnson 's  A Dictionary of the English Language , published in 1755, included the word.  Johnson defined it  [ vague ]  with two poems, one by  Jonathan Swift , the other by  Sir John Suckling . [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4939", "text": "Benjamin Franklin prepared  an essay on the topic  for the Royal Academy of Brussels in 1781 urging scientific study. In 1607, a group of  Members of Parliament  had written a ribald poem entitled  The Parliament Fart , as a symbolic protest against the conservatism of the  House of Lords  and the king,  James I . [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4940", "text": "While not one of  George Carlin 's original  seven dirty words , he noted in a later routine that the word  fart  ought to be added to \"the list\" of words that were not acceptable (for broadcast) in any context (which have non-offensive meanings), and described television as (then) a \"fart-free zone\". [ 18 ] [ 19 ]   Thomas Wolfe  had the phrase \"a fizzing and sulphuric fart\" cut out of his 1929 work  Look Homeward, Angel  by his publisher.  Ernest Hemingway , who had the same publisher, accepted the principle that \"fart\" could be cut, on the grounds that  words should not be used purely to shock. [ 20 ]  The  hippie  movement in the 1970s saw a new definition develop, with the use of \"fart\" as a personal noun, to describe a \"detestable person, or someone of small stature or limited mental capacity\", gaining wider and more open usage as a result. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4941", "text": "Rhyming slang  developed the alternative form \"raspberry tart\", later shortened to \"raspberry\", and occasionally abbreviated further to \"razz\".  This was associated with the phrase \" blowing a raspberry \". [ 22 ]  The word has become more prevalent, and now features in children's literature, such as the  Walter the Farting Dog  series of children's books,  Robert Munsch 's  Good Families Don't  and  The Gas We Pass  by Shinta Cho."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4942", "text": "The  fauces ,  isthmus of fauces , or the  oropharyngeal isthmus  is the opening at the back of the  mouth  into the  throat . [ 1 ]  It is a narrow passage between the  velum  and the base of the  tongue . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4943", "text": "The fauces is a part of the  oropharynx  directly behind the  oral cavity  as a subdivision, bounded superiorly by the  soft palate , laterally by the  palatoglossal  and  palatopharyngeal arches , and inferiorly by the  tongue . The arches form the  pillars of the fauces . The anterior pillar is the palatoglossal arch formed of the  palatoglossus muscle . The posterior pillar is the palatopharyngeal arch formed of the  palatopharyngeus muscle . Between these two arches on the lateral walls of the oropharynx is the  tonsillar fossa  which is the location of the  palatine tonsil . [ 3 ]  The arches are also known together as the  palatine arches ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4944", "text": "Each arch runs downwards, laterally and forwards, from the soft palate to the side of the tongue. The approximation of the arches due to the contraction of the palatoglossal muscles constricts the fauces, and is essential to  swallowing ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4945", "text": "Inflammation of the fauces, known as  faucitis , is seen in animals. In cats, faucitis is usually a secondary disease to  gingivitis  but can be a primary disease. In this species faucitis is usually caused by  bacterial  and  viral infections  although  food allergies  need to be excluded in any diagnosis. Treatment is  symptomatic  and includes  broad-spectrum antibiotics  and in severe cases where cats are inappetant,  corticosteroids  (often given as  depot forms , e.g.  depomedrol ) or  chemotherapy  (e.g.  chlorambucil )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4946", "text": "A  fecal plug  (sometimes referred to as a  tappen ) is a significant biological phenomenon observed in  bears  and other animals during  hibernation . It is a dense mass of hardened  feces  that forms in the  colon  due to having remained in the intestine so long that the intestinal walls have absorbed the fluids out of it, leaving it dry and hard. [ 1 ]  An erroneous speculation still repeated in popular literature today is that bears prepare for hibernation by eating indigestible plant material to purge their digestive tracts and form a rectal plug that prevents further eating. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4947", "text": "The fecal plug forms as the bear enters hibernation, a period characterized by a significant decrease in the animal's metabolic rate. During this time, bears do not eat, drink, urinate, or defecate. The plug consists of various materials ingested in the period leading up to hibernation, including undigested food, shed intestinal cells, ingested bedding materials, and even small rocks or soil particles consumed during grooming. A notable component of the plug is bits of dried,  callused  skin from the bear's  footpads , which the bear may chew or lick during the later stages of hibernation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4948", "text": "The primary function of the fecal plug is to prevent defecation during the months of hibernation, aiding in maintaining the bear's energy conservation. It acts as a physical blockage, ensuring that the bear remains in a state of minimal digestive activity. [ citation needed ]  This adaptation is crucial for the bear's survival, as it allows for the conservation of energy and resources in an environment where food is scarce."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4949", "text": "Upon the conclusion of hibernation in spring, the bear expels the fecal plug. This typically occurs near the entrance of the den and signifies the bear's return to its regular physiological functions. The expulsion of the plug is often one of the first activities a bear undertakes after emerging from its den, marking the end of its hibernation period."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4950", "text": "The study of fecal plugs provides valuable insights into bear biology, particularly their hibernation habits and digestive processes. Researchers analyze the composition of the plugs to understand more about bear diet and health before hibernation. This research also contributes to broader ecological studies, as it helps in understanding the role of bears in their natural habitats."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4951", "text": "While the fecal plug is most notably associated with bears, similar phenomena have been observed in other hibernating animals. Understanding these similarities and differences can provide deeper insights into the evolutionary adaptations for hibernation across different species."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4952", "text": "Bears play a significant role in their ecosystems, and the process of hibernation, including the formation and expulsion of fecal plugs, is part of this role. The nutrients and materials contained in expelled plugs can have an impact on the local flora and fauna, contributing to the  nutrient cycle  in bear habitats."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4953", "text": "The fecal plug of bears has also found a place in human culture and history. Indigenous peoples and early naturalists have observed and documented this phenomenon, contributing to our understanding and the mythology surrounding bears and hibernation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4954", "text": "Hibernation"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4955", "text": "Flatulence  is the expulsion of gas from the  intestines  via the anus, commonly referred to as  farting . \"Flatus\" is the medical word for gas generated in the  stomach  or bowels. [ 1 ]  A proportion of intestinal gas may be swallowed environmental air, and hence flatus is not entirely generated in the stomach or bowels. The scientific study of this area of medicine is termed  flatology . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4956", "text": "Flatus is brought to the  rectum  and pressurized by  muscles  in the intestines. It is normal to pass flatus (\"to fart\"), though volume and frequency vary greatly among individuals. It is also normal for intestinal gas to have a  feculent  or unpleasant odor, which may be intense. The noise commonly associated with flatulence is produced by the  anus  and  buttocks , which act together in a manner similar to that of an  embouchure . Both the sound and odor are sources of  embarrassment , annoyance or amusement ( flatulence humor ). In many societies, flatus is a  taboo . Thus, many people either let their flatus out quietly or even hold it completely. [ 3 ] [ 4 ]  However, holding the gases inside is not healthy. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4957", "text": "There are several general symptoms related to intestinal gas: pain,  bloating  and abdominal distension, excessive flatus volume, excessive flatus odor, and gas incontinence. Furthermore,  eructation  (colloquially known as \"burping\") is sometimes included under the topic of flatulence. [ 7 ]  When excessive or malodorous, flatus can be a sign of a health disorder, such as  irritable bowel syndrome ,  celiac disease  or  lactose intolerance . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4958", "text": "Non-medical definitions of the term include \"the uncomfortable condition of having gas in the stomach and bowels\", or \"a state of excessive gas in the alimentary canal\". These definitions highlight that many people consider \"bloating\",  abdominal distension  or increased volume of intestinal gas, to be synonymous with the term flatulence (although this is technically inaccurate)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4959", "text": "Colloquially, flatulence may be referred to as \"farting\", \"pumping\", \"trumping\", [ 9 ]  \"blowing off\", \"pooting\", \"passing gas\", \"breaking wind\", \"backfiring\", \"tooting\", \"beefing\", or simply (in  American English ) \"gas\" or ( British English ) \"wind\". Derived terms include  vaginal flatulence , otherwise known as a  queef ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4960", "text": "Generally speaking, there are four different types of complaints that relate to intestinal gas, which may present individually or in combination."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4961", "text": "Patients may complain of bloating as  abdominal distension , discomfort and pain from \"trapped wind\". In the past, functional bowel disorders such as  irritable bowel syndrome  that produced symptoms of bloating were attributed to increased production of intestinal gas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4962", "text": "However, three significant pieces of evidence refute this theory. First, in normal subjects, even very high rates of gas infusion into the small intestine (30 \u00a0 mL/min) is tolerated without complaints of pain or bloating and harmlessly passed as flatus per rectum. [ 10 ]  Secondly, studies aiming to quantify the total volume of gas produced by patients with irritable bowel syndrome (some including gas emitted from the mouth by eructation) have consistently failed to demonstrate increased volumes compared to healthy subjects. The proportion of hydrogen produced may be increased in some patients with irritable bowel syndrome, but this does not affect the total volume. [ 11 ]  Thirdly, the volume of flatus produced by patients with irritable bowel syndrome who have pain and abdominal distension would be tolerated in normal subjects without any complaints of pain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4963", "text": "Patients who complain of bloating frequently can be shown to have objective increases in abdominal girth, often increased throughout the day and then resolving during  sleep . The increase in girth combined with the fact that the total volume of flatus is not increased led to studies aiming to image the distribution of intestinal gas in patients with bloating. They found that gas was not distributed normally in these patients: there was segmental gas pooling and focal distension. [ 10 ]  In conclusion, abdominal distension, pain and bloating symptoms are the result of abnormal intestinal gas dynamics rather than increased flatus production."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4964", "text": "The range of volumes of flatus in normal individuals varies hugely (476\u20131,491\u2009mL/24\u2009h). [ 2 ]  All intestinal gas is either swallowed environmental air, present intrinsically in foods and beverages, or the result of gut fermentation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4965", "text": "Swallowing small amounts of air occurs while eating and drinking. This is emitted from the mouth by eructation (burping) and is normal. Excessive swallowing of environmental air is called  aerophagia , and has been shown in a few case reports to be responsible for increased flatus volume. This is, however, considered a rare cause of increased flatus volume. Gases contained in food and beverages are likewise emitted largely through eructation, e.g., carbonated beverages."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4966", "text": "Endogenously produced intestinal gases make up 74 percent of flatus in normal subjects. The volume of gas produced is partially dependent upon the composition of the intestinal microbiota, which is normally very resistant to change, but is also very different in different individuals. Some patients are predisposed to increased endogenous gas production by virtue of their gut microbiota composition. [ 10 ]  The greatest concentration of gut bacteria is in the colon, while the small intestine is normally nearly sterile. Fermentation occurs when unabsorbed food residues arrive in the colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4967", "text": "Therefore, even more than the composition of the microbiota, diet is the primary factor that dictates the volume of flatus produced. [ 10 ]  Diets that aim to reduce the amount of undigested fermentable food residues arriving in the colon have been shown to significantly reduce the volume of flatus produced. Again, increased volume of intestinal gas will not cause bloating and pain in normal subjects. Abnormal intestinal gas dynamics will create pain, distension, and bloating, regardless of whether there is high or low total flatus volume."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4968", "text": "Although flatus possesses an odor, this may be abnormally increased in some patients and cause social distress to the patient. Increased odor of flatus presents a distinct clinical issue from other complaints related to intestinal gas. [ 12 ]  Some patients may exhibit over-sensitivity to bad flatus odor, and in extreme forms,  olfactory reference syndrome  may be diagnosed. Recent informal research found a correlation between flatus odor and both loudness and humidity content. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4969", "text": "\"Gas incontinence\" could be defined as loss of voluntary control over the passage of flatus. It is a recognised subtype of  faecal incontinence , and is usually related to minor disruptions of the continence mechanisms. Some consider gas incontinence to be the first, sometimes only, symptom of faecal incontinence. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4970", "text": "Intestinal gas is composed of varying quantities of exogenous sources and endogenous sources. [ 15 ]  The exogenous gases are swallowed ( aerophagia ) when eating or drinking or increased swallowing during times of excessive salivation (as might occur when nauseated or as the result of  gastroesophageal reflux  disease). The  endogenous  gases are produced either as a by-product of digesting certain types of food, or of incomplete  digestion , as is the case during  steatorrhea . Anything that causes food to be incompletely digested by the  stomach  or  small intestine  may cause flatulence when the material arrives in the large intestine, due to  fermentation  by  yeast  or  prokaryotes  normally or abnormally present in the  gastrointestinal tract ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4971", "text": "Flatulence-producing foods are typically high in certain  polysaccharides , especially  oligosaccharides  such as  inulin . Those foods include  beans ,  lentils ,  dairy products ,  onions ,  garlic ,  spring onions ,  leeks ,  turnips ,  swedes ,  radishes ,  sweet potatoes ,  potatoes ,  cashews ,  Jerusalem artichokes ,  oats ,  wheat , and  yeast  in  breads .  Cauliflower ,  broccoli ,  cabbage ,  Brussels sprouts  and other  cruciferous vegetables  that belong to the genus  Brassica  are commonly reputed to not only increase flatulence, but to increase the pungency of the flatus. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4972", "text": "In beans, endogenous gases seem to arise from complex oligosaccharides ( carbohydrates ) that are particularly resistant to digestion by mammals, but are readily digestible by  microorganisms  ( methane-producing  archaea;  Methanobrevibacter smithii ) that inhabit the  digestive tract . These oligosaccharides pass through the small intestine largely unchanged, and when they reach the large intestine,  bacteria  ferment them, producing copious amounts of flatus. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4973", "text": "When excessive or malodorous, flatus can be a sign of a health disorder, such as  irritable bowel syndrome ,  celiac disease ,  non-celiac gluten sensitivity  or  lactose intolerance . It can also be caused by certain medicines, such as  ibuprofen ,  laxatives ,  antifungal  medicines or  statins . [ 8 ] [ 19 ]  Some infections, such as  giardiasis , are also associated with flatulence. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4974", "text": "Interest in the causes of flatulence was spurred by high-altitude  flight  and  human spaceflight ; the low  atmospheric pressure , confined conditions, and stresses peculiar to those endeavours were cause for concern. [ 18 ]  In the field of mountaineering, the phenomenon of  high altitude flatus expulsion  was first recorded over two hundred years ago."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4975", "text": "Flatus (intestinal gas) is mostly produced as a byproduct of bacterial fermentation in the gastrointestinal (GI) tract, especially the  colon . [ 21 ]  There are reports of  aerophagia  (excessive air swallowing) causing excessive intestinal gas, but this is considered rare. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4976", "text": "Over 99% of the volume of flatus is composed of odorless gases. [ 2 ]  These include  oxygen ,  nitrogen ,  carbon dioxide ,  hydrogen  and  methane . Nitrogen is not produced in the gut, but a component of environmental air. Patients who have excessive intestinal gas that is mostly composed of nitrogen have aerophagia. [ 23 ]  Hydrogen, carbon dioxide and methane are all produced in the gut and contribute 74% of the volume of flatus in normal subjects. [ 24 ]  Methane and hydrogen are  flammable , and so  flatus can be ignited  if it contains adequate amounts of these components. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4977", "text": "Not all humans produce flatus that contains methane. For example, in one study of the  faeces  of nine adults, only five of the samples contained  archaea  capable of producing methane. [ 26 ]  The prevalence of methane over hydrogen in human flatus may correlate with obesity, constipation and irritable bowel syndrome, as archaea that oxidise hydrogen into methane promote the metabolism's ability to absorb fatty acids from food. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4978", "text": "The remaining trace (<1% volume) compounds contribute to the odor of flatus. Historically, compounds such as  indole ,  skatole ,  ammonia  and  short chain fatty acids  were thought to cause the odor of flatus. More recent evidence proves that the major contribution to the odor of flatus comes from a combination of volatile  sulfur  compounds. [ 2 ] [ 28 ]   Hydrogen sulfide ,  methyl mercaptan  (also known as  methanethiol ),  dimethyl sulfide ,  dimethyl disulfide  and  dimethyl trisulfide  are present in flatus. The benzopyrrole volatiles  indole  and  skatole  have an odor of mothballs,  and therefore probably do not contribute greatly to the characteristic odor of flatus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4979", "text": "In one study, hydrogen sulfide concentration was shown to correlate convincingly with perceived bad odor of flatus, followed by methyl mercaptan and dimethyl sulfide. [ 23 ]  This is supported by the fact that hydrogen sulfide may be the most abundant volatile sulfur compound present. These results were generated from subjects who were eating a diet high in  pinto beans  to stimulate flatus production."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4980", "text": "Others report that methyl mercaptan was the greatest contributor to the odor of flatus in patients not under any specific dietary alterations. [ 2 ]  It has now been demonstrated that methyl mercaptan, dimethyl sulfide, and hydrogen sulfide (described as decomposing vegetables, unpleasantly sweet/wild radish and rotten eggs respectively) are all present in human flatus in concentrations above their smell perception thresholds. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4981", "text": "It is recognized that increased dietary sulfur-containing amino acids significantly increases the odor of flatus. It is therefore likely that the odor of flatus is created by a combination of volatile sulfur compounds, with minimal contribution from non-sulfur volatiles. [ 23 ]  This odor can also be caused by the presence of large numbers of microflora  bacteria  or the presence of faeces in the rectum. Diets high in protein, especially sulfur-containing amino acids, have been demonstrated to significantly increase the odor of flatus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4982", "text": "Normal flatus volume is 476 to 1491 mL per 24 hours. [ 2 ] [ 21 ]  This variability between individuals is greatly dependent upon diet. Similarly, the number of flatus episodes per day is variable; the normal range is given as 8\u201320 per day. [ 23 ]  The volume of flatus associated with each flatulence event again varies (5\u2013375\u00a0mL). [ 2 ] [ 21 ] [ 24 ]  The volume of the first flatulence upon waking in the morning is significantly larger than those during the day. [ 2 ]  This may be due to buildup of intestinal gas in the colon during sleep, the peak in peristaltic activity in the first few hours after waking or the strong prokinetic effect of rectal distension on the rate of transit of intestinal gas. [ 10 ]  It is now known that gas is moved along the gut independently of solids and liquids, and this transit is more efficient in the erect position compared to when supine. [ 10 ]  It is thought that large volumes of intestinal gas present low resistance, and can be propelled by subtle changes in gut tone, capacitance and proximal contraction and distal relaxation. This process is thought not to affect solid and liquid intra-lumenal contents. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4983", "text": "Researchers investigating the role of sensory nerve endings in the anal canal did not find them to be essential for retaining fluids in the anus, and instead speculate that their role may be to distinguish between flatus and faeces, thereby helping detect a need to defecate or to signal the end of defecation. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4984", "text": "The sound varies depending on the volume of gas, the size of the opening that the air is being pushed through, which is affected by the state of tension in the  sphincter muscle , and the  force  or  velocity  of the  gas  being propelled, as well as other factors, such as whether the gas was caused by swallowed air. [ 30 ] [ 31 ]  Among humans, flatulence occasionally happens accidentally, such as incidentally to  coughing [ 32 ]  or  sneezing  or during  orgasm ; on other occasions, flatulence can be voluntarily elicited by tensing the rectum or \"bearing down\" on stomach or bowel muscles and subsequently relaxing the anal sphincter, resulting in the expulsion of flatus. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4985", "text": "Since problems involving intestinal gas present as different (but sometimes combined) complaints, the management is cause-related."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4986", "text": "While not affecting the production of the gases themselves,  surfactants  (agents that lower  surface tension ) can reduce the disagreeable sensations associated with flatulence, by aiding the dissolution of the gases into liquid and solid faecal matter. [ 33 ]  Preparations containing  simethicone  reportedly operate by promoting the coalescence of smaller bubbles into larger ones more easily passed from the body, either by  burping  or flatulence. Such preparations do not decrease the total amount of gas generated in or passed from the colon, but make the bubbles larger and thereby allowing them to be passed more easily. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4987", "text": "Other drugs including  prokinetics ,  lubiprostone , antibiotics and probiotics are also used to treat bloating in patients with functional bowel disorders such as irritable bowel syndrome, and there is some evidence that these measures may reduce symptoms. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4988", "text": "A flexible tube, inserted into the  rectum , can be used to collect intestinal gas in a flatus bag. This method is occasionally needed in a hospital setting, when the patient is unable to pass gas normally. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4989", "text": "One method of reducing the volume of flatus produced is dietary modification, reducing the amount of fermentable carbohydrates. This is the theory behind diets such as the  low-FODMAP diet  (a diet low in fermentable oligosaccharides, disaccharides, monosaccharides, alcohols, and polyols). [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4990", "text": "Most starches, including potatoes, corn, noodles, and wheat, produce gas as they are broken down in the large intestine. [ 15 ]  Intestinal gas can be reduced by fermenting the beans, and making them less gas-inducing, or by cooking them in the liquor from a previous batch. For example, the fermented bean product  miso  is less likely to produce as much intestinal gas. Some  legumes  also stand up to prolonged cooking, which can help break down the oligosaccharides into simple sugars. Fermentative lactic acid bacteria such as  Lactobacillus casei  and  Lactobacillus plantarum  reduce flatulence in the human intestinal tract. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4991", "text": "Probiotics  ( live yogurt ,  kefir , etc.) are reputed to reduce flatulence when used to restore balance to the normal  intestinal flora . [ 38 ]  Live (bioactive) yogurt contains, among other lactic bacteria,  Lactobacillus acidophilus , which may be useful in reducing flatulence.  L. acidophilus  may make the intestinal environment more acidic, supporting a natural balance of the fermentative processes.  L. acidophilus  is available in supplements.  Prebiotics , which generally are non-digestible oligosaccharides, such as  fructooligosaccharide , generally increase flatulence in a similar way as described for lactose intolerance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4992", "text": "Digestive enzyme  supplements may significantly reduce the amount of flatulence caused by some components of foods not being digested by the body and thereby promoting the action of microbes in the small and large  intestines . It has been suggested that  alpha-galactosidase   enzymes , which can digest certain complex sugars, are effective in reducing the volume and frequency of flatus. [ 39 ]  The  enzymes   alpha-galactosidase ,  lactase ,  amylase ,  lipase ,  protease ,  cellulase ,  glucoamylase ,  invertase , malt  diastase ,  pectinase , and  bromelain  are available, either individually or in combination blends, in commercial products."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4993", "text": "The  antibiotic   rifaximin , often used to treat  diarrhea  caused by the  microorganism   E. coli , may reduce both the production of intestinal gas and the frequency of flatus events. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4994", "text": "Bismuth"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4995", "text": "The  odor  created by flatulence is commonly treated with  bismuth subgallate , available under the name Devrom. Bismuth subgallate is commonly used by individuals who have had  ostomy  surgery,  bariatric surgery ,  faecal incontinence  and  irritable bowel syndrome . [ 41 ] [ 42 ]   Bismuth subsalicylate  is a compound that binds hydrogen sulfide, and one study reported a dose of 524\u00a0mg four times a day for 3\u20137 days bismuth subsalicylate yielded a >95% reduction in faecal hydrogen sulfide release in both humans and rats. [ 43 ] \nAnother bismuth compound, bismuth subnitrate was also shown to bind to hydrogen sulfide. [ 44 ]  Another study showed that bismuth acted synergistically with various antibiotics to inhibit sulfate-reducing gut bacteria and sulfide production. [ 45 ]  Some authors proposed a theory that hydrogen sulfide was involved in the development of  ulcerative colitis  and that bismuth might be helpful in the management of this condition. [ 46 ]  However, bismuth administration in rats did not prevent them from developing ulcerative colitis despite reduced hydrogen sulfide production. [ 46 ]  Also, evidence suggests that colonic hydrogen sulfide is largely present in bound forms, probably sulfides of iron and other metals. [ 2 ]  Rarely, serious bismuth toxicity may occur with higher doses. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4996", "text": "Activated charcoal"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4997", "text": "Despite being an ancient treatment for various digestive complaints,  activated charcoal  did not produce reduction in both the total flatus volume nor the release of sulfur-containing gasses, and there was no reduction in abdominal symptoms (after 0.52 \u00a0 g activated charcoal four times a day for one week). [ 48 ]  The authors suggested that saturation of charcoal binding sites during its passage through the gut was the reason for this. A further study concluded that activated charcoal (4 \u00a0 g) does not influence gas formation in vitro or in vivo. [ 49 ]  Other authors reported that activated charcoal was effective. A study in 8 dogs concluded activated charcoal (unknown oral dose) reduced hydrogen sulfide levels by 71%. In combination with yucca schidigera, and zinc acetate, this was increased to an 86% reduction in hydrogen sulfide, although flatus volume and number was unchanged. [ 50 ]  An early study reported activated charcoal (unknown oral dose) prevented a large increase in the number of flatus events and increased breath hydrogen concentrations that normally occur following a gas-producing meal. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4998", "text": "Garments and external devices"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_4999", "text": "In 1998, Chester \"Buck\" Weimer of  Pueblo, Colorado , received a patent for the first  undergarment  that contained a replaceable  charcoal filter . The undergarments are  air-tight  and provide a pocketed  escape hole  in which a charcoal filter can be inserted. [ 52 ]  In 2001 Weimer received the  Ig Nobel Prize  for Biology for his invention. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5000", "text": "A similar product was released in 2002, but rather than an entire undergarment, consumers are able to purchase an insert similar to a  pantiliner  that contains activated charcoal. [ 54 ]  The inventors, Myra and Brian Conant of  Mililani, Hawaii , still claim on their website to have discovered the undergarment product in 2002 (four years after Chester Weimer filed for a patent for his product), but state that their tests \"concluded\" that they should release an insert instead. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5001", "text": "Flatus incontinence where there is involuntary passage of gas, is a type of  faecal incontinence , and is managed similarly."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5002", "text": "In many  cultures , flatulence in public is regarded as embarrassing, but, depending on context, may also be considered humorous. [ 56 ]  People will often strain to hold in the passing of gas when in polite company, or position themselves to silence or conceal the passing of gas. In other cultures, [ example needed ]  it may be no more embarrassing than  coughing ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5003", "text": "While the act of passing flatus in some cultures is generally considered to be an unfortunate occurrence in public settings, flatulence may, in casual circumstances and especially among children, be used as either a humorous supplement to a joke (\"pull my finger\"), or as a comic activity in and of itself. The social acceptability of flatulence-based humour in entertainment and the mass media varies over the course of time and between cultures. A sufficient number of entertainers have performed using their flatus to lead to the coining of the term  flatulist . The  whoopee cushion  is a joking device invented in the early 20th century for simulating a fart. In 2008, a farting application for the  iPhone  earned nearly $10,000 in one day. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5004", "text": "A  farting  game named  Touch Wood  was documented by  John Gregory Bourke  in the 1890s. [ 58 ]  It was known as  Safety  in the 20th century in the U.S., and is still played by children as of 2011. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5005", "text": "In January 2011, the  Malawi   Minister of Justice ,  George Chaponda , said that  Air Fouling Legislation  would make public \"farting\" illegal in his country. When reporting the story, the media satirised Chaponda's statement with punning headlines. Later, the minister withdrew his statement. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5006", "text": "Flatulence is often blamed as a significant source of  greenhouse gases , owing to the erroneous belief that the methane released by  livestock  is in the flatus. [ 61 ]  While livestock account for around 20% of global  methane emissions , [ 62 ]  90\u201395% of that is released by  exhaling  or  burping . [ 63 ]  In cows, gas and burps are produced by methane-generating microbes called  methanogens , which live inside the cow's digestive system. Proposals for reducing methane production in cows include the feeding of supplements such as  oregano  and  seaweed , and the genetic engineering of gut biome microbes to produce less methane. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5007", "text": "Since New Zealand produces large amounts of agricultural products, it has the unique position of having higher methane emissions from livestock compared to other greenhouse gas sources. The New Zealand government is a signatory to the  Kyoto Protocol  and therefore attempts to reduce  greenhouse emissions . To achieve this, an  agricultural emissions research levy  was proposed, which promptly became known as a \" fart tax \" or \"flatulence tax\". It encountered opposition from farmers, farming lobby groups and opposition politicians."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5008", "text": "Historical comment on the ability to fart at will is observed as early as  Saint Augustine 's  The City of God  (5th century A.D.). Augustine mentions \"people who produce at will without any stench such rhythmical sounds from their fundament that they appear to be making music even from that quarter.\" [ 64 ]  Intentional passing of gas and its use as entertainment for others appear to have been somewhat well known in pre-modern Europe, according to mentions of it in medieval and later literature, including  Rabelais . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5009", "text": "Le P\u00e9tomane  (\"the Fartomaniac\") was a famous French performer in the 19th century who, as well as many  professional farters  before him, did flatulence impressions and held shows. The performer  Mr. Methane  carries on le P\u00e9tomane's tradition today. Also, a 2002 fiction film  Thunderpants  revolves around a boy named Patrick Smash who has an ongoing flatulence problem from the time of his birth. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5010", "text": "Since the 1970s, farting has increasingly been featured in film, especially comedies such as  Blazing Saddles  and  Scooby-Doo . [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5011", "text": "In the popular vulgar cartoon series \" South Park ,\" characters sometimes watch a  show-within-a-show  called \"The  Terrance and Phillip  Show\" whose humor primarily revolves around flatulence."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5012", "text": "People find other peoples' flatus unpleasant, but are unfazed by, and may even enjoy, the scent of their own. [ 67 ]  While there has been little research carried out upon the subject, some speculative guesses have been made as to why this might be so. For example, one explanation for this phenomenon is that people are very familiar with the scent of their own flatus, and that survival in nature may depend on the detection of and reaction to foreign scents. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5013", "text": "Some people have Eproctophilla, the  fetish  of flatulence, finding  sexual gratification  and  pleasure  from either the sound of the gas, smells from the gas, feeling of the gas, some combination of the three, or all three."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5014", "text": "Foregut fermentation  is a form of  digestion  that occurs in the  foregut  of some animals such as the  hamster rat ,  langur monkey , and the  hippopotamus . [ 1 ]  It has  evolved independently  in several groups of mammals, and also in the  hoatzin , a bird species."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5015", "text": "Foregut fermentation is employed by  ruminants  and  pseudoruminants , some  rodents  and some  marsupials . [ 2 ]  It has also evolved in  colobine  monkeys and in  sloths . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5016", "text": "This  vertebrate anatomy \u2013related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5017", "text": "The  Gal4 transcription factor  is a positive regulator of gene expression of galactose-induced genes. [ 1 ]  This protein represents a large fungal family of transcription factors, Gal4 family, which includes over 50 members in the yeast  Saccharomyces cerevisiae  e.g. Oaf1, Pip2, Pdr1, Pdr3, Leu3. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5018", "text": "Gal4 recognizes genes with UAS G , an  upstream activating sequence , and activates them. In yeast cells, the principal targets are GAL1 ( galactokinase ), GAL10 ( UDP-glucose 4-epimerase ), and GAL7 ( galactose-1-phosphate uridylyltransferase ), three enzymes required for galactose metabolism. This binding has also proven useful in constructing the  GAL4/UAS system , a technique for controlling expression in insects. [ 3 ]  In yeast, Gal4 is by default repressed by Gal80, and activated in the presence of  galactose  as Gal3 binds away Gal80. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5019", "text": "Two executive domains, DNA binding and activation domains, provide key function of the Gal4 protein conforming to most of the transcription factors."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5020", "text": "Gal4 N-terminus is a zinc finger and belongs to the  Zn(2)-C6  fungal family. It forms a Zn \u2013 cysteines thiolate cluster, [ 5 ] [ 6 ]  and specifically recognizes UAS G  in GAL1 promoter.  [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5021", "text": "Localised to the C-terminus, belongs to the nine amino acids  transactivation domain  family, 9aaTAD, together with Oaf1, Pip2, Pdr1, Pdr3, but also  p53 ,  E2A ,  MLL . [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5022", "text": "Galactose  induces Gal4 mediated transcription albeit Glucose causes severe repression. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5023", "text": "As a part of the Gal4 regulation, inhibitory protein Gal80 recognises and binds to the Gal4 region (853-874 aa). [ 13 ] [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5024", "text": "The inhibitory protein Gal80 is sequestered by regulatory protein Gal3 in Galactose dependent manner. This allows for Gal4 to work when there is galactose. [ 16 ] [ 4 ] [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5025", "text": "The Gal4 loss-of-function mutant gal4-64 (1-852 aa, deletion of the Gal4 C-terminal 29 aa) lost both interaction with Gal80 and activation function. [ 19 ] [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5026", "text": "In the Gal4 reverted mutant Gal4C-62 mutant, [ 22 ]  a sequence (QTAY N AFMN) with the 9aaTAD pattern emerged and restored activation function of the Gal4 protein."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5027", "text": "The activation domain Gal4 is inhibited by C-terminal domain in some Gal4 constructs. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5028", "text": "The Gal4 activation function is mediated by  MED15  (Gal11). [ 25 ] [ 26 ] [ 27 ] [ 28 ] [ 29 ] [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5029", "text": "The Gal4 protein interacts also with other mediators of transcription as are Tra1, [ 32 ] [ 33 ] [ 34 ]  TAF9, [ 35 ]  and SAGA/MED15 complex. [ 36 ] [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5030", "text": "A subunit of the 26 S proteasome Sug2 regulatory protein has a molecular and functional interaction with Gal4 function. [ 38 ] [ 39 ]  Proteolytic turnover of the Gal4 transcription factor is not required for function in vivo. [ 40 ]  The native Gal4 monoubiquitination protects from 19S-mediated destabilizing under inducing conditions. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5031", "text": "The broad use of the Gal4 is in yeast  two-hybrid screening  to screen or to assay protein-protein interactions in eukaryotic cells from yeast to human."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5032", "text": "In the  GAL4/UAS system , the Gal4 protein and Gal4 upstream activating region (UAS) are used to study the gene expression and function in organisms such as the fruit fly. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5033", "text": "The Gal4 and inhibitory protein Gal80 have found application in a genetics technique for creating individually labeled homozygous cells called  MARCM  (Mosaic analysis with a repressible cell marker)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5034", "text": "In  vertebrates , the  gallbladder , also known as the  cholecyst , is a small hollow  organ  where  bile  is stored and concentrated before it is released into the  small intestine . In humans, the pear-shaped gallbladder lies beneath the  liver , although the structure and position of the gallbladder can vary significantly among animal species. It receives bile, produced by the liver, via the  common hepatic duct , and stores it. The bile is then released via the  common bile duct  into the  duodenum , where the bile helps in the digestion of  fats ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5035", "text": "The gallbladder can be affected by  gallstones , formed by material that cannot be dissolved \u2013 usually  cholesterol  or  bilirubin , a product of  hemoglobin  breakdown. These may cause significant pain, particularly in the upper-right corner of the abdomen, and are often treated with removal of the gallbladder (called a  cholecystectomy ).  Cholecystitis , inflammation of the gallbladder, has a wide range of causes, including result from the impaction of gallstones, infection, and autoimmune disease."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5036", "text": "The human gallbladder is a hollow grey-blue  organ  that sits in a shallow depression below the right lobe of the  liver . [ 2 ]  In adults, the gallbladder measures approximately 7 to 10 centimetres (2.8 to 3.9 inches) in length and 4 centimetres (1.6\u00a0in) in diameter when fully distended. [ 3 ]  The gallbladder has a capacity of about 50 millilitres (1.8 imperial fluid ounces). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5037", "text": "The gallbladder is shaped like a pear, with its tip opening into the  cystic duct . [ 4 ]  The gallbladder is divided into three sections: the  fundus ,  body , and  neck . The  fundus  is the rounded base, angled so that it faces the  abdominal wall . The  body  lies in a depression in the surface of the lower liver. The  neck  tapers and is continuous with the  cystic duct , part of the  biliary tree . [ 2 ]  The gallbladder fossa, against which the fundus and body of the gallbladder lie, is found beneath the junction of  hepatic segments  IVB and V. [ 5 ]  The cystic duct unites with the  common hepatic duct  to become the  common bile duct . At the junction of the neck of the gallbladder and the cystic duct, there is an out-pouching of the gallbladder wall forming a mucosal fold known as \" Hartmann 's pouch\". [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5038", "text": "Lymphatic drainage of the gallbladder follows the cystic node, which is located between the cystic duct and the common hepatic duct. Lymphatics from the lower part of the organ drain into lower  hepatic lymph nodes . All the lymph finally drains into  celiac lymph nodes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5039", "text": "The gallbladder wall is composed of a number of layers. The innermost surface of the gallbladder wall is lined by a single layer of  columnar cells  with a  brush border  of  microvilli , very similar to intestinal absorptive cells. [ 2 ]  Underneath the epithelium is an underlying  lamina propria , a  muscular layer , an outer perimuscular layer and  serosa . Unlike elsewhere in the intestinal tract, the gallbladder does not have a  muscularis mucosae , and the muscular fibres are not arranged in distinct layers. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5040", "text": "The  mucosa , the inner portion of the gallbladder wall, consists of a  lining  of a  single layer of columnar  cells, with cells possessing small hair-like attachments called  microvilli . [ 2 ]  This sits on a thin layer of connective tissue, the  lamina propria . [ 6 ]  The mucosa is curved and collected into tiny outpouchings called  rugae . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5041", "text": "A muscular layer sits beneath the mucosa. This is formed by  smooth muscle , with fibres that lie in longitudinal, oblique and transverse directions, and are not arranged in separate layers. The muscle fibres here contract to expel bile from the gallbladder. [ 6 ]  A distinctive feature of the gallbladder is the presence of  Rokitansky\u2013Aschoff sinuses , deep outpouchings of the mucosa that can extend through the muscular layer, and which indicate  adenomyomatosis . [ 7 ]  The muscular layer is surrounded by a layer of connective and  fat  tissue. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5042", "text": "The outer layer of the fundus of gallbladder, and the surfaces not in contact with the liver, are covered by a thick  serosa , which is exposed to the  peritoneum . [ 2 ]  The serosa contains blood vessels and lymphatics. [ 6 ]  The surfaces in contact with the liver are covered in  connective tissue . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5043", "text": "The gallbladder varies in size, shape, and position among different people. [ 2 ]  Rarely, two or even three gallbladders may coexist, either as separate bladders draining into the cystic duct, or sharing a common branch that drains into the cystic duct. Additionally, the gallbladder may fail to form at all. Gallbladders with two lobes separated by a  septum  may also exist. These abnormalities are not likely to affect function and are generally asymptomatic. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5044", "text": "The location of the gallbladder in relation to the liver may also vary, with documented variants including gallbladders found within, [ 9 ]  above, on the left side of, behind, and detached or suspended from the liver. Such variants are very rare: from 1886 to 1998, only 110 cases of left-lying liver, or less than one per year, were reported in scientific literature. [ 10 ] [ 11 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5045", "text": "An  anatomical variation  can occur, known as a  Phrygian cap , which is an innocuous fold in the fundus, named after its resemblance to the  Phrygian cap . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5046", "text": "The gallbladder develops from an  endodermal  outpouching of the embryonic gut tube. [ 13 ]  Early in development, the human embryo has three  germ layers  and abuts an embryonic  yolk sac . During the second week of  embryogenesis , as the embryo grows, it begins to surround and envelop portions of this sac. The enveloped portions form the basis for the adult gastrointestinal tract. Sections of this  foregut  begin to differentiate into the organs of the gastrointestinal tract, such as the  esophagus ,  stomach , and  intestines . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5047", "text": "During the fourth week of embryological development, the stomach rotates. The stomach, originally lying in the midline of the embryo, rotates so that its body is on the left. This rotation also affects the part of the gastrointestinal tube immediately below the stomach, which will go on to become the  duodenum . By the end of the fourth week, the developing duodenum begins to spout a small outpouching on its right side, the  hepatic diverticulum , which will go on to become the  biliary tree . Just below this is a second outpouching, known as the  cystic diverticulum , that will eventually develop into the gallbladder. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5048", "text": "The main functions of the gallbladder are to store and concentrate  bile , also called gall, needed for the digestion of fats in food. Produced by the liver, bile flows through small vessels into the larger  hepatic ducts  and ultimately through the  cystic duct  (parts of the  biliary tree ) into the gallbladder, where it is stored. At any one time, 30 to 60 millilitres (1.0 to 2.0\u00a0US\u00a0fl\u00a0oz) of bile is stored within the gallbladder. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5049", "text": "When food containing fat enters the  digestive tract , it stimulates the  secretion  of  cholecystokinin  (CCK) from  I cells  of the duodenum and jejunum. In response to cholecystokinin, the gallbladder rhythmically contracts and releases its contents into the  common bile duct , eventually draining into the  duodenum . The bile  emulsifies  fats in partly digested food, thereby assisting their absorption. Bile consists primarily of water and  bile salts , and also acts as a means of eliminating  bilirubin , a product of  hemoglobin  metabolism, from the body. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5050", "text": "The bile that is secreted by the liver and stored in the gallbladder is not the same as the bile that is secreted by the gallbladder. During gallbladder storage of bile, it is concentrated 3\u201310 fold [ 16 ]  by removal of some water and electrolytes. This is through the  active transport  of sodium and chloride ions [ 17 ]  across the epithelium of the gallbladder, which creates an  osmotic pressure  that also causes water and other electrolytes to be reabsorbed. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5051", "text": "A function of the gallbladder appears to be protection against  carcinogenesis  as indicated by  observations that removal of the gallbladder ( cholecystectomy ) increases subsequent cancer risk.  For instance, a systematic review and meta analysis of eighteen studies concluded that cholecystectomy has a harmful effect on the risk of right-sided colon cancer. [ 18 ]   Another recent study reported a significantly increased total cancer risk, including increased risk of several different types of cancer, after cholecystectomy. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5052", "text": "Gallstones  form when the bile is  saturated , usually with either  cholesterol  or  bilirubin . [ 20 ]  Most gallstones do not cause symptoms, with stones either remaining in the gallbladder or passed along the  biliary system . [ 21 ]  When symptoms occur, severe \"colicky\" pain in the upper right  quadrant  of the abdomen is often felt. [ 20 ]  If the  stone blocks the gallbladder , inflammation known as  cholecystitis  may result. If the stone lodges in the biliary system,  jaundice  may occur; if the stone blocks the  pancreatic duct ,  pancreatitis  may occur. [ 21 ]  Gallstones are diagnosed using  ultrasound . [ 20 ]  When a symptomatic gallstone occurs, it is often managed by waiting for it to be passed naturally. [ 21 ]  Given the likelihood of recurrent gallstones, surgery to remove the gallbladder is often considered. [ 21 ]  Some medication, such as  ursodeoxycholic acid , may be used;  lithotripsy , a non-invasive mechanical procedure used to break down the stones, may also be used. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5053", "text": "Known as  cholecystitis , inflammation of the gallbladder is commonly caused by obstruction of the duct with gallstones, which is known as  cholelithiasis . Blocked bile accumulates, and pressure on the gallbladder wall may lead to the release of substances that cause inflammation, such as  phospholipase . There is also the risk of bacterial infection. An inflamed gallbladder is likely to cause sharp and localised pain, fever, and tenderness in the upper, right corner of the abdomen, and may have a positive  Murphy's sign . Cholecystitis is often managed with rest and antibiotics, particularly  cephalosporins  and, in severe cases,  metronidazole . Additionally the gallbladder may need to be removed surgically if inflammation has progressed far enough. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5054", "text": "A  cholecystectomy  is a procedure in which the gallbladder is removed. It may be removed because of recurrent gallstones and is considered an  elective procedure . A cholecystectomy may be an  open  procedure, or a  laparoscopic  one. In the surgery, the gallbladder is removed from the neck to the fundus, [ 22 ]  and so bile will drain directly from the liver into the  biliary tree . About 30 percent of patients may experience some degree of  indigestion  following the procedure, although severe complications are much rarer. [ 21 ]  About 10 percent of surgeries lead to a chronic condition of  postcholecystectomy syndrome . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5055", "text": "Biliary injury (bile duct injury) is the traumatic damage of the  bile ducts . It is most commonly an  iatrogenic  complication of  cholecystectomy  \u2014 surgical removal of  gall bladder , but can also be caused by other operations or by  major trauma . The risk of biliary injury is more during laparoscopic cholecystectomy than during open cholecystectomy. Biliary injury may lead to several complications and may even cause death if not diagnosed in time and managed properly. Ideally biliary injury should be managed at a center with facilities and expertise in  endoscopy ,  radiology  and surgery. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5056", "text": "Biloma is collection of  bile  within the  abdominal cavity . It happens when there is a bile leak, for example after surgery for removing the gallbladder ( laparoscopic cholecystectomy ), with an incidence of 0.3\u20132%. Other causes are biliary surgery,  liver biopsy ,  abdominal trauma , and, rarely, spontaneous perforation. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5057", "text": "Cancer of the gallbladder is uncommon and mostly occurs in later life. When cancer occurs, it is mostly of the glands lining the surface of the gallbladder ( adenocarcinoma ). [ 21 ]  Gallstones are thought to be linked to the formation of cancer. Other risk factors include large (>1\u00a0cm)  gallbladder polyps  and having a highly calcified  \"porcelain\" gallbladder . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5058", "text": "Cancer of the gallbladder can cause attacks of biliary pain, yellowing of the skin ( jaundice ), and weight loss. A large gallbladder may be able to be felt in the abdomen.  Liver function tests  may be elevated, particularly involving  GGT  and  ALP , with ultrasound and CT scans being considered  medical imaging  investigations of choice. [ 21 ]  Cancer of the gallbladder is managed by removing the gallbladder, however, as of 2010, [update]  the prognosis remains poor. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5059", "text": "Cancer of the gallbladder may also be found incidentally after surgical removal of the gallbladder, with 1\u20133% of cancers identified in this way.  Gallbladder polyps  are mostly benign growths or lesions resembling growths that form in the gallbladder wall, [ 26 ]  and are only associated with cancer when they are larger in size (>1\u00a0cm). [ 21 ]  Cholesterol polyps, often associated with  cholesterolosis  (\"strawberry gallbladder\", a change in the gallbladder wall due to excess  cholesterol [ 27 ] ), often cause no symptoms and are thus often detected in this way. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5060", "text": "Tests used to investigate for gallbladder disease include  blood tests  and  medical imaging . A  full blood count  may reveal an increased white cell count suggestive of inflammation or infection. Tests such as  bilirubin  and  liver function tests  may reveal if there is inflammation linked to the biliary tree or gallbladder, and whether this is associated with inflammation of the liver, and a  lipase  or  amylase  may be elevated if there is  pancreatitis . Bilirubin may rise when there is obstruction of the flow of bile. A  CA 19-9  level may be taken to investigate for cholangiocarcinoma. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5061", "text": "An  ultrasound  is often the first  medical imaging  test performed when gallbladder disease such as gallstones are suspected. [ 21 ]  An  abdominal X-ray  or  CT scan  is another form of imaging that may be used to examine the gallbladder and surrounding organs. [ 21 ]  Other imaging options include MRCP ( magnetic resonance cholangiopancreatography ),  ERCP  and percutaneous or intraoperative  cholangiography . [ 21 ]  A  cholescintigraphy  scan is a  nuclear imaging  procedure used to assess the condition of the gallbladder. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5062", "text": "Most  vertebrates  have gallbladders, but the form and arrangement of the bile ducts may vary considerably. In many species, for example, there are several separate ducts running to the intestine, rather than the single common bile duct found in humans. Several species of  mammals  (including  horses ,  deer ,  rats , and  laminoids ), [ 29 ] [ 30 ]  several species of  birds  (such as pigeons and some  psittacine  species),  lampreys  and all  invertebrates  do not have a gallbladder. [ 31 ] [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5063", "text": "The bile from several species of bears is used in  traditional Chinese medicine ;  bile bears  are kept alive in captivity while their bile is extracted, in an industry characterized by  animal cruelty . [ 33 ] [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5064", "text": "Depictions of the gallbladder and biliary tree are found in  Babylonian  models found from 2000 BCE, and in ancient  Etruscan  model from 200 BCE, with models associated with divine worship. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5065", "text": "Diseases of the gallbladder are known to have existed in humans since antiquity, with gallstones found in the mummy of Princess Amenen of  Thebes  dating to 1500 BCE. [ 35 ] [ 36 ]  Some historians believe the death of  Alexander the Great  may have been associated with an acute episode of cholecystitis. [ 35 ]  The existence of the gallbladder has been noted since the 5th century, but it is only relatively recently that the function and the diseases of the gallbladder has been documented, [ 36 ]  particularly in the last two centuries. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5066", "text": "The first descriptions of gallstones appear to have been in the  Renaissance , perhaps because of the low incidence of gallstones in earlier times owing to a diet with more cereals and vegetables and less meat. [ 37 ]  Anthonius Benevinius in 1506 was the first to draw a connection between symptoms and the presence of gallstones. [ 37 ]   Ludwig Georg Courvoisier , after examining a number of cases in 1890 that gave rise to the  eponymous   Courvoisier's law , stated that in an enlarged, nontender gallbladder, the cause of  jaundice  is unlikely to be gallstones. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5067", "text": "The first surgical removal of a gallstone (cholecystolithotomy) was in 1676 by physician Joenisius, who removed the stones from a spontaneously occurring  biliary fistula . [ 35 ]  Stough Hobbs in 1867 performed the first recorded  cholecystotomy , [ 37 ]  although such an operation was in fact described earlier by French surgeon  Jean Louis Petit  in the mid eighteenth century. [ 35 ]  German surgeon  Carl Langenbuch  performed the first cholecystectomy in 1882 for a sufferer of cholelithiasis. [ 36 ]  Before this, surgery had focused on creating a  fistula  for drainage of gallstones. [ 35 ]  Langenbuch reasoned that given several other species of mammal have no gallbladder, humans could survive without one. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5068", "text": "The debate whether surgical removal of the gallbladder or simply gallstones was preferred was settled in the 1920s, with the consensus that removal of the gallbladder was preferred. [ 36 ]  It was only in the mid and late parts of the twentieth century that medical imaging techniques such as use of  contrast medium  and  CT scans  were used to view the gallbladder. [ 35 ]  The first  laparoscopic  cholecystectomy performed by  Erich M\u00fche  of Germany in 1985, although French surgeons Phillipe Mouret and Francois Dubois are often credited for their operations in 1987 and 1988 respectively. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5069", "text": "To have \"gall\" is associated with bold, belligerent behaviour, whereas to have \"bile\" is associated with sourness. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5070", "text": "In the  Chinese medicine , the gallbladder ( \u81bd ) is associated with the  Wuxing  element of wood, in excess its emotion is belligerence and in deficiency cowardice and judgement, in the Chinese language it is related to a myriad of  idioms , including using terms such as \"a body completely [of] gall\" ( \u6e3e\u8eab\u662f\u81bd ) to describe a forward person, and \"single, alone gallbladder hero\" ( \u5b64\u81bd\u82f1\u96c4 ) to describe a lone hero, or \"they have a lot of gall to talk like that\". [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5071", "text": "In the  Zangfu  theory of  Chinese medicine  it is an extraordinary Fu or  yang  organ, as it holds bile. The gallbladder not only has a digestive role, but is seen as the seat of decision-making and judgement. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5072", "text": "Ganeden, Inc.  is a privately held United States  probiotic  ingredient manufacturer that sells its products to makers of foods and  dietary supplements . It is based in  Mayfield Heights, Ohio  and was founded in 1997 in  San Diego, California  by Sean Farmer. The company's name, Ganeden, was derived from the Hebrew \" Gan Eden \", meaning  Garden of Eden . [ 1 ]  The company moved to Ohio in 2000. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5073", "text": "In 2011, Ganeden sold two of its probiotic brands, Sustenex and Digestive Advantage, to  Schiff Nutrition International . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5074", "text": "In 2017, the Irish-based  Kerry Group  acquired Ganeden for an undisclosed amount. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5075", "text": "Gastric glands  are  glands  in the lining of the  stomach  that play an essential role in the  process of digestion . Their secretions make up the  digestive gastric juice . The gastric glands open into  gastric pits  in the  mucosa . The gastric mucosa is covered in  surface mucous cells  that produce the  mucus  necessary to protect the stomach's  epithelial lining  from  gastric acid  secreted by  parietal cells  in the glands, and from  pepsin , a secreted  digestive enzyme . Surface mucous cells follow the indentations and partly line the gastric pits. Other mucus secreting cells are found in the necks of the glands. These are  mucous neck cells  that produce a different kind of mucus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5076", "text": "There are two types of gastric gland, the  exocrine   oxyntic gland , and the  endocrine   pyloric gland . The major type of gastric gland is the oxyntic gland that is present in the fundus and the body of the stomach making up about 80 per cent of the stomach area. These glands are often referred to simply as the  gastric glands .  The oxyntic gland contains the  parietal cells  that produce  hydrochloric acid  and  intrinsic factor , and  chief cells  that produce  pepsinogen  and  gastric lipase ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5077", "text": "The pyloric gland is found in the  pyloric region , the remaining 20 per cent of the stomach. The pyloric glands are mainly in the  pyloric antrum . The pyloric gland secretes  gastrin  from its  G cells . Pyloric glands are similar in structure to the oxyntic glands but have hardly any parietal cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5078", "text": "The gastric glands are glands in the lining of the stomach that play an essential role in the process of  digestion . All of the glands have mucus-secreting  foveolar cells  (also known as surface mucous cells) that line the stomach and partly line the  gastric pits , and mucus-secreting  mucous neck cells  in the necks of the gastric glands. [ 1 ]   Mucus  lines the entire stomach as  gastric mucosa  protecting the stomach lining from the effects of  hydrochloric acid  produced by the parietal cells and released from the oxyntic glands."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5079", "text": "Gastric glands are mostly  exocrine glands [ 2 ]  and are all located beneath the gastric pits within the gastric mucosa. [ 3 ]  The gastric mucosa is pitted with innumerable gastric pits which each house 3-5 gastric glands. [ 4 ]  The cells of the exocrine glands (oxyntic glands) are mucous neck cells,  chief cells , and  parietal cells . [ 4 ]  Mucous neck cells produce mucus, parietal cells secrete  hydrochloric acid  and  intrinsic factor , chief cells secrete  pepsinogen  and  gastric lipase . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5080", "text": "The other type of gastric gland is the  pyloric gland  which is an  endocrine gland  that secretes the hormone  gastrin  produced by its  G cells ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5081", "text": "The secretions of the different exocrine gastric gland cells produce a watery, acidic fluid into the stomach lumen called gastric juice. [ 5 ] [ 6 ]  Gastric juice contains water, hydrochloric acid, intrinsic factor, pepsinogen, and salts. Adults produce around two to three litres of gastric juice per day. [ 5 ]  The composition of the fluid varies according to the time of eating, and the rates of activity of the various cells. The cells are more active after eating. The composition of the gastric juice electrolytes is related to its rate of secretion: when secretion increases, the concentration of sodium decreases, and the concentration of hydrogen increases. There is always a higher level of potassium ions in the fluid than in the plasma. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5082", "text": "The glands are named for the region of the stomach that they occupy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5083", "text": "The  cardiac glands  are found in the  cardia  of the stomach which is the part nearest to the heart, enclosing the opening where the esophagus joins to the stomach. Cardiac glands primarily secrete mucus. [ 7 ]  They are fewer in number than the other gastric glands and are more shallowly positioned in the mucosa. There are two kinds - either  simple tubular  with short ducts  or   compound racemose  resembling the  duodenal   Brunner's glands . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5084", "text": "The  fundic glands  (or  oxyntic glands ), are found in the  fundus  and body of the stomach. They are simple almost straight tubes, two or more of which open into a single duct.  Oxyntic  means acid-secreting and they secrete  hydrochloric acid  (HCl) and  intrinsic factor . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5085", "text": "The  pyloric glands  are located in the  antrum  of the  pylorus . They secrete  gastrin  produced by their  G cells . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5086", "text": "There are millions of  gastric pits  (also known as  foveolae )  in the gastric mucosa and their necessary narrowness determines the tubular form of the gastric gland. More than one tube allows for the accommodation of more than one cell type. The form of each gastric gland is similar; they are all described as having a neck region that is closest to the pit entrance, and basal regions on the lower parts of the tubes. [ 9 ]  The epithelium from the gastric mucosa travels into the pit and at the neck the epithelial cells change to short columnar granular cells. These cells almost fill the tube and the remaining lumen is continued as a very fine channel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5087", "text": "Cells found in the gastric glands include mucous neck cells,  chief cells ,  parietal cells ,  G cells , and  enterochromaffin-like cells  (ECLs). The first cells of all of the glands are mucus-secreting  foveolar cells that line the gastric pits. The mucus produced here is less acidic than that produced by the mucous neck cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5088", "text": "Fundic glands found in the fundus and also in the body have another two cell types\u2013gastric  chief cells  and  parietal cells  (oxyntic cells)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5089", "text": "Fundic gland polyposis  is a medical syndrome where the  fundus  and the body of the  stomach  develop many  fundic gland   polyps ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5090", "text": "Pernicious anemia  is caused when damaged parietal cells fail to produce the intrinsic factor necessary for the absorption of vitamin B12. This is the most common cause of  vitamin B12 deficiency ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5091", "text": "List of distinct cell types in the adult human body"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5092", "text": "This article incorporates text in the  public domain  from the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5093", "text": "A  gastric shield  is an organ in the digestive tract of  bivalves ,  tusk shells , and some  gastropods  against which a  crystalline style  typically rotates, in an action resembling that of a  mortar and pestle . The gastric shield is permeated by microcanals which transmit digestive enzymes from the stomach, and serves to protect the cells of the stomach lining from the abrasive effects of the style. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5094", "text": "2520"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5095", "text": "14459"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5096", "text": "ENSG00000184502"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5097", "text": "ENSMUSG00000017165"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5098", "text": "P01350"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5099", "text": "P48757"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5100", "text": "NM_000805"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5101", "text": "NM_010257"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5102", "text": "NP_000796"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5103", "text": "NP_034387"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5104", "text": "Gastrin  is a  peptide hormone  that stimulates secretion of  gastric acid  (HCl) by the  parietal cells  of the  stomach  and aids in gastric motility. It is released by  G cells  in the  pyloric antrum  of the stomach,  duodenum , and the  pancreas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5105", "text": "Gastrin binds to  cholecystokinin B receptors  to stimulate the release of histamines in enterochromaffin-like cells, and it induces the insertion of K + /H +  ATPase pumps into the apical membrane of parietal cells (which in turn increases H +  release into the stomach cavity). Its release is stimulated by  peptides  in the  lumen  of the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5106", "text": "In humans, the  GAS  gene is located on the long arm of the  seventeenth chromosome  (17q21). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5107", "text": "Gastrin is a linear  peptide hormone  produced by  G cells  of the duodenum and in the  pyloric antrum  of the  stomach . It is secreted into the bloodstream. The encoded polypeptide is preprogastrin, which is cleaved by enzymes in  posttranslational modification  to produce progastrin (an intermediate, inactive precursor) and then gastrin in various forms, primarily the following three:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5108", "text": "Also,  pentagastrin  is an artificially synthesized, five amino acid sequence identical to the last five amino acid sequence at the  C-terminus  end of gastrin.\nThe numbers refer to the  amino acid  count."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5109", "text": "Gastrin is released in response to certain stimuli.  These include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5110", "text": "Gastrin release is inhibited by: [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5111", "text": "The presence of gastrin stimulates  parietal cells  of the stomach to  secrete   hydrochloric acid  (HCl)/gastric acid.  This is done both directly on the parietal cell and indirectly via binding onto  CCK2/gastrin receptors  on  ECL cells  in the stomach, which respond by releasing  histamine , which in turn acts in a paracrine manner on parietal cells stimulating them to secrete  H+ ions . This is the major stimulus for acid secretion by parietal cells. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5112", "text": "Along with the above-mentioned function, gastrin has been shown to have additional functions as well:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5113", "text": "Factors influencing secretion of gastrin can be divided into 2 categories: [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5114", "text": "In the  Zollinger\u2013Ellison syndrome , gastrin is produced at excessive levels, often by a  gastrinoma  gastrin-producing tumor, mostly benign of the  duodenum  or the  pancreas . To investigate for hypergastrinemia high blood levels of gastrin, a \" pentagastrin  test\" can be performed. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5115", "text": "In autoimmune  gastritis , the immune system attacks the  parietal cells  leading to  hypochlorhydria  low stomach acid secretion.  This results in an elevated gastrin level in an attempt to compensate for increased pH in the stomach.  Eventually, all the parietal cells are lost and  achlorhydria  results leading to a loss of  negative feedback  on gastrin secretion. Plasma gastrin concentration is elevated in virtually all individuals with  mucolipidosis type IV  (mean 1507 pg/mL; range 400-4100 pg/mL) (normal 0-200 pg/mL) secondary to a constitutive achlorhydria. This finding facilitates the diagnosis of patients with this neurogenetic disorder. [ 18 ]  Additionally, elevated gastrin levels may be present in chronic gastritis resulting from  H. pylori  infection. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5116", "text": "Its existence was first suggested in 1905 by the British physiologist John Sydney Edkins, [ 20 ] [ 21 ]  and gastrins were isolated in 1964 by  Hilda Tracy  and  Roderic Alfred Gregory  at the  University of Liverpool . [ 22 ]  In 1964 the structure of gastrin was determined. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5117", "text": "The  gastrointestinal tract  ( GI tract ,  digestive tract ,  alimentary canal ) is the tract or passageway of the  digestive system  that leads from the  mouth  to the  anus . The GI tract contains all the major  organs  of the digestive system, in humans and other animals, including the  esophagus ,  stomach , and  intestines . Food taken in through the mouth is  digested  to extract  nutrients  and absorb  energy , and the waste expelled at the anus as  feces .  Gastrointestinal  is an adjective meaning of or pertaining to the stomach and intestines."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5118", "text": "Most animals  have a \"through-gut\" or complete digestive tract. Exceptions are more primitive ones:  sponges  have small pores ( ostia ) throughout their body for digestion and a larger dorsal pore ( osculum ) for excretion,  comb jellies  have both a ventral mouth and dorsal anal pores, while  cnidarians  and  acoels  have a single pore for both digestion and excretion. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5119", "text": "The human gastrointestinal tract consists of the  esophagus ,  stomach, and intestines, and is divided into the upper and lower gastrointestinal tracts. [ 3 ]  The GI tract includes all structures between the  mouth  and the  anus , [ 4 ]  forming a continuous passageway that includes the main organs of digestion, namely, the  stomach ,  small intestine , and  large intestine . The complete  human digestive system  is made up of the gastrointestinal tract plus the accessory organs of digestion (the  tongue ,  salivary glands ,  pancreas ,  liver  and  gallbladder ). [ 5 ]  The tract may also be divided into  foregut ,  midgut , and  hindgut , reflecting the  embryological  origin of each segment. The whole human GI tract is about nine meters (30 feet) long at  autopsy . It is considerably shorter in the living body because the intestines, which are tubes of  smooth muscle tissue , maintain constant  muscle tone  in a halfway-tense state but can relax in spots to allow for local distention and  peristalsis . [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5120", "text": "The gastrointestinal tract contains the  gut microbiota , with some 1,000 different  strains  of  bacteria  having diverse roles in the maintenance of  immune health  and  metabolism , and many other  microorganisms . [ 8 ] [ 9 ] [ 10 ]  Cells of the GI tract release  hormones  to help regulate the digestive process. These  digestive hormones , including  gastrin ,  secretin ,  cholecystokinin , and  ghrelin , are mediated through either  intracrine  or  autocrine  mechanisms, indicating that the cells releasing these hormones are conserved structures throughout  evolution . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5121", "text": "The structure and function can be described both as  gross anatomy  and as  microscopic anatomy  or  histology . The tract itself is divided into upper and lower tracts, and the intestines  small  and  large  parts. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5122", "text": "The upper gastrointestinal tract consists of the  mouth ,  pharynx ,  esophagus ,  stomach , and  duodenum . [ 13 ] \nThe exact demarcation between the upper and lower tracts is the  suspensory muscle of the duodenum . This differentiates the embryonic borders between the foregut and midgut, and is also the division commonly used by clinicians to describe  gastrointestinal bleeding  as being of either \"upper\" or \"lower\" origin. Upon  dissection , the duodenum may appear to be a unified organ, but it is divided into four segments based on function, location, and internal anatomy. The four segments of the duodenum are as follows (starting at the stomach, and moving toward the jejunum):  bulb , descending, horizontal, and ascending. The suspensory muscle attaches the superior border of the ascending duodenum to the  jejunum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5123", "text": "The suspensory muscle is an important anatomical landmark that shows the formal division between the duodenum and the jejunum, the first and second parts of the small intestine, respectively. [ 14 ]  This is a thin muscle which is derived from the  embryonic   mesoderm ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5124", "text": "The lower gastrointestinal tract includes most of the  small intestine  and all of the  large intestine . [ 15 ]  In  human anatomy , the  intestine  ( bowel  or  gut ; Greek:  \u00e9ntera ) is the segment of the gastrointestinal tract extending from the pyloric sphincter of the  stomach  to the  anus  and as in other mammals, consists of two segments: the  small intestine  and the  large intestine . In humans, the small intestine is further subdivided into the  duodenum ,  jejunum , and  ileum  while the large intestine is subdivided into the  cecum , ascending, transverse, descending, and sigmoid  colon ,  rectum , and  anal canal . [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5125", "text": "The  small intestine  begins at the  duodenum  and is a tubular structure, usually between 6 and 7 m long. [ 18 ]  Its  mucosal  area in an adult human is about 30\u00a0m 2  (320\u00a0sq\u00a0ft). [ 19 ]  The combination of the  circular folds , the villi, and the microvilli increases the absorptive area of the mucosa about 600-fold, making a total area of about 250\u00a0m 2  (2,700\u00a0sq\u00a0ft) for the entire small intestine. [ 20 ]  Its main function is to absorb the products of digestion (including carbohydrates, proteins, lipids, and vitamins) into the bloodstream. There are three major divisions:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5126", "text": "The  large intestine , also called the colon, forms an arch starting at the  cecum  and ending at the  rectum  and  anal canal . It also includes the  appendix , which is attached to the  cecum . Its length is about 1.5 m, and the area of the mucosa in an adult human is about 2\u00a0m 2  (22\u00a0sq\u00a0ft). [ 19 ]  Its main function is to absorb water and salts. The colon is further divided into:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5127", "text": "The gut is an  endoderm -derived structure. At approximately the sixteenth day of human development, the  embryo  begins to fold  ventrally  (with the embryo's ventral surface becoming  concave ) in two directions: the sides of the embryo fold in on each other and the head and tail fold toward one another. The result is that a piece of the  yolk sac , an  endoderm -lined structure in contact with the  ventral  aspect of the embryo, begins to be pinched off to become the primitive gut. The yolk sac remains connected to the gut tube via the  vitelline duct . Usually, this structure regresses during development; in cases where it does not, it is known as  Meckel's diverticulum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5128", "text": "During  fetal  life, the primitive gut is gradually patterned into three segments:  foregut ,  midgut , and  hindgut . Although these terms are often used in reference to segments of the primitive gut, they are also used regularly to describe regions of the definitive gut as well."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5129", "text": "Each segment of the gut is further specified and gives rise to specific gut and gut-related structures in later development. Components derived from the gut proper, including the  stomach  and  colon , develop as swellings or dilatations in the cells of the primitive gut. In contrast, gut-related derivatives \u2014 that is, those structures that derive from the primitive gut but are not part of the gut proper, in general, develop as out-pouchings of the primitive gut. The blood vessels supplying these structures remain constant throughout development. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5130", "text": "The gastrointestinal tract has a form of general histology with some differences that reflect the specialization in functional anatomy. [ 22 ]  The GI tract can be divided into four concentric layers in the following order:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5131", "text": "The mucosa is the innermost layer of the gastrointestinal tract. The mucosa surrounds the  lumen , or open space within the tube. This layer comes in direct contact with digested food ( chyme ). The mucosa is made up of:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5132", "text": "The mucosae are highly specialized in each organ of the gastrointestinal tract to deal with the different conditions. The most variation is seen in the epithelium."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5133", "text": "The submucosa consists of a dense irregular layer of connective tissue with large blood vessels, lymphatics, and nerves branching into the mucosa and  muscularis externa . It contains the  submucosal plexus , an  enteric nervous plexus , situated on the inner surface of the  muscularis externa ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5134", "text": "The  muscular layer  consists of an inner circular layer and a  longitudinal  outer layer. The circular layer prevents food from traveling backward and the longitudinal layer shortens the tract. The layers are not truly longitudinal or circular, rather the layers of muscle are helical with different pitches. The inner circular is helical with a steep pitch and the outer longitudinal is helical with a much shallower pitch. [ 23 ]  Whilst the muscularis externa is similar throughout the entire gastrointestinal tract, an exception is the stomach which has an additional inner oblique muscular layer to aid with grinding and mixing of food. The muscularis externa of the stomach is composed of the inner oblique layer, middle circular layer, and the outer longitudinal layer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5135", "text": "Between the circular and longitudinal muscle layers is the  myenteric plexus . This controls peristalsis. Activity is initiated by the pacemaker cells, (myenteric  interstitial cells of Cajal ). The gut has intrinsic peristaltic activity ( basal electrical rhythm ) due to its self-contained enteric nervous system. The rate can be modulated by the rest of the  autonomic nervous system . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5136", "text": "The coordinated contractions of these layers is called  peristalsis  and propels the food through the tract. Food in the GI tract is called a bolus (ball of food) from the mouth down to the stomach. After the stomach, the food is partially digested and semi-liquid, and is referred to as  chyme . In the large intestine, the remaining semi-solid substance is referred to as  faeces . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5137", "text": "The outermost layer of the gastrointestinal tract consists of several layers of  connective tissue ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5138", "text": "Intraperitoneal  parts of the GI tract are covered with  serosa . These include most of the  stomach , first part of the  duodenum , all of the  small intestine ,  caecum  and  appendix ,  transverse colon ,  sigmoid colon  and  rectum . In these sections of the gut, there is a clear boundary between the gut and the surrounding tissue. These parts of the tract have a  mesentery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5139", "text": "Retroperitoneal  parts are covered with  adventitia . They blend into the surrounding tissue and are fixed in position. For example, the retroperitoneal section of the duodenum usually passes through the  transpyloric plane . These include the  esophagus ,  pylorus  of the stomach, distal  duodenum ,  ascending colon ,  descending colon  and  anal canal . In addition, the  oral cavity  has adventitia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5140", "text": "Approximately 20,000 protein coding genes are expressed in human cells and 75% of these genes are expressed in at least one of the different parts of the digestive organ system. [ 24 ] [ 25 ]  Over 600 of these genes are more specifically expressed in one or more parts of the GI tract and the corresponding proteins have functions related to digestion of food and uptake of nutrients. Examples of specific proteins with such functions are  pepsinogen PGC  and the  lipase LIPF , expressed in  chief cells , and gastric  ATPase ATP4A  and  gastric intrinsic factor GIF , expressed in  parietal cells  of the stomach mucosa. Specific proteins expressed in the stomach and duodenum involved in defence include  mucin  proteins, such as  mucin 6  and  intelectin-1 . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5141", "text": "The time taken for food to transit through the gastrointestinal tract varies on multiple factors, including age, ethnicity, and gender. [ 27 ] [ 28 ]  Several techniques have been used to measure transit time, including radiography following a  barium -labeled meal, breath  hydrogen  analysis,  scintigraphic  analysis following a  radiolabeled  meal, [ 29 ]  and simple ingestion and spotting of  corn kernels . [ 30 ]  It takes 2.5 to 3 hours for 50% of the contents to leave the stomach. [ medical citation needed ]  The rate of digestion is also dependent of the material being digested, as food composition from the same meal may leave the stomach at different rates. [ 31 ]  Total emptying of the stomach takes around 4\u20135 hours, and transit through the colon takes 30 to 50 hours. [ 29 ] [ 32 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5142", "text": "The gastrointestinal tract forms an important part of the  immune system . [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5143", "text": "The surface area of the digestive tract is estimated to be about 32 square meters, or about half a badminton court. [ 19 ]  With such a large exposure (more than three times larger than the  exposed surface of the skin ), these immune components function to prevent pathogens from entering the blood and lymph circulatory systems. [ 35 ]  Fundamental components of this protection are provided by the  intestinal mucosal barrier , which is composed of physical, biochemical, and immune elements elaborated by the intestinal mucosa. [ 36 ]  Microorganisms also are kept at bay by an extensive immune system comprising the  gut-associated lymphoid tissue  (GALT)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5144", "text": "There are additional factors contributing to protection from pathogen invasion. For example, low  pH  (ranging from 1 to 4) of the stomach is fatal for many  microorganisms  that enter it. [ 37 ]  Similarly,  mucus  (containing  IgA   antibodies ) neutralizes many pathogenic microorganisms. [ 38 ]  Other factors in the GI tract contribution to immune function include  enzymes  secreted in the  saliva  and  bile ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5145", "text": "Beneficial bacteria also can contribute to the homeostasis of the gastrointestinal immune system. For example,  Clostridia , one of the most predominant bacterial groups in the GI tract, play an important role in influencing the dynamics of the gut's immune system. [ 39 ]  It has been demonstrated that the intake of a high fiber diet could be responsible for the induction of  T-regulatory cells  (Tregs). This is due to the production of  short-chain fatty acids  during the fermentation of plant-derived nutrients  such as  butyrate  and  propionate .  Basically, the butyrate induces the differentiation of Treg cells by enhancing  histone H3   acetylation  in the promoter and conserved non-coding sequence regions of the  FOXP3  locus, thus regulating the  T cells , resulting in the reduction of the inflammatory response and allergies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5146", "text": "The large intestine contains multiple types of  bacteria  that can break down molecules the human body cannot process alone, [ 40 ]  demonstrating a  symbiotic  relationship. These bacteria are responsible for gas production at  host\u2013pathogen interface , which is released as  flatulence . Intestinal bacteria can also participate in biosynthesis reactions. For example, certain strains in the large intestine produce vitamin B 12 ; [ 41 ]  an essential compound in humans for things like DNA synthesis and red blood cell production. [ 42 ]  However, the primary function of the large intestine is water absorption from digested material (regulated by the  hypothalamus ) and the reabsorption of  sodium  and nutrients. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5147", "text": "Beneficial  intestinal bacteria  compete with potentially harmful  bacteria  for space and \"food\", as the intestinal tract has limited resources. A ratio of 80\u201385% beneficial to 15\u201320% potentially harmful bacteria is proposed for maintaining  homeostasis . [ citation needed ]  An imbalanced ratio results in  dysbiosis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5148", "text": "Enzymes  such as  CYP3A4 , along with the  antiporter  activities, are also instrumental in the intestine's role of  drug metabolism  in the detoxification of  antigens  and  xenobiotics . [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5149", "text": "In most  vertebrates , including  amphibians ,  birds ,  reptiles ,  egg-laying mammals , and some  fish , the gastrointestinal tract ends in a  cloaca  and not an  anus . In the cloaca, the  urinary system  is fused with the genito-anal pore.  Therians  (all mammals that do not lay eggs, including humans) possess separate anal and uro-genital openings. The females of the subgroup  Placentalia  have even separate urinary and genital openings."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5150", "text": "During  early development , the asymmetric position of the bowels and inner organs is initiated (see also  axial twist theory )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5151", "text": "Ruminants  show many specializations for digesting and  fermenting  tough plant material, consisting of  additional stomach compartments ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5152", "text": "Many birds and other animals have a specialised stomach in the digestive tract called a  gizzard  used for grinding up food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5153", "text": "Another feature found in a range of animals is the  crop . In birds this is found as a pouch alongside the esophagus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5154", "text": "In 2020, the oldest known fossil digestive tract, of an extinct wormlike organism in the  Cloudinidae  was discovered; it lived during the late  Ediacaran   period  about 550 million years ago. [ 45 ] [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5155", "text": "A through-gut (one with both mouth and anus) is thought to have evolved within the  nephrozoan  clade of  Bilateria , after their ancestral ventral orifice (single, as in  cnidarians  and  acoels ; re-evolved in nephrozoans like  flatworms ) stretched antero-posteriorly, before the middle part of the stretch would get narrower and closed fully, leaving an anterior orifice (mouth) and a posterior orifice (anus plus  genital opening ). A stretched gut without the middle part closed is present in another branch of bilaterians, the extinct  proarticulates . This and the  amphistomic  development (when both mouth and anus develop from the gut stretch in the embryo) present in some nephrozoans (e.g.  roundworms ) are considered to support this hypothesis. [ 47 ] [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5156", "text": "There are many diseases and conditions that can affect the gastrointestinal system, including  infections ,  inflammation  and  cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5157", "text": "Various  pathogens , such as  bacteria  that cause  foodborne illnesses , can induce  gastroenteritis  which results from  inflammation  of the stomach and small intestine.  Antibiotics  to treat such bacterial infections can decrease the  microbiome  diversity of the gastrointestinal tract, and further enable inflammatory mediators. [ 49 ]  Gastroenteritis is the most common disease of the GI tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5158", "text": "Diverticular disease  is a condition that is very common in older people in industrialized countries.  It usually affects the large intestine but has been known to affect the small intestine as well.   Diverticulosis  occurs when pouches form on the intestinal wall.  Once the pouches become inflamed it is known as  diverticulitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5159", "text": "Inflammatory bowel disease  is an inflammatory condition affecting the bowel walls, and includes the subtypes  Crohn's disease  and  ulcerative colitis . While Crohn's can affect the entire gastrointestinal tract, ulcerative colitis is limited to the large intestine. Crohn's disease is widely regarded as an  autoimmune disease . Although ulcerative colitis is often treated as though it were an autoimmune disease, there is no consensus that it actually is such."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5160", "text": "Functional gastrointestinal disorders  the most common of which is  irritable bowel syndrome . Functional constipation and  chronic functional abdominal pain  are other functional disorders of the intestine that have physiological causes but do not have identifiable structural, chemical, or infectious pathologies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5161", "text": "Several symptoms can indicate problems with the gastrointestinal tract, including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5162", "text": "Gastrointestinal surgery  can often be performed in the outpatient setting.  In the United States in 2012, operations on the digestive system accounted for 3 of the 25 most common ambulatory surgery procedures and constituted 9.1 percent of all outpatient ambulatory surgeries. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5163", "text": "Various methods of imaging the gastrointestinal tract include the  upper  and  lower gastrointestinal series :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5164", "text": "Intestines from animals other than humans are used in a number of ways.  From each species of  livestock  that is a source of  milk , a corresponding  rennet  is obtained from the intestines of milk-fed  calves .   Pig  and  calf  intestines are eaten, and pig intestines are used as  sausage  casings. Calf intestines supply  calf-intestinal alkaline phosphatase  (CIP), and are used to make  goldbeater's skin .\nOther uses are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5165", "text": "The  gastrointestinal hormones  (or  gut hormones ) constitute a group of  hormones  secreted by  enteroendocrine cells  in the  stomach ,  pancreas , and  small intestine  that control various functions of the digestive organs. Later studies showed that most of the gut peptides, such as  secretin ,  cholecystokinin  or  substance P , were found to play a role of  neurotransmitters  and  neuromodulators  in the central and peripheral nervous systems. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5166", "text": "Enteroendocrine cells do not form glands but are spread throughout the digestive tract. They exert their autocrine and paracrine actions that integrate gastrointestinal function. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5167", "text": "The gastrointestinal hormones [ 3 ]  can be divided into three main groups based upon their  chemical structure ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5168", "text": "Ghrelin  is a peptide hormone released from the stomach and liver and is often referred to as the \"hunger hormone\" since high levels of it are found in individuals that are fasting. Ghrelin agonistic treatments can be used to treat illnesses such as anorexia and loss of appetites in cancer patients. Ghrelin treatments for obesity are still under intense scrutiny and no conclusive evidence has been reached. This hormone stimulates growth hormone release.\n Amylin  controls glucose homeostasis and gastric motility"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5169", "text": "Glucose-dependent insulinotropic polypeptide  possesses an acute influence on food intake through its effects on adipocytes"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5170", "text": "Oxyntomodulin  plays a role in controlling acid secretion and satiation"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5171", "text": "The  gastrointestinal wall  of the  gastrointestinal tract  is made up of four layers of specialised tissue. From the inner cavity of the gut (the  lumen ) outwards, these are the  mucosa , the  submucosa , the  muscular layer  and the  serosa  or  adventitia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5172", "text": "The mucosa is the innermost layer of the gastrointestinal tract. It surrounds the lumen of the tract and comes into direct contact with digested food ( chyme ). The mucosa itself is made up of three layers: [ 1 ]  the  epithelium , where most digestive, absorptive and secretory processes occur; the  lamina propria , a layer of  connective tissue , and the  muscularis mucosae , a thin layer of  smooth muscle ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5173", "text": "The submucosa contains nerves including the  submucous plexus  (also called Meissner's plexus), blood vessels and elastic fibres with collagen, that stretches with increased capacity but maintains the shape of the intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5174", "text": "The muscular layer surrounds the submucosa. It comprises layers of  smooth muscle  in longitudinal and circular orientation that also helps with continued bowel movements ( peristalsis ) and the movement of digested material out of and along the gut. In between the two layers of muscle lies the  myenteric plexus  (also called plexus)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5175", "text": "The  serosa / adventitia  are the final layers. These are made up of loose  connective tissue  and coated in  mucus  so as to prevent any friction damage from the intestine rubbing against other tissue. The serosa is present if the tissue is  within the peritoneum , and the adventitia if the tissue is  retroperitoneal ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5176", "text": "When viewed under the  microscope , the gastrointestinal wall has a consistent general form, but with certain parts differing along its course."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5177", "text": "The mucosa is the innermost layer of the gastrointestinal tract. It surrounds the cavity ( lumen ) of the tract and comes into direct contact with digested food ( chyme ). The mucosa is made up of three layers: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5178", "text": "The epithelium, the most exposed part of the mucosa, is a  glandular epithelium  with many  goblet cells . Goblet cells secrete  mucus , which lubricates the passage of food along and protects the intestinal wall from digestive enzymes. In the small intestine,  villi  are folds of the mucosa that increase the surface area of the intestine. The villi contain a  lacteal , a vessel connected to the  lymph system  that aids in the removal of  lipids  and tissue fluids.  Microvilli  are present on the epithelium of a villus and further increase the surface area over which absorption can take place. Numerous  intestinal glands  as pocket-like invaginations are present in the underlying tissue. In the large intestines, villi are absent and a flat surface with thousands of glands is observed. Underlying the epithelium is the lamina propria, which contains myofibroblasts, blood vessels, nerves, and several different immune cells, and the  muscularis mucosa  which is a layer of smooth muscle that aids in the action of continued  peristalsis  and  catastalsis  along the gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5179", "text": "The epithelial lining of the mucosa, differs along the gastrointestinal tract. [ 1 ]  The epithelium is described as stratified if it consists of multiple layers of cells, and simple if it is made up of one layer of cells. Terms used to describe the shape of the cells in it - columnar if column-shaped, and squamous if flat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5180", "text": "Transition between the different types of epithelium occurs at  the junction between the oesophagus and stomach ; between the  stomach and duodenum , between the  ileum and caecum , and at the  pectinate line  of the  anus . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5181", "text": "The submucosa consists of a dense and irregular layer of connective tissue with  blood vessels , lymphatics, and nerves branching into the mucosa and muscular layer. It contains the  submucous plexus , and  enteric nervous plexus , situated on the inner surface of the muscular layer. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5182", "text": "The  muscular layer  consists of two layers of muscle, the inner and outer layer. [ 3 ]  The muscle of the inner layer is arranged in circular rings around the tract, whereas the muscle of the outer layer is arranged longitudinally. The stomach has an extra layer, an inner oblique muscular layer. [ 1 ]  Between the two muscle layers is the  myenteric plexus  (Auerbach's plexus). This controls peristalsis. Activity is initiated by the pacemaker cells ( interstitial cells of Cajal ). The gut has intrinsic peristaltic activity ( basal electrical rhythm ) due to its self-contained enteric nervous system. The rate can, of course, be modulated by the rest of the  autonomic nervous system ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5183", "text": "The layers are not truly longitudinal or circular, rather the layers of muscle are helical with different pitches. The inner circular is helical with a steep pitch and the outer longitudinal is helical with a much shallower pitch."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5184", "text": "The coordinated contractions of these layers is called  peristalsis  and propels the food through the tract. Food in the GI tract is called a  bolus  (ball of food) from the mouth down to the stomach. After the stomach, the food is partially digested and semi-liquid, and is referred to as  chyme . In the large intestine the remaining semi-solid substance is referred to as faeces. The circular muscle layer prevents food from travelling backward and the longitudinal layer shortens the tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5185", "text": "The thickness of the muscular layer varies in each part of the tract:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5186", "text": "The outermost layer of the gastrointestinal wall consists of several layers of  connective tissue  and is either of  serosa  (below the diaphragm) or  adventitia  above the diaphragm. [ 4 ] [ 1 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5187", "text": "Regions of the gastrointestinal tract within the peritoneum (called  Intraperitoneal ) are covered with  serosa . This structure consists of connective tissue covered by a simple squamous epithelium, called the mesothelium, which reduces frictional forces during digestive movements. The intraperitoneal regions include most of the  stomach , first part of the  duodenum , all of the  small intestine ,  caecum  and  appendix ,  transverse colon ,  sigmoid colon  and  rectum . In these sections of the gut there is clear boundary between the gut and the surrounding tissue. These parts of the tract have a  mesentery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5188", "text": "Regions of the gastrointestinal tract behind the peritoneum (called  retroperitoneal ) are covered with  adventitia . They blend into the surrounding tissue and are fixed in position (for example, the retroperitoneal section of the duodenum usually passes through the  transpyloric plane ). The retroperitoneal regions include the  oral cavity ,  esophagus ,  pylorus  of the stomach, distal  duodenum ,  ascending colon ,  descending colon  and  anal canal . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5189", "text": "The gastrointestinal wall can be affected in a number of conditions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5190", "text": "An  ulcer  is something that's eroded through the epithelium of the wall. Ulcers that affect the tract include  peptic ulcers  and  perforated ulcer  is one that has eroded completely through the layers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5191", "text": "The gastrointestinal wall is inflamed in a number of conditions. This is called  esophagitis ,  gastritis ,  duodenitis ,  ileitis , and  colitis  depending on the parts affected. It can be due to infections or other conditions, including  coeliac disease , and  inflammatory bowel disease  affects the layers of the gastrointestinal tract in different ways.  Ulcerative colitis  involves the colonic mucosa.  Crohn's disease  may produce inflammation in all layers in any part of the gastrointestinal tract and so can result in transmural  fistulae ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5192", "text": "Invasion of tumours through the layers of the gastrointestinal wall is used in  staging  of tumour spread. This affects treatment and prognosis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5193", "text": "The normal thickness of the small intestinal wall is 3\u20135\u00a0mm, [ 6 ]  and 1\u20135\u00a0mm in the large intestine. [ 7 ]  Focal, irregular and asymmetrical gastrointestinal wall thickening suggests a malignancy. [ 7 ]  Segmental or diffuse gastrointestinal wall thickening is most often due to ischemic, inflammatory or infectious disease. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5194", "text": "A  gastrolith , also called a  stomach stone  or  gizzard stone , is a  rock  held inside a  gastrointestinal tract . Gastroliths in some species are retained in the muscular  gizzard  and used to grind food in animals lacking suitable grinding  teeth . In other species the rocks are ingested and pass through the digestive system and are frequently replaced. The  grain size  depends upon the size of the animal and the gastrolith's role in digestion. Other species use gastroliths as  ballast . [ 1 ]  Particles ranging in size from  sand  to  cobble  have been documented."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5195", "text": "Gastrolith comes from the  Greek  \u03b3\u03b1\u03c3\u03c4\u03ae\u03c1 ( gast\u0113r ), meaning \"stomach\", and \u03bb\u03af\u03b8\u03bf\u03c2 ( lithos ), meaning \"stone\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5196", "text": "Among living  vertebrates , gastroliths are common among  crocodiles ,  alligators ,  herbivorous   birds ,  seals  and  sea lions . Domestic  fowl  require access to  grit .  Stones swallowed by  ostriches  can exceed a length of 10 centimetres (3.9\u00a0in) [ citation needed ] . Apparent microgastroliths have also been found in frog tadpoles. [ 2 ]  Ingestion of silt and gravel by tadpoles of various  anuran  (frog) species has been observed to improve buoyancy control. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5197", "text": "Some  extinct  animals such as  sauropod   dinosaurs  appear to have used stones to grind tough plant matter. A rare example of this is the Early Cretaceous theropod  Caudipteryx  zoui  from northeastern China, which was discovered with a series of small stones, interpreted as gastroliths, in the area of its skeleton that would have corresponded with its abdominal region. Aquatic animals, such as  plesiosaurs , may have used them as ballast, to help balance themselves or to decrease their buoyancy, as  crocodiles  do. [ 3 ]  Research indicates that the presence of gastroliths in  elasmosaurid plesiosaurs  differs from that of the  short-necked plesiosaurs .  While some  fossil  gastroliths are rounded and polished, many stones in living birds are not polished at all. Gastroliths associated with  dinosaur  fossils can weigh several kilograms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5198", "text": "Certain crayfish store gastroliths in their stomachs. Crayfish living in freshwater store these gastroliths as the presence of calcium is limited in freshwater. These gastroliths serve as a calcium source for molting. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5199", "text": "In 1906,  George Reber Weiland  reported the presence of worn and polished quartz pebbles associated with the remains of  plesiosaurs  and  sauropod   dinosaurs  and interpreted these stones as gastroliths. [ 7 ]  In 1907,  Barnum Brown  found gravel in close association with the fossil remains of the duck-billed  hadrosaur   Claosaurus  and interpreted it as gastroliths.  Brown was among the first paleontologists to recognize that dinosaurs used gastroliths in their digestive systems to aid in the grinding of food. [ 8 ]   Other paleontologists over the years were unconvinced. In 1932,  Friedrich von Huene  found stones in Late Triassic sediments, in association with the fossil remains of the  prosauropod   Sellosaurus  and interpreted them as gastroliths. [ 9 ]   In 1934, the Howe Quarry, a fossil location in northwestern Wyoming also yielded dinosaur bones with their associated gastroliths.  In 1942,  William Lee Stokes  recognized the presence of gastroliths in the remains of sauropod dinosaurs recovered from Late Jurassic  strata ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5200", "text": "Geologists  usually require several pieces of evidence before they will accept that a rock was used by a dinosaur to aid its  digestion .  First, it should be rounded on all edges (and some are polished) because inside a dinosaur's gizzard any genuine gastrolith would have been acted upon by other stones and fibrous materials in a process similar to the action of a  rock tumbler . Second, the stone must be unlike the rock found in its geological vicinity, i.e., its geologic context. Many gastroliths have been found in fine grained lake, mud, and swamp deposits. These environs are calm water deposits and could not carry pebbles and cobbles (unlike a river or beach). Oliver Wings also argues that the stone must be found with the  fossils  of the dinosaur which ingested it. [ citation needed ]  It is this last criterion that causes trouble in identification, as smooth stones found without context can (possibly erroneously in some cases) be dismissed as having been polished by water or wind.  Christopher H. Whittle  (1988,9) pioneered  scanning electron microscope  analysis of wear patterns on gastroliths. Wings (2003) found that  ostrich  gastroliths would be deposited outside the skeleton if the carcass was deposited in an aquatic environment for as little as a few days following death. He concludes that this is likely to hold true for all birds (with the possible exception of  moa ) due to their air-filled bones which would cause a carcass deposited in water to float for the time it needs to rot sufficiently to allow gastroliths to escape."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5201", "text": "Gastroliths can be distinguished from stream- or beach-rounded rocks by several criteria: gastroliths are highly polished on the higher surfaces, with little or no polish in depressions or crevices, often strongly resembling the surface of worn animal teeth. Stream- or beach-worn rocks, particularly in a high-impact environment, show less polishing on higher surfaces, often with many small pits or cracks on these higher surfaces. Finally, highly polished gastroliths often show long microscopic rilles, defined by Whittle as \"longitudinal gashes, deeper than one millimeter and longer than one centimeter at a magnification of 50 times\". [ 10 ]  These are presumably caused by contact with stomach acid. Since most gastroliths were scattered when the animal died and many entered a stream or beach environment, some gastroliths show a mixture of these wear features. Others were undoubtedly swallowed by other dinosaurs and highly polished gastroliths may have been swallowed repeatedly."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5202", "text": "None of the gastroliths examined in a 2001 study of  Cedarosaurus  gastroliths had the \"soapy\" texture popularly used to distinguish gastroliths from other types of clast. [ 11 ]  The researchers dismissed using a soapy texture to identify gastroliths as \"unreliable\". [ 11 ]  Gastroliths tended to be universally dull, although the colors represented were varied including black, dark brown, purplish red and grey-blue. [ 11 ]  Reflectance values greater than 50% are very diagnostic for identifying gastroliths. [ 11 ]  Clasts from beaches and streams tended to have reflectance values of less than 35%. [ 12 ]  Less than ten percent of beach clasts have reflectance values lying between 50 and 80%. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5203", "text": "The American Museum of Natural History  Photograph # 311488 demonstrates an articulated skeleton of a  Psittacosaurus mongoliensis , from the  Ondai Sair Formation , Lower  Cretaceous   Period  of  Mongolia , showing a collection of about 40 gastroliths inside the  rib cage , about midway between shoulder and pelvis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5204", "text": "Gastroliths have sometimes been called  Morrison stones  because they are often found in the  Morrison Formation  (named after the town of  Morrison , west of  Denver ,  Colorado ), a late  Jurassic  formation roughly 150 million years old. Some gastroliths are made of  petrified wood . Most known instances of preserved  sauropod  gastroliths are from  Jurassic  animals. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5205", "text": "The  Early Cretaceous   Cedar Mountain Formation  of Central  Utah  is full of highly polished red and black  cherts , and other rounded quartzose clasts, which may partly represent gastroliths. The cherts may themselves contain fossils of ancient animals, such as corals. These stones do not appear to be associated with stream deposits and are rarely more than fist-sized, which is consistent with the idea that they are gastroliths."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5206", "text": "Most known instances of preserved  sauropod  gastroliths are from  Jurassic  animals. [ 14 ]  The largest known gastroliths found in association with sauropod skeletons are approximately ten centimeters in length. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5207", "text": "In 2001  Frank Sanders ,  Kim Manley , and  Kenneth Carpenter  published a study on 115 gastroliths discovered in association with a  Cedarosaurus  specimen. [ 16 ]  The stones were identified as gastroliths on the basis of their tight spatial distribution, partial matrix support, and an edge-on orientation indicative of their being deposited while the carcass still had soft tissue. [ 16 ]  Their high surface  reflectance  values are consistent with other known dinosaur gastroliths. [ 16 ]   Nearly all of the  Cedarosaurus  gastroliths were found within a .06 m volume [ clarification needed ]  of space in the gut region of the skeleton. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5208", "text": "The total mass of the gastroliths themselves was 7 kilograms (15\u00a0lb). [ 18 ]  Most were less than 10 millilitres (0.35\u00a0imp\u00a0fl\u00a0oz; 0.34\u00a0US\u00a0fl\u00a0oz) in volume. [ 19 ]  The least massive clast was 0.1 grams (0.0035\u00a0oz) and the most was 715 grams (25.2\u00a0oz), with most of them being toward the smaller end of that range. [ 19 ]  The clasts tended to be close to spherical in shape, although the largest specimens were also the most irregular. [ 19 ]  The largest gastroliths contributed the most to the total surface area of the set. [ 20 ]  Some gastroliths were so large and irregularly shaped that they may have been difficult to swallow. [ 20 ]  The gastroliths were mostly composed of  chert , with some  sandstone ,  siltstone , and  quartzite  clasts also included. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5209", "text": "Since some of the most irregular gastroliths are also the largest, it is unlikely that they were ingested by accident. [ 20 ]   Cedarosaurus  may have found irregular clasts to be attractive potential gastroliths or was not selective about shape. [ 20 ]  The clasts were generally of dull coloration, suggesting that color was not a major factor for the sauropod's decision making. [ 16 ]  The high surface area to volume ratio of the largest clasts suggests that the gastroliths may have broken down ingested plant material by grinding or crushing it. [ 13 ]  The sandstone clasts tended to be fragile and some broke in the process of collection. [ 11 ]  The sandstone gastroliths may have been rendered fragile after deposition by loss of cement caused by the external chemical environment. [ 21 ]  If the clasts had been that fragile while the animal was alive, they probably rolled and tumbled in the digestive tract. [ 13 ]  If they were more robust, they could have served as part of a ball-mill system. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5210", "text": "Paleontologists  and geologists are researching new methods of identifying gastroliths that have been found disassociated from animal remains, because of the important information they can provide, if indeed they are trace fossils. If the validity of such gastroliths can be verified, it may be possible to trace gastrolithic rocks back to their original source area where the dinosaur first swallowed the rock. This may provide important information on how dinosaurs migrated. Because the number of suspected gastroliths is substantial, they might provide significant new information and insights into the lives and behaviour of dinosaurs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5211", "text": "The  gastrovascular cavity  is the primary organ of  digestion  and  circulation  in two major animal phyla: the  Coelenterates  or cnidarians (including  jellyfish  and  corals ) and  Platyhelminthes  (flatworms). The cavity may be extensively branched into a system of canals. In cnidarians, the gastrovascular system is also known as the  coelenteron , and is commonly known as a \"blind gut\" or \"blind sac\", since food enters and waste exits through the same orifice."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5212", "text": "The  radially symmetrical  cnidarians have a sac-like body in two distinct layers, the epidermis and  gastrodermis , with a jellylike layer called the  mesoglea  between. Extracellular digestion takes place within the central cavity of the sac-like body.  This cavity has only one opening to the outside which, in most cnidarians, is surrounded by  tentacles  for capturing prey."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5213", "text": "This article about anatomy of the phylum  Cnidaria  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5214", "text": "This  flatworm - (or platyhelminth-) related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5215", "text": "Gulp: Adventures on the Alimentary Canal  is a nonfiction work by science author  Mary Roach , published in April 2013 by  W.W. Norton & Company ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5216", "text": "The book covers 17 topics:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5217", "text": "Gut microbiota ,  gut microbiome , or  gut flora  are the  microorganisms , including  bacteria ,  archaea ,  fungi , and  viruses , that live in the  digestive tracts  of  animals . [ 1 ] [ 2 ]  The gastrointestinal  metagenome  is the aggregate of all the  genomes  of the gut  microbiota . [ 3 ] [ 4 ]  The  gut  is the main location of the  human microbiome . [ 5 ]  The gut microbiota has broad impacts, including effects on  colonization , resistance to  pathogens , maintaining the  intestinal epithelium , metabolizing dietary and pharmaceutical compounds, controlling immune function, and even behavior through the  gut\u2013brain axis . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5218", "text": "The microbial composition of the gut microbiota varies across regions of the digestive tract. The  colon  contains the highest microbial density of any human-associated microbial community studied so far, representing between 300 and 1000 different  species . [ 6 ]  Bacteria are the largest and to date, best studied component and 99% of gut bacteria come from about 30 or 40 species. [ 7 ]  About 55% of the dry mass of  feces  is bacteria. [ 8 ]  Over 99% of the bacteria in the gut are  anaerobes , but in the  cecum ,  aerobic bacteria  reach high densities. [ 5 ]  It is estimated that the human gut microbiota have around a hundred times as many  genes  as there are in the  human genome ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5219", "text": "In humans, the gut microbiota has the highest numbers and species of bacteria compared to other areas of the body. [ 9 ]  The approximate number of bacteria composing the gut microbiota is about 10 13 \u201310 14  (10,000 to 100,000 billion). [ 10 ]   In humans, the gut flora is established at birth and gradually transitions towards a state resembling that of adults by the age of two, [ 11 ]  coinciding with the development and maturation of the  intestinal epithelium  and  intestinal mucosal barrier . This barrier is essential for supporting a symbiotic relationship with the gut flora while providing protection against pathogenic organisms. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5220", "text": "The relationship between some gut microbiota and humans is not merely  commensal  (a non-harmful coexistence), but rather a  mutualistic  relationship. [ 5 ] :\u200a700\u200a  Some human gut microorganisms benefit the host by  fermenting   dietary fiber  into  short-chain fatty acids  (SCFAs), such as  acetic acid  and  butyric acid , which are then absorbed by the host. [ 9 ] [ 14 ]  Intestinal  bacteria  also play a role in synthesizing certain  B vitamins  and  vitamin K  as well as metabolizing  bile acids ,  sterols , and  xenobiotics . [ 5 ] [ 14 ]  The systemic importance of the SCFAs and other compounds they produce are like  hormones  and the gut flora itself appears to function like an  endocrine organ . [ 14 ]  Dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions. [ 9 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5221", "text": "The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes. [ 9 ] [ 15 ]  A  systematic review  from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of probiotic bacteria and identified those that had the most potential to be useful for certain  central nervous system disorders . [ 16 ]  It should also be highlighted that the Mediterranean diet, rich in vegetables and fibers, stimulates the activity and growth of beneficial bacteria for the brain. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5222", "text": "The microbial composition of the gut microbiota varies across the digestive tract. In the  stomach  and  small intestine , relatively few species of bacteria are generally present. [ 6 ] [ 18 ]   Fungi ,  protists ,  archaea , and  viruses  are also present in the gut flora, but less is known about their activities. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5223", "text": "Many species in the gut have not been studied outside of their hosts because they cannot be  cultured . [ 18 ] [ 7 ] [ 20 ]  While there are a small number of core microbial species shared by most individuals, populations of microbes can vary widely. [ 21 ]  Within an individual, their microbial populations stay fairly constant over time, with some alterations occurring due to changes in lifestyle, diet and age. [ 6 ] [ 22 ]  The  Human Microbiome Project  has set out to better describe the  microbiota  of the human gut and other body locations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5224", "text": "The four dominant  bacterial phyla  in the human gut are  Bacillota  (Firmicutes),  Bacteroidota ,  Actinomycetota , and  Pseudomonadota . [ 23 ]  Most bacteria belong to the genera  Bacteroides ,  Clostridium ,  Faecalibacterium , [ 6 ] [ 7 ]   Eubacterium ,  Ruminococcus ,  Peptococcus ,  Peptostreptococcus , and  Bifidobacterium . [ 6 ] [ 7 ]  Other genera, such as  Escherichia  and  Lactobacillus , are present to a lesser extent. [ 6 ]  Species from the genus  Bacteroides  alone constitute about 30% of all bacteria in the gut, suggesting that this genus is especially important in the functioning of the host. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5225", "text": "Fungal genera that have been detected in the gut include  Candida ,  Saccharomyces ,  Aspergillus ,  Penicillium ,  Rhodotorula ,  Trametes ,  Pleospora ,  Sclerotinia ,  Bullera , and  Galactomyces , among others. [ 24 ] [ 25 ]   Rhodotorula  is most frequently found in individuals with  inflammatory bowel disease  while  Candida  is most frequently found in individuals with hepatitis\u00a0B cirrhosis and chronic hepatitis\u00a0B. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5226", "text": "Due to the prevalence of fungi in the natural environment, determining which genera and species are permanent members of the gut  mycobiome  is difficult. [ 26 ] [ 27 ]  Research is underway as to whether  Penicillium  is a permanent or transient member of the gut flora, obtained from dietary sources such as  cheese , though several species in the genus are known to survive at temperatures around 37\u00b0C, around the same as the  core body temperature . [ 27 ]   Saccharomyces cerevisiae , brewer's yeast, is known to reach the intestines after being ingested and can be responsible for the condition  auto-brewery syndrome  in cases where it is overabundant, [ 27 ] [ 28 ] [ 29 ]  while  Candida albicans  is likely a permanent member, and is believed to be acquired at birth through  vertical transmission . [ 30 ] [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5227", "text": "Archaea  constitute another large class of gut flora which are important in the metabolism of the bacterial products of fermentation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5228", "text": "Industrialization  is associated with changes in the microbiota and the reduction of diversity could drive certain species to extinction; in 2018, researchers proposed a  biobank  repository of human microbiota. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5229", "text": "An  enterotype  is a classification of living organisms based on its bacteriological  ecosystem  in the human gut microbiome not dictated by age, gender, body weight, or national divisions. [ 32 ]  There are indications that long-term diet influences enterotype. [ 33 ]  Three human enterotypes have been proposed, [ 32 ] [ 34 ]  but their value has been questioned. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5230", "text": "Due to the high acidity of the  stomach , most microorganisms cannot survive there. The main bacteria of the  gastric microbiota  belong to five major phyla:  Firmicutes ,  Bacteroidetes ,  Actinobacteria ,  Fusobacteriota , and  Proteobacteria . The dominant genera are  Prevotella ,  Streptococcus ,  Veillonella ,  Rothia  , and  Haemophilus . [ 36 ]  The interaction between the pre-existing gastric microbiota with the introduction of  H.\u00a0pylori  may influence  disease progression . [ 36 ]  When there is a presence of  H.\u00a0pylori  it becomes the dominant of the microbiota. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5231", "text": "The small intestine contains a trace amount of microorganisms due to the proximity and influence of the stomach.  Gram-positive   cocci  and  rod-shaped bacteria  are the predominant microorganisms found in the small intestine. [ 5 ]  However, in the distal portion of the small intestine alkaline conditions support gram-negative bacteria of the  Enterobacteriaceae . [ 5 ]  The bacterial flora of the small intestine aid in a wide range of intestinal functions. The bacterial flora provide regulatory signals that enable the development and utility of the gut. Overgrowth of bacteria in the small intestine can lead to intestinal failure. [ 39 ]  In addition the large intestine contains the largest bacterial ecosystem in the human body. [ 5 ]  About 99% of the large intestine and feces flora are made up of obligate anaerobes such as  Bacteroides  and  Bifidobacterium. [ 40 ]  Factors that disrupt the microorganism population of the large intestine include antibiotics, stress, and parasites. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5232", "text": "Bacteria make up most of the flora in the  colon [ 41 ]  and accounts for 60%  of  fecal  nitrogen. [ 6 ]  This fact makes feces an ideal source of gut flora for any tests and experiments by extracting the nucleic acid from fecal specimens, and bacterial 16S rRNA gene sequences are generated with bacterial primers. This form of testing is also often preferable to more invasive techniques, such as biopsies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5233", "text": "Five  phyla  dominate the intestinal microbiota:  Bacteroidota ,  Bacillota  (Firmicutes),  Actinomycetota ,  Pseudomonadota , and  Verrucomicrobiota \u00a0\u2013 with Bacteroidota and Bacillota constituting 90% of the composition. [ 42 ]  Somewhere between 300 [ 6 ]  and 1000 different  species  live in the gut, [ 18 ]  with most estimates at about 500. [ 43 ] [ 44 ]  However, it is probable that 99% of the bacteria come from about 30 or 40 species, with  Faecalibacterium prausnitzii  (phylum firmicutes) being the most common species in healthy adults. [ 7 ] [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5234", "text": "Research suggests that the relationship between gut  flora  and humans is not merely  commensal  (a non-harmful coexistence), but rather is a  mutualistic ,  symbiotic  relationship. [ 18 ]  Though people can survive with no gut flora, [ 43 ]  the microorganisms perform a host of useful functions, such as  fermenting  unused energy substrates, training the  immune system  via end products of metabolism like  propionate  and  acetate , preventing growth of harmful species, regulating the development of the gut, producing vitamins for the host (such as  biotin  and  vitamin K ), and producing hormones to direct the host to store fats. [ 5 ]  Extensive modification and imbalances of the gut microbiota and its microbiome or gene collection are associated with obesity. [ 46 ]  However, in certain conditions, some species are thought to be capable of causing  disease  by causing  infection  or increasing  cancer  risk for the host. [ 6 ] [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5235", "text": "Fungi  and  protists  also make up a part of the gut flora, but less is known about their activities. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5236", "text": "The  human virome  is mostly  bacteriophages . [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5237", "text": "There are common patterns of microbiome composition evolution during life. [ 49 ]  In general, the diversity of microbiota composition of fecal samples is significantly higher in adults than in children, although interpersonal differences are higher in children than in adults. [ 50 ]  Much of the maturation of microbiota into an adult-like configuration happens during the first three years of life. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5238", "text": "As the microbiome composition changes, so does the composition of bacterial proteins produced in the gut. In adult microbiomes, a high prevalence of enzymes involved in  fermentation ,  methanogenesis  and the metabolism of  arginine ,  glutamate ,  aspartate  and  lysine  have been found. In contrast, in infant microbiomes the dominant enzymes are involved in  cysteine  metabolism and fermentation pathways. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5239", "text": "Gut microbiome composition depends on the geographic origin of populations. Variations in a trade-off of  Prevotella , the representation of the  urease  gene, and the representation of genes encoding glutamate synthase/degradation or other enzymes involved in amino acids degradation or vitamin biosynthesis show significant differences between populations from the US,  Malawi , or Amerindian origin. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5240", "text": "The US population has a high representation of enzymes encoding the degradation of  glutamine  and enzymes involved in vitamin and  lipoic acid  biosynthesis; whereas Malawi and Amerindian populations have a high representation of enzymes encoding glutamate synthase and they also have an overrepresentation of  \u03b1-amylase  in their microbiomes. As the US population has a diet richer in fats than Amerindian or Malawian populations which have a corn-rich diet, the diet is probably the main determinant of the gut bacterial composition. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5241", "text": "Further studies have indicated a large difference in the composition of microbiota between European and rural African children. The fecal bacteria of children from  Florence  were compared to that of children from the small rural village of  Boulpon  in  Burkina Faso . The diet of a typical child living in this village is largely lacking in fats and animal proteins and rich in polysaccharides and plant proteins. The fecal bacteria of European children were dominated by  Firmicutes  and showed a marked reduction in biodiversity, while the fecal bacteria of the Boulpon children was dominated by  Bacteroidetes . The increased biodiversity and different composition of the gut microbiome in African populations may aid in the digestion of normally indigestible plant polysaccharides and also may result in a reduced incidence of non-infectious colonic diseases. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5242", "text": "On a smaller scale, it has been shown that sharing numerous common environmental exposures in a family is a strong determinant of individual microbiome composition. This effect has no genetic influence and it is consistently observed in culturally different populations. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5243", "text": "Malnourished  children have less mature and less diverse gut microbiota than healthy children, and changes in the microbiome associated with nutrient scarcity can in turn be a pathophysiological cause of malnutrition. [ 52 ] [ 53 ]  Malnourished children also typically have more potentially pathogenic gut flora, and more  yeast  in their mouths and throats. [ 54 ]  Altering diet may lead to changes in gut microbiota composition and diversity. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5244", "text": "Researchers with the American Gut Project and Human Microbiome Project found that twelve microbe families varied in abundance based on the race or ethnicity of the individual. The strength of these associations is limited by the small sample size: the American Gut Project collected data from 1,375 individuals, 90% of whom were white. [ 56 ]  The Healthy Life in an Urban Setting (HELIUS) study in Amsterdam found that those of Dutch ancestry had the highest level of gut microbiota diversity, while those of South Asian and  Surinamese  descent had the lowest diversity. The study results suggested that individuals of the same race or ethnicity have more similar microbiomes than individuals of different racial backgrounds. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5245", "text": "As of 2020, at least two studies have demonstrated a link between an individual's  socioeconomic status  (SES) and their gut microbiota. A study in  Chicago  found that individuals in higher SES neighborhoods had greater microbiota diversity. People from higher SES neighborhoods also had more abundant  Bacteroides  bacteria. Similarly, a study of  twins  in the United Kingdom found that higher SES was also linked with a greater gut diversity. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5246", "text": "As of 2023, a study suggests that antibiotics, especially those used in the treatment of broad-spectrum bacterial infections, have negative effects on the gut microbiota. [ 57 ]  The study also states that there are many experts on intestinal health concerned that antibody usage has reduced the diversity of the gut microbiota, many of the strains are lost, and if there is a re-emergence of the bacteria, is gradual and long-term.  [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5247", "text": "The establishment of a gut flora is crucial to the health of an adult, as well as the functioning of the gastrointestinal tract. [ 59 ]  In humans, a gut flora similar to an adult's is formed within one to two years of birth as microbiota are acquired through parent-to-child transmission and transfer from food, water, and other environmental sources. [ 60 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5248", "text": "The traditional view of the  gastrointestinal tract  of a normal  fetus  is that it is sterile, although this view has been challenged in the past few years. [ timeframe? ] [ 61 ]  Multiple lines of evidence have begun to emerge that suggest there may be bacteria in the intrauterine environment. In humans, research has shown that microbial colonization may occur in the fetus [ 62 ]  with one study showing  Lactobacillus  and  Bifidobacterium  species were present in placental biopsies. [ 63 ]  Several  rodent studies  have demonstrated the presence of bacteria in the amniotic fluid and placenta, as well as in the  meconium  of babies born by sterile cesarean section. [ 64 ] [ 65 ]  In another study, researchers administered a culture of bacteria orally to pregnant mice, and detected the bacteria in the offspring, likely resulting from transmission between the digestive tract and amniotic fluid via the blood stream. [ 66 ]  However, researchers caution that the source of these intrauterine bacteria, whether they are alive, and their role, is not yet understood. [ 67 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5249", "text": "During birth and rapidly thereafter, bacteria from the mother and the surrounding environment colonize the infant's gut. [ 12 ]  The exact sources of bacteria are not fully understood, but may include the birth canal, other people (parents, siblings, hospital workers), breastmilk, food, and the general environment with which the infant interacts. [ 68 ]  Research has shown that the microbiome of babies born  vaginally  differs significantly from that of babies delivered by  caesarean section  and that vaginally born babies got most of their gut bacteria from their mother, while the microbiota of babies born by caesarean section had more bacteria associated with hospital environments. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5250", "text": "During the first year of life, the composition of the gut flora is generally simple and changes a great deal with time and is not the same across individuals. [ 12 ]  The initial bacterial population are generally  facultative anaerobic organisms ; investigators believe that these initial colonizers decrease the oxygen concentration in the gut, which in turn allows obligately anaerobic bacteria like  Bacteroidota ,  Actinomycetota , and  Bacillota  to become established and thrive. [ 12 ]  Breast-fed babies become dominated by  bifidobacteria , possibly due to the contents of  bifidobacterial growth factors  in breast milk, and by the fact that breast milk carries prebiotic components, allowing for healthy bacterial growth. [ 63 ] [ 70 ]  Breast milk also contains higher levels of Immunoglobulin A (IgA) to help with the tolerance and regulation of the baby's immune system. [ 71 ]  In contrast, the microbiota of  formula-fed  infants is more diverse, with high numbers of  Enterobacteriaceae ,  enterococci , bifidobacteria,  Bacteroides , and clostridia. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5251", "text": "Caesarean section,  antibiotics , and  formula feeding  may alter the gut microbiome composition. [ 63 ]  Children treated with antibiotics have less stable, and less diverse floral communities. [ 73 ]  Caesarean sections have been shown to be disruptive to mother-offspring transmission of bacteria, which impacts the overall health of the offspring by raising risks of disease such as  celiac disease ,  asthma , and  type \u00a0 1 diabetes . [ 63 ]  This further evidences the importance of a healthy gut microbiome. Various methods of microbiome restoration are being explored, typically involving exposing the infant to maternal vaginal contents, and oral probiotics. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5252", "text": "When the study of gut flora began in 1995, [ 74 ]  it was thought to have three key roles: direct defense against  pathogens , fortification of host defense by its role in developing and maintaining the  intestinal epithelium  and inducing antibody production there, and metabolizing otherwise indigestible compounds in food.  Subsequent work discovered its role in training the developing immune system, and yet further work focused on its role in the  gut\u2013brain axis . [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5253", "text": "The gut flora community plays a direct role in defending against pathogens by fully colonising the space, making use of all available nutrients, and by secreting compounds known as  cytokines  that kill or inhibit unwelcome organisms that would compete for nutrients with it. [ 76 ]  Different strains of gut bacteria cause the production of different cytokines. Cytokines are chemical compounds produced by our immune system for initiating the  inflammatory response  against infections. Disruption of the gut flora allows competing organisms like  Clostridioides difficile  to become established that otherwise are kept in abeyance. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5254", "text": "In humans, a gut flora similar to an adult's is formed within one to two years of birth. [ 12 ]  As the gut flora gets established, the lining of the intestines \u2013 the intestinal epithelium and the intestinal mucosal barrier that it secretes \u2013 develop as well, in a way that is tolerant to, and even supportive of, commensalistic microorganisms to a certain extent and also provides a barrier to pathogenic ones. [ 12 ]  Specifically,  goblet cells  that produce the mucosa proliferate, and the mucosa layer thickens, providing an outside mucosal layer in which \"friendly\" microorganisms can anchor and feed, and an inner layer that even these organisms cannot penetrate. [ 12 ] [ 13 ]  Additionally, the development of  gut-associated lymphoid tissue  (GALT), which forms part of the intestinal epithelium and which detects and reacts to pathogens, appears and develops during the time that the gut flora develops and established. [ 12 ]  The GALT that develops is tolerant to gut flora species, but not to other microorganisms. [ 12 ]  GALT also normally becomes tolerant to food to which the infant is exposed, as well as digestive products of food, and gut flora's  metabolites  (molecules formed from metabolism) produced from food. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5255", "text": "The human  immune system  creates  cytokines  that can drive the immune system to produce inflammation in order to protect itself, and that can tamp down the immune response to maintain  homeostasis  and allow healing after insult or injury. [ 12 ]  Different bacterial species that appear in gut flora have been shown to be able to drive the immune system to create cytokines selectively; for example  Bacteroides fragilis  and some  Clostridia  species appear to drive an anti-inflammatory response, while some  segmented filamentous bacteria  drive the production of inflammatory cytokines. [ 12 ] [ 77 ]  Gut flora can also regulate the production of  antibodies  by the immune system. [ 12 ] [ 78 ]  One function of this regulation is to cause  B cells  to class switch to  IgA . In most cases B cells need activation from  T helper cells  to induce  class switching ; however, in another pathway, gut flora cause  NF-kB  signaling by intestinal epithelial cells which results in further signaling molecules being secreted. [ 79 ]  These signaling molecules interact with B cells to induce class switching to IgA. [ 79 ]  IgA is an important type of antibody that is used in mucosal environments like the gut. It has been shown that IgA can help diversify the gut community and helps in getting rid of bacteria that cause inflammatory responses. [ 80 ]  Ultimately, IgA maintains a healthy environment between the host and gut bacteria. [ 80 ]  These cytokines and antibodies can have effects outside the gut, in the lungs and other tissues. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5256", "text": "The immune system can also be altered due to the gut bacteria's ability to produce  metabolites  that can affect cells in the immune system. For example  short-chain fatty acids  (SCFA) can be produced by some gut bacteria through  fermentation . [ 81 ]  SCFAs stimulate a rapid increase in the production of innate immune cells like  neutrophils ,  basophils  and  eosinophils . [ 81 ]  These cells are part of the innate immune system that try to limit the spread of infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5257", "text": "Without gut flora, the human body would be unable to utilize some of the undigested  carbohydrates  it consumes, because some types of gut flora have  enzymes  that human cells lack for breaking down certain  polysaccharides . [ 14 ]  Rodents raised in a  sterile  environment and lacking in gut flora need to eat 30% more  calories  just to remain the same weight as their normal counterparts. [ 14 ]  Carbohydrates that humans cannot  digest  without bacterial help include certain  starches ,  fiber ,  oligosaccharides , and  sugars  that the body failed to digest and absorb like  lactose  in the case of  lactose intolerance  and  sugar alcohols ,  mucus  produced by the gut, and proteins. [ 9 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5258", "text": "Bacteria turn carbohydrates they ferment into  short-chain fatty acids  by a form of fermentation called  saccharolytic fermentation . [ 44 ]  Products include  acetic acid ,  propionic acid  and  butyric acid . [ 7 ] [ 44 ]  These materials can be used by host cells, providing a major source of energy and nutrients. [ 44 ]  Gases (which are involved in  signaling [ 86 ]  and may cause  flatulence ) and  organic acids , such as  lactic acid , are also produced by fermentation. [ 7 ]  Acetic acid is used by  muscle , propionic acid facilitates  liver  production of  ATP , and butyric acid provides energy to gut cells. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5259", "text": "Gut flora also synthesize vitamins like  biotin  and  folate , and facilitate absorption of  dietary minerals , including magnesium, calcium, and iron. [ 6 ] [ 22 ]   Methanobrevibacter smithii  is unique because it is not a species of bacteria, but rather a member of  domain   Archaea , and is the most abundant  methane -producing archaeal species in the human gastrointestinal microbiota. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5260", "text": "Gut microbiota also serve as a source of vitamins K and B 12 , which are not produced by the body or produced in little amount. [ 88 ] [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5261", "text": "Bacteria that degrade cellulose (such as  Ruminococcus ) are prevalent among  great apes , ancient human societies,  hunter-gatherer  communities, and even modern rural populations. However, they are rare in industrialized societies. Human-associated strains have acquired genes that can degrade specific plant fibers such as  maize ,  rice , and  wheat . Bacterial strains found in primates can also degrade  chitin , a polymer abundant in insects, which are part of the diet of many nonhuman  primates . The decline of these bacteria in the human gut were\u00a0likely influenced by the shift toward western lifestyles. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5262", "text": "The human  metagenome  (i.e., the genetic composition of an individual and all microorganisms that reside on or within the individual's body) varies considerably between individuals. [ 91 ] [ 92 ]  Since the total number of microbial cells in the human body (over 100\u00a0trillion) greatly outnumbers  Homo sapiens  cells (tens of trillions), [ note 1 ] [ 91 ] [ 93 ]  there is considerable potential for interactions between drugs and an individual's microbiome, including: drugs altering the composition of the  human microbiome ,  drug metabolism  by microbial enzymes modifying the drug's  pharmacokinetic  profile, and microbial drug metabolism affecting a drug's clinical efficacy and  toxicity  profile. [ 91 ] [ 92 ] [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5263", "text": "Apart from carbohydrates, gut microbiota can also metabolize other  xenobiotics  such as drugs,  phytochemicals , and food toxicants. More than 30 drugs have been shown to be metabolized by gut microbiota. [ 95 ]  The microbial metabolism of drugs can sometimes inactivate the drug. [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5264", "text": "The gut microbiota is an enriched community that contains diverse genes with huge biochemical capabilities to modify drugs, especially those taken by mouth. [ 97 ]  Gut microbiota can affect drug metabolism via direct and indirect mechanisms. [ 98 ]  The direct mechanism is mediated by the microbial enzymes that can modify the chemical structure of the administered drugs. [ 99 ]  Conversely, the indirect pathway is mediated by the microbial metabolites which affect the expression of host metabolizing enzymes such as  cytochrome P450 . [ 100 ] [ 98 ]  The effects of the gut microbiota on the pharmacokinetics and bioavailability of the drug have been investigated a few decades ago. [ 101 ] [ 102 ] [ 103 ]  These effects can be varied; it could activate the inactive drugs such as lovastatin, [ 104 ]  inactivate the active drug such as  digoxin [ 105 ]  or induce drug toxicity as in  irinotecan . [ 106 ]  Since then, the impacts of the gut microbiota on the pharmacokinetics of many drugs were heavily studied. [ 107 ] [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5265", "text": "The human gut microbiota plays a crucial role in modulating the effect of the administered drugs on the human. Directly, gut microbiota can synthesize and release a series of enzymes with the capability to metabolize drugs such as microbial biotransformation of L-dopa by decarboxylase and dehydroxylase enzymes. [ 99 ]  On the contrary, gut microbiota may also alter the metabolism of the drugs by modulating the host drug metabolism. This mechanism can be mediated by microbial metabolites or by modifying host metabolites which in turn change the expression of host metabolizing enzymes. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5266", "text": "A large number of studies have demonstrated the metabolism of over 50 drugs by the gut microbiota. [ 107 ] [ 98 ]  For example, lovastatin (a cholesterol-lowering agent) which is a lactone prodrug is partially activated by the human gut microbiota forming active acid hydroxylated metabolites. [ 104 ]  Conversely, digoxin (a drug used to treat Congestive Heart Failure) is inactivated by a member of the gut microbiota (i.e.  Eggerthella   lanta ). [ 108 ]   Eggerthella   lanta  has a cytochrome-encoding operon up-regulated by digoxin and associated with digoxin-inactivation. [ 108 ]  Gut microbiota can also modulate the efficacy and toxicity of chemotherapeutic agents such as irinotecan. [ 109 ]  This effect is derived from the microbiome-encoded \u03b2-glucuronidase enzymes which recover the active form of the irinotecan causing gastrointestinal toxicity. [ 110 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5267", "text": "This microbial community in the gut has a huge biochemical capability to produce distinct secondary metabolites that are sometimes produced from the metabolic conversion of dietary foods such as  fibers , endogenous biological compounds such as  indole  or  bile acids . [ 111 ] [ 112 ] [ 113 ]  Microbial metabolites especially short chain fatty acids (SCFAs) and secondary bile acids (BAs) play important roles for the human in health and disease states. [ 114 ] [ 115 ] [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5268", "text": "One of the most important bacterial metabolites produced by the gut microbiota is secondary bile acids (BAs). [ 113 ]  These metabolites are produced by the bacterial biotransformation of the primary bile acids such as cholic acid  (CA) and chenodeoxycholic acid (CDCA) into secondary bile acids (BAs) lithocholic acid (LCA) and deoxy cholic acid (DCA) respectively. [ 117 ]  Primary bile acids which are synthesized by hepatocytes and stored in the gall bladder possess hydrophobic characters. These metabolites are subsequently metabolized by the gut microbiota into secondary metabolites with increased hydrophobicity. [ 117 ]  Bile salt hydrolases (BSH) which are conserved across gut microbiota phyla such as  Bacteroides ,  Firmicutes , and  Actinobacteria  responsible for the first step of secondary bile acids metabolism. [ 117 ]  Secondary bile acids (BAs) such as DCA and LCA have been demonstrated to inhibit both  Clostridioides difficile  germination and outgrowth. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5269", "text": "The gut microbiota is important for maintaining homeostasis in the intestine. Development of  intestinal cancer  is associated with an imbalance in the natural microflora (dysbiosis). [ 118 ]   The secondary bile acid  deoxycholic acid  is associated with alterations of the microbial community that lead to increased intestinal carcinogenesis. [ 118 ]   Increased exposure of the colon to secondary bile acids resulting from dysbiosis can cause  DNA damage , and such damage can produce carcinogenic mutations in cells of the colon. [ 119 ]  The high density of bacteria in the  colon  (about 10 12  per ml.) that are subject to dysbiosis compared to the relatively low density in the  small intestine  (about 10 2  per ml.) may account for the greater than 10-fold higher incidence of cancer in the colon compared to the small intestine. [ 119 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5270", "text": "The gut microbiota contributes to digestion and immune modulation, as it plays a role in the gut-brain axis, where microbial metabolites such as short-chain fatty acids and neurotransmitters influence brain function and behavior. The gut\u2013brain axis is the biochemical signaling that takes place between the  gastrointestinal tract  and the  central nervous system . [ 75 ]  That term has been expanded to include the role of the gut flora in the interplay; the term \"microbiome\u2013\u2013brain axis\" is sometimes used to describe paradigms explicitly including the gut flora. [ 75 ] [ 120 ] [ 121 ]  Broadly defined, the gut\u2013brain axis includes the central nervous system,  neuroendocrine  and  neuroimmune  systems including the  hypothalamic\u2013pituitary\u2013adrenal axis  (HPA axis), sympathetic and parasympathetic arms of the  autonomic nervous system  including the  enteric nervous system , the  vagus nerve , and the gut  microbiota . [ 75 ] [ 121 ]  Studies show links between gut dysbiosis and mental health conditions, indicating a complex interaction that impacts mood and cognitive functions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5271", "text": "A  systematic review  from 2016 examined the preclinical and small human trials that have been conducted with certain commercially available strains of  probiotic  bacteria and found that among those tested,  Bifidobacterium  and  Lactobacillus   genera  ( B. longum ,  B. breve ,  B. infantis ,  L. helveticus ,  L. rhamnosus ,  L. plantarum , and  L. casei ), had the most potential to be useful for certain  central nervous system disorders . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5272", "text": "Altering the numbers of gut bacteria, for example by taking  broad-spectrum antibiotics , may affect the host's health and ability to digest food. [ 122 ]  Antibiotics can cause  antibiotic-associated diarrhea  by irritating the  bowel  directly, changing the levels of microbiota, or allowing  pathogenic  bacteria to grow. [ 7 ]  Another harmful effect of antibiotics is the increase in numbers of  antibiotic-resistant bacteria  found after their use, which, when they invade the host, cause illnesses that are difficult to treat with antibiotics. [ 122 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5273", "text": "Changing the numbers and species of gut microbiota can reduce the body's ability to ferment carbohydrates and metabolize  bile  acids and may cause  diarrhea . Carbohydrates that are not broken down may absorb too much water and cause runny stools, or lack of SCFAs produced by gut microbiota could cause diarrhea. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5274", "text": "A reduction in levels of native bacterial species also disrupts their ability to inhibit the growth of harmful species such as  C. difficile  and  Salmonella  Kedougou, and these species can get out of hand, though their overgrowth may be incidental and not be the true cause of diarrhea. [ 6 ] [ 7 ] [ 122 ]  Emerging treatment protocols for C. difficile infections involve fecal microbiota transplantation of donor feces (see  Fecal transplant ). [ 123 ]  Initial reports of treatment describe success rates of 90%, with few side effects. Efficacy is speculated to result from restoring bacterial balances of bacteroides and firmicutes classes of bacteria. [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5275", "text": "The composition of the gut microbiome also changes in severe illnesses, due not only to antibiotic use but also to such factors as  ischemia  of the gut, failure to eat, and  immune compromise . Negative effects from this have led to interest in  selective digestive tract decontamination , a treatment to kill only pathogenic bacteria and allow the re-establishment of healthy ones. [ 125 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5276", "text": "Antibiotics alter the population of the microbiota in the  gastrointestinal tract , and this may change the intra-community metabolic interactions, modify caloric intake by using carbohydrates, and globally affect host metabolic, hormonal, and immune homeostasis. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5277", "text": "There is reasonable evidence that taking probiotics containing  Lactobacillus  species may help prevent antibiotic-associated diarrhea and that taking probiotics with  Saccharomyces  (e.g.,  Saccharomyces boulardii   ) may help to prevent  Clostridioides difficile  infection following systemic antibiotic treatment. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5278", "text": "The gut microbiota of a woman changes as  pregnancy  advances, with the changes similar to those seen in  metabolic syndromes  such as diabetes. The change in gut microbiota causes no ill effects. The newborn's gut microbiota resemble the mother's first-trimester samples. The diversity of the microbiome decreases from the first to third trimester, as the numbers of certain species go up. [ 63 ] [ 128 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5279", "text": "Probiotics  contain live  microorganisms . When consumed, they are believed to provide health benefits by altering the microbiome composition. [ 129 ] [ 130 ] [ 131 ]  Current research explores using probiotics as a way to restore the microbial balance of the  intestine  by stimulating the immune system and inhibiting pro-inflammatory  cytokines . [ 129 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5280", "text": "With regard to gut microbiota,  prebiotics  are typically non-digestible,  fiber  compounds that pass undigested through the upper part of the  gastrointestinal tract  and stimulate the growth or activity of advantageous gut flora by acting as  substrate  for them. [ 44 ] [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5281", "text": "Synbiotics  refers to  food ingredients  or  dietary supplements  combining probiotics and prebiotics in a form of  synergism . [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5282", "text": "The term \"pharmabiotics\" is used in various ways, to mean:  pharmaceutical formulations  (standardized manufacturing that can obtain regulatory approval as a drug) of probiotics,  prebiotics , or  synbiotics ; [ 134 ]  probiotics that have been genetically engineered or otherwise optimized for best performance (shelf life, survival in the digestive tract, etc.); [ 135 ]  and the natural products of gut flora metabolism (vitamins, etc.). [ 136 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5283", "text": "There is some evidence that treatment with some probiotic strains of bacteria may be effective in  irritable bowel syndrome , [ 137 ] [ 138 ]  abdominal bloating  [ 139 ] and  chronic idiopathic constipation . Those organisms most likely to result in a decrease of symptoms have included:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5284", "text": "Feces of about 10\u201315% of people consistently floats in toilet water ('floaters'), while the rest produce feces that sinks ('sinkers') and production of gas causes feces to float. [ 143 ]  While conventional mice often produce 'floaters', gnotobiotic germfree mice no gut microbiota (bred in germfree isolator) produce 'sinkers', and gut microbiota colonization in germfree mice leads to food transformation to microbial biomass and enrichment of multiple gasogenic bacterial species that turns the 'sinkers' into 'floaters'. [ 144 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5285", "text": "Tests for whether non-antibiotic drugs may impact human gut-associated bacteria were performed by  in vitro  analysis on more than 1000 marketed drugs against 40 gut bacterial strains, demonstrating that 24% of the drugs inhibited the growth of at least one of the bacterial strains. [ 145 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5286", "text": "Bacteria in the digestive tract can contribute to and be affected by disease in various ways. The presence or overabundance of some kinds of bacteria may contribute to inflammatory disorders such as  inflammatory bowel disease . [ 6 ]  Additionally, metabolites from certain members of the gut flora may influence host signalling pathways, contributing to disorders such as  obesity  and  colon cancer . [ 6 ]  Some gut bacteria may also cause  infections  and  sepsis , for example when they are allowed to  pass from the gut into the rest of the body . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5287", "text": "Helicobacter pylori  infection can initiate formation of stomach ulcers when the bacteria penetrate the stomach epithelial lining, then causing an  inflammatory phagocytotic response . [ 146 ]  In turn, the inflammation damages parietal cells which release excessive  hydrochloric acid  into the stomach and produce less of the protective mucus. [ 147 ]  Injury to the stomach lining, leading to  ulcers , develops when gastric acid overwhelms the defensive properties of cells and inhibits endogenous  prostaglandin  synthesis,  reduces mucus and bicarbonate secretion, reduces mucosal blood flow, and lowers resistance to injury. [ 147 ]  Reduced protective properties of the stomach lining increase vulnerability to further injury and ulcer formation by stomach acid,  pepsin , and bile salts. [ 146 ] [ 147 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5288", "text": "Normally- commensal bacteria  can harm the host if they extrude from the intestinal tract. [ 12 ] [ 13 ]   Translocation , which occurs when bacteria leave the gut through its  mucosal  lining, can occur in a number of different diseases. [ 13 ]  If the gut is perforated, bacteria invade the  interstitium , causing a potentially fatal  infection . [ 5 ] :\u200a715"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5289", "text": "The two main types of  inflammatory bowel diseases ,  Crohn's disease  and  ulcerative colitis , are  chronic  inflammatory disorders of the gut; the causes of these diseases are unknown and issues with the gut flora and its relationship with the host have been implicated in these conditions. [ 15 ] [ 148 ] [ 149 ] [ 150 ]  Additionally, it appears that interactions of gut flora with the gut\u2013brain axis have a role in IBD, with physiological stress mediated through the  hypothalamic\u2013pituitary\u2013adrenal axis  driving changes to intestinal epithelium and the gut flora in turn releasing factors and metabolites that trigger signaling in the  enteric nervous system  and the  vagus nerve . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5290", "text": "The diversity of gut flora appears to be significantly diminished in people with inflammatory bowel diseases compared to healthy people; additionally, in people with ulcerative colitis, Proteobacteria and Actinobacteria appear to dominate; in people with Crohn's,  Enterococcus faecium  and several Proteobacteria appear to be over-represented. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5291", "text": "There is reasonable evidence that correcting gut flora imbalances by taking probiotics with  Lactobacilli  and  Bifidobacteria  can reduce visceral pain and gut inflammation in IBD. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5292", "text": "Irritable bowel syndrome  is a result of stress and chronic activation of the HPA axis; its symptoms include abdominal pain, changes in bowel movements, and an increase in proinflammatory cytokines. Overall, studies have found that the luminal and mucosal microbiota are changed in irritable bowel syndrome individuals, and these changes can relate to the type of irritation such as diarrhea or  constipation . Also, there is a decrease in the diversity of the microbiome with low levels of fecal Lactobacilli and Bifidobacteria, high levels of facultative  anaerobic bacteria  such as  Escherichia coli , and increased ratios of Firmicutes: Bacteroidetes. [ 121 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5293", "text": "With asthma, two hypotheses have been posed to explain its rising prevalence in the developed world. The  hygiene hypothesis  posits that children in the developed world are not exposed to enough microbes and thus may contain lower prevalence of specific bacterial taxa that play protective roles. [ 151 ]  The second hypothesis focuses on the  Western pattern diet , which lacks  whole grains  and  fiber  and has an overabundance of  simple sugars . [ 15 ]  Both hypotheses converge on the role of short-chain fatty acids (SCFAs) in  immunomodulation . These bacterial fermentation metabolites are involved in immune signalling that prevents the triggering of asthma and lower SCFA levels are associated with the disease. [ 151 ] [ 152 ]  Lacking protective genera such as  Lachnospira ,  Veillonella ,  Rothia  and  Faecalibacterium  has been linked to reduced SCFA levels. [ 151 ]  Further, SCFAs are the product of bacterial fermentation of fiber, which is low in the Western pattern diet. [ 15 ] [ 152 ]  SCFAs offer a link between gut flora and immune disorders, and as of 2016, this was an active area of research. [ 15 ]  Similar hypotheses have also been posited for the rise of food and other allergies. [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5294", "text": "The connection between the gut microbiota and  diabetes mellitus type\u00a01  has also been linked to SCFAs, such as  butyrate  and acetate. Diets yielding butyrate and acetate from bacterial fermentation show increased  T reg  expression. [ 154 ]   T reg  cells  downregulate   effector T cells , which in turn reduces the  inflammatory response  in the gut. [ 155 ]  Butyrate is an energy source for colon cells. butyrate-yielding diets thus decrease  gut permeability  by providing sufficient energy for the formation of  tight junctions . [ 156 ]  Additionally, butyrate has also been shown to decrease insulin resistance, suggesting gut communities low in butyrate-producing microbes may increase chances of acquiring  diabetes mellitus type\u00a02 . [ 157 ]  Butyrate-yielding diets may also have potential  colorectal cancer  suppression effects. [ 156 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5295", "text": "The gut flora have been implicated in obesity and  metabolic syndrome  due to a key role in the digestive process; the Western pattern diet appears to drive and maintain changes in the gut flora that in turn change how much energy is derived from food and how that energy is used. [ 150 ] [ 158 ]  One aspect of a  healthy diet  that is often lacking in the  Western-pattern diet  is fiber and other complex carbohydrates that a healthy gut flora require flourishing; changes to gut flora in response to a Western-pattern diet appear to increase the amount of energy generated by the gut flora which may contribute to obesity and metabolic syndrome. [ 127 ]  There is also evidence that microbiota influence eating behaviours based on the preferences of the microbiota, which can lead to the host consuming more food eventually resulting in obesity. It has generally been observed that with higher gut microbiome diversity, the microbiota will spend energy and resources on competing with other microbiota and less on manipulating the host. The opposite is seen with lower gut microbiome diversity, and these microbiotas may work together to create host food cravings. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5296", "text": "Additionally, the liver plays a dominant role in  blood glucose  homeostasis by maintaining a balance between the uptake and storage of glucose through the metabolic pathways of  glycogenesis  and  gluconeogenesis . Intestinal lipids regulate glucose homeostasis involving a gut\u2013brain\u2013liver axis. The direct administration of lipids into the upper intestine increases the long chain fatty  acyl-coenzyme A  (LCFA-CoA) levels in the upper intestines and suppresses glucose production even under subdiaphragmatic  vagotomy  or gut vagal  deafferentation . This interrupts the neural connection between the brain and the gut and blocks the upper intestinal lipids' ability to inhibit glucose production. The gut\u2013brain\u2013liver axis and gut microbiota composition can regulate the glucose homeostasis in the liver and provide potential therapeutic methods to treat obesity and diabetes. [ 159 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5297", "text": "Just as gut flora can function in a feedback loop that can drive the development of obesity, there is evidence that restricting intake of calories (i.e.,  dieting ) can drive changes to the composition of the gut flora. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5298", "text": "The composition of the human gut microbiome is similar to that of the other great apes. However, humans' gut biota has decreased in diversity and changed in composition since our evolutionary split from  Pan . [ 160 ]  Humans display increases in Bacteroidetes, a bacterial phylum associated with diets high in animal protein and fat, and decreases in Methanobrevibacter and Fibrobacter, groups that ferment complex plant polysaccharides. [ 160 ]  These changes are the result of the combined dietary, genetic, and cultural changes humans have undergone since evolutionary divergence from  Pan . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5299", "text": "In addition to humans and vertebrates, some insects also have complex and diverse gut microbiota that play key nutritional roles. [ 2 ]  Microbial communities associated with  termites  can constitute a majority of the weight of the individuals and perform important roles in the digestion of  lignocellulose  and  nitrogen fixation . [ 161 ]  It is known that the disruption of gut microbiota of termites using agents like antibiotics [ 162 ]  or  boric acid [ 163 ]  (a common agent used in preventative treatment) causes severe damage to digestive function and leads to the rise of opportunistic pathogens. [ 163 ]  These communities are host-specific, and closely related insect species share comparable similarities in gut microbiota composition. [ 164 ] [ 165 ]  In  cockroaches , gut microbiota have been shown to assemble in a deterministic fashion, irrespective of the  inoculum ; [ 166 ]  the reason for this host-specific assembly remains unclear. Bacterial communities associated with insects like termites and cockroaches are determined by a combination of forces, primarily diet, but there is some indication that host  phylogeny  may also be playing a role in the selection of lineages. [ 164 ] [ 165 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5300", "text": "For more than 51 years it has been known that the administration of low doses of antibacterial agents promotes the growth of farm animals to increase weight gain. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5301", "text": "In a study carried out on  mice  the ratio of  Firmicutes  and  Lachnospiraceae  was significantly elevated in animals treated with subtherapeutic doses of different antibiotics. By analyzing the caloric content of faeces and the concentration of small chain fatty acids (SCFAs) in the GI tract, it was concluded that the changes in the composition of microbiota lead to an increased capacity to extract calories from otherwise indigestible constituents, and to an increased production of SCFAs. These findings provide evidence that antibiotics perturb not only the composition of the GI microbiome but also its metabolic capabilities, specifically with respect to SCFAs. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5302", "text": "The  gut\u2013brain axis  is the two-way biochemical signaling that takes place between the  gastrointestinal tract  (GI tract) and the  central nervous system  (CNS). [ 2 ]  The term \" microbiota\u2013gut\u2013brain axis \" highlights the role of  gut microbiota  in these  biochemical signaling  . [ 3 ] [ 2 ]  Broadly defined, the gut\u2013brain axis includes the  central nervous system ,  neuroendocrine  system,  neuroimmune systems , the  hypothalamic\u2013pituitary\u2013adrenal axis  (HPA axis),  sympathetic  and  parasympathetic  arms of the  autonomic nervous system , the  enteric nervous system ,  vagus nerve , and the gut microbiota. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5303", "text": "Chemicals released by the  gut microbiome  can influence  brain  development, starting from birth. A review from 2015 states that the gut microbiome influences the  CNS  by \"regulating brain chemistry and influencing neuro-endocrine systems associated with stress response, anxiety and memory function\". [ 4 ]  The gut, sometimes referred to as the \"second brain\", may use the same type of neural network as the  CNS , suggesting why it could have a role in brain function and  mental health . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5304", "text": "The bidirectional communication is done by  immune ,  endocrine ,  humoral  and neural connections between the gastrointestinal tract and the central nervous system. [ 4 ]  More research suggests that the  gut microbiome  influence the function of the brain by releasing the following chemicals:  cytokines ,  neurotransmitters ,  neuropeptides ,  chemokines , endocrine messengers and microbial  metabolites  such as \"short-chain fatty acids, branched chain amino acids, and  peptidoglycans \". [ 6 ]  These chemical signals are then transported to the brain via the  blood ,  neuropod cells ,  nerves ,  endocrine cells , [ 7 ] [ 8 ]  where they impact different metabolic processes. Studies have confirmed that  gut microbiome  contribute to range of brain functions controlled by the  hippocampus ,  prefrontal cortex  and  amygdala  (responsible for  emotions  and  motivation ) and act as a key node in the gut-brain behavioral axis. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5305", "text": "While  Irritable bowel syndrome  (IBS) is the only disease confirmed to be directly influenced by the gut microbiome, many disorders (such as  anxiety ,  autism ,  depression  and  schizophrenia ) have been reportedly linked to the gut-brain axis as well. [ 6 ] [ 10 ] [ 7 ]  According to a study from 2017, \" probiotics  have the ability to restore normal microbial balance, and therefore have a potential role in the treatment and prevention of anxiety and depression\". [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5306", "text": "The first of the brain\u2013gut interactions shown, was the  cephalic phase of digestion , in the release of gastric and pancreatic secretions in response to sensory signals, such as the smell and sight of food. This was first demonstrated by  Pavlov  through  Nobel prize  winning research in 1904. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5307", "text": "As of October 2016, most of the work done on the role of gut microbiota in the gut\u2013brain axis had been conducted in animals, or on characterizing the various  neuroactive compounds  that gut microbiota can produce. Studies with humans \u2013 measuring variations in gut microbiota between people with various psychiatric and neurological conditions or when stressed, or measuring effects of various  probiotics  (dubbed \" psychobiotics \" in this context) \u2013 had generally been small and were just beginning to be generalized. [ 14 ]  Whether changes to the gut microbiota are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut\u2013brain axis, remain unclear. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5308", "text": "The  enteric nervous system  is one of the main divisions of the  nervous system  and consists of a mesh-like system of  neurons  that governs the function of the  gastrointestinal system ; it has been described as a \"second brain\" for several reasons. The enteric nervous system can operate autonomously. It normally communicates with the  central nervous system  (CNS) through the  parasympathetic  (e.g., via the  vagus nerve ) and  sympathetic  (e.g., via the  prevertebral ganglia ) nervous systems. However,  vertebrate  studies show that when the  vagus nerve  is severed, the enteric nervous system continues to function. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5309", "text": "In vertebrates, the enteric nervous system includes  efferent neurons ,  afferent neurons , and  interneurons , all of which make the enteric nervous system capable of carrying reflexes in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the motor neurons control  peristalsis  and churning of intestinal contents. Other neurons control the secretion of  enzymes . The enteric nervous system also makes use of more than 30  neurotransmitters , most of which are identical to the ones found in CNS, such as  acetylcholine ,  dopamine , and  serotonin . More than 90% of the body's serotonin lies in the gut, as well as about 50% of the body's dopamine; the dual function of these neurotransmitters is an active part of gut\u2013brain research. [ 17 ] [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5310", "text": "The first of the gut\u2013brain interactions was shown to be between the sight and smell of food and the release of gastric secretions, known as the  cephalic phase , or cephalic response of digestion. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5311", "text": "The  gut microbiota  is the complex community of  microorganisms  that live in the  digestive tracts  of humans and other animals. The gut  metagenome  is the aggregate of all the  genomes  of gut microbiota. [ 24 ]  The gut is one niche that  human microbiota  inhabit. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5312", "text": "In humans, the gut microbiota has the largest quantity of bacteria and the greatest number of species, compared to other areas of the body. [ 26 ]  In humans, the gut flora is established at one to two years after birth; by that time, the  intestinal epithelium  and the  intestinal mucosal barrier  that it secretes have co-developed in a way that is tolerant to, and even supportive of, the gut flora and that also provides a barrier to  pathogenic organisms . [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5313", "text": "The relationship between gut microbiota and humans is not merely  commensal  (a non-harmful coexistence), but rather a  mutualistic  relationship. [ 25 ]  Human gut microorganisms benefit the host by collecting the energy from the  fermentation  of undigested  carbohydrates  and the subsequent absorption of  short-chain fatty acids  (SCFAs),  acetate ,  butyrate , and  propionate . [ 26 ] [ 29 ]  Intestinal  bacteria  also play a role in synthesizing  vitamin B  and  vitamin K  as well as metabolizing  bile acids ,  sterols , and  xenobiotics . [ 25 ] [ 29 ]  The systemic importance of the SCFAs and other compounds they produce are like  hormones  and the gut flora itself appears to function like an  endocrine organ ; [ 29 ]  dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions. [ 26 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5314", "text": "The composition of human gut microbiota changes over time, when the diet changes, and as overall health changes. [ 26 ] [ 30 ]  In general, the average human has over 1000 species of bacteria in their gut microbiome, with Bacteroidetes and Firmicutes being the dominant phyla. Diets higher in processed foods and unnatural chemicals can negatively alter the ratios of these species, while diets high in whole foods can positively alter the ratios. Additional health factors that may skew the composition of the gut microbiota are  antibiotics  and  probiotics . Antibiotics have severe impacts on gut microbiota, ridding of both good and bad bacteria. Without proper rehabilitation, it can be easy for harmful bacteria to become dominant. Probiotics may help to mitigate this by supplying healthy bacteria into the gut and replenishing the richness and diversity of the gut microbiota. There are many strains of probiotics that can be administered depending on the needs of a specific individual. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5315", "text": "The gut\u2013brain axis, a bidirectional neurohumoral communication system, is important for maintaining  homeostasis  and is regulated through the  central  and  enteric nervous systems  and the neural, endocrine, immune, and metabolic pathways, and especially including the  hypothalamic\u2013pituitary\u2013adrenal axis  (HPA axis). [ 2 ]  That term has been expanded to include the role of the gut microbiota as part of the \"microbiome-gut-brain axis\", a linkage of functions including the gut microbiota. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5316", "text": "Interest in the field was sparked by a 2004 study (Nobuyuki Sudo and Yoichi Chida) showing that germ-free mice (genetically homogeneous laboratory mice, birthed and raised in an antiseptic environment) showed an exaggerated HPA axis response to stress, compared to non-GF laboratory mice. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5317", "text": "The gut microbiota can produce a range of neuroactive molecules, such as  acetylcholine ,  catecholamines ,  \u03b3-aminobutyric acid ,  histamine ,  melatonin , and  serotonin , which are essential for regulating peristalsis and sensation in the gut. [ 32 ]  Changes in the composition of the gut microbiota due to diet, drugs, or disease correlate with changes in levels of circulating  cytokines , some of which can affect brain function. [ 32 ]  The gut microbiota also release molecules that can directly activate the  vagus nerve , which transmits information about the state of the intestines to the brain. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5318", "text": "Likewise, chronic or acutely stressful situations activate the  hypothalamic\u2013pituitary\u2013adrenal axis , causing changes in the gut microbiota and  intestinal epithelium , and possibly having  systemic effects . [ 32 ]  Additionally, the  cholinergic anti-inflammatory pathway , signaling through the vagus nerve, affects the gut epithelium and microbiota. [ 32 ]   Hunger  and satiety are integrated in the brain, and the presence or absence of food in the gut and types of food present also affect the composition and activity of gut microbiota. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5319", "text": "Most of the work that has been done on the role of gut microbiota in the gut\u2013brain axis has been conducted in animals, including the highly artificial germ-free mice. As of 2016, studies with humans measuring changes to gut microbiota in response to stress, or measuring effects of various probiotics, have generally been small and cannot be generalized; whether changes to gut microbiota are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut\u2013brain axis, remains unclear. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5320", "text": "The concept is of special interest in  autoimmune diseases  such as  multiple sclerosis . [ 33 ]  This process is thought to be regulated via the gut microbiota, which ferment indigestible dietary fibre and resistant starch; the fermentation process produces  short chain fatty acids  (SCFAs) such as propionate, butyrate, and acetate. [ 34 ]  \nThe history of ideas about a relationship between the gut and the mind dates from the nineteenth century.  [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5321", "text": "While  Irritable bowel syndrome  (IBS) is the only disease confirmed to be directly influenced by the gut microbiome, many disorders such as  anxiety ,  autism ,  depression  and  schizophrenia  have been linked to the gut-brain axis as well. [ 6 ] [ 36 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5322", "text": "Skin conditions  such as  acne  were proposed as early as 1930, [ 37 ]  to be related to emotional states which altered the gut microbiome leading to  systemic inflammation . Such conditions that have been improved by the use of  probiotics . [ 38 ]  Studies have shown overlapping mechanisms in  psoriasis  and depression; psoriasis causing disturbances in the gut microbiota that reflect in the brain causing depression that in turn can cause the stress that affects the microbiome. [ 39 ]  Probiotics may reduce symptoms of depression through the vagus nerve and sympathetic pathways."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5323", "text": "Irritable bowel syndrome (IBS) can cause many abdominal issues such as symptoms of constipation, diarrhea, gas, bloating, and abdominal pain. IBS can be stress-induced and flare-ups are associated with bouts of stress. The gut-brain axis may explain this. The use of probiotics has been shown to help to restore a balance of helpful and harmful bacteria. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5324", "text": "Brain function is dependent on multiple  neuropeptides  including  dopamine ,  GABA  and  serotonin , that are controlled in the gut microbiota. Imbalances in the gut microbiota intensifies  anxiety  as both the immune and metabolic pathways are affected. Specific microbes can lead to increased anxiety due to the activation of  c-Fos  proteins. These proteins serve as indicators of neuronal activation. Probiotics have beneficial impacts on anxiety. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5325", "text": "Studies have shown that children with  autism  are four times more likely to develop gastrointestinal disorders. The severity of their behavioral symptoms is proportional to the severity of their gastrointestinal issues. Many children with autism have high  focal levels of  HMGB1 . [ 42 ]   [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5326", "text": "Different neurotrophins play a role in schizophrenia. One of the main ones is called Brain-Derived Neurotrophic Factor (BDNF). BDNF has been associated with schizophrenia and is believed to be a part of the molecular mechanism that has to do with cognitive dysfunction during neurodevelopmental changes. Those who have been diagnosed with schizophrenia tend to exhibit lower levels of BDNF in blood and levels of BDNF are also lower in the cortex and hippocampus. Levels of butyric acid have also been shown to be different between schizophrenic patients and non-schizophrenic patients. It is important to note that studies regarding the link between the gut-brain axis and schizophrenia are limited and further studies are underway.  [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5327", "text": "Braak's theory  proposed that  gut dysbiosis  in Parkinson's causes the aggregation of  alpha-synuclein  in the gastrointestinal tract before its spreading to the brain. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5328", "text": "The gut-brain microbiota abnormalities that contribute to Parkinson's disease, supports the idea that it originates in the gut and spreads. The route would be from the gut to the central nervous system, through the vagus nerve. Gastrointestinal syndromes are known to be dysphagia, gastroparesis, and constipation among others, contributing to the risk of Parkinson's disease. From the understanding of these diseases, the disease modifying therapies are known to be aspects that help prevent the progress of these diseases that focus on the gut-brain axis. Relevant therapies are the Vagus nerve stimulation, the Fecal microbiota transplantation, the use of Rifaximun and other drugs directed towards the gut. \n [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5329", "text": "Microbial derived secondary  bile acids  produced in the gut may influence cognitive function. [ 47 ]   Altered bile acid profiles occur in cases of  mild cognitive impairment  and  Alzheimer's disease  with an increase in  cytotoxic  secondary bile acids and a decrease in primary bile acids. [ 48 ]   These findings suggest a role of the gut  microbiome  in the progression to Alzheimer's disease. [ 48 ]  In contrast to the cytotoxic effect of secondary bile acids, the bile acid  tauroursodeoxycholic acid  may be beneficial in the treatment of  neurodegenerative diseases . [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5330", "text": "As more bile acids are absorbed via apical sodium-bile acid transporters, there is a significant increase in age-related cognitive impairment. Levels of serum conjugated primary bile acids were monitored and increased levels revealed ammonia accumulation in the brain. These increased levels of ammonia led to hippocampal synapse loss. Because the hippocampus is largely responsible for memory, the loss of these synapses can have profound impacts on the memories of those affected.  [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5331", "text": "4KKI ,  4KKJ"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5332", "text": "6947"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5333", "text": "n/a"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5334", "text": "ENSG00000134827"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5335", "text": "P20061"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5336", "text": "NM_001062"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5337", "text": "NP_001053"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5338", "text": "Haptocorrin  (HC) also known as  transcobalamin-1  ( TC-1 ) or  cobalophilin  is a  transcobalamin   protein  that in humans is encoded by the  TCN1   gene . [ 3 ]  One essential function of haptocorrin is protection of the acid-sensitive  vitamin B 12  while it moves through the stomach. A second function is serum HC binding of the great majority of circulating vitamin B 12 , rendering it unavailable for take-up by cells. This is conjectured to be a circulating storage function."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5339", "text": "Haptocorrin (HC), also commonly known as the R-protein, or the R-factor, or previously referred to as transcobalamin I, is a unique  glycoprotein  produced by the salivary glands of the oral cavity, in response to ingestion of food. This protein binds strongly to vitamin B 12  in what is an intricate and necessary mechanism to protect this vitamin from the acidic environment of the stomach. [ 4 ] :\u200a44\u200a  Vitamin B 12  is an essential water-soluble vitamin, the deficiency of which creates anemia ( macrocytic anemia ), decreased bone marrow cell production ( anemia ,  pancytopenia ), neurological problems, as well as metabolic issues ( methylmalonyl-CoA acidosis ). [ 4 ] :\u200a50\u201351"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5340", "text": "Vitamin B 12  is therefore an important vitamin for the body to absorb. Despite its vital role however, vitamin B 12  is structurally very sensitive to the  hydrochloric acid  found in the stomach secretions, and easily denatures in that environment before it has a chance to be absorbed by the small intestine.  Found in fresh animal products (such as liver), vitamin B 12  attaches haptocorrin, which has a high affinity for its molecular structure. [ 5 ]  Coupled together vitamin B 12  and haptocorrin create a complex. This haptocorrin\u2013B 12  complex is impervious to the insult of the stomach acid, and passes on via the  pylorus  to the  duodenum . In the duodenum pancreatic  proteases  (a component of  pancreatic juice ) cleave haptocorrin, releasing vitamin B 12  in its free form."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5341", "text": "The same cells in the stomach that produce gastric hydrochloric acid, the  parietal cells , also produce a molecule called the  intrinsic factor  (IF), which binds the B 12  after its release from haptocorrin by digestion, and without which only 1% of vitamin B 12  is absorbed. Intrinsic factor (IF) is a glycoprotein, with a molecular weight of 45 kDa. In the duodenum, the free vitamin B 12  attaches to the intrinsic factor (IF) to create a vitamin B 12 \u2013IF complex. This complex then travels through the small bowel and reaches the terminal tertiary portion of the small intestine, called the  ileum . The ileum is the longest of all portions of the small intestine, and has on its surface specialized receptors called  cubilin  receptors, that identify the B 12 \u2013IF complexes and take them up into the circulation via  endocytosis -mediated absorption. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5342", "text": "Separate from the digestive absorption function, serum HC binds 80-90% of circulating B 12 , rendering it unavailable for cellular delivery by  transcobalamin II . This is conjectured to be a circulating storage function. [ 7 ]  Several serious, even life-threatening diseases cause elevated serum HC, measured as abnormally high serum vitamin B 12  while at the same time manifesting as a vitamin deficiency because of insufficient vitamin bound to transcobalamin II. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5343", "text": "The  hepatopancreas ,  digestive gland  or  midgut gland  is an organ of the  digestive tract  of  arthropods  and  molluscs . It provides the functions which in  mammals  are provided separately by the  liver  and  pancreas , including the production of digestive  enzymes , and absorption of digested food. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5344", "text": "Arthropods, especially  detritivores  in the Order  Isopoda , Suborder Oniscidea ( woodlice ), have been shown to be able to store  heavy metals  in their hepatopancreas. [ 3 ]  This could lead to  bioaccumulation  through the  food chain  and implications for  food web  destruction, if the accumulation gets high enough in polluted areas; for example, high metal concentrations are seen in  spiders  of the genus  Dysdera  which feed on  woodlice , including their hepatopancreas, the major metal storage organ of isopods in  polluted  sites. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5345", "text": "The hepatopancreas is a centre for  lipid metabolism  and for storage of lipids in  gastropods . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5346", "text": "Some species in the genus  Phyllodesmium  contains active  zooxanthellae  of the genus  Symbiodinium  in the hepatopancreas. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5347", "text": "Heyndrickxia coagulans  (formerly  Bacillus coagulans ) is a  lactic acid \u2013forming bacterial species. This species was transferred to  Weizmannia  in 2020, [ 1 ]  then to  Heyndrickxia  in 2023. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5348", "text": "H. coagulans  is a  Gram-positive ,  catalase -positive, spore-forming,  motile ,  facultative anaerobe  rod that measures approximately 0.9\u00a0\u03bcm by 3.0\u00a0\u03bcm to 5.0\u00a0\u03bcm. It may appear  Gram negative  when entering the  stationary phase  of growth. The optimum temperature for growth is 50\u00a0\u00b0C (122\u00a0\u00b0F); the range of temperatures tolerated is 30\u201355\u00a0\u00b0C (86\u2013131\u00a0\u00b0F).  IMViC  tests  VP and MR ( methyl red ) are positive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5349", "text": "The species was first isolated and described in 1915 by B.W. Hammer at the Iowa Agricultural Experiment Station as a cause of an outbreak of coagulation in  evaporated milk  packed by an Iowa  condensary . [ 3 ]  Separately isolated in 1935 and described as  Lactobacillus sporogenes  in the fifth edition of  Bergey's Manual of Systematic Bacteriology , it exhibits characteristics typical of both genera  Lactobacillus  and  Bacillus ; its taxonomic position between the families  Lactobacillaceae  and  Bacillaceae  was often debated. However, in the seventh edition of  Bergey's , it was finally transferred to the genus  Bacillus . DNA-based technology was used in distinguishing between the two genera of bacteria, which are  morphologically  similar and possess similar  physiological  and  biochemical  characteristics. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5350", "text": "In 2020, further genetic evidence shows that it is sufficiently different from other members of  Bacillus  to be transferred into its own genus. As a result, it became the  type species  of  Weizmannia . [ 1 ]  In 2023, even further genetic evidence shows that  Weizmannia  was not sufficiently distinct from  Heyndrickxia  to be an independent genus; as a result, all members of  Weizmannia  were moved to  Heyndrickxia . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5351", "text": "H. coagulans  has been added by the  EFSA  to their Qualified Presumption of Safety list [ 6 ]  and has been approved for veterinary purposes as  GRAS  by the  U.S. Food and Drug Administration 's Center for Veterinary Medicine, as well as by the  European Union , and is listed by  AAFCO  for use as a direct-fed microbial in livestock production. It is often used in veterinary applications, especially as a  probiotic  in pigs, cattle, poultry, and shrimp. Many references to use of this bacterium in humans exist, especially in improving the  vaginal flora , [ 7 ] [ 8 ] [ 9 ]  improving abdominal pain and bloating in  irritable bowel syndrome  patients, [ 10 ]  and increasing immune response to viral challenges. [ 11 ]  There is evidence from animal research that suggests that  H.\u00a0coagulans  is effective in both treating as well as preventing recurrence of  Clostridioides difficile  associated diarrhea . [ 12 ]  Further, one animal research study showed that it can alter inflammatory processes in the context of  multiple sclerosis . [ 13 ]  One strain of this bacterium has also been assessed for safety as a food ingredient. [ 14 ]   Spores are activated in the acidic environment of the stomach and begin germinating and proliferating in the intestine. Sporeforming  H.\u00a0coagulans  strains are used in some countries as probiotics for patients on antibiotics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5352", "text": "H. coagulans  is often marketed as  Lactobacillus sporogenes  or a 'sporeforming lactic acid bacterium' probiotic, but this is an outdated name due to taxonomic changes in 1939. Although  H.\u00a0coagulans  does produce L+ lactic acid , the bacterium used in these products is not a lactic-acid bacterium, as  Bacillaceae  species do not belong to the  lactic acid bacteria  ( Lactobacillales ). By definition, lactic acid bacteria ( Lactobacillus ,  Bifidobacterium ) do not form spores. Therefore, using the name  Lactobacillus sporogenes  is scientifically incorrect. [ 4 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5353", "text": "The 2023 name  H. coagulans  is nowhere as common as the former name  Bacillus coagulans . The former name remains  valid  under the  Prokaryotic Code ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5354", "text": "Hindgut fermentation  is a digestive process seen in  monogastric   herbivores  (animals with a simple, single-chambered  stomach ).    Cellulose  is digested with the aid of  symbiotic  microbes including  bacteria ,  archaea , and  eukaryotes . [ 1 ]  The  microbial   fermentation  occurs in the digestive organs that follow the  small intestine : the  cecum  and  large intestine .  Examples of  hindgut  fermenters include  proboscideans  and large  odd-toed ungulates  such as  horses  and  rhinos , as well as small animals such as  rodents ,  rabbits  and  koalas . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5355", "text": "In contrast,  foregut fermentation  is the form of cellulose digestion seen in  ruminants  such as  cattle  which have a four-chambered stomach, [ 3 ]  as well as in  sloths ,  macropodids , some  monkeys , and one bird, the  hoatzin . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5356", "text": "Hindgut fermenters generally have a  cecum  and large intestine that are much larger and more complex than those of a foregut or  midgut  fermenter. [ 5 ]  Research on small cecum fermenters such as  flying squirrels , rabbits and lemurs has revealed these mammals to have a GI tract about 10-13 times the length of their body. [ 6 ]   This is due to the high intake of  fiber  and other hard to digest compounds that are characteristic to the diet of monogastric herbivores. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5357", "text": "Easily digestible food is processed in the gastrointestinal tract & expelled as regular feces.  But in order to get nutrients out of hard to digest fiber, some smaller hindgut fermenters, like  lagomorphs  (rabbits, hares, pikas), ferment fiber in the cecum (at the small and large intestine junction) and then expel the contents as  cecotropes , which are reingested ( cecotrophy ).  The cecotropes are then absorbed in the small intestine to utilize the nutrients. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5358", "text": "This process is also beneficial in allowing for restoration of the microflora population, or  gut flora . These microbes are found in the gastrointestinal tract and can act as protective agents that strengthen the  immune system . Small hindgut fermenters have the ability to expel their microflora, which is useful during the acts of  hibernation ,  estivation  and  torpor ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5359", "text": "While foregut fermentation is generally considered more efficient, and monogastric animals cannot digest cellulose as efficiently as ruminants, [ 5 ]  hindgut fermentation allows animals to consume small amounts of low-quality forage all day long and thus survive in conditions where ruminants might not be able to obtain nutrition adequate for their needs. While ruminants require a good deal of time resting between meals, hindgut fermenters are able to take in smaller meals more frequently, allowing them to eat and move more readily. [ 8 ]   The large hindgut fermenters are bulk feeders: they ingest large quantities of low-nutrient food, which they process more rapidly than would be possible for a similarly sized foregut fermenter. The main food in that category is grass, and grassland grazers move over long distances to take advantage of the growth phases of grass in different regions. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5360", "text": "The ability to process food more rapidly than foregut fermenters gives hindgut fermenters an advantage at very large body size, as they are able to accommodate significantly larger food intakes. The largest extant and prehistoric  megaherbivores , elephants and  indricotheres  (a type of rhino), respectively, have been hindgut fermenters. [ 10 ]  Study of the rates of evolution of larger maximum body mass in different terrestrial mammalian groups has shown that the fastest growth in body mass over time occurred in hindgut fermenters ( perissodactyls ,  rodents   and  proboscids ). [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5361", "text": "Hindgut fermenters are subdivided into two groups based on the relative size of various digestive organs in relationship to the rest of the system:  colonic  fermenters tend to be larger species such as horses, and cecal fermenters are smaller animals such as rabbits and rodents. [ 2 ]  However, in spite of the terminology, colonic fermenters such as horses make extensive use of the cecum to break down cellulose. [ 12 ] [ 13 ]  Also, colonic fermenters typically have a proportionally longer large intestine than small intestine, whereas cecal fermenters have a considerably enlarged cecum compared to the rest of the digestive tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5362", "text": "In addition to mammals, several insects are also hindgut fermenters, the best studied of which are the  termites , which are characterised by an enlarged \"paunch\" of the hindgut that also houses the bulk of the gut microbiota. [ 14 ]  Digestion of wood particles in lower termites is accomplished inside the phagosomes of gut flagellates, but in the flagellate-free higher termites, this appears to be accomplished by fibre-associated bacteria. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5363", "text": "In  humans , the  anus  ( pl. :  anuses  or  ani ; from  Latin   \u0101nus , \"ring\", \"circle\") [ 1 ] [ 2 ]  is the external opening of the  rectum  located inside the  intergluteal cleft . Two  sphincters  control the exit of  feces  from the body during an act of  defecation , which is the primary function of the anus. These are the  internal anal sphincter  and the  external anal sphincter , which are circular  muscles  that normally maintain constriction of the orifice and which relax as required by normal physiological functioning. The inner sphincter is involuntary and the outer is voluntary. Above the anus is the  perineum , which is also located beneath the  vulva  or  scrotum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5364", "text": "In part owing to its exposure to feces, a number of medical conditions may affect the anus, such as  hemorrhoids . [ 3 ]  The anus is the site of potential  infections  and other conditions, including  cancer  (see  anal cancer ). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5365", "text": "With  anal sex , the anus can play a role in  sexuality . Attitudes toward anal sex vary, and it is illegal in some countries. [ 5 ]  The anus is often considered a  taboo  part of the body, [ 5 ]  and is known by many, usually vulgar,  slang  terms. Some  sexually transmitted infections  including  HIV/AIDS  and  anal warts  can be spread via anal sex."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5366", "text": "The anus is the final part of the  gastrointestinal tract , and directly continues from the  rectum , passing through the  pelvic floor . The top and bottom of the anus are surrounded by the  internal  and  external anal sphincters , two muscular rings which control defecation. [ 6 ] :\u200a397\u200a \nThe anus is surrounded in its length by folds called  anal valves , which converge at a line known as the  pectinate line . This represents the point of transition between the  hindgut  and the  ectoderm  in the embryo. Below this point, the mucosa of the internal anus becomes skin. [ 6 ]   :\u200a397\u200a  The pectinate line is also the division between the internal and external anus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5367", "text": "The anus receives blood from the  inferior rectal artery  and innervation from the  inferior rectal nerves , which branch from the  pudendal nerve . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5368", "text": "The pseudostratified columnar  epithelium  of the gastrointestinal tract transitions to stratified squamous epithelium at the pectinate line. The stratified squamous epithelium gradually accumulates  sebaceous  and  apocrine glands . [ 8 ] :\u200a285"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5369", "text": "During  puberty , as testosterone triggers  androgenic hair  growth on the body,  pubic hair  begins to appear around the anus. Although initially sparse, it fills out by the end of puberty, if not earlier. In some genetic populations, androgenic hair is less common."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5370", "text": "Intra-rectal pressure builds as the rectum fills with feces, pushing the feces against the walls of the  anal canal . Contractions of abdominal and pelvic floor muscles can create intra-abdominal pressure, which further increases intra-rectal pressure. The internal anal sphincter (an involuntary muscle) responds to the pressure by relaxing, thus allowing the feces to enter the canal. The rectum shortens as feces are pushed into the anal canal and  peristaltic waves  push the feces out of the rectum. Relaxation of the internal and external anal sphincters allows the feces to exit from the anus, finally, as the  levator ani  muscles pull the anus up over the exiting feces."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5371", "text": "Anal fissures  are tears in the external lining of the lining (mucosa) of the anus. These are exquisitely painful, with pain occurring after a motion is passed; other symptoms may include minor bleeding, discharge, or itch. [ 9 ]  Generally, fissures are due to injury to the mucosa, or because of a poor local blood supply that prevents proper healing, with spasm of the external anal sphincter contributing. [ 9 ]  The external anal sphincter can be relaxed by the application of  glyceryl trinitrate  creams, and  constipation  is managed with  laxatives  and improving hydration. [ 9 ]  Some fissures may require  botulinum toxin  injection; worst cases may require surgical intervention, such as \"lateral internal  anal sphincterotomy  or advancement anoplasty\" [ clarification needed ] . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5372", "text": "Hemorrhoids  are visible blood vessels from the internal or external  venous plexuses  of the anus. Haemorrhoids may; cause bleeding after passing a motion; be painful; cause an itch; or  prolapse  out of the anus. [ 9 ]  Haemorrhoids are often associated with straining due to constipation, and  pregnancy . [ 9 ]  Usually, haemorrhoids are managed with medications to  make motions more soft  and prevent straining during constipation. Some haemorrhoids require surgery to manage, which may involve  placing a band around the haemorrhoid , in order for it to lose blood supply; or surgical excision. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5373", "text": "Other"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5374", "text": "Anal abscesses  usually result from infection of the normal glands of the anus, or sometimes because of  Crohn's disease . [ 9 ]  They usually occur to the sides of the sphincters, and between the internal and external sphincters, either on the surface, or deeper. They may get bigger, enlarging in the direction of the rectum, and resulting in an abnormal connection called an  anorectal fistula . They are usually managed with surgical drainage [ 9 ]  and antibiotics. [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5375", "text": "Additional"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5376", "text": "Anal cancer , also called \"anal carcinoma\", and  anal intraepithelial neoplasia . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5377", "text": "Itchiness, called  pruritus ani , can affect the anus area. It is most often due to long-term exposure of the anus to faeces, with reasons including diseases of the anus such as haemorrhoids, fistulas and fissures; poor hygiene or chronic diarrhoea; local infections such as  tapeworm  and  thrush ; or skin conditions such as  psoriasis  and  contact dermatitis . If there is a specific cause identified, the cause may be treated to relieve the itch. Otherwise, treatment includes keeping the area clean and dry, ceasing topical creams and ointments, and potentially bulk-forming laxatives to reduce the chance of faecal contamination. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5378", "text": "Damage or injury to the anal sphincter ( patulous anus  in more severe cases) as a result of damage during surgery, such as to the  perineal  region, or resulting from  anal sex ; can lead to  flatus  and/or  fecal incontinence , chronic constipation and  megacolon . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5379", "text": "The anus has a relatively high concentration of  nerve endings  and can be an  erogenous zone , which can make anal intercourse pleasurable if performed properly. The pudendal nerve that branches to supply the external anal sphincter also branches to the  dorsal nerve of the clitoris  and the  dorsal nerve of the penis . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5380", "text": "In addition to nerve endings, pleasure from anal intercourse may be aided by the close proximity between the anus and the  prostate  for males, and  vagina ,  clitoral   legs  and anal area for females. This is because of indirect stimulation of the prostate and vagina or clitoral legs. [ 14 ] [ 15 ] [ 16 ]  For a male insertive partner, the tightness of the anus can be a source of pleasure via the tactile pressure on the penis. [ 17 ] [ 18 ]  Pleasure from the anus can also be achieved through  anal masturbation ,  anal fingering , [ 5 ]   facesitting ,  anilingus , and other penetrative and  non-penetrative acts . Anal stretching or  fisting  is pleasurable for some, but it poses a more serious threat of damage due to the deliberate stretching of the anal and rectal tissues; its injuries include anal sphincter lacerations and rectal and  sigmoid colon  (rectosigmoid) perforation, which might result in death. [ 19 ]  Lubricant and  condoms  are widely regarded as a necessity while performing anal sex, as well as a slow and cautious penetration. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5381", "text": "Anal intercourse is sometimes referred to as  sodomy  or buggery, and is considered  taboo  in a number of legal systems. It has been, and in some  jurisdictions  continues to be, a crime carrying severe punishment. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5382", "text": "To prevent diseases of the anus [ citation needed ]  and to promote general hygiene, humans often clean the exterior of the anus after emptying the bowels. A rinse with water from a  bidet  or a wipe with  toilet paper  is often used for this purpose, though anal cleansing practices vary greatly between cultures."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5383", "text": "Shaving, trimming,  depilatory  (hair removal), or  Brazilian waxing  can clear the  perineum  of hair."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5384", "text": "Anal bleaching  is a process in which the anus and perineum is lightened.  Perineum sunning  is a process in which the anus is  sun tanned  by deliberate exposure to sunlight, resulting in a darkening of the area. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5385", "text": "A true  anal piercing  is rare because it may interfere with the function of the anus and cause infections. Surface piercings of the perineum are easier to care for and much more common."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5386", "text": "Some people have their anuses  tattooed ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5387", "text": "The anus has many slang terms including  asshole ,  butthole  (and their respective British equivalents  arsehole ,  bumhole ),  cornhole , and  bunghole ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5388", "text": "In  human anatomy , the  mouth  is the first portion of the  alimentary canal  that receives  food  and produces  saliva . [ 2 ]  The  oral mucosa  is the mucous membrane  epithelium  lining the inside of the mouth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5389", "text": "In addition to its primary role as the beginning of the  digestive system , the mouth also plays a significant role in  communication . While primary aspects of the  voice  are produced in the  throat , the  tongue ,  lips , and  jaw  are also needed to produce the range of sounds included in  speech ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5390", "text": "The mouth consists of two regions, the  vestibule  and the  oral cavity proper . The mouth, normally moist, is lined with a  mucous membrane , and contains the  teeth .  The lips mark the transition from mucous membrane to  skin , which covers most of the  body ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5391", "text": "The mouth consists of two regions: the vestibule and the oral cavity proper. The vestibule is the area between the teeth, lips and cheeks. [ 3 ]  The oral cavity is bounded at the sides and in front by the  alveolar process  (containing the  teeth ) and at the back by the  isthmus of the fauces . Its roof is formed by the  hard palate . The floor is formed by the  mylohyoid muscles  and is occupied mainly by the anterior two-thirds of the  tongue . A  mucous membrane  \u2013 the  oral mucosa , lines the sides and under surface of the tongue to the  gums , and lines the inner aspect of the jaw ( mandible ). It receives secretions from the  submandibular  and  sublingual   salivary glands . The posterior border of the oral cavity (ie, junction between the oral cavity and the  oropharynx ) includes the junction of the  hard palate  and the  soft palate  superiorly, the  circumvallate papillae  of the  tongue  inferiorly, and the  retromolar trigone ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5392", "text": "The  lips  come together to close the opening of the mouth, forming a line between the upper and lower lip. In  facial expression , this  mouth line  is iconically shaped like an up-open  parabola  in a  smile , and like a down-open parabola in a  frown . A  down-turned mouth  means a mouth line forming a down-turned parabola, and when permanent can be normal. Also, a  down-turned mouth  can be part of the presentation of  Prader\u2013Willi syndrome . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5393", "text": "The teeth and the  periodontium  (the  tissues  that support the teeth) are innervated by the  maxillary  and  mandibular nerves  \u2013 divisions of the  trigeminal nerve . Maxillary (upper) teeth and their associated  periodontal ligament  are innervated by the superior alveolar nerves, branches of the maxillary division, termed the  posterior superior alveolar nerve ,  anterior superior alveolar nerve , and the variably present  middle superior alveolar nerve . These nerves form the  superior dental plexus  above the maxillary teeth. The mandibular (lower) teeth and their associated periodontal ligament are innervated by the  inferior alveolar nerve , a branch of the mandibular division. This nerve runs inside the mandible, within the  inferior alveolar canal  below the mandibular teeth, giving off branches to all the lower teeth ( inferior dental plexus ). [ 5 ] [ 6 ]  The  oral mucosa  of the gingiva (gums) on the  facial  (labial) aspect of the maxillary  incisors ,  canines  and  premolar  teeth is innervated by the superior labial branches of the  infraorbital nerve . The posterior superior alveolar nerve supplies the gingiva on the facial aspect of the maxillary  molar  teeth. The gingiva on the  palatal  aspect of the maxillary teeth is innervated by the  greater palatine nerve  apart from in the incisor region, where it is the  nasopalatine nerve  (long sphenopalatine nerve). The gingiva of the  lingual  aspect of the mandibular teeth is innervated by the sublingual nerve, a branch of the  lingual nerve . The gingiva on the facial aspect of the mandibular incisors and canines is innervated by the  mental nerve , the continuation of the inferior alveolar nerve emerging from the  mental foramen . The gingiva of the buccal (cheek) aspect of the mandibular molar teeth is innervated by the  buccal nerve  (long buccal nerve). [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5394", "text": "The  philtrum  is the vertical depression formed between the  philtral ridges  between the upper lip and the nasal septum, formed where the  nasomedial  and  maxillary  processes meet during  embryo development . When these processes fail to fuse fully, a  cleft lip ,  cleft palate , or both can result."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5395", "text": "The  nasolabial folds  are the deep creases of tissue that extend from the nose to the sides of the mouth. One of the first signs of age on the human face is the increase in prominence of the nasolabial folds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5396", "text": "The mouth plays an important role in  eating ,  drinking , and speaking.  Mouth breathing  refers to the act of breathing through the mouth (as a temporary backup system) if there is an obstruction to  breathing through the nose , which is the designated breathing organ for the human body. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5397", "text": "Infants  are born with a  sucking reflex , by which they  instinctively  know to suck for nourishment using their lips and  jaw .\nThe mouth also helps in  chewing  and  biting  food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5398", "text": "For some disabled people, especially many disabled artists, who through illness, accident or congenital disability have lost dexterity, their mouths take the place of their hands, when typing, texting, writing, making  drawings ,  paintings  and other works of art by maneuvering brushes and other tools, in addition to the basic oral functions.  Mouth painters  hold the brush in their mouth or between their teeth and maneuver it with their tongue and cheek muscles, but mouth painting can be strenuous for neck and jaw muscles since the head has to perform the same back and forth movement as a hand does when painting. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5399", "text": "A  male  mouth can hold, on average, 71.2\u00a0ml (2.51\u00a0imp\u00a0fl\u00a0oz; 2.41\u00a0US\u00a0fl\u00a0oz), while a  female  mouth holds 55.4\u00a0ml (1.95\u00a0imp\u00a0fl\u00a0oz; 1.87\u00a0US\u00a0fl\u00a0oz). [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5400", "text": "Gastric  hydrogen potassium ATPase , also known as  H + /K +  ATPase , is an  enzyme  which functions to acidify the stomach. [ 1 ]  It is a member of the  P-type ATPases , also known as E 1 -E 2  ATPases due to its two states. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5401", "text": "The gastric hydrogen potassium  ATPase  or H + /K +  ATPase is the  proton pump  of the  stomach . It exchanges potassium from the intestinal  lumen  with  cytoplasmic   hydronium [ 2 ]  and is the enzyme primarily responsible for the acidification of the stomach contents and the activation of the digestive enzyme  pepsin [ 3 ]  (see  gastric acid )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5402", "text": "The H + /K +  ATPase is found in  parietal cells , which are highly specialized  epithelial  cells located in the inner cell lining of the stomach called the gastric  mucosa . Parietal cells possess an extensive secretory membrane system and the H + /K +  ATPase is the major protein constituent of these membranes. A small amount of H + /K +  ATPase is also found in the  renal medulla . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5403", "text": "The H + /K +  ATPase is a heterodimeric  protein , the product of 2 genes. The gene  ATP4A [ 4 ]  encodes the H + /K +  ATPase \u03b1 subunit, and is a ~1000-amino acid protein that contains the catalytic sites of the enzyme and forms the pore through the cell membrane that allows the transport of ions. Hydronium ions bind to two active sites present in the \u03b1 subunit. [ 5 ]  The \u03b1 subunit also has a phosphorylation site (Asp 385 ). [ 6 ]  The gene  ATP4B [ 7 ]  encodes the \u03b2 subunit of the H + /K +  ATPase, which is a ~300-amino acid protein with a 36-amino acid N-terminal cytoplasmic domain, a single transmembrane domain, and a highly glycosylated extracellular domain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5404", "text": "The H + /K +  ATPase \u03b2 subunit stabilizes the H + /K +  ATPase \u03b1 subunit and is required for function of the enzyme. The \u03b2 subunit prevents the pump from running in reverse, [ 8 ]  and it also appears to contain signals that direct the heterodimer to membrane destinations within the cell, although some of these signals are subordinate to signals found in H + /K +  ATPase \u03b1 subunit."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5405", "text": "The structure of H + /K +  ATPase has been determined for humans, dogs, hogs, rats, and rabbits and is 98% homologous across all species. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5406", "text": "H + /K +  ATPase is a P 2 -type ATPase, a member of the eukaryotic class of  P-type ATPases . [ 9 ]  Like the Ca 2+  and the Na + /K +  ATPases, the H + /K +  ATPase functions as an \u03b1, \u03b2 protomer. [ 10 ]  Unlike other eukaryotic ATPases, the H + /K +  ATPase is electroneutral, transporting one proton into the stomach lumen per potassium ion retrieved from the gastric lumen. [ 9 ]  As an ion pump the H + /K +  ATPase is able to transport ions against a concentration gradient using energy derived from the hydrolysis of ATP. Like all P-type ATPases, a phosphate group is transferred from  adenosine triphosphate  (ATP) to the H + /K +  ATPase during the transport cycle. This phosphate transfer powers a conformational change in the enzyme that helps drive ion transport. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5407", "text": "The hydrogen potassium ATPase is activated indirectly by  gastrin  that causes  ECL cells  to release  histamine . [ 11 ]  The histamine binds to H2 receptors on the parietal cell, activating a  cAMP-dependent pathway  which causes the enzyme to move from the cytoplasmic tubular membranes to deeply folded canaliculi of the stimulated parietal cell. [ 2 ]  Once localized, the enzyme alternates between two conformations, E1 and E2, to transport ions across the membrane."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5408", "text": "The E1 conformation binds a phosphate from ATP and hydronium ion on the cytoplasmic side. The enzyme then changes to the E2 conformation, allowing hydronium to be released in the lumen. The E2 conformation binds potassium, and reverts to the E1 conformation to release phosphate and K +  into the cytoplasm where another ATP can be hydrolyzed to repeat the cycle. [ 2 ]  The \u03b2 subunit prevents the E2-P conformation from reverting to the E1-P conformation, making proton pumping unidirectional. [ 8 ]  The number of ions transported per ATP varies from 2H + /2K +  to 1H + /1K + depending on the pH of the stomach. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5409", "text": "Inhibiting the hydrogen potassium pump to decrease stomach acidity has been the most common method of treating diseases including  gastroesophageal reflux disease  (GERD/GORD) and  peptic ulcer  disease (PUD). [ 13 ]  Reducing acidity alleviates disease symptoms but does not treat the actual cause of GERD (abnormal relaxation of the esophageal sphincter) or PUD ( Helicobacter pylori  and  NSAIDs ). [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5410", "text": "Three drug classes have been used to inhibit H + /K + -ATPases.  H 2 -receptor antagonists , like  cimetidine  (Tagamet), inhibit the signaling pathway that leads to activation of the ATPase. This type of inhibitor is effective in treating ulcers but does not prevent them from forming, and patients develop tolerance to them after about one week, leading to a 50% reduction in efficacy. [ 15 ]   Proton pump inhibitors  (PPIs) were later developed, starting with Timoprazole in 1975. [ 15 ]  PPIs are acid-activated  prodrugs  that inhibit the hydrogen-potassium ATPase by binding covalently to active pumps. [ 16 ]  Current PPIs like  Omeprazole  have a short half-life of approximately 90 minutes. [ 17 ]  Acid pump antagonists (APAs) or potassium-competitive acid blockers (PCABs) are a third type of inhibitor that blocks acid secretion by binding to the K +  active site. [ 15 ]  APAs provide faster inhibition than PPIs since they do not require acid activation.  Revaprazan  was the first APA used clinically in east Asia, and other APAs are being developed since they appear to provide better acid control in clinical trials. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5411", "text": "Inactivation of the proton pump can also lead to health problems. A study in mice by Krieg et al. [ 18 ]  found that a mutation of the pump's \u03b1-subunit led to  achlorhydria , resulting in problems with iron absorption, leading to iron deficiency and  anemia . The use of PPIs has not been correlated with an elevated risk of anemia, so the H + /K + -ATPase is thought to aid iron absorption but is not necessarily required. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5412", "text": "Current association of dementia and PPIs have been documented in Germany and in research articles denoting how Benzimidazole derivatives,  Astemizole  (AST) and  Lansoprazole  (LNS) interact with anomalous aggregates of tau protein ( neurofibrillary tangles ). [ 19 ] [ 20 ] [ 21 ]  Current theories include the non-selective blockade of sodium-potassium pumps in the brain causing osmotic imbalances or swelling in the cells. [auth opinion]\nInteraction of PPIs with other drug affecting the sodium-potassium pump, e.g., digoxin, warfarin etc., has been well documented. [ 22 ] \nMemory has been associated with astrocytes and the alpha3 subunit of adenosine receptor found in hydrogen/Sodium-potassium pumps may be a focal point in dementia. [ 23 ] [ 24 ] [ 25 ] \nChronic use of PPIs may cause down regulation of alpha3 subunit increasing damage to astrocytes. [ 26 ] \nOsteopetrosis via TCIRG1 gene has a strong association with pre-senile dementia. [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5413", "text": "The  ileocecal fold  (or  ileocaecal fold ) is an  anatomical  structure of the human abdomen formed by a layer of  peritoneum  between the  ileum  and   cecum . The upper border of the ileocecal fold is fixed to the ileum opposite its  mesenteric  attachment, and the lower border passes over the  ileocecal junction  to join the  mesentery of the appendix  (and sometimes the  appendix  itself as well). Behind the ileocecal fold is the inferior ileocecal fossa. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5414", "text": "The ileocecal fold is also called a  ligament ,  veil , or  bloodless fold of Treves  (after English surgeon  Sir Frederick Treves ). [ 1 ]  Despite the latter name, the ileocecal fold in fact often contains a vessel. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5415", "text": "This article incorporates text in the  public domain  from  page 1160  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5416", "text": "Ileus  is a disruption of the normal  propulsive  ability of the  intestine . It can be caused by lack of  peristalsis  or by  mechanical obstruction . [ 1 ] \nThe word 'ileus' derives from  Ancient Greek     \u03b5\u1f30\u03bb\u03b5\u03cc\u03c2  (eile\u00f3s) \u00a0'intestinal obstruction'. The term 'subileus' refers to a partial obstruction. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5417", "text": "Symptoms of ileus include, but are not limited to: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5418", "text": "Decreased propulsive ability may be broadly classified as caused either by bowel obstruction or by intestinal  atony  or paralysis. However, instances with symptoms and signs of a bowel obstruction occur, but with the absence of a mechanical obstruction, mainly in acute colonic  pseudo-obstruction ,  Ogilvie's syndrome . [ 3 ]  In 2023 the US  FDA  reported gastrointestinal ileus as an  adverse effect  of the medication  semaglutide , with frequency and causal relationship unknown. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5419", "text": "A bowel obstruction is generally a mechanical obstruction of the gastrointestinal tract and can occur anywhere from the Ligament of Treitz to the anus. When the obstruction affects only the small intestine, it is generally referred to as a small bowel obstruction to distinguish it from a colonic obstruction, which may or may not affect the small intestine. The distinction helps to narrow the possible causes and treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5420", "text": "Common causes of small bowel obstruction include post-operative adhesions, hernias, intussusception, and intraabdominal tumors. Common causes of colonic obstruction include primary colon cancer,  volvulus  and post-operative adhesions. When the ileocecal valve is competent, colonic obstruction may manifest as gaseous distention of the colon, but not the small intestine; when the ileocecal valve is incompetent, it does not prevent retrograde passage of air and stool and a colonic obstruction will cause dilation of both large and small bowel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5421", "text": "Bowel obstructions can be partial or complete. They can be differentiated on imaging by the intestinal gas pattern. Partial obstructions will have gas distal to the obstruction, whereas a complete obstruction will not. Sounds of \"rushes and tinkles\" are associated with partial obstructions [ 5 ]  and represent brief passages of fluid and gas (respectively) through the partial obstruction. Complete obstructions do not make these sounds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5422", "text": "Paralytic ileus is paralysis of the intestine, whether or not complete, sufficient to prohibit the passage of food through the intestine and lead to intestinal blockage.  It causes constipation and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are heard because the bowel is inactive. [ citation needed ]   It is a common side effect of some types of surgery, termed postsurgical ileus. It can also result from certain drugs and from various injuries and illnesses, such as  acute pancreatitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5423", "text": "A temporary paralysis of a portion of the intestines occurs typically after abdominal surgery. Since the intestinal content of this portion is unable to move forward, food or drink should be avoided until  peristaltic  sound is heard, by  auscultation  (use of a stethoscope) of the area where this portion lies. Intestinal atony or paralysis may be caused by inhibitory neural reflexes, inflammation or other implication of neurohumoral peptides. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5424", "text": "Traditionally,  nothing by mouth  was considered to be mandatory in all cases, but gentle feeding by enteral  feeding tube  may help to restore motility by triggering the gut's normal feedback signals, so this is the recommended management initially. [ 7 ]  When the patient has severe, persistent signs that motility is completely disrupted,  nasogastric suction  and  parenteral nutrition  may be required until passage is restored. In such cases, continuing aggressive enteral feeding causes a risk of perforating the gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5425", "text": "Several options are available in the case of paralytic ileus. Most treatment is supportive. If caused by medication, the offending agent is discontinued or reduced. Bowel movements may be stimulated by prescribing  lactulose ,  erythromycin  or, in severe cases that are thought to have a neurological component (such as  Ogilvie's syndrome ),  neostigmine . There is also evidence from a systematic review of  randomized controlled trials  that chewing gum, as a form of ' sham feeding ', may stimulate gastrointestinal motility in the post-operative period and reduce the duration of postoperative ileus. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5426", "text": "If possible the underlying cause is corrected (e.g. replace electrolytes)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5427", "text": "Ileus is a cause of  colic  in horses due to functional obstruction of the intestines. It is most commonly seen in horses postoperatively, especially following colic surgery. [ 9 ]  Horses experiencing ileus are at risk for gastric rupture due to rapid reflux build-up, and require intense medical management with frequent nasogastric intubation. [ 9 ]  Ileus may increase  adhesion  formation, because intestinal segments have more prolonged contact and intestinal distention causes serosal injury and  ischemia . It is usually treated with aggressive fluid support,  prokinetics , and anti-inflammatories. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5428", "text": "ICD-10  coding reflects both impaired-peristalsis senses and mechanical-obstruction senses of the term as modified by various adjectives. [ 1 ]  Some authors have argued for trying to reserve the term for the impaired-peristalsis senses, [ 10 ] [ 11 ]  under which  prescription  certain older terms such as \" gallstone  ileus\" and \" meconium  ileus\", although now technically  misnomers , are still accepted as correct owing to their long-established usage. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5429", "text": "Ingestion   is the consumption of a substance by an  organism . In  animals , it normally is accomplished by taking in a substance through the  mouth  into the  gastrointestinal tract , such as through  eating  or  drinking . In  single-celled organisms , ingestion takes place by absorbing a substance through the  cell membrane ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5430", "text": "Besides  nutritional  items, substances that may be ingested include  medication  (where ingestion is termed  oral administration ),  recreational drugs , and substances considered inedible, such as  foreign bodies  or  excrement . Ingestion is a common route taken by  pathogenic   organisms  and  poisons  entering the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5431", "text": "Ingestion can also refer to a mechanism picking up something and making it enter an internal hollow of that mechanism, e.g. \" a  grille  was fitted to prevent the pump from ingesting  driftwood \"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5432", "text": "Some  pathogens  are  transmitted  via ingestion, including  viruses ,  bacteria , and  parasites . Most commonly, this takes place via the  faecal-oral route . An intermediate step is often involved, such as  drinking water  contaminated by  faeces  or  food  prepared by workers who fail to practice adequate  hand-washing , and is more common in regions where  untreated   sewage  is common.  Diseases  transmitted via the fecal-oral route include  hepatitis A ,  polio , and  cholera ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5433", "text": "Some pathogenic organisms are typically ingested by other routes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5434", "text": "Disk batteries , also called button cells, are often mistakenly ingested, particularly by  children  and the  elderly . They may be mistaken for a  medication   pill  because of their size and shape, or they may be swallowed after being held in the mouth while the battery is being changed. Battery ingestion can cause medical problems including blocked  airway ,  vomiting ,  irritability , persistent  drooling , and  rash  (due to  nickel  metal  allergy ). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5435", "text": "Pica  is an abnormal appetite for non- nutritive  objects or for food items in a form not normally eaten, such as  flour .  Coprophagia  is the consumption of  feces , an  abnormal ingestive behavior  common in some animals."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5436", "text": "Interstitial cells of Cajal  (ICC) are  interstitial cells  found in the  gastrointestinal tract . There are different types of ICC with different functions. ICC and another type of interstitial cell, known as  platelet-derived growth factor receptor alpha  (PDGFR\u03b1) cells, are electrically coupled to  smooth muscle cells  via  gap junctions , that work together as an  SIP functional syncytium . [ 2 ]   Myenteric  interstitial cells of Cajal (ICC-MY) serve as pacemaker cells that generate the bioelectrical events known as  slow waves . [ 3 ]  Slow waves conduct to smooth muscle cells and cause phasic contractions. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5437", "text": "The picture to the right shows an isolated Interstitial cell of Cajal from the Myenteric plexus of the mouse small intestine grown in a primary cell culture. This cell type can be characterized morphologically as having a small cell body often triangular or stellate-shaped with several long processes branching out into secondary and tertiary extensions - these processes often contact smooth muscle cells. They have contractile behaviour in both the cell body and the extended processes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5438", "text": "These cells are derived from  mesoderm , [ 6 ]  unlike the  enteric neurons  that arise from neural crest cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5439", "text": "Intramuscular Interstitial cells of Cajal (ICC-IM) are involved in mediating responses to neurotransmission. [ 7 ]   All ICC in the gastrointestinal tract express calcium-activated chloride channels encoded by the gene  ANO1 .  These channels are activated by release of calcium in ICC and are important for both the pacemaker activity of ICC and their responses to neurotransmitters.  A recent review noted that  carbachol  increases ICC activity through this channel. [ 8 ] [ 9 ]   ANO1-knockout mice fail to produce slow waves and ANO1 channel inhibitors block slow waves. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5440", "text": "ICC are also thought to be present in other types of smooth muscle tissues. But with few exceptions the function of these cells is not well understood and currently an area of active  research ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5441", "text": "ICC serve as  electrical  pacemakers and generate spontaneous electrical  slow waves  in the gastrointestinal (GI) tract.  Electrical slow waves spread from ICC to  smooth muscle cells  and the resulting depolarization initiates  calcium ion  entry and contraction.  Slow waves organize gut contractions into phasic contractions that are the basis for  peristalsis  and  segmentation . [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5442", "text": "The frequency of ICC pacemaker activity differs in different regions of the GI tract: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5443", "text": "ICC also mediate neural input from  enteric   motor neurons . Animals lacking ICC have greatly reduced responses to the  neurotransmitter   acetylcholine , released from excitatory motor neurons, and to the  transmitter   nitric oxide , released from  inhibitory motor neurons . Loss of ICC in  disease , therefore, may interrupt normal neural control of gastrointestinal (GI) contractions and lead to  functional GI disorders , such as  irritable bowel syndrome . [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5444", "text": "ICC also express mechano-sensitive mechanisms that cause these cells to respond to stretch. Stretching GI muscles can affect the  resting potentials  of ICC and affect the frequency of pacemaker activity.   Carbachol  increases ICC activity through  ANO1  activation. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5445", "text": "ICC are also critical in the propagation of electrical slow waves.  ICC form a network through which slow wave activity can propagate. If this network is broken, then 2 regions of muscle will function independently. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5446", "text": "ICCs are thought to be the cells from which  gastrointestinal stromal tumours  (GISTs) arise. [ 11 ]  Also, abnormalities in the ICC network is one cause of  chronic intestinal pseudo-obstruction . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5447", "text": "The interstitial cells of Cajal are named after  Santiago Ram\u00f3n y Cajal , [ 13 ]  a  Spanish   pathologist  and  Nobel laureate ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5448", "text": "In  histology , an  intestinal gland  (also  crypt of  Lieberk\u00fchn  and  intestinal crypt ) is a  gland  found in between  villi  in the  intestinal epithelial  lining of the  small intestine  and  large intestine  (or colon). The glands and intestinal villi are covered by  epithelium , which contains multiple types of  cells :  enterocytes  (absorbing water and electrolytes),  goblet cells  (secreting mucus),  enteroendocrine cells  (secreting hormones), cup cells,  myofibroblast ,  tuft cells , and at the base of the gland,  Paneth cells  (secreting anti-microbial peptides) and  stem cells ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5449", "text": "Intestinal glands are found in the  epithelia  of the  small intestine , namely the  duodenum ,  jejunum , and  ileum , and in the  large intestine  (colon), where they are sometimes called  colonic crypts . Intestinal glands of the small intestine contain a base of replicating  stem cells ,  Paneth cells  of the  innate immune system , and  goblet cells , which produce mucus. [ 1 ]  In the colon, crypts do not have Paneth cells. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5450", "text": "The  enterocytes  in the small intestinal  mucosa  contain  digestive enzymes  that digest specific foods while they are being absorbed through the epithelium. These enzymes include  peptidase ,  sucrase ,  maltase ,  lactase  and intestinal  lipase . This is in contrast to the  gastric glands  of the  stomach  where  chief cells  secrete  pepsinogen ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5451", "text": "Also, new epithelium is formed here, which is important because the cells at this site are continuously worn away by the passing food. The basal (further from the  intestinal lumen ) portion of the crypt contains multipotent  stem cells . During each  mitosis , one of the two daughter cells remains in the crypt as a stem cell, while the other differentiates and migrates up the side of the crypt and eventually into the  villus . These stem cells can differentiate into either an absorptive ( enterocytes ) or secretory ( Goblet cells ,  Paneth cells ,  enteroendocrine cells ) lineages. [ 3 ]  Both  Wnt  and  Notch  signaling pathways play a large role in regulating cell proliferation and in intestinal  morphogenesis  and  homeostasis . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5452", "text": "Loss of proliferation control in the crypts is thought to lead to  colorectal cancer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5453", "text": "Intestinal juice ( also called  succus entericus [ 5 ] ) refers to the clear to pale yellow watery secretions from the glands lining the  small intestine  walls. The  Brunner's glands  secrete large amounts of alkaline mucus in response to (1) tactile or irritating stimuli on the duodenal mucosa; (2) vagal stimulation, which increases Brunner's glands secretion concurrently with increase in stomach secretion; and (3) gastrointestinal hormones, especially  secretin . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5454", "text": "Its function is to complete the process begun by  pancreatic juice ; the  enzyme   trypsin  exists in pancreatic juice in the inactive form  trypsinogen , it is activated by the intestinal  enterokinase  in intestinal juice. Trypsin can then activate other protease enzymes and catalyze the reaction pro-colipase \u2192 colipase.   Colipase  is necessary, along with  bile salts , to enable  lipase  function.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5455", "text": "Intestinal juice also contains  hormones ,  digestive enzymes ,  mucus , substances to neutralize  hydrochloric acid  coming from the  stomach . Various  exopeptidase  which further digests  polypeptides  into  amino acids  complete the digestion of  proteins . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5456", "text": "The intestinal glands in the colon are often referred to as colonic crypts. The  epithelial  inner surface of the colon is punctuated by invaginations, the colonic crypts. The colon crypts are shaped like microscopic thick-walled test tubes with a central hole down the length of the tube (the crypt  lumen ). Four tissue sections are shown here, two (A and B) cut across the long axes of the crypts and two (C and D) cut parallel to the long axes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5457", "text": "In these images the cells have been  stained  to show a brown-orange color if the cells produce a  mitochondrial  protein called  cytochrome c oxidase subunit I  (CCOI or COX-1).  The  nuclei  of the cells (located at the outer edges of the cells lining the walls of the crypts) are stained blue-gray with  haematoxylin . As seen in panels C and D, crypts are about 75 to about 110 cells long. The average crypt circumference is 23 cells. [ 8 ]  From the images, an average is shown to be about 1,725 to 2530 cells per colonic crypt. Another measure was attained giving a range of 1500 to 4900 cells per colonic crypt. [ 9 ]  Cells are produced at the crypt base and migrate upward along the crypt axis before being shed into the colonic  lumen  days later. [ 8 ]   There are 5 to 6 stem cells at the bases of the crypts. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5458", "text": "As estimated from the image in panel A, there are about 100 colonic crypts per square millimeter of the colonic epithelium. [ 10 ]   The length of the human colon is, on average 160.5\u00a0cm (measured from the bottom of the cecum to the colorectal junction) with a range of 80\u00a0cm to 313\u00a0cm. [ 11 ]  The average inner circumference of the colon is 6.2\u00a0cm. [ 10 ]  Thus, the inner surface epithelial area of the human colon has an area, on average, of about 995 cm 2 , which includes 9,950,000 (close to 10 million) crypts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5459", "text": "In the four tissue sections shown here, many of the intestinal glands have cells with a  mitochondrial DNA  mutation in the CCOI gene and appear mostly white, with their main color being the blue-gray staining of the nuclei.  As seen in panel B, a portion of the stem cells of three crypts appear to have a mutation in CCOI, so that 40% to 50% of the cells arising from those stem cells form a white segment in the cross cut area."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5460", "text": "Overall, the percentage of crypts deficient for CCOI is less than 1% before age 40, but then increases linearly with age. [ 7 ]  Colonic crypts deficient for CCOI reaches, on average, 18% in women and 23% in men, by 80\u201384 years of age. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5461", "text": "Crypts of the colon can reproduce by fission, as seen in panel C, where a crypt is dividing to form two crypts, and in panel B where at least one crypt appears to be fissioning.  Most crypts deficient in CCOI are in clusters of crypts (clones of crypts) with two or more CCOI-deficient crypts adjacent to each other (see panel D). [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5462", "text": "Crypt  inflammation  is known as  cryptitis  and characterized by the presence of  neutrophils  between the  enterocytes .  A severe cryptitis may lead to a crypt  abscess ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5463", "text": "Pathologic processes that lead to Crohn's disease, i.e. progressive intestinal crypt destruction, are associated with branching of the crypts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5464", "text": "Causes of crypt branching include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5465", "text": "Intestinal glands contain adult stem cells referred to as  intestinal stem cells . [ 12 ]  These cells have been used in the field of stem biology to further understand  stem cell niches , [ 13 ]  and to generate intestinal  organoids . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5466", "text": "The crypts of Lieberk\u00fchn are named after the eighteenth-century German anatomist  Johann Nathanael Lieberk\u00fchn ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5467", "text": "The  intestinal mucosal barrier , also referred to as  intestinal barrier , refers to the property of the  intestinal mucosa  that ensures adequate containment of undesirable  luminal  contents within the intestine while preserving the ability to absorb  nutrients . The separation it provides between the body and the gut prevents the uncontrolled translocation of luminal contents into the body proper. Its role in protecting the mucosal tissues and  circulatory system  from exposure to  pro-inflammatory molecules , such as  microorganisms ,  toxins , and  antigens  is vital for the maintenance of health and well-being. [ 1 ] [ 2 ] [ 3 ]  Intestinal mucosal barrier dysfunction has been implicated in numerous health conditions such as:  food allergies ,  microbial infections ,  irritable bowel syndrome ,  inflammatory bowel disease ,  celiac disease ,  metabolic syndrome ,  non-alcoholic fatty liver disease ,  diabetes , and  septic shock . [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5468", "text": "The intestinal mucosal barrier is a  heterogeneous  entity composed of physical, biochemical, and immune elements elaborated by the intestinal mucosa. The central component is the  intestinal epithelial layer , which provides physical separation between the lumen and the body. The secretion of various molecules into the lumen reinforces the barrier function on the extra-epithelial side, while a variety of immune cells provide additional protection below the epithelial layer. [ 3 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5469", "text": "Mucus  forms a layer (or layers, in the case of the  colon ) that separates the bulk of the luminal contents from the intestinal epithelium. The mucus consists of a highly  glycosylated   hydrated gel  formed by  mucin molecules  that are secreted by  goblet cells . The mucus prevents large particles from contacting the epithelial cell layer while allowing small molecules to pass. The mucus also facilitates passage of the luminal contents along the length of the intestines, protects the epithelial cells from  digestive enzymes , and prevents the direct contact of microorganisms with the epithelial layer. [ 1 ] [ 5 ] [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5470", "text": "The  intestinal epithelium  is the foremost component of the intestinal mucosal barrier. It consists of the layer of epithelial cells lining the intestine. Crucial for forming an effective barrier is the precise control of the  paracellular pathway  (a route for translocation of molecules between cells). Sealing of the space between adjacent cells is mediated by  junctional complexes  formed by protein connections elaborated by each individual cell. [ 1 ]  In addition to its protective function, the intestinal epithelium controls the selective uptake of beneficial ions, nutrients, and other substances from the lumen into the body. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5471", "text": "The  commensal microbial species  that inhabit the gut are considered by some to be part of the intestinal mucosal barrier. The  gut microbiota  can influence barrier function both directly, by stimulating epithelial cell proliferation and secretion of  IL-8 , and indirectly by producing  short-chain fatty acids , which are an important energy source for colonic epithelial cells (colonocytes). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5472", "text": "The  bile  produced by the  liver  to aid in the digestion of  lipids  has  bactericidal  properties. [ 7 ]  The  gastric acid  produced by the stomach can also kill microorganisms. [ 8 ]  Both contribute to intestinal barrier function although they are not produced by the intestinal mucosa."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5473", "text": "Specialised secretory epithelial cells called  Paneth cells  secrete abundant quantities  human \u03b1-defensins  into the intestinal lumen of healthy individuals. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5474", "text": "Lysozyme  is another defensive molecule secreted by Paneth cells into the lumen. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5475", "text": "Reg3\u03b3  is an antibacterial  lectin  secreted by Paneth cells that serves to prevent microorganisms from coming into contact with the epithelial layer. [ 3 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5476", "text": "Antimicrobial peptides (AMPs) , which are a diverse array of molecules that kill bacteria and fungi, are secreted by Paneth cells into the lumen. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5477", "text": "Secretory immunoglobulin A (sIgA)  is produced by  plasma cells  in the lamina propria and transported into the lumen by intestinal epithelial cells. [ 7 ]  SIgA blocks epithelial-specific  receptors  on pathogens, thereby preventing their attachment to epithelial cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5478", "text": "A variety of immune cells reside in the  lamina propria  which underlies the intestinal epithelium. These include  dendritic cells (DCs) ,  macrophages ,  intraepithelial lymphocytes  (IEL),  T regulatory cells (T Regs) ,  TCD4+ lymphocytes ,  B lymphocytes , and  plasma cells . [ 6 ]  This population provides immune protection that is characterised by the rapid detection and killing of microorganisms that penetrate the intestinal epithelium. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5479", "text": "Intestinal barrier integrity is malleable and multiple mechanisms have been shown to be capable of modulating intestinal permeability (a measure of intestinal barrier function). [ 4 ]  Modulating factors include  cytokines ,  immune cells , and exogenous factors. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5480", "text": "Intestinal permeability  is a measurement of intestinal mucosal barrier function and is defined as \"the facility with which intestinal epithelium allows molecules to pass through by non-mediated  passive diffusion .\" [ 11 ]  Permeability in this respect is mostly related to the measurable passage of ions and small inert molecules. Standard methods for measurement include tissue electrical resistance for in vitro testing and passage of ingested inert molecules of specific molecular weights into the urine for in vivo testing. [ 12 ] [ 13 ]  For example, in vivo testing using  lactulose  /  mannitol  consists of ingesting 5 g lactulose and 2 g mannitol followed by determination of urinary concentrations of lactulose and mannitol 5 hours after ingestion. The percentage lactulose excretion and the lactulose mannitol ratio in the urine are calculated and used as a measure of intestinal permeability. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5481", "text": "A disrupted intestinal mucosal barrier can allow passage of microbes, microbial products, and  foreign antigens  into the mucosa and the body proper. This can result in activation of the  immune system  and secretion of  inflammatory mediators . Certain immune responses might, in turn, cause cellular damage that could result in further barrier dysfunction. [ 7 ]  Defects in intestinal mucosal barrier function with the accompanying translocation of microbes and their products have been linked with a variety of conditions, [ 3 ]  some of which are thought to additionally require a  genetic predisposition . [ 15 ]  Both intestinal and extra-intestinal autoimmune disorders can result. [ 15 ]  Intestinal barrier dysfunction is thought to be precondition for and  exacerbating factor  of numerous autoimmune and inflammatory conditions, including  food allergies ,  inflammatory bowel diseases ,  celiac disease  and  diabetes . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5482", "text": "Intestinal barrier dysfunction may be a critical factor for antigen sensitisations and the  IgE / mast cell -mediated  anaphylactic  effector phase of food allergies. The development of food allergies depend on the antigen coming into contact with components of the mucosal immune system. This leads to antigen sensitisation and dietary antigen-specific CD4+  Th2 cell  and IgE production. The hypothesis is that intestinal barrier dysfunction allows dietary antigens to cross the intestinal barrier, come into contact with the mucosal immune system, and trigger an antigen-specific immune response. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5483", "text": "Reduced intestinal barrier function correlates with the severity of symptoms experienced by food allergy sufferers. Oral challenge with the implicated allergen results in an increased lactulose/mannitol ratio in the urine (a measure of intestinal permeability). [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5484", "text": "An emerging model of inflammatory bowel disease (IBD)  pathogenesis  postulates three prerequisite factors: 1) degradation of intestinal barrier function, 2) translocation of luminal contents into the lamina propria and subsequent exposure to immune cells, and 3) an inappropriate immune response. Although intestinal barrier dysfunction is clearly implicated in the development of inflammatory bowel disease, it is unclear what initiates the self-perpetuating cycle that leads to disease exacerbation. Nevertheless, there is a growing body of evidence that implicates increased intestinal permeability as a primary  etiologic factor  of inflammatory bowel disease pathogenesis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5485", "text": "Altered intestinal barrier function may play a role in the development of celiac disease. By allowing  gliadin , the causative agent of celiac disease, to cross the intestinal barrier, inappropriate activation of the immune system can occur. Celiac disease sufferers have been shown to have elevated intestinal permeability and altered tight junctions. Moreover, these disruptions persist in patients who successfully maintain a  gluten-free diet . Data also exist demonstrating that increased intestinal permeability is present prior to onset of celiac disease. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5486", "text": "A combination of genetics, dysregulated intestinal barrier function, and inappropriate immune responses has been hypothesised to play a role in  type 1 diabetes . Elevated intestinal permeability has been reported observed in patients at disease onset. The resulting increase in exposure to antigens can trigger  autoimmune  destruction of  beta cells  in the  pancreas . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5487", "text": "Defects in intestinal mucosal barrier function have also been implicated in  irritable bowel syndrome ,  metabolic syndrome ,  non-alcoholic fatty liver disease , and  septic shock . [ 3 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5488", "text": "Psychological  and  physical stress  can induce a variety of alterations in intestinal function. These include changes in  gut motility ,  intestinal permeability , ion flux,  fluid balance  and mucus secretion. Furthermore, acute and chronic stress in  animal models  has shown that stress can cause degradation of intestinal barrier function. [ 4 ]  Psychological stress can influence the clinical outcome of  inflammatory bowel disease  and  irritable bowel syndrome . Long-term stress has been shown to be positively associated with an increased propensity for relapse of  ulcerative colitis . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5489", "text": "Cummings adopted the term mucosal barrier in 2004 to describe the \"complex structure that separates the internal milieu from the luminal environment.\" [ 16 ]  More recently, intestinal barrier has been used by gastroenterologists, immunologists and microbiologists to emphasise the component of the intestine that protects the body from microorganisms and their toxins. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5490", "text": "Intestinal permeability  is a term describing the control of material passing from inside the  gastrointestinal tract  through the  cells  lining the  gut wall , into the rest of the body. The intestine normally exhibits some permeability, which allows nutrients to pass through the gut, while also maintaining a barrier function to keep potentially harmful substances (such as  antigens ) from leaving the intestine and migrating to the body more widely. [ 1 ]  In a healthy human intestine, small particles (< 4  \u00c5  in radius) can migrate through  tight junction   claudin  pore pathways, [ 2 ]  and particles up to 10\u201315 \u00c5 (3.5  kDa ) can transit through the paracellular space uptake route. [ 3 ]  There is some evidence abnormally increased intestinal permeability may play a role in some chronic diseases and inflammatory conditions. [ 4 ]  The most well understood condition with observed increased intestinal permeability is  celiac disease . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5491", "text": "The barrier formed by the  intestinal epithelium  separates the external environment (the contents of the intestinal  lumen ) from the body [ 6 ]  and is the most extensive and important  mucosal surface  of the body. [ 7 ]  However, the intestinal mucin can also be barriers for the host antimicrobial peptides, thus plays a bidirectional barrier for host-microbial interaction. [ 8 ]  The intestinal epithelium is composed of a single layer of cells and serves two crucial functions. First, it acts as a barrier, preventing the entry of harmful substances such as foreign  antigens ,  toxins  and  microorganisms . [ 6 ] [ 9 ]  Second, it acts as a selective filter which facilitates the uptake of dietary  nutrients ,  electrolytes , water and various other beneficial substances from the intestinal lumen. [ 6 ]  Selective permeability is mediated via two major routes: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5492", "text": "One way in which intestinal permeability is modulated is via  CXCR3  receptors in cells in the  intestinal epithelium , which respond to  zonulin . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5493", "text": "Gliadin  (a glycoprotein present in wheat) activates zonulin signaling in all people who eat  gluten , irrespective of the genetic expression of  autoimmunity . This leads to increased intestinal permeability to macromolecules. [ 4 ] [ 12 ] [ 5 ]  Bacterial infections such as  cholera , select enteric viruses, parasites, and stress can all modulate intestinal tight junction structure and function, and these effects may contribute to the development of chronic intestinal disorders. [ 4 ] [ 13 ] [ 12 ]  So called absorption modifying excipients, investigated for the possibility of increasing intestinal drug absorption, can increase the gut permeability. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5494", "text": "Most people do not experience adverse symptoms, but the opening of intercellular tight junctions (increased intestinal permeability) can act as a trigger for diseases that can affect any organ or tissue depending on genetic predisposition. [ 4 ] [ 5 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5495", "text": "Increased intestinal permeability is a factor in several diseases, such as  celiac disease , [ 16 ]   irritable bowel syndrome ,  [ 17 ]   type 1 diabetes , [ 18 ]   type 2 diabetes , [ 16 ]   rheumatoid arthritis ,  spondyloarthropathies , [ 19 ]   inflammatory bowel disease , [ 4 ] [ 20 ]   schizophrenia , [ 21 ] [ 22 ]  certain types of  cancer , [ 4 ]   obesity , [ 23 ]   fatty liver , [ 24 ]   atopy  and  allergic  diseases, [ 18 ]  among others. In the majority of cases, increased permeability develops prior to disease, [ 4 ]  but the cause\u2013effect relationship between increased intestinal permeability in most of these diseases is not clear. [ 20 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5496", "text": "A well studied model is celiac disease, in which increased intestinal permeability appears secondary to the abnormal immune reaction induced by gluten and allows fragments of gliadin protein to get past the intestinal epithelium, triggering an immune response at the intestinal submucosa level that leads to diverse gastrointestinal or extra-gastrointestinal symptoms. [ 26 ] [ 27 ]   Other environmental triggers may contribute to alter permeability in celiac disease, including intestinal infections and iron deficiency. [ 26 ]  Once established, this increase of permeability might self-sustain the inflammatory immune responses and perpetuate a vicious cycle. [ 26 ]  Eliminating gluten from the diet leads to normalization of intestinal permeability and the autoimmune process shuts off. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5497", "text": "In normal physiology,  glutamine  plays a key role in signalling in  enterocytes  that are part of the intestinal barrier, but it is not clear if  supplementing the diet  with glutamine is helpful in conditions where there is increased intestinal permeability. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5498", "text": "Prebiotics  and certain  probiotics  such as  E. coli  strain Nissle 1917  have been found to reduce increased intestinal permeability. [ 12 ]   Lactobacillus rhamnosus , [ 30 ]   Lactobacillus reuteri , [ 30 ]  and  Faecalibacterium prausnitzii [ 31 ]  have also been shown to significantly reduce increased intestinal permeability."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5499", "text": "Larazotide acetate  (previously known as AT-1001) is a zonulin receptor antagonist that has been probed in clinical trials. It seems to be a drug candidate for use in conjunction with a  gluten-free diet  in people with celiac disease, with the aim to reduce the intestinal permeability caused by gluten and its passage through the epithelium, and therefore mitigating  the resulting cascade of immune reactions. [ 27 ] [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5500", "text": "Genetic disruption of arginase-2 in mouse attenuates the onset of senescence and extends lifespan. [ 33 ] [ 34 ] \nArginase inhibitors have been developed to reduce the effect of NO on intestinal permeability. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5501", "text": "\" Leaky gut syndrome \" is a hypothetical, medically unrecognized condition. [ 20 ]  It has been popularized by some  nutritionists  and practitioners of  alternative medicine  who claim that  restoring normal functioning  of the  gut wall  can cure many systemic health conditions. However, reliable source evidence to support this claim has not been published. Nor has there been published any reliable evidence that the treatments promoted for so-called \"leaky gut syndrome\"\u2014including nutritional supplements,  probiotics , [ 12 ]  herbal remedies, (or low- FODMAP  diets; low-sugar, antifungal, or  gluten-free  diets)\u2014have any beneficial effect for most of the conditions they are claimed to help. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5502", "text": "Exercise-induced stress can diminish intestinal barrier function. [ 35 ] [ 36 ] [ 37 ]  In humans, the level of physical activity modulates the gastrointestinal  microbiota , an increased intensity and volume of exercise may lead to gut  dysbiosis , and supplementation may keep  gut microbiota  in  biodiversity , especially with intense exercise. [ 38 ]  In mice, exercise reduced the richness of the microbial community, but increased the distribution of bacterial communities. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5503", "text": "Intraepithelial lymphocytes  ( IEL ) are  lymphocytes  found in the  epithelial  layer of mammalian  mucosal linings , such as the  gastrointestinal (GI) tract  and  reproductive tract . [ 1 ]  However, unlike other  T cells , IELs do not need priming. Upon encountering antigens, they immediately release  cytokines  and cause killing of infected target cells. In the GI tract, they are components of  gut-associated lymphoid tissue  (GALT). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5504", "text": "Intestinal IELs are long-lived resistant effector cells spread along the entire length of intestine, where they patrol the space between intestinal  epithelial cells  (IEC) and the  basement membrane  (the intraepithelial space). Epithelium of  small intestine  contains approximately 1 IEL per 10  enterocytes . [ 3 ]  Due to their constant exposure to of antigens at mucosal barrier, they have unique antigen-experienced activated phenotypes and they constantly express  CD103  (\u03b1E integrin), that is distinct from the conventional T cells in the intestine. [ 3 ]  IELs are mainly T cells with mixture of subsets. They are divided into two groups \u2013 conventional and unconventional IELs. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5505", "text": "In mice both groups are retained in almost equal proportions. [ 5 ]  In humans, the majority of IELs are alpha beta T cells. 15% of IELs are gamma delta T cells and thus represent a minor component of human IELs. However, IELs significantly increase under certain conditions, such as  celiac disease . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5506", "text": "The majority of IELs (80%) are  CD3+ , and over 75% of these also express  CD8 . IELs can be divided into two major subsets based on their CD8 coreceptor expression. [ 5 ]  One subset of IELs typically express activation marker CD8\u03b1\u03b1 and some IELs express CD8\u03b1\u03b2 +  marker (CD8\u03b1\u03b2 promotes  TCR  activation, whereas CD8\u03b1\u03b1 suppresses TCR signals)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5507", "text": "In both humans and mice IELs express higher levels of  CD103 , activation marker  CD69 ,  granzyme B  and  perforin  cytolytic granules.  CD25  expression is lower in comparison with effector memory T cells. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5508", "text": "Expression of CD8\u03b1\u03b1 is an important phenotypic marker of IELs, but not all IELs subpopulations express this molecule. CD8\u03b1\u03b1  homodimer  is an alternative isoform to classical  CD8 \u03b1\u03b2 heterodimer, which is expressed on conventional  CD8 T-cells . CD8\u03b1\u03b1 is mainly expressed by effector or mature antigen-experienced cells in the gut. This molecule can bind  MHC I , but, opposed to the function of CD8\u03b1\u03b2, CD8\u03b1\u03b1 reduces sensitivity of  TCR  towards antigens. Thus, when recognizing MHC I, CD8\u03b1\u03b1 functions as a repressor of activation. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5509", "text": "CD8\u03b1\u03b1 can also recognize thymus leukemia (TL) antigen, which is a  non-classical MHC I  molecule that is expressed in  thymus  and in intestinal epithelium. Interaction between TL and CD8\u03b1\u03b1 does not serve for migration of IELs into the epithelium, but it is important for modulating immune response of IELs. [ 9 ]  It has been suggested that cross-talk between TL and CD8\u03b1\u03b1 might regulate IELs survival and proliferation. [ 8 ]  More accurately, TL prevents proliferation of IELs, when there is co-occurrence of weak TCR stimulation. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5510", "text": "Induced IELs (TCR\u03b1\u03b2+ CD8\u03b1\u03b2 + ) are generated from  naive T cells  during an  immune response . TCR\u03b1\u03b2 +  CD8\u03b1\u03b1 (natural IELs) cells differentiate in the  thymus . [ 6 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5511", "text": "Development and cytolytic activation are independent of live micro-organisms but they become cytolytic in response to the exogenous antigenic substances other than live micro-organisms in the gut. IEL T cells acquire their activated memory phenotype post-thymically, in response to  antigens  encountered in the periphery. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5512", "text": "Their role in immune system is crucial because IELs provide a first line of defense at this extensive barrier with the outside world. All IEL T cells are antigen-experienced T cells, which typically display a cytotoxic functional phenotype. IELs mediate antigen-specific delayed-type hypersensitivity (DTH) responses, exhibit virus-specific CTL function, to express  natural killer  (NK)-like activity and produce a local  graft-versus-host reaction (GVHR)  when transferred to semiallogeneic hosts. IELs are also able to produce a variety of  cytokines  which are characteristically produced by T h 1- and T h 2-type cells and can also provide help for  B cell  responses. [ 6 ] [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5513", "text": "An elevated IEL population, as determined by biopsy, typically indicates ongoing inflammation within the mucosa.  In diseases such as  celiac sprue , IEL elevation throughout the small intestine is one of many specific markers. [ 1 ]  IELs have heightened activated status that can lead to inflammatory disease such as IBD, promote cancer development and progression, [ 12 ]  or become the malignant cells in  enteropathy-associated T-cell lymphoma , a lymphoma that is a complication of celiac sprue. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5514", "text": "Alternatively, elevated IEL populations can be a marker for developing neoplasia in the tissue such as found in  cervical  and  prostate  cancers, as well as some  colorectal cancers , particularly those associated with  Lynch syndrome  (hereditary non-polyposis colon cancer <HNPCC>). [ 15 ]  IELs themselves can, when chronically activated, undergo mutation that can lead to  lymphoma . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5515", "text": "IELs can be divided into different subpopulations based on molecular markers expression, mainly by expression of TCR and CD8\u03b1\u03b1, and by origin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5516", "text": "Also termed conventional IELs, express TCR\u03b1\u03b2 together with CD4 or CD8\u03b1\u03b2 and are derived from antigen-experienced T cells that home to intraepithelial space. Contrary to natural IELs, induced IELs are the progeny of  MHCI -restricted CD8\u03b1\u03b2 or  MHCII -restricted CD4 na\u00efve T cells that further undergo a post-thymic differentiation. These cells express activation markers ( CD44 ,  CD69 ) and unlike natural TCR + IELs express  CD2 ,  CD5 ,  CD28 ,  LFA-1 , and  Thy1 . Upon the entry into the intestinal epithelium, these cells can start express also CD8\u03b1\u03b1. [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5517", "text": "TCR\u03b1\u03b2 + CD4 +  IELs arise from conventional peripheral  CD4 +  T-cells . These cells migrate into the intestinal epithelium as effector or tissue-resident memory T cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5518", "text": "In mice, up to 50% of these IELs can express CD8\u03b1\u03b1 homodimer, which they acquire in the intestinal epithelium after external stimuli such as  TGF-\u03b2 ,  IFN-\u03b3 ,  IL-27  and  retinoic acid . Function of TCR\u03b1\u03b2 +  CD4 +  CD8\u03b1\u03b1 +  IELs is unclear. Even though they express granzymes and have cytolytic properties, it has been suggested that they can also have regulatory properties in the context of chronic intestinal inflammation. [ 3 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5519", "text": "These IELs emerge from peripherally activated conventional CD8 +  T-cells and home to the intestinal epithelium, where they function as effector or memory cells. They continuously express  integrin \u03b27 ,  granzyme B ,  CD103  and  CD69  and produce lower amounts of  TNF-\u03b1  and  IFN-\u03b3  as opposed to the conventional  CD8 +  T-cells . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5520", "text": "Some of these cells also express CD8\u03b1\u03b1 homodimer and can be pathogenic during  coeliac disease  in humans. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5521", "text": "These DP IELs are subset of induced IELs, which are CD4 +  IELs with some functions of CD8 +  IELs and under physiological condition their number in the intestine is very small. During the intestinal inflammation, levels of DP IELs significantly increase. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5522", "text": "DP IELs develop independently of the  thymus  and contrary to natural IELs, these cells increase with age, especially when they are exposed to  exogenous antigens . Their migration into the intestinal epithelium depends mainly on the luminal bacteria and the dietary antigens. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5523", "text": "DP IELs induction is directed by the transcriptional regulation. During the development of IELs, CD4 +  T cells downregulate ThPOK and instead start to express  Runx3  transcription factor, because CD4 + CD8aa +  IELs have low levels of ThPOK expression while the expression of Runx3 is very high. T-bet inducing environment is also required for the Runx3 upregulation, most likely containing  IFN-y ,  IL-27 ,  IL-15  and  Retionic acid  (RA). [ 19 ]  RA have the ability to induce an expression of the intetsine-homing receptors, such as  \u03b14\u03b27-integrin  and CC-chemokine receptor 9 ( CCR9 ). [ 20 ]  Another transcription factor responsible for DP IELs induction is the  Aryl hydrocarbon receptor  (AhR). AhR is ligand-dependent transcription factor, and its activation is responsible for ThPOK downregulation. AhR is activated by  indole  metabolites of  tryptophan  induced by microbiota, such as  Lactobacillus reuteri . [ 21 ]  Therefore, the DP IELs induction is dependent on the microbiota composition and the diet."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5524", "text": "The function of CD4CD8aa IELs is due to their CD8 phenotype and  granzyme B  expression to prevent pathogens from invading and to maintain integrity of the intestinal epithelial barrier. Their CD4 phenotype is responsible for  IL-10  and  TGF-\u03b2  secretion that prevents Th1-induced inflammation in the intestine, therefore their role can be complementary to T regulatory cells. [ 18 ] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5525", "text": "DP IELs probably play role in intestinal homeostasis because of their immunosuppressive function. But for their cytotoxic responses they may play an important role in the pathological process of  IBD . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5526", "text": "Also termed unconventional IELs, express either TCR\u03b1\u03b2 or TCR\u03b3\u03b4 and do not express either CD4 or CD8\u03b1\u03b2, but express CD8\u03b1\u03b1 homodimers. In contrast to induced TCR +  IELs lack expression of CD2, CD5, CD28, LFA-1, and Thy1. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5527", "text": "In mice, these IELs are the most abundant at birth and with age their numbers decrease. In humans, these cells are present during gestation but are very rare in adulthood. TCR\u03b1\u03b2 +  IELs develop in thymus where they undergo agonist positive selection and thereby are self-reactive. Nevertheless, they have regulatory properties and protect against  colitis  in animal experiments. These cells are influenced by normal intestinal  microbiota  and  vitamin D .  NOD2  receptor expressed by  antigen presenting cells  and epithelial cells in the intestine recognizes microbes and triggers the production of  IL-15  cytokine, which promotes TCR\u03b1\u03b2 + CD8\u03b1\u03b1 +  IELs. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5528", "text": "TCR\u03b3\u03b4 +  IELs develop outside of thymus and their maintenance and function in the intestinal epithelium is influenced by a cross-talk with enterocytes. Moreover, they can migrate through the epithelium with the help of interactions with epithelial cells. [ 23 ]  Most of these cells express V\u03b37 in mice and V\u03b34 in humans. Their function resides in the protection of the intestinal barrier against pathogens early in the infection and later they quench the inflammation and protect the barrier from tissue damage. The mechanism is not clear, but TCR\u03b3\u03b4 +  IELs have cytotoxic properties and can produce cytokines  TGF-\u03b2 ,  TNF-\u03b1 ,  IFN-\u03b3 ,  IL-13  and  IL-10  and  antimicrobial peptides , all of which can contribute to the diverse functions. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5529", "text": "Similar functions have been found in the context of  colitis , where these cells seem to have pathogenic role at the beginning, whereas later they protect the epithelium against tissue damage. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5530", "text": "IELs that do not express TCR."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5531", "text": "These cells show properties of  NK cells . In humans, they are elevated during  Crohn\u00b4s disease  and in mice, they are pathogenic during colitis. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5532", "text": "These innate lymphocytes express homodimer CD8\u03b1\u03b1 and CD3 and develop outside of thymus. They have cytotoxic and phagocytic properties, express  MHC II  and thereby can present antigens to conventional CD4 +  T-cells. iCD8\u03b1 protect against bacterial infections and promotes experimental colitis. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5533", "text": "These cells are very similar to iCD8\u03b1 population and it is unclear if this is a different subset of cells or only precursors of iCD8\u03b1. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5534", "text": "IEL of the GI tract"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5535", "text": "A  Kock pouch  is a continent pouch formed by the terminal  ileum  after  colectomy .  The procedure was detailed and first performed in 1969 by Dr.  Nils Kock .  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5536", "text": "Kock pouch ileostomy is indicated for patients who are unfit for  ileal pouch anal anastomosis  (IPAA) because the anus and anal sphincter will be removed during the operation; and patients who develop severe  incontinence  after IPAA. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5537", "text": "A Kock pouch need not be created during the initial colectomy surgery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5538", "text": "The pouch has a volume of 500ml to 1000ml so that  feces  can be stored temporarily and the patient need not carry a  stoma bag . This improves the patient's quality of life. A valve is constructed by  intussusception  of the terminal ileum, [ 2 ]  thereby containing the stored feces. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5539", "text": "Lactase persistence  or  lactose tolerance  is the continued activity of the  lactase   enzyme  in adulthood, allowing the  digestion  of  lactose  in  milk . In most  mammals , the activity of the enzyme is dramatically reduced after  weaning . [ 1 ]  In some human populations though, lactase persistence has recently  evolved [ 2 ]  as an  adaptation  to the consumption of nonhuman milk and dairy products beyond infancy. Lactase persistence is very high among northern Europeans, especially  Irish people . Worldwide, most people are lactase  non -persistent, [ 1 ]  and are affected by varying degrees of  lactose intolerance  as adults. However, lactase persistence and lactose intolerance can overlap."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5540", "text": "The distribution of the lactase persistence (LP)  phenotype , or the ability to digest lactose into adulthood, is not homogeneous in the world. Lactase persistence frequencies are highly variable. In Europe, the distribution of the lactase persistence phenotype is  clinal , with frequencies ranging from 15\u201354% in the south-east to 89\u201396% in the north-west. [ 3 ]  For example, only 17% of  Greeks  and 14% of  Sardinians  are predicted to possess this phenotype, while around 80% of  Finns   and  Hungarians  and 100% of  Irish people  are predicted to be lactase persistent. [ 4 ]  Similarly, the frequency of lactase-persistence is clinal in India, a 2011 study of 2,284 individuals identifying a prevalence of LP in the  Ror  community, of  Haryana , in the North West, of 48.95%, declining to 1.5% in the  Andamanese , of the South East, and 0.8% in the Tibeto-Burman communities, of the North East. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5541", "text": "High frequencies of lactase persistence are also found in some places in Sub-Saharan Africa [ 7 ] [ 8 ] \nand in the Middle East. [ 9 ] [ 10 ] \nBut the most common situation is intermediate to low lactase persistence: intermediate (11 to 32%) in Central Asia, [ 11 ]  low (<=5%) in  Native Americans , East Asians, most Chinese populations [ 2 ]  and some African populations. [ 3 ] [ 4 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5542", "text": "In Africa, the distribution of lactase persistence is \"patchy\": [ 12 ] [ 13 ] [ 3 ]  high variations of frequency are observed in neighbouring populations, for example between  Beja  and  Nilotes  from Sudan. [ 14 ]  This makes the study of lactase persistence distribution more difficult. [ 4 ]  High percentages of lactase persistence phenotype are found in traditionally  pastoralist  populations like  Fulani  and  Bedouins . [ 3 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5543", "text": "Lactase persistence is prevalent in  Nguni  and certain other pastoralist populations of South Africa as a result of the dairy they consume in their diet. Lactase persistence amongst Nguni people is, however, less common than in Northern European populations because traditionally, their consumption of dairy came primarily in the form of  amasi  (known as Maas in Afrikaans), which is lower in lactose than fresh, raw milk as a result of the fermentation process it goes through. [ 16 ] [ 17 ] [ 15 ] [ 18 ] [ 19 ] [ 20 ] [ 21 ] [ 22 ] [ 23 ] [ excessive citations ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5544", "text": "Multiple studies indicate that the presence of the two  phenotypes  \"lactase persistent\" (derived phenotype) and \"lactase nonpersistent\" ( hypolactasia ) is genetically programmed, and that lactase persistence is not necessarily conditioned by the consumption of lactose after the suckling period. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5545", "text": "The lactase persistent phenotype involves high  mRNA  expression, high lactase activity, and thus the ability to digest lactose, while the lactase nonpersistent phenotype involves low mRNA expression and low lactase activity. [ 26 ]  The enzyme lactase is encoded by the gene  LCT . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5546", "text": "Hypolactasia is known to be recessively and autosomally inherited, which means that individuals with the nonpersistent phenotype are  homozygous  and received the two copies of a low lactase-activity  allele  (the ancestral allele) from their parents, who may be homozygous or at least  heterozygous  for the allele. [ 24 ]  Only one high-activity allele is required to be lactase persistent. [ 24 ] [ 25 ]  Lactase persistence behaves as a dominant trait because half levels of lactase activity are sufficient to show significant digestion of lactose. [ 1 ]   Cis-acting  transcriptional silence of the lactase gene is responsible for the hypolactasia phenotype. [ 24 ] [ 25 ]  Furthermore, studies show that only eight cases were found where the parents of a child with lactase persistence were both hypolactasic. [ 1 ]  While a variety of genetic, as well as nutritional, factors determine lactase expression, no evidence has been found for adaptive alteration of lactase expression within an individual in response to changes in lactose consumption levels. [ 1 ]  The two distinct phenotypes of hypolactasia are: Phenotype I, characterized by reduced synthesis of precursor LPH, and phenotype II, associated with ample precursor synthesis, but reduced conversion of the protein to its mature molecular form. [ 27 ] \nThe lactase enzyme has two active sites which break down lactose. The first is at Glu1273 and the second is at Glu1749, which separately break down lactose into two separate kinds of molecules. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5547", "text": "At least six mutations ( single-nucleotide polymorphisms  \u2013 SNPs) have been associated with lactase expression. [ 28 ]  They are all located in a region of the gene  MCM6  upstream of  LCT . This region is considered as an enhancer region for the transcription of  LCT . [ 29 ] [ 30 ] [ 31 ]  The first identified genetic variant associated with lactase persistence is C/T*\u221213910. [ 32 ]  The ancestral allele is C and the derived allele \u2013 associated with lactase persistence \u2013 is T. In the same study, another variant was found to also correlate with the phenotype in most of the cases: G*/A-22018. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5548", "text": "Other alleles associated with lactase persistence have been identified: G/C*-14010, [ 15 ]  C/G*-13907, [ 15 ] [ 13 ] [ 33 ]  and T/G*-13915. [ 34 ]  This variant is described as part of a compound allele with T/C*3712 in. [ 31 ]  These three variants are widespread in some populations. Rare variants were reported in a few studies, like the G/A*14107 in the Xhosa [ 35 ]  and the Fulani (from Mali); [ 28 ]  the C/T*13906 in the Fulani (from Mali). [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5549", "text": "Lactase-persistence alleles vary in their geographic distributions. Within European and populations of European ancestry, they are almost entirely correlated with the presence of the \u221213,910 C/T mutation in the enhancer region of the lactase gene ( LCT ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5550", "text": "This differs from lactase persistence allelic distributions in the rest of the world, particularly in Africa and in the Middle East, where several alleles coexist. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5551", "text": "The T/G*-13915 allele is found mostly in populations from East and North Africa and the Middle East. The allele G/C*-14010 was identified in East Africa. [ 36 ]  The C/G*13907 allele was described in Sudan and Ethiopia. [ 15 ] [ 33 ] [ 37 ]  The \"European\" allele T*13910 allele is also found in some populations from Africa, including the Fulani (from Mali, [ 28 ]  Sudan, [ 38 ]  and Cameroon [ 33 ] ) and the Khoe from South Africa. [ 20 ] [ 22 ]  This allele has also been found in Central Asia. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5552", "text": "It is not known how exactly the different variants described above regulate  LCT  expression. None of the mutations so far identified have been shown to be exclusively causal for lactase persistence, and it is possible that there are more alleles to be discovered. [ 39 ]  If we focus on the \"European variant\", the position \u221213910 has an enhancer function on the lactase promoter (the promoter facilitates the transcription of the  LCT  gene). T\u221213910 is a greater enhancer than C\u221213910, so this mutation is thought to be responsible for the differences in lactase expression, [ 40 ]  although not enough evidence is found to prove that lactase persistence is only caused by C\u221213910\u2192T\u221213910. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5553", "text": "In addition, it was shown in one study involving a Finnish population that the lactase gene has a higher expression when G\u221222018 is combined with T-13910. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5554", "text": "Lactase persistence is a textbook example of  natural selection  in humans: it has been reported to present stronger selection pressure than any other known human gene. [ 24 ]  However, the specific reasons as to why lactase persistence confers a selective advantage \"remain open to speculation\". [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5555", "text": "Several pieces of evidence for positive selection acting at the T*-13910 allele were given: it is located in a stretch of homozygosity of c. 1\u00a0Mb; [ 42 ]  the strength of selection is similar to that estimated for the resistance to malaria. [ 2 ]  Haplotype inferences were performed on data from Central Asia populations; selection was detected there as well \u2013 though less strong than in European populations. [ 11 ]  Thus, even if T*13910 may not be causative for lactase persistence, it was selected during human evolutionary history."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5556", "text": "The other variants were also proved to be under selection. The C*-14010 allele is located on a particularly long stretch of homozygosity (>\u00a02\u00a0Mb). [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5557", "text": "The compound allele G*-13915 & C*-3712 was proved to be located on a long stretch of homozygosity (1.1\u00a0Mb [ 15 ]  to 1.3\u00a0Mb [ 31 ] )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5558", "text": "The ability to digest lactose is not an evolutionary novelty in human populations. Nearly all mammals begin life with the ability to digest lactose. This trait is advantageous during the infant stage, because milk serves as the primary source for nutrition. As weaning occurs, and other foods enter the diet, milk is no longer consumed. As a result, the ability to digest lactose no longer provides a distinct fitness advantage. [ 43 ]   This is evident in examining the mammalian lactase gene ( LCT ), whose expression decreases after the weaning stage, resulting in a lowered production of lactase enzymes. [ 43 ]  When these enzymes are produced in low quantities, lactase non-persistence (LNP) results. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5559", "text": "The ability to digest fresh milk through adulthood is genetically coded for by different variants which are located upstream of the  LCT  gene and which differ among populations. Those variants are found at very high frequencies in some populations and show signatures of selection. There are two notable hypotheses with dissimilar theories which try to explain why lactase persistence phenotype has been positively selected. [ 3 ]  The first one, known as the cultural-historical hypothesis, states that the main reason for LP is the introduction of dairy-based food products into the diet, [ 3 ]  while the reverse-cause hypothesis argues that dairy consumption was embraced by the societies which were already high in LP frequency. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5560", "text": "The  gene\u2013culture coevolution  hypothesis of the positive selection of the lactase persistence phenotype is based on the observation that pastoralist populations often present high levels of lactase persistence. According to this hypothesis, the reason of selection is the nutritional advantage of being lactase persistent. [ 2 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5561", "text": "Individuals who expressed lactase-persistent phenotypes would have had a significant advantage in nutritional acquisition. [ 38 ]  This is especially true for societies in which the domestication of milk-producing animals and pastoralism became a main way of life. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5562", "text": "The combination of pastoralism and lactase persistence genes would have allowed individuals the advantage of niche construction, meaning they would have had less competition for resources by deriving a secondary food source, milk. [ 44 ]  Milk as a nutrition source may have been more advantageous than meat, as its rate of renewal is significantly faster. Rather than having to raise and slaughter animals, one cow or goat could repeatedly serve as a resource with fewer time and energy constraints. The competitive advantage conferred on lactose-tolerant individuals would have given rise to strong selective pressures for this genotype, especially in times of starvation and famine, which in turn gave rise to higher frequencies in lactase persistence within the populations. Milk is also generally less contaminated than water, which decreases exposure to pathogens or parasites. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5563", "text": "By contrast, for societies which did not engage in pastoral behaviors, no selective advantage exists for lactase persistence. Mutations which may have developed allelic variations which code for lactase production into adulthood are simply neutral mutations. They seemingly confer no fitness benefit to individuals. As a result, no selection has perpetuated the spread of these allelic variants, and the lactase persistence genotype and phenotype remains rare. [ 1 ]  For example, in East Asia, historical sources also attest that the  Chinese  did not consume milk, whereas the nomads who lived on the borders did. This reflects modern distributions of intolerance. China is particularly notable as a place of poor tolerance, whereas in  Mongolia  and the  Asian steppes , milk and dairy products are a main nutrition source. The nomads also make an alcoholic beverage, called  airag  or  kumis , from mare's milk, although the  fermentation  process reduces the amount of lactose present. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5564", "text": "Two scenarios have been proposed for the gene\u2013culture coevolution hypothesis: either lactase persistence developed and was selected after the onset of pastoralist practices (culture-historical hypothesis); or pastoralism spread only in populations where lactase persistence was already at high frequencies (reverse-cause hypothesis). There are exceptions to the hypothesis like the hunter-gatherers  Hadza  (Tanzania) with a prevalence of lactase persistence phenotype of 50%. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5565", "text": "The evolution of lactase persistence in response to pastoral behavior can be seen as an example of the  Baldwin effect , by which animals' behavior affects the selection pressure they are under. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5566", "text": "The consumption of  lactose  has been shown to benefit humans with lactase persistence through adulthood. For example, the 2009 British Women's Heart and Health Study [ 47 ]  investigated the effects on women's health of the alleles that coded for lactase persistence.  Where the C  allele  indicated lactase nonpersistence and the T allele indicated lactase persistence, the study found that women who were homozygous for the C allele exhibited worse health than women with a C and a T allele and women with two T alleles.  Women who were CC reported more hip and wrist fractures, more  osteoporosis , and more  cataracts  than the other groups. [ 48 ]  They also were on average 4\u20136\u00a0mm shorter than the other women, as well as slightly lighter in weight. [ 48 ]   In addition, factors such as metabolic traits, socioeconomic status, lifestyle, and fertility were found to be unrelated to the findings, indicating that health improvements for these women were due to dairy products consumption and exhibited lactase persistence. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5567", "text": "Another possibility is the calcium absorption hypothesis. [ 13 ] [ 48 ]  Lactose favors the intestinal absorption of calcium; it helps maintaining it in a soluble form. This can be advantageous in regions of low sunlight exposure where Vitamin D, necessary for the transport of calcium, is a limiting factor. The lactase persistence gene has been shown to correlate with higher levels of Vitamin D. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5568", "text": "The correlation between lactase persistence frequencies and latitude in 33 populations in Europe was found to be positive and significant, while the correlation between lactase persistence and longitude was not, suggesting that high levels of lactose assimilation were indeed useful in areas of low sunlight in northern Europe. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5569", "text": "Increased calcium absorption helps to prevent  rickets  and  osteomalacia . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5570", "text": "A hypothesis specific to arid climate was proposed: [ 51 ]  here, milk is not only a source of nutrients, but also a source of fluid, which could be particularly advantageous during epidemics of gastrointestinal diseases like cholera (where water is contaminated).\nHuman populations differ in the prevalence of genotypic lactase persistence, phenotypic lactose tolerance, and habitual milk consumptions. (Vliert, et al, 2018). An individual's capacity to absorb milk is widespread under three conditions. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5571", "text": "One study suggested that lactase persistence was selected for parallel to malaria resistance in the Fulani from Mali. [ 28 ]  Proposed mechanisms are: nutritional advantage of milk; low content of  p -aminobenzoic acid compared to non-milk diets; intake of immunomodulators contained in milk."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5572", "text": "Although the selective advantages of lactase persistence have been discussed, there have been studies of ethnic groups whose populations, despite relying heavily on milk consumption, currently have a low frequency of lactase persistence. [ 13 ]  A study of 303 individuals from the Beja tribe and 282 individuals from various Nilotic tribes in Sudan discovered a sharp difference between the distribution of lactase phenotypes of the two populations. Lactase persistence was determined with  hydrogen breath tests . The frequency of lactose malabsorbers was 18.4% in members of Beja tribes over the age of 30, and 73.3% in members of Nilotic tribes over the age of 30. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5573", "text": "According to the gene-culture coevolution hypothesis, the ability to digest lactose into adulthood (lactase persistence)  became advantageous to humans after the invention of  animal husbandry  and the domestication of animal species that could provide a consistent source of milk.  Hunter-gatherer  populations before the  Neolithic Revolution  were overwhelmingly lactose intolerant, [ 53 ] [ 54 ]  as are modern hunter-gatherers. Genetic studies suggest that the oldest mutations associated with lactase persistence only reached appreciable levels in human populations in the last 10,000 years. [ 55 ] [ 2 ]  This correlates with the beginning of animal domestication, which occurred during the Neolithic transition. Therefore, lactase persistence is often cited as an example of both  recent human evolution [ 15 ]  and, as lactase persistence is a genetic trait but animal husbandry a cultural trait,  gene-culture coevolution  in the mutual human-animal  symbiosis  initiated with the advent of  agriculture . [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5574", "text": "Depending on the populations, one or the other hypothesis for the selective advantage of lactase persistence is more relevant: In Northern Europe, the calcium absorption hypothesis might be one of the factors leading to the strong selection coefficients, [ 57 ]  whereas in African populations, where vitamin D deficiency is not as much of an issue, the spread of the allele is most closely correlated with the added calories and nutrition from pastoralism. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5575", "text": "Several  genetic markers  for lactase persistence have been identified, and these show that lactase persistence has multiple origins in different parts of the world (i.e. it is an example of  convergent evolution ). In particular, it has been hypothesized [ 58 ]  that the T*13910 variant appeared at least twice independently. Indeed, it is observed on two different haplotypes: H98, the more common (among others in the Finnish and in the Fulani); and H8 H12, related to geographically restricted populations. The common version is relatively older. The H98 variant \u2013 most common among Europeans \u2013 is estimated to have risen to significant frequencies about 7,500 years ago in the central  Balkans  and  Central Europe , a place and time roughly corresponding to the archaeological  Linear Pottery culture  and  Star\u010devo cultures . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5576", "text": "The T*13910 variant is also found in North Africans. Thus it probably originated earlier than 7500 ya, in the  Near East , but the earliest farmers did not have high levels of lactase persistence and did not consume significant amounts of unprocessed milk. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5577", "text": "Some hypotheses regarding the evolutionary history of lactase persistence in given regions of the world are described below."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5578", "text": "Concerning Europe, the model proposed for the spread of lactase persistence combines selection and demographic processes. [ 47 ] [ 36 ] [ 3 ] [ 13 ]  Some studies used modelling approaches to investigate the role of genetic drift. [ 3 ]  According to some models, the spread of lactase persistence in Europe can be attributed primarily to a form of  genetic drift . [ 47 ]  Evidence can also come from other fields, for example written historical records: Roman authors recorded that the people of northern Europe, particularly  Britain  and  Germany , drank unprocessed milk. This corresponds very closely with modern European distributions of lactose intolerance, where the people of Britain, Germany, and Scandinavia have a high tolerance, and those of southern Europe, especially Italy, have a lower tolerance. [ 41 ]  The lower tolerance in southern Europe can be explained by genetic drift alone but the higher tolerance in northern Europe may be a result of positive selection. [ 3 ]  2017 reports, by 23AndMe, indicated 40.4% of its customers, who self identified as European, carried a single copy of the mutated 13910C/T allele and a further 42% carried two copies of the Lactase persistence mutation. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5579", "text": "A 2015 genome-wide scan for selection using DNA gathered from 230 ancient West Eurasians who lived between 6500 and 300 BCE found that the earliest appearance of the allele responsible for lactase persistence occurred in an individual who lived in central Europe between 2450 and 2140 BCE. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5580", "text": "A 2021  archaeogenetics  study found that lactase persistence rose swiftly in early  Iron Age Britain , a thousand years before it became widespread in mainland Europe, which suggests that milk became a very important foodstuff in Britain at this time. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5581", "text": "In Central Asia, the causal polymorphism for lactase persistence is the same as in Europe (T*13910, rs4988235), suggesting genetic diffusion between the two geographical regions. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5582", "text": "It is indicated that the allele responsible for lactase persistence (T*13910) may have arisen in  Central Asia , based on the higher frequency of lactase persistence among Kazakhs who have the lowest proportion of \"western\" gene pool inferred from admixture analysis from autosomal microsatellite data. [ 11 ]  This, in turn, could also be an indirect genetic proof of early domestication of horses for milk products as recently attested from archaeological remains. [ 11 ] [ 63 ]  In Kazakhs, traditionally herders, lactase persistence frequency is estimated to 25\u201332%, of which only 40.2% have symptoms and 85\u201392% of the individuals are carriers of the T*13910 allele. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5583", "text": "In South Asia, the dominant causal polymorphism for lactase persistence is the same as in Europe (T*13910, rs4988235), suggesting genetic diffusion between the two geographical regions. A 2012 study, of 2284 individual across the region, identified an average frequency of 10.3% for the mutation, though varying in prevalence from 0.8% among the Tibeto-Burman speakers to 18.4% among Indo-European speakers; the west of India hosting the highest incidents of the derived allele. Additionally approximately 3.4% of the population possessed one of the other known mutations. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5584", "text": "The situation is more complex in  Africa , where all five main lactase persistence variants are found. [ 65 ] [ 15 ] [ 19 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5585", "text": "The presence of T*13910 alleles among the Khoe pastoralists is ascribed to gene flow from Europe. However, the presence of other alleles signals gene flow from East Africa. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5586", "text": "It has been hypothesized that the G*13915 variant dispersed from the Middle East, [ 65 ]  in association with the domestication of the  Arabian camel . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5587", "text": "The G-14009 mutation is based in Ethiopia. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5588", "text": "The G*13907 variant is concentrated among  Afroasiatic  speakers in  Northeast Africa . [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5589", "text": "The C*14010 allele is today most common among pastoralist groups inhabiting eastern Africa, from where it is thought to have spread along with pastoralism into parts of southern Africa. [ 65 ] [ 19 ] [ 20 ] [ 67 ]  Ultimately, the C*14010 lactase persistence variant is believed to have arrived from the Sahara in areas that were previously inhabited by Afroasiatic-speaking populations. This was deduced from the existence of animal husbandry- and milking-related loanwords of Afroasiatic origin in various  Nilo-Saharan  and  Niger-Congo  languages, as well as from the earliest appearance of processed milk lipids on ceramics which were found at the  Tadrart Acacus  archaeological site in  Libya  (radiocarbon-dated to c. 7,500 BP, close to the estimated age of the C*14010 mutation). [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5590", "text": "The evolutionary processes driving the rapid spread of lactase persistence in some populations are not known. [ 1 ]  Among some populations inhabiting East Africa, lactase persistence has gone from negligible to near-ubiquitous frequencies in just 3000 years, suggesting a very strong  selective pressure . [ 15 ]  Some studies also proposed that selection for lactase persistence is not as strong as supposed ( soft selective sweep ), and that its strength varies a lot depending on particular environmental conditions. [ 13 ] \nPost animal domestication, individuals gained the ability to tolerate lactose after weaning from infancy. This offered a crucial advantage to humans through natural selection by creating genetic variances. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5591", "text": "Neolithic   agriculturalists , who may have resided in  Northeast Africa  and the  Near East , may have been the source population for lactase persistence variants, including \u201313910*T, and may have been subsequently supplanted by later migrations of peoples. [ 70 ]  The  Sub-Saharan   West African  Fulani, the  North African   Tuareg , and  European agriculturalists , who are descendants of these Neolithic agriculturalists, share the lactase persistence variant \u201313910*T. [ 70 ]  While shared by Fulani and Tuareg herders, compared to the Tuareg variant, the Fulani variant of \u201313910*T has undergone a longer period of haplotype differentiation. [ 70 ]  The  Fulani  lactase persistence variant \u201313910*T may have spread, along with cattle  pastoralism , between 9686 BP and 7534 BP, possibly around 8500 BP; corroborating this timeframe for the Fulani, by at least 7500 BP, there is evidence of herders engaging in the act of  milking  in the Central  Sahara . [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5592", "text": "Lactose  malabsorption  is typical for adult mammals, and lactase persistence is a phenomenon likely linked to human interactions in the form of dairying.\nMost mammals lose the ability to digest lactose once they are old enough to find their own source of nourishment away from their mothers. [ 71 ]  After  weaning , or the transition from being milk-fed to consuming other types of food, their ability to produce lactase naturally diminishes as it is no longer needed. For example, in the time a piglet in one study aged from five to 18 days, it lost 67% of its lactose absorption ability. [ 72 ]  While nearly all humans can normally digest lactose for the first 5 to 7 years of their lives, [ 71 ]  most mammals stop producing lactase much earlier. Cattle can be  weaned  from their mothers' milk at 6 months to a year of age. [ 73 ]  Lambs are regularly weaned around 16 weeks old. [ 74 ]  Such examples suggest that lactase persistence is a uniquely human phenomenon. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5593", "text": "Some examples exist of factors that can cause the lactase persistence phenotype in the absence of any genetic variant associated with LP. Individuals may lack the alleles for lactase persistence, but still tolerate dairy products in which lactose is broken down by the fermentation process (e.g. cheese, yogurt). [ 75 ]  Also, healthy colonic gut bacteria may also aid in the breakdown of lactose, allowing those without the genetics for lactase persistence to gain the benefits from milk consumption. [ 75 ] [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5594", "text": "A lactose tolerance test may be conducted by asking test subjects to fast overnight, then sampling blood to establish a baseline glucose level. Lactose solution is then given to the subjects to drink, and blood glucose levels are checked at 20 minute intervals for an hour. The subjects who show a substantial rise in their blood glucose level are considered lactose tolerant. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5595", "text": "A  hydrogen breath test  is often used to detect lactose intolerance. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5596", "text": "A  lacteal  is a  lymphatic capillary  that absorbs dietary  fats  in the  villi  of the  small intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5597", "text": "Triglycerides are emulsified by  bile  and  hydrolyzed  by the enzyme  lipase , resulting in a mixture of  fatty acids , di- and  monoglycerides . [ 1 ]  These then pass from the intestinal lumen into the  enterocyte , where they are re-esterified to form  triglyceride . The triglyceride is then combined with  phospholipids ,  cholesterol   ester , and  apolipoprotein B 48 to form  chylomicrons . These chylomicrons then pass into the lacteals, forming a milky substance known as  chyle . The lacteals merge to form larger lymphatic vessels that transport the chyle to the  thoracic duct  where it is emptied into the bloodstream at the  subclavian vein . [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5598", "text": "At this point, the fats are in the bloodstream in the form of chylomicrons. Once in the blood, chylomicrons are subject to delipidation by  lipoprotein lipase . Eventually, enough lipid has been lost and additional apolipoproteins gained, that the resulting particle (now referred to as a chylomicron remnant) can be taken up by the  liver . From the liver, the fat released from chylomicron remnants can be re-exported to the blood as the triglyceride component of  very low-density lipoproteins . Very low-density lipoproteins are also subject to delipidation by vascular lipoprotein lipase, and deliver fats to tissues throughout the body.  In particular, the released fatty acids can be stored in  adipose  cells as triglycerides. As triglycerides are lost from very low-density lipoproteins, the lipoprotein particles become smaller and denser (since protein is denser than lipid) and ultimately become  low-density lipoproteins . LDL particles are highly  atherogenic . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5599", "text": "In contrast to any other route of absorption from the small intestine, the lymphatic system avoids  first pass metabolism ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5600", "text": "Lacticaseibacillus casei  is an organism that belongs to the largest genus in the family  Lactobacillaceae , a  lactic acid bacteria  (LAB), that was previously classified as  Lactobacillus casei . [ 1 ]  This bacteria has been identified as  facultatively anaerobic  or microaerophilic, acid-tolerant, non-spore-forming bacteria."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5601", "text": "This species is a non-sporing, rod-shaped, gram positive microorganism that can be found within the reproductive and digestive tract of the human body. [ 2 ]  Since  L. casei  can survive in a variety of environmental habitats, it has and continues to be extensively studied by health scientists. Commercially,  L. casei  is used in fermenting dairy products and its application as a  probiotic . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5602", "text": "In bacteraemia, it is regarded to be similar in pathogenicity to Lactobacillus and associated with  infective endocarditis . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5603", "text": "The taxonomy of the  L. casei  group  has been debated for several years because researchers struggled to differentiate between the strains of  L. casei  and  L. paracasei  using methods of traditional bacteriology, i.e. phenotypic, physiological, and biochemical similarities. In the 1990s, researchers began to realize that the  type strain  for  L. casei , ATCC 393, does not quite match most other strains classified as \"L. casei\" by then. To solve this discrapency, Dellaglio  et al.  argued to simply replace the type with ATCC 334, which is closer to these \"other strains\", and to bury the name \"L. paracasei\". This argument was not accepted by the  ICSP , which ruled in 1994 [ 5 ]  and 2008 that the type strain should not be changed. ICSP also mentions that ATCC 334 is a strain of  L. paracasei , meaning that it's the aforementioned \"other strains\" that need to be moved to  paracasei . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5604", "text": "The next major event in taxonomic revision came with Zheng  et al.  2020, which split  Lactobacillus  into several genera on phylogenomic grounds.  L. casei  was made the  type species  of  Lacticaseibacillus , containing more than 20 species. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5605", "text": "As of December 2023, the accepted taxonomy under the  species complex  is as follows: [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5606", "text": "The most common application of  L. casei  is industrial, specifically for  dairy  production. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5607", "text": "Lacticaseibacillus casei  is typically the dominant species of nonstarter lactic acid bacteria (i.e. contaminant bacteria [ 10 ] ) present in ripening  cheddar cheese , and, recently, the complete genome sequence of  L. casei   ATCC  334 has become available. [ dubious  \u2013  discuss ]   L. casei  is also the dominant species in naturally fermented Sicilian  green olives . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5608", "text": "A commercial beverage containing  L. casei  strain Shirota has been shown to inhibit the  in vivo  growth of  Helicobacter pylori , but when the same beverage was consumed by humans in a small trial,  H. pylori  colonization decreased only slightly, and the trend was not statistically significant. [ 12 ]  Some  L. casei  strains are considered to be  probiotic , and may be effective in alleviation of gastrointestinal pathogenic bacterial diseases. According to  World Health Organization , those properties have to be demonstrated on each specific strain\u2014including human clinical studies\u2014to be valid. [ 13 ]   L. casei  has been combined with other probiotic strains of bacteria in randomized trials studying its effects in preventing  antibiotic-associated diarrhea  (AAD) and  Clostridioides difficile  infections (CDI), and patients in the trials who were not given the placebo had significantly lower rates of AAD or CDI (depending on the trial) with no adverse effects reported. [ 14 ]  Additionally, trials have shown significantly shorter recovery times in children suffering from acute diarrhea (primarily caused by rotavirus) when given different  L. casei  treatments when compared to placebo. [ 15 ]  Studies suggest that  lactobacilli  are a safe and effective treatment for acute and infectious diarrhea. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5609", "text": "In the preparation of food,  L. casei  bacteria can be used in the natural  fermentation  of beans to lower levels of the compounds causing flatulence upon digestion. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5610", "text": "Another strain that has been studied is \"01\", also known as \"Lc-01\" or  Lacticaseibacillus casei -01. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5611", "text": "Among the best-documented probiotic strains of  L. casei ,  L. casei  DN-114001 ( Actimel/DanActive ) and  L. casei  Shirota ( Yakult ) have been extensively studied [ 19 ]  and are widely available as  functional foods ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5612", "text": "The genomes of these two strains have been sequenced from commercial yogurt, re-designated \"LcA\" and \"LcY\" respectively. They were found to be extremely closely related. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5613", "text": "In the past few years, many studies have been conducted in the decolorization of  azo dyes  by lactic acid bacteria such as  L. casei  TISTR 1500,  L. paracasei ,  Oenococcus oeni , etc. With the  azoreductase  activity, mono- and diazo bonds are degraded completely, and generate other aromatic compounds as intermediates. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5614", "text": "The following table includes the colony, morphological, physiological, and biochemical characteristics of  L. casei . [ 22 ] [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5615", "text": "Lactic acid bacteria (LAB) is widely exploited for its probiotic and fermenting properties, so understanding how its genetic material is exchanged was crucial for researchers. A wide variety of comparative analyses were used to determine that  horizontal gene transfer  (HGT) influenced the evolution of the  Lactobacillus  genus. [ 25 ]  HGT in  L. casei  includes  transformation ,  conjugation , and  transduction . The mobile genetic elements found within the genome, known as  mobilomes , play an important role in  Lactobacillaceae  transfer. This includes  insertion sequences ,  bacteriophages ,  integrons ,  plasmids ,  genomic islands , and  transposons . [ 26 ]  Within LAB, they are responsible for metabolizing different molecules, hydrolyzing proteins, resisting antibiotics, DNA, and phages, and modifying genetic elements. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5616", "text": "The first form of gene transfer used by  Lactobacillus  is transformation. This includes the uptake of naked DNA by a recipient bacterial cell to gain the genetic information of a donor cell. [ 28 ]  This occurs after a donor bacterium has undergone  autolysis  and its DNA fragments are left within the free extracellular fluid. [ 29 ]  The recipient bacterium will then ingest the DNA fragments and will result in either a bacterial cell with a plasmid or recombination of the recipient DNA will transpire within the chromosome."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5617", "text": "The next form of transfer is conjugation, a process that involves the transfer of DNA from a  Lactobacillus  donor to a recipient via cell-to-cell contact or direct cytoplasmic contact. [ 30 ]  In this process, the recipient cell is known as the  transconjugant . [ 31 ]  Once the cells come together, fragments of DNA are directly transferred from the donor to the transconjugant. This is mediated by pheromone-induced cell aggregation and mobilization proteins since many of the plasmids are unable to transfer on their own. [ 25 ]  Afterward, the mating cells will separate and a recombinant cell will be produced after homologous recombination. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5618", "text": "Finally, transduction in  Lactobacillus  cells is a bacteriophage-mediated transfer of plasmid or chromosomal genetic information. [ 32 ]  To initiate this process, a bacteriophage must first infect the donor cell so that  lysis  of the cell will occur. At this point, the cell lysate will be filled with phages that carry donated genome fragments and the recipient cell will be injected with abnormal phage. This will result in a recombination cell whether the cell is infected after homologous recombination or after the infection occurs by bacteriophage integrase. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5619", "text": "Lacticaseibacillus rhamnosus  (previously  Lactobacillus rhamnosus [ 1 ] ) is a  bacterium  that originally was considered to be a subspecies of  L. casei , but genetic research found it to be a separate species in the  L. casei  clade, which also includes  L. paracasei  and  L. zeae . [ 2 ] [ 3 ]  It is a short  Gram-positive  homofermentative  facultative anaerobic  non-spore-forming rod that often appears in chains. Some strains of  L. rhamnosus  bacteria are being used as  probiotics , and are particularly useful in treating infections of the female urogenital tract, most particularly very difficult to treat cases of  bacterial vaginosis  (or \"BV\"). [ 4 ]  The species  Lacticaseibacillus rhamnosus  and  Limosilactobacillus reuteri   are commonly found in the healthy female genito-urinary tract and are helpful to regain control of dysbiotic bacterial overgrowth during an active infection.  L. rhamnosus  sometimes is used in  dairy products  such as fermented milk and as non-starter-lactic acid bacterium (NSLAB) in long-ripened cheese. [ 5 ]  While frequently considered a beneficial organism,  L. rhamnosus  may not be as beneficial to certain subsets of the population; in rare circumstances, especially those primarily involving  weakened immune system  or infants, it may cause  endocarditis . [ 6 ]  Despite the rare infections caused by  L. rhamnosus , the species is included in the list of bacterial species with qualified presumed safety (QPS) status of the  European Food Safety Agency . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5620", "text": "Lacticaseibacillus rhamnosus  is considered a nomadic organism [ 8 ]  and strains have been isolated from many different environments including the vagina and the gastrointestinal tract.  L. rhamnosus  strains have the capacity for strain-specific gene functions that are required to adapt to a large range of environments. [ 9 ]  Its core  genome  contains 2,164 genes, out of 4,711 genes in total (the  pan-genome ). [ 9 ]  The accessory genome is overtaken by genes encoding carbohydrate transport and metabolism,  extracellular polysaccharides ,  biosynthesis ,  bacteriocin  production,  pili  production, the  CRISPR-Cas system , the clustered regularly interspaced short palindromic repeat ( CRISPR ) loci, and more than 100 transporter functions and mobile genetic elements such as  phages ,  plasmid  genes, and  transposons . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5621", "text": "The genome of the specific strain  L. rhamnosus  LRB, in this case, taken from a human baby tooth, consists of a circular chromosome of 2,934,954 bp with 46.78% GC content. [ 10 ]  This genome contains 2,749 total genes with 2,672 that are total protein-coding sequences. [ 10 ]  This sample did not contain any plasmids. [ 10 ]  The most extensively studied strain,  L. rhamnosus  GG, a gut isolate, consists of a genome of 3,010,111 bp. Therefore, the LRB genome is shorter than GG\u2019s genome. LRB lacks the spaCBA gene cluster of GG and is not expected to produce functional pili (6). [ 10 ]  This difference may help explain why each strain lives in a different habitat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5622", "text": "Lacticaseibacillus rhamnosus  GG (ATCC 53103) is a  strain  of  L. rhamnosus  that was isolated in 1983 from the intestinal tract of a healthy human being; filed for a patent on 17 April 1985, by  Sherwood Gorbach  and Barry Goldin, [ 11 ]  the 'GG' derives from the first letters of their surnames. [ 12 ]  The patent refers to a strain of \" L. acidophilus  GG\" with  American Type Culture Collection  (ATCC) accession number 53103; later reclassified as a strain of  L. rhamnosus . The patent claims the  L. rhamnosus  GG (ATCC 53103) strain is acid- and bile-stable, has a great  avidity  for human intestinal mucosal cells, and produces  lactic acid . Since the discovery of the  L. rhamnosus  GG (ATCC 53103) strain, it has been studied extensively on its various health benefits and currently  L. rhamnosus  GG (ATCC 53103) strain is the world's most studied probiotic bacterium with more than 800 scientific studies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5623", "text": "The genome sequence of  Lactobacillus rhamnosus  GG (ATCC 53103) has been decoded in 2009. [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5624", "text": "In 1983,  L. rhamnosus  GG was isolated from the intestinal tract of a healthy human by Sherwood Gorbach and Barry Goldin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5625", "text": "While  L. rhamnosus  GG (ATCC 53103) is able to survive the acid and bile of the stomach and intestine, [ 15 ]  is claimed to colonize the digestive tract, and to balance intestinal microbiota, evidence suggests that  L. rhamnosus , comparable to virtually all probiotic lactobacilli, is only a transient inhabitant and not  autochthonous . [ 16 ]   Lactobacillus rhamnosus  GG binds to the gut mucosa. [ 17 ]  These features make it a favorable organism for the investigation of probiotic supplementation as a potential treatment for a variety of disease states."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5626", "text": "Lacticaseibacillus rhamnosus  GG is beneficial in the prevention of  rotavirus   diarrhea  in children. Prevention and treatment of various types of  diarrhea  have been shown in children and in adults. [ 18 ] [ 19 ]   L. rhamnosus  GG can be beneficial in the prevention of antibiotic-associated diarrhea and nosocomial diarrhea and this has been recently supported by European guidelines. [ 20 ] [ 21 ] [ 22 ]   Lactobacillus rhamnosus  GG may reduce the risk of traveler's diarrhea. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5627", "text": "A position paper published by ESPGHAN Working Group for Probiotics and Prebiotics based on a systematic review and  randomized controlled trials  (RCTs) suggested that  L. rhamnosus  GG (low quality of evidence, strong recommendation) may be considered in the management of children with acute  gastroenteritis  in addition to  rehydration therapy . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5628", "text": "Lacticaseibacillus rhamnosus  GG has been found to be ineffective for treating eczema. [ 25 ]  However in one non-randomized clinical observation [ 26 ]  dealing with resistant childhood atopic eczema, a substantial improvement in quality of life was reported in pediatric patients given Lactobacillus rhamnosus as a supplement."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5629", "text": "The use of  L. rhamnosus  GG for  probiotic  therapy has been linked with rare cases of  sepsis  in certain risk groups, primarily those with a  weakened immune system  and infants. [ 27 ]  Ingestion of GG is considered to be safe and data show a significant growth in the consumption of  L. rhamnosus  GG at the population level did not lead to an increase in  Lactobacillus   bacteraemia  cases. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5630", "text": "Lacticaseibacillus rhamnosus  GR-1 was originally found in the urethra of a healthy female and is nowadays a model strain for vaginal probiotics. A genome comparison between  L. rhamnosus  GG and  L. rhamnosus  GR-1 shows that GR-1 lacks  spaCBA -encoded pili, an important adhesin in  L. rhamnosus  GG adhesion to the intestinal epithelial cells. [ 29 ]  In contrast,  L. rhamnosus  GR-1 utilises  lectin -like proteins to attach to carbohydrates on the surface of the target cell. Lectin-like proteins preferentially bind to nonkeratinized stratified squamous cells which are found in the urethra and vagina. The lectin-like protein 1 purified from  L. rhamnosus  GR-1 is found to prevent infection by the uropathogenic  E. coli  UTI89 by inhibiting its adhesion to epithelial cells and by disrupting its  biofilm  formation. [ 30 ]  Additionally, it can increase biofilm formation in other beneficial lactobacilli that inhabit the vagina."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5631", "text": "Salminen MK, Rautelin H, Tynkkynen S, Poussa T, Saxelin M, Valtonen V, J\u00e4rvinen A (January 2004). \"Lactobacillus bacteremia, clinical significance, and patient outcome, with special focus on probiotic L. rhamnosus GG\".  Clinical Infectious Diseases .  38  (1):  62\u2013 9.  doi : 10.1086/380455 .  PMID \u00a0 14679449 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5632", "text": "Lactiplantibacillus plantarum  (formerly  Lactobacillus arabinosus  and  Lactobacillus plantarum ) [ 3 ]  is a widespread member of the genus  Lactiplantibacillus  and commonly found in many fermented food products as well as anaerobic plant matter. [ 4 ]   L. plantarum  was first isolated from  saliva . Based on its ability to temporarily persist in plants, the insect intestine and in the intestinal tract of vertebrate animals, it was designated as a nomadic organism. [ 5 ] [ 6 ]   L. plantarum  is Gram positive, bacilli shaped bacterium.  L. plantarum  cells are rods with rounded ends, straight, generally 0.9\u20131.2 \u03bcm wide and 3\u20138 \u03bcm long, occurring singly, in pairs or in short chains. [ 7 ]   L. plantarum  has one of the largest  genomes  known among the  lactic acid bacteria  and is a very flexible and versatile species. It is estimated to grow between pH 3.4 and 8.8. [ 8 ]   Lactiplantibacillus plantarum  can grow in the temperature range 12\u00a0\u00b0C to 40\u00a0\u00b0C. [ 9 ]  The viable counts of the \"L. plantarum\" stored at refrigerated condition (4\u00a0\u00b0C) remained high, while a considerable reduction in the counts was observed stored at room temperature (25 \u00b1 1\u00a0\u00b0C). [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5633", "text": "Lactiplantibacillus plantarum  are homofermentative,  aerotolerant   Gram-positive bacteria  that grow at 15\u00a0\u00b0C (59\u00a0\u00b0F), but not at 45\u00a0\u00b0C (113\u00a0\u00b0F), and produce both isomers of  lactic acid  ( D and L ).  Many lactobacilli including  L. plantarum  are unusual in that they can respire oxygen and express  cytochromes \u00a0if heme and menaquinone are present in the growth medium. [ 11 ] [ 12 ]  In the absence of heme and menaquinone, oxygen is consumed by NADH-peroxidase with  hydrogen peroxide  as intermediate and water as end product. [ 11 ] [ 12 ]   The peroxide, it is presumed, acts as a weapon to exclude competing bacteria from the food source. In place of the protective enzyme  superoxide dismutase  present in almost all other oxygen-tolerant cells, this organism accumulates millimolar quantities of  manganese   polyphosphate . Manganese is also used by  L. plantarum  in a  pseudo-catalase  to lower reactive oxygen levels. Because the chemistry by which manganese complexes protect the cells from oxygen damage is subverted by  iron , these cells contain virtually no iron atoms; in contrast, a cell of  Escherichia coli  of comparable volume contains over one-million iron atoms. Because of this,  L. plantarum  cannot be used to create active enzymes that require a  heme  complex, such as true catalases. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5634", "text": "L. plantarum  can also reduce insoluble terminal electron acceptors, such as iron oxides or solid electrodes through extracellular electron transfer when riboflavin and quinone (such as 1 4-dihydroxy-2-naphthoic acid, DHNA) are present. [ 14 ] [ 15 ]   L. plantarum  uses extracellular electron transfer to increase the NAD + /NADH ratio, accelerate fermentation, generate more ATP through the substrate-level phosphorylation, and accumulate more biomass. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5635", "text": "Lactiplantibacillus plantarum , like many lactobacilli, can be cultured using  MRS  media. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5636", "text": "The genome sequencing of the lactic acid bacterium  L. plantarum  WCFS1 shows more molecular details. The chromosome contains 3,308,274 base pairs. [ 17 ]  The GC content of  L. plantarum  is 44.45% with the average protein count 3063. According to the experiment from Wageningen Centre for Food Sciences, the rRNA number of  L. plantarum  WCFS1 is 15, and the number or tRNA is 70. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5637", "text": "Lactiplantibacillus plantarum  is the most common bacterium used in  silage   inoculants . During the anaerobic conditions of ensilage, these organisms quickly dominate the microbial population, and, within 48 hours, they begin to produce lactic and acetic acids via the  Embden-Meyerhof Pathway , further diminishing their competition. Under these conditions,  L. plantarum  strains producing high levels of  heterologous  proteins have been found to remain highly competitive. This quality could allow this species to be utilized as an effective biological pretreatment for  lignocellulosic biomass . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5638", "text": "Lactiplantibacillus plantarum  is commonly found in milk products, meat and a lot of vegetable fermentations including  sauerkraut , pickles, brined  olives , Korean  kimchi , Nigerian  Ogi ,  sourdough , and other fermented plant material, and also some  cheeses ,  fermented sausages , and  stockfish .  The high levels of this organism in food also makes it an ideal candidate for the development of  probiotics . In a 2008 study by Juana Frias et al.,  L. plantarum  was applied to reduce the allergenicity of  soy flour . The result showed that, compared to other microbes,  L. plantarum -fermented soy flour showed the highest reduction in  IgE   immunoreactivity  (96\u201399%), depending upon the sensitivity of the plasma used.  L. plantarum   is also found in  dadiah , a traditional fermented  buffalo  milk of the  Minangkabau people , native to  Sumatra ,  Indonesia . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5639", "text": "Lactobacillus plantarum  strain K21 is a  gram-positive   bacteria  isolated from  fermented  vegetables. It has the ability to hydrolyze  bile salt  when it is provided as a supplement. In fat mice, K21 also reduces the levels of  cholesterol  and  triglyceride , and inhibits the accumulation of lipid in 3T3-L1  preadipocytes .\nFurthermore, it reduces the level of plasma  leptin , mitigates liver damage and alleviates  glucose intolerance . Finally K21 inhibits body weight gain and fat mass accumulation. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5640", "text": "Because it is abundant, of human origin, and easy to grow,  L. plantarum  has been tested for health effects. It has been identified as a probiotic, which suggests its value for further research and application. [ 21 ]   L. plantarum  has significant antioxidant activities and also helps to maintain  intestinal permeability . [ 22 ]  It is able to suppress the growth of gas-producing bacteria in the intestines and may benefit some patients who suffer from  IBS . [ 23 ]  It helps to create microbe balance and stabilize digestive enzyme patterns. [ 17 ]   Lactiplantibacillus plantarum  has been found in experiments to increase  hippocampal   brain derived neurotrophic factor , which means  L. plantarum  may have a beneficial role in the treatment of depression. [ 24 ]  The ability of  L. plantarum  to survive in the  human gastro-intestinal tract  makes it a possible  in vivo  delivery vehicle for therapeutic compounds or proteins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5641", "text": "Lactiplantibacillus plantarum  is a constituent in  VSL#3 . This proprietary, standardized formulation of live bacteria may be used in combination with conventional therapies to treat  ulcerative colitis  and requires a prescription. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5642", "text": "The ability of  L. plantarum  to produce antimicrobial substances helps them survive in the  gastrointestinal tract  of humans. The antimicrobial substances produced have shown significant effect on  Gram-positive  and  Gram-negative bacteria . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5643", "text": "As a result of initial  HIV  infection, the gut has been found to be a prime center of immune activity. [ 26 ]   The immune systems'  Paneth cells  of the gut attack HIV by producing  interleukin 1 beta  (IL-1\u03b2), which results in extensive collateral damage\u2014sloughing of tight intestinal lining, witnessed as severe  diarrhea . This destruction of the gut lining allows fungal pathogens to invade, e.g.,  Cryptococcus  species, resulting in an  AIDS-defining illness  such as  cryptococcosis , representing 60% to 70% of all AIDS-defining cases, [ 27 ]  but not necessarily only the gut. In  rhesus macaques ,  L. plantarum  is able to reduce (destroy) IL-1\u03b2, resolving inflammation, and accelerating gut repair within hours. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5644", "text": "The entire  genome  has recently been sequenced, and  promoter  libraries have been developed for both conditional and constitutive gene expression, adding to the utility of  L. plantarum . It is also commonly employed as the indicative organism in  niacin   bioassay  experiments, in particular,  AOAC International  Official Method 944.13, as it is a niacin  auxotroph . [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5645", "text": "Lactose intolerance  is caused by a lessened ability or a complete inability to digest  lactose , a sugar found in  dairy products . [ 1 ]  Humans vary in the amount of lactose they can tolerate before symptoms develop. [ 1 ]  Symptoms may include  abdominal pain ,  bloating ,  diarrhea ,  flatulence , and  nausea . [ 1 ]  These symptoms typically start thirty minutes to two hours after eating or drinking something containing lactose, [ 1 ]  with the severity typically depending on the amount consumed. [ 1 ]  Lactose intolerance does not cause damage to the  gastrointestinal tract . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5646", "text": "Lactose intolerance is due to the lack of the  enzyme   lactase  in the  small intestines  to break lactose down into  glucose  and  galactose . [ 3 ]  There are four types: primary, secondary, developmental, and congenital. [ 1 ]  Primary lactose intolerance occurs as the amount of lactase declines as people grow up. [ 1 ]  Secondary lactose intolerance is due to injury to the small intestine. Such injury could be the result of infection,  celiac disease ,  inflammatory bowel disease , or other diseases. [ 1 ] [ 4 ]  Developmental lactose intolerance may occur in  premature babies  and usually improves over a short period of time. [ 1 ]  Congenital lactose intolerance is an extremely rare  genetic disorder  in which little or no lactase is made from birth. [ 1 ]  The reduction of lactase production starts typically in late childhood or early adulthood, [ 1 ]  but prevalence increases with age. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5647", "text": "Diagnosis may be confirmed if symptoms resolve following eliminating lactose from the diet. [ 1 ]  Other supporting tests include a  hydrogen breath test  and a  stool acidity test . [ 1 ]  Other conditions that may produce similar symptoms include  irritable bowel syndrome ,  celiac disease , and  inflammatory bowel disease . [ 1 ]  Lactose intolerance is different from a  milk allergy . [ 1 ]  Management is typically by decreasing the amount of lactose in the diet, taking  lactase supplements , or treating the underlying disease. [ 1 ] [ 6 ]  People are typically able to drink at least one cup of milk without developing symptoms, with greater amounts tolerated if drunk with a meal or throughout the day. [ 1 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5648", "text": "Worldwide, around 65% of adults are affected by lactose malabsorption. [ 5 ] [ 8 ]  Other  mammals  usually lose the ability to digest lactose after  weaning . Lactose intolerance is the  ancestral state  of all humans before the  recent evolution  of  lactase persistence  in some cultures, which extends lactose tolerance into adulthood. [ 9 ]  Lactase persistence evolved in several populations independently, probably as an adaptation to the  domestication  of  dairy animals  around 10,000 years ago. [ 10 ] [ 11 ]  Today the prevalence of lactose tolerance varies widely between regions and ethnic groups. [ 5 ]  The ability to digest lactose is most common in people of Northern European descent, and to a lesser extent in some parts of the Middle East and Africa. [ 5 ] [ 8 ]  Lactose intolerance is most common among people of East Asian descent, with 90% lactose intolerance, people of Jewish descent, in many  African countries  and  Arab countries , and among people of Southern European descent (notably amongst Greeks and Italians).  Traditional food  cultures reflect local variations in tolerance [ 5 ]  and historically many societies have adapted to low levels of tolerance by making  dairy products  that contain less lactose than fresh milk. [ 12 ]  The  medicalization  of lactose intolerance as a disorder has been attributed to biases in research history, since most early studies were conducted amongst populations which are normally tolerant, [ 9 ]  as well as the cultural and economic importance and impact of milk in countries such as the United States. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5649", "text": "Lactose intolerance  primarily refers to a syndrome with one or more symptoms upon the consumption of food substances containing  lactose sugar . Individuals may be lactose intolerant to varying degrees, depending on the severity of these symptoms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5650", "text": "Hypolactasia  is the term specifically for the  small intestine  producing little or no  lactase enzyme . [ 14 ]  If a person with hypolactasia consumes lactose sugar, it results in  lactose malabsorption . [ 2 ]  The digestive system is unable to process the lactose sugar, and the unprocessed sugars in the gut produce the symptoms of  lactose intolerance ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5651", "text": "Lactose intolerance is not an  allergy , because it is not an immune response, but rather a sensitivity to dairy caused by a deficiency of lactase enzyme.  Milk allergy , occurring in about 2% of the population, is a separate condition, with distinct symptoms that occur when the presence of milk proteins trigger an immune reaction. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5652", "text": "The principal manifestation of lactose intolerance is an adverse reaction to products containing lactose (primarily milk), including abdominal  bloating  and  cramps ,  flatulence ,  diarrhea ,  nausea ,  borborygmi , and  vomiting  (particularly in  adolescents ). These appear one-half to two hours after consumption. [ 1 ]  The severity of these signs and symptoms typically increases with the amount of lactose consumed; most lactose-intolerant people can tolerate a certain level of lactose in their diets without ill effects. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5653", "text": "Because lactose intolerance is not an allergy, it does not produce  allergy symptoms  (such as itching,  hives , or  anaphylaxis )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5654", "text": "Lactose intolerance is a consequence of  lactase  deficiency, which may be genetic ( primary hypolactasia  and  primary congenital alactasia ) or environmentally induced ( secondary or acquired hypolactasia ). In either case, symptoms are caused by insufficient levels of lactase in the lining of the  duodenum . Lactose, a  disaccharide  molecule found in milk and dairy products, cannot be directly absorbed through the wall of the small intestine into the bloodstream, so, in the absence of lactase, passes intact into the  colon . [ citation needed ]   Bacteria  in the colon can metabolise lactose, and the resulting  fermentation  produces copious amounts of gas (a mixture of  hydrogen ,  carbon dioxide , and  methane ) that causes the various abdominal symptoms. The unabsorbed sugars and fermentation products also raise the  osmotic pressure  of the colon, causing an increased flow of water into the bowels (diarrhea). [ 18 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5655", "text": "Lactose intolerance in infants (congenital lactase deficiency) is caused by mutations in the  LCT  gene. The  LCT  gene provides the instructions for making lactase. Mutations are believed to interfere with the function of lactase, causing affected infants to have a severely impaired ability to digest lactose in breast milk or formula. [ 19 ]  Lactose intolerance in adulthood is a result of gradually decreasing activity (expression) of the  LCT  gene after infancy, which occurs in most humans. The specific DNA sequence in the  MCM6  gene helps control whether the  LCT  gene is turned on or off. [ 20 ]  At least several thousand years ago, some humans developed a mutation in the  MCM6  gene that keeps the  LCT  gene turned on even after breast feeding is stopped. [ 21 ]  Populations that are lactose intolerant lack this mutation.  The  LCT  and  MCM6  genes are both located on the long arm (q) of chromosome 2 in region 21. The locus can be expressed as 2q21. [ 21 ]  The lactase deficiency also could be linked to certain heritages and varies widely. A 2016 study of over 60,000 participants from 89 countries found regional prevalence of lactose malabsorption was \"64% (54\u201374) in Asia (except Middle East), 47% (33\u201361) in eastern Europe, Russia, and former Soviet Republics, 38% (CI 18\u201357) in Latin America, 70% (57\u201383) in the Middle East, 66% (45\u201388) in northern Africa, 42% (13\u201371) in northern America, 45% (19\u201371) in Oceania, 63% (54\u201372) in sub-Saharan Africa, and 28% (19\u201337) in northern, southern and western Europe.\" [ 5 ]  According to Johns Hopkins Medicine, lactose intolerance is more common in Asian Americans, African Americans, Mexican Americans, and Native Americans. [ 22 ]  Analysis of the DNA of 94 ancient skeletons in Europe and Russia concluded that the mutation for lactose tolerance appeared about 4,300 years ago and spread throughout the European population. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5656", "text": "Some human populations have developed  lactase persistence , in which lactase production continues into adulthood probably as a response to the benefits of being able to digest milk from farm animals. Some have argued that this links intolerance to  natural selection  favoring lactase-persistent individuals, but it is also consistent with a physiological response to decrease lactase production when it is not needed in cultures in which dairy products are not an available food source. [ 24 ]  Although populations in Europe, India, Arabia, and Africa were first thought to have high rates of lactase persistence because of a single mutation, lactase persistence has been traced to a number of mutations that occurred independently. [ 11 ]  Different alleles for lactase persistence have developed at least three times in East African populations, with persistence extending from 26% in  Tanzania  to 88% in the  Beja  pastoralist population in  Sudan . [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5657", "text": "The accumulation of  epigenetic  factors, primarily  DNA methylation , in the extended LCT region, including the gene  enhancer  located in the  MCM6  gene near C/T-13910 SNP, may also contribute to the onset of lactose intolerance in adults. [ 26 ] [ 27 ]  Age-dependent expression of  LCT  in mice intestinal epithelium has been linked to DNA methylation in the gene enhancer. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5658", "text": "Lactose intolerance is classified according to its causes as:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5659", "text": "In order to assess lactose intolerance, intestinal function is challenged by ingesting more dairy products than can be readily digested.  Clinical symptoms typically appear within 30 minutes, but may take up to two hours, depending on other foods and activities. [ 35 ]   Substantial variability in response (symptoms of nausea, cramping, bloating, diarrhea, and flatulence) is to be expected, as the extent and severity of lactose intolerance varies among individuals. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5660", "text": "The next step is to determine whether it is due to primary lactase deficiency or an underlying disease that causes secondary lactase deficiency. [ 2 ]  Physicians should investigate the presence of undiagnosed  coeliac disease ,  Crohn's disease , or other  enteropathies  when secondary lactase deficiency is suspected and infectious gastroenteritis has been ruled out. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5661", "text": "Lactose intolerance is distinct from  milk allergy , an immune response to cow's milk proteins. They may be distinguished in diagnosis by giving lactose-free milk, producing no symptoms in the case of lactose intolerance, but the same reaction as to normal milk in the presence of a milk allergy. A person can have both conditions. If positive confirmation is necessary, four tests are available. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5662", "text": "In a  hydrogen breath test , the most accurate lactose intolerance test, after an overnight fast, 25 grams of lactose (in a solution with water) are swallowed. If the lactose cannot be digested, enteric bacteria metabolize it and produce hydrogen, which, along with methane, if produced, can be detected on the patient's breath by a clinical gas chromatograph or compact solid-state detector. The test takes about 2.5 hours to complete. If the hydrogen levels in the patient's breath are high, they may have lactose intolerance. This test is not usually done on babies and very young children, because it can cause severe diarrhea. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5663", "text": "In conjunction, measuring blood glucose level every 10 to 15 minutes after ingestion will show a \"flat curve\" in individuals with lactose malabsorption, while the lactase persistent will have a significant \"top\", with a typical elevation of 50% to 100%, within one to two hours. However, due to the need for frequent blood sampling, this approach has been largely replaced by breath testing. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5664", "text": "After an overnight fast, blood is drawn and then 50 grams of lactose (in aqueous solution) are swallowed. Blood is then drawn again at the 30-minute, 1-hour, 2-hour, and 3-hour marks.  If the lactose cannot be digested, blood glucose levels will rise by less than 20\u00a0mg/dl. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5665", "text": "This test can be used to diagnose lactose intolerance in infants, for whom other forms of testing are risky or impractical. [ 41 ]  The infant is given lactose to drink. If the individual is tolerant, the lactose is digested and absorbed in the small intestine; otherwise, it is not digested and absorbed, and it reaches the colon. The bacteria in the colon, mixed with the lactose, cause acidity in stools. Stools passed after the ingestion of the lactose are tested for level of acidity. If the stools are acidic, the infant is intolerant to lactose. [ 42 ] \nStool pH in lactose intolerance is less than 5.5."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5666", "text": "An intestinal biopsy must confirm lactase deficiency following discovery of elevated hydrogen in the hydrogen breath test. [ 43 ]   Modern techniques have enabled a bedside test, identifying presence of lactase enzyme on upper gastrointestinal endoscopy instruments. [ 44 ]   However, for research applications such as  mRNA  measurements, a specialist laboratory is required."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5667", "text": "Chromatography can be used to separate and identify undigested sugars present in faeces. Although lactose may be detected in the faeces of people with lactose intolerance, this test is not considered reliable enough to conclusively diagnose or exclude lactose intolerance. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5668", "text": "Genetic tests may be useful in assessing whether a person has primary lactose intolerance. Lactase activity persistence in adults is associated with two  polymorphisms : C/T 13910 and G/A 22018 located in the  MCM6  gene. [ 28 ]  These polymorphisms may be detected by  molecular biology  techniques at the  DNA  extracted from blood or saliva samples; genetic kits specific for this diagnosis are available. The procedure consists of extracting and amplifying DNA from the sample, following with a hybridation protocol in a strip. Colored bands are obtained as result, and depending on the different combinations, it would be possible to determine whether the patient is lactose intolerant. This test allows a noninvasive definitive diagnostic. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5669", "text": "When lactose intolerance is due to secondary lactase deficiency, treatment of the underlying disease may allow lactase activity to return to normal levels. [ 6 ]  In people with celiac disease, lactose intolerance normally reverts or improves several months after starting a  gluten-free diet , but temporary dietary restriction of lactose may be needed. [ 4 ] [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5670", "text": "People with primary lactase deficiency cannot modify their body's ability to produce lactase. [ 1 ]  In societies where lactose intolerance is the norm, it is not considered a condition that requires treatment. However, where dairy is a larger component of the normal diet, a number of efforts may be useful. There are four general principles in dealing with lactose intolerance: avoidance of dietary lactose, substitution to maintain nutrient intake, regulation of calcium intake, and use of enzyme substitute. [ 43 ]  Regular consumption of dairy food by lactase deficient individuals may also reduce symptoms of intolerance by promoting colonic bacteria adaptation. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5671", "text": "The primary way of managing the symptoms of lactose intolerance is to limit the intake of lactose to a level that can be tolerated. [ 47 ]  Lactase deficient individuals vary in the amount of lactose they can tolerate, [ 1 ]  and some report that their tolerance varies over time, depending on health status and pregnancy. [ 48 ] [ 49 ]  However, as a rule of thumb, people with primary lactase deficiency and no small intestine injury are usually able to consume at least 12 grams of lactose per sitting without symptoms, or with only mild symptoms, with greater amounts tolerated if consumed with a meal or throughout the day. [ 1 ] [ 49 ] [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5672", "text": "Lactose is found primarily in  dairy products , which vary in the amount of lactose they contain:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5673", "text": "There used to be [ 59 ]  a lack of standardization on how lactose is measured and reported in food. The different molecular weights of anhydrous lactose or lactose monohydrate result in up to 5% difference. [ 60 ]  One source recommends using the \"carbohydrates\" or \"sugars\" part of the nutritional label as surrogate for lactose content, [ 57 ]  but such \"lactose by difference\" values are not assured to correspond to real lactose content. [ 59 ]  The stated dairy content of a product also varies according to manufacturing processes and labelling practices, and commercial terminology varies between languages and regions. [ 43 ]  As a result, absolute figures for the amount of lactose consumed (by weight) may not be very reliable."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5674", "text": "Kosher  products labeled  pareve  or  fleishig  are free of milk. However, if a \"D\" (for \"dairy\") is present next to the circled \"K\", \"U\", or other  hechsher , the food product likely contains milk solids, [ 61 ]  although it may also simply indicate the product was produced on equipment shared with other products containing milk derivatives."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5675", "text": "Lactose is also a commercial  food additive  used for its texture, flavor, and adhesive qualities. It is found in additives labelled as  casein ,  caseinate ,  whey ,  lactoserum ,  milk solids ,  modified milk ingredients , etc. [ citation needed ]  As such, lactose is found in foods such as processed meats ( sausages / hot dogs , sliced meats,  p\u00e2t\u00e9s ), [ 61 ]  gravy stock powder,  margarines , [ 62 ]  sliced  breads , [ 63 ] [ 64 ]  breakfast cereals,  potato chips , [ 65 ]   processed foods ,  medications , prepared meals, meal replacements (powders and bars), protein supplements (powders and bars), and even  beers  in the  milk stout  style. Some barbecue sauces and liquid cheeses used in fast-food restaurants may also contain lactose. When dining out, carrying lactose intolerance cards that explain dietary restrictions in the local language can help communicate needs to restaurant staff. [ 66 ]  Lactose is often used as the primary filler (main ingredient) in most prescription and non-prescription solid pill form medications, though product labeling seldom mentions the presence of 'lactose' or 'milk', and neither do product monograms provided to pharmacists, and most pharmacists are unaware of the very wide scale yet common use of lactose in such medications until they contact the supplier or manufacturer for verification. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5676", "text": "Plant-based milks  and derivatives such as  soy milk ,  rice milk ,  almond milk ,  coconut milk ,  hazelnut  milk,  oat milk ,  hemp milk , macadamia nut milk, and  peanut milk  are inherently lactose-free.  Low-lactose and lactose-free versions of foods are often available to replace dairy-based foods for those with lactose intolerance. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5677", "text": "When lactose avoidance is not possible, or on occasions when a person chooses to consume such items, then enzymatic lactase supplements may be used. [ 68 ] [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5678", "text": "Lactase enzymes similar to those produced in the small intestines of humans are produced industrially by  fungi  of the  genus   Aspergillus . The enzyme,  \u03b2-galactosidase , is available in tablet form in a variety of doses, in many countries without a prescription. It functions well only in high-acid environments, such as that found in the human gut due to the addition of gastric juices from the stomach. Unfortunately, too much acid can denature it, [ 70 ]  so it should not be taken on an empty stomach. Also, the enzyme is ineffective if it does not reach the small intestine by the time the problematic food does. Lactose-sensitive individuals can experiment with both timing and dosage to fit their particular needs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5679", "text": "While essentially the same process as normal intestinal lactose digestion, direct treatment of milk employs a different variety of industrially produced lactase. This enzyme, produced by  yeast  from the genus  Kluyveromyces , takes much longer to act, must be thoroughly mixed throughout the product, and is destroyed by even mildly acidic environments. Its main use is in producing the lactose-free or lactose-reduced dairy products sold in supermarkets. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5680", "text": "Regular consumption of dairy foods containing lactose can promote a colonic bacteria adaptation, enhancing a favorable microbiome, which allows people with primary lactase deficiency to diminish their intolerance and to consume more dairy foods. [ 46 ] [ 49 ] [ 72 ]  The way to induce tolerance is based on progressive exposure, consuming smaller amounts frequently, distributed throughout the day. [ 73 ]  Lactose intolerance can also be managed by ingesting live yogurt cultures containing  lactobacilli  that are able to digest the lactose in other dairy products. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5681", "text": "Worldwide, about 65% of people experience some form of lactose intolerance as they age past infancy, but there are significant differences between populations and regions. As few as 5% of northern Europeans are lactose intolerant, while as many as 90% of adults in parts of Asia are lactose intolerant. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5682", "text": "In northern European countries, early adoption of dairy farming conferred a selective evolutionary advantage to individuals that could tolerate lactose. This led to higher frequencies of lactose tolerance in these countries. For example, almost 100% of  Irish people  are predicted to be lactose tolerant. [ 77 ]  Conversely, regions of the south, such as Africa, did not adopt dairy farming as early and tolerance from milk consumption did not occur the same way as in northern Europe. [ 46 ]  Lactose intolerance is common among people of Jewish descent, as well as from West Africa, the Arab countries, Greece, and Italy. [ 76 ]  Different populations will present certain gene constructs depending on the evolutionary and cultural pre-settings of the geographical region. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5683", "text": "Greater lactose tolerance has come about in two ways. [ 78 ]  Some populations have developed genetic changes to allow the digestion of lactose:  lactase persistence . [ 78 ]  Other populations developed cooking methods like milk fermentation. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5684", "text": "Lactase persistence in humans evolved relatively recently (in the last 10,000 years) among some populations. Around 8,000 years ago in modern-day Turkey, humans became reliant on newly-domesticated animals that could be milked; such as cows, sheep, and goats. This resulted in higher frequency of lactase persistence. [ 79 ]  Lactase persistence became high in regions such as Europe, Scandinavia, the Middle East and Northwestern India. However, most people worldwide remain lactase  non -persistent. [ 9 ]  Populations that raised animals not used for milk tend to have 90\u2013100 percent of a lactose intolerant rate. [ 80 ]  For this reason, lactase persistence is of some interest to the fields of  anthropology ,  human genetics , and  archaeology , which typically use the genetically derived persistence/non-persistence terminology. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5685", "text": "The rise of dairy and producing dairy related products from cow milk alone, varies across different regions of the world, aside from genetic predisposition. [ 46 ]  The process of turning milk into cheese dates back earlier than 5200 BC. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5686", "text": "DNA analysis in February 2012 revealed that  \u00d6tzi  was lactose intolerant, supporting the theory that lactose intolerance was still common at that time, despite the increasing spread of agriculture and dairying. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5687", "text": "Genetic analysis shows lactase persistence has developed several times in different places independently in an example of  convergent evolution . [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5688", "text": "It was not until relatively recently that  medicine  recognised the worldwide prevalence of lactose intolerance and its genetic causes. Its symptoms were described as early as  Hippocrates  (460\u2013370 BC), [ 84 ]  but until the 1960s, the prevailing assumption was that tolerance was the norm. Intolerance was explained as the result of a milk allergy, intestinal pathogens, or as being  psychosomatic  \u2013 it being recognised that some cultures did not practice dairying, and people from those cultures often reacted badly to consuming milk. [ 85 ] [ 86 ]  Two reasons have been given for this misconception. One was that early research was conducted solely on European-descended populations, which have an unusually low incidence of lactose intolerance [ 87 ]  and an extensive cultural history of dairying. As a result, researchers wrongly concluded that tolerance was the global norm. Another reason is that lactose intolerance tends to be under-reported: lactose intolerant individuals can tolerate at least some lactose before they show symptoms, and their symptoms differ in severity. The large majority of people are able to digest some quantity of milk, for example in tea or coffee, without developing any adverse effects. [ 16 ]   Fermented dairy products , such as cheese, also contain significantly less lactose than plain milk. Therefore, in societies where tolerance is the norm, many lactose intolerant people who consume only small amounts of dairy, or have only mild symptoms, may be unaware that they cannot digest lactose."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5689", "text": "Eventually, in the 1960s, it was recognised that lactose intolerance was correlated with  race  in the United States. [ 88 ] [ 89 ] [ 90 ]  Subsequent research revealed that lactose intolerance was more common globally than tolerance, [ 91 ] [ 92 ] [ 93 ] [ 94 ] [ 95 ]  and that the variation was due to genetic differences, not an adaptation to cultural practices. [ 86 ] [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5690", "text": "Most  mammals  normally cease to produce lactase and become lactose intolerant after  weaning . [ 9 ]  The downregulation of lactase expression in  mice  could be attributed to the accumulation of  DNA methylation  in the  Lct  gene and the adjacent  Mcm6  gene. [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5691", "text": "The  large intestine , also known as the  large bowel , is the last part of the  gastrointestinal tract  and of the  digestive system  in  tetrapods . Water is absorbed here and the remaining waste material is stored in the  rectum  as  feces  before being removed by  defecation . [ 1 ]  The  colon  (progressing from the  ascending colon  to the  transverse , the  descending  and finally the  sigmoid colon ) is the longest portion of the large intestine, and the terms \"large intestine\" and \"colon\" are often used interchangeably, but most sources define the large intestine as the combination of the  cecum , colon,  rectum , and  anal canal . [ 1 ] [ 2 ] [ 3 ]  Some other sources exclude the anal canal. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5692", "text": "In humans, the large intestine begins in the right  iliac region  of the  pelvis , just at or below the  waist , where it is joined to the end of the  small intestine  at the cecum, via the  ileocecal valve . It then continues as the colon  ascending  the  abdomen , across the width of the  abdominal cavity  as the  transverse colon , and then  descending  to the rectum and its endpoint at the   anal canal . [ 7 ]  Overall, in humans, the large intestine is about 1.5 metres (5\u00a0ft) long, which is about one-fifth of the whole length of the human gastrointestinal tract. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5693", "text": "The  colon  of the large intestine is the last part of the  digestive system . It has a segmented appearance due to a series of saccules called  haustra . [ 9 ]  It extracts  water  and  salt  from  solid wastes  before they are  eliminated  from the body and is the site in which the  fermentation  of unabsorbed material by the  gut microbiota  occurs. Unlike the  small intestine , the colon does not play a major role in absorption of foods and nutrients. About 1.5 litres or 45 ounces of water arrives in the colon each day. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5694", "text": "The colon is the longest part of the large intestine and its average length in the adult human is 65 inches or 166\u00a0cm (range of 80 to 313\u00a0cm) for males, and 61 inches or 155\u00a0cm (range of 80 to 214\u00a0cm) for females. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5695", "text": "In  mammals , the large intestine consists of the  cecum  (including the  appendix ), colon (the longest part),  rectum , and  anal canal . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5696", "text": "The four sections of the colon are: the  ascending colon ,  transverse colon ,  descending colon , and  sigmoid colon . These sections turn at the  colic flexures ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5697", "text": "The parts of the colon are either intraperitoneal or behind it in the  retroperitoneum . Retroperitoneal organs, in general, do not have a complete covering of  peritoneum , so they are fixed in location. Intraperitoneal organs are completely surrounded by peritoneum and are therefore mobile. [ 12 ]  Of the colon, the ascending colon, descending colon and rectum are retroperitoneal, while the cecum, appendix, transverse colon and sigmoid colon are intraperitoneal. [ 13 ]  This is important as it affects which organs can be easily accessed during surgery, such as a  laparotomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5698", "text": "In terms of diameter, the cecum is the widest, averaging slightly less than 9\u00a0cm in healthy individuals, and the transverse colon averages less than 6\u00a0cm in diameter. [ 14 ]  The descending and sigmoid colon are slightly smaller, with the sigmoid colon averaging 4\u20135\u00a0cm (1.6\u20132.0\u00a0in) in diameter. [ 14 ] [ 15 ]  Diameters larger than certain thresholds for each colonic section can be diagnostic for  megacolon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5699", "text": "The  cecum  is the first section of the large intestine and is involved in digestion, while the  appendix  which develops embryologically from it, is not involved in digestion and is considered to be part of the  gut-associated lymphoid tissue . The function of the appendix is uncertain, but some sources believe that it has a role in housing a sample of the  gut microbiota , and is able to help to repopulate the colon with microbiota if depleted during the course of an immune reaction. The appendix has also been shown to have a high concentration of lymphatic cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5700", "text": "The ascending colon is the first of four main sections of the large intestine. It is connected to the small intestine by a section of bowel called the cecum. The ascending colon runs upwards through the abdominal cavity toward the transverse colon for approximately eight inches (20\u00a0cm)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5701", "text": "One of the main functions of the colon is to remove the water and other key nutrients from waste material and recycle it. As the waste material exits the small intestine through the  ileocecal valve , it will move into the cecum and then to the ascending colon where this process of extraction starts. The waste material is pumped upwards toward the transverse colon by  peristalsis . The ascending colon is sometimes attached to the  appendix  via  Gerlach's valve . In  ruminants , the ascending colon is known as the  spiral colon . [ 16 ] [ 17 ] [ 18 ] \nTaking into account all ages and sexes, colon cancer occurs here most often (41%). [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5702", "text": "The transverse colon is the part of the colon from the  hepatic flexure , also known as the right colic, (the turn of the colon by the  liver ) to the  splenic flexure  also known as the left colic, (the turn of the colon by the  spleen ). The transverse colon hangs off the  stomach , attached to it by a large fold of  peritoneum   called the  greater omentum . On the posterior side, the transverse colon is connected to the posterior abdominal wall by a  mesentery  known as the  transverse mesocolon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5703", "text": "The transverse colon is encased in  peritoneum , and is therefore mobile (unlike the parts of the colon immediately before and after it)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5704", "text": "The proximal two-thirds of the transverse colon is perfused by the  middle colic artery , a branch of the  superior mesenteric artery  (SMA), while the latter third is supplied by branches of the  inferior mesenteric artery  (IMA). The \"watershed\" area between these two blood supplies, which represents the embryologic division between the  midgut  and  hindgut , is an area sensitive to  ischemia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5705", "text": "The descending colon is the part of the colon from the splenic flexure to the beginning of the sigmoid colon. One function of the descending colon in the digestive system is to store feces that will be emptied into the rectum. It is  retroperitoneal  in two-thirds of humans. In the other third, it has a (usually short) mesentery. [ 20 ]  The arterial supply comes via the  left colic artery . The descending colon is also called the  distal gut , as it is further along the gastrointestinal tract than the proximal gut. Gut flora are very dense in this region."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5706", "text": "The sigmoid colon is the part of the large intestine after the descending colon and before the rectum. The name  sigmoid  means S-shaped (see  sigmoid ; cf.  sigmoid sinus ). The walls of the sigmoid colon are muscular and contract to increase the pressure inside the colon, causing the  stool  to move into the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5707", "text": "The sigmoid colon is supplied with blood from several branches (usually between 2 and 6) of the  sigmoid arteries , a branch of the IMA. The IMA terminates as the  superior rectal artery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5708", "text": "Sigmoidoscopy  is a common diagnostic technique used to examine the sigmoid colon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5709", "text": "The  rectum  is the last section of the large intestine. It holds the formed feces awaiting elimination via defecation.\nIt is about 12\u00a0cm long. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5710", "text": "The  cecum  \u2013 the first part of the large intestine"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5711", "text": "The  taenia coli  run the length of the large intestine.  Because the taenia coli are shorter than the large bowel itself, the colon becomes  sacculated , forming the  haustra  of the colon which are the shelf-like intraluminal projections. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5712", "text": "Arterial  supply to the colon comes from branches of the  superior mesenteric artery  (SMA) and  inferior mesenteric artery  (IMA). Flow between these two systems communicates via the  marginal artery of the colon  that runs parallel to the colon for its entire length. Historically, a structure variously identified as the arc of Riolan or meandering mesenteric artery (of Moskowitz) was thought to connect the  proximal  SMA to the proximal IMA. This variably present structure would be important if either vessel were occluded. However, at least one review of the literature questions the existence of this vessel, with some experts calling for the abolition of these terms from future medical literature. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5713", "text": "Venous  drainage usually mirrors colonic arterial supply, with the  inferior mesenteric vein  draining into the  splenic vein , and the  superior mesenteric vein  joining the splenic vein to form the  hepatic portal vein  that then enters the  liver .  Middle rectal veins  are an exception, delivering blood to  inferior vena cava  and bypassing the liver. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5714", "text": "Lymphatic drainage  from the ascending colon and proximal two-thirds of the  transverse colon  is to the  ileocolic lymph nodes  and the  superior mesenteric lymph nodes , which drain into the  cisterna chyli . [ 25 ]  The lymph from the distal one-third of the  transverse colon , the  descending colon , the sigmoid colon, and the upper  rectum  drain into the inferior mesenteric and colic lymph nodes. [ 25 ]  The lower rectum to the anal canal above the pectinate line drain to the internal ileocolic nodes. [ 26 ]  The anal canal below the pectinate line drains into the superficial  inguinal  nodes. [ 26 ]  The  pectinate line  only roughly marks this transition."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5715", "text": "Sympathetic supply: superior & inferior mesenteric ganglia;\nparasympathetic supply: vagus & sacral plexus (S2-S4) [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5716", "text": "The endoderm, mesoderm and ectoderm are germ layers that develop in a process called gastrulation. Gastrulation occurs early in human development. The gastrointestinal tract is derived from these layers. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5717", "text": "One variation on the normal anatomy of the colon occurs when extra loops form, resulting in a colon that is up to five metres longer than normal. This condition, referred to as  redundant colon , typically has no direct major health consequences, though rarely  volvulus  occurs, resulting in obstruction and requiring immediate medical attention. [ 28 ] [ 29 ]  A significant indirect health consequence is that use of a standard adult  colonoscope  is difficult and in some cases impossible when a redundant colon is present, though specialized variants on the instrument (including the pediatric variant) are useful in overcoming this problem. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5718", "text": "The wall of the large intestine is lined with simple columnar  epithelium  with  invaginations .  The invaginations are called the  intestinal glands  or colonic crypts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5719", "text": "The colon crypts are shaped like microscopic thick walled test tubes with a central hole down the length of the tube (the crypt  lumen ). Four tissue sections are shown here, two cut across the long axes of the crypts and two cut parallel to the long axes.  In these images the cells have been stained by  immunohistochemistry  to show a brown-orange color if the cells produce a  mitochondrial  protein called  cytochrome c oxidase subunit I  (CCOI).  The  nuclei  of the cells (located at the outer edges of the cells lining the walls of the crypts) are stained blue-gray with  haematoxylin . As seen in panels C and D, crypts are about 75 to about 110 cells long.  Baker et al. [ 32 ]  found that the average crypt circumference is 23 cells.  Thus, by the images shown here, there are an average of about 1,725 to 2,530 cells per colonic crypt.  Nooteboom et al. [ 33 ]  measuring the number of cells in a small number of crypts reported a range of 1,500 to 4,900 cells per colonic crypt.  Cells are produced at the crypt base and migrate upward along the crypt axis before being shed into the colonic  lumen  days later. [ 32 ]   There are 5 to 6 stem cells at the bases of the crypts. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5720", "text": "As estimated from the image in panel A, there are about 100 colonic crypts per square millimeter of the colonic epithelium. [ 34 ]   Since the average length of the human colon is 160.5\u00a0cm [ 11 ]  and the average inner circumference of the colon is 6.2\u00a0cm, [ 34 ]  the inner surface epithelial area of the human colon has an average area of about 995\u00a0cm 2 , which includes 9,950,000 (close to 10 million) crypts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5721", "text": "In the four tissue sections shown here, many of the intestinal glands have cells with a  mitochondrial DNA  mutation in the  CCOI  gene and appear mostly white, with their main color being the blue-gray staining of the nuclei.  As seen in panel B, a portion of the stem cells of three crypts appear to have a mutation in  CCOI , so that 40% to 50% of the cells arising from those stem cells form a white segment in the cross cut area."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5722", "text": "Overall, the percent of crypts deficient for CCOI is less than 1% before age 40, but then increases linearly with age. [ 31 ]  Colonic crypts deficient for CCOI in women reaches, on average, 18% in women and 23% in men by 80\u201384 years of age. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5723", "text": "Crypts of the colon can reproduce by fission, as seen in panel C, where a crypt is fissioning to form two crypts, and in panel B where at least one crypt appears to be fissioning.  Most crypts deficient in CCOI are in clusters of crypts (clones of crypts) with two or more CCOI-deficient crypts adjacent to each other (see panel D). [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5724", "text": "About 150 of the many thousands of  protein coding genes  expressed in the large intestine, some are specific to the mucous membrane in different regions and include  CEACAM7 . [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5725", "text": "The large intestine absorbs water and any remaining absorbable nutrients from the food before sending the indigestible matter to the rectum. The colon absorbs vitamins that are created by the colonic bacteria, such as  thiamine ,  riboflavin , and  vitamin K  (especially important as the daily ingestion of vitamin K is not normally enough to maintain adequate  blood coagulation ). [ 36 ] [ citation needed ] [ 37 ]  It also compacts feces, and stores fecal matter in the rectum until it can be discharged via the  anus  in  defecation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5726", "text": "The large intestine also secretes K+ and Cl-. Chloride secretion increases in cystic fibrosis.\nRecycling of various nutrients takes place in the colon. Examples include fermentation of carbohydrates, short chain fatty acids, and urea cycling. [ 38 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5727", "text": "The  appendix  contains a small amount of  mucosa-associated lymphoid tissue  which gives the appendix an undetermined role in immunity. However, the appendix is known to be important in fetal life as it contains  endocrine  cells that release biogenic amines and peptide hormones important for  homeostasis  during early growth and development. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5728", "text": "By the time the  chyme  has reached this tube, most  nutrients  and 90% of the water have been absorbed by the body. Indeed, as demonstrated by the commonality of  ileostomy  procedures, it is possible for many people to live without large portions of their large intestine, or even without it completely. At this point only some  electrolytes  like  sodium ,  magnesium , and  chloride  are left as well as indigestible parts of ingested food (e.g., a large part of ingested  amylose , starch which has been shielded from digestion heretofore, and  dietary fiber , which is largely indigestible  carbohydrate  in either soluble or insoluble form). As the chyme moves through the large intestine, most of the remaining  water  is removed, while the chyme is mixed with  mucus  and  bacteria  (known as  gut flora ), and becomes feces. The  ascending colon  receives fecal material as a liquid. The muscles of the colon then move the watery waste material forward and slowly absorb all the excess water, causing the stools to gradually solidify as they move along into the  descending colon . [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5729", "text": "The bacteria break down some of the  fiber  for their own nourishment and create  acetate ,  propionate , and  butyrate  as waste products, which in turn are used by the cell lining of the colon for nourishment. [ 41 ]  No protein is made available. In humans, perhaps 10% of the undigested carbohydrate thus becomes available, though this may vary with diet; [ 42 ]  in other animals, including other apes and primates, who have proportionally larger colons, more is made available, thus permitting a higher portion of plant material in the diet.  The large intestine [ 43 ]  produces no digestive  enzymes  \u2014  chemical digestion  is completed in the  small intestine  before the chyme reaches the large intestine. The  pH  in the colon varies between 5.5 and 7 (slightly  acidic  to neutral). [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5730", "text": "Water absorption at the colon typically proceeds against a  transmucosal   osmotic pressure   gradient . The  standing gradient osmosis  is the reabsorption of water against the osmotic gradient in the intestines. Cells occupying the intestinal lining pump sodium ions into the intercellular space, raising the osmolarity of the intercellular fluid. This  hypertonic  fluid creates an osmotic pressure that drives water into the lateral intercellular spaces by osmosis via  tight junctions  and adjacent cells, which then in turn moves across the  basement membrane  and into the  capillaries , while more sodium ions are pumped again into the intercellular fluid. [ 45 ]  Although water travels down an osmotic gradient in each individual step, overall, water usually travels against the osmotic gradient due to the pumping of sodium ions into the intercellular fluid. This allows the large intestine to absorb water despite the blood in capillaries being  hypotonic  compared to the fluid within the intestinal lumen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5731", "text": "The large intestine houses over 700 species of  bacteria  that perform a variety of functions, as well as  fungi ,  protozoa , and  archaea . Species diversity varies by geography and diet. [ 46 ]  The microbes in a human distal gut often number in the vicinity of 100 trillion, and can weigh around 200 grams (0.44 pounds). This mass of mostly symbiotic microbes has recently been called the latest human organ to be \"discovered\" or in other words, the \"forgotten organ\". [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5732", "text": "The large intestine absorbs some of the products formed by the bacteria inhabiting this region. Undigested  polysaccharides  (fiber) are metabolized to short-chain fatty acids by bacteria in the large intestine and absorbed by  passive diffusion . The bicarbonate that the large intestine secretes helps to neutralize the increased acidity resulting from the formation of these fatty acids. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5733", "text": "These bacteria also produce large amounts of  vitamins , especially  vitamin K  and  biotin  (a  B vitamin ), for absorption into the blood. Although this source of vitamins, in general, provides only a small part of the daily requirement, it makes a significant contribution when dietary vitamin intake is low. An individual who depends on absorption of vitamins formed by bacteria in the large intestine may become vitamin-deficient if treated with  antibiotics  that inhibit the vitamin producing species of bacteria as well as the intended disease-causing bacteria. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5734", "text": "Other bacterial products include gas ( flatus ), which is a mixture of  nitrogen  and  carbon dioxide , with small amounts of the gases  hydrogen ,  methane , and  hydrogen sulfide . Bacterial  fermentation  of undigested  polysaccharides  produces these. Some of the fecal odor is due to  indoles , metabolized from the amino acid tryptophan. The normal flora is also essential in the development of certain tissues, including the cecum and  lymphatics . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5735", "text": "They are also involved in the production of cross-reactive antibodies. These are antibodies produced by the immune system against the normal flora, that are also effective against related pathogens, thereby preventing infection or invasion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5736", "text": "The two most prevalent phyla of the colon are  Bacillota  and  Bacteroidota . The ratio between the two seems to vary widely as reported by the Human Microbiome Project. [ 50 ]   Bacteroides  are implicated in the initiation of  colitis  and  colon cancer .  Bifidobacteria  are also abundant, and are often described as 'friendly bacteria'. [ 51 ] [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5737", "text": "A  mucus  layer protects the large intestine from attacks from colonic  commensal bacteria . [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5738", "text": "Following are the most common diseases or disorders of the colon:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5739", "text": "Colonoscopy  is the  endoscopic  examination of the large intestine and the  distal  part of the  small bowel  with a  CCD camera  or a  fiber optic  camera on a flexible tube passed through the  anus . It can provide a visual diagnosis (e.g.  ulceration ,  polyps ) and grants the opportunity for  biopsy  or removal of suspected  colorectal cancer  lesions. Colonoscopy can remove polyps as small as one millimetre or less. Once polyps are removed, they can be studied with the aid of a microscope to determine if they are precancerous or not. It takes 15 years or fewer for a polyp to turn cancerous."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5740", "text": "Colonoscopy is similar to  sigmoidoscopy \u2014the difference being related to which parts of the colon each can examine. A colonoscopy allows an examination of the entire colon (1200\u20131500\u00a0mm in length). A sigmoidoscopy allows an examination of the distal portion (about 600\u00a0mm) of the colon, which may be sufficient because benefits to cancer survival of colonoscopy have been limited to the detection of lesions in the distal portion of the colon. [ 54 ] [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5741", "text": "A sigmoidoscopy is often used as a screening procedure for a full colonoscopy, often done in conjunction with a stool-based test such as a fecal occult blood test (FOBT), fecal immunochemical test (FIT), or multi-target stool DNA test (Cologuard) or blood-based test, SEPT9 DNA methylation test (Epi proColon). [ 57 ]  About 5% of these screened patients are referred to colonoscopy. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5742", "text": "Virtual colonoscopy , which uses 2D and 3D imagery reconstructed from  computed tomography  (CT) scans or from  nuclear magnetic resonance  (MR) scans, is also possible, as a totally  non-invasive  medical test, although it is not standard and still under investigation regarding its diagnostic abilities. Furthermore, virtual colonoscopy does not allow for therapeutic maneuvers such as polyp/tumour removal or biopsy nor visualization of lesions smaller than 5 millimeters.  If a growth or polyp is detected using CT colonography, a standard colonoscopy would still need to be performed. Additionally, surgeons have lately been using the term  pouchoscopy  to refer to a colonoscopy of the  ileo-anal pouch ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5743", "text": "The large intestine is truly distinct only in  tetrapods , in which it is almost always separated from the small intestine by an  ileocaecal valve . In most vertebrates, however, it is a relatively short structure running directly to the anus, although noticeably wider than the small intestine. Although the caecum is present in most  amniotes , only in mammals does the remainder of the large intestine develop into a true colon. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5744", "text": "In some small mammals, the colon is straight, as it is in other tetrapods, but, in the majority of mammalian species, it is divided into ascending and descending portions; a distinct transverse colon is typically present only in  primates . However, the taeniae coli and accompanying haustra are not found in either  carnivorans  or  ruminants . The rectum of mammals (other than  monotremes ) is derived from the  cloaca  of other vertebrates, and is, therefore, not truly  homologous  with the \"rectum\" found in these species. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5745", "text": "In some fish, there is no true large intestine, but simply a short rectum connecting the end of the digestive part of the gut to the cloaca. In  sharks , this includes a  rectal gland  that secretes salt to help the animal maintain  osmotic  balance with the seawater. The gland somewhat resembles a caecum in structure but is not a homologous structure. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5746", "text": "This article incorporates text in the  public domain  from  page 1177  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5747", "text": "Limosilactobacillus reuteri  is a  lactic acid bacterium  found in a variety of natural environments, including the  gastrointestinal tract  of humans and other animals. It does not appear to be pathogenic and may have health effects."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5748", "text": "At the turn of the 20th century,  L. reuteri  was recorded in scientific classifications of  lactic acid bacteria , [ 1 ]  though at this time it was mistakenly grouped as a member of  Lactobacillus fermentum . In the 1960s, further work by  microbiologist   Gerhard Reuter , for whom the species eventually was named, reclassified the species as  L. fermentum  biotype II. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5749", "text": "Significant differences were found between biotype II and other biotypes of  L. fermentum , to the point that in 1980 it was identified as a distinct species and the formal species identity,  L. reuteri , was proposed. [ 3 ]  In April 2020,  L. reuteri  was reassigned to the genus  Limosilactobacillus . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5750", "text": "Limosilactobacillus reuteri  is found in a variety of natural environments. It has been isolated from many foods, especially meats and dairy products. [ 2 ] [ 5 ] [ 6 ]  It appears to be essentially ubiquitous in the animal kingdom, having been found in the  gastrointestinal tracts  and feces of healthy humans, [ 7 ]   sheep ,  chickens , [ 8 ]   pigs , [ 9 ]  and  rodents . [ 10 ]  It is the only species to constitute a \"major component\" of the  Lactobacillus  species present in the gut of each of the tested host animals, [ 11 ]  and each host seems to harbor its own specific strain of  L. reuteri . [ 10 ] [ 12 ]  It is possible that  L. reuteri  contributes to the health of its host organism in some manner. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5751", "text": "Limosilactobacillus reuteri  is present as a dominant member of  fermenting  organisms in type II  sourdoughs ; several metabolic traits of  L. reuteri , including  exopolysaccharide  formation and conversion of  glutamine  to  glutamate , improve bread quality.  [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5752", "text": "Limosilactobacillus reuteri  is known to produce  reuterin , [ 15 ]  reutericin 6 [ 16 ]  and  reutericyclin . [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5753", "text": "In the late 1980s,  Walter Dobrogosz , Ivan Casas and colleagues discovered that  L. reuteri  produced a novel broad-spectrum  antibiotic  substance via the organism's  fermentation  of  glycerol . They named this substance reuterin, after Reuter. [ 15 ]  Reuterin is a multiple-compound  dynamic equilibrium  (HPA system, HPA) consisting of 3-hydroxypropionaldehyde, its  hydrate , and its  dimer . [ 19 ] [ 20 ]  At concentrations above 1.4  M , the HPA dimer was predominant. However, at concentrations relevant for biological systems, HPA hydrate was the most abundant, followed by the  aldehyde  form. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5754", "text": "Reuterin inhibits the growth of some harmful  Gram-negative  and  Gram-positive  bacteria, along with  yeasts ,  fungi  and  protozoa . [ 22 ]  Researchers found that  L. reuteri  can secrete sufficient amounts of reuterin to achieve the desired antimicrobial effects. Furthermore, since about four to five times the amount of reuterin is needed to kill \"good\" gut bacteria (i.e.  L. reuteri  and other  Lactobacillus  species) as \"bad\", this would allow  L. reuteri  to remove gut invaders without harming other gut microbiota. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5755", "text": "Some studies questioned whether reuterin production is essential for  L. reuteri ' s health-promoting activity. The discovery that it produces an antibiotic substance led to a great deal of further research. In early 2008,  L. reuteri  was confirmed to be capable of producing reuterin in the  gastrointestinal tract , improving its ability to inhibit the growth of  E. coli . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5756", "text": "The gene cluster controlling the biosynthesis of reuterin and  cobalamin  in the  L. reuteri  genome is a  genomic island  acquired from an anomalous source. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5757", "text": "Although  L. reuteri  occurs naturally in humans, it is not found in all individuals. Dietary supplementation can sustain high levels of it in those with deficiencies. Oral intake of  L. reuteri  has been shown to effectively colonize the  intestines  of healthy individuals. Colonization begins within days of  ingestion , although levels drop months later if intake is stopped. [ 25 ]   L. reuteri  is found in  breast milk . [ 26 ]  Oral intake on the mother's part increases the amount of  L. reuteri  present in her milk, and the likelihood that it will be transferred to the child. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5758", "text": "Manipulation of gut microbiota is a complex process that may cause bacteria-host interactions. [ 28 ]  Although  probiotics  in general are considered safe, concerns exist about their use in certain cases. [ 28 ] [ 29 ]  Some people, such as those with  compromised immune systems ,  short bowel syndrome ,  central venous catheters ,  heart valve disease , and  premature infants , may be at higher risk for adverse events. [ 30 ]  Rarely, consumption of probiotics may cause  bacteremia ,  fungemia  and  sepsis , potentially fatal infections, in children with compromised immune systems or who are already critically ill. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5759", "text": "One of the better documented effects of  L. reuteri  is a significant reduction of symptom duration in pediatric  diarrheal  disease. [ 32 ] [ 33 ] [ 34 ]   L. reuteri  is effective as a  prophylactic  for this illness; children fed it while healthy are less likely to fall ill with diarrhea. [ 35 ]  With regard to prevention of gut infections, comparative research found  L. reuteri  to be more potent than other probiotics. [ 36 ] [ 37 ]  Animal research found it to reduce motor complexes and thus  intestinal motility . [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5760", "text": "Limosilactobacillus reuteri  may be effective treating  necrotizing enterocolitis  in preterm infants. Meta-analysis of randomized studies suggests that  L. reuteri  can reduce the incidence of  sepsis  and shorten the required duration of hospital treatment in this population. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5761", "text": "Limosilactobacillus reuteri  is an effective treatment against infant  colic . [ 40 ] [ 41 ] [ 42 ]  Studies suggest that colicky infants treated with  L. reuteri  experience a reduction in time spent crying compared to those treated with  simethicone [ 43 ]  or placebo. [ 44 ]  However, colic is still poorly understood, and it is not clear why or how  L. reuteri  ameliorates its symptoms. One theory holds that affected infants cry because of gastrointestinal discomfort; if this is the case, it is plausible that  L. reuteri  somehow acts to lessen this discomfort, since its primary residence is inside the gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5762", "text": "Limosilactobacillus reuteri  have a pronounced anti-helicobacter activity and its use as adjuvant therapy of  H. pylori  in children appears to be very promising, especially in the case of detection of infection with  H. pylori  with no absolute indication of eradication. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5763", "text": "Growing evidence indicates  L. reuteri  is capable of fighting the gut  pathogen   Helicobacter pylori , which causes  peptic ulcers  and is endemic in parts of the developing world. One study showed dietary supplementation of  L. reuteri  alone reduces, but does not eradicate,  H. pylori  in the gut. [ 46 ]  Another study found the addition of  L. reuteri  to  omeprazole  therapy dramatically increased (from 0% to 60%) the cure rate of  H. pylori -infected patients compared to the drug alone. [ 47 ]  Yet another study showed that  L. reuteri  effectively suppressed  H. pylori  infection and decreased the occurrence of dyspeptic symptoms, although it did not improve the outcome of antibiotic therapy. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5764", "text": "Llimosilactobacillus reuteri  has the potential to suppress  H. Pylori  infection and may lead to an improvement of H. Pylori-associated gastrointestinal symptoms, [ 49 ]  reducing specific symptoms such as diarrhea and frequent abdominal distention. [ 50 ]  In the future,  L. reuteri  can become a central part of a strategy to avoid using antibiotics and fighting antibiotic resistance in  H. pylori  infections [ 51 ]  and besides fighting  antibiotics resistance ,  L. reuteri  may be a great alternative treatment for  H. pylori  causing fewer side effects than antibiotics. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5765", "text": "Limosilactobacillus reuteri  may be capable of promoting dental health, as it has been proven to kill  Streptococcus mutans , a bacterium responsible for  tooth decay . A screen of several probiotic bacteria found  L. reuteri  was the only tested species able to block  S. mutans . Before testing in humans began, another study showed  L. reuteri  had no harmful effects on  teeth .  Clinical trials  proved that people whose  mouths  are colonized with  L. reuteri  (via dietary supplementation) have significantly less  S. mutans . [ 53 ]  Since these studies were short-term, it is not known whether  L. reuteri  prevents tooth decay. However, since it is able to reduce the numbers of an important decay-causing bacterium, this would be expected."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5766", "text": "Gingivitis  may be ameliorated by consumption of  L. reuteri . Patients afflicted with severe gingivitis showed decreased  gum  bleeding,  plaque  formation and other gingivitis-associated symptoms compared with placebo after chewing  gum  containing  L. reuteri . [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5767", "text": "Lactobacillus reuteri  and other probiotics may influence the  gut microbiome  in ways that protect against  bone loss , common in post-menopausal women.\n [ 55 ] [ 56 ] [ 57 ] [ 58 ] [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5768", "text": "By protecting against many common infections,  L. reuteri  promotes overall wellness in both children and adults.  Double-blind ,  randomized  studies in  child care  centers have found  L. reuteri -fed infants fall sick less often, require fewer doctor visits and are absent fewer days from the center compared to placebo and to the competing probiotic  Bifidobacterium lactis . [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5769", "text": "Similar results have been found in adults; those consuming  L. reuteri  daily end up falling ill 50% less often, as measured by their decrease use of sick leave. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5770", "text": "Scientific studies that require harming the subjects (for example, exposing them to a dangerous  virus ) cannot be conducted in  humans . Therefore, many of  L. reuteri's  benefits have been studied only in different animal species, such as pigs and  mice ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5771", "text": "In general, animal studies on  L. reuteri  are done using the species-specific strain of the bacterium."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5772", "text": "Limosilactobacillus reuteri  confers a high level of resistance to the  pathogen   Salmonella typhimurium , halving  mortality rates  in mice. [ 62 ]  The same is true for chickens [ 63 ]  and turkeys;  L. reuteri  greatly moderates the morbidity and mortality caused by this dangerous food-borne pathogen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5773", "text": "Limosilactobacillus reuteri  is effective in stopping harmful strains of  E. coli  from affecting their hosts. A study performed in chickens showed  L. reuteri  was as potent as the antibiotic  gentamicin  in preventing  E. coli -related deaths. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5774", "text": "The  protozoic   parasite   Cryptosporidium parvum  causes severe watery diarrhea, which can become life-threatening in  immunocompromised  (as in individuals infected with  HIV ) patients.  L. reuteri  is known to lessen the symptoms of  C. parvum  infection in mice [ 65 ]  and pigs. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5775", "text": "Some protective effect against the yeast  Candida albicans  has been found in mice, but in this case,  L. reuteri  did not work as well as other probiotic organisms, such as  L. acidophilus  and  L. casei . [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5776", "text": "In juvenile commercial  livestock , such as turkey poults and piglets,  body weight  and growth rate are good health indicators. Animals raised in the dirty, crowded environments of  commercial farms  are generally less healthy (and therefore weigh less) than their counterparts born and bred in cleaner spaces. In turkeys, for example, this phenomenon is known as \"poult growth depression\", or PGD. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5777", "text": "Supplementing the diets of these young animals with  L. reuteri  helps them to largely overcome the stresses imposed by unhealthy environs. Commercial turkeys fed  L. reuteri  from birth had nearly a 10% higher adult body weight than their peers raised in the same conditions. [ 68 ]  A similar study on piglets showed  L. reuteri  is at least as effective as synthetic  antibiotics  in improving body weight under crowded conditions. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5778", "text": "The mechanism by which  L. reuteri  is able to support healthy growth is not entirely understood. It possibly serves to protect against illness caused by  S. typhimurium  and other pathogens (see above), which are much more common in crowded commercial farms. However, other studies found that it can help when the growth depression is caused entirely by a lack of  dietary protein , and not by contagious disease. [ 70 ]  This raises the possibility that  L. reuteri  somehow improves the intestines' ability to absorb and process  nutrients . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5779", "text": "Treating  colonic  tissue from rats with  acetic acid  causes an injury similar to the human condition  ulcerative colitis . Treating the injured tissue with  L. reuteri  immediately after removing the acid almost completely reverses any ill effects, [ 71 ]  leading to the possibility that  L. reuteri  may be beneficial in the treatment of human colitis patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5780", "text": "In addition to its role in  digestion , the intestinal wall is also vital in preventing harmful bacteria, endotoxins, [ 72 ]  etc., from \"leaking\" into the bloodstream. This leaking, known as  bacterial \"translocation\" , can lead to lethal conditions such as  sepsis . In humans, translocation is more likely to occur following such events as  liver  injury and ingestion of some  poisons . In  rodent studies ,  L. reuteri  was found to greatly reduce the amount of bacterial translocation following either the surgical removal of the liver [ 73 ]  or injection with  D-galactosamine , [ 74 ]  a chemical which causes liver damage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5781", "text": "The  anticancer  drug  methotrexate  causes severe  enterocolitis  in high doses.  L. reuteri  greatly mitigates the symptoms of methotrexate-induced enterocolitis in rats, one of which is bacterial translocation. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5782", "text": "In mice, the absence of  L. reuteri  has been causally linked to maternal diet. [ 72 ]  A gut microbial imbalance, lacking in  L. reuteri , was linked to behavioral abnormalities consistent with  autism  in humans. [ 72 ]  These symptoms were reversible by supplementing  L. reuteri . [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5783", "text": "The  lips  are a horizontal pair of  soft   appendages  attached to the  jaws  and are the most visible part of the  mouth  of many  animals , including  humans . [ 1 ]   Vertebrate  lips are soft, movable and serve to facilitate the  ingestion  of  food  (e.g.  suckling  and  gulping ) and the  articulation  of sound and  speech . Human lips are also a  somatosensory  organ, and can be an  erogenous zone  when used in  kissing  and other acts of  intimacy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5784", "text": "The upper and lower lips are referred to as the  labium superius oris  and  labium inferius oris , respectively. [ 2 ] [ 3 ]   The juncture where the lips meet the surrounding skin of the mouth area is the  vermilion border , [ 4 ]  and the typically reddish area within the borders is called the vermilion zone. [ 5 ]   The vermilion border of the upper lip is known as the  Cupid's bow . [ 6 ]   The fleshy protuberance located in the center of the upper lip is a  tubercle  known by various terms including the procheilon (also spelled  prochilon ), the \"tuberculum labii superioris\", and the \"labial tubercle\". [ 7 ]   The vertical groove extending from the procheilon to the  nasal septum  is called the  philtrum . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5785", "text": "The skin of the lip, with three to five cellular layers, is very thin compared to typical face skin, which has up to 16 layers. With light skin color, the lip skin contains fewer  melanocytes  (cells which produce melanin  pigment , which give skin its color). Because of this, the  blood vessels  appear through the skin of the lips, which leads to their notable red coloring. With darker skin color this effect is less prominent, as in this case the skin of the lips contains more melanin and thus is visually darker.  The skin of the lip forms the border between the exterior skin of the face, and the interior  mucous membrane  of the inside of the mouth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5786", "text": "The lip skin is not hairy and does not have  sweat glands . Therefore, it does not have the usual protection layer of sweat and body oils which keep the skin smooth, inhibit pathogens, and regulate warmth. For these reasons, the lips dry out faster and become  chapped  more easily."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5787", "text": "The lower lip is formed from the  mandibular prominence , a branch of the  first pharyngeal arch . The lower lip covers the anterior  body of the mandible . It is lowered by the  depressor labii inferioris muscle  and the  orbicularis oris  borders it inferiorly."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5788", "text": "The upper lip covers the  anterior surface of the body of the maxilla . Its upper half is of usual skin color and has a depression at its center, directly under the nasal septum, called the  philtrum , which is Latin for \"lower nose\", while its lower half is a markedly different, red-colored skin tone more similar to the color of the inside of the mouth, and the term  vermillion  refers to the colored portion of either the upper or lower lip."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5789", "text": "It is raised by the  levator labii superioris  and is connected to the  lower lip  by the thin lining of the lip itself."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5790", "text": "Thinning of the vermilion of the upper lip and flattening of the  philtrum  are two of the facial characteristics of  fetal alcohol syndrome , a lifelong  disability  caused by the mother's consumption of alcohol during pregnancy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5791", "text": "The skin of the lips is  stratified squamous epithelium . The mucous membrane is represented by a large area in the  sensory cortex , and is therefore highly sensitive. The  frenulum labii inferioris  is the  frenulum  of the lower lip. The  frenulum labii superioris  is the frenulum of the upper lip."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5792", "text": "The  facial artery  is one of the six non-terminal branches of the  external carotid artery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5793", "text": "This artery supplies both lips by its superior and inferior labial branches. Each of the two branches  bifurcate  and  anastomose  with their companion branch from the other terminal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5794", "text": "The muscles acting on the lips are considered part of the muscles of  facial expression .  All muscles of facial expression are derived from the  mesoderm  of the second  pharyngeal arch  and are therefore supplied (motor supply) by the nerve of the second pharyngeal arch, the  facial nerve  (7th  cranial nerve ). The muscles of facial expression are all specialized members of the  panniculus carnosus , which attach to the  dermis  and so wrinkle or dimple the overlying skin. Functionally, the muscles of facial expression are arranged in groups around the  orbits , nose, and mouth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5795", "text": "The muscles acting on the lips:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5796", "text": "Because they have their own muscles and bordering muscles, the lips are easily movable. Lips are used for eating functions, like holding food or to get it in the mouth. In addition, lips serve to close the mouth airtight shut, to hold food and drink inside, and to keep out unwanted objects. Through making a narrow  funnel  with the lips, the suction of the mouth is increased. This suction is essential for babies to  breast feed . Lips can also be used to suck in other contexts, such as sucking on a straw to drink liquids."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5797", "text": "The lips serve for creating different sounds\u2014mainly  labial ,  bilabial , and  labiodental  consonant sounds as well as  vowel rounding \u2014and thus are an important part of the speech apparatus.  The lips enable  whistling  and the performing of wind instruments such as the trumpet,  clarinet , flute, and saxophone. People who have  hearing loss  may unconsciously or consciously  lip read  to understand speech without needing to perceive the actual sounds, and visual cues from the lips affect the perception of what sounds have been heard, for example the  McGurk effect ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5798", "text": "The lip has many  nerve endings   and reacts as part of the  tactile  (touch) senses.  Lips are very sensitive to touch, warmth, and cold.  It is therefore an important aid for exploring unknown objects for babies and toddlers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5799", "text": "Because of their high number of nerve endings, the lips are an  erogenous zone . The lips therefore play a crucial role in  kissing  and other acts of intimacy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5800", "text": "A woman's lips are also a visible expression of her fertility. In studies performed on the science of human attraction, psychologists have concluded that a woman's facial and sexual attractiveness is closely linked to the makeup of her hormones during puberty and development.  Contrary to the effects of  testosterone  on a man's facial structure, the effects of a woman's  oestrogen  levels serve to maintain a relatively \"childlike\" and youthful facial structure during puberty and during final maturation.  It has been shown that the more oestrogen a woman has, the larger her eyes and the fuller her lips, characteristics which are perceived as more feminine. [ 9 ]   Surveys performed by sexual psychologists [ who? ]  have also found that universally, men find a woman's full lips to be more sexually attractive than lips that are less so. [ citation needed ]   A woman's lips are therefore sexually attractive to males because they serve as a biological indicator of a woman's health and fertility.  A woman's lipstick (or  collagen   lip enhancement ) attempts to take advantage of this fact by creating the illusion that a woman has more oestrogen than she actually has and thus that she is more fertile and attractive. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5801", "text": "Lip size is linked to sexual attraction in both men and women. Women are attracted to men with masculine lips that are more middle size and not too big or too small; they are to be rugged and sensual. In general, the researchers found that a small nose, big eyes and voluptuous lips are sexually attractive both in men and women. [ 11 ]  The lips may temporarily swell during sexual arousal due to engorgement with blood. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5802", "text": "The lips contribute substantially to  facial expressions . The lips visibly express emotions such as a  smile  or frown, iconically by the curve of the lips forming an up-open or down-open arc, respectively. Lips can also be made pouty when whining or perky to be provocative."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5803", "text": "The function of the abrupt change in skin structure between the lips and surrounding face (in particular, the function of the less keratinized  vermillion  and the  white roll ) is not completely understood. [ 12 ]  Possible reasons for the difference may include advantages to somatosensory function, better communication of facial expressions, and/or emphasis of the lips' slight  sexual dimorphism  as a  secondary sex characteristic ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5804", "text": "As an organ of the body, the lip can be a focus of disease or show symptoms of a disease:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5805", "text": "Lips are often viewed as a symbol of sensuality and sexuality. This has many origins; above all, the lips are a very sensitive erogenous and tactile organ. Furthermore, in many cultures of the world, a woman's mouth and lips are veiled because of their representative association with the vulva, and because of their role as a woman's secondary sexual organ. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5806", "text": "As part of the mouth, the lips are also associated with the symbolism associated with the mouth as orifice by which food is taken in.  The lips are also linked symbolically to neonatal psychology (see for example  oral stage  of the psychology according to  Sigmund Freud )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5807", "text": "Lip piercing  or  lip augmentation  is sometimes carried out for cosmetic reasons. Products designed for use on the lips include lipstick,  lip gloss  and  lip balm ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5808", "text": "In most vertebrates, the lips are relatively unimportant folds of tissue lying just outside the jaws. However, in  mammals , they become much more prominent, being separated from the jaws by a deep cleft [ citation needed ]  (a notable exception being the  naked mole-rat , whose lips close behind the front teeth). [ 20 ]  They are also more mobile in mammals than in other groups since it is only in this group that they have any attached muscles. In some  teleost  fish, the lips may be modified to carry sensitive  barbels . In birds and turtles, the lips are hard and  keratinous , forming a solid  beak . [ 21 ]   Clevosaurids  like  Clevosaurus  are notable for the presence of bone \"lips\"; in these species the tooth-like jaw projections common to all  sphenodontians  form a beak-like edge around the jaws, protecting the teeth within. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5809", "text": "The following is a  list of intestinal stem cell marker genes,  including their name and known function."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5810", "text": "In the adult  intestine , the  crypts of Lieberk\u00fchn  are the niche for  epithelial   stem cells  and contain all proliferative stem and progenitor cells. Differentiating cells exit the cell cycle and migrate out of the crypts and onto the surface epithelium of the intestine, where they perform their physiological role (e.g., nutrient absorption by enterocytes; mucous secretion by goblet cells) and are eventually shed into the lumen. [ 1 ]  Intestinal stem cells were first identified as such in the 1970s. Cheng and Leblond used autoradiography of phagosomes to track the fate of cells at the base of the crypts, and determined that slender cells interspersed among Paneth cells at the crypt base could give rise to all of the other cell types that constituted the intestinal epithelium. [ 2 ]   Due to their narrow shape and location, these cells were called crypt base columnar cells (CBCs). Potten and colleagues used a combination of DNA labeling and assessment of the response of the epithelium to high-dose radiation to identify label-retaining cells (LRCs) as putative stem cells, which were typically located around four cell positions above the bottom of the crypt, and were therefore also called \"+4 cells\". [ 3 ] [ 4 ]  Later work suggested that these \"+4 cells\" may function as reserve or back-up stem cells, and further suggested that they divide slowly relative to the other progenitor cells in the crypt. Thus, these cells are also called quiescent stem cells. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5811", "text": "The stem cell zone model states that the CBC stem cells reside in a stem-cell-permissive environment. These cycling stem cells regularly generate progeny, which subsequently exit the niche and pass through the \u201ccommon origin of differentiation\u201d around position +5, where they commit toward the various individual lineages. Progenitors mature as they migrate upward onto the villus. Maturing Paneth cell progenitors migrate downward, with the oldest Paneth cells residing at the very base of the crypt. [ 6 ]  In accordance with the stem cell zone model proposing that, during their upward migration, CBC stem cells would only gradually lose their self-renewal capacity, it was shown in vivo that transient amplifying cells can revert to Lgr5+ CBC stem cells after damage, presumably by direct contact with Paneth cells. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5812", "text": "More recently modern genetics techniques, primarily using transgenic mice, have been used to identify genes that are specifically expressed or highly enriched in the intestinal stem cells. Below, a table of intestinal stem cell  \"marker\" genes  is given, along with a notation if this marks active of CBC stem cells, or quiescent/reserve/+4 stem cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5813", "text": "Additional possible markers:\t\nCD24\nCD44v6\nActive beta-catenin\nPcdh8  21419747"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5814", "text": "The  major duodenal papilla  (papilla of Vater) is a rounded projection in the  duodenum  into which the  common bile duct  and  pancreatic duct  drain. The major duodenal papilla is, in most people, the primary mechanism for the secretion of  bile  and other enzymes that facilitate  digestion ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5815", "text": "The major duodenal papilla is situated in the second part of the  duodenum , 7\u201310\u00a0cm from the  pylorus , at the level of the second or third  lumbar vertebrae . It is surrounded by the  sphincter of Oddi , a circular muscle, and receives a mixture of pancreatic enzymes and  bile  from the  Ampulla of Vater , which drains both the  pancreatic duct  and  biliary system . [ 2 ]   The junction between the  foregut  and  midgut  occurs directly below the major duodenal papilla. [ 3 ]   :\u200a274\u200a  The major duodenal papilla projects less than a centimetre into the  lumen  of the duodenum. [ 4 ]  It appears rounded and is often covered by a fold on the uppermost side of the papilla; that is, the side which receives contents from the stomach. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5816", "text": "The major duodenal papilla is seen from the duodenum as lying within a  mucosal  fold. The  minor duodenal papilla  is situated 2\u00a0cm proximal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5817", "text": "The major duodenal papilla is occasionally found in the junction between the descending and horizontal parts of the duodenum, or in the horizontal part of the duodenum; a case study of 1000 people demonstrated this in 12 and 8% respectively. [ 4 ]  in the third part of the duodenum, the level of the vertebrae may be L2-3, and in about 10% of people, it may not receive  bile . Additionally, in a small number of people, the primary papilla for draining the pancreas may in fact be the  accessory pancreatic duct . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5818", "text": "Pancreatic enzymes and bile drain into the duodenum from both the  pancreatic duct  and  biliary system . [ 4 ]  This facilitates the digestion of food; particularly proteins (pancreatic enzymes), and fat-soluble vitamins (bile)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5819", "text": "The minor papilla drains the duct of Santorini, superior in position to the major papilla. In pancreatic divisum, in which the minor papilla drains the bulk of pancreatic secretions and major drains a minority of secretions (opposite of normal), a Santorinicele may develop leading to obstructed secretions/reflux resulting in pancreatitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5820", "text": "The major duodenal papilla was first illustrated by  Gottfreid Bidloo  in 1685, although is sometimes called the  papilla of Vater , after  German   anatomist   Abraham Vater . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5821", "text": "The  mesenteric arteries  take blood from the aorta and distribute it to a large portion of the  gastrointestinal tract ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5822", "text": "Both the  superior  and  inferior  mesenteric arteries arise from the  abdominal aorta . [ 1 ]  Each of these arteries travel through the  mesentery , within which they branch several times before reaching the gut. In humans, many of these branches are named, but in smaller animals the branches are more variable. In some animals, including humans, branches of these arteries join with the  marginal artery of the colon , which means that occlusion of one of the main arteries does not necessarily lead to the death of the part of the gut that it usually supplies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5823", "text": "The term  mesenteric artery  is also used to describe smaller branches of these vessels which, particularly in smaller animals, provide a significant source of vascular resistance. These branches have a dense innervation by  sympathetic  nerves, allowing the brain to control their diameter and hence the resistance to blood flow to the gut. This is of particular importance when blood flow is required elsewhere, such as in exercise or shock, where a large proportion of the blood is required to supply the needs of  skeletal muscle ; by constricting the smaller mesenteric vessels, the resistance of blood flow to the gut increases, and hence blood flows more readily to other organs. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5824", "text": "In  human anatomy , the  mesentery , an  organ  that attaches the  intestines  to the  posterior abdominal wall , comprises the double fold of the  peritoneum . It helps (among other functions) in storing  fat  and allowing  blood vessels ,  lymphatics , and  nerves  to supply the intestines. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5825", "text": "The  mesocolon   (the part of the mesentery that attaches the colon to the abdominal wall) was formerly thought to be a fragmented structure, with all named parts\u2014the ascending, transverse, descending, and sigmoid  mesocolons , the  mesoappendix , and the  mesorectum \u2014separately terminating their insertion into the posterior abdominal wall. [ 2 ]  However, in 2012, new  microscopic  and  electron microscopic   examinations  showed the mesocolon to be a single structure derived from the  duodenojejunal flexure  and extending to the distal mesorectal layer. [ 2 ] [ 3 ]  Thus the mesentery is an  internal organ . [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5826", "text": "The mesentery of the  small intestine  arises from the  root of the mesentery  (or  mesenteric root ) and is the part connected with the structures in front of the  vertebral column . The root is narrow, about 15\u00a0cm long, 20\u00a0cm in width, and is directed obliquely from the  duodenojejunal flexure  at the left side of the second  lumbar vertebra  to the right  sacroiliac joint . The root of the mesentery extends from the duodenojejunal flexure to the  ileocaecal junction . This section of the small intestine is located centrally in the abdominal cavity and lies behind the transverse colon and the  greater omentum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5827", "text": "The mesentery becomes attached to the  colon  at the gastrointestinal margin and continues as the several regions of the mesocolon. The parts of the mesocolon take their names from the part of the colon to which they attach. These are the transverse mesocolon attaching to the transverse colon, the sigmoid mesocolon attaching to the sigmoid colon, the mesoappendix attaching to the appendix, and the mesorectum attaching to the upper third of the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5828", "text": "The mesocolon regions were traditionally taught to be separate sections with separate insertions into the posterior abdominal wall. In 2012, the first detailed observational and  histological  studies of the mesocolon were undertaken and this revealed several new findings. [ 6 ]  The study included 109 patients undergoing open, elective, total abdominal  colectomy . Anatomical observations were recorded during the surgery and on the post-operative specimens."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5829", "text": "These studies showed that the mesocolon is continuous from the ileocaecal to the rectosigmoid level. It was also shown that a mesenteric confluence occurs at the ileocaecal and rectosigmoid junctions, as well as at the  hepatic and splenic flexures  and that each confluence involves peritoneal and omental attachments. The proximal rectum was shown to originate at the confluence of the mesorectum and mesosigmoid. A plane occupied by perinephric fascia was shown to separate the entire apposed small intestinal mesentery and the mesocolon from the  retroperitoneum . Deep in the  pelvis , this fascia coalesces to give rise to  presacral fascia . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5830", "text": "Flexural anatomy is frequently described as a difficult area. It is simplified when each flexure is considered as being centered on a mesenteric contiguity. The ileocaecal flexure arises at the point where the ileum is continuous with the caecum around the ileocaecal mesenteric flexure. Similarly, the  hepatic flexure  is formed between the right mesocolon and transverse mesocolon at the mesenteric confluence. The colonic component of the hepatic flexure is draped around this mesenteric confluence. Furthermore, the  splenic flexure  is formed by the mesenteric confluence between the transverse and left mesocolon. The colonic component of the splenic flexure occurs lateral to the mesenteric confluence. At every flexure, a continuous peritoneal fold lies outside the colonic/mesocolic complex tethering this to the posterior abdominal wall. [ 2 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5831", "text": "The  transverse mesocolon  is that section of the mesentery attached to the  transverse colon  that lies between the  colic flexures ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5832", "text": "The  sigmoid mesocolon  is that region of the mesentery to which the  sigmoid colon  is attached at the gastrointestinal mesenteric margin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5833", "text": "The  mesoappendix  is the portion of the mesentery connecting the  ileum  to the  appendix . It may extend to the tip of the appendix. It encloses the  appendicular artery  and vein, as well as  lymphatic  vessels, nerves, and often a  lymph node ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5834", "text": "The  mesorectum  is that part attached to the upper third of the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5835", "text": "Understanding the macroscopic structure of the mesenteric organ meant that associated structures\u2014the peritoneal folds and congenital and omental adhesions\u2014could be better appraised. The small intestinal mesenteric fold occurs where the small intestinal mesentery folds onto the posterior abdominal wall and continues laterally as the right mesocolon. During mobilization of the small intestinal mesentery from the posterior abdominal wall, this fold is incised, allowing access to the interface between the small intestinal mesentery and the retroperitoneum. The fold continues at the inferolateral boundary of the ileocaecal junction and turn  cephalad  as the right paracolic peritoneal fold. This fold is divided during lateral to medial mobilization, permitting the surgeon to serially lift the right colon and associated mesentery off the underlying fascia and retroperitoneum. At the hepatic flexure, the right lateral peritoneal fold turns and continues medially as the hepatocolic peritoneal fold. Division of the fold in this location permits separation of the colonic component of the hepatic flexure and mesocolon off the retroperitoneum. [ 2 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5836", "text": "Interposed between the hepatic and splenic flexures, the greater omentum adheres to the transverse colon along a further band or fold of peritoneum. Dissection through this allows access to the cephalad (top) surface of the transverse mesocolon. Focal adhesions frequently tether the greater omentum to the cephalad aspect of the transverse mesocolon. The left colon is associated with a similar anatomic configuration of peritoneal folds; the splenic peritoneal fold is contiguous with the left lateral paracolic peritoneal fold at the splenic flexure. Division of the latter similarly allows for the separation of the left colon and associated mesentery off the underlying fascia and frees it from the retroperitoneum. The left lateral paracolic peritoneal fold continues distally at the lateral aspect of the mobile component of the mesosigmoid. [ 2 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5837", "text": "Determination of the macroscopic structure of the mesenteric organ allowed a recent characterisation of the histological and electron microscopic properties. [ 7 ]  The microscopic structure of the mesocolon and associated fascia is consistent from ileocecal to mesorectal levels. A surface  mesothelium  and underlying connective tissue is universally apparent.  Adipocytes  lobules within the body of the mesocolon are separated by fibrous  septa  arising from submesothelial connective tissue. Where apposed to the retroperitoneum, two mesothelial layers separate the mesocolon and underlying retroperitoneum. Between these is  Toldt's fascia , a discrete layer of connective tissue. Lymphatic channels are evident in mesocolic connective tissue and in Toldt's fascia. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5838", "text": "The  primitive gut  is suspended from the posterior abdominal wall by the  dorsal mesentery . The gastrointestinal tract and associated dorsal mesentery are subdivided into  foregut ,  midgut , and  hindgut  regions based on the respective blood supply. The foregut is supplied by the  celiac trunk , the midgut is supplied by the  superior mesenteric artery  (SMA), and the hindgut is supplied by the  inferior mesenteric artery  (IMA). This division is established by the fourth week of  development . After this, the midgut undergoes a period of rapid elongation, forcing it to herniate through the  navel . During herniation, the midgut  rotates  90\u00b0 anti-clockwise around the axis of the SMA and forms the midgut loop. The cranial portion of the loop moves to the right and the caudal portion of the loop moves toward the left. This  rotation  occurs at about the eighth week of development. The  cranial  portion of the loop will develop into the jejunum and most of the ileum, while the  caudal  part of the loop eventually forms the terminal portion of the ileum, the  ascending colon  and the initial two-thirds of the transverse colon. As the foetus grows larger, the mid-gut loop is drawn back through the umbilicus and undergoes a further 180\u00b0 rotation, completing a total of 270\u00b0 rotation. At this point, about 10 weeks, the  caecum  lies close to the  liver . From here it moves in a cranial to caudal direction to eventually lie in the lower right portion of the abdominal cavity. This process brings the ascending colon to lie vertically in the lateral right portion of the abdominal cavity apposed to the posterior abdominal wall. The descending colon occupies a similar position on the left side. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5839", "text": "During these topographic changes, the dorsal mesentery undergoes corresponding changes. Most anatomical and embryological textbooks say that after adopting a final position, the ascending and descending mesocolons disappear during embryogenesis.  Embryology\u2014An Illustrated Colour Text , \"most of the mid-gut retains the original dorsal mesentery, though parts of the duodenum derived from the mid-gut do not. The mesentery associated with the ascending colon and descending colon is resorbed, bringing these parts of the colon into close contact with the body wall.\" [ 9 ]  In  The Developing Human , the author states, \"the mesentery of the ascending colon fuses with the parietal peritoneum on this wall and disappears; consequently the ascending colon also becomes retroperitoneal\". [ 10 ]  To reconcile these differences, several theories of embryologic mesenteric development\u2014including the \"regression\" and \"sliding\" theories\u2014have been proposed, but none has been widely accepted. [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5840", "text": "The portion of the  dorsal mesentery  that attaches to the  greater curvature  of the  stomach , is known as the  dorsal mesogastrium . The part of the dorsal mesentery that suspends the  colon  is termed the  mesocolon . The dorsal mesogastrium develops into the  greater omentum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5841", "text": "The development of the  septum transversum  takes part in the formation of the  diaphragm , while the caudal portion into which the  liver  grows forms the  ventral mesentery . The part of the ventral mesentery that attaches to the  stomach  is known as the  ventral mesogastrium . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5842", "text": "The  lesser omentum  is formed, by a thinning of the  mesoderm  or ventral mesogastrium, which attaches the stomach and  duodenum  to the anterior  abdominal wall . By the subsequent growth of the liver, this leaf of mesoderm is divided into two parts \u2013 the  lesser omentum  between the stomach and liver, and the  falciform  and  coronary ligaments  between the liver and the abdominal wall and diaphragm. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5843", "text": "In the adult, the ventral mesentery is the part of the  peritoneum  closest to the  navel ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5844", "text": "Clarifications of the mesenteric anatomy have facilitated a clearer understanding of diseases involving the mesentery, examples of which include  malrotation  and  Crohn's disease  (CD). In CD, the mesentery is frequently thickened, rendering  hemostasis  challenging. In addition, fat wrapping\u2014creeping fat\u2014involves extension of mesenteric fat over the circumference of contiguous gastrointestinal tract, and this may indicate increased mesothelial plasticity. The relationship between mesenteric derangements and mucosal manifestations in CD points to a pathobiological overlap; some authors say that CD is mainly a mesenteric disorder that secondarily affects the GIT and systemic circulation. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5845", "text": "Thrombosis  of the  superior mesenteric vein  can cause  mesenteric ischemia  also known as  ischemic bowel . Mesenteric ischemia can also result from the formation of a  volvulus , a twisted loop of the small intestine that when it wraps around itself and also encloses the mesentery too tightly can cause  ischemia . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5846", "text": "The rationalization of mesenteric and peritoneal fold anatomy permits the surgeon to differentiate both from intraperitoneal adhesions\u2014also called congenital adhesions. These are highly variable among patients and occur in several locations. Congenital adhesions occur between the lateral aspect of the peritoneum overlying the mobile component of the mesosigmoid and the parietal peritoneum in the left iliac fossa. During the lateral to the medial approach of mobilizing of the mesosigmoid, these must be divided first before the peritoneum proper can be accessed. Similarly, focal adhesions occur between the undersurface of the greater omentum and the cephalad aspect of the transverse mesocolon. These can be accessed after dividing the peritoneal fold that links the greater omentum and transverse colon. Adhesions here must be divided to separate the greater omentum off the transverse mesocolon, thus allowing access to the lesser sac proper. [ 2 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5847", "text": "While the total mesorectal excision (TME) operation has become the surgical gold standard for the management of rectal cancer, this is not so for colon cancer. [ 2 ] [ 14 ] \nRecently, the surgical principles underpinning TME in rectal cancer have been extrapolated to colonic surgery. [ 15 ] [ 16 ]  Total or complete mesocolic excision (CME), use planar surgery and extensive mesenterectomy (high tie) to minimise breach of the mesentery and maximise lymph nodes yield. Application of this T/CME reduces local five-year recurrence rates in colon cancer from 6.5% to 3.6%, while cancer-related five-year survival rates in patients resected for cure increased from 82.1% to 89.1%. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5848", "text": "Recent radiologic appraisals of the mesenteric organ have been conducted in the context of the contemporary understanding of mesenteric organ anatomy. When this organ is divided into non-flexural and flexural regions, these can readily be differentiated in most patients on CT imaging. Clarification of the radiological appearance of the human mesentery resonates with the suggestions of Dodds and enables a clearer conceptualization of mesenteric derangements in disease states. [ 18 ]  This is of immediate relevance in the spread of cancer from colon cancer and perforated diverticular disease, and in pancreatitis where fluid collections in the lesser sac dissect the mesocolon from the retroperitoneum and thereby extend distally within the latter. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5849", "text": "Mesentery has been known for thousands of years, however it was unclear whether mesentery is a single organ or there are several mesenteries. [ 20 ] [ better\u00a0source\u00a0needed ]  The classical anatomical description of the mesocolon is credited to British surgeon  Sir Frederick Treves  in 1885, [ 21 ]  although a description of the membrane as a single structure dates back to at least  Leonardo da Vinci . [ 22 ]  Treves is known for performing the first  appendectomy  in England in 1888; he was surgeon to both  Queen Victoria  and  King Edward VII . [ 23 ]  He studied the human mesentery and peritoneal folds in 100 cadavers and described the right and left mesocolons as vestigial or absent in the human adult. Accordingly, the small intestinal mesentery, transverse, and sigmoid mesocolons all terminated or attached at their insertions into the posterior abdominal wall. [ 21 ] [ 23 ]  These assertions were included in mainstream surgical, anatomical, embryological, and radiologic literature for more than a century. [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5850", "text": "Almost 10 years before Treves, the Austrian anatomist  Carl Toldt  described the persistence of all portions of the mesocolon into adulthood. [ 26 ]   Toldt was professor of anatomy in Prague and Vienna; he published his account of the human mesentery in 1879. Toldt identified a fascial plane between the mesocolon and the underlying retroperitoneum, formed by the fusion of the visceral peritoneum of the mesocolon with the parietal peritoneum of the retroperitoneum; this later became known as Toldt's fascia. [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5851", "text": "In 1942, anatomist  Edward Congdon  also demonstrated that the\nright and left mesocolons persisted into adulthood and remained separate from the retroperitoneum\u2014extraretroperitoneal. [ 28 ]  Radiologist  Wylie J. Dodds  described this concept in 1986. [ 18 ]  Dodds extrapolated that unless the mesocolon remained an extraretroperitoneal structure\u2014separate from the retroperitoneum\u2014only then would the radiologic appearance of the mesentery and peritoneal folds be reconciled with actual anatomy. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5852", "text": "Descriptions of the mesocolon by Toldt, Congdon, and Dodds have largely been ignored in mainstream literature until recently. A formal appraisal of the mesenteric organ anatomy was conducted in 2012; it echoed the findings of Toldt, Congdon, and Dodds. [ 6 ]  The single greatest advance in this regard was the identification of the mesenteric organ as being contiguous, as it spans the gastrointestinal tract from duodenojejunal flexure to mesorectal level. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5853", "text": "In 2012 it was discovered that the mesentery was a single organ, which precipitated advancement in colon and rectum surgery [ 29 ]  and in sciences related to  anatomy  and  development ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5854", "text": "The word \"mesentery\" and its  Neo-Latin  equivalent  mesenterium  ( / \u02cc m \u025b z \u0259 n \u02c8 t \u025b r i \u0259 m / ) use the  combining forms   mes-  +  enteron , ultimately from ancient Greek  \u03bc\u03b5\u03c3\u03ad\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd  ( mesenteron ), from  \u03bc\u03ad\u03c3\u03bf\u03c2  ( m\u00e9sos , \"middle\") +  \u1f14\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd  ( \u00e9nteron , \"gut\"), yielding \"mid-intestine\" or \"midgut\". The adjectival form is \"mesenteric\" ( / \u02cc m \u025b z \u0259 n \u02c8 t \u025b r \u026a k / )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5855", "text": "An improved understanding of mesenteric structure and histology has enabled a formal characterization of mesenteric lymphangiology. [ 7 ]   Stereologic  assessments of the lymphatic vessels demonstrate a rich lymphatic network embedded within the mesenteric connective tissue lattice. On average, vessels occur every 0.14\u00a0mm (0.0055\u00a0in), and within 0.1\u00a0mm (0.0039\u00a0in) from the mesocolic surfaces\u2014anterior and posterior. Lymphatic channels have also been identified in Toldt's fascia, though the significance of this is unknown. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5856", "text": "( Wayback Machine  copy)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5857", "text": "Methanogens  are a group of  microorganisms  that produce  methane  as a byproduct of their metabolism. They play an important role in the digestive system of  ruminants . The  digestive tract  of ruminants contains four major parts:  rumen ,  reticulum ,  omasum  and  abomasum . The food with saliva first passes to the rumen for breaking into smaller particles and then moves to the reticulum, where the food is broken into further smaller particles. Any indigestible particles are sent back to the rumen for  rechewing . The majority of  anaerobic microbes  assisting the cellulose breakdown occupy the rumen and initiate the fermentation process. The animal absorbs the fatty acids, vitamins and nutrient content on passing the partially digested food from the rumen to the omasum. This decreases the pH level and initiates the release of enzymes for further breakdown of the food which later passes to the abomasum to absorb remaining nutrients before excretion. This process takes about 9\u201312 hours."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5858", "text": "Some of the microbes in the ruminant digestive system are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5859", "text": "Migrating motor complex , also known as  migrating myoelectric complex ,  migratory motor complex ,  migratory myoelectric complex  and  MMC , is a cyclic, recurring motility pattern that occurs in the stomach and small bowel during  fasting ; it is interrupted by  feeding . [ 1 ]  A pattern of electrical activity is also observed in the  gastrointestinal tract  in a regular cycle during this interdigestive period."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5860", "text": "MMC was discovered and characterized in fasting dogs in 1969 by Dr. Joseph H. Szurszewski at the  Mayo Clinic . [ 2 ]  He also showed that this activity stops upon eating a meal, and suggested that it induces a motor activity that acts as an \"interdigestive housekeeper\" in the small intestine. [ 2 ]  These motor complexes trigger  peristaltic waves , which facilitate transportation of indigestible substances such as  bone ,  fiber , and  foreign bodies  from the  stomach , through the  small intestine , past the  ileocecal sphincter , and into the  colon . MMC activity varies widely across individuals and within an individual when measured on different days. The MMC occurs every 90\u2013230 minutes during the interdigestive phase (i.e., between meals) and is responsible for the  rumbling  experienced when hungry. [ 3 ] [ 4 ]  It also serves to transport  bacteria  from the small intestine to the large intestine and to inhibit the migration of colonic bacteria into the  terminal ileum ; an impairment to the MMC typically results in  small intestinal bacterial overgrowth . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5861", "text": "The MMC originates mostly in the stomach\u2014although ~25% will arise from the  duodenum  or proximal  jejunum \u2014and can travel to the distal end of the  ileum . [ 6 ]  They consist of four distinct phases:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5862", "text": "Movements of the small bowel are believed to be controlled by the central and enteric nervous systems, intestinal muscles, and numerous peptides and hormones. For example, the MMC is thought to be initiated by  motilin , and it does not directly depend on extrinsic nerves. [ 7 ]  Additionally, gastrin, insulin, cholecystokinin, glucagon, and secretin have been reported to disrupt the MMC."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5863", "text": "Eating interrupts the MMC. For example, one study found that a continental breakfast of 450 Kcal causes the MMC to disappear for 213 \u00b1 48 minutes. [ 8 ]  The number of calories and nature of food determine the length of the disruption with fats causing a longer disruption than carbohydrates which in turn cause a longer disruption than protein. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5864", "text": "Most of the cleaning waves in the MMC happen at night while we are asleep. For many people this will be sufficient to help maintain a healthy, balanced environment in the digestive tract. For others, it may be beneficial to space out food intake to allow for a couple cleaning waves to occur between meals throughout the day as well. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5865", "text": "Autoimmunity following infection by a pathogen producing  CdtB , such as  C. jejuni , may be the leading cause of MMC impairment. [ 11 ]   Narcotics  are also known to impair the MMC. [ 12 ]  Stress has been shown to reduce MMC activity as well. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5866", "text": "Patients with  SIBO  and  IBS  have on average a third as many MMC phase III events with those events being roughly 30% shorter on average. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5867", "text": "Drugs used to enhance gastrointestinal motility are generally referred to as  prokinetics . Serotonin induces phase III of the MMC, and so serotonin receptor agonists are commonly administered as prokinetics. [ 15 ]  Motilin administration causes phase III contractions, and so motilin agonists are another common prokinetic. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5868", "text": "Eradication of bacterial overgrowth has been shown to partially restore MMC activity. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5869", "text": "An  elemental diet  has been hypothesized to partially restore MMC function. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5870", "text": "A  monogastric  organism has a simple single-chambered  stomach  (one stomach). Examples of monogastric  omnivores  include  humans ,  pigs ,  hamsters  and  rats . Furthermore, there are monogastric  carnivores  such as  cats . [ 1 ]  A monogastric organism is contrasted with  ruminant  organisms (which have four-chambered complex stomachs), such as  cattle ,  goats , and  sheep .  Herbivores with monogastric digestion can digest  cellulose  in their diets by way of symbiotic gut  bacteria . However, their ability to extract energy from cellulose digestion is less efficient than in ruminants. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5871", "text": "Herbivores digest cellulose by microbial   fermentation . Monogastric herbivores which can digest  cellulose  nearly as well as ruminants are called  hindgut fermenters , while ruminants are called  foregut fermenters . [ 3 ]   These are subdivided into two groups based on the relative size of various digestive organs in relationship to the rest of the system:  colonic  fermenters tend to be larger species such as horses and  rhinos , and  cecal  fermenters are smaller animals such as rabbits and rodents. [ 4 ]   Great apes  derive significant amounts of  phytanic acid  from the  hindgut fermentation  of plant materials. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5872", "text": "Monogastrics cannot digest the fiber molecule cellulose as efficiently as ruminants, though the ability to digest cellulose varies amongst species. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5873", "text": "A monogastric digestive system works as soon as the food enters the mouth.  Saliva  moistens the food and begins the digestive process. (Note that horses have no (or negligible amounts of)  amylase  in their saliva). After being swallowed, the food passes from the  esophagus  into the stomach, where  stomach acid  and  enzymes  help to break down the food. Once food leaves the stomach and enters the small intestine, the  pancreas  secretes enzymes and alkali to neutralize the stomach acid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5874", "text": "This  biology  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5875", "text": "The  mouth  is the  body orifice  through which many  animals   ingest  food and  vocalize . The  body cavity  immediately behind the mouth opening, known as the  oral cavity  (or  cavum oris  in  Latin ), [ 2 ]  is also the first part of the  alimentary canal , which leads to the  pharynx  and the  gullet . In  tetrapod   vertebrates , the mouth is bounded on the outside by the  lips  and  cheeks  \u2014 thus the oral cavity is also known as the  buccal cavity  (from Latin  bucca , meaning \"cheek\") [ 3 ]  \u2014 and contains the  tongue  on the inside. Except for some groups like  birds  and  lissamphibians , vertebrates usually have  teeth  in their mouths, [ 4 ]  although some  fish  species have  pharyngeal teeth  instead of oral teeth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5876", "text": "Most  bilaterian   phyla , including  arthropods ,  molluscs  and  chordates , have a two-opening  gut tube  with a mouth at one end and an  anus  at the other. Which end forms first in  ontogeny  is a criterion used to classify bilaterian animals into  protostomes  and  deuterostomes ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5877", "text": "In the first  multicellular animals , there was probably no mouth or gut and food particles were engulfed by the cells on the exterior surface by a process known as  endocytosis . The particles became enclosed in  vacuoles  into which enzymes were secreted and  digestion  took place  intracellularly . The digestive products were absorbed into the cytoplasm and diffused into other cells. This form of digestion is used nowadays by simple organisms such as  Amoeba  and  Paramecium  and also by  sponges  which, despite their large size, have no mouth or gut and capture their food by endocytosis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5878", "text": "However,  most animals  have a mouth and a gut, the lining of which is continuous with the  epithelial cells  on the surface of the body. A few animals which live parasitically originally had guts but have secondarily lost these structures. The original gut of  diploblastic  animals probably consisted of a mouth and a one-way gut. Some modern invertebrates still have such a system: food being ingested through the mouth, partially broken down by enzymes secreted in the gut, and the resulting particles engulfed by the other cells in the gut lining. Indigestible waste is ejected through the mouth. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5879", "text": "In animals at least as complex as an  earthworm , the  embryo  forms a dent on one side, the  blastopore , which deepens to become the  archenteron , the first phase in the formation of the  gut . In deuterostomes, the blastopore becomes the anus while the gut eventually tunnels through to make another opening, which forms the mouth. In the protostomes, it used to be thought that the blastopore formed the mouth ( proto\u2013  meaning \"first\") while the anus formed later as an opening made by the other end of the gut. More recent research, however, shows that in protostomes the edges of the slit-like blastopore close up in the middle, leaving openings at both ends that become the mouth and anus. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5880", "text": "Apart from sponges and  placozoans , almost all animals have an internal gut cavity, which is lined with gastrodermal cells. In less advanced invertebrates such as the  sea anemone , the mouth also acts as an anus. Circular muscles around the mouth are able to relax or contract in order to open or close it. A fringe of tentacles thrusts food into the cavity and it can gape widely enough to accommodate large prey items. Food passes first into a  pharynx  and digestion occurs extracellularly in the  gastrovascular cavity . [ 7 ]   Annelids  have simple tube-like guts, and the possession of an anus allows them to separate the digestion of their foodstuffs from the absorption of the nutrients. [ 8 ] \nMany molluscs have a  radula , which is used to scrape microscopic particles off surfaces. [ 9 ]  In invertebrates with hard exoskeletons, various mouthparts may be involved in feeding behaviour. Insects have a range of mouthparts suited to their mode of feeding. These include mandibles, maxillae and labium and can be modified into suitable appendages for chewing, cutting, piercing, sponging and sucking. [ 10 ]   Decapods  have six pairs of mouth appendages, one pair of mandibles, two pairs of maxillae and three of  maxillipeds . [ 11 ]  Sea urchins have a set of five sharp calcareous plates, which are used as jaws and are known as  Aristotle's lantern . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5881", "text": "In vertebrates, the first part of the digestive system is the  buccal cavity , commonly known as the mouth. The buccal cavity of a fish is separated from the opercular cavity by the  gills . Water flows in through the mouth, passes over the gills and exits via the  operculum  or  gill slits . Nearly all fish have  jaws  and may seize food with them but most feed by opening their jaws, expanding their pharynx and sucking in food items. The food may be held or chewed by teeth located in the jaws, on the roof of the mouth, on the pharynx or on the  gill arches . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5882", "text": "Nearly all amphibians are carnivorous as adults. Many catch their prey by flicking out an elongated tongue with a sticky tip and drawing it back into the mouth, where they hold the prey with their jaws. They then swallow their food whole without much chewing. [ 14 ]  They typically have many small hinged  pedicellate teeth , the bases of which are attached to the jaws, while the crowns break off at intervals and are replaced. Most amphibians have one or two rows of teeth in both jaws but some frogs lack teeth in the lower jaw. In many amphibians, there are also  vomerine teeth  attached to the bone in the roof of the mouth. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5883", "text": "The mouths of reptiles are largely similar to those of mammals. The  crocodilians  are the only reptiles to have teeth anchored in  sockets  in their jaws. [ 16 ]  They are able to replace each of their approximately 80 teeth up to 50 times during their lives. [ 17 ]  Most reptiles are either carnivorous or insectivorous, but turtles are often herbivorous. Lacking teeth that are suitable for efficiently chewing of their food, turtles often have  gastroliths  in their stomach to further grind the plant material. [ 18 ]  Snakes have a very flexible lower jaw, the two halves of which are not rigidly attached, and numerous other joints in their skull. These modifications allow them to open their mouths wide enough to swallow their prey whole, even if it is wider than they are. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5884", "text": "Birds do not have teeth, relying instead on other means of gripping and macerating their food. Their  beaks  have a range of sizes and shapes according to their diet and are composed of elongated mandibles. The upper mandible may have a nasofrontal hinge allowing the beak to open wider than would otherwise be possible. The exterior surface of beaks is composed of a thin, horny sheath of  keratin . [ 20 ]  Nectar feeders such as  hummingbirds  have specially adapted brushy tongues for sucking up nectar from flowers. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5885", "text": "In mammals, the buccal cavity is typically roofed by the  hard  and  soft palates , floored by the  tongue  and surrounded by the  cheeks ,  salivary glands , and upper and lower  teeth . The upper teeth are embedded in the  upper jaw  and the lower teeth in the  lower jaw , which articulates with the  temporal bones  of the  skull . The  lips  are soft and fleshy folds which shape the entrance into the mouth. The buccal cavity empties through the  pharynx  into the  oesophagus . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5886", "text": "Crocodilians  living in the tropics can gape with their mouths to provide cooling by  evaporation  from the mouth lining. [ 23 ]  Some mammals rely on panting for  thermoregulation  as it increases evaporation of water across the moist surfaces of the lungs, the tongue and mouth. Birds also avoid overheating by gular fluttering, flapping the wings near the gular (throat) skin, similar to panting in mammals. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5887", "text": "Various animals use their mouths in threat displays. They may gape widely, exhibit their teeth prominently, or flash the startling colours of the mouth lining. This display allows each potential combatant an opportunity to assess the weapons of their opponent and lessens the likelihood of actual combat being necessary. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5888", "text": "A number of species of bird use a  gaping , open beak in their fear and threat displays. Some augment the display by hissing or breathing heavily, while others clap their beaks. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5889", "text": "Mouths are also used as part of the mechanism for producing sounds for communication. To produce sounds, air is forced from the lungs over  vocal cords  in the larynx. In humans, the pharynx, soft palate, hard palate,  alveolar ridge , tongue, teeth and lips are termed  articulators  and play their part in the production of  speech . Varying the position of the tongue in relation to the other articulators or moving the lips restricts the airflow from the lungs in different ways and changes the mouth's resonating properties, producing a range of different sounds. [ 27 ]  In frogs, the sounds can be amplified using sacs in the throat region. The vocal sacs can be inflated and deflated and act as resonators to transfer the sound to the outside world. [ 28 ]  A bird's song is produced by the flow of air over a vocal organ at the base of the  trachea , the  syrinx . For each burst of song, the bird opens its beak and closes it again afterwards. The beak may move slightly and may contribute to the resonance but the song originates elsewhere. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5890", "text": "Mucoid plaque  (or mucoid cap or rope) is a  pseudoscientific  term used by some  alternative medicine  advocates to describe what is claimed to be a combination of harmful  mucus-like  material and food residue that they say coats the  gastrointestinal tract  of most people. The term was coined by Richard Anderson, a  naturopath  and  entrepreneur , who sells a range of products that claim to \"cleanse\" the body of such purported plaques. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5891", "text": "Many such \" colon cleansing \" products are promoted to the public on websites that have been described as making misleading medical claims. [ 2 ]  The presence of laxatives,  bentonite clay , and fibrous thickening agents in some of these \"cleansing agents\" has led to suggestions that the products themselves produce the excreted matter regarded as the plaque. [ 2 ] [ 3 ] \nThe concept of a 'mucoid plaque' has been dismissed by medical experts as having no anatomical or physiological basis. [ 4 ] [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5892", "text": "Various forms of colon cleansing were popular in the 19th and early 20th century. [ 7 ]  In 1932, Bastedo wrote in the  Journal of the American Medical Association  about his observation of mucus masses being removed during a colon irrigation procedure: \"When one sees the dirty gray, brown or blackish sheets, strings and rolled up wormlike masses of tough mucus with a rotten or dead-fish odor that are obtained by colon irrigations, one does not wonder that these patients feel ill and that they obtain relief and show improvement as the result of the irrigation.\" [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5893", "text": "While colonic irrigation enjoyed a vogue in the early 20th century as a possible cure for numerous diseases, subsequent research showed that it was useless and potentially harmful. [ 9 ]  With the scientific rationale for \"colon cleansing\" disproven, the idea fell into disrepute as a form of  quackery , with a 2005 medical review stating that \"there is no evidence to support this ill-conceived theory that has been long abandoned by the scientific community.\" [ 10 ]   Similarly, in response to claims that colon cleansing removes \"toxins\", Bennett Roth, a gastroenterologist at the  University of California , stated that \"there is absolutely no science to this whatsoever. There is no such thing as getting rid of quote-unquote 'toxins.' The colon was made to carry stool. This is total baloney.\" [ 11 ]  The preoccupation with such bowel management products has been described as a \"quaint and amusing chapter in the history of weird medical beliefs.\" [ 12 ]  Nevertheless, interest in colonic \" autointoxication \" as a cause of illness, and in colonic irrigation as a cure, enjoyed a revival in  alternative medicine  at the end of the 20th century. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5894", "text": "The term \"mucoid plaque\" was coined and popularized by  naturopath  and  entrepreneur  Richard Anderson, who sells a range of products that claim to cleanse the body of such purported plaques by causing them to be eliminated. [ 1 ]   Anderson describes a mucoid plaque as a rubbery, ropey, generally green  gel -like mucus film that covers the  epithelial cells  of the  hollow organs , particularly of the  alimentary canal . Anderson also claims the plaque can impair digestion and the absorption of nutrients, hold  pathogens , and cause illnesses such as  diarrhea ,  bowel cancer ,  allergies  and skin conditions. Based on these claims, he promotes efforts to remove the plaque, and sells a range of products to this end. [ 3 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5895", "text": "Though Anderson argues that his beliefs are backed by scientific research, his claims are primarily supported by  anecdotal evidence  rather than  empirical data , and doctors have noted the absence of mucoid plaques. Anderson claims this is due to medical textbooks failing to cover the concept, which results in doctors not knowing what to look for. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5896", "text": "Practicing  physicians  have dismissed the concept of mucoid plaque as a  hoax  and a \"non-credible concept\". [ 4 ]  A pathologist at the  University of Texas  School of Medicine addressed Anderson's claims directly, saying that he has \"seen several thousand intestinal biopsies and have never seen any 'mucoid plaque.' This is a complete fabrication with no anatomic basis.\" [ 1 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5897", "text": "Another pathologist, Edward Friedlander, noted that, in his experience, he has never observed anything resembling a \"toxic bowel settlement\", and that some online photographs actually depict what he recognises as a  blood clot . [ 6 ]  Commenting on claims that waste material can adhere to the colon, Douglas Pleskow, a gastroenterologist at  Beth Israel Deaconess Medical Center , stated, \"that is the urban legend. In reality, most people clear their GI tract within three days.\" [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5898", "text": "In a review of websites promoting products that claim to remove 'mucoid rope' or plaque from consumers' intestines, Howard Hochster of  New York University  wrote that these websites are \"abundant, quasi-scientific, and unfortunately convincing to a biologically uneducated public.\" He noted that although such sites are entertaining, they are disturbing in that they promote a belief that has no basis in physiology. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5899", "text": "Hochster also noted that a preparation marketed to remove mucoid plaque contains laxatives and bulky fibrous ingredients. Thus, the rope-like fecal material expelled from people who consume this product \"certainly is a result of the figs and senna in this preparation,\" rather than any sort of pathologic 'plaque'. [ 2 ]  Other 'colon cleanser' products contain bentonite clay that, when ingested, would also result in production of bulky stools. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5900", "text": "In many cases, customers purchase supplement products that are said to help the body excrete the so-called 'mucoid plaque'. The customer may consume a number of pills, and then within 12\u201348 hours, will pass a rope-like fecal material in their subsequent bowel movements. This fecal material is said to be the 'mucoid plaque'. However, analysis of supplements consumed by the customer shows that the active ingredient is very similar to that of clay used in clumping cat litter. This clay takes a negative mould of the large intestine which is then excreted during the customer's next bowel movement.  [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5901", "text": "The  muscularis mucosae  (or  lamina muscularis mucosae ) is a thin layer ( lamina ) of  muscle  of the  gastrointestinal tract , located outside the  lamina propria , and separating it from the  submucosa . It is present in a continuous fashion from the  esophagus  to the upper  rectum  (the exact nomenclature of the rectum's muscle layers is still being debated). A discontinuous muscularis mucosae\u2013like muscle layer is present in the  urinary tract , from the  renal pelvis  to the  bladder ; as it is discontinuous, it should not be regarded as a true muscularis mucosae."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5902", "text": "In the  gastrointestinal tract , the term  mucosa  or  mucous membrane  refers to the combination of  epithelium , lamina propria, and (where it occurs) muscularis mucosae. [ 1 ]   The etymology suggests this, since the Latin names translate to \"the mucosa's own special layer\" ( lamina propria mucosae ) and \"muscular layer of the mucosa\" ( lamina muscularis mucosae )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5903", "text": "The muscularis mucosae is composed of several thin layers of  smooth muscle fibers  oriented in different ways which keep the mucosal surface and underlying  glands  in a constant state of gentle agitation to expel contents of glandular  crypts  and enhance contact between epithelium and the contents of the  lumen ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5904", "text": "Stacey E. Mills\u00a0\u2014 Histology for Pathologists: 3rd (third) Edition, page 670.  ISBN \u00a0 9780781762410"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5905", "text": "Nitrosamines  (or more formally  N -nitrosamines ) are  organic compounds  produced by industrial processes. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5906", "text": "The  chemical structure  is  R 2 N\u2212N=O , where R is usually an  alkyl group . [ 2 ]  They feature a  nitroso  group ( NO + ) that are \"probable human carcinogens\", [ 3 ]  bonded to a deprotonated  amine . Most nitrosamines are  carcinogenic  in animals. [ 4 ]  A 2006 systematic review supports a \"positive association between nitrite and nitrosamine intake and  gastric cancer , between meat and processed meat intake and gastric cancer and  oesophageal cancer , and between preserved fish, vegetable and smoked food intake and gastric cancer, but is not conclusive\". [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5907", "text": "The organic chemistry of nitrosamines is well developed with regard to their syntheses, their structures, and their reactions. [ 7 ] [ 8 ]  They usually are produced by the reaction of  nitrous acid  ( HNO 2 ) and secondary amines, although other  nitrosyl  sources (e.g.  N 2 O 4 ,  NOCl ,  RONO ) have the same effect: [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5908", "text": "The nitrous acid usually arises from protonation of a  nitrite . This synthesis method is relevant to the generation of nitrosamines under some biological conditions. [ 10 ]   The nitrosation is also reversible, particularly in acidic solutions of  nucleophiles . [ 11 ]   Aryl  nitrosamines rearrange to give a  para -nitroso aryl amine in the  Fischer-Hepp rearrangement . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5909", "text": "With regards to structure, the  C 2 N 2 O  core of nitrosamines is planar, as established by  X-ray crystallography . The N-N and N-O distances are 132 and 126 pm, respectively in  dimethylnitrosamine , [ 13 ]  one of the simplest members of a large class of N-nitrosamines"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5910", "text": "Nitrosamines are not directly carcinogenic. Metabolic activation is required to convert them to the  alkylating agents  that modify bases in DNA, inducing mutations. The specific alkylating agents vary with the nitrosamine, but all are proposed to feature  alkyldiazonium  centers. [ 14 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5911", "text": "In 1956, two British scientists, John Barnes and Peter Magee, reported that a simple member of the large class of N-nitrosamines,  dimethylnitrosamine , produced liver  tumours  in rats. Subsequent studies showed that approximately 90% of the 300 nitrosamines tested were  carcinogenic  in a wide variety of animals. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5912", "text": "A common way ordinary consumers are exposed to nitrosamines is through tobacco use and cigarette smoke. [ 14 ]   Tobacco-specific nitrosamines  also can be found in American  dip snuff ,  chewing tobacco , and to a much lesser degree,  snus  (127.9\u00a0 ppm  for American dip snuff compared to 2.8\u00a0ppm in Swedish snuff or snus). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5913", "text": "Nitroso  compounds react with  primary amines  in acidic environments to form  nitrosamines , which human metabolism converts to mutagenic  diazo compounds .  Small amounts of nitro and nitroso compounds form during meat  curing ; the toxicity of these compounds  preserves  the meat against  bacterial infection .  After curing completes, the concentration of these compounds appears to degrade over time.  Their presence in finished products has been tightly regulated since several food-poisoning cases in the early 20th century, [ 17 ]  but consumption of large quantities of processed meats can still cause a slight elevation in  gastric  and  oesophageal cancer  risk today. [ 18 ] [ 19 ] [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5914", "text": "For example, during the 1970s, certain  Norwegian  farm animals began exhibiting elevated levels of  liver cancer .  These animals had been fed  herring   meal  preserved with  sodium nitrite . The sodium nitrite had reacted with  dimethylamine  in the fish and produced  dimethylnitrosamine . [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5915", "text": "The effects of nitroso compounds vary dramatically across the gastrointestinal tract, and with diet.  Nitroso compounds present in stool do not induce nitrosamine formation, because stool has neutral  pH . [ 23 ] [ 24 ]   Stomach acid  catalyzes nitrosamine compound formation and is the main location of the reaction during digestion. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5916", "text": "The formation process is inhibited when amine concentration is low (e.g. a low-protein diet or no fermented food).  The process may also be inhibited in the case of high  vitamin\u00a0C (ascorbic acid)  or  erythorbic acid [ 26 ]  concentration (e.g. high-fruit diet). [ 27 ] [ 28 ] [ 29 ]  However, when 10% of the meal is fat, the effect reverses, and ascorbic acid markedly increases nitrosamine formation. [ 25 ] [ 30 ]  Vitamin C and erythorbic acid are already commonly used in the meat industry because they enhance the binding of nitrite to myoglobin, encouraging the formation of the desired pink color. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5917", "text": "There have been recalls for various medications due to the presence of nitrosamine impurities. There have been recalls for  angiotensin II receptor blockers ,  ranitidine ,  valsartan , Duloxetine, and others."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5918", "text": "The US  Food and Drug Administration  published guidance about the control of nitrosamine impurities in medicines. [ 32 ] [ 33 ]   Health Canada  published guidance about nitrosamine impurities in medications [ 34 ]  and a list of established acceptable intake limits of nitrosamine impurities in medications. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5919", "text": "In biochemistry,  nitrosamines  are a class of compounds that can form during  food   digestion .  The presence of their precursors,  nitrites , in  cured meats , is controversial, because of a small connection to cancer risk."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5920", "text": "Nitroso  compounds react with  primary amines  in acidic environments to form  nitrosamines , which human metabolism converts to mutagenic  diazo compounds .  Small amounts of nitro and nitroso compounds form during meat  curing ; the toxicity of these compounds  preserves  the meat against  bacterial infection .  After curing completes, the concentration of these compounds appears to degrade over time.  Their presence in finished products has been tightly regulated since several food-poisoning cases in the early 20th century, [ 1 ]  but consumption of large quantities of processed meats can still cause a slight elevation in  gastric  and  oesophageal cancer  risk today. [ 2 ] [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5921", "text": "For example, during the 1970s, certain  Norwegian  farm animals began exhibiting elevated levels of  liver cancer .  These animals had been fed  herring   meal  preserved with  sodium nitrite . The sodium nitrite had reacted with  dimethylamine  in the fish and produced  dimethylnitrosamine . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5922", "text": "The effects of nitroso compounds vary dramatically across the gastrointestinal tract, and with diet.  Nitroso compounds present in stool do not induce nitrosamine formation, because stool has neutral  pH . [ 7 ] [ 8 ]   Stomach acid  catalyzes nitrosamine compound formation and is the main location of the reaction during digestion. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5923", "text": "The formation process is inhibited when amine concentration is low (e.g. a low-protein diet or no fermented food).  The process may also be inhibited in the case of high  vitamin\u00a0C (ascorbic acid)  or  erythorbic acid [ 10 ]  concentration (e.g. high-fruit diet). [ 11 ] [ 12 ] [ 13 ]  However, when 10% of the meal is fat, the effect reverses, and ascorbic acid markedly increases nitrosamine formation. [ 9 ] [ 14 ]  Vitamin C and erythorbic acid are already commonly used in the meat industry because they enhance the binding of nitrite to myoglobin, encouraging the formation of the desired pink color. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5924", "text": "In  organic chemistry ,  nitroso  refers to a  functional group  in which the  nitric oxide  ( \u2212N=O ) group is attached to an organic  moiety . As such, various nitroso groups can be categorized as  C -nitroso compounds (e.g., nitroso alkanes ;  R\u2212N=O ),  S -nitroso compounds ( nitrosothiols ;  RS\u2212N=O ),  N -nitroso compounds (e.g.,  nitrosamines ,  RN(\u2212R\u2019)\u2212N=O ), and  O -nitroso compounds ( alkyl nitrites ;  RO\u2212N=O )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5925", "text": "Nitroso compounds can be prepared by the reduction of  nitro compounds [ 1 ]  or by the oxidation of  hydroxylamines . [ 2 ]  \nOrtho-nitrosophenols may be produced by the  Baudisch reaction . In the  Fischer\u2013Hepp rearrangement , aromatic 4-nitrosoanilines are prepared from the corresponding  nitrosamines ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5926", "text": "Nitrosoarenes typically participate in a  monomer\u2013dimer equilibrium .  The azobenzene  N , N'- dioxide (Ar( \u2013 O)N + = + N(O \u2013 )Ar) dimers, which are often pale yellow, are generally favored in the solid state, whereas the deep-green monomers are favored in dilute solution or at higher temperatures.  They exist as  cis  and  trans  isomers . [ 4 ]   The central \"double bond\" in the dimer in fact has a bond order of about 1.5. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5927", "text": "When stored in  protic media ,  primary  and  secondary  nitrosoalkanes  isomerize  to  oximes . [ 6 ]   Some tertiary nitrosoalkanes also isomerize to oximes through C-C bond fission, particularly if the bond is  electron-poor . [ 7 ]   Nitrosophenols and naphthols isomerize to the oxime  quinone  in solution, but reversibly; nitrosophenol ethers typically dealkylate to facilitate the isomerization.  Nitroso tertiary anilines generally do not dealkylate in that way. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5928", "text": "Due to the stability of the nitric oxide  free radical , nitroso organyls tend to have very low C\u2013N  bond dissociation energies : nitrosoalkanes have BDEs on the order of 30\u201340\u00a0kcal/mol (130\u2013170\u00a0kJ/mol), while nitrosoarenes have BDEs on the order of 50\u201360\u00a0kcal/mol (210\u2013250\u00a0kJ/mol).  As a consequence, they are generally heat- and light-sensitive.  Compounds containing O\u2013(NO) or N\u2013(NO) bonds generally have even lower bond dissociation energies.  For instance,  N -nitrosodiphenylamine , Ph 2 N\u2013N=O, has a N\u2013N bond dissociation energy of only 23\u00a0kcal/mol (96\u00a0kJ/mol). [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5929", "text": "Organonitroso compounds serve as a  ligands  giving  transition metal nitroso complexes . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5930", "text": "Many reactions make use of an intermediate nitroso compound, such as the  Barton reaction  and  Davis\u2013Beirut reaction , as well as the synthesis of  indoles , for example:  Baeyer\u2013Emmerling indole synthesis ,  Bartoli indole synthesis . In the  Saville reaction , mercury is used to replace a nitrosyl from a thiol group."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5931", "text": "C -nitroso compounds are used in organic synthesis as synthons in some well-documented chemical reactions such as hetero Diels-Alder (HDA), nitroso-ene and nitroso-aldol reactions. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5932", "text": "Nitrosyls are non-organic compounds containing the NO group, for example directly bound to the metal via the N atom, giving a metal\u2013NO moiety. Alternatively, a  nonmetal  example is the common reagent  nitrosyl chloride  ( Cl\u2212N=O ). Nitric oxide is a stable  radical , having an unpaired electron. Reduction of nitric oxide gives the nitrosyl  anion ,  NO \u2212 :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5933", "text": "Oxidation of NO yields the  nitrosonium   cation ,  NO + :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5934", "text": "Nitric oxide can serve as a  ligand  forming  metal nitrosyl complexes  or just metal nitrosyls. These complexes can be viewed as adducts of  NO + ,  NO \u2212 , or some intermediate case."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5935", "text": "Nitroso  compounds react with  primary amines  in acidic environments to form  nitrosamines , which human metabolism converts to mutagenic  diazo compounds .  Small amounts of nitro and nitroso compounds form during meat  curing ; the toxicity of these compounds  preserves  the meat against  bacterial infection .  After curing completes, the concentration of these compounds appears to degrade over time.  Their presence in finished products has been tightly regulated since several food-poisoning cases in the early 20th century, [ 12 ]  but consumption of large quantities of processed meats can still cause a slight elevation in  gastric  and  oesophageal cancer  risk today. [ 13 ] [ 14 ] [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5936", "text": "For example, during the 1970s, certain  Norwegian  farm animals began exhibiting elevated levels of  liver cancer .  These animals had been fed  herring   meal  preserved with  sodium nitrite . The sodium nitrite had reacted with  dimethylamine  in the fish and produced  dimethylnitrosamine . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5937", "text": "The effects of nitroso compounds vary dramatically across the gastrointestinal tract, and with diet.  Nitroso compounds present in stool do not induce nitrosamine formation, because stool has neutral  pH . [ 18 ] [ 19 ]   Stomach acid  catalyzes nitrosamine compound formation and is the main location of the reaction during digestion. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5938", "text": "The formation process is inhibited when amine concentration is low (e.g. a low-protein diet or no fermented food).  The process may also be inhibited in the case of high  vitamin\u00a0C (ascorbic acid)  or  erythorbic acid [ 21 ]  concentration (e.g. high-fruit diet). [ 22 ] [ 23 ] [ 24 ]  However, when 10% of the meal is fat, the effect reverses, and ascorbic acid markedly increases nitrosamine formation. [ 20 ] [ 25 ]  Vitamin C and erythorbic acid are already commonly used in the meat industry because they enhance the binding of nitrite to myoglobin, encouraging the formation of the desired pink color. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5939", "text": "The   omasum , also known as the  bible , [ 1 ]  the  fardel , [ 1 ]  the  manyplies [ 1 ]  and the  psalterium , [ 1 ]  is the third compartment of the  stomach  in  ruminants . The omasum comes after the  rumen  and  reticulum  and before the  abomasum . Different ruminants have different omasum structures and function based on the food that they eat and how they developed through evolution. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5940", "text": "The omasum can be found on the right side of the cranial portion of the rumen. [ 3 ]  It receives food from the  reticulum  through the reticulo-omasal orifice [ 3 ]  and provides food to the abomasum through the omaso-abomasal orifice. [ 4 ]   The omasum is spherical [ 5 ]  to crescent shape [ 6 ]  and has multiple leaflets similar to that of a book [ 7 ]  called omasal laminae. [ 4 ]   The omasal laminae are made of thin muscular layers covered with a nonglandular mucous membrane. [ 4 ]  The omasal laminae come from the sides of the large curvature and project towards the inside of the omasum, extending from the reticulo-omasal orifice to the omaso-abomasal orifice. [ 8 ] [ 4 ]  They greatly increase the surface area of the omasum. [ 3 ] [ 9 ]  The laminae are covered in omasal papillae that are claw-like in some ruminants or blunt cones in others. [ 4 ] [ 2 ]  These papillae further increase the surface area but they also provide increased friction against the food particles. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5941", "text": "The function of the omasum is not completely understood. [ 5 ]  During the second contraction phase of the reticulum,  the reticule-omasal sphincter opens for a few seconds allowing a small volume of finely dispersed and well-fermented ingesta to enter the omasum. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5942", "text": "The omasum has two physiological compartments: omasal canal that transfers food from the reticulum to the omasum, and the inter-laminate recesses between the mucosal laminae which provide the area for absorption. [ 2 ]  The omasum is where food particles that are small enough get transferred into the abomasum for enzymatic digestion. [ 5 ] [ 2 ]  In ruminants with a more sophisticated omasum [ example needed ] , the large surface area [ 9 ]  allows it to play a key role in the absorption of water,  electrolytes , [ 2 ] [ 4 ]  volatile fatty acids, minerals, and the fermentation of food. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5943", "text": "Young ruminants that are still drinking milk have an esophageal groove that allows milk to bypass the rumen and go straight from the esophagus to the omasum. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5944", "text": "An early version of the omasum is seen in early ruminants like  duikers  and  muntjacs , where it is a little more than a strainer sieve which prevents un-chewed foods from entering the  abomasum . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5945", "text": "The smallest omasum belongs to ruminants that consume high quality diets like the  moose  and  roe deer , while the largest belongs to those who are un-selective grass and roughage eaters like cattle and sheep. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5946", "text": "The omasum is not only bigger in grass and roughage eaters but there is greater differentiation in the book-like structure; seen as an increase in the number of laminae. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5947", "text": "The  pectinate line  ( dentate line ) is a line which divides the upper two-thirds and lower third of the  anal canal .  Developmentally, this line represents the  hindgut - proctodeum  junction."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5948", "text": "It is an important anatomical landmark in humans, and forms the boundary between the anal canal and the  rectum  according to the anatomic definition. [ 1 ]  Colorectal surgeons instead define the anal canal as the zone from the anal verge to the anorectal ring (palpable structure formed by the  external anal sphincter  and the  puborectalis muscle ). [ 1 ]  Several distinctions can be made based upon the location of a structure relative to the pectinate line:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5949", "text": "Peristalsis  ( / \u02cc p \u025br \u026a \u02c8 s t \u00e6 l s \u026a s /   PERR -ih- STAL -siss ,  US  also  /- \u02c8 s t \u0254\u02d0 l -/   -\u2060 STAWL - ) [ 1 ]  is a  type of  intestinal motility , characterized by  radially symmetrical  contraction and relaxation of  muscles  that propagate in a  wave  down a tube, in an  anterograde  direction. Peristalsis is progression of coordinated contraction of involuntary circular muscles, which is preceded by a simultaneous contraction of the longitudinal muscle and relaxation of the circular muscle in the lining of the gut. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5950", "text": "In much of a  digestive tract , such as the human gastrointestinal tract,  smooth muscle tissue  contracts in sequence to produce a peristaltic wave, which propels a ball of  food  (called a  bolus  before being transformed into  chyme  in the stomach) along the tract. The peristaltic movement comprises relaxation of circular smooth muscles, then their contraction behind the chewed material to keep it from moving backward, then longitudinal contraction to push it forward."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5951", "text": "Earthworms  use a similar mechanism to drive their locomotion, [ 3 ] [ self-published source? ]  and some modern machinery imitate this design. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5952", "text": "The word comes from  Neo-Latin  and is derived from the  Greek   peristellein , \"to wrap around,\" from  peri -, \"around\" +  stellein , \"draw in, bring together; set in order\". [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5953", "text": "Peristalsis is generally directed caudal, that is, towards the  anus . This sense of direction might be attributable to the polarisation of the  myenteric plexus . Because of the reliance of the peristaltic reflex on the myenteric plexus, it is also referred to as the myenteric reflex. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5954", "text": "The food bolus causes a stretch of the gut  smooth muscle  that causes  serotonin  to be secreted to sensory neurons, which then get activated. These sensory neurons, in turn, activate neurons of the  myenteric plexus , which then proceed to split into two  cholinergic  pathways: a retrograde and an anterograde. Activated neurons of the retrograde pathway release  substance molecules alsoP  and  acetylcholine  to contract the smooth muscle behind the bolus. The activated neurons of the anterograde pathway instead release  nitric oxide  and  vasoactive intestinal polypeptide  to relax the smooth muscle caudal to the bolus. This allows the food bolus to effectively be pushed forward along the digestive tract. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5955", "text": "After food is chewed into a bolus, it is  swallowed  and moved through the esophagus. Smooth muscles contract behind the bolus to prevent it from being squeezed back into the mouth. Then rhythmic, unidirectional waves of contractions work to rapidly force the food into the stomach. The  migrating motor complex  (MMC) helps trigger peristaltic waves. This process works in one direction only, and its sole esophageal function is to move food from the mouth into the stomach (the MMC also functions to clear out remaining food in the stomach to the small bowel and remaining particles in the small bowel into the colon). [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5956", "text": "In the esophagus, two types of peristalsis occur:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5957", "text": "During  vomiting , the propulsion of food up the esophagus and out the mouth comes from the contraction of the  abdominal muscles ; peristalsis does not reverse in the esophagus. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5958", "text": "When a peristaltic wave reaches at the end of the  esophagus , the  cardiac sphincter  (gastroesophageal sphincter) opens, allowing the passage of bolus into the stomach. The gastroesophageal sphincter normally remains closed and does not allow the stomach's food contents to move back. The churning movements of the stomach's thick muscular wall blend the food thoroughly with the acidic  gastric juice , producing a mixture called the  chyme . The  muscularis layer  of the stomach is thickest and maximum peristalsis occurs here. After short intervals, the  pyloric sphincter  keeps on opening and closing so the chyme is fed into the intestine in installments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5959", "text": "Once processed and digested by the stomach, the semifluid chyme is passed through the  pyloric sphincter  into the  small intestine . Once past the stomach, a typical peristaltic wave lasts only a few seconds, traveling at only a few centimeters per second. Its primary purpose is to mix the chyme in the intestine rather than to move it forward in the intestine. Through this process of mixing and continued digestion and absorption of nutrients, the chyme gradually works its way through the small intestine to the  large intestine . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5960", "text": "In contrast to peristalsis,  segmentation contractions  result in that churning and mixing without pushing materials further down the digestive tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5961", "text": "Although the  large intestine  has peristalsis of the type that the small intestine uses, it is not the primary propulsion. Instead, general contractions called mass action contractions occur one to three times per day in the large intestine, propelling the chyme (now feces) toward the rectum. Mass movements often tend to be triggered by meals, as the presence of chyme in the stomach and duodenum prompts them ( gastrocolic reflex ). Minimum peristalsis is found in the  rectum  part of the large intestine as a result of the thinnest  muscularis layer ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5962", "text": "The human  lymphatic system  has no central pump. Instead,  lymph   circulates  through peristalsis in the lymph capillaries as well as valves in the capillaries, compression during contraction of adjacent skeletal muscle, and arterial pulsation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5963", "text": "During  ejaculation , the smooth muscle in the walls of the  vasa deferentia  contract reflexively in peristalsis, propelling  sperm  from the  testicles  to the  urethra . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5964", "text": "The  earthworm  is a limbless  annelid  worm with a  hydrostatic skeleton  that moves by peristalsis. Its hydrostatic skeleton consists of a fluid-filled body cavity surrounded by an extensible body wall. The worm moves by radially constricting the anterior portion of its body, increasing length via hydrostatic pressure. This constricted region propagates posteriorly along the worm's body. As a result, each segment is extended forward, then relaxes and re-contacts the substrate, with hair-like  setae  preventing backward slipping. [ 11 ]  Various other invertebrates, such as  caterpillars  and  millipedes , also move by peristalsis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5965", "text": "A  peristaltic pump  is a positive-displacement pump in which a motor pinches advancing portions of a flexible tube to propel a fluid within the tube. The pump isolates the fluid from the machinery, which is important if the fluid is abrasive or must remain sterile."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5966", "text": "Robots have been designed that use peristalsis to achieve locomotion, as the earthworm uses it. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5967", "text": "The  peritrophic matrix  (from the prefix  peri- , meaning around, and  -trophic , referring to nutrition(food)) or  peritrophic membrane  is a semi-permeable, non-cellular structure which surrounds the food  bolus  in an organism's  midgut . Although they are often found in  insects , [ 1 ]  peritrophic matrixes are found in seven different  phyla . [ 2 ]  The peritrophic matrix serves several functions, including improvement of  digestion , protection against mechanical and chemical damage and serving as a barrier to infection by  pathogens . [ 3 ]   Such peritrophic envelopes are also of great ecological importance in marine environments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5968", "text": "The peritrophic matrix is composed of regularly arranged  chitin  microfibrils, (3\u201313% of matrix mass), and species specific  proteins  (20\u201355%) embedded in a  proteoglycan  matrix. [ 4 ] [ 5 ]  The peritrophic matrix also includes very small pores which allow for passage of small  molecules  into and out of the matrix. Thus, due to size limitations (pores reach a maximum size of 10\u00a0nm) larger, unwanted materials taken in while feeding are trapped and  excreted  along with the matrix. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5969", "text": "Type I formation of a peritrophic matrix is thought to be the  ancestral  method, and is found in the majority of  organisms  that produce a peritrophic matrix. In type I formation, the peritrophic matrix is secreted by the entire midgut, and is formed simply by delamination from the surface of the midgut  epithelium . [ 3 ]  Type I formation usually occurs as a response to  feeding , but can also be produced continually. When formed in response to feeding, a single matrix is secreted by the midgut epithelium. This matrix surrounds the food bolus and is later excreted along with unwanted materials present in the food bolus after digestion. When formed continually, as in the insect family  Acrididae  (locusts), multiple peritrophic matrixes are secreted and surround the food bolus, creating a peritrophic envelope. When no food bolus is present, peritrophic matrixes that are secreted are rapidly passed in excrement. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5970", "text": "Type II formation of a peritrophic matrix is considered to be a  derived  technique, and is found only in some families of the  diptera ,  dermaptera ,  embioptera  and  lepidoptera  orders of insects. [ 3 ]  In type II formation, the peritrophic matrix is produced by a specialized group of cells present on the  proventriculus  of the anterior midgut. [ 6 ]  Type II formation is a continuous process which is carried out regardless of the presence or absence of a food bolus. Thus, the peritrophic matrix is secreted as an unbroken, concentric, \u201csleeve like\u201d structure. Although the peritrophic matrix is secreted continually, the presence of a food bolus significantly increases the rate of production. In addition, the presence of a food bolus stimulates the production of multiple matrices which surround the bolus. Following the secretion of a primary peritrophic matrix, subsequent matrices are secreted underneath the first matrix to create a layered peritrophic envelope. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5971", "text": "In many organisms the primary function of the peritrophic matrix is to improve  digestion . Following feeding, the food bolus is surrounded by the peritrophic matrix, effectively isolating it from the  midgut   epithelium . This isolation creates two distinct compartments within the midgut, the endoperitrophic space and ectoperitrophic space. This compartmentalization of the midgut provides three general advantages: prevention of non-specific binding of undigested material to the epithelium wall, conservation and concentration of  enzymes  and  substrates  and rapid removal of indigestible molecules. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5972", "text": "Prevention of non-specific binding is particularly important, as it increases the efficiency of the  absorption  process by filtering out undigested material which would otherwise block access to the midgut  epithelium . Due to the small pore size of the matrix, only small molecules which have been broken down by enzymes or can already be effectively absorbed come in contact with the midgut epithelium. The remaining materials, undigested food and unwanted molecules, are kept within the matrix until they can be broken down by  enzymes  or excreted. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5973", "text": "Concentrating enzymes and food substrate within the endoperitrophic space significantly decreases the time required for digestion in the midgut. In addition, since enzymes are small enough to easily move into and out of the peritrophic matrix, they are rarely lost when the matrix, along with its contents still in the endoperitrophic space, is excreted. A counterflow of fluid in the ectoperitrophic space also helps recycle enzymes, thus maximizing their efficacy. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5974", "text": "The presence of a peritrophic matrix significantly simplifies the excretion process. Rather than having to continually sift through a mixture of digestible and unwanted molecules, digestible molecules are quickly broken down by enzymes, removed from the matrix and absorbed. Once the digestive process is completed, unwanted molecules are kept confined within the endoperitrophic space and excreted along with the matrix. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5975", "text": "Although the peritrophic matrix is a very thin layer of compounds (type I matrixes reach a maximum thickness of 20\u00a0\u03bcm, type II matrixes reach a maximum thickness of 2\u00a0\u03bcm), it can withstand mechanical  pressure  strains up to 500 mmH2O. [ 3 ]  This capacity to expand prevents the food bolus from rupturing the delicate epithelial layer while assisting the passage of food through the gut."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5976", "text": "Much like indigestible molecules present in the food bolus, many  toxins  are too large to pass through the small pores of the peritrophic matrix. For example, some insects that are resistant to the  insecticide   DDT  shed large amounts of the toxin in the peritrophic matrix. In addition, some smaller toxins bind with specific surface proteins present in the peritrophic matrix. This binding is particularly important for blood-feeding insects. Heme groups, which are components of  hemoglobin , an oxygen carrying protein present in vertebrate blood, act as strong  oxidizers  in insects. Although this  oxidizing agent  is safe in vertebrates, it is very damaging to insects. However,  heme  groups ingested in a blood meal bind to proteins on the peritrophic matrix, enabling insects to safely feed on blood. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5977", "text": "Organisms that take in food often infected with pathogens, such as  blood-feeding insects , also depend on the peritrophic matrix to filter out the disease agents, which are often too large to fit through the matrix pores. This benefit in particular is thought to be an important driving force in the evolution of peritrophic matrices, as many insects feeding on foods with low pathogen levels lack the ability to produce a peritrophic matrix. This trend is highlighted by  mosquitoes , as blood-feeding female mosquitoes produce a peritrophic matrix while nectar-feeding males do not. [ 9 ]  A significant trend can also be observed in the type of peritrophic matrix produced by blood-feeding insects that are capable of transmitting disease. The majority of blood-feeding insects that are good disease  vectors  produce a type I matrix. In comparison, blood-feeding insects that produce a type II matrix, which provides a more impenetrable barrier to pathogens, are rarely disease vectors."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5978", "text": "Many pathogens are too large to fit through the small pores of the peritrophic matrix, and thus have evolved specialized mechanisms of evading being filtered out by the matrix. Since type I peritrophic matrixes are secreted in response to the presence of a food bolus in the midgut, some pathogens simply invade the epithelial cells before the matrix is excreted. Many helminth  microfilaria  and  arboviruses  (arthropod borne viruses) are transmitted to the mosquito in their infective form and are able to immediately invade mosquito tissue. [ 9 ]  However, other pathogens such as the malaria protozoan must first develop into an infective stage within the midgut before invading other tissues. These pathogens secrete  chitinase  and  proteinase  enzymes which dissolve the chitin microfibrils and proteins present in the peritrophic matrix. These enzymes open large holes in the membrane, allowing the pathogen to infect the epithelium and other tissues in the insect. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5979", "text": "The  pharynx  ( pl. :  pharynges ) is the part of the  throat  behind the  mouth  and  nasal cavity , and above the  esophagus  and  trachea  (the tubes going down to the  stomach  and the  lungs  respectively). It is found in vertebrates and invertebrates, though its structure varies across species. The pharynx carries food to the esophagus and air to the  larynx . The flap of cartilage called the  epiglottis  stops food from entering the larynx."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5980", "text": "In humans, the pharynx is part of the  digestive system  and the  conducting zone  of the  respiratory system . (The conducting zone\u2014which also includes the  nostrils  of the  nose , the  larynx ,  trachea ,  bronchi , and  bronchioles \u2014filters, warms and moistens air and conducts it into the  lungs ). [ 1 ]  The human pharynx is conventionally divided into three sections: the  nasopharynx ,  oropharynx , and  laryngopharynx ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5981", "text": "In humans, two sets of  pharyngeal muscles  form the pharynx and determine the shape of its  lumen . They are arranged as an inner layer of longitudinal muscles and an outer circular layer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5982", "text": "The upper portion of the pharynx, the nasopharynx, extends from the base of the  skull  to the upper surface of the  soft palate . [ 2 ]  It includes the space between the  internal nares  and the soft palate and lies above the oral cavity. The  adenoids , also known as the pharyngeal tonsils, are  lymphoid tissue  structures located in the posterior wall of the nasopharynx.  Waldeyer's tonsillar ring  is an annular arrangement of lymphoid tissue in both the nasopharynx and oropharynx. The nasopharynx is lined by  respiratory epithelium  that is pseudostratified, columnar, and ciliated."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5983", "text": "Polyps  or  mucus  can obstruct the nasopharynx, as can congestion due to an upper respiratory infection. The  auditory tube , which connects the middle ear to the pharynx, opens into the nasopharynx at the pharyngeal opening of the auditory tube. The opening and closing of the auditory tubes serves to equalize the barometric pressure in the middle ear with that of the ambient atmosphere."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5984", "text": "The anterior aspect of the nasopharynx communicates through the  choanae  with the nasal cavities. On its lateral wall is the  pharyngeal opening of the auditory tube , somewhat triangular in shape and bounded behind by a firm prominence, the  torus tubarius  or cushion, caused by the medial end of the cartilage of the tube that elevates the  mucous membrane .\nTwo folds arise from the cartilaginous opening:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5985", "text": "The oropharynx lies behind the oral cavity, extending from the  uvula  to the level of the  hyoid bone . It opens anteriorly, through the  isthmus faucium , into the mouth, while in its lateral wall, between the  palatoglossal arch  and the  palatopharyngeal arch , is the  palatine tonsil . [ 4 ]  The anterior wall consists of the base of the tongue and the  epiglottic vallecula ; the lateral wall is made up of the tonsil, tonsillar fossa, and tonsillar (faucial) pillars; the superior wall consists of the inferior surface of the soft palate and the uvula. Because both food and air pass through the pharynx, a flap of connective tissue called the  epiglottis  closes over the  glottis  when food is swallowed to prevent  aspiration . The oropharynx is lined by non-keratinized squamous stratified epithelium."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5986", "text": "The  HACEK  organisms ( H aemophilus ,  A ctinobacillus actinomycetemcomitans ,  C ardiobacterium hominis ,  E ikenella corrodens ,  K ingella ) are part of the normal oropharyngeal flora, which grow slowly, prefer a carbon dioxide-enriched atmosphere, and share an enhanced capacity to produce  endocardial  infections, especially in young children. [ 5 ]   Fusobacterium  is a pathogen. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5987", "text": "The laryngopharynx, ( Latin :  pars laryngea pharyngis ), also known as  hypopharynx , is the  caudal  part of the pharynx; it is the part of the throat that connects to the esophagus. It lies inferior to the epiglottis and extends to the location where this common pathway diverges into the respiratory ( laryngeal ) and digestive ( esophageal ) pathways. At that point, the laryngopharynx is continuous with the esophagus posteriorly. The esophagus conducts food and fluids to the stomach; air enters the larynx anteriorly. During swallowing, food has the \"right of way\", and air passage temporarily stops. Corresponding roughly to the area located between the 4th and 6th  cervical vertebrae , the superior boundary of the laryngopharynx is at the level of the  hyoid bone . The laryngopharynx includes three major sites: the  pyriform sinus , postcricoid area, and the posterior pharyngeal wall. Like the oropharynx above it, the laryngopharynx serves as a passageway for food and air and is lined with a  stratified squamous epithelium . It is innervated by the  pharyngeal plexus  and by the  recurrent laryngeal nerve ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5988", "text": "The vascular supply to the laryngopharynx includes the  superior thyroid artery , the  lingual artery  and the  ascending pharyngeal artery . The primary neural supply is from both the  vagus  and  glossopharyngeal  nerves. The vagus nerve provides an  auricular branch  also termed \"Arnold's nerve\" which also supplies the external auditory canal, thus laryngopharyngeal cancer can result in referred  ear pain . This nerve is also responsible for the  ear-cough reflex  in which stimulation of the ear canal results in a person coughing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5989", "text": "The pharynx moves food from the mouth to the esophagus. It also moves air from the  nasal  and  oral  cavities to the  larynx . It is also used in human speech, as  pharyngeal consonants  are articulated here, and it acts as a  resonating chamber  during phonation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5990", "text": "Inflammation of the pharynx, or  pharyngitis , is the painful inflammation of the throat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5991", "text": "Pharyngeal cancer  is a cancer that originates in the neck and/or throat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5992", "text": "Waldeyer's tonsillar ring  is an anatomical term collectively describing the annular arrangement of lymphoid tissue in the pharynx. Waldeyer's ring circumscribes the naso- and oropharynx, with some of its tonsillar tissue located above and some below the soft palate (and to the back of the oral cavity). It is believed that Waldeyer's ring prevents the invasion of microorganisms from going into the air and food passages and this helps in the defense mechanism of the respiratory and alimentary systems. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5993", "text": "The word  pharynx  ( / \u02c8 f \u00e6r \u026a \u014b k s / [ 8 ] [ 9 ] ) is derived from the  Greek  \u03c6\u03ac\u03c1\u03c5\u03b3\u03be  ph\u00e1rynx , meaning \"throat\". Its plural form is  pharynges   / f \u0259 \u02c8 r \u026a n d\u0292 i\u02d0 z /  or  pharynxes   / \u02c8 f \u00e6r \u026a \u014b k s \u0259 z / , and its adjective form is  pharyngeal  ( / \u02cc f \u00e6 r \u026a n \u02c8 d\u0292 i\u02d0 \u0259l /   or   / f \u0259 \u02c8 r \u026a n d\u0292 i \u0259l / )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5994", "text": "All vertebrates have a pharynx, used in both feeding and respiration. The pharynx arises during development in all vertebrates through a series of six or more outpocketings on the lateral sides of the head. These outpocketings are  pharyngeal arches , and they give rise to a number of different structures in the skeletal, muscular, and circulatory systems. The structure of the pharynx varies across the vertebrates. It differs in dogs, horses, and ruminants. In dogs, a single duct connects the nasopharynx to the nasal cavity. The tonsils are a compact mass that points away from the lumen of the pharynx. In the horse, the auditory tube opens into the guttural pouch and the tonsils are diffuse and raised slightly. Horses are unable to breathe through the mouth as the free apex of the rostral epiglottis lies dorsal to the soft palate in a normal horse. In  ruminants , the tonsils are a compact mass that points towards the lumen of the pharynx."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5995", "text": "Pharyngeal arches are characteristic features of vertebrates whose origin can be traced back through  chordates  to basal  deuterostomes  who also share endodermal outpocketings of the pharyngeal apparatus. Similar patterns of gene expression can be detected in the developing pharynx of  amphioxi  and  hemichordates . However, the vertebrate pharynx is unique in that it gives rise to  endoskeletal  support through the contribution of  neural crest  cells. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5996", "text": "Pharyngeal jaws  are a \"second set\" of  jaws  contained within the pharynx of many species of fish, distinct from the primary (oral) jaws. Pharyngeal jaws have been studied in  moray eels  where their specific action is noted. When the moray bites  prey , it first bites normally with its oral jaws, capturing the prey. Immediately thereafter, the pharyngeal jaws are brought forward and bite down on the prey to grip it; they then retract, pulling the prey down the eel's esophagus, allowing it to be swallowed. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5997", "text": "Invertebrates  also have a pharynx. Invertebrates with a pharynx include the  tardigrades , [ 12 ]   annelids  and  arthropods , [ 13 ]  and the  priapulids  (which have an eversible pharynx). [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5998", "text": "The \"pharynx\" of the  nematode  worm is a muscular food pump in the head, triangular in cross-section, that grinds food and transports it directly to the intestines. A one-way valve connects the pharynx to the excretory canal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_5999", "text": "This article incorporates text in the  public domain  from  page 1141  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6000", "text": "General"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6001", "text": "The  nervous system , and  endocrine system  collaborate in the  digestive system  to control gastric secretions, and motility associated with the movement of food throughout the  gastrointestinal tract , including  peristalsis , and  segmentation contractions ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6002", "text": "Gastric activity involved in digestion is divided into three  phases of digestion  known as the  cephalic phase , the gastric phase, and the intestinal phase. These phases overlap and all three can occur simultaneously. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6003", "text": "A fourth phase of acid secretion is known as the basal state which occurs in the times between meals (interdigestive phase). The level of acid secretion during these times is regulated by body weight, individual, number of parietal cells, and time of day. Acid secretion is lowest in the morning before awakening and highest at night. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6004", "text": "The cephalic phase of digestion is the stage in which the stomach responds to the mere sight, smell, taste, or thought of food. About 20% of total acid secretion occurs before food enters the stomach. These sensory and mental inputs converge on the hypothalamus to induce the responses needed for preparing the  gastrointestinal tract  for food processing, which relays signals to the  medulla oblongata . [ 3 ]  Vagus nerve fibers from the medulla stimulate the parasympathetic nervous system of the stomach which, in turn, stimulates gastric secretion (via parietal and G cells). [ 1 ]  This enhanced secretory activity brought on by the thought or sight of food is a conditioned reflex. It only occurs when food is desired. When appetite is depressed this part of the cephalic reflex is inhibited."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6005", "text": "Sensory stimuli from food activate dorsal motor nucleus of  vagus nerve  in the  medulla  (activating the  parasympathetic nervous system ). Insulin induced hypoglycemia also stimulates the vagus nerve. This results in four distinct physiological events."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6006", "text": "1) In the body of the stomach, the vagal postganglionic muscarinic nerves release  acetylcholine  (ACh) which stimulates  parietal cell  H+ secretion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6007", "text": "2) In the lamina propria of the body of the stomach the ACh released from the vagal endings triggers histamine secretion from  ECL cells . Histamine also stimulates H+ secretion from parietal cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6008", "text": "3) In the antrum, peptidergic postganglionic parasympathetic vagal neurons and other enteric nervous system neurons release GRP which stimulates antral  G cells  to produce and release  gastrin . Gastrin stimulates  gastric acid  secretion by directly stimulating parietal cells as well as by promoting histamine secretion by ECL cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6009", "text": "4) In both the antrum and corpus, the vagus nerve inhibits  delta cells  (D cells), thus reducing their release of somatostatin and reducing background inhibition of gastrin release. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6010", "text": "Gastric chief cells  are primarily activated by ACh. However the decrease in pH caused by activation of parietal cells further activates gastric chief cells. Alternatively, acid in the  duodenum  can stimulate  S cells  to secrete  secretin  which acts on an endocrine path to deactivate gastric chief cells."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6011", "text": "50-60% of total gastric acid secretion occurs during this phase. The gastric phase is a period in which swallowed food and semidigested protein (peptides and amino acids) activate gastric activity.   Ingested food stimulates gastric activity in two ways: by stretching the stomach and by gastric contents stimulating receptors in the stomach. [ 2 ]   Stretch activates two reflexes: a short reflex mediated through the myenteric nerve plexus, and a long reflex mediated through the vagus nerves and brainstem. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6012", "text": "1.)  Vagovagal reflex : Distention, or stretching, activates an afferent pathway which in turn stimulates efferent response from the dorsal nucleus of the vagus nerve. Stimulation of acid secretion occurs as it does in the cephalic phase."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6013", "text": "2.) Local ENS Pathway: Activated ENS releases ACh stimulating parietal cells to secrete acid. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6014", "text": "As dietary protein is digested, it breaks down into smaller peptides and amino acids, which directly stimulate the G cells to secrete even more gastrin \u2013 a positive feedback loop that accelerates protein digestion. As discussed earlier gastrin stimulates by activating parietal cells and stimulating ECL to produce histamine (histamine stimulates parietal cells to produce acid). [ 2 ]  Small peptides also buffer stomach acid so the pH does not fall excessively low."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6015", "text": "Gastric secretion is stimulated chiefly by three chemicals:  acetylcholine  (ACh),  histamine , and  gastrin .  ACh is secreted by  parasympathetic  nerve fibers of both the short and long reflex ,.ml; pathways.   Histamine  is a paracrine secretion from the enteroendocrine cells in the gastric glands.   Gastrin  is a hormone produced by enteroendocrine G cells in the pyloric glands. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6016", "text": "All three of these stimulate parietal cells to secrete  hydrochloric acid  and intrinsic factor.  The chief cells secrete  pepsinogen  in response to gastrin and especially Ach, and ACh also stimulates mucus secretion. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6017", "text": "Low intragastric pH stimulates antral D cells to release  somatostatin . Somatostatin inhibits gastrin release from G cells. Reduced gastrin secretion reduces acid secretion. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6018", "text": "5-10% of gastric secretion occurs during this phase. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6019", "text": "The intestinal phase is a stage in which the  duodenum  responds to arriving  chyme  and moderates gastric activity through hormones and nervous reflexes.  The  duodenum  initially enhances gastric secretion, but soon inhibits it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6020", "text": "The presence of partially digested proteins and amino acids in the duodenum stimulates acid secretion in the stomach by four methods:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6021", "text": "1.) Peptones stimulate duodenal  G cells  to secrete gastrin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6022", "text": "2.) Peptones stimulate an unknown endocrine cell to release an additional humoral signal, \"enterooxytonin\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6023", "text": "3.) Amino acids absorbed by the duodenum stimulate acid secretion by unknown mechanisms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6024", "text": "4.) Osmolarity due to products of digestion stimulate acid secretion"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6025", "text": "The acid and semi-digested fats in the  duodenum  trigger the enterogastric reflex \u2013 the  duodenum  sends inhibitory signals to the stomach by way of the enteric nervous system, and sends signals to the medulla that (1) inhibit the vagal nuclei, thus reducing vagal stimulation of the stomach, and (2) stimulate sympathetic neurons, which send inhibitory signals to the stomach.  Chyme also stimulates duodenal enteroendocrine cells to release secretin and cholecystokinin.  They primarily stimulate the pancreas and gall bladder, but also suppress gastric secretion and motility.  The effect of this is that gastrin secretion declines and the pyloric sphincter contracts tightly to limit the admission of more chyme into the duodenum.  This gives the duodenum time to work on the chyme it has already received before being loaded with more. [ 1 ]  \nThe enteroendocrine cells also secrete glucose dependent insulinotropic peptide.  Originally called gastric-inhibitory peptide, it is no longer thought to have a significant effect on the stomach, but to be more concerned with stimulating insulin secretion in preparation for processing the nutrients about to be absorbed by the small intestine. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6026", "text": "There is small continuous basal secretion of gastric acid between meals of usually less than 10 mEq/hour. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6027", "text": "The  basal electrical rhythm  controls the smooth muscle of the stomach and intestines, and controls the actions of  peristalsis , and  segmentation contractions ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6028", "text": "The  polythyridium  is a component of the gut that surrounds the entrance of the intestine in  priapulids  of genus  Tubiluchus . It comprises tuberculate and hairy plates associated with a strong muscle. These plates may help to keep unwanted particles out of the gut. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6029", "text": "This  animal anatomy \u2013related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6030", "text": "This  protostome -related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6031", "text": "Potential renal acid load  (PRAL) is a measure of the acid that the body produces after ingesting a food. This is different from pH, which is the acidity of a food before being consumed. [ 1 ] [ 2 ]  PRAL is a different acidity measure than the food ash measurement. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6032", "text": "Some acidic foods actually have a negative PRAL measurement, meaning they reduce acidity in the stomach. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6033", "text": "A low PRAL diet (not to be confused with an  alkaline diet ) can lower acidity in the stomach, which can be helpful for people suffering  GERD  or Acid Reflux. However, it does not lower the pH of blood and therefore cannot treat osteoporosis or other conditions. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6034", "text": "This  medical  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6035", "text": "Prebiotics  are compounds in food that foster growth or activity of beneficial  microorganisms  such as bacteria and fungi. [ 1 ]  The most common environment concerning their effects on human health is the gastrointestinal tract, where prebiotics can alter the composition of organisms in the  gut   microbiome ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6036", "text": "Dietary prebiotics are typically nondigestible  fiber  compounds that pass undigested through the upper part of the  gastrointestinal tract  and help growth or activity of advantageous bacteria in the  colon  by acting as  substrates  for them. [ 1 ]  They were first identified and named by Marcel Roberfroid in 1995. [ 1 ] [ 2 ]  Depending on the jurisdiction, they may have regulatory scrutiny as  food additives  for the  health claims  made for marketing purposes. Common prebiotics used in food manufacturing include  beta-glucan  from  oats ,  resistant starch  from grains and beans, and  inulin  from  chicory root ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6037", "text": "The definition of prebiotics and the food ingredients that can fall under this classification, has evolved since its first definition in 1995. [ 3 ]  In its earliest definition, the term prebiotics was used to refer to non-digestible food ingredients that were beneficial to the host through their selective stimulation of specific bacteria within the  colon . [ 3 ] [ 4 ]  Further research has suggested that selective stimulation has not been scientifically demonstrated. [ 5 ]  As a result of research suggesting that prebiotics could impact microorganisms outside of the colon, in 2016 the  International Scientific Association for Probiotics and Prebiotics  (ISAPP) produced the following definition of prebiotics: a  substrate  that is selectively used by a host microorganism to produce a health benefit. [ 3 ]  In 2021, The Global Prebiotic Association (GPA) defined a prebiotic as a product or ingredient that is utilized in the microbiota producing a health or performance benefit. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6038", "text": "Compounds that can be classified as prebiotics must also meet the following criteria: [ 3 ] [ 4 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6039", "text": "Thus, consumption of prebiotics may facilitate the health of the host. [ 7 ]  Based on the previous classifications, plant-derived carbohydrate compounds called  oligosaccharides  as well as resistant starch are the main source of prebiotics that have been identified. [ 8 ] [ 4 ] [ 9 ] [ 10 ]  Specifically,  fructans  and  galactans  are two oligosaccharide sources which have been found to stimulate the activity and growth of beneficial bacterial colonies in the gut. [ 7 ] [ 3 ]  Fructans are a category of carbohydrate consisting of  fructooligosaccharides  (FOS) and  inulins , while galactans consist of  galactooligosaccharides . [ 3 ]  Resistant starch has been shown to shift the intestinal bacteria, as well as improve biomarkers for numerous health conditions. [ 11 ] [ 12 ] [ 13 ]   Other dietary fibers also fit the definition of prebiotics, such as  pectin , [ 14 ]   beta-glucans , [ 15 ]  and  xylooligosaccharides . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6040", "text": "The  European Food Safety Authority  (EFSA), the regulatory agency for product labeling, differentiates between \"prebiotic\" and \"dietary fiber\", stating that \"a  cause and effect relationship  has not been established between the consumption of the food constituents which are the subject of the health claims and a beneficial physiological effect related to increasing numbers of gastrointestinal microbiota\". [ 17 ]  Consequently, under EFSA rules individual ingredients cannot be labeled as prebiotics, but only as dietary fiber and with no implication of health benefits. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6041", "text": "When the prebiotic concept was first introduced in 1995, the primary focus was on the effects that prebiotics confer on  Bifidobacteria  and  Lactobacillus . [ 3 ] [ 4 ] [ 18 ]  With improved mechanistic techniques in recent years, the current prebiotic targets have expanded to a wider range of microbes, including  Roseburia  spp.,  Eubacterium  spp.,  Akkermansia  spp.,  Christensenella  spp.,  Propionibacterium  spp. and  Faecalibacterium  spp. [ 19 ]  These bacteria have been highlighted as key  probiotics  and beneficial gut bacteria as they may have several beneficial effects on the host in terms of improving digestion (including but not limited to enhancing mineral absorption) [ 20 ]  and the effectiveness and intrinsic strength of the immune system. [ 21 ]  Both  Bifidobacteria  and  Lactobacillus  have been shown to have differing prebiotic specificity and to selectively ferment prebiotic fiber based on the enzymes characteristic of the bacterial population. [ 22 ]  Thus,  Lactobacilli  prefer inulin and fructooligosaccharides, while  Bifidobacteria  display specificity for inulin, fructooligosaccharides, xylooligosaccharides and galactooligosaccharides. [ 22 ]   Studies have also shown that prebiotics, besides helping growth of beneficial gut bacteria, can also inhibit detrimental and potentially pathogenic microbes in the gut, [ 9 ] [ 4 ]  such as  clostridia . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6042", "text": "Fermentation  is the main  mechanism of action  by which prebiotics are used by beneficial bacteria in the colon. [ 7 ] [ 4 ]  Both  Bifidobacteria  and  Lactobacillus  are bacterial populations which use  saccharolytic  metabolism to break down substrates. [ 4 ]  The bifidobacterial  genome  contains many  genes  that encode for carbohydrate-modifying enzymes as well as genes that encode for carbohydrate uptake proteins. The presence of these genes indicates that  Bifidobacteria  contain specific metabolic pathways specialized for the fermentation and metabolism of plant-derived oligosaccharides, or prebiotics. These pathways in  Bifidobacteria  ultimately produce  short chain fatty acids , [ 4 ] [ 7 ]  which have diverse  physiological  roles in body functions. [ 23 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6043", "text": "Prebiotic sources must be proven to confer a benefit to the host in order to be classified as a prebiotic. [ 3 ]  Fermentable  carbohydrates  derived from  fructans  and  xylans  are one well documented example of prebiotics. [ 3 ]  Resistant starch from starchy foods are also well documented prebiotics and have historically been the highest source of prebiotics in the diet, as 4-10% of starch in mixed diets has been shown to reach the large intestine. [ 24 ]  One study reported that individuals consuming a traditional diet in Africa consumed 38 grams of resistant starch/day. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6044", "text": "An endogenous source of prebiotics in humans is human  breast milk , which contains  oligosaccharides  structurally similar to  galactooligosaccharides , referred to as human milk oligosaccharides. [ 26 ] [ 9 ] [ 22 ] [ 3 ]  Human milk oligosaccharides were found to increase the  Bifidobacteria  bacterial population in breastfed infants, and to strengthen the infant immune system. [ 3 ] [ 9 ]  Furthermore, human milk oligosaccharides help establish a healthy intestinal microbiota composition in newborns. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6045", "text": "Indigestible carbohydrate compounds classified as prebiotics are a type of  fermentable  fiber, and thus can be classified as  dietary fiber . [ 4 ]  However, not all dietary fiber can be classified as a prebiotic source. [ 4 ]  In addition to the food sources highlighted in the following table, raw oats, [ 18 ]   unrefined barley , [ 18 ]   yac\u00f3n , [ 18 ]  and whole grain  breakfast cereals [ 4 ]  are also classified as prebiotic fiber sources. The predominant type of prebiotic fiber may vary according to the food. For instance, oats and barley have high amounts of  beta-glucans , fruit and berries contain  pectins , seeds contain  gums , onions and  Jerusalem artichokes  are rich in  inulin  and  oligofructose , and bananas and legumes contain  resistant starch . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6046", "text": "While there is no broad consensus on an ideal daily serving of prebiotics, recommendations typically range from 4\u00a0to 8 grams (0.14\u20130.28\u00a0oz) for general digestive health support, to 15 grams (0.53\u00a0oz) or more for those with active digestive disorders. Given an average 6 grams (0.21\u00a0oz) serving, below are the amounts of prebiotic foods required to achieve a daily serving of prebiotic fiber:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6047", "text": "Preliminary research has demonstrated potential effects on calcium and other mineral absorption, [ 29 ]   immune system  effectiveness, [ 30 ] [ 31 ]   bowel  acidity, reduction of  colorectal cancer  risk, [ 32 ]   inflammatory bowel disease  ( Crohn's disease  or  ulcerative colitis ), [ 33 ]   hypertension [ 34 ]  and  defecation  frequency. [ 35 ]  Prebiotics may be effective in decreasing the number of infectious episodes needing antibiotics and the total number of infections in children aged 0\u201324 months. [ 31 ] [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6048", "text": "No good evidence shows that prebiotics are effective in preventing or treating allergies. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6049", "text": "While research demonstrates that prebiotics lead to increased production of  short-chain fatty acids  (SCFA), [ 38 ]  more research is required to establish a direct causal connection. Prebiotics may be beneficial to  inflammatory bowel disease  or Crohn's disease through production of SCFA as nourishment for colonic walls, and mitigation of ulcerative colitis symptoms. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6050", "text": "The sudden addition of substantial quantities of prebiotics to the diet may result in an increase in  fermentation , leading to increased gas production,  bloating  or  bowel movement . [ 40 ]  Production of SCFA and fermentation quality are reduced during long-term diets of low fiber intake. [ 41 ]  Until bacterial flora are gradually established to rehabilitate or restore intestinal bacteria, nutrient absorption may be impaired and colonic transit time temporarily increased with a rapid addition of higher prebiotic intake. [ 40 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6051", "text": "Genetically modified plants  have been created in research labs with upregulated inulin production. [ 43 ] [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6052", "text": "Probiotics  are live  microorganisms  promoted with claims that they provide health benefits when consumed, generally by improving or restoring the  gut microbiota . [ 1 ] [ 2 ]  Probiotics are considered  generally safe to consume , but may cause  bacteria - host  interactions and unwanted  side effects  in rare cases. [ 3 ] [ 4 ] [ 5 ]  There is some evidence that probiotics are beneficial for some conditions, such as helping to ease some symptoms of irritable bowel syndrome (IBS). However, many claimed health benefits, such as treating eczema, lack substantial scientific support. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6053", "text": "The first discovered probiotic was a certain strain of  bacillus  in Bulgarian yoghurt, called  Lactobacillus bulgaricus . The discovery was made in 1905 by Bulgarian physician and microbiologist  Stamen Grigorov . The modern-day theory is generally attributed to Russian  Nobel Prize  laureate  \u00c9lie Metchnikoff , who postulated around 1907 that  yoghurt -consuming Bulgarian peasants lived longer. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6054", "text": "A growing probiotics market has led to the need for stricter requirements for  scientific substantiation  of putative benefits conferred by microorganisms claimed to be probiotic. [ 7 ]  Although some evidence claimed benefits are marketed towards using probiotic, such as reducing  gastrointestinal  discomfort, improving  immune health , [ 8 ]  relieving  constipation , or avoiding the  common cold , such claims are strain-specific and cannot be extrapolated to other strains. [ 7 ] [ 9 ] [ 10 ]  As of 2019, numerous applications for approval of  health claims  by European manufacturers of probiotic  dietary supplements  have been rejected by the  European Food Safety Authority  for insufficient evidence of beneficial mechanism or efficacy. [ 8 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6055", "text": "An October 2001 report by the  World Health Organization  (WHO) defines probiotics as \"live microorganisms which when administered in adequate amounts confer a health benefit on the host.\" [ 12 ] [ 13 ]  Following this definition, a  working group  convened by the  Food and Agriculture Organization  (FAO)/WHO in May 2002 issued the  Guidelines for the Evaluation of Probiotics in Food . [ 14 ]  A consensus definition of the term  probiotics , based on available information and scientific evidence, was adopted after the aforementioned joint expert consultation between the  FAO  of the  United Nations  and the WHO. This effort was accompanied by local governmental and supra-governmental regulatory bodies' requirements to better characterize health claims substantiations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6056", "text": "That first global effort was further developed in 2010; two expert groups of academic scientists and industry representatives made recommendations for the evaluation and validation of probiotic health claims. [ 15 ] [ 16 ]  The same principles emerged from those two groups as were expressed in the \"Guidelines\" of FAO/WHO in 2002. This definition, though widely adopted, is not acceptable to the  European Food Safety  Authority because it embeds a health claim that is not measurable. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6057", "text": "A group of scientific experts assembled in Canada in October 2013 to discuss the scope and appropriate use of the term \"probiotic\", adjusting the definition to be \"live microorganisms that, when administered in adequate amounts, confer a health benefit on the host.\" [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6058", "text": "Live probiotic  cultures  are part of  fermented dairy products , other  fermented  foods, and probiotic-fortified foods. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6059", "text": "Lactic acid bacteria  (LAB), which are food fermenting bacteria, have the ability to prevent food spoilage and can improve the nutritive value of the foods they inhabit. Acid fermentation (as well as salting), remains one of the most practical methods of preservation of fresh vegetables, cereal gruels, and milk-cereal mixtures due to its low cost and energy requirements. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6060", "text": "Fermented products  that contain lactic acid bacteria include vegetables such as  pickled vegetables , [ 20 ]   kimchi , [ 20 ] [ 21 ]   pao cai , [ 22 ]  and  sauerkraut ; [ 23 ]   sourdough bread  or bread-like products made without  wheat  or  rye flour , amino acid/peptide meat-flavored sauces and pastes produced by fermentation of cereals and legumes; fermented cereal-fish-shrimp mixtures and fermented meats; [ 19 ]  soy products such as  tempeh , [ 24 ]   miso , [ 25 ]  and  soy sauce ; [ 26 ]  dairy products such as  yogurt ,  kefir , [ 27 ]   buttermilk ; [ 28 ]  and non-dairy products such as  bee pollen . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6061", "text": "More precisely, sauerkraut contains the bacteria  Leuconostoc mesenteroides ,  Lactobacillus plantarum , Pediococcus pentosaceus,  Lactobacillus brevis , Leuconostoc citreum, Leuconostoc argentinum,  Lactobacillus paraplantarum , Lactobacillus coryniformis , and  Weissella  spp. [ 30 ]  Kimchi contains the bacteria  Leuconostoc  spp.,  Weissella  spp., and  Lactobacillus  spp. Pao cai contains  L. pentosus,\u2009L. plantarum\u2009, Leuconostoc mesenteroides\u2009, L. brevis, L. lactis , and  L. fermentum .\nA list of many other bacteria found in several Asian fermented fruits and vegetables also is available. [ 31 ] [ 32 ]  Kefir contains  Lactobacillus acidophilus ,  Bifidobacterium bifidum ,  Streptococcus thermophilus ,  Lactobacillus delbrueckii  subsp.  bulgaricus, Lactobacillus helveticus,  Lactobacillus kefiranofaciens , Lactococcus lactis , and  Leuconostoc  species. [ 33 ] [ 34 ]  Buttermilk contains either  Lactococcus lactis  or  L. bulgaricus . Other acidic bacteria, said to be probiotic, [ 35 ] [ 36 ]  can be found in  kombucha , including  Gluconacetobacter xylinus , [ 37 ] [ 38 ]   Zygosaccharomyces  sp.,  Acetobacter pasteurianus,  Acetobacter aceti , and  Gluconobacter oxydans . [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6062", "text": "It is incorrect to think that a higher colony forming units (CFU) count corresponds to greater efficacy - rather, probiotic efficacy is strain- and disease specific. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6063", "text": "The manipulation of the gut microbiota is complex and may cause bacteria-host interactions. [ 5 ]  Though probiotics are considered safe, some have concerns about their safety in certain cases. [ 5 ] [ 41 ]  Some people, such as those with  immunodeficiency ,  short bowel syndrome ,  central venous catheters , and  cardiac valve disease , and premature infants, may be at higher risk for adverse events. [ 3 ]  In severely ill people with  inflammatory bowel disease , a risk exists for the passage of viable bacteria from the gastrointestinal tract to the internal organs (bacterial translocation) as a consequence of  bacteremia , which can cause adverse health consequences. [ 5 ]  Rarely, consumption of probiotics by children with lowered immune system function or who are already critically ill may result in bacteremia or  fungemia  (i.e., bacteria or fungi in the blood), which can lead to  sepsis , a potentially fatal disease. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6064", "text": "Probiotic supplements typically contain between one and ten billion  colony-forming units  (CFUs) per dose. [ 42 ]  A higher number of CFUs does not provide additional probiotic effects, but may have unintended consequences of causing digestive discomfort, such as bloating, gas, and diarrhea. [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6065", "text": "Lactobacillus  species have been suggested to contribute to obesity in humans, but no evidence of this relationship has been found. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6066", "text": "In 2015, the global retail market value for probiotics was US$41 billion, including sales of probiotic  supplements , fermented milk products, and yogurt, which alone accounted for 75% of total consumption. [ 45 ]  Innovation in probiotic products in 2015 was mainly from supplements, which produced US$4 billion and was projected to grow 37% globally by 2020. [ 45 ]  Consumption of yogurt products in China has increased by 20% per year since 2014. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6067", "text": "As of 2019 [update] , the  European Food Safety Authority  has rejected all petitions by commercial manufacturers for health claims on probiotic products in Europe due to insufficient evidence for a  cause-and-effect mechanism  for benefit,  thus inconclusive proof of effectiveness. [ 7 ] [ 8 ] [ 11 ]  The  European Commission  placed a ban on putting the word \"probiotic\" on the packaging of products because such labeling misleads consumers to believe a health benefit is provided by the product when no scientific proof exists to demonstrate that health effect. [ 7 ] [ 47 ] [ 48 ] [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6068", "text": "In the United States, the  Food and Drug Administration  (FDA) and  Federal Trade Commission  (FTC) have issued warning letters and imposed punishment on various manufacturers of probiotic products whose labels claim to treat a disease or condition. [ 10 ] [ 50 ] [ 51 ]   Food product labeling  requires language approved by the FDA, so probiotic manufacturers have received warning letters for making disease or treatment claims. [ 10 ] [ 51 ]  The FTC has taken punitive actions, including a US$21 million fine coordinated by 39 different state governments against a major probiotic manufacturer for deceptive advertising and exaggerated claims of health benefits for yogurt and probiotic dairy drink. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6069", "text": "In  Vietnam , the Vietnam Food Administration (VFA) under the  Ministry of Health , in collaboration with other relevant authorities, oversees and addresses violations related to probiotic products. This includes issuing warnings, imposing administrative penalties, [ 52 ]  demanding product recalls [ 53 ] [ 54 ]  and coordinating with other agencies. [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6070", "text": "The  National Yogurt Association  (NYA) of the United States gives a \"Live & Active Cultures Seal\" to refrigerated yogurt products that contain 100 million cells per gram, or frozen yogurt products that contain 10 million cells per gram at the time of manufacture. [ 57 ]  In 2002, the FDA and WHO recommended that \"the minimum viable numbers of each probiotic strain at the end of the shelf-life\" be reported on labeling, [ 58 ]  but most companies that give a number report the viable cell count at the date of manufacture, a number that could be much higher than that which exists at consumption. [ 59 ]  Because of the variability in storage conditions and time before eating, exactly how many active culture cells remain at the time of consumption is difficult to determine. The survival of probiotics was strongly dependent on the storage temperature and remarkable viability loss occurred in room temperature compared to refrigerated storage. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6071", "text": "Probiotics have received renewed attention in the 21st century from product manufacturers, research studies, and consumers. Their history can be traced to the first use of cheese and fermented products, which were well-known to the  Greeks  and  Romans  who recommended their consumption. [ 61 ]  The  fermentation  of dairy foods represents one of the oldest techniques for  food preservation . [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6072", "text": "The original modern hypothesis of the positive role played by certain bacteria was first introduced by  Russian  scientist and  Nobel laureate   \u00c9lie Metchnikoff , who in 1907 suggested that it would be possible to modify the  gut microbiota  and to replace harmful microbes with useful microbes. [ 63 ]  Metchnikoff, at that time a professor at the  Pasteur Institute  in  Paris , proposed the hypothesis that the  aging  process results from the activity of  putrefactive  ( proteolytic ) microbes producing toxic substances in the  large bowel . Proteolytic bacteria such as  clostridia , which are part of the normal gut microbiota, produce toxic substances including  phenols ,  indols , and  ammonia  from the  digestion  of  proteins . According to  Metchnikoff , these compounds were responsible for what he called \"intestinal  autointoxication \", which would cause the physical changes associated with old age. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6073", "text": "At that time,  milk fermented  with  lactobacillales  were known to inhibit the growth of proteolytic bacteria because of the low  pH  produced by the fermentation of  lactose . Metchnikoff had also observed that certain rural populations in Europe, for example in Bulgaria and the Russian steppes, who lived largely on milk fermented by lactic-acid bacteria, were exceptionally long-lived. Based on these observations, Metchnikoff proposed that consumption of fermented milk would \"seed\" the  intestine  with harmless lactic-acid bacteria and decrease the intestinal pH, and that this would suppress the growth of proteolytic bacteria. Metchnikoff himself introduced in his diet  sour milk  fermented with the bacteria he called \"Bulgarian Bacillus\" and believed his health benefited. Friends in Paris soon followed his example and physicians began prescribing the sour-milk diet for their patients. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6074", "text": "Bifidobacteria  was first isolated from a breastfed infant by Henry Tissier, who also worked at the  Pasteur Institute . The isolated bacterium named  Bacillus bifidus communis [ 66 ]  was later renamed to the genus  Bifidobacterium . [ 67 ]  Tissier found that bifidobacteria are dominant in the gut microbiota of  breast-fed  babies and he observed clinical benefits from treating infant diarrhea with bifidobacteria."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6075", "text": "During an outbreak of  shigellosis  in 1917, German professor Alfred Nissle isolated a strain of  Escherichia coli  from the feces of a soldier who was not affected by the disease. [ 68 ]  Methods of treating infectious diseases were needed at that time when antibiotics were not yet available, and Nissle used the  E. coli  Nissle 1917 strain  in acute gastrointestinal infectious  salmonellosis  and  shigellosis . [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6076", "text": "In 1920, Rettger and Cheplin reported that Metchnikoff's \"Bulgarian Bacillus\", later called  Lactobacillus delbrueckii  subsp.  bulgaricus , could not live in the human intestine. [ 70 ] [ non-primary source needed ]  They conducted experiments involving rats and humans volunteers, feeding them with  Lactobacillus acidophilus . They observed the disappearance of the pathogenic protist  Balantidium coli  as well as of other gas-producing bacteria. [ 70 ]  Rettger further explored the possibilities of  L. acidophilus , and reasoned that bacteria originating from the gut were more likely to produce the desired effect in this environment. In 1935, certain strains of  L. acidophilus  were found very active when implanted in the human digestive tract. [ 71 ] [ non-primary source needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6077", "text": "Contrasting antibiotics, probiotics were defined as microbially derived factors that stimulate the growth of other microorganisms. In 1989, Roy Fuller suggested a definition of probiotics that have been widely used: \"A live microbial feed supplement which beneficially affects the host animal by improving its intestinal microbial balance.\" [ 72 ]  Fuller's definition emphasizes the requirement of viability for probiotics and introduces the aspect of a beneficial effect on the host."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6078", "text": "The term \"probiotic\" originally referred to microorganisms that have effects on other microorganisms. [ 73 ]  The concept of probiotics involved the notion that substances secreted by one microorganism stimulated the growth of another microorganism. The term was used again [ 74 ]  to describe tissue extracts that stimulated microbial growth. The term probiotics was taken up by Parker, [ 75 ]  who defined the concept as, \"Organisms and substances that have a beneficial effect on the host animal by contributing to its intestinal microbial balance.\" Later, the definition was greatly improved by Fuller, [ 72 ]  whose explanation was very close to the definition used today. Fuller described probiotics as a \"live microbial feed supplement which beneficially affects the host animal by improving its intestinal microbial balance.\" He stressed two important claims for probiotics: the viable nature of probiotics and the capacity to help with intestinal balance."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6079", "text": "In the following decades, intestinal lactic-acid bacterial species with alleged health-beneficial properties were introduced as probiotics, including  Lactobacillus rhamnosus ,  Lactobacillus casei , and  Lactobacillus johnsonii . [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6080", "text": "Some literature gives the word a full Greek  etymology , [ 77 ] [ 78 ]  but it appears to be a composite of the Latin preposition  pro , meaning 'for', and the Greek adjective \u03b2\u03b9\u03c9\u03c4\u03b9\u03ba\u03cc\u03c2 ( bi\u014dtikos ), meaning 'fit for life, lively', [ 79 ]  the latter deriving from the noun \u03b2\u03af\u03bf\u03c2 ( bios ), meaning 'life'. [ 80 ]  The term contrasts etymologically with the term  antibiotic , although it is not a complete  antonym . The related term  prebiotic  comes from the Latin  prae , meaning 'before', and refers to a substance that is not digested, but rather may be  fermented  to promote the growth of beneficial intestinal microorganisms. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6081", "text": "As food products or dietary supplements, probiotics are under preliminary research to evaluate if they provide any effect on health. [ 2 ] [ 7 ] [ 82 ]  In all cases proposed as health claims to the  European Food Safety Authority , the scientific evidence remains insufficient to prove a cause-and-effect relationship between consumption of probiotic products and any health benefit. [ 7 ] [ 83 ]  There is no scientific basis for extrapolating an effect from a tested strain to an untested strain. [ 2 ] [ 84 ] [ 85 ]  Improved health through gut flora modulation appears to be directly related to long-term dietary changes. [ 7 ] [ 86 ]  Claims that some lactobacilli may contribute to  weight gain  in some humans [ 87 ] [ 88 ]  remain controversial. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6082", "text": "There is inconsistency in the results of different groups of 3488 children as reported in a Cochrane review. [ 90 ]  Also, it shows no significant difference regarding the adverse effects between probiotic and the other comparators. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6083", "text": "Only limited, low-quality evidence exists to indicate that probiotics are helpful for treating people with  milk allergy . [ 91 ]  A 2015 review showed low-quality evidence that probiotics given directly to infants with  eczema , or in infants whose mothers used probiotics during the  last trimester of pregnancy  and breastfeeding, had lower risk of eczema. [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6084", "text": "It is unclear whether probiotic supplementation helps with childhood  asthma , as the quality of research evidence is low. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6085", "text": "Antibiotics are a common treatment for children, with 11% to 40% of antibiotic-treated children developing  diarrhea . [ 94 ]   Antibiotic-associated diarrhea  (AAD) results from an imbalance in the colonic microbiota caused by antibiotic therapy. [ 94 ]  These microbial community alterations result in changes in  carbohydrate metabolism , with decreased  short-chain fatty acid  absorption and osmotic diarrhea as a result. A 2015  Cochrane review  concluded that a protective effect of some probiotics existed for AAD in children. [ 94 ]  The known risks of using probiotics for treating  Clostridioides difficile  outweighs the uncertain benefits. [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6086", "text": "Probiotic treatment might reduce the incidence and severity of AAD as indicated in several  meta-analyses . [ 96 ] [ 97 ] [ 98 ]  For example, treatment with probiotic formulations including   L. rhamnosus  may reduce the risk of AAD, improve stool consistency during antibiotic therapy, and enhance the immune response after vaccination. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6087", "text": "The potential efficacy of probiotics to treat AAD depends on the probiotic strains and dosage. [ 100 ] [ 101 ]  One review recommended for children  L. rhamnosus  or  Saccharomyces boulardii  at 5 to 40 billion colony-forming units/day, given the modest number needed to treat and the likelihood that adverse events are very rare. [ 94 ]  The same review stated that probiotic use should be avoided in pediatric populations at risk for  adverse events , such as severely debilitated or  immune-compromised  children. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6088", "text": "Probiotic treatment of bacterial vaginosis is the application or ingestion of  bacterial species found in the healthy vagina  to cure the infection of bacteria causing  bacterial vaginosis . This treatment is based on the observation that 70% of healthy females have a group of bacteria in the genus  Lactobacillus  that dominate the population of organisms in the vagina. Specific strains of lactobacilli inhibit the growth of bacteria causing BV by producing H 2 O 2 , lactic acid, and/or bacteriocins, and/or inhibit the adherence of  Gardnerella vaginalis  to the vaginal epithelium, which prevents the infection from occurring in the vagina. [ 102 ]  Currently, the success of probiotic treatment has been mixed, since the use of probiotics to restore healthy populations of  Lactobacillus  has not been standardized.  Often, standard antibiotic treatment is used at the same time that probiotics are being tested. In addition, some groups of women respond to treatment based upon ethnicity, age, number of sexual partners, pregnancy, and the pathogens causing bacterial vaginosis. [ 103 ]  In 2013, researchers found that administration of  hydrogen peroxide -producing strains, such as  L. acidophilus  and  L. rhamnosus , were able to normalize vaginal pH and rebalance the  vaginal microbiota , preventing and alleviating bacterial vaginosis. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6089", "text": "As of 2017 [update] , only limited evidence indicated any direct link between  high blood pressure  and gut microbiota. [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6090", "text": "A 2002 meta-analysis that included five double-blind trials examining the short-term (2\u20138 weeks) effects of a yogurt with probiotic strains on serum cholesterol levels found little effect of 8.5\u00a0mg/dL (0.22\u00a0mmol/L) (4% decrease) in  total cholesterol  concentration, and a decrease of 7.7\u00a0mg/dL (0.2\u00a0mmol/L) (5% decrease) in serum  LDL  concentration. [ 106 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6091", "text": "A 2019 meta-analysis found low-quality evidence for probiotics having a small improvement in  depression  and  anxiety . [ 107 ]  A 2020 review found probiotics might improve depression, but more studies are needed. [ 108 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6092", "text": "Some probiotics are suggested as a possible treatment for various forms of  gastroenteritis . [ 109 ]  As a treatment for infectious diarrhea, probiotics are of no benefit to people who have the condition for more than two days, and there is no evidence they lessen the duration of diarrhea overall. [ 110 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6093", "text": "Probiotics are commonly given to breastfeeding mothers and their young children to prevent eczema ( dermatitis ), but no good evidence shows efficacy for this purpose. [ 111 ]  There is little evidence to support the use of probiotics to treat  atopic dermatitis , and some risk of  adverse effects . [ 112 ]  The  American Academy of Dermatology  stated: \"The use of probiotics/prebiotics for the treatment of patients with established atopic dermatitis is not recommended due to inconsistent evidence\". [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6094", "text": "According to an umbrella review of meta-analyses of randomized controlled trials, probiotics supplementation reduces glucose homeostasis. This can be an effective therapy for lowering high blood sugar levels unless the body becomes  hypoglycemic ; caution and glucose monitoring are necessary to avoid this.  [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6095", "text": "Some strains of lactic acid bacteria (LAB) may affect  Helicobacter pylori  infections (which may cause  peptic ulcers ) in adults when used in combination with standard medical treatments, but no standard in medical practice or regulatory approval exists for such treatment. [ 115 ]  The only peer-reviewed treatments for  H. pylori  to date all include various Antibiotic Regimens. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6096", "text": "Some strains of LAB may affect  pathogens  by means of  competitive inhibition  (i.e., by competing for growth) and some evidence suggests they may improve immune function by increasing the number of  IgA -producing plasma cells and increasing or improving  phagocytosis , as well as increasing the proportion of  T lymphocytes  and natural killer cells. [ 117 ] [ 118 ]  LAB products might aid in the treatment of acute diarrhea and possibly affect  rotavirus  infections in children and travelers' diarrhea in adults, [ 117 ] [ 118 ]  but no products are approved for such indications. There are weak evidence probiotics might lower the incidence of acute upper respiratory tract infections in adults, they were better than placebo or no treatment. [ 119 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6097", "text": "Probiotics do not appear to change the risk of infection in older people. [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6098", "text": "The use of oral probiotic supplements to modify the composition and behavior of the microbiome has been considered as a possible therapy for both induction and maintenance of remission in people with Crohn's disease and ulcerative colitis. A Cochrane review in 2020 did not find clear evidence of improved remission likelihood, nor lower adverse events, in people with Crohn's disease, following probiotic treatment.  [ 121 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6099", "text": "For ulcerative colitis, there is low-certainty evidence that probiotic supplements may increase the probability of clinical remission.  [ 122 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects.  [ 122 ] Although there was no clear evidence of greater remission when probiotic supplements were compared with  5\u2010aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy.  [ 122 ]  Whereas in people who are already in remission, it is unclear whether probiotics help to prevent future relapse, either as a monotherapy or  combination therapy .  [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6100", "text": "Probiotics are under study for their potential to affect  irritable bowel syndrome , although uncertainty remains around which type of probiotic works best, and around the size of possible effect. [ 124 ] [ 125 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6101", "text": "Several clinical studies provide evidence for the potential of probiotics to lower the risk of  necrotizing enterocolitis  and mortality in premature infants. One meta-analysis indicated that probiotics reduce these risks by more than 50% compared with controls but that further, large, high-quality trials were needed to inform policy and practice. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6102", "text": "A Cochrane systematic review found no good evidence that probiotics were of benefit in reducing the risk of  gestational diabetes , but good evidence that they increased the risk of  pre-eclampsia . For this reason, the use of probiotics in pregnancy was advised against. [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6103", "text": "A 2017 review based on moderate to low-quality evidence suggests that probiotics may be helpful in relieving pain in the short term in children with recurrent abdominal pain, but the proper strain and dosage are not known. [ 128 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6104", "text": "A clinical study investigating the impact of probiotics in relieving the signs and symptoms of  dry eye  revealed promising results for the ophthalmic formulation of  Latilactobacillus sakei , while the oral probiotic demonstrated no discernible benefits. [ 129 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6105", "text": "There is limited evidence indicating probiotics are of benefit in the management of infection or inflammation of the  urinary tract . [ 130 ]  One literature review found  Lactobacillus  probiotic supplements appeared to increase vaginal lactobacilli levels, thus reducing the incidence of vaginal infections in otherwise healthy adult women. [ 131 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6106", "text": "Supplements such as tablets, capsules, powders, and sachets containing bacteria have been studied.  However, probiotics taken orally can be destroyed by the acidic conditions of the stomach.  As of 2010, a number of  microencapsulation  techniques were being developed to address this problem. [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6107", "text": "Preliminary research is evaluating the potential  physiological  effects of multiple probiotic strains, as opposed to a single strain. [ 133 ] [ 134 ]  As the human gut may contain tens of thousands of microbial species, one theory indicates that this diverse environment may benefit from consuming multiple probiotic strains, an effect that remains scientifically unconfirmed. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6108", "text": "Only preliminary evidence exists for most probiotic health claims. Even for the most studied probiotic  strains , few have been sufficiently developed in basic and clinical research to warrant approval for  health claim  status by a regulatory agency such as the FDA or EFSA, and as of 2010 [update] , no claims had been approved by those two agencies. [ 7 ]  Some experts are skeptical about the efficacy of different probiotic strains and believe that not all subjects benefit from probiotics. [ 7 ] [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6109", "text": "Multiple studies have shown that there is a significant difference in the survival rate of Lactobacillus and Bifidobacterium under refrigerated (4\u00b0C) and room temperature (25\u00b0C) storage conditions. At room temperature (25\u00b11\u00b0C), the number of\u00a0 probiotics decreased by 5 to 6 logarithmic units (down to 1/100,000) after 90 days of storage. In contrast, no significant change in the number of probiotics was observed under refrigerated conditions (4 \u00b1 1\u00b0C). [ 136 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6110", "text": "First, probiotics must be alive when administered. [ 72 ] [ 137 ] [ 138 ]  One of the concerns throughout the  scientific literature  resides in the viability and reproducibility on a large scale of observed results for specific studies, as well as the viability and stability during use and storage, and finally the ability to survive in stomach acids and then in the intestinal ecosystem. [ 7 ] [ failed verification ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6111", "text": "Second, probiotics must have undergone controlled evaluation to document  health benefits  in the target host. Only products that contain live organisms shown in reproducible human studies to confer a health benefit may claim to be probiotic. [ 7 ] [ 139 ] [ 140 ]  The correct definition of health benefit, backed with solid scientific evidence, is a strong element for the proper identification and assessment of the effect of a probiotic. This aspect is a challenge for scientific and industrial investigations because several difficulties arise, such as variability in the site for probiotic use (oral, vaginal, intestinal) and mode of application. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6112", "text": "Third, the probiotic candidate must be a taxonomically defined microbe or combination of microbes ( genus ,  species , and strain level). It is commonly admitted that most effects of probiotics are strain-specific and cannot be extended to other probiotics of the same genus or species. [ 137 ]  This calls for precise identification of the strain, i.e.  genotypic  and  phenotypic  characterization of the tested microorganism. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6113", "text": "Fourth, probiotics must be safe for their intended use. The 2002 FAO/WHO guidelines recommend that, though bacteria may be generally recognized as safe (GRAS), the safety of the potential probiotic be assessed by the  minimum  required tests:  [ 141 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6114", "text": "In Europe, EFSA adopted a premarket system for the safety assessment of microbial species used in food and feed productions to set priorities for the need for risk assessment. The assessment is made for certain microorganisms; if the result is favorable, it leads to \"Qualified Presumption of Safety\"  status. [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6115", "text": "Psychobiotics  is a term used in preliminary research to refer to  live bacteria  that, when ingested in appropriate amounts, might confer a  mental health  benefit by affecting  microbiota  of the host organism. [ 1 ]  Whether bacteria might play a role in the  gut-brain axis  is under research. A 2020 literature review suggests that the consumption of psychobiotics could be considered as a viable option to restore mental health [ 2 ]  although lacking  randomized controlled trials  on clear mental health outcomes in humans. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6116", "text": "In experimental probiotic psychobiotics, the bacteria most commonly used are  gram-positive bacteria , such as  Bifidobacterium  and  Lactobacillus  families, as these do not contain  lipopolysaccharide  chains, reducing the likelihood of an  immunological response . [ 1 ]   Prebiotics  are substances, such as  fructans  and  oligosaccharides , that induce the growth or activity of beneficial  microorganisms , such as bacteria on being  fermented  in the gut. [ 1 ] [ 5 ]  Multiple bacterial species contained in a single probiotic broth is known as a polybiotic. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6117", "text": "Psychobiotics are probiotics that influence the gut-brain axis, the bidirectional communication network linking the gastrointestinal system and the brain. By positively modulating the gut microbiota, psychobiotics can impact the production of neurotransmitters, reduce inflammation, and enhance neural signaling, which may improve mental health and alleviate symptoms of neurological disorders. This highlights their potential as a therapeutic tool for maintaining a healthy gut-brain connection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6118", "text": "A 2021 review showed that treating anxiety in young people with psychobiotics had no significant effect. [ 7 ]  This study highlights the gut microbiome's role in brain function and mental health is a growing research area, particularly during adolescence, a critical period for gut-brain axis development. This study systematically reviewed and analyzed the effects of psychobiotic interventions on anxiety in youth (ages 10\u201324). Among 5416 studies identified, 14 were reviewed, and 10 included in the meta-analysis, involving 617 participants. The results showed minimal efficacy of psychobiotics in reducing anxiety, with a pooled standard mean difference of \u22120.03, indicating no significant effect. Despite limited evidence, future research focusing on mechanisms, causality, and youth perspectives is essential for advancing psychobiotic use in mental health management."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6119", "text": "Another  2022  article highlights how the nervous system disorders affect millions globally each year, sparking interest in the potential of probiotics to support the gut-brain axis alongside traditional treatments. Psychobiotics, a type of probiotic, have shown promise in improving gut microbiota and alleviating symptoms of central nervous system (CNS) disorders. This study reviewed their impact on conditions like autism spectrum disorders, Parkinson's disease, multiple sclerosis, depression, and insomnia, among others. The findings suggest that psychobiotic-containing functional foods could be an effective tool for improving mental health and managing CNS disorders."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6120", "text": "There is a need for more diverse human studies, mainly because those that exist have contradictory outcomes. [ 3 ] [ 4 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6121", "text": "Several species of bacteria have been used in probiotic psychobiotic research: [ 6 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6122", "text": "Putrefaction  is the fifth  stage of death , following  pallor mortis ,  livor mortis ,  algor mortis , and  rigor mortis . This process references the breaking down of a body of an  animal   post-mortem . In broad terms, it can be viewed as the decomposition of  proteins , and the eventual breakdown of the cohesiveness between tissues, and the liquefaction of most organs. This is caused by the decomposition of organic matter by bacterial or fungal digestion, which causes the release of gases that infiltrate the body's tissues, and leads to the deterioration of the tissues and organs. \nThe approximate time it takes putrefaction to occur is dependent on various factors. Internal factors that affect the rate of putrefaction include the age at which death has occurred, the overall structure and condition of the body, the cause of death, and external injuries arising before or after death. External factors include environmental temperature, moisture and air exposure, clothing, burial factors, and light exposure.  Body farms  are facilities that study the way various factors affect the putrefaction process."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6123", "text": "The first signs of putrefaction are signified by a greenish discoloration on the outside of the skin, on the abdominal wall corresponding to where the large intestine begins, as well as under the surface of the liver."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6124", "text": "Certain substances, such as  carbolic acid ,  arsenic ,  strychnine , and  zinc chloride , can be used to delay the process of putrefaction in various ways based on their chemical make up."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6125", "text": "In  thermodynamic  terms, all organic tissues are composed of chemical energy, which, when not maintained by the  constant biochemical maintenance  of the living organism, begin to chemically break down due to the reaction with water into  amino acids , known as  hydrolysis . The breakdown of the proteins of a decomposing body is a  spontaneous process .  Protein hydrolysis  is accelerated as the  anaerobic bacteria  of the  digestive tract  consume, digest, and excrete the cellular proteins of the body."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6126", "text": "The bacterial digestion of the cellular proteins weakens the tissues of the body. As the proteins are continuously broken down to smaller components, the bacteria excrete gases and  organic compounds , such as the  functional-group   amines   putrescine  (from  ornithine ) and  cadaverine  (from  lysine ), which carry the noxious odor of rotten flesh. Initially, the gases of putrefaction are constrained within the body cavities, but eventually diffuse through the adjacent tissues, and then into the  circulatory system . Once in the blood vessels, the putrid gases infiltrate and diffuse to other parts of the body and the limbs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6127", "text": "The visual result of gaseous tissue-infiltration is notable bloating of the torso and limbs. The increased internal pressure of the continually rising volume of gas further stresses, weakens, and separates the tissues constraining the gas. In the course of putrefaction, the skin tissues of the body eventually rupture and release the bacterial gas. As the anaerobic bacteria continue consuming, digesting, and excreting the tissue proteins, the body's decomposition progresses to the stage of  skeletonization . This continued consumption also results in the production of  ethanol  by the bacteria, which can make it difficult to determine the  blood alcohol content  (BAC) in autopsies, particularly in bodies recovered from water. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6128", "text": "Generally, the term  decomposition  encompasses the biochemical processes that occur from the physical death of the person (or animal) until the skeletonization of the body. Putrefaction is one of seven stages of  decomposition ; as such, the term  putrescible  identifies all organic matter (animal and human) that is  biochemically  subject to putrefaction. In the matter of death by poisoning, the putrefaction of the body is chemically delayed by poisons such as  antimony ,  arsenic ,  carbolic acid  (phenol),  nux vomica  (plant),  strychnine  (pesticide), and  zinc chloride ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6129", "text": "The rough timeline of events during the putrefaction stage is as follows:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6130", "text": "Order of organs' decomposition in the body: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6131", "text": "The rate of putrefaction is greatest in air, followed by water, soil, and earth. The exact rate of putrefaction is dependent upon many factors such as weather, exposure and location. Thus, refrigeration at a morgue or funeral home can retard the process, allowing for burial in three days or so following death without  embalming .  The rate increases dramatically in tropical climates. The first external sign of putrefaction in a body lying in air is usually a greenish discoloration of the skin over the region of the  cecum , which appears in 12\u201324 hours. The first internal sign is usually a greenish discoloration on the undersurface of the liver."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6132", "text": "Various factors affect the rate of putrefaction. [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6133", "text": "Environmental temperature: Decomposition is accelerated by high atmospheric or environmental temperature, with putrefaction speed optimized between 21\u00a0\u00b0C (70\u00a0\u00b0F) and 38\u00a0\u00b0C (100\u00a0\u00b0F), further sped along by high levels of humidity. This optimal temperature assists in the chemical breakdown of the tissue and promotes microorganism growth. Decomposition nearly stops below 0\u00a0\u00b0C (32\u00a0\u00b0F) or above 48\u00a0\u00b0C (118\u00a0\u00b0F)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6134", "text": "Moisture and air exposure: Putrefaction is ordinarily slowed by the body being submerged in water, due to diminished exposure to air. Air exposure and moisture can both contribute to the introduction and growth of microorganisms, speeding degradation. In a hot and dry environment, the body can undergo a process called mummification where the body is completely dehydrated and bacterial decay is inhibited."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6135", "text": "Clothing: Loose-fitting clothing can speed up the rate of putrefaction, as it helps to retain body heat. Tight-fitting clothing can delay the process by cutting off blood supply to tissues and eliminating nutrients for bacteria to feed on."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6136", "text": "Manner of burial: Speedy burial can slow putrefaction. Bodies within deep graves tend to decompose more slowly due to the diminished influences of changes in temperature. The composition of graves can also be a significant contributing factor, with dense, clay-like soil tending to speed putrefaction while dry and sandy soil slows it."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6137", "text": "Light exposure: Light can also contribute indirectly, as flies and insects prefer to lay eggs in areas of the body not exposed to light, such as the crevices formed by the eyelids and nostrils. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6138", "text": "Age at time of death: Stillborn fetuses and infants putrefy slowly due to their sterility. Otherwise, however, younger people generally putrefy more quickly than older people. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6139", "text": "Condition of the body: A body with a greater fat percentage and less lean body mass will have a faster rate of putrefaction, as fat retains more heat and it carries a larger amount of fluid in the tissues. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6140", "text": "Cause of death: The cause of death has a direct relationship to putrefaction speed, with bodies that died from acute violence or accident generally putrefying slower than those that died from infectious diseases. Certain poisons, such as  potassium cyanide  or  strychnine , may also delay putrefaction, while chronic alcoholism and cocaine use will speed it. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6141", "text": "External injuries: Antemortem or postmortem injuries can speed putrefaction as injured areas can be more susceptible to invasion by bacteria. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6142", "text": "Certain poisonous substances to the body can delay the process of putrefaction. They include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6143", "text": "Embalming  is the process of preserving human remains by delaying decomposition. This is acquired through the use of embalming fluid, which is a mixture of formaldehyde, methanol, and various other solvents. The most common reasons to preserve the body are for viewing purposes at a funeral, for above-ground interment or distant transportation of the deceased, and for medical or religious practices."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6144", "text": "Body farms  subject donated cadavers to various environmental conditions to study the process of human decomposition. [ 7 ]  These include The University of Tennessee's Forensic Anthropologic Facility, Western Carolina Universities Osteology Research Station (FOREST), Texas State University's Forensic Anthropology Research Facility (FARF), Sam Houston State University's Southeast Texas Applied Forensic Science Facility (STAFS), Southern Illinois University's Complex for Forensic Anthropology Research, and Colorado Mesa University's Forensic Investigation Research Station. The Australian Facility for Taphonomic Experimental Research, near  Sydney , is the first body farm located outside of the United States  [ 8 ]  In the United Kingdom there are several facilities which, instead of using human remains or cadavers, use dead pigs to study the decomposition process. Pigs are less likely to have infectious diseases than human cadavers, and are more readily available without any concern for ethical issues, but a human body farm is still highly sought after for further research. [ 9 ]  Each body farm is unique in its environmental make-up, giving researchers a broader knowledge, and allowing research into how different environmental factors can affect the rate of decomposition significantly such as humidity, sun exposure, rain or snow, altitude level and more."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6145", "text": "In  alchemy , putrefaction is the same as  fermentation , whereby a substance is allowed to rot or decompose undisturbed.  In some cases, the commencement of the process is facilitated with a small sample of the desired material to act as a \"seed\", a technique akin to the use of a  seed crystal  in  crystallization . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6146", "text": "The  pylorus  ( / p a\u026a \u02c8 l \u0254\u02d0r \u0259 s /  or  / p \u026a \u02c8 l o\u028a r \u0259 s / ) connects the  stomach  to the  duodenum . The pylorus is considered as having two parts, the  pyloric antrum  (opening to the body of the stomach) and the  pyloric canal  (opening to the duodenum). The  pyloric canal  ends as the  pyloric orifice , which marks the junction between the stomach and the duodenum. The orifice is surrounded by a  sphincter , a band of muscle, called the  pyloric sphincter .\nThe word  pylorus  comes from  Greek  \u03c0\u03c5\u03bb\u03c9\u03c1\u03cc\u03c2, via  Latin . The word  pylorus  in Greek means \"gatekeeper\", related to \"gate\" ( Greek :  pyle ) and is thus linguistically related to the word \" pylon \". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6147", "text": "The pylorus is the furthest part of the stomach that connects to the  duodenum . It is divided into two parts, the  antrum , which connects to the body of the stomach, and the  pyloric canal , which connects to the duodenum. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6148", "text": "The antrum  also called the  gastric antrum  or the  pyloric antrum  is the initial portion of the pyloric region. It is near the bottom of the stomach, proximal to the pyloric sphincter, which separates the stomach and the duodenum.  It may temporarily become partially or completely shut off from the remainder of the stomach during  digestion  by  peristaltic  contraction of the prepyloric  sphincter ; it is  demarcated , sometimes, from the pyloric canal by a slight groove."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6149", "text": "The  pyloric canal  ( Latin :  canalis pyloricus ) is the opening between the stomach and the duodenum. [ 3 ]  The wall thickness of the pyloric canal is up to 3 millimeters (mm) in infants younger than 30 days, [ 4 ]  and up to 8\u00a0mm in adults. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6150", "text": "The  pyloric sphincter , or  valve , is a strong ring of smooth muscle at the end of the pyloric canal which lets food pass from the stomach to the duodenum. It controls the outflow of gastric contents into the duodenum. [ 6 ]  It receives  sympathetic  innervation from the  celiac ganglion ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6151", "text": "Under  microscopy , the pylorus contains numerous  glands , including  gastric pits , which constitute about half the depth of the pyloric  mucosa .  They consist of two or three short closed tubes opening into a common duct or mouth. These tubes are wavy, and are about one-half the length of the duct. The duct is lined by  columnar cells , continuous with the epithelium lining the surface of the  mucous membrane  of the stomach, the tubes by shorter and more cubical cell which are finely granular. The glands contain mucous cells and  G cells  that secrete  gastrin . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6152", "text": "The pylorus also contains scattered  parietal cells  and  neuroendocrine cells . These  endocrine  cells include  D cells , which release  somatostatin , [ 8 ]  responsible for shutting off acid secretion. (There is a second hormone-sensitive population near the  fundus .)\nUnstriated muscles, which are entirely involuntary, are located at the pylorus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6153", "text": "The pylorus is one component of the  gastrointestinal system . Food from the  stomach , as  chyme , passes through the pylorus to the  duodenum . The pylorus, through the pyloric sphincter, regulates entry of food from the stomach into the duodenum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6154", "text": "In such conditions as  stomach cancer , tumours may partly block the pyloric canal. A special tube can be implanted surgically to connect the stomach to the duodenum so as to facilitate the passage of food from one to the other. The surgery to place this tube is called a  gastroduodenostomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6155", "text": "Pyloric stenosis  refers to a pylorus that is narrow. This is due to congenital  hypertrophy  of the pyloric sphincter. The lumen of the pylorus is narrower, and less food is able to pass through. This problem is often detected in the early weeks of life. When it is present, a newborn baby may projectile vomit after eating, but despite vomiting remain hungry. Pyloric stenosis may be managed by the insertion of a  stent , or through surgical cutting of the pyloric sphincter, a  pyloromyotomy . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6156", "text": "The  rectum  ( pl. :  rectums  or  recta ) is the final straight portion of the  large intestine  in humans and some other  mammals , and the  gut  in others. Before expulsion through the  anus  or  cloaca , the rectum stores the  feces  temporarily. The adult human rectum is about 12 centimetres (4.7\u00a0in) long, [ 2 ]  and begins at the rectosigmoid junction (the end of the  sigmoid colon ) at the level of the third sacral vertebra or the sacral promontory depending upon what definition is used. [ 3 ]  Its diameter is similar to that of the sigmoid colon at its commencement, but it is dilated near its termination, forming the  rectal ampulla . [ 4 ]  It terminates at the level of the anorectal ring (the level of the  puborectalis  sling) or the  dentate line , again depending upon which definition is used. [ 3 ]  In humans, the rectum is followed by the  anal canal , which is about 4 centimetres (1.6\u00a0in) long, before the gastrointestinal tract terminates at the  anal verge . The word rectum comes from the  Latin   r\u0113ctum   intest\u012bnum , meaning  straight intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6157", "text": "The human rectum is a part of the  lower gastrointestinal tract . The rectum is a continuation of the  sigmoid colon , and connects to the  anus . The rectum follows the shape of the  sacrum  and ends in an expanded section called an ampulla where  feces  is stored before its release via the  anal canal . An ampulla (from  Latin    bottle ) is a cavity, or the dilated end of a duct, shaped like a Roman  ampulla . [ 5 ]  The rectum joins with the sigmoid colon at the level of  S3 , and joins with the anal canal as it passes through the  pelvic floor  muscles. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6158", "text": "Unlike other portions of the colon, the rectum does not have distinct  taeniae coli . [ 6 ]  The taeniae blend with one another in the sigmoid colon five centimeters above the rectum, becoming a singular longitudinal muscle that surrounds the rectum on all sides for its entire length. [ 7 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6159", "text": "The blood supply of the rectum changes between the top and bottom portions. [ 8 ]  The top two thirds is supplied by the  superior rectal artery . The lower third is supplied by the  middle  and  inferior rectal arteries . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6160", "text": "The superior rectal artery is a single artery that is a continuation of the  inferior mesenteric artery , when it crosses the  pelvic brim . [ 8 ]  It enters the mesorectum at the level of S3, and then splits into two branches, which run at the lateral back part of the rectum, and then the sides of the rectum. These then end in branches in the submucosa, which join with ( anastamose ) with branches of the middle and inferior rectal arteries. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6161", "text": "The microanatomy of the wall of the rectum is similar to the rest of the  gastrointestinal tract ; [ 9 ]  namely, that it possesses a mucosa with a lining of  a single layer of column-shaped cells  with mucus-secreting  goblet cells  interspersed, resting on a  lamina propria , with a layer of smooth muscle called  muscularis mucosa . This sits on an underlying  submucosa  of connective tissue, surrounded by a  muscularis propria  of two bands of muscle, an inner circular band and an outer longitudinal one. [ 10 ]  There are a higher concentration of goblet cells in the rectal mucosa than other parts of the gastrointestinal tract. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6162", "text": "The lining of the rectum changes sharply at the line where the rectum meets the  anus . Here, the lining changes from the column-shaped cells of the rectum to  multiple layers of flat cells . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6163", "text": "The rectum acts as a temporary storage site for feces. The rectum receives fecal material from the  descending colon , transmitted through regular muscle contractions called  peristalsis . [ 11 ]  As the rectal walls expand due to the materials filling it from within, stretch receptors from the  nervous system  located in the rectal walls stimulate the desire to pass feces, a process called  defecation . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6164", "text": "An  internal  and  external anal sphincter , and resting contraction of the  puborectalis , prevent leakage of feces ( fecal incontinence ). As the rectum becomes more distended, the sphincters relax and a  reflex  expulsion of the contents of the rectum occurs. Expulsion occurs through contractions of the muscles of the rectum. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6165", "text": "The urge to voluntarily defecate occurs after the rectal pressure increases to beyond 18 mmHg; and reflex expulsion at 55 mmHg. In voluntary defecation, in addition to contraction of the rectal muscles and relaxation of the external anal sphincter, abdominal muscle contraction, and relaxation of the puborectalis muscle occurs. This acts to make the angle between the rectum and anus straighter, and facilitate defecation. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6166", "text": "For the diagnosis of certain ailments, a  rectal exam  may be done. These include  faecal impaction ,  prostatic cancer  and  benign prostatic hypertrophy  in men,  faecal incontinence , and internal  haemorrhoids . [ 12 ]  Forms of  medical imaging  used to examine the rectum include  CT scans  and MRI scans. An  ultrasound  probe may be inserted into the rectum to view nearby structures such as the prostate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6167", "text": "Colonoscopy  and  sigmoidoscopy  are forms of  endoscopy  that use a guided camera to directly view the rectum. The instruments may have the ability to take  biopsies  if needed, for diagnosis of diseases such as  cancer . A  proctoscope  is another instrument that is used to visualise the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6168", "text": "Body temperature  can also be taken in the rectum. Rectal temperature can be taken by inserting a  medical thermometer  not more than 25\u00a0mm (0.98\u00a0in) into the rectum via the  anus . A  mercury thermometer  should be inserted for 3 to 5 minutes; a digital thermometer should remain inserted until it beeps. Normal rectal temperature generally ranges from 36 to 38\u00a0\u00b0C (97 to 100\u00a0\u00b0F) and is about 0.5\u00a0\u00b0C (32.9\u00a0\u00b0F) above oral (mouth) temperature and about 1\u00a0\u00b0C (34\u00a0\u00b0F) above  axilla  (armpit) temperature. [ citation needed ]  Availability of less invasive temperature-taking methods including tympanic (ear) and forehead thermometers has facilitated reduced use of this method."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6169", "text": "Some medications are also administered via the rectum ( Latin :  per rectum ). [ 13 ]  By their definitions, suppositories are inserted, and enemas are injected into the rectum. [ 14 ] [ 15 ]  Medications might be given via the rectum to relieve constipation, to treat conditions near the rectum, such as fissures or haemorrhoids, or to give medications that are systemically active when taking them by mouth is not possible. [ 16 ]  People do not tend to like medications administered by this route because of both cultural issues, discomfort, and issues that may affect the medication working, such as leakage. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6170", "text": "One cause of  constipation  is  faecal impaction  in the rectum, in which a dry, hard  stool  forms. [ citation needed ]  Constipation is most commonly due to dietary and lifestyle factors such as inadequate  hydration , immobility, and lack of dietary fibre, although there are many potential causes. [ 17 ]  Such causes may include obstruction because of narrowing, local disease (such as Crohn's disease, fissures or haemorrhoids), or diseases affecting the neurological control of the bowel, or slow bowel transit time, including  spinal cord injury  and  multiple sclerosis ; use of medications such as  opioids , and conditions such as  diabetes mellitus , as well as severe illness. [ 17 ]  High calcium levels and  low thyroid activity  may also cause constipation. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6171", "text": "Testing may be carried out to investigate the cause. This may include  blood tests  such as  biochemistry ,  calcium  levels,  thyroid function tests . [ 17 ]  A digital rectal examination may be performed to see if there is stool in the rectum, and whether there is an obstruction. [ 17 ]  When symptoms such as weight loss, bleeding through the rectum, or pain are present, additional investigations such as a  CT scan  may be ordered. [ 17 ]  If constipation persists despite simple treatments, testing may also include  anal manometry  to measure pressures in the anus and rectum, electrophysiological studies, and magnetic resonance proctography. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6172", "text": "In general however, constipation is treated by improving factors such as hydration, exercise, and dietary fibre. [ 17 ]   Laxatives  may be used. Constipation that persists may require enemas or suppositories. Sometimes, use of the fingers or hand (manual evacuation) is required. [ citation needed ]  Although  peristalsis  in the colon delivers material to the rectum, laxatives such as  bisacodyl  or  senna  that induce peristalsis in the large bowel do not appear to initiate peristalsis in the rectum. They induce a sensation of rectal fullness and contraction that frequently leads to defecation, but without the distinct waves of activity characteristic of peristalsis. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6173", "text": "Other diseases of the rectum include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6174", "text": "Due to the proximity of the anterior wall of the rectum to the  vagina  in females or to the  prostate  in males, and the shared nerves thereof, the rectum is an  erogenous zone  and its  stimulation  or penetration can result in  sexual arousal . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6175", "text": "English  rectum  is derived from the Latin  intestinum rectum [ 20 ]  'straight gut', [ 21 ] [ 22 ]  a  calque [ 23 ] [ 24 ]  of  Ancient Greek  \u1f00\u03c0\u03b5\u03c5\u03b8\u03c5\u03c3\u03bc\u03ad\u03bd\u03bf\u03bd \u1f14\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd, derived from \u1f00\u03c0\u03b5\u03c5\u03b8\u03cd\u03bd\u03b5\u03b9\u03bd,  to make straight , [ 25 ]  and \u1f14\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd,  gut , [ 25 ]  attested in the writings of Greek  physician   Galen . [ 23 ] [ 24 ]  During his anatomic investigations on animal corpses, Galen observed the rectum to be straight instead of curved as in humans. [ 23 ] [ 24 ]  The expressions \u1f00\u03c0\u03b5\u03c5\u03b8\u03c5\u03c3\u03bc\u03ad\u03bd\u03bf\u03bd \u1f14\u03bd\u03c4\u03b5\u03c1\u03bf\u03bd and intestinum rectum are therefore not appropriate descriptions of the rectum in humans.  Apeuthysmenon [ 26 ]   is the Latinization of \u1f00\u03c0\u03b5\u03c5\u03b8\u03c5\u03c3\u03bc\u03ad\u03bd\u03bf\u03bd and  euthyenteron [ 27 ]  has a similar meaning  (\u03b5\u1f50\u03b8\u03cd\u03c2 'straight [ 25 ] ). Much of the knowledge of the anatomy of the rectum comes from detailed descriptions provided by  Andreas Vesalius  in 1543. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6176", "text": "The  reticulum  is the second chamber in the four-chamber  alimentary canal  of a  ruminant  mammal.  Anatomically it is the smaller portion of the  reticulorumen  along with the  rumen . Together these two compartments make up 84% of the volume of the total stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6177", "text": "The reticulum is colloquially referred to as the  honeycomb ,  bonnet' , [ 1 ]  or  kings-hood . [ 1 ]   When cleaned and used for food, it is called \" tripe \"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6178", "text": "Heavy or dense feed and foreign objects will settle here. It is the site of  hardware disease  in cattle and because of the proximity to the heart this disease can be life-threatening."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6179", "text": "The internal mucosa has a honeycomb shape. When looking at the reticulum with ultrasonography it is a crescent-shaped structure with a smooth contour. [ 2 ]  The reticulum is adjacent to the diaphragm, lungs, abomasum, rumen and liver. The heights of the reticular crests and depth of the structures vary across ruminant animal species. [ 3 ]   Grazing  ruminants have higher crests than  browsers . However, general reticulum size is fairly constant across ruminants of differing body size and feeding type."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6180", "text": "Why nature selected the honeycomb shape as the internal mucosal structure of the reticulum. The main function of the reticulum is to store higher-density particles and generate biphasic contraction for the separation of food particles governed by the large amount of water in the reticulum. In The internal anatomical structure of the reticulum, the Honeycomb resembles the classical organic benzene structure; it is the most favourite structure of the nature. A hexagon has six sides, which allows it to distribute forces evenly across its structure, making it more stable and resistant to deformation. Additionally, the angles of a hexagon are evenly spaced, which helps to evenly distribute stress and prevent weak points, it has the angle that releases the most tension i.e.;120 degrees. The hexagon uses the least amount of material to hold the most weight that\u2019s why higher density particles remain stay in the reticulum. High density particles may settle into the honeycomb structures and can be found after death. It is during the contractions of the reticulum that sharp objects can penetrate the wall and make their way to the heart. The hexagon is considered one of the strongest shapes in nature due to its ability to distribute force evenly and efficient. Hexagonal structures allow water molecules (with their one atom of oxygen and two of hydrogen) to group up together in the most efficient way and help in food particles separation. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6181", "text": "In a mature cow, the reticulum can hold around 5 gallons of liquid. The rumen and reticulum are very close in structure and function and can be considered as one organ. They are separated only by a muscular fold of tissue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6182", "text": "In immature ruminants, a reticular groove is formed by the muscular fold of the reticulum. This allows milk to pass by the reticulorumen straight into the abomasum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6183", "text": "The fluid contents of the reticulum play a role in particle separation. This is true both in domestic and wild ruminants. The separation takes place through biphasic contractions. In the first contraction, there is sending large particles back into the rumen while the reticulo-omasal orifice allows the passage of finer particles. In the second contraction, the reticulum contracts completely so the empty reticulum can refill with contents from the rumen. These contents are then sorted in the next biphasic contraction. [ 3 ]  The contractions occur in regular intervals. High density particles may settle into the honeycomb structures and can be found after death. It is during the contractions of the reticulum that sharp objects can penetrate the wall and make their way to the heart. Some ruminants, such as goats, also have monophasic contractions in addition to the biphasic contractions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6184", "text": "Retroperistalsis  is the reverse of the involuntary  smooth muscle  contractions of  peristalsis . It usually occurs as a precursor to  vomiting . Local irritation of the stomach, such as bacteria or food poisoning, activates the  emetic center  of the brain which in turn signals an imminent  vomiting reflex . Retroperistalsis begins in the small intestine and  pyloric sphincter . [ 1 ]  Food then moves in the opposite direction, often from the  duodenum  into the  stomach ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6185", "text": "Retroperistalsis occurs pathologically during vomiting and physiologically at the first part of the duodenum where it protects from high acidity of food, and also at the  terminal ileum , where an amount of water and  electrolytes  are absorbed to assist  defecation . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6186", "text": "The  rumen , also known as a  paunch , is the largest stomach compartment in  ruminants .  [ 1 ]  The rumen and the reticulum make up the  reticulorumen  in  ruminant  animals. [ 2 ]  The diverse  microbial  communities in the rumen allows it to serve as the primary site for microbial  fermentation  of ingested feed, which is often fiber-rich roughage typically indigestible by  mammalian  digestive systems. [ 2 ] [ 3 ]  The rumen is known for containing unique microbial networks within its multiple sac compartments to break down nutrients into usable energy and fatty acids.  [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6187", "text": "The rumen is composed of five muscular sacs: cranial sac, ventral sac, dorsal sac, caudodorsal sac, and caudoventral blind sac. Each of these areas contain unique microbial communities, environments, and physical abilities that influence digestion.  [ 1 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6188", "text": "The outer lining of the rumen, known as the epithelium, serves as a protective layer and contributes to the metabolic processing of  fermentation  products.  [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6189", "text": "The inner lining of the rumen wall is covered in small fingerlike projections called papillae, which aid in nutrient absorption. [ 1 ]  The  reticulum  is lined with ridges that form a  hexagonal   honeycomb  pattern. [ 1 ]  These features increase the surface area of the  reticulorumen  wall, facilitating the absorption of  volatile fatty acids  and capture of smaller digesta particles. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6190", "text": "The rumen and the  reticulum  differ with regard to the makeup of the lining but account for approximately 80% of total  ruminant  stomach volume.  [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6191", "text": "Digestion in the rumen and  reticulorumen  occurs through  fermentation  by diverse  microbe  communities to optimize resources from nutrient dense feed. [ 5 ]  Millions of  microorganisms , including  bacteria ,  archaea ,  viruses ,  fungi , and  protozoa , are known to reside in the  reticulorumen  and are essential to digest structural  carbohydrates , like  lignocellulose  ( hemicellulose  and  cellulose ), non-structural  carbohydrates  ( starch ,  sugar , and  pectin ),  lipids , and  nitrogenous compounds  ( proteins ,  peptides , and  amino acids ). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6192", "text": "Both non-structural and structural carbohydrates are  hydrolysed  to  monosaccharides  or  disaccharides  by microbial  enzymes . The resulting  mono - and  disaccharides  are transported into the microbes.  Once within microbial cell walls, the  mono - and  disaccharides   may be assimilated into microbial biomass or fermented to  volatile fatty acids  (VFAs), such as  acetate ,  propionate ,  butyrate ,  lactate ,  valerate  and other  branched-chain  VFAs via  glycolysis  and other biochemical pathways to yield energy for the microbial cell. [ 1 ] [ 3 ]   Most VFAs are absorbed across the  reticulorumen  wall, directly into the bloodstream, and are used by the ruminant as substrates for energy production and  biosynthesis . [ 1 ] [ 6 ]  Some  branched chain VFAs  are incorporated into the  lipid membrane  of rumen microbes. VFAs provide large amounts of energy for ruminants and are critical to the health of the rumen and its microbiome. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6193", "text": "Lipids ,  lignin ,  minerals , and  vitamins  play a less prominent role in digestion than carbohydrates and protein, but they are still critical in many ways.  Lipids  are partly hydrolysed and hydrogenated, and  glycerol , if present in the lipid, is fermented. Lipids are otherwise inert in the rumen. Some carbon from carbohydrate or protein may be used for  de novo synthesis  of microbial lipid.  High levels of lipid, particularly unsaturated lipid, in the rumen are thought to poison microbes and suppress fermentation activity.  Lignin , a phenolic compound, is recalcitrant to digestion, through it can be solubilized by fungi. Lignin is thought to shield associated nutrients from digestion and hence limits degradation. Minerals are absorbed by microbes and are necessary to their growth.  Microbes in turn synthesize many vitamins, such as  cyanocobalamin , in great quantities\u2014often great enough to sustain the ruminant even when vitamins are highly deficient in the diet."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6194", "text": "The protein ingested is either  degradable intake protein  or  undegradable intake protein , or  rumen bypass protein .  [ 1 ]  Protein is hydrolysed to  peptides  and  amino acids  by microbial enzymes, which are subsequently transported across the microbial cell wall for assimilation into cell biomass, primarily.  Peptides, amino acids, ammonia, and other sources of nitrogen originally present in the feed can also be used directly by microbes with little to no hydrolysis. In situations in which nitrogen for microbial growth is in excess, protein and its derivatives can also be fermented to produce energy, yielding  ammonia . Excess  ammonia  is absorbed by the rumen and converted into  urea  in the liver. Non-amino acid nitrogen is used for synthesis of microbial amino acids. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6195", "text": "Ruminants  have access to food-sourced protein and microbial proteins produced by the  microbes  in the rumen. [ 1 ]  This creates a  symbiotic  relationship between the  ruminant  and the  microbial  communities, as the  microbes  can be used as a protein source when washed into the  abomasum  section of the digestive tract. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6196", "text": "Digested food (digesta) in the rumen is not uniform, but rather stratified into gas, liquid, and particles of different sizes, densities, and other physical characteristics. Additionally, the digesta is subject to extensive mixing and complicated flow paths upon entry into the rumen. Though they may seem trivial at first, these complicated stratification, mixing, and flow patterns of digesta are a key aspect of digestive activity in the ruminant and thus warrant detailed discussion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6197", "text": "After being swallowed, food travels down the  oesophagus  and is deposited in the  dorsal  part of the reticulum. Contractions of the reticulorumen propel and mix the recently ingested feed into the ruminal mat.  The mat is a thick mass of digesta, consisting of partially degraded, long, fibrous material.  Most material in the mat has been recently ingested, and as such, has considerable fermentable substrate remaining.  Microbial fermentation proceeds rapidly in the mat, releasing many gases.  Some of these gases are trapped in the mat, causing the mat to be buoyant.  As fermentation proceeds, fermentable substrate is exhausted, gas production decreases, and particles lose buoyancy due to loss of entrapped gas.  Digesta in the mat hence goes through a phase of increasing buoyancy followed by decreasing buoyancy.  Simultaneously, the size of digesta particles\u2013relatively large when ingested\u2013is reduced by microbial fermentation and, later, rumination. Incomplete digestion of plant material here will result in the formation of a type of  bezoar  called Phytobezoars. At a certain point, particles are dense and small enough that they may \u201cfall\u201d through the rumen mat into the ventral sac below, or they may be swept out of the rumen mat into the reticulum by liquid gushing through the mat during ruminal contractions. Once in the ventral sac, digesta continues to ferment at decreased rates, further losing buoyancy and decreasing in particle size.  It is soon swept into the ventral reticulum by ruminal contractions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6198", "text": "In the ventral reticulum, less dense, larger digesta particles may be propelled up into the oesophagus and mouth during contractions of the reticulum.  Digesta is chewed in the mouth in a process known as  rumination , then expelled back down the oesophagus and deposited in the dorsal sac of the reticulum, to be lodged and mixed into the ruminal mat again.  Denser, small particles stay in the ventral reticulum during reticular contraction, and then during the next contraction may be swept out of the reticulorumen with liquid through the  reticulo-omasal orifice , which leads to the next chamber in the ruminant animal's alimentary canal, the  omasum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6199", "text": "Water and saliva enter through the rumen to form a liquid pool.  Liquid will ultimately escape from the reticulorumen from absorption through the wall, or through passing through the reticulo-omasal orifice, as digesta does.  However, since liquid cannot be trapped in the mat as digesta can, liquid passes through the rumen much more quickly than digesta does.  Liquid often acts as a carrier for very small digesta particles, such that the dynamics of small particles is similar to that of liquid."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6200", "text": "The uppermost area of the rumen, the headspace, is filled with  gases  (such as  methane ,  carbon dioxide , and, to a much lower degree,  hydrogen ) released from  fermentation  and  anaerobic respiration  of food. These gases are regularly expelled from the reticulorumen through the mouth, in a process called  eructation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6201", "text": "The different sacs of the rumen allow for varying ecological niches for microbes in the reticulorumen, including  bacteria ,  protozoa ,  fungi ,  archaea , and  viruses . [ 7 ]  Each microbial community depends on a variety of enzymes to breakdown  lignocellulose , nonstructural  carbohydrates ,  nitrogenous compounds , and  lipids . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6202", "text": "Bacteria, along with  protozoa , are the predominant microbes and by mass account for 40-60% of total microbial matter in the rumen. [ 8 ] [ 9 ]  They are categorized into several functional groups, such as  fibrolytic ,  amylolytic , and  proteolytic  types, which preferentially digest structural carbohydrates, non-structural carbohydrates, and protein, respectively.  Protozoa  (40-60% of microbial mass) derive their nutrients through  phagocytosis  of other microbes, and degrade and digest feed  carbohydrates , especially starch and sugars, and protein. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6203", "text": "Ruminal  fungi  make up 5-10% of microbes and are absent on diets poor in fibre. [ 9 ]   Fungi occupy an important niche in the rumen because they hydrolyse some ester linkages between  lignin  and  hemicellulose  or  cellulose , and help break down digesta particles.   Archaea , approximately 3% of total microbes, are mostly  autotrophic  methanogens and produce  methane  through  anaerobic respiration . [ 9 ]   Most of the hydrogen produced by  bacteria ,  protozoa  and  fungi  is used by these  methanogens  to reduce  carbon dioxide  to  methane . [ 9 ]   Viruses  are present in unknown numbers and have not been well studied.  However, they can  lyse  microbes, releasing their contents for other microbes to assimilate and ferment in a process called  microbial recycling , although recycling through the predatory activities of protozoa is quantitatively more important. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6204", "text": "Microbes  in the  reticulorumen  eventually flow out into the  omasum  and the remainder of the  alimentary canal .  Under normal  fermentation  conditions the environment in the  reticulorumen  is weakly acidic and is populated by microbes that are adapted to a pH between roughly 5.5 and 6.5; since the abomasum is strongly acidic (pH 2 to 4), it acts as a barrier that largely kills  reticulorumen   flora  and  fauna  as they flow into it. [ 1 ]   Subsequently, microbial  biomass  is digested in the  small intestine  and smaller molecules (mainly  amino acids ) are absorbed and transported in the portal vein to the liver. [ 1 ]   The digestion of these  microbes  in the small intestine is a major source of nutrition, as microbes usually supply some 60 to 90% of the total amount of amino acids absorbed. On starch-poor diets, they also provide the predominant source of glucose absorbed from the small intestinal contents. [ 1 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6205", "text": "The feed contained within the reticulorumen, known as \"paunch waste\", has been studied as a fertiliser for use in  sustainable agriculture . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6206", "text": "At birth, the rumen  organ , rumen  epithelium , and rumen  microbiota  are not fully developed and are metabolically nonfunctional. [ 3 ]  The developing rumen does not display the level of keratinization seen in the mature organ. [ 3 ]   Generally, the most receptive time for rumen development is between the  postnatal  and  weaning  periods. Over this period, rumen organ and  epithelium  growth, along with the establishment of rumen  microbiota , will prove to be essential to rumen development. [ 11 ]  This process is influenced by the introduction of solid food and the establishment of  fermentation  in the rumen. [ 3 ]  Additionally, there must be an adequate amount of  short chain fatty acids , produced during  fermentation , to properly develop the papillae. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6207", "text": "Papillae  growth in rumen  epithelium  is essential for rumen functionality. Papillae increase the surface area inside of the rumen and allow for a considerable increase in nutrient  absorption  inside of the rumen. [ 1 ]  Distinguishing a developed from an undeveloped rumen is simplified by observing the carpeting of tissue surrounding the interior of the rumen, as an undeveloped rumen maintains a smooth, papillae-lacking outer surface, and a developed rumen possesses thick, papillae-full walls. [ 3 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6208", "text": "Due to ruminants being born with a sterile  gastrointestinal tract , the developing rumen must be exposed to an array of microflora at an early stage. Specific diets in which  microflora  promote an  anaerobic  environment suitable for fermentation in the rumen are favored. [ 11 ]  Furthermore, feeds must be tailored to the needs of the specific  ruminants , as developing  ruminants  who have been on a strict liquid feed diet will possess different  microflora  when compared to that of a developing  ruminant  fed with a combination of a dry and liquid feed. [ 3 ]  This is due to the nutrients ingested by the animal not entering into the rumen stomach compartment, as it is instead bypassed by the reflexive closure of the  esophageal  groove. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6209", "text": "The most abundant bacteria present in the rumen microbiome include  Prevotella ,  Butyrivibrio , and  Ruminococcus . [ 13 ]  This is due to ruminant organisms ingesting high-forage, commonly grass-based diets. Their typical high-forage diets cause this significant demand for cellulose digesting bacteria to be ever-present. Other bacteria, such as  Lachnospira multiparus, Prevotella ruminicola,  and  Butyrivibrio fibrisolvens , play essential roles in the creation of  volatile fatty acids  (VFAs). [ 13 ]  Specific feeds can stimulate this extensive bacterial growth in the rumen and therefore aid in the production of these volatile fatty acids, which play a major role in rumen epithelium growth, capillary development, and papillae formation. [ 14 ]  Previous research identified the significant impact of volatile fatty acids on rumen development through the effects of the inter-ruminal insertion of  acetate ,  propionate , and  butyrate . [ 15 ]  The most visually notable and impactful of these volatile fatty acids was butyrate, which is synthesized naturally in ruminants through multiple anaerobic fermentation pathways of dietary substrates. [ 16 ]  Butyrate, mainly expressed in epithelial tissue lining, is involved in regulating a plethora of ruminant epithelial cell genes. Generally, butyrate regulates gene expression by acting on cell cycle control pathways. [ 17 ]  In the epithelial wall of the rumen, butyrate regulates epithelial cell gene expression to increase blood flow and papilla proliferation. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6210", "text": "Developing feeds to support the microbiome growth of both production and pet ruminant animals is vital; both for the overall health of the maturing animal and for reducing the costs associated with raising that animal. In the production animal realm, feeding can account for up to 75% of the overall cost associated with that animal, making it crucial to identify and satisfy the nutritional demands of the rumen. [ 18 ]  Sampling microbial DNA from rumen epithelial cells has led to the identification of microbial genes and functional pathways associated with animal growth factors. [ 19 ]  Microbial clusters in the rumen possess genes associated with many animal growth-related factors. Protein encoding genes that encode for bacterial cell functions, such as  aguA, ptb , K01188, and  murD , also are associated with the animal\u2019s average daily weight gain. [ 18 ]  Furthermore, vitamin B12 related genes, including  cobD, tolC, and fliN,  are also related to the daily feed intake of the animal. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6211", "text": "S cells  are cells which release  secretin , found in the  jejunum  and  duodenum . [ 1 ]  They are stimulated by a drop in  pH  to 4 or below in the  small intestine 's lumen. The released secretin will increase the secretion of  bicarbonate  (HCO 3 \u2212 ) into the lumen, via the  pancreas . This is primarily accomplished by an increase in  cyclic AMP  that activates  CFTR  to release chloride anions into the lumen. The luminal Cl \u2212  is then involved in a  bicarbonate transporter protein  exchange, in which the chloride is reabsorbed by the cell and HCO 3 \u2212  is secreted into the  lumen . S cells are also one of the main producers of  cyclosamatin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6212", "text": "Saccharomyces cerevisiae  ( / \u02cc s \u025br \u0259 \u02c8 v \u026a s i . i\u02d0 / ) ( brewer's yeast  or  baker's yeast ) is a species of  yeast  (single-celled  fungal  microorganisms). The species has been instrumental in  winemaking ,  baking , and  brewing  since ancient times. It is believed to have been originally isolated from the skin of  grapes . [ a ]  It is one of the most intensively studied  eukaryotic   model organisms  in  molecular  and  cell biology , much like  Escherichia coli  as the model  bacterium . It is the microorganism which causes many common types of  fermentation .  S.\u00a0cerevisiae  cells are round to ovoid, 5\u201310\u00a0 \u03bcm  in diameter. It reproduces by  budding . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6213", "text": "Many  proteins  important in human biology were first discovered by studying their  homologs  in yeast; these proteins include  cell cycle  proteins,  signaling proteins , and protein-processing  enzymes .  S. cerevisiae  is currently the only yeast cell known to have  Berkeley bodies  present, which are involved in particular secretory pathways.  Antibodies  against  S.\u00a0cerevisiae  are found in 60\u201370% of patients with  Crohn's disease  and 10\u201315% of patients with  ulcerative colitis , and may be useful as part of a panel of serological markers in differentiating between inflammatory bowel diseases (e.g. between ulcerative colitis and Crohn's disease), their localization and severity. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6214", "text": "\" Saccharomyces \" derives from  Latinized   Greek  and means \"sugar-mould\" or \"sugar-fungus\",  saccharon  (\u03c3\u03ac\u03ba\u03c7\u03b1\u03c1\u03bf\u03bd) being the combining form \"sugar\" and  myces  (\u03bc\u03cd\u03ba\u03b7\u03c2) being \" fungus \". [ 3 ] [ 4 ]   cerevisiae  comes from Latin and means \"of beer\". [ 5 ]   Other names for the organism are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6215", "text": "This species is also the main source of  nutritional yeast  and  yeast extract . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6216", "text": "In the 19th century, bread bakers obtained their yeast from beer brewers, and this led to sweet-fermented breads such as the Imperial \" Kaisersemmel \" roll, [ 7 ] \nwhich in general lacked the sourness created by the acidification typical of  Lactobacillus . However, beer brewers slowly switched from top-fermenting ( S. cerevisiae ) to bottom-fermenting ( S. pastorianus ) yeast. The  Vienna Process  was developed in 1846. [ 8 ] \nWhile the innovation is often popularly credited for using steam in baking ovens, leading to a different crust characteristic, it is notable for including procedures for high milling of grains (see Vienna grits [ 9 ] ),\ncracking them incrementally instead of mashing them with one pass; as well as better processes for growing and harvesting top-fermenting yeasts, known as press-yeast. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6217", "text": "Refinements in microbiology following the work of  Louis Pasteur  led to more advanced methods of culturing pure strains. In 1879, Great Britain introduced specialized growing vats for the production of  S. cerevisiae , and in the United States around the turn of the 20th century centrifuges were used for concentrating the yeast, [ 11 ] \nturning yeast production into a major industrial process which simplified its distribution, reduced unit costs and contributed to the commercialization and commoditization of bread and beer. Fresh \"cake yeast\" became the standard leaven for bread bakers in much of the Western world during the early 20th century. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6218", "text": "During  World War II ,  Fleischmann's  developed a  granulated  active dry yeast for the United States armed forces, which did not require refrigeration and had a longer shelf-life and better temperature tolerance than fresh yeast; it is still the standard yeast for US military recipes. The company created yeast that would rise twice as fast, cutting down on baking time.  Lesaffre  would later create instant yeast in the 1970s, which has gained considerable use and market share at the expense of both fresh and dry yeast in their various applications. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6219", "text": "In nature, yeast cells are found primarily on ripe fruits such as grapes (before maturation, grapes are almost free of yeasts). [ 13 ]   S. cerevisiae  can also be found year-round in the bark of  oak trees . [ 14 ]  Since  S. cerevisiae  is not airborne, it requires a vector to move. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6220", "text": "Queens of social wasps overwintering as adults ( Vespa crabro  and  Polistes  spp.) can harbor yeast cells from autumn to spring and transmit them to their progeny. [ 16 ]  The intestine of  Polistes dominula , a social wasp, hosts  S. cerevisiae  strains as well as  S. cerevisiae  \u00d7  S. paradoxus  hybrids. Stefanini et al. (2016) showed that the intestine of  Polistes dominula  favors the mating of  S. cerevisiae  strains, both among themselves and with  S. paradoxus  cells by providing environmental conditions prompting cell  sporulation  and spores germination. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6221", "text": "The optimum temperature for growth of  S. cerevisiae  is 30\u201335\u00a0\u00b0C (86\u201395\u00a0\u00b0F). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6222", "text": "Two forms of yeast cells can survive and grow:  haploid  and  diploid . The haploid cells undergo a simple  lifecycle  of  mitosis  and growth, and under conditions of high stress will, in general, die. This is the  asexual  form of the fungus. The diploid cells (the preferential 'form' of yeast) similarly undergo a simple lifecycle of mitosis and  growth . The rate at which the mitotic cell cycle progresses often differs substantially between haploid and diploid cells. [ 18 ]  Under conditions of  stress , diploid cells can undergo  sporulation , entering  meiosis  and producing four haploid  spores , which can subsequently mate. This is the  sexual  form of the  fungus . Under optimal conditions, yeast cells can double their population every 100\u00a0minutes. [ 19 ] [ 20 ]  However, growth rates vary enormously between strains and between environments. [ 21 ]  Mean  replicative  lifespan is about 26\u00a0cell divisions. [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6223", "text": "In the wild, recessive deleterious mutations accumulate during long periods of  asexual reproduction  of diploids, and are purged during  selfing : this purging has been termed \"genome renewal\". [ 24 ] [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6224", "text": "All  strains  of  S.\u00a0cerevisiae  can grow  aerobically  on  glucose ,  maltose , [ 26 ]  and  trehalose [ 27 ]  and fail to grow on  lactose  and  cellobiose . However, growth on other  sugars  is variable.  Galactose  and  fructose  are shown to be two of the best fermenting sugars. The ability of yeasts to use different sugars can differ depending on whether they are grown aerobically or anaerobically. Some strains cannot grow anaerobically on  sucrose  and trehalose. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6225", "text": "All strains can use  ammonia  and  urea  as the sole  nitrogen  source, but cannot use  nitrate , since they lack the ability to reduce them to  ammonium   ions . They can also use most  amino acids , small  peptides , and nitrogen bases as nitrogen sources.  Histidine ,  glycine ,  cystine , and  lysine  are, however, not readily used.  S.\u00a0cerevisiae  does not excrete  proteases , so extracellular protein cannot be metabolized."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6226", "text": "Yeasts  also have a requirement for  phosphorus , which is assimilated as a dihydrogen phosphate ion, and  sulfur , which can be assimilated as a  sulfate  ion or as organic sulfur compounds such as the  amino acids  methionine and cysteine. Some metals, like  magnesium ,  iron ,  calcium , and  zinc , are also required for good growth of the yeast."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6227", "text": "Concerning organic requirements, most strains of  S. cerevisiae  require  biotin . [ 28 ]  Indeed, a  S. cerevisiae -based growth assay laid the foundation for the isolation, crystallization, and later structural determination of biotin. Most strains also require  pantothenate  for full growth. In general,  S. cerevisiae  is prototrophic for vitamins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6228", "text": "Yeast has two mating types,  a  and \u03b1 ( alpha ), which show primitive aspects of sex differentiation. [ 29 ]  As in many other eukaryotes, mating leads to  genetic recombination , i.e. production of novel combinations of chromosomes. Two  haploid  yeast cells of opposite mating type can mate to form  diploid  cells that can either  sporulate  to form another generation of haploid cells or continue to exist as diploid cells. Mating has been exploited by biologists as a tool to combine genes, plasmids, or proteins at will. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6229", "text": "The mating pathway employs a  G protein-coupled receptor ,  G protein ,  RGS protein , and three-tiered  MAPK  signaling cascade that is homologous to those found in humans. This feature has been exploited by biologists to investigate basic mechanisms of  signal transduction  and  desensitization . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6230", "text": "Growth in yeast is synchronized with the growth of the  bud , which reaches the size of the mature cell by the time it separates from the parent cell. In well nourished, rapidly growing yeast  cultures , all the cells have buds, since bud formation occupies the whole  cell cycle . Both mother and daughter cells can initiate bud formation before cell separation has occurred. In yeast cultures growing more slowly, cells lacking buds can be seen, and bud formation only occupies a part of the cell cycle. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6231", "text": "Cytokinesis  enables budding yeast  Saccharomyces cerevisiae  to divide into two daughter cells.  S. cerevisiae  forms a bud which can grow throughout its cell cycle and later leaves its mother cell when mitosis has completed. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6232", "text": "S. cerevisiae  is relevant to cell cycle studies because it divides asymmetrically by using a polarized cell to make two daughters with different fates and sizes. Similarly,  stem cells  use asymmetric division for self-renewal and differentiation. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6233", "text": "For many cells, M phase does not happen until S phase is complete. However, for entry into mitosis in  S. cerevisiae  this is not true. Cytokinesis begins with the budding process in late G1 and is not completed until about halfway through the next cycle. The assembly of the spindle can happen before S phase has finished duplicating the chromosomes. [ 30 ]  Additionally, there is a lack of clearly defined G2 in between M and S. Thus, there is a lack of extensive regulation present in higher eukaryotes. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6234", "text": "When the daughter emerges, the daughter is two-thirds the size of the mother. [ 32 ]  Throughout the process, the mother displays little to no change in size. [ 33 ]  The RAM pathway is activated in the daughter cell immediately after cytokinesis is complete. This pathway makes sure that the daughter has separated properly. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6235", "text": "Two interdependent events drive cytokinesis in  S. cerevisiae . The first event is contractile  actomyosin ring  (AMR) constriction and the second event is formation of the primary  septum  (PS), a chitinous cell wall structure that can only be formed during cytokinesis. The PS resembles in animals the process of extracellular matrix remodeling. [ 32 ]  When the AMR constricts, the PS begins to grow. Disrupting AMR misorients the PS, suggesting that both have a dependent role. Additionally, disrupting the PS also leads to disruptions in the AMR, suggesting both the actomyosin ring and primary septum have an interdependent relationship. [ 34 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6236", "text": "The AMR, which is attached to the cell membrane facing the cytosol, consists of actin and myosin II molecules that coordinate the cells to split. [ 30 ]  The ring is thought to play an important role in ingression of the plasma membrane as a contractile force. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6237", "text": "Proper coordination and correct positional assembly of the contractile ring depends on septins, which is the precursor to the septum ring. These GTPases assemble complexes with other proteins. The septins form a ring at the site where the bud will be created during late G1. They help promote the formation of the actin-myosin ring, although this mechanism is unknown. It is suggested they help provide structural support for other necessary cytokinesis processes. [ 30 ]  After a bud emerges, the septin ring forms an hourglass. The septin hourglass and the myosin ring together are the beginning of the future division site. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6238", "text": "The septin and AMR complex progress to form the primary septum consisting of glucans and other chitinous molecules sent by vesicles from the Golgi body. [ 36 ]  After AMR constriction is complete, two secondary septums are formed by glucans. How the AMR ring dissembles remains poorly unknown. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6239", "text": "Microtubules do not play as significant a role in cytokinesis compared to the AMR and septum. Disruption of microtubules did not significantly impair polarized growth. [ 37 ]  Thus, the AMR and septum formation are the major drivers of cytokinesis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6240", "text": "When researchers look for an organism to use in their studies, they look for several traits. Among these are size, [ clarification needed ]  short generation time, accessibility [ clarification needed ] , ease of manipulation, genetics, [ clarification needed ]  conservation of mechanisms, [ clarification needed ]  and potential economic benefit. [ citation needed ]  The yeast species  Schizosaccharomyces pombe  and  S. cerevisiae  are both well studied; these two species diverged approximately  600\u00a0to\u00a0300  million years ago , and are significant tools in the study of  DNA damage  and  repair mechanisms . [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6241", "text": "S. cerevisiae  has developed as a  model organism  because it scores favorably on a number of criteria."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6242", "text": "For more than five decades  S. cerevisiae  has been studied as a model organism to better understand aging and has contributed to the identification of more mammalian genes affecting aging than any other model organism. [ 41 ]  Some of the topics studied using yeast are  calorie restriction , as well as in genes and cellular pathways involved in  senescence . The two most common methods of measuring aging in yeast are Replicative Life Span (RLS), which measures the number of times a cell divides, and Chronological Life Span (CLS), which measures how long a cell can survive in a non-dividing stasis state. [ 41 ]  Limiting the amount of glucose or amino acids in the  growth medium  has been shown to increase RLS and CLS in yeast as well as other organisms. [ 42 ]  At first, this was thought to increase RLS by up-regulating the sir2 enzyme; however, it was later discovered that this effect is independent of  sir2 . Over-expression of the genes sir2 and fob1 has been shown to increase RLS by preventing the accumulation of  extrachromosomal rDNA circles , which are thought to be one of the causes of senescence in yeast. [ 42 ]  The effects of dietary restriction may be the result of a decreased signaling in the TOR cellular pathway. [ 41 ]  This pathway modulates the cell's response to nutrients, and mutations that decrease TOR activity were found to increase CLS and RLS. [ 41 ] [ 42 ]  This has also been shown to be the case in other animals. [ 41 ] [ 42 ]  A yeast mutant lacking the genes  Sch9  and  Ras2  has recently been shown to have a tenfold increase in chronological lifespan under conditions of calorie restriction and is the largest increase achieved in any organism. [ 43 ] [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6243", "text": "Mother cells give rise to progeny buds by mitotic divisions, but undergo replicative  aging  over successive generations and ultimately die. However, when a mother cell undergoes  meiosis  and  gametogenesis ,  lifespan  is reset. [ 45 ]  The replicative potential of  gametes  ( spores ) formed by aged cells is the same as gametes formed by young cells, indicating that age-associated damage is removed by meiosis from aged mother cells. This observation suggests that during meiosis removal of age-associated damages leads to  rejuvenation . However, the nature of these damages remains to be established."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6244", "text": "During starvation of non-replicating  S. cerevisiae  cells,  reactive oxygen species  increase leading to the accumulation of  DNA damages  such as apurinic/apyrimidinic sites and double-strand breaks. [ 46 ]   Also in non-replicating cells the ability to  repair  endogenous double-strand breaks declines during chronological  aging . [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6245", "text": "S. cerevisiae  reproduces by mitosis as diploid cells when nutrients are abundant. However, when starved, these cells undergo meiosis to form haploid spores. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6246", "text": "Evidence from studies of  S. cerevisiae  bear on the adaptive function of meiosis and  recombination .  Mutations  defective in genes essential for meiotic and mitotic recombination in  S. cerevisiae  cause increased sensitivity to  radiation  or  DNA damaging chemicals . [ 49 ] [ 50 ]  For instance, gene  rad52  is required for both meiotic recombination [ 51 ]  and mitotic recombination. [ 52 ]   Rad52  mutants have increased sensitivity to killing by  X-rays ,  Methyl methanesulfonate  and the DNA cross-linking agent  8-methoxypsoralen-plus-UVA , and show reduced meiotic recombination. [ 50 ] [ 51 ] [ 53 ]  These findings suggest that  recombination repair  during meiosis and mitosis is needed for repair of the different damages caused by these agents."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6247", "text": "Ruderfer et al. [ 49 ]  (2006) analyzed the ancestry of natural  S. cerevisiae  strains and concluded that  outcrossing  occurs only about once every 50,000 cell divisions. Thus, it appears that in nature, mating is likely most often between closely related yeast cells. Mating occurs when haploid cells of  opposite mating type  MATa and MAT\u03b1 come into contact. Ruderfer et al. [ 49 ]  pointed out that such contacts are frequent between closely related yeast cells for two reasons. The first is that cells of opposite mating type are present together in the same  ascus , the sac that contains the cells directly produced by a single meiosis, and these cells can mate with each other. The second reason is that haploid cells of one mating type, upon cell division, often produce cells of the opposite mating type with which they can mate. The relative rarity in nature of meiotic events that result from  outcrossing  is inconsistent with the idea that production of  genetic variation  is the main selective force maintaining meiosis in this organism. However, this finding is consistent with the alternative idea that the main selective force maintaining meiosis is enhanced recombinational repair of DNA damage, [ 54 ]  since this benefit is realized during each meiosis, whether or not out-crossing occurs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6248", "text": "S. cerevisiae  was the first eukaryotic  genome  to be completely sequenced. [ 55 ]  The genome sequence was released to the  public domain  on April 24, 1996. Since then, regular updates have been maintained at the  Saccharomyces  Genome Database . This  database  is a highly annotated and cross-referenced database for yeast researchers. Another important  S.\u00a0cerevisiae  database is maintained by the Munich Information Center for Protein Sequences (MIPS). Further information is located at the  Yeastract  curated repository. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6249", "text": "The  S. cerevisiae  genome is composed of about 12,156,677  base pairs  and 6,275  genes , compactly organized on 16 chromosomes. [ 55 ]  Only about 5,800 of these genes are believed to be functional. It is estimated at least 31% of yeast genes have  homologs  in the human genome. [ 57 ]  Yeast genes are classified using gene symbols (such as Sch9) or systematic names. In the latter case the 16 chromosomes of yeast are represented by the letters A to P, then the gene is further classified by a sequence number on the left or right arm of the chromosome, and a letter showing which of the two DNA strands contains its coding sequence. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6250", "text": "Examples:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6251", "text": "The availability of the  S.\u00a0cerevisiae  genome sequence and a set of deletion mutants covering 90% of the yeast genome [ 59 ]  has further enhanced the power of  S.\u00a0cerevisiae  as a model for understanding the regulation of eukaryotic cells. A project underway to analyze the genetic interactions of all double-deletion mutants through  synthetic genetic array  analysis will take this research one step further. The goal is to form a functional map of the cell's processes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6252", "text": "As of 2010 [update]  a model of genetic interactions is most comprehensive yet to be constructed, containing \"the interaction profiles for ~75% of all genes in the Budding yeast\". [ 60 ]  This model was made from 5.4 million two-gene comparisons in which a double  gene knockout  for each combination of the genes studied was performed. The effect of the double knockout on the  fitness  of the cell was compared to the expected fitness. Expected fitness is determined from the sum of the results on fitness of single-gene knockouts for each compared gene. When there is a change in fitness from what is expected, the genes are presumed to interact with each other. This was tested by comparing the results to what was previously known. For example, the genes Par32, Ecm30, and Ubp15 had similar interaction profiles to genes involved in the Gap1-sorting module cellular process. Consistent with the results, these genes, when knocked out, disrupted that process, confirming that they are part of it. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6253", "text": "From this, 170,000 gene interactions were found and genes with similar interaction patterns were grouped together. Genes with similar genetic interaction profiles tend to be part of the same pathway or biological process. [ 61 ]  This information was used to construct a global network of gene interactions organized by function. This network can be used to predict the function of uncharacterized genes based on the functions of genes they are grouped with. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6254", "text": "Approaches that can be applied in many different fields of biological and medicinal science have been developed by yeast scientists. These include  yeast two-hybrid  for studying  protein interactions  and  tetrad analysis . Other resources, include a gene deletion library including ~4,700 viable haploid single gene deletion strains. A  GFP fusion strain library  used to study protein localisation and a  TAP tag library  used to purify protein from yeast cell extracts. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6255", "text": "Stanford University's  yeast deletion project  created  knockout mutations  of every gene in the  S.\u00a0cerevisiae  genome to determine their function. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6256", "text": "The yeast genome is highly accessible to manipulation, hence it is an excellent model for genome engineering."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6257", "text": "The international Synthetic Yeast Genome Project (Sc2.0 or  Saccharomyces cerevisiae version 2.0 ) aims to build an entirely designer, customizable, synthetic  S. cerevisiae  genome from scratch that is more stable than the wild type. In the synthetic genome all  transposons ,  repetitive elements  and many  introns  are removed, all UAG  stop codons  are replaced with UAA, and  transfer RNA  genes are moved to a novel  neochromosome . As of March\u00a02017 [update] , 6 of the 16 chromosomes have been synthesized and tested. No significant fitness defects have been found. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6258", "text": "All 16 chromosomes can be fused into one single chromosome by successive end-to-end chromosome fusions and  centromere  deletions. The single-chromosome and wild-type yeast cells have nearly identical  transcriptomes  and similar phenotypes. The giant single chromosome can support cell life, although this strain shows reduced growth across environments, competitiveness,  gamete  production and viability. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6259", "text": "Among other microorganisms, a sample of living  S.\u00a0cerevisiae  was included in the  Living Interplanetary Flight Experiment , which would have completed a three-year interplanetary round-trip in a small capsule aboard the Russian  Fobos-Grunt  spacecraft, launched in late 2011. [ 65 ] [ 66 ]  The goal was to test whether selected  organisms  could survive a few years in  deep space  by flying them through interplanetary space. The experiment would have tested one aspect of  transpermia , the hypothesis that  life  could survive space travel, if protected inside rocks blasted by impact off one planet to land on another. [ 65 ] [ 66 ] [ 67 ]  Fobos-Grunt's mission ended unsuccessfully, however, when it failed to escape low Earth orbit. The spacecraft along with its instruments fell into the Pacific Ocean in an uncontrolled re-entry on January 15, 2012. The next planned exposure mission in deep space using  S. cerevisiae  is  BioSentinel . (see:  List of microorganisms tested in outer space )"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6260", "text": "Saccharomyces cerevisiae  is used in brewing beer, when it is sometimes called a  top-fermenting  or top-cropping yeast. It is so called because during the fermentation process its hydrophobic surface causes the  flocs  to adhere to CO 2  and rise to the top of the fermentation vessel. Top-fermenting yeasts are fermented at higher temperatures than the lager yeast  Saccharomyces pastorianus , and the resulting beers have a different flavor from the same beverage fermented with a lager yeast. \"Fruity esters\" may be formed if the yeast undergoes temperatures near 21\u00a0\u00b0C (70\u00a0\u00b0F), or if the fermentation temperature of the beverage fluctuates during the process. Lager yeast normally ferments at a temperature of approximately 5\u00a0\u00b0C (41\u00a0\u00b0F) or 278 k, where  Saccharomyces cerevisiae  becomes dormant. A variant yeast known as  Saccharomyces cerevisiae  var.  diastaticus  is a beer spoiler which can cause secondary fermentations in packaged products. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6261", "text": "In May 2013, the  Oregon  legislature made  S. cerevisiae  the  official state microbe  in recognition of the impact craft beer brewing has had on the state economy and the state's identity. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6262", "text": "S. cerevisiae  is used in baking; the carbon dioxide generated by the fermentation is used as a  leavening agent  in bread and other baked goods. Historically, this use was closely linked to the brewing industry's use of yeast, as bakers took or bought the  barm  or yeast-filled foam from brewing  ale  from the brewers (producing the  barm cake ); today, brewing and baking yeast strains are somewhat different. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6263", "text": "Saccharomyces cerevisiae  is the main source of nutritional yeast, which is sold commercially as a food product. It is popular with vegans and vegetarians as an ingredient in cheese substitutes, or as a general food additive as a source of vitamins and minerals, especially amino acids and B-complex vitamins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6264", "text": "Owing to the high cost of commercial CO 2  cylinder systems,  CO 2  injection  by yeast is one of the most popular  DIY  approaches followed by aquaculturists for providing CO 2  to underwater aquatic plants. The yeast culture is, in general, maintained in plastic bottles, and typical systems provide one bubble every 3\u20137 seconds. Various approaches have been devised to allow proper absorption of the gas into the water. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6265", "text": "Saccharomyces cerevisiae  is used as a  probiotic  in humans and animals. The strain  Saccharomyces cerevisiae var. boulardii  is industrially manufactured and used clinically as a medication."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6266", "text": "Several clinical and experimental studies have shown that  S. cerevisiae var. boulardii  is, to lesser or greater extent, useful for prevention or treatment of several gastrointestinal diseases. [ 71 ]  Moderate quality evidence has shown  S. cerevisiae var. boulardii  reduces risk of antibiotic-associated diarrhoea both in adults [ 72 ] [ 71 ] [ 73 ]  and in children [ 72 ] [ 71 ]  and to reduce risk of adverse effects of  Helicobacter pylori  eradication therapy. [ 74 ] [ 71 ] [ 73 ]  There is some evidence to support efficacy of  S. cerevisiae var. boulardii  in prevention (but not treatment) of traveler's diarrhoea [ 71 ] [ 73 ]  and, at least as an adjunct medication, in treatment of acute diarrhoea in adults and children and of persistent diarrhoea in children. [ 71 ]  It may also reduce symptoms of  allergic rhinitis. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6267", "text": "Administration of  S. cerevisiae var. boulardii  is considered generally safe. [ 73 ]  In clinical trials it was well tolerated by patients, and adverse effects rate was similar to that in control groups (i. e. groups with  placebo  or no treatment). [ 72 ]  No case of  S. cerevisiae var. boulardii  fungemia has been reported during clinical trials. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6268", "text": "In clinical practice, however, cases of  fungemia , caused by  S. cerevisiae var. boulardii  are reported. [ 73 ] [ 71 ]  Patients with  compromised immunity  or those with central vascular catheters are at special risk. Some researchers have recommended avoiding use of  S. cerevisiae var. boulardii  as treatment in such patients. [ 73 ]  Others suggest only that caution must be exercised with its use in risk group patients. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6269", "text": "Saccharomyces cerevisiae  is proven to be an  opportunistic human pathogen , though of relatively low  virulence . [ 76 ]  Despite widespread use of this microorganism at home and in industry, contact with it very rarely leads to infection. [ 77 ] \n Saccharomyces cerevisiae  was found in the skin, oral cavity, oropharinx, duodenal mucosa, digestive tract, and vagina of healthy humans [ 78 ]  (one review found it to be reported for 6% of samples from human intestine [ 79 ] ). Some specialists consider  S. cerevisiae  to be a part of the  normal microbiota  of the gastrointestinal tract, the respiratory tract, and the vagina of humans, [ 80 ]  while others believe that the species cannot be called a true  commensal  because it originates in food. [ 79 ] [ 81 ]  Presence of  S. cerevisiae  in the human digestive system may be rather transient; [ 81 ]  for example, experiments show that in the case of oral administration to healthy individuals it is eliminated from the intestine within 5 days after the end of administration. [ 79 ] [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6270", "text": "Under certain circumstances, such as  degraded immunity ,  Saccharomyces cerevisiae  can cause infection in humans. [ 77 ] [ 76 ]  Studies show that it causes 0.45\u20131.06% of the cases of  yeast-induced vaginitis . In some cases, women suffering from  S. cerevisiae -induced vaginal infection were intimate partners of bakers, and the strain was found to be the same that their partners  used for baking . As of 1999, no cases of  S. cerevisiae -induced vaginitis in women, who worked in bakeries themselves, were reported in scientific literature. Some cases were linked by researchers to the use of the yeast in home baking. [ 76 ]  Cases of infection of  oral cavity  and  pharynx  caused by  S. cerevisiae  are also known. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6271", "text": "Occasionally   Saccharomyces cerevisiae  causes  invasive infections  (i. e. gets into the bloodstream or other normally sterile body fluid or into a deep site tissue, such as  lungs ,  liver  or  spleen ) that can go  systemic  (involve multiple organs). Such conditions are life-threatening. [ 76 ] [ 81 ]  More than 30% cases of  S. cerevisiae  invasive infections lead to death even if treated. [ 81 ]   S. cerevisiae  invasive infections, however, are much rarer than invasive infections caused by  Candida albicans [ 76 ] [ 82 ]  even in patients weakened by cancer. [ 82 ]   S. cerevisiae  causes 1% to 3.6%  nosocomial  cases of  fungemia . [ 81 ]  A comprehensive review of  S. cerevisiae  invasive infection cases found all patients to have at least one predisposing condition. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6272", "text": "Saccharomyces cerevisiae  may enter the bloodstream or get to other deep sites of the body by translocation from  oral  or  enteral   mucosa  or through contamination of intravascular catheters (e. g.  central venous catheters ). [ 80 ]  Intravascular catheters, antibiotic therapy and compromised immunity are major predisposing factors for  S. cerevisiae  invasive infection. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6273", "text": "A number of cases of  fungemia  were caused by intentional ingestion of living  S. cerevisiae  cultures for dietary or therapeutic reasons, including use of  Saccharomyces boulardii  (a strain of  S. cerevisiae   which is used as a  probiotic  for treatment of certain forms of  diarrhea ). [ 76 ] [ 81 ]   Saccharomyces boulardii  causes about 40% cases of invasive  Saccharomyces  infections [ 81 ]  and is more likely (in comparison to other  S. cerevisiae  strains) to cause invasive infection in humans without general problems with immunity, [ 81 ]  though such adverse effect is very rare relative to  Saccharomyces boulardii  therapeutic administration. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6274", "text": "S. boulardii  may contaminate intravascular catheters through hands of medical personnel involved in administering probiotic preparations of  S. boulardii  to patients. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6275", "text": "Systemic infection usually occurs in patients who have their  immunity compromised  due to severe illness ( HIV/AIDS ,  leukemia , other forms of  cancer ) or certain medical procedures ( bone marrow transplantation ,  abdominal surgery ). [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6276", "text": "A case was reported when a  nodule  was  surgically excised  from a lung of a man employed in baking business, and examination of the tissue revealed presence of  Saccharomyces cerevisiae . Inhalation of  dry baking yeast powder  is supposed to be the source of infection in this case. [ 84 ] [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6277", "text": "Not all strains of  Saccharomyces cerevisiae  are equally virulent towards humans. Most environmental strains are not capable of growing at temperatures above 35\u00a0\u00b0C (i. e. at temperatures of living body of humans and other  mammalian ). Virulent strains, however, are capable of growing at least above 37\u00a0\u00b0C  and often up to 39\u00a0\u00b0C (rarely up to 42\u00a0\u00b0C). [ 78 ]  Some industrial strains are also capable of growing above 37\u00a0\u00b0C. [ 76 ]   European Food Safety Authority  (as of 2017) requires that all  S. cerevisiae  strains capable of growth above 37\u00a0\u00b0C that are added to the food or feed chain in viable form must, as to be qualified presumably safe, show no resistance to antimycotic drugs used for treatment of yeast infections. [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6278", "text": "The ability to grow at elevated temperatures is an important factor for strain's virulence but not the sole one. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6279", "text": "Other traits that are usually believed to be associated with virulence are: ability to produce certain enzymes such as  proteinase [ 76 ]  and  phospholipase , [ 78 ]  invasive growth [ 78 ]  (i.e. growth with intrusion into the nutrient medium), ability to adhere to mammalian cells, [ 78 ]  ability to survive in the presence of  hydrogen peroxide [ 78 ]  (that is used by  macrophages  to kill foreign microorganisms in the body) and other abilities allowing the yeast to resist or influence immune response of the host body. [ 78 ]  Ability to form branching chains of cells, known as  pseudohyphae  is also sometimes said to be associated with virulence, [ 76 ] [ 78 ]  though some research suggests that this trait may be common to both virulent and non-virulent strains of  Saccharomyces cerevisiae . [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6280", "text": "Footnotes"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6281", "text": "Citations"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6282", "text": "Satiety  ( /s\u0259\u02c8ta\u026a.\u0259.ti/   s\u0259-TYE-\u0259-tee ) is a state or condition of fullness gratified beyond the point of satisfaction, the opposite of  hunger . Following satiation (meal termination), satiety is a feeling of fullness lasting until the next meal. [ 1 ]  When food is present in the  GI tract  after a meal, satiety signals overrule hunger signals, but satiety slowly fades as hunger increases."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6283", "text": "The satiety center in animals is located in  ventromedial nucleus  of the  hypothalamus . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6284", "text": "Satiety is signaled through the vagus nerve as well as circulating hormones. During intake of a meal, the stomach must stretch to accommodate this increased volume. This gastric accommodation activates stretch receptors in the proximal (upper) portion of the stomach. These receptors then signal through  afferent  vagus nerve fibers to the hypothalamus, increasing satiety. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6285", "text": "In addition, as the food moves into the duodenum, duodenal cells release multiple substances that affect digestion and satiety.  Glucagon-like peptide-1  (GLP-1) is an  incretin  released by the duodenum that inhibits relaxation of the stomach. This inhibition causes increased stretch of the stomach, increasing activation of proximal gastric stretch receptors. It also slows overall gut motility, increasing the duration of satiety. [ 3 ]  This effect is used to increase weight loss and treat obesity through GLP-1 agonists. [ 4 ]   Cholecystokinin  (CCK) is gut peptide produced by the duodenum in response to fat and proteins. CCK has the effect of slowing gut motility and increasing satiety as well as activating release of pancreatic digestive enzymes and bile from the gallbladder. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6286", "text": "6343"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6287", "text": "20287"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6288", "text": "ENSG00000070031 ENSG00000274473"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6289", "text": "ENSMUSG00000038580"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6290", "text": "P09683"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6291", "text": "Q08535"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6292", "text": "NM_021920"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6293", "text": "NM_011328 NM_001287171 NM_001309439"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6294", "text": "NP_068739"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6295", "text": "NP_001274100 NP_001296368 NP_035458"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6296", "text": "Secretin  is a  hormone  that regulates  water homeostasis  throughout the body and influences the environment of the  duodenum  by regulating secretions in the  stomach ,  pancreas , and  liver . It is a  peptide hormone  produced in the  S cells  of the duodenum, which are located in the  intestinal glands . [ 5 ]  In humans, the secretin peptide is encoded by the  SCT   gene . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6297", "text": "Secretin helps regulate the  pH  of the duodenum by inhibiting the secretion of  gastric acid  from the  parietal cells  of the stomach and stimulating the production of  bicarbonate  from the  ductal cells  of the pancreas. [ 7 ] [ 8 ]  It also stimulates the secretion of bicarbonate and water by  cholangiocytes  in the bile duct, protecting it from  bile acids  by controlling the pH and promoting the flow in the duct. [ 9 ]  Meanwhile, in concert with secretin's actions, the other main hormone simultaneously issued by the duodenum,  cholecystokinin  (CCK), stimulates the  gallbladder  to contract, delivering its stored bile."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6298", "text": "Prosecretin  is a precursor to secretin, which is present in digestion. Secretin is stored in this unusable form, and is activated by  gastric acid . This indirectly results in the neutralisation of duodenal pH, thus ensuring no damage is done to the small intestine by the aforementioned acid. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6299", "text": "In 2007, secretin was discovered to play a role in  osmoregulation  by acting on the  hypothalamus ,  pituitary gland , and  kidney . [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6300", "text": "In 1902,  William Bayliss  and  Ernest Starling  were studying how the nervous system controls the process of digestion. [ 13 ]  It was known that the pancreas secreted digestive juices in response to the passage of food (chyme) through the pyloric sphincter into the duodenum. They discovered (by cutting all the nerves to the pancreas in their experimental animals) that this process was not, in fact, governed by the nervous system. They determined that a substance secreted by the intestinal lining stimulates the pancreas after being transported via the bloodstream. They named this intestinal secretion  secretin . This type of 'chemical messenger' substance is now called a  hormone , a term coined by Starling in 1905. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6301", "text": "Secretin is frequently erroneously stated to have been the first hormone identified. [ 15 ]  However, British researchers  George Oliver  and  Edward Albert Sch\u00e4fer  had already published their findings of an adrenal extract increasing blood pressure and heart rate in brief reports in 1894 and a full publication in 1895, making  adrenaline  the first discovered hormone. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6302", "text": "Secretin is initially synthesized as a 120 amino acid precursor protein known as  prosecretin . This precursor contains an  N-terminal  signal peptide, spacer, secretin itself (residues 28\u201354), and a 72-amino acid  C-terminal  peptide. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6303", "text": "The mature secretin peptide is a linear  peptide hormone , which is composed of 27  amino acids  and has a  molecular weight  of 3055. A helix is formed in the amino acids between positions 5 and 13. The amino acids sequences of secretin have some similarities to that of  glucagon ,  vasoactive intestinal peptide  (VIP), and  gastric inhibitory peptide  (GIP). Fourteen of 27 amino acids of secretin reside in the same positions as in glucagon, 7 the same as in VIP, and 10 the same as in GIP. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6304", "text": "Secretin also has an amidated  carboxyl-terminal  amino acid which is valine. [ 19 ]  The sequence of amino acids in secretin is H\u2013 His - Ser - Asp - Gly - Thr - Phe - Thr - Ser - Glu - Leu - Ser - Arg - Leu - Arg - Asp - Ser - Ala - Arg - Leu - Gln - Arg - Leu - Leu - Gln - Gly - Leu - Val \u2013NH 2 . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6305", "text": "Secretin is synthesized in cytoplasmic secretory granules of S-cells, which are found mainly in the  mucosa  of the  duodenum , and in smaller numbers in the  jejunum  of the  small intestine . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6306", "text": "Secretin is released into circulation and/or intestinal lumen in response to low duodenal pH that ranges between 2 and 4.5 depending on species; the acidity is due to  hydrochloric acid  in the  chyme  that enters the duodenum from the stomach via the  pyloric sphincter . [ 21 ]  Also, the secretion of secretin is increased by the products of protein digestion bathing the mucosa of the upper small intestine. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6307", "text": "Secretin release is inhibited by  H 2  antagonists , which reduce gastric acid secretion. As a result, if the pH in the duodenum increases above 4.5, secretin cannot be released. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6308", "text": "Secretin primarily functions to neutralize the pH in the  duodenum , allowing digestive  enzymes  from the pancreas (e.g.,  pancreatic amylase  and  pancreatic lipase ) to function optimally. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6309", "text": "Secretin targets the  pancreas ; pancreatic centroacinar cells have  secretin receptors  in their plasma membrane. As secretin binds to these receptors, it stimulates adenylate cyclase activity and converts  ATP  to  cyclic AMP . [ 25 ]  Cyclic AMP acts as second messenger in intracellular signal transduction and causes the organ to secrete a  bicarbonate -rich fluid that flows into the  intestine . Bicarbonate is a base that neutralizes the acid, thus establishing a pH favorable to the action of other digestive enzymes in the small intestine. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6310", "text": "Secretin also increases water and bicarbonate secretion from duodenal  Brunner's glands  to buffer the incoming  protons  of the acidic chyme, [ 24 ]  and also reduces acid secretion by  parietal cells  of the  stomach . [ 27 ]  It does this through at least three mechanisms: 1) By stimulating release of  somatostatin , 2) By inhibiting release of  gastrin  in the  pyloric antrum , and 3) By direct  downregulation  of the parietal cell acid secretory mechanics. [ 28 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6311", "text": "It counteracts  blood glucose  concentration spikes by triggering increased  insulin  release from pancreas, following oral  glucose  intake. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6312", "text": "Secretin modulates  water  and  electrolyte  transport in  pancreatic duct  cells, [ 30 ]  liver  cholangiocytes , [ 31 ]  and  epididymis  epithelial cells. [ 32 ]  It is found [ 33 ]  to play a role in the  vasopressin -independent regulation of  renal water reabsorption . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6313", "text": "Secretin is found in the magnocellular neurons of the paraventricular and supraoptic nuclei of the  hypothalamus  and along the neurohypophysial tract to  neurohypophysis . During increased osmolality, it is released from the  posterior pituitary . In the hypothalamus, it activates  vasopressin  release. [ 12 ]  It is also needed to carry out the central effects of angiotensin II. In the absence of secretin or its receptor in the gene knockout animals, central injection of angiotensin II was unable to stimulate water intake and vasopressin release. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6314", "text": "It has been suggested that abnormalities in such secretin release could explain the abnormalities underlying type D  syndrome of inappropriate antidiuretic hormone hypersecretion  (SIADH). [ 12 ]  In these individuals, vasopressin release and response are normal, although abnormal renal expression, translocation of  aquaporin 2 , or both are found. [ 12 ]  It has been suggested that \"Secretin as a neurosecretory hormone from the posterior pituitary, therefore, could be the long-sought vasopressin independent mechanism to solve the riddle that has puzzled clinicians and physiologists for decades.\" [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6315", "text": "Secretin and its receptor are found in discrete nuclei of the hypothalamus, including the  paraventricular nucleus  and the  arcuate nucleus , which are the primary brain sites for regulating body energy homeostasis. It was found that both central and peripheral injection of Sct reduce food intake in mouse, indicating an anorectic role of the peptide. This function of the peptide is mediated by the  central melanocortin system . [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6316", "text": "Secretin is used in diagnostic tests for pancreatic function; secretin is injected and the pancreatic output can then be imaged with  magnetic resonance imaging , a noninvasive procedure, or secretions generated as a result can gathered either through an endoscope or through tubes inserted through the mouth, down into the duodenum. [ 36 ] [ 37 ] [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6317", "text": "A recombinant human secretin has been available since 2004 for these diagnostic purposes. [ 39 ]   There were problems with the availability of this agent from 2012 to 2015. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6318", "text": "A wave of enthusiasm for secretin as a possible treatment for  autism  arose in the 1990s based on a hypothetical gut-brain connection; as a result the NIH ran a series of clinical trials that showed that secretin was not effective, which brought an end to popular interest. [ 41 ] [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6319", "text": "A high-affinity and optimized secretin receptor antagonist (Y10,c[E16,K20],I17,Cha22,R25)sec(6-27) has been designed and developed which has allowed the structural characterization of secreting inactive conformation. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6320", "text": "Segmentation contractions  (or  movements ) are a type of  intestinal motility ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6321", "text": "Unlike  peristalsis , which predominates in the  esophagus ,  segmentation contractions  occur in the  large intestine  and  small intestine , while predominating in the latter. While peristalsis involves one-way motion in the caudal direction, segmentation contractions move  chyme  in both directions, which allows greater mixing with the secretions of the intestines.  Segmentation involves contractions of the circular muscles in the digestive tract, while peristalsis involves rhythmic contractions of the longitudinal muscles in the  gastrointestinal tract .  Unlike peristalsis, segmentation actually can slow progression of chyme through the system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6322", "text": "The  septum transversum  is a thick mass of cranial  mesenchyme , formed in the  embryo , that gives rise to parts of the  thoracic diaphragm  and the  ventral mesentery  of the foregut in the developed human being and other mammals."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6323", "text": "The septum transversum originally arises as the most cranial part of the  mesenchyme  on day 22. [ 1 ]  During craniocaudal folding, it assumes a position cranial to the developing heart at the level of the cervical vertebrae. [ 1 ]  During subsequent weeks the dorsal end of the embryo grows much faster than its ventral counterpart resulting in an  apparent descent  of the ventrally located septum transversum. At week 8, it can be found at the level of the thoracic vertebrae. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6324", "text": "After successful craniocaudal folding the septum transversum picks up innervation from the adjacent  ventral rami  of spinal nerves C3, C4 and C5, thus forming the precursor of the  phrenic nerve . During the descent of the septum, the  phrenic nerve  is carried along and assumes its descending pathway."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6325", "text": "During embryonic development of the  thoracic diaphragm ,  myoblast  cells from the septum invade the other components of the diaphragm. They thus give rise to the motor and sensory innervation of the muscular diaphragm by the  phrenic nerve ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6326", "text": "The  cranial  part of the septum transversum gives rise to the  central tendon  of the diaphragm, [ 1 ]  and is the origin of the  myoblasts  that invade the  pleuroperitoneal  folds resulting in the formation of the muscular diaphragm. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6327", "text": "The  caudal  part of the septum transversum is invaded by the  hepatic diverticulum  which divides within it to form the liver and thus gives rise to the  ventral mesentery  of the foregut, which in turn is the precursor of the  lesser omentum , the  visceral peritoneum  of the  liver  and the  falciform ligament ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6328", "text": "Though not derived from the septum transversum, development of the liver is highly dependent upon signals originating here.   Bone morphogenetic protein 2  (BMP-2),  BMP-4  and  BMP-7  produced from the septum transversum join  fibroblast growth factor  (FGF) signals from the cardiac  mesoderm  induce part of the foregut to differentiate towards a hepatic fate. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6329", "text": "The  sigmoid colon  (or  pelvic colon ) is the part of the  large intestine  that is closest to the  rectum  and  anus . It forms a loop that averages about 35\u201340 centimetres (14\u201316\u00a0in) in length. The loop is typically shaped like a Greek letter sigma (\u03c2) or Latin letter S (thus  sigma  +  -oid ). This part of the colon normally lies within the  pelvis , but due to its freedom of movement it is liable to be displaced into the  abdominal cavity . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6330", "text": "The sigmoid colon begins at the  superior aperture  of the  lesser pelvis , where it is continuous with the  iliac colon , and passes transversely across the front of the  sacrum  to the right side of the pelvis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6331", "text": "It then curves on itself and turns toward the left to reach the middle line at the level of the third piece of the  sacrum , where it bends downward and ends in the  rectum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6332", "text": "Its function is to expel solid and gaseous waste from the gastrointestinal tract. The curving path it takes toward the anus allows it to store gas in the superior arched portion, enabling the colon to expel gas without excreting faeces simultaneously."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6333", "text": "The sigmoid colon is completely surrounded by  peritoneum  (and thus is not  retroperitoneal ), which forms a  mesentery  ( sigmoid mesocolon ), which diminishes in length from the center toward the ends of the loop, where it disappears, so that the loop is fixed at its junctions with the  iliac colon  and rectum, but enjoys a considerable range of movement in its central portion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6334", "text": "Pelvic splanchnic nerves  are the primary source for  parasympathetic  innervation.   Lumbar splanchnic nerves  provide  sympathetic  innervation via the  inferior mesenteric ganglion ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6335", "text": "Behind the sigmoid colon are the  external iliac vessels , ovary, obturator nerve, the left  piriformis , and left  sacral plexus  of nerves."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6336", "text": "In front, it is separated from the  bladder  in the  male , and the  uterus  in the  female , by some coils of the  small intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6337", "text": "Diverticulosis  often occurs in the sigmoid colon in association with increased intraluminal pressure and focal weakness in the colonic wall. It is a common cause of  hematochezia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6338", "text": "Volvulus  occurs when a portion of the bowel twists around its mesentery, which can lead to obstruction and  infarction . Volvulus in the elderly commonly occurs in the sigmoid colon, whereas in infants and children it is more likely to occur in the midgut. This may correct itself spontaneously or the rotation may continue until the blood supply of the gut is cut off completely."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6339", "text": "This article incorporates text in the  public domain  from  page 1182  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6340", "text": "Simeticone  ( INN ), also known as  simethicone  ( USAN ), is an  anti-foaming agent  used to reduce  bloating , discomfort or pain caused by excessive gas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6341", "text": "Simeticone is used to relieve the symptoms of excessive gas in the  gastrointestinal tract , namely bloating, burping, and flatulence. [ 2 ] [ 3 ]  While there is a lack of conclusive evidence that simeticone is effective for this use,\u2063 [ 4 ] [ 5 ] [ failed verification ]  studies have shown that it can relieve symptoms of  functional dyspepsia [ 6 ]  and  functional bloating . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6342", "text": "It has not been fully established that simeticone is useful to treat  colic  in babies, [ 8 ]  and it is not recommended for this purpose. [ 5 ]  A study in the United Kingdom reported that according to parental perception simeticone helped infant colic in some cases. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6343", "text": "Simeticone can also be used for suspected  postoperative   abdominal discomfort  in infants. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6344", "text": "Simeticone does not have any serious side effects. [ 11 ]  Two uncommon side effects (occurring in 1 in 100 to 1 in 1,000 patients) are constipation and nausea. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6345", "text": "Simeticone is a non-systemic  surfactant  which decreases the surface tension of gas bubbles in the GI tract. [ 11 ]  This allows gas bubbles to leave the GI tract as  flatulence  or  belching . [ 11 ]  Simeticone does not reduce or prevent the formation of gas. [ 13 ]  Its effectiveness has been shown in several  in vitro  studies. [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6346", "text": "Simeticone is a mixture of  dimethicone  and  silicon dioxide . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6347", "text": "The INN name is \"simeticone\", which was added to the INN recommended list in 1999. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6348", "text": "Simeticone is marketed under many brand names and in many  combination drugs ; it is also marketed as a veterinary drug. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6349", "text": "Brand names include A.F., Acid Off, Aero Red, Aero-OM, Aero-Sim, Aerocol, Aerox, Aesim, Aflat, Air-X, Anaflat, Antiflat, Baby Rest, Bicarsim, Bicarsim Forte, Blow-X, Bobotic, Bobotik, Carbogasol, Colic E, Colin, Cuplaton, Degas, Dentinox, Dermatix, Digesta, Dimetikon Meda, Disflatyl, Disolgas, Elugan N, Elzym, Endo-Paractol, Enterosilicona, Espaven Antigas, Espumisan, Espumisan L, Flacol, Flapex, Flatidyl, Flatoril, Flatulex, Flucolic, Gas X, Gas-X, Gaselab, Gaseoflat, Gaseoflatex, Gaseophar, Gaseoplus, Gaseovet, Gaservol, Gasimetin, Gasnil, Gasofilm, Gastrex, Gastrosen, Gazim X, Gazix, Geludrox-HS, Genasyme, Ilio-Funkton, Imogas, Imogaze, Imonogas, Infacalm, Infacol, Infacolic, Lefax, Lefaxin, Lefoam, Logastin, Luftal, Maxi Flat, Meteosim, Metiorisan, Metsil, Mylanta, Mylicon, Mylicongas, Mylom, Mymus, Nanog, Neodrop, Neogasol, Neolanta, Orocure, Ovol, Pedicon, Phazin, Phazyme, Polysilane Junior, Restime, Rugby Gas Relief, Sab Simplex, Salinal, Semecon, Semeth, Sicongast, Siflat, Silbione, Siligas, Silipin, Sim, Simcone, Simecon, Simecrin, Simedill, Simegut, Simet, Simethicon, Simethicone, Simetic, Simeticon, Simeticona, Simeticone, Sim\u00e9ticone, Simeticonum, Simetigast, Simflat, Simicol, Simicon, Wilcon, Wind-eze and WindSetlers. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6350", "text": "It is also marketed as a  combination drug : [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6351", "text": "It is also marketed as a veterinary drug under the brands Birp and Methysilox."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6352", "text": "The  small intestine  or  small bowel  is an  organ  in the  gastrointestinal tract  where most of the  absorption  of  nutrients  from food takes place.  It lies between the  stomach  and  large intestine , and receives  bile  and  pancreatic juice  through the  pancreatic duct  to aid in  digestion . The small intestine is about 5.5 metres (18 feet) long and folds many times to fit in the abdomen. Although it is longer than the large intestine, it is called the small intestine because it is narrower in diameter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6353", "text": "The small intestine has three distinct regions \u2013 the  duodenum ,  jejunum , and  ileum . The duodenum, the shortest, is where preparation for absorption through small finger-like protrusions called  villi  begins. [ 2 ]  The jejunum is specialized for the absorption through its lining by  enterocytes : small nutrient particles which have been previously digested by  enzymes  in the duodenum.  The main function of the ileum is to absorb  vitamin B 12 ,  bile salts , and whatever products of digestion that were not absorbed by the jejunum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6354", "text": "The length of the small intestine can vary greatly, from as short as 3 metres (10 feet) to as long as  10.5\u00a0m ( 34 + 1 \u2044 2 \u00a0ft), also depending on the measuring technique used. [ 3 ]  The typical length in a living person is  3\u20135\u00a0m (10\u2013 16 + 1 \u2044 2 \u00a0ft). [ 4 ] [ 5 ]  The length depends both on how tall the person is and how the length is measured. [ 3 ]  Taller people generally have a longer small intestine and measurements are generally longer after death and when the bowel is empty. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6355", "text": "It is approximately  1.5 centimetres ( 5 \u2044 8  inch) in diameter in  newborns  after 35 weeks of  gestational age , [ 7 ]  and  2.5\u20133\u00a0cm (1\u2013 1 + 1 \u2044 8 \u00a0in) in diameter in adults. On  abdominal X-rays , the small intestine is considered to be abnormally dilated when the diameter exceeds 3\u00a0cm. [ 8 ] [ 9 ]  On  CT scans , a diameter of over 2.5\u00a0cm is considered abnormally dilated. [ 8 ] [ 10 ]  The surface area of the human  small intestinal mucosa , due to enlargement caused by folds, villi and microvilli, averages 30 square metres (320\u00a0sq\u00a0ft). [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6356", "text": "The small intestine is divided into three structural parts."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6357", "text": "The jejunum and ileum are suspended in the  abdominal cavity  by  mesentery . The mesentery is part of the  peritoneum . Arteries, veins, lymph vessels and nerves travel within the mesentery. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6358", "text": "The small intestine receives a blood supply from the  celiac trunk  and the  superior mesenteric artery . These are both branches of the  aorta . The duodenum receives blood from the  coeliac trunk  via the  superior pancreaticoduodenal artery  and from the superior mesenteric artery via the  inferior pancreaticoduodenal artery . These two arteries both have  anterior and posterior  branches that meet in the midline and  anastomose .  The jejunum and ileum receive blood from the superior mesenteric artery. [ 14 ]  Branches of the superior mesenteric artery form a series of arches within the mesentery known as  arterial arcades , which may be several layers deep. Straight blood vessels known as  vasa recta  travel from the arcades closest to the ileum and jejunum to the organs themselves. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6359", "text": "The three sections of the small intestine look similar to each other at a microscopic level, but there are some important differences. The parts of the intestine are as follows:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6360", "text": "About 20,000 protein coding genes are  expressed  in human cells and 70% of these genes are expressed in the normal duodenum. [ 15 ] [ 16 ]  Some 300 of these genes are more specifically expressed in the duodenum with very few genes expressed only in the small intestine. The corresponding specific proteins are expressed in glandular cells of the mucosa, such as  fatty acid binding protein   FABP6 .  Most of the more specifically expressed genes in the small intestine are also expressed in the duodenum, for example  FABP2  and the  DEFA6  protein expressed in secretory granules of  Paneth cells . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6361", "text": "The small intestine develops from the  midgut  of the  primitive gut tube . [ 18 ]  By the fifth week of  embryological  life, the  ileum  begins to grow longer at a very fast rate, forming a U-shaped fold called the  primary intestinal loop . The loop grows so fast in length that it outgrows the abdomen and protrudes through the  umbilicus . By week 10, the loop retracts back into the abdomen. Between weeks six and ten the small intestine rotates anticlockwise, as viewed from the front of the embryo. It rotates a further 180 degrees after it has moved back into the abdomen. This process creates the twisted shape of the  large intestine . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6362", "text": "Food from the stomach is allowed into the duodenum through the  pylorus  by a muscle called the pyloric sphincter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6363", "text": "The small intestine is where most chemical digestion takes place. Many of the  digestive enzymes  that act in the small intestine are secreted by the  pancreas  and  liver  and enter the small intestine via the  pancreatic duct . Pancreatic enzymes and  bile  from the gallbladder enter the small intestine in response to the hormone  cholecystokinin , which is produced in the response to the presence of nutrients.  Secretin , another hormone produced in the small intestine, causes additional effects on the pancreas, where it promotes the release of  bicarbonate  into the duodenum in order to neutralize the potentially harmful acid coming from the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6364", "text": "The three major classes of nutrients that undergo digestion are  proteins ,  lipids  (fats) and  carbohydrates :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6365", "text": "Digested food is now able to pass into the blood vessels in the wall of the intestine through either  diffusion  or  active transport . The small intestine is the site where most of the nutrients from ingested food are absorbed. The inner wall, or mucosa, of the small intestine, is lined with  intestinal epithelium , a  simple columnar epithelium . Structurally, the mucosa is covered in wrinkles or flaps called  circular folds , which are considered permanent features in the mucosa. They are distinct from  rugae  which are considered non-permanent or temporary allowing for distention and contraction. From the circular folds project microscopic finger-like pieces of tissue called  villi  ( Latin  for \"shaggy hair\"). The individual epithelial cells also have finger-like projections known as  microvilli . The functions of the circular folds, the villi, and the microvilli are to increase the amount of surface area available for the absorption of  nutrients , and to limit the loss of said nutrients to intestinal fauna."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6366", "text": "Each villus has a network of  capillaries  and fine lymphatic vessels called  lacteals  close to its surface. The epithelial cells of the villi transport nutrients from the lumen of the intestine into these capillaries (amino acids and carbohydrates) and lacteals (lipids). The absorbed substances are transported via the blood vessels to different organs of the body where they are used to build complex substances such as the proteins required by our body. The material that remains undigested and unabsorbed passes into the large intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6367", "text": "Absorption of the majority of nutrients takes place in the  jejunum , with the following notable exceptions:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6368", "text": "The small intestine supports the body's  immune system . [ 20 ]   The presence of  gut flora  appears to contribute positively to the host's immune system.\n Peyer's patches , located within the ileum of the small intestine, are an important part of the digestive tract's local immune system. They are part of the lymphatic system, and provide a site for antigens from potentially harmful bacteria or other microorganisms in the digestive tract to be sampled, and subsequently presented to the immune system. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6369", "text": "The small intestine is a complex organ, and as such, there are a very large number of possible conditions that may affect the function of the small bowel. A few of them are listed below, some of which are common, with up to 10% of people being affected at some time in their lives, while others are vanishingly rare."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6370", "text": "The small intestine is found in all  tetrapods  and also in  teleosts , although its form and length vary enormously between species. In teleosts, it is relatively short, typically around one and a half times the length of the fish's body. It commonly has a number of  pyloric caeca , small pouch-like structures along its length that help to increase the overall surface area of the organ for digesting food. There is no ileocaecal valve in teleosts, with the boundary between the small intestine and the  rectum  being marked only by the end of the digestive epithelium. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6371", "text": "In tetrapods, the  ileocaecal valve  is always present, opening into the colon. The length of the small intestine is typically longer in tetrapods than in teleosts, but is especially so in  herbivores , as well as in mammals and  birds , which have a higher  metabolic rate  than  amphibians  or  reptiles . The lining of the small intestine includes microscopic folds to increase its surface area in all vertebrates, but only in mammals do these develop into true villi. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6372", "text": "The boundaries between the duodenum, jejunum, and ileum are somewhat vague even in humans, and such distinctions are either ignored when discussing the anatomy of other animals, or are essentially arbitrary. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6373", "text": "There is no small intestine as such in non-teleost fish, such as  sharks ,  sturgeons , and  lungfish . Instead, the digestive part of the gut forms a  spiral intestine , connecting the stomach to the rectum. In this type of gut, the intestine itself is relatively straight but has a long fold running along the inner surface in a spiral fashion, sometimes for dozens of turns. This valve greatly increases both the surface area and the effective length of the intestine. The lining of the spiral intestine is similar to that of the small intestine in teleosts and non-mammalian tetrapods. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6374", "text": "In  lampreys , the spiral valve is extremely small, possibly because their diet requires little digestion.  Hagfish  have no spiral valve at all, with digestion occurring for almost the entire length of the intestine, which is not subdivided into different regions. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6375", "text": "In  traditional Chinese medicine , the  small intestine  is a  yang  organ. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6376", "text": "The  Solitary lymphatic nodules  (or  solitary follicles ) are structures found in the  small intestine  and  large intestine ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6377", "text": "The solitary lymphatic nodules are found scattered throughout the  mucous membrane  of the small intestine, but are most numerous in the lower part of the  ileum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6378", "text": "Their free surfaces are covered with rudimentary  villi , except at the summits, and each gland is surrounded by the openings of the intestinal glands."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6379", "text": "Each consists of a dense interlacing  retiform  tissue closely packed with  lymph -corpuscles, and permeated with an abundant capillary network."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6380", "text": "The interspaces of the retiform tissue are continuous with larger lymph spaces which surround the gland, through which they communicate with the  lacteal  system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6381", "text": "They are situated partly in the submucous tissue, partly in the mucous membrane, where they form slight projections of its  epithelial  layer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6382", "text": "The solitary lymphatic nodules of the large intestine are most abundant in the  cecum  and  vermiform process , but are irregularly scattered also over the rest of the intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6383", "text": "They are similar to those of the small intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6384", "text": "This article incorporates text in the  public domain  from  page 1176  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6385", "text": "The  sphincter of Boyden  (also known as the  choledochal sphincter ) is a  sphincter  located in the  common bile duct  before it joins with the  pancreatic duct  to form the  ampulla of vater . This sphincter controls the flow of  bile  into the pancreatic duct and it helps in filling up of the  gallbladder  with  bile ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6386", "text": "The sphincter of Boyden is a smooth muscle sphincter surrounding the  common bile duct  (ductus choledocus). [ 1 ] [ 2 ]  It occurs just before the junction with the  pancreatic duct , where the  ampulla of Vater  is formed. [ 1 ]  Occasionally, some fibres also surround the pancreatic duct. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6387", "text": "It is subdivided into two parts - pars superior and pars inferior. The pars inferior is the strongest component of the  sphincter of Oddi complex . [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6388", "text": "The sphincter of Boyden controls the flow of  bile  from the  common bile duct  into the  pancreatic duct . [ 1 ]  This helps with filling of the  gallbladder  with  bile ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6389", "text": "Its contractions regulate the passage of bile into the  gall bladder  or the  duodenum . [ 4 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6390", "text": "This is named after the American anatomist  Edward Allen Boyden  (1886-1976)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6391", "text": "The  sphincter of Oddi  (also  hepatopancreatic sphincter  or  Glisson's sphincter ), abbreviated as  SO , [ 1 ]  is a muscular valve that in some animals, including humans, controls the flow of  bile  and  pancreatic juice  out of the gallbladder and pancreas respectively through the  ampulla of Vater  into the second part of the  duodenum . It is named after  Ruggero Oddi ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6392", "text": "The sphincter of Oddi is a circular muscle band ( sphincter ) that surrounds the  major duodenal papilla . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6393", "text": "The sphincter regulates the secretion of pancreatic juice and bile into the duodenum. [ 3 ]  It also prevents reflux of duodenal contents into the ampulla of Vater. [ 4 ]  By preventing reflux of the contents of the duodenum, the sphincter of Oddi prevents the accumulation of particulate matter and sludge in the bile ducts, reducing the risk of  cholangitis . The sphincter of Oddi also allows retrograde filling of the gallbladder. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6394", "text": "The sphincter of Oddi is relaxed by the hormone  cholecystokinin [ 6 ] [ 7 ]  via  vasoactive intestinal peptide . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6395", "text": "Pancreatitis  can result from a failure of pancreatic secretions to drain properly. One possible cause of impaired drainage of pancreatic juice is blockage of the sphincter of Oddi. A common cause of blockage is a  gallstone  in the  common bile duct . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6396", "text": "Opiates may cause spasms of the sphincter of Oddi, leading to increased serum amylase levels. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6397", "text": "The sphincter was described for the first time by  Ruggero Oddi  when he was a young student in 1887. [ 10 ]  This description followed extensive research into the physiology of dogs and detailed  histological  examinations of humans and many other species. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6398", "text": "In many mammals (including  mice ,  guinea pigs ,  dogs , and  opossums ), the  smooth muscle  around the  ampulla of Vater  does not form a sphincter. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6399", "text": "Spiral folds of cystic duct [ 2 ] [ 1 ]  (also known as the  spiral mucosal folds , [ 3 ]   spiral valves of Cina , [ citation needed ]   Amussat valve , or  Cina valves ) are a series of crescenteric, spirally arranged  mucosal  folds [ 4 ] [ 2 ]  in the proximal part of [ 2 ]  the  cystic duct . [ 4 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6400", "text": "The folds are 2-10 in number. They project into the lumen of the duct. They are continuous with the folds of the neck of the gallbladder. [ 4 ]  They are arranged in a somewhat spiral manner. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6401", "text": "The spiral valves are supported by underlying smooth  muscle  fibers. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6402", "text": "The function of the valves is not known. [ 4 ]  Since the structures' discovery, various functions have been proposed, including the structural support to the cystic duct, and moderation of the speed of passage of bile through the duct in either direction [ 3 ]  Their role has been commonly ascribed to the regulation of bile flow, however, [ 4 ] [ 3 ]  they may instead maintain patency of the duct (i.e. keep the duct open) [ 4 ] [ 5 ] [ 3 ]  as the duct is thin and tortuous and thus prone to kinking; the observation that the folds are more prominent in younger individuals in whom the duct is also thinner supports this hypothesis. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6403", "text": "The presence of the spiral folds, in combination with the tortuosity of the cystic duct, makes  endoscopic   cannulation  and  catheterization  of the cystic duct extremely difficult. The valves of Cina are susceptible to  lacerations  and were once a serious obstacle to the surgical canalization, which has since been overcome by newer technologies. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6404", "text": "On ultrasound, valves of Cina are echogenic. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6405", "text": "Stercobilin  is a  tetrapyrrolic   bile pigment  and is one end-product of  heme   catabolism . [ 1 ] [ 2 ]  It is the chemical responsible for the brown color of  human feces  and was originally isolated from feces in 1932. Stercobilin (and related  urobilin ) can be used as a marker for biochemical identification of fecal pollution levels in rivers. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6406", "text": "Stercobilin results from breakdown of the heme  moiety  of hemoglobin found in  erythrocytes  (red blood cells).  Macrophages  break down senescent erythrocytes and break the heme down into  biliverdin , which rapidly reduces to free  bilirubin . Bilirubin binds tightly to  plasma  proteins (especially  albumin ) in the blood stream and is transported to the liver, where it is conjugated with one or two  glucuronic acid  residues into  bilirubin diglucuronide , and secreted into the small intestine as  bile . In the small intestine, some bilirubin glucuronide is converted back to bilirubin via bacterial enzymes in the terminal ileum.  This bilirubin is further converted to colorless  urobilinogen  by the bacterial enzyme bilirubin reductase. [ 4 ]  Urobilinogen that remains in the colon can either be reduced to  stercobilinogen  and finally oxidized to stercobilin, or it can be directly reduced to stercobilin. Stercobilin is responsible for the brown color of human feces. Stercobilin is then excreted in the feces. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6407", "text": "In  obstructive jaundice , no bilirubin reaches the small intestine, meaning that there is no formation of stercobilinogen. The lack of stercobilin and other bile pigments causes feces to become clay-colored. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6408", "text": "An analysis of two infants suffering from  cholelithiasis  observed that a substantial amount of stercobilin was present in brown pigment gallstones. This study suggested that brown pigment gallstones could form spontaneously in infants suffering from bacterial infections of the biliary tract. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6409", "text": "A 1996 study by McPhee et al. suggested that stercobilin and other related pyrrolic pigments \u2014 including urobilin, biliverdin, and xanthobilirubic acid \u2014 has potential to function as a new class of HIV-1  protease inhibitors  when delivered at low micromolar concentrations. These pigments were selected due to a similarity in shape to the successful HIV-1 protease inhibitor  Merck  L-700,417 ( N , N -bis(2-hydroxy-1-indanyl)-2,6-diphenylmethyl-4-hydroxy-1,7-heptandiamide). Further research is suggested to study the pharmacological efficacy of these pigments. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6410", "text": "The  stomach  is a muscular,  hollow organ  in the  upper gastrointestinal tract  of  humans  and many other animals, including several  invertebrates . The stomach has a dilated structure and functions as a vital organ in the  digestive system . The stomach is involved in the  gastric phase of digestion , following the  cephalic phase  in which the sight and smell of food and the act of  chewing  are stimuli.  In the stomach a chemical breakdown of food takes place by means of secreted   digestive enzymes  and  gastric acid ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6411", "text": "The stomach is located between the  esophagus  and the  small intestine .  The  pyloric sphincter  controls the passage of partially digested food ( chyme ) from the stomach into the  duodenum , the first and shortest part of the small intestine, where  peristalsis  takes over to move this through the rest of the intestines."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6412", "text": "In the  human digestive system , the stomach lies between the  esophagus  and the  duodenum  (the first part of the  small intestine ). It is in the  left upper quadrant  of the  abdominal cavity . The top of the stomach lies against the  diaphragm . Lying behind the stomach is the  pancreas . A large double fold of visceral  peritoneum  called the  greater omentum  hangs down from the  greater curvature  of the stomach. Two  sphincters  keep the contents of the stomach contained; the  lower esophageal sphincter   (found in the cardiac region), at the junction of the esophagus and stomach, and the  pyloric sphincter  at the junction of the stomach with the duodenum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6413", "text": "The stomach is surrounded by  parasympathetic  (inhibitor) and  sympathetic  (stimulant)  plexuses  (networks of  blood vessels  and  nerves  in the  anterior  gastric,  posterior ,  superior  and  inferior , celiac and myenteric), which regulate both the secretory activity of the stomach and the motor (motion) activity of its muscles."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6414", "text": "The stomach is  distensible , and can normally expand to hold about one litre of food. [ 3 ]  In a newborn human baby the stomach will only be able to hold about 30 millilitres. The maximum stomach volume in adults is between 2 and 4 litres, [ 4 ] [ 5 ]  although volumes of up to 15 litres have been observed in extreme circumstances. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6415", "text": "The human stomach can be divided into four sections, beginning at the cardia followed by the fundus, the body and the pylorus. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6416", "text": "The cardia is defined as the region following the \"z-line\" of the  gastroesophageal junction , the point at which the  epithelium  changes from  stratified squamous  to  columnar . Near the cardia is the lower esophageal sphincter. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6417", "text": "The  stomach bed  refers to the structures upon which the  stomach rests in mammals. [ 10 ] [ 11 ]  These include the  tail of the pancreas ,  splenic artery , left  kidney , left  suprarenal gland ,  transverse colon  and its  mesocolon , and the  left crus of diaphragm , and the  left colic flexure . The term was introduced around 1896 by Philip Polson of the Catholic University School of Medicine, Dublin. However this was brought into disrepute by surgeon anatomist J Massey. [ 12 ] [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6418", "text": "The lesser curvature of the human stomach is supplied by the  right gastric artery  inferiorly and the  left gastric artery  superiorly, which also supplies the cardiac region. The greater curvature is supplied by the  right gastroepiploic artery  inferiorly and the  left gastroepiploic artery  superiorly. The fundus of the stomach, and also the upper portion of the greater curvature, is supplied by the  short gastric arteries , which arise from the splenic artery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6419", "text": "The two sets of  gastric lymph nodes  drain the stomach's tissue fluid into the lymphatic system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6420", "text": "Like the other parts of the  gastrointestinal wall , the human stomach wall from inner to outer, consists of a  mucosa ,  submucosa ,  muscular layer ,  subserosa  and  serosa . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6421", "text": "The inner part of the stomach wall is the  gastric mucosa  a mucous membrane that forms the lining of the stomach. the membrane consists of an outer layer of  columnar epithelium , a  lamina propria , and a thin layer of  smooth muscle  called the  muscularis mucosa . Beneath the mucosa lies the  submucosa , consisting of  fibrous connective tissue . [ 17 ]   Meissner's plexus  is in this layer interior to the oblique muscle layer. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6422", "text": "Outside of the submucosa lies the muscular layer. It consists of three layers of muscular fibres, with fibres lying at angles to each other. These are the inner oblique, middle circular, and outer longitudinal layers. [ 19 ]  The presence of the inner oblique layer is distinct from other parts of the gastrointestinal tract, which do not possess this layer. [ 20 ]  The stomach contains the thickest muscular layer consisting of three layers, thus maximum peristalsis occurs here."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6423", "text": "The  outer longitudinal layer  is responsible for moving the semi-digested food towards the pylorus of the stomach through muscular shortening."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6424", "text": "To the outside of the muscular layer lies a  serosa , consisting of layers of connective tissue continuous with the  peritoneum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6425", "text": "Smooth mucosa along the inside of the lesser curvature forms a passageway - the  gastric canal   that fast-tracks liquids entering the stomach, to the pylorus. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6426", "text": "The mucosa lining the stomach is lined with  gastric pits , which receive  gastric juice , secreted by between 2 and 7  gastric glands . [ citation needed ]  Gastric juice is an acidic fluid containing  hydrochloric acid  and digestive enzymes. [ 21 ]  The glands contains a number of cells, with the function of the glands changing depending on their position within the stomach. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6427", "text": "Within the body and fundus of the stomach lie the  fundic glands . In general, these glands are lined by column-shaped cells that secrete a protective layer of  mucus  and  bicarbonate . Additional cells present include  parietal cells  that secrete hydrochloric acid and  intrinsic factor ,  chief cells  that secrete  pepsinogen  (this is a precursor to pepsin- the highly acidic environment converts the pepsinogen to pepsin), and neuroendocrine cells that secrete  serotonin . [ 22 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6428", "text": "Glands differ where the stomach meets the esophagus and near the pylorus. [ 23 ]  Near the  gastroesophageal junction  lie  cardiac glands , which primarily secrete mucus. [ 22 ]  They are fewer in number than the other gastric glands and are more shallowly positioned in the mucosa. There are two kinds - either simple  tubular glands  with short ducts  or  compound racemose  resembling the  duodenal   Brunner's glands . [ citation needed ]  Near the pylorus lie  pyloric glands  located in the antrum of the pylorus. They secrete mucus, as well as  gastrin  produced by their  G cells . [ 24 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6429", "text": "About 20,000  protein-coding genes  are expressed in human cells and nearly 70% of these genes are expressed in the normal stomach. [ 25 ] [ 26 ]  Just over 150 of these genes are more specifically expressed in the stomach compared to other organs, with only some 20 genes being highly specific. The corresponding specific proteins expressed in stomach are mainly involved in creating a suitable environment for handling the digestion of food for uptake of nutrients. Highly stomach-specific proteins include  gastrokine-1  expressed in the mucosa;  pepsinogen  and  gastric lipase , expressed in  gastric chief cells ; and a gastric  ATPase  and  gastric intrinsic factor , expressed in  parietal cells . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6430", "text": "In the early part of the  development of the human embryo , the ventral part of the embryo abuts the  yolk sac . During the third week of development, as the embryo grows, it begins to surround parts of the yolk sac. The enveloped portions form the basis for the adult gastrointestinal tract. [ 28 ]  The sac is surrounded by a network of  vitelline arteries and veins . Over time, these arteries consolidate into the three main arteries that supply the developing gastrointestinal tract: the  celiac artery ,  superior mesenteric artery , and  inferior mesenteric artery . The areas supplied by these arteries are used to define the  foregut ,  midgut , and  hindgut . [ 28 ]  The surrounded sac becomes the primitive gut. Sections of this gut begin to differentiate into the organs of the gastrointestinal tract, and the esophagus, and stomach form from the foregut. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6431", "text": "As the stomach rotates during early development, the dorsal and ventral mesentery rotate with it; this rotation produces a space anterior to the expanding stomach called the greater sac, and a space posterior to the stomach called the lesser sac. After this rotation the dorsal mesentery thins and forms the greater  omentum , which is attached to the greater curvature of the stomach. The ventral mesentery forms the lesser omentum, and is attached to the developing  liver . In the adult, these connective structures of omentum and mesentery form the  peritoneum , and act as an insulating and protective layer while also supplying organs with  blood  and lymph vessels as well as nerves. [ 29 ]  Arterial supply to all these structures is from the  celiac trunk , and venous drainage is by the  portal venous system . Lymph from these organs is drained to the prevertebral celiac nodes at the origin of the celiac artery from the  aorta ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6432", "text": "In the  human digestive system , a  bolus  (a small rounded mass of  chewed up  food) enters the stomach through the  esophagus  via the  lower esophageal sphincter . The stomach releases  proteases  (protein-digesting  enzymes  such as  pepsin ), and  hydrochloric acid , which kills or inhibits  bacteria  and provides the acidic  pH  of 2 for the  proteases  to work. Food is churned by the stomach through  peristaltic  muscular contractions of the wall \u2013 reducing the volume of the bolus, before looping around the fundus [ 30 ]  and the  body of stomach  as the boluses are converted into  chyme  (partially digested food). Chyme slowly passes through the  pyloric sphincter  and into the  duodenum  of the  small intestine , where the extraction of nutrients begins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6433", "text": "Gastric juice  in the stomach also contains  pepsinogen .  Hydrochloric acid  activates this inactive form of enzyme into the active form, pepsin. Pepsin breaks down proteins into  polypeptides ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6434", "text": "Within a few moments after food enters the stomach, mixing waves begin to occur at intervals of approximately 20 seconds. A mixing wave is a unique type of  peristalsis  that mixes and softens the food with gastric juices to create chyme. The initial mixing waves are relatively gentle, but these are followed by more intense waves, starting at the body of the stomach and increasing in force as they reach the pylorus."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6435", "text": "The pylorus, which holds around 30 mL of chyme, acts as a filter, permitting only liquids and small food particles to pass through the mostly, but not fully, closed  pyloric sphincter . In a process called  gastric emptying , rhythmic mixing waves force about 3 mL of chyme at a time through the pyloric sphincter and into the duodenum. Release of a greater amount of chyme at one time would overwhelm the capacity of the small intestine to handle it. The rest of the chyme is pushed back into the body of the stomach, where it continues mixing. This process is repeated when the next mixing waves force more chyme into the duodenum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6436", "text": "Gastric emptying is regulated by both the stomach and the duodenum. The presence of chyme in the duodenum activates receptors that inhibit gastric secretion. This prevents additional chyme from being released by the stomach before the duodenum is ready to process it. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6437", "text": "The fundus stores both undigested food and gases that are released during the process of chemical digestion. Food may sit in the fundus of the stomach for a while before being mixed with the chyme. While the food is in the fundus, the digestive activities of  salivary amylase  continue until the food begins mixing with the acidic chyme. Ultimately, mixing waves incorporate this food with the chyme, the acidity of which inactivates salivary amylase and activates  lingual lipase . Lingual lipase then begins breaking down triglycerides into free fatty acids, and mono- and diglycerides."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6438", "text": "The breakdown of protein begins in the stomach through the actions of hydrochloric acid, and the enzyme  pepsin ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6439", "text": "The stomach can also produce  gastric lipase , which can help digesting fat."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6440", "text": "The contents of the stomach are completely emptied into the duodenum within two to four hours after the meal is eaten. Different types of food take different amounts of time to process. Foods heavy in carbohydrates empty fastest, followed by high-protein foods. Meals with a high triglyceride content remain in the stomach the longest. Since enzymes in the small intestine digest fats slowly, food can stay in the stomach for 6 hours or longer when the duodenum is processing fatty chyme. However, this is still a fraction of the 24 to 72 hours that full digestion typically takes from start to finish. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6441", "text": "Although the absorption in the human digestive system is mainly a function of the small intestine, some absorption of certain small molecules nevertheless does occur in the stomach through its lining. This includes:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6442", "text": "The  parietal cells  of the human stomach are responsible for producing  intrinsic factor , which is necessary for the absorption of  vitamin B12 . B12 is used in cellular metabolism and is necessary for the production of  red blood cells , and the functioning of the  nervous system ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6443", "text": "Chyme from the stomach is slowly released into the  duodenum  through coordinated  peristalsis  and opening of the pyloric sphincter. The movement and the flow of chemicals into the stomach are controlled by both the  autonomic nervous system  and by the various  digestive hormones  of the digestive system:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6444", "text": "Other than gastrin, these hormones all act to turn off the stomach action. This is in response to food products in the  liver  and gall bladder, which have not yet been absorbed. The stomach needs to push food into the small intestine only when the intestine is not busy. While the intestine is full and still digesting food, the stomach acts as storage for food."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6445", "text": "Epidermal growth factor  (EGF) results in cellular proliferation, differentiation, and survival. [ 36 ]   EGF is a low-molecular-weight polypeptide first purified from the mouse submandibular gland, but since then found in many human tissues including the  submandibular gland , and the  parotid gland . Salivary EGF, which also seems to be regulated by dietary inorganic  iodine , also plays an important physiological role in the maintenance of oro-esophageal and gastric tissue integrity. The biological effects of salivary EGF include healing of oral and gastroesophageal ulcers, inhibition of gastric acid secretion, stimulation of DNA synthesis, and mucosal protection from intraluminal injurious factors such as gastric acid, bile acids, pepsin, and trypsin and from physical, chemical, and bacterial agents. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6446", "text": "The human stomach has  receptors responsive to  sodium glutamate [ 38 ]  and this information is passed to the  lateral hypothalamus  and  limbic system  in the  brain  as a  palatability  signal through the  vagus nerve . [ 39 ]  The stomach can also sense, independently of tongue and oral taste receptors,  glucose , [ 40 ]   carbohydrates , [ 41 ]   proteins , [ 41 ]  and  fats . [ 42 ]  This allows the brain to link  nutritional  value of foods to their tastes. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6447", "text": "This syndrome defines the association between thyroid disease and chronic gastritis, which was first described in the 1960s. [ 43 ]  This term was coined also to indicate the presence of thyroid autoantibodies or autoimmune thyroid disease in patients with pernicious anemia, a late clinical stage of atrophic gastritis. [ 44 ]  In 1993, a more complete investigation on the stomach and thyroid was published, [ 45 ]  reporting that the thyroid is, embryogenetically and  phylogenetically, derived from a primitive stomach, and that the thyroid cells, such as primitive gastroenteric cells, migrated and specialized in uptake of iodide and in storage and elaboration of iodine compounds during vertebrate evolution. In fact, the stomach and thyroid share iodine-concentrating ability and many morphological and functional similarities, such as cell polarity and apical microvilli, similar organ-specific antigens and associated autoimmune diseases, secretion of glycoproteins (thyroglobulin and mucin) and peptide hormones, the digesting and readsorbing ability, and lastly, similar ability to form iodotyrosines by peroxidase activity, where iodide acts as an electron donor in the presence of H 2 O 2 . In the following years, many researchers published reviews about this syndrome. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6448", "text": "A  series of radiographs  can be used to examine the stomach for various disorders. This will often include the use of a  barium swallow . Another method of examination of the stomach, is the use of an  endoscope . A  gastric emptying study  is considered the gold standard to assess the gastric emptying rate. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6449", "text": "A large number of studies have indicated that most cases of  peptic ulcers , and  gastritis , in humans are caused by  Helicobacter pylori  infection, and an association has been seen with the development of  stomach cancer . [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6450", "text": "A  stomach rumble  is actually noise from the intestines."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6451", "text": "In humans, many  bariatric surgery  procedures involve the stomach, in order to lose weight. A  gastric band  may be placed around the cardia area, which can adjust to limit intake. The  anatomy of the stomach may be modified , or the stomach may be  bypassed entirely ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6452", "text": "Surgical removal of the stomach is called a  gastrectomy , and removal of the cardia area is a called a  cardiectomy .  \"Cardiectomy\" is a term that is also used to describe the removal of the  heart . [ 49 ] [ 50 ] [ 51 ]  A gastrectomy may be carried out because of gastric cancer or severe perforation of the stomach wall."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6453", "text": "Fundoplication  is stomach surgery in which the fundus is wrapped around the lower esophagus and stitched into place.  It is used to treat  gastroesophageal reflux disease (GERD) . [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6454", "text": "The word  stomach  is derived from  Greek   stomachos  ( \u03c3\u03c4\u03cc\u03bc\u03b1\u03c7\u03bf\u03c2 ), ultimately from  stoma  ( \u03c3\u03c4\u03cc\u03bc\u03b1 ) 'mouth'. [ 53 ]   Gastro-  and  gastric  (meaning 'related to the stomach') are both derived from Greek  gaster  ( \u03b3\u03b1\u03c3\u03c4\u03ae\u03c1 ) 'belly'. [ 54 ] [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6455", "text": "Although the precise shape and size of the stomach varies widely among different vertebrates, the relative positions of the esophageal and duodenal openings remain relatively constant. As a result, the organ always curves somewhat to the left before curving back to meet the pyloric sphincter. However,  lampreys ,  hagfishes ,  chimaeras ,  lungfishes , and some  teleost  fish have no stomach at all, with the esophagus opening directly into the intestine. These animals all consume diets that require little storage of food, no predigestion with gastric juices, or both. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6456", "text": "The gastric lining is usually divided into two regions, an anterior portion lined by fundic glands and a posterior portion lined with pyloric glands. Cardiac glands are unique to  mammals , and even then are absent in a number of species. The distributions of these glands vary between species, and do not always correspond with the same regions as in humans. Furthermore, in many non-human mammals, a portion of the stomach anterior to the cardiac glands is lined with epithelium essentially identical to that of the esophagus.  Ruminants , in particular, have a complex four-chambered stomach. The first three chambers ( rumen ,  reticulum , and  omasum ) are all lined with esophageal mucosa, [ 57 ]  while the final chamber functions like a  monogastric  stomach, which is called the  abomasum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6457", "text": "In  birds  and  crocodilians , the stomach is divided into two regions. Anteriorly is a narrow tubular region, the  proventriculus , lined by fundic glands, and connecting the true stomach to the  crop . Beyond lies the powerful muscular  gizzard , lined by pyloric glands, and, in some species, containing stones that the animal swallows to help grind up food. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6458", "text": "In  insects , there is also a crop. The insect stomach is called the  midgut ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6459", "text": "Information about the stomach in  echinoderms  or  molluscs  can be found under the respective articles."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6460", "text": "A  stomach rumble , also known as a  bowel sound ,  peristaltic sound ,  abdominal sound ,  bubble gut  or  borborygmus  (pronounced  / \u02cc b \u0254\u02d0r b \u0259 \u02c8 r \u026a \u0261 m \u0259 s / ; plural  borborygmi ), is a rumbling, growling or gurgling noise produced by movement of the contents of the  gastrointestinal tract  as they are propelled through the  small intestine  by a series of  muscle contractions  called  peristalsis . [ 1 ]  A trained healthcare provider can listen to these intestinal noises with a  stethoscope , but they may be audible enough to be heard with the naked ear as the fluid and gas move forward in the  intestines  (in the vicinity of, but not actually within the  stomach ). The lack of bowel sounds is indicative of  ileus ,  intestinal obstruction , or some other serious pathology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6461", "text": "The scientific name borborygmus is related to the 16th-century French word  borborygme , itself from Latin, ultimately from Ancient Greek \u03b2\u03bf\u03c1\u03b2\u03bf\u03c1\u03c5\u03b3\u03bc\u03cc\u03c2 ( borborygm\u00f3s ). The Greek term is probably   onomatopoetic  in origin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6462", "text": "Other causes of stomach rumbles:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6463", "text": "If symptoms are minimal, treat by:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6464", "text": "Avoid foods such as beans and peas along with coarse grains and dried fruits. Limiting consumption of coffee, tea, and alcohol is recommended."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6465", "text": "The word  borborygmic  has been used in literature to describe noisy plumbing. In  Ada ,  Vladimir Nabokov  wrote: \"All the toilets and waterpipes in the house had been suddenly seized with borborygmic convulsions\".\nIn  A Long Way Down  (New York: Harper, 1959, p.\u00a054), Elizabeth Fenwick wrote: \"The room was very quiet, except for its borborygmic old radiator\". [ 6 ] \n Graham Greene 's  short story  \" Alas, Poor Maling \" tells the tale of a luckless individual whose borborygmus takes the form of irritating noises that he has recently heard."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6466", "text": "The word  borborygmus  has also been used in journalism to describe political turbulence. In an article in  The Atlantic ,  Graeme Wood [ 7 ]  used the word to describe the effects of mass refugee migration into Europe: \"Central Europe had to digest a massive refugee flow from Syria and Afghanistan, and the resulting borborygmus upended European politics and enabled a populist wave that has yet to crest.\""}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6467", "text": "The  submucosa  (or  tela submucosa ) is a thin layer of  tissue  in various  organs  of the  gastrointestinal ,  respiratory , and  genitourinary  tracts. It is the layer of  dense irregular connective tissue  that supports the mucosa ( mucous membrane ) and joins it to the  muscular layer , the bulk of overlying  smooth muscle  (fibers running circularly within layer of longitudinal muscle)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6468", "text": "The submucosa ( sub-  +  mucosa ) is to a mucous membrane what the  subserosa  ( sub-  +  serosa ) is to a  serous membrane ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6469", "text": "Blood vessels ,  lymphatic vessels , and  nerves  (all supplying the  mucosa ) will run through here. In the intestinal wall, tiny  parasympathetic  ganglia are scattered around forming the  submucous plexus  (or \"Meissner's plexus\") where  preganglionic  parasympathetic neurons synapse with  postganglionic  nerve fibers that supply the  muscularis mucosae . Histologically, the wall of the alimentary canal shows four distinct layers (from the lumen moving out): mucosa, submucosa, muscularis externa, and either a  serous membrane  or an  adventitia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6470", "text": "In the  gastrointestinal tract  and the  respiratory tract  the submucosa contains the  submucosal glands  that secrete  mucus ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6471", "text": "Identification of the submucosa plays an important role in diagnostic and therapeutic  endoscopy , where special  fibre-optic  cameras are used to perform procedures on the  gastrointestinal tract .  Abnormalities of the submucosa, such as  gastrointestinal stromal tumors , usually show integrity of the mucosal surface."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6472", "text": "The submucosa is also identified in  endoscopic ultrasound  to identify the depth of tumours and to identify other abnormalities.  An injection of  dye ,  saline , or  epinephrine  into the submucosa is imperative in the safe removal of certain  polyps ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6473", "text": "Endoscopic mucosal  resection  involves removal of the mucosal layer, and in order to be done safely, a submucosal injection of dye is performed to ensure integrity at the beginning of the procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6474", "text": "Female uterine submucosal layers are liable to develop fibroids during pregnancy and are often excised upon discovery. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6475", "text": "Small intestinal  submucosa (SIS) is submucosal  tissue  in the  small intestines  of  vertebrates .  SIS is harvested (typically from pigs) for  transplanted  structural material in several  clinical  applications, typically  biologic meshes . They have low  immunogenicity .  Some uses under investigation include a  scaffold  for  intervertebral disc  regeneration. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6476", "text": "Unlike other scaffold materials, the  resorbable  SIS  extracellular matrix  (SIS-ECM) scaffold is replaced by well-organized host tissues, including differentiated  skeletal muscle . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6477", "text": "A scientific article published in March 2018 [ 5 ]  proposed a revision of the anatomical definition of the submucosa. They first saw a non compact tissue which should be submucosa using a technology called  endomicroscopy . They hypothesised that the submucosa was not compact as it was previously seen on histological analysis but form a reticular pattern. To confirm their findings, they performed fixed samples of bile duct into a freezing media in order to conserve the shape of the submucosa. They then performed a histological analysis and with several staining techniques, they described the submucosa as a network of collagenous bands separating open, formerly  fluid-filled spaces. Theses spaces are bordered by fibroblast-like cells  CD34  positive. However, these cells are devoid of ultrastructural features indicative of endothelial differentiation, including pinocytotic vesicles and Weibel-Palade bodies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6478", "text": "The  suspensory muscle of duodenum  (also known as  suspensory ligament of duodenum ,  Treitz's muscle  or  ligament of Treitz [ 1 ] ) is a thin  muscle  connecting the junction between the  duodenum  and  jejunum  (the  small intestine 's first and second parts, respectively), as well as the  duodenojejunal flexure  to  connective tissue  surrounding the  superior mesenteric  and  coeliac arteries . The suspensory muscle most often connects to both the third and fourth parts of the duodenum, as well as the duodenojejunal flexure, although the attachment is quite variable."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6479", "text": "The suspensory muscle marks the formal division between the duodenum and the jejunum. This division is used to mark the difference between the  upper and lower gastrointestinal tracts , which is relevant in  clinical medicine  as it may determine the source of gastrointestinal bleeding."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6480", "text": "The suspensory muscle is derived from  mesoderm  and plays a role in the  embryological  rotation of the gut, by offering a point of fixation for the rotating gut. It is also thought to help digestion by widening the angle of the duodenojejunal flexure.  Superior mesenteric artery syndrome  is a rare abnormality caused by a congenitally short suspensory muscle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6481", "text": "The  duodenum  and the  jejunum  are the first and second parts of the  small intestine , respectively. The suspensory muscle of the duodenum marks their formal division. [ 2 ]  The suspensory muscle arises from the  right crus  of the  diaphragm  as it passes around the  esophagus , continues as  connective tissue  around the stems of the  celiac trunk  (celiac artery) and  superior mesenteric artery , passes behind the  pancreas , and enters the upper part of the  mesentery , inserting into the junction between the duodenum and jejunum, the duodenojejunal flexure. [ 3 ]  Here, the muscles are continuous with the muscular layers of the duodenum. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6482", "text": "Considerable  anatomic variation  exists, in terms of length and point of attachment. [ 4 ]  Despite the classical description, the muscle only solely attaches to the duodenojejunal flexure in about 8% of people; it is far more common, 40 to 60% of the time to attach additionally to the third and fourth parts of the duodenum; and 20 to 30%  of the time it only attaches to the third and fourth parts. Moreover, separate multiple attachments are not that uncommon. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6483", "text": "According to some authors, who use the original description by Treitz, the muscle may be divided into two sections: a ligamentous portion attaching the  right crus of diaphragm  to the connective tissue surrounding the  coeliac artery  and superior mesenteric artery; and a lower muscular portion from the connective tissue attaching to the duodenum. The superior portion is also described as the  Hilfsmuskel . [ 3 ] [ 4 ]  These two parts are now considered anatomically distinct, with the  suspensory muscle  referring solely to the lower structure attaching at the duodenum. [ 1 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6484", "text": "The ligament contains a slender band of skeletal muscle from the diaphragm and a fibromuscular band of smooth muscle from the horizontal and ascending parts of the duodenum. When it contracts, by virtue of connections to the third and fourth parts of the duodenum, the suspensory muscle of the duodenum widens the angle of the duodenojejunal flexure, allowing movement of the intestinal contents. [ 1 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6485", "text": "Embryologically , the suspensory muscle of the duodenum is derived from  mesoderm . It plays an important role in the embryological rotation of the small intestine as the superior retention band. [ 1 ] [ 3 ] :\u200a48"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6486", "text": "This ligament is an important  anatomical  landmark of the duodenojejunal flexure, separating the  upper and lower gastrointestinal tracts . For example,  bloody vomit  or  melena , black tarry stools, usually indicate a gastrointestinal bleed from a location in the upper gastrointestinal tract. In contrast,  hematochezia , bright red blood or clots in the stool, usually indicates gastrointestinal bleeding from the lower part of the gastrointestinal tract. [ 6 ]  It is an especially important landmark to note when looking at the bowel for the presence of  malrotation of the gut , a syndrome often suspected in young children when they have episodes of recurrent vomiting. Visualising a normal location of the ligament of Treitz in radiological images is critical in ruling out malrotation of the gut in a child;  it is abnormally located when malrotation is present. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6487", "text": "During a  Whipple's procedure , commonly used to treat  pancreatic cancer  by removing the  pancreas , duodenum, and part of the jejunum, the ligament of Treitz is separated from the duodenum and preserved. When the remaining jejunum is  anastamosed  with the  pylorus  of the  stomach , it may be passed through the ligament. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6488", "text": "Superior mesenteric artery syndrome  (SMA) is an extremely rare life-threatening condition that can either be congenital and chronic, or induced and acute. SMA Syndrome is characterised by compression of the duodenum between the  abdominal aorta  and the superior mesenteric artery, and may\u2014when congenital\u2014result from a short suspensory muscle. One surgical treatment is  Strong's operation , which involves cutting the suspensory muscle, though this is not often carried out. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6489", "text": "The suspensory muscle of the duodenum was first named in 1853 by  V\u00e1clav Treitz , as the  musculus suspensorius duodeni  (in Latin), and described as consisting of a lower muscular portion with a broad base, and an upper tendinous portion blending with connective tissue around the origins of the superior mesenteric and coeliac arteries. It is commonly termed the  ligament of Treitz  by  clinicians  and as the  suspensory muscle of the duodenum  by  anatomists . It has also been likened to \"a  polar ice cap \u00a0... a structure that many refer to but few have seen.\" [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6490", "text": "Synbiotics  refer to  food ingredients  or  dietary supplements  combining  probiotics  and  prebiotics  in a form of  synergism , hence synbiotics. [ 1 ]  The synbiotic concept was first introduced as \"mixtures of probiotics and prebiotics that beneficially affect the host by improving the survival and implantation of live microbial dietary supplements in the  gastrointestinal tract , by selectively stimulating the growth and/or by activating the metabolism of one or a limited number of health-promoting  bacteria , thus improving host welfare\". [ 2 ]  As of 2018, the research on this concept is preliminary, with no high-quality evidence from  clinical research  that such benefits exist."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6491", "text": "Synbiotics may be complementary synbiotics, where each component is independently chosen for its potential effect on host health, or synergistic synbiotics, where the prebiotic component is chosen to support the activity of the chosen probiotic. [ 3 ]  Research is evaluating if synbiotics can be optimized, (known as 'optibiotics') [ 3 ]  which are purported to enhance the growth and health benefits of existing probiotics. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6492", "text": "Probiotics are live bacteria which are intended to colonize the large intestine, although as of 2018, there is no evidence that adding dietary bacteria to healthy people has any added effect. [ 5 ]  A prebiotic is a food or dietary supplement product that may induce the growth or activity of beneficial microorganisms. A prebiotic may be a  fiber , but a fiber is not necessarily a prebiotic. [ 3 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6493", "text": "Using prebiotics and probiotics in combination may be described as synbiotic, but the  United Nations Food & Agriculture Organization   recommends that the term \"synbiotic\" be used only if the net health benefit is synergistic. [ 7 ]  Synbiotic formulations in combination with pasteurized breast milk are under preliminary clinical research for their potential to ameliorate  necrotizing enterocolitis  in infants, although there was insufficient evidence to warrant recommending synbiotics for this use as of 2016. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6494", "text": "TNO (gastro-) Intestinal Models  (\u201cTIM\u201d) is a system of models mimicking the digestive tract. The system was developed by TNO, the  Netherlands Organisation for Applied Scientific Research . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6495", "text": "The models are dynamic computer controlled multi-compartmental systems with adjustable parameters for the physiological conditions of the stomach and intestine. Temperature, peristalsis, bile secretion, secretion of saliva, stomach and pancreas enzymes are all fully adjustable. \nThe TIM systems are being used to study the behavior of oral products during transit through the stomach, the small intestine and large intestine. Commonly performed studies concern the digestibility of food and food components, the bioaccessibility for absorption of pharmaceutical compounds, proteins, fat, minerals and (water- and fat-soluble) vitamins.  [ 2 ] \n [ 3 ] \n [ 4 ] \n [ 5 ] \n [ 6 ] \n [ 7 ] \n [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6496", "text": "There are different models for the stomach and small intestine ( TIM-1  and  Tiny-TIM ) and a model simulating the physiological conditions of the  colon  ( TIM-2 )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6497", "text": "The  TIM-1  system consists of a stomach compartment and 3 compartments for the  small intestine , the duodenum, jejunum and ileum. The  Tiny-TIM  system consists of a stomach compartment and one single compartment for the small intestine. Samples can be harvested for analysis from these models from any compartment at any time."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6498", "text": "TIM-2  simulates the colon, containing the  microbiota  as found in human colon. This model serves as a tool to study fermentation of non-digestible food components (fibers and prebiotics) and the release of drugs  specifically targeted for the colon. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6499", "text": "The  tongue  is a  muscular   organ  in the  mouth  of a typical  tetrapod . It manipulates food for chewing and swallowing as part of the  digestive process , and is the primary organ of taste. The tongue's upper surface (dorsum) is covered by  taste buds  housed in numerous  lingual papillae . It is sensitive and kept moist by  saliva  and is richly supplied with  nerves  and  blood vessels . The tongue also serves as a natural means of cleaning the teeth. [ 2 ]  A major function of the tongue is to enable speech in humans and  vocalization  in other animals."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6500", "text": "The human tongue is divided into two parts, an  oral  part at the front and a  pharyngeal  part at the back. The left and right sides are also separated along most of its length by a vertical section of  fibrous tissue  (the  lingual septum ) that results in a groove, the median sulcus, on the tongue's surface."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6501", "text": "There are two groups of glossal muscles. The four intrinsic muscles alter the shape of the tongue and are not attached to bone. The four paired extrinsic muscles change the position of the tongue and are anchored to bone."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6502", "text": "The word  tongue  derives from the  Old English   tunge , which comes from  Proto-Germanic  * tung\u014dn . [ 3 ]  It has  cognates  in other  Germanic languages \u2014for example  tonge  in  West Frisian ,  tong  in  Dutch  and  Afrikaans ,  Zunge  in  German ,  tunge  in  Danish  and  Norwegian , and  tunga  in  Icelandic ,  Faroese  and  Swedish . The  ue  ending of the word seems to be a fourteenth-century attempt to show \"proper pronunciation\", but it is \"neither etymological nor phonetic\". [ 3 ]  Some used the spelling  tunge  and  tonge  as late as the sixteenth century."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6503", "text": "The tongue is a  muscular hydrostat  that forms part of the floor of the  oral cavity . The left and right sides of the tongue are separated by a vertical section of fibrous tissue known as the  lingual septum . This division is along the length of the tongue save for the very back of the pharyngeal part and is visible as a groove called the median sulcus. The human tongue is divided into  anterior and posterior  parts by the terminal sulcus, which is a \"V\"-shaped groove. The apex of the terminal sulcus is marked by a blind foramen, the foramen cecum, which is a remnant of the median  thyroid diverticulum  in early  embryonic development . The anterior  oral  part is the visible part situated at the front and makes up roughly two-thirds the length of the tongue. The posterior  pharyngeal  part is the part closest to the  throat , roughly one-third of its length. These parts differ in terms of their  embryological development  and  nerve supply ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6504", "text": "The anterior tongue is, at its apex, thin and narrow. It is directed forward against the lingual surfaces of the lower  incisor  teeth. The posterior part is, at its root, directed backward, and connected with the  hyoid bone  by the  hyoglossi  and  genioglossi  muscles and the  hyoglossal membrane , with the  epiglottis  by three  glossoepiglottic folds  of mucous membrane, with the  soft palate  by the  glossopalatine arches , and with the  pharynx  by the  superior pharyngeal constrictor muscle  and the  mucous membrane . It also forms the anterior wall of the  oropharynx ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6505", "text": "The average length of the human tongue from the  oropharynx  to the tip is 10\u00a0cm. [ 4 ]  The average weight of the human tongue from adult males is 99g and for adult females 79g. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6506", "text": "In  phonetics  and  phonology , a distinction is made between the  tip  of the tongue and the  blade  (the portion just behind the tip).  Sounds made with the tongue tip are said to be  apical , while those made with the tongue blade are said to be  laminal ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6507", "text": "The upper surface of the tongue is called the dorsum, and is divided by a groove into symmetrical halves by the  median sulcus . The  foramen cecum  marks the end of this division (at about 2.5\u00a0cm from the root of the tongue) and the beginning of the  terminal sulcus . The foramen cecum is also the point of attachment of the  thyroglossal duct  and is formed during the descent of the  thyroid diverticulum  in  embryonic development ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6508", "text": "The terminal sulcus is a shallow groove that runs forward as a shallow groove in a  V  shape from the foramen cecum, forwards and outwards to the margins (borders) of the tongue. The terminal sulcus divides the tongue into a posterior  pharyngeal  part and an anterior  oral  part. The pharyngeal part is supplied by the  glossopharyngeal nerve  and the oral part is supplied by the  lingual nerve  (a branch of the mandibular branch (V3) of the  trigeminal nerve ) for somatosensory perception and by the  chorda tympani  (a branch of the  facial nerve ) for  taste perception ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6509", "text": "Both parts of the tongue develop from different  pharyngeal arches ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6510", "text": "On the undersurface of the tongue is a fold of mucous membrane called the  frenulum  that tethers the tongue at the midline to the floor of the mouth. On either side of the frenulum are small prominences called  sublingual caruncles  that the major salivary  submandibular glands  drain into."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6511", "text": "The eight muscles of the human tongue are classified as either  intrinsic  or  extrinsic . The four intrinsic muscles act to change the shape of the tongue, and are not attached to any bone. The four extrinsic muscles act to change the position of the tongue, and are anchored to bone."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6512", "text": "The four extrinsic muscles originate from bone and extend to the tongue. They are the  genioglossus , the  hyoglossus  (often including the  chondroglossus ) the  styloglossus , and the  palatoglossus . Their main functions are altering the tongue's position allowing for protrusion, retraction, and side-to-side movement. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6513", "text": "The genioglossus arises from the  mandible  and protrudes the tongue. It is also known as the tongue's \"safety muscle\" since it is the only muscle that propels the tongue forward."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6514", "text": "The hyoglossus, arises from the  hyoid bone  and retracts and depresses the tongue. The chondroglossus is often included with this muscle."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6515", "text": "The styloglossus arises from the  styloid process  of the  temporal bone  and draws the sides of the tongue up to create a trough for swallowing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6516", "text": "The palatoglossus arises from the  palatine aponeurosis , and depresses the  soft palate , moves the  palatoglossal fold  towards the midline, and elevates the back of the tongue during swallowing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6517", "text": "Four paired intrinsic muscles of the tongue originate and insert within the tongue, running along its length. They are the  superior longitudinal muscle , the  inferior longitudinal muscle , the  vertical muscle , and the  transverse muscle . These muscles alter the shape of the tongue by lengthening and shortening it, curling and uncurling its apex and edges as in  tongue rolling , and flattening and rounding its surface. This provides shape and helps facilitate speech, swallowing, and eating. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6518", "text": "The superior longitudinal muscle runs along the upper surface of the tongue under the mucous membrane, and functions to shorten and curl the tongue upward. It originates near the  epiglottis , at the  hyoid bone , from the median fibrous septum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6519", "text": "The inferior longitudinal muscle lines the sides of the tongue, and is joined to the styloglossus muscle. It functions to shorten and curl the tongue downward."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6520", "text": "The vertical muscle is located in the middle of the tongue, and joins the superior and inferior longitudinal muscles. It functions to flatten the tongue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6521", "text": "The transverse muscle divides the tongue at the middle, and is attached to the  mucous membranes  that run along the sides. It functions to lengthen and narrow the tongue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6522", "text": "The tongue receives its  blood  supply primarily from the  lingual artery , a branch of the  external carotid artery . The  lingual veins  drain into the  internal jugular vein . The floor of the mouth also receives its blood supply from the lingual artery. [ 6 ]  There is also a secondary blood supply to the root of tongue from the  tonsillar branch of the facial artery  and the  ascending pharyngeal artery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6523", "text": "An area in the neck sometimes called the  Pirogov triangle  is formed by the intermediate tendon of the  digastric muscle , the posterior border of the  mylohyoid muscle , and the  hypoglossal  nerve. [ 7 ] [ 8 ]  The lingual artery is a good place to stop severe  hemorrhage  from the tongue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6524", "text": "Innervation of the tongue consists of motor fibers,  special sensory  fibers for taste, and  general sensory  fibers for sensation. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6525", "text": "Innervation of taste and sensation is different for the anterior and posterior part of the tongue because they are derived from different embryological structures ( pharyngeal arch  1 and pharyngeal arches 3 and 4, respectively). [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6526", "text": "The tip of tongue drains to the submental nodes. The left and right halves of the anterior two-thirds of the tongue drains to  submandibular lymph nodes , while the posterior one-third of the tongue drains to the jugulo-omohyoid nodes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6527", "text": "The upper surface of the tongue is covered in  masticatory mucosa , a type of  oral mucosa , which is of  keratinized stratified squamous epithelium . Embedded in this are numerous  papillae , some of which house the  taste buds  and their  taste receptors . [ 10 ]  The lingual papillae consist of  filiform ,  fungiform ,  vallate  and  foliate papillae , [ 6 ]  and only the filiform papillae are not associated with any taste buds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6528", "text": "The tongue can divide itself in dorsal and ventral surface. The dorsal surface is a stratified squamous keratinized epithelium, which is characterized by numerous mucosal projections called papillae. [ 11 ]  The lingual papillae covers the dorsal side of the tongue towards the front of the terminal groove. The ventral surface is stratified squamous non-keratinized epithelium which is smooth. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6529", "text": "The tongue begins to develop in the fourth week of  embryonic development  from a median swelling \u2013 the  median tongue bud  (tuberculum impar) of the  first pharyngeal arch . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6530", "text": "In the fifth week a pair of  lateral lingual swellings , one on the right side and one on the left, form on the first pharyngeal arch. These lingual swellings quickly expand and cover the median tongue bud. They form the anterior part of the tongue that makes up two-thirds of the length of the tongue, and continue to develop through  prenatal development . The line of their fusion is marked by the  median sulcus . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6531", "text": "In the fourth week, a swelling appears from the second  pharyngeal arch , in the midline, called the  copula . During the fifth and sixth weeks, the copula is overgrown by a swelling from the third and fourth arches (mainly from the third arch) called the  hypopharyngeal eminence , and this develops into the posterior part of the tongue (the other third and the posterior most part of the tongue is developed from the fourth pharyngeal arch). The hypopharyngeal eminence develops mainly by the growth of  endoderm  from the third pharyngeal arch. The boundary between the two parts of the tongue, the anterior from the first arch and the posterior from the third arch is marked by the terminal sulcus. [ 13 ]  The terminal sulcus is shaped like a  V  with the tip of the V situated posteriorly. At the tip of the terminal sulcus is the  foramen cecum , which is the point of attachment of the  thyroglossal duct  where the embryonic  thyroid  begins to descend. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6532", "text": "Chemicals that stimulate  taste receptor  cells are known as  tastants . Once a tastant is dissolved in  saliva , it can make contact with the  plasma membrane  of the gustatory hairs, which are the sites of taste  transduction . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6533", "text": "The tongue is equipped with many  taste buds  on its  dorsal  surface, and each taste bud is equipped with taste receptor cells that can sense particular classes of tastes. Distinct types of taste receptor cells respectively detect substances that are sweet, bitter, salty, sour, spicy, or taste of  umami . [ 15 ]  Umami receptor cells are the least understood and accordingly are the type most intensively under research. [ 16 ]  There is a  common misconception  that different sections of the tongue are exclusively responsible for different  basic tastes . Although widely taught in schools in the form of the  tongue map , this is incorrect; all taste sensations come from all regions of the tongue, although certain parts are more sensitive to certain tastes. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6534", "text": "The tongue is an important accessory organ in the digestive system. The tongue is used for crushing food against the hard palate, during mastication and manipulation of food for softening prior to swallowing. The  epithelium  on the tongue's upper, or dorsal surface is  keratinised . Consequently, the tongue can grind against the hard palate without being itself damaged or irritated. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6535", "text": "The tongue is one of the primary articulators in the production of  speech , and this is facilitated by both the extrinsic muscles that move the tongue and the intrinsic muscles that change its shape. Specifically, different  vowels  are  articulated  by changing the tongue's height and retraction to alter the  resonant  properties of the  vocal tract . These resonant properties amplify specific  harmonic frequencies  ( formants ) that are different for each vowel, while attenuating other harmonics. For example, [a] is produced with the tongue  lowered and centered  and [i] is produced with the tongue  raised and fronted .  Consonants  are articulated by constricting airflow through the vocal tract, and many consonants feature a constriction between the tongue and some other part of the vocal tract. For example,  alveolar consonants  like [s] and [n] are articulated with the tongue against the  alveolar ridge , while  velar consonants  like [k] and [g] are articulated with the tongue dorsum against the soft palate (velum). Tongue shape is also relevant to speech articulation, for example in  retroflex consonants , where the tip of the tongue is curved backward."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6536", "text": "The tongue plays a role in  physical intimacy  and  sexuality . The tongue is part of the  erogenous zone  of the mouth and can be used in intimate contact, as in the  French kiss  and in  oral sex ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6537", "text": "A  congenital disorder  of the tongue is that of  ankyloglossia  also known as  tongue-tie . The tongue is  tied  to the floor of the mouth by a very short and thickened  frenulum  and this affects speech, eating, and swallowing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6538", "text": "The tongue is prone to several  pathologies  including  glossitis  and other  inflammations  such as  geographic tongue , and  median rhomboid glossitis ;  burning mouth syndrome ,  oral hairy leukoplakia ,  oral candidiasis  (thrush),  black hairy tongue , bifid tongue (due to failure in fusion of two lingual swellings of first pharyngeal arch) and  fissured tongue ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6539", "text": "There are several types of  oral cancer  that mainly affect the tongue. Mostly these are  squamous cell carcinomas . [ 19 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6540", "text": "Food debris,  desquamated   epithelial cells  and  bacteria  often form a visible tongue coating. [ 21 ]  This coating has been identified as a major factor contributing to  bad breath  (halitosis), [ 21 ]  which can be managed by using a  tongue cleaner ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6541", "text": "The  sublingual  region underneath the front of the tongue is an ideal location for the  administration  of certain medications into the body. The  oral mucosa  is very thin underneath the tongue, and is underlain by a plexus of veins. The sublingual route takes advantage of the highly  vascular  quality of the oral cavity, and allows for the speedy application of medication into the cardiovascular system, bypassing the gastrointestinal tract. This is the only convenient and efficacious  route of administration  (apart from  Intravenous therapy ) of  nitroglycerin  to a patient suffering chest pain from  angina pectoris ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6542", "text": "The muscles of the tongue evolved in  amphibians  from  occipital   somites . Most amphibians show a proper tongue after their  metamorphosis . [ 22 ]  As a consequence, most  tetrapod  animals\u2014amphibians, reptiles, birds, and mammals\u2014have tongues (the  frog  family of  pipids  lack tongue). In mammals such as  dogs  and  cats , the tongue is often used to clean the fur and body by  licking . The tongues of these species have a very rough texture, which allows them to remove oils and parasites. Some dogs have a tendency to consistently lick a part of their foreleg, which can result in a  skin condition  known as a  lick granuloma . A dog's tongue also acts as a heat regulator. As a dog increases its exercise the tongue will increase in size due to greater blood flow. The tongue hangs out of the dog's mouth and the moisture on the tongue will work to cool the bloodflow. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6543", "text": "Some animals have tongues that are specially adapted for catching prey. For example,  chameleons ,  frogs ,  pangolins  and  anteaters  have  prehensile  tongues."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6544", "text": "Other animals may have organs that are  analogous  to tongues, such as a  butterfly 's  proboscis  or a  radula  on a  mollusc , but these are not  homologous  with the tongues found in vertebrates and often have little resemblance in function. For example, butterflies do not lick with their proboscides; they suck through them, and the proboscis is not a single organ, but two jaws held together to form a tube. [ 25 ]  Many species of fish have small folds at the base of their mouths that might informally be called tongues, but they lack a muscular structure like the true tongues found in most  tetrapods . [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6545", "text": "The tongue can serve as a  metonym  for  language . For example, the  New Testament  of the Bible, in the Book of  Acts of the Apostles ,  Jesus ' disciples on the Day of  Pentecost  received a type of  spiritual gift : \"there appeared unto them cloven tongues like as of fire, and it sat upon each of them. And they were all filled with the  Holy Ghost , and began to speak with other tongues\u00a0....\", which amazed the crowd of  Jewish  people in  Jerusalem , who were from various parts of the  Roman Empire  but could now understand what was being preached. The phrase  mother tongue  is used as a child's first language.  Many languages [ 28 ]  have the same word for \"tongue\" and \" language \", as did the  English language  before the  Middle Ages ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6546", "text": "A common temporary failure in word  retrieval  from  memory  is referred to as the    tip-of-the-tongue   phenomenon . The expression  tongue in cheek  refers to a statement that is not to be taken entirely seriously \u2013 something said or done with subtle ironic or sarcastic humour. A  tongue twister  is a phrase very difficult to pronounce. Aside from being a  medical condition , \"tongue-tied\" means being unable to say what you want due to confusion or restriction. The phrase \"cat got your tongue\" refers to when a person is speechless. To \"bite one's tongue\" is a phrase which describes holding back an opinion to avoid causing offence. A \"slip of the tongue\" refers to an unintentional utterance, such as a  Freudian slip . The \"gift of tongues\" refers to when one is uncommonly gifted to be able to speak in a foreign language, often as a type of  spiritual gift .  Speaking in tongues  is a common phrase used to describe  glossolalia , which is to make smooth, language-resembling sounds that is no true spoken language itself. A deceptive person is said to have a  forked tongue , and a smooth-talking person is said to have a  silver tongue ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6547", "text": "Sticking one's tongue out at someone is considered a childish gesture of  rudeness  or defiance in many countries; the act may also have sexual connotations, depending on the way in which it is done. However, in  Tibet  it is considered a greeting. [ 29 ]  In 2009, a farmer from  Fabriano , Italy, was convicted and fined by  Italy's highest court  for sticking his tongue out at a neighbor with whom he had been arguing - proof of the affront had been captured with a cell-phone camera. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6548", "text": "Tongue piercing  and  splitting  have become more common in western countries in recent decades. [ when? ]  One study found that one-fifth of young adults in Israel had at least one type of oral piercing, most commonly the tongue. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6549", "text": "Protruding tongues appear in the art of several  Polynesian cultures . [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6550", "text": "The tongues of some animals are consumed and sometimes prized as delicacies. Hot-tongue sandwiches frequently appear on menus in  kosher   delicatessens  in America.  Taco de lengua  ( lengua  being Spanish for tongue) is a taco filled with  beef tongue , and is especially popular in Mexican cuisine. As part of Colombian gastronomy, Tongue in Sauce (Lengua en Salsa) is a dish prepared by frying the tongue and adding tomato sauce, onions and salt.  Tongue can also be prepared as  birria . Pig and beef tongue are consumed in Chinese cuisine.  Duck  tongues are sometimes employed in  Sichuan  dishes, while  lamb 's tongue is occasionally employed in Continental and contemporary American cooking. Fried  cod  \"tongue\" is a relatively common part of fish meals in  Norway  and in  Newfoundland . In  Argentina  and  Uruguay  cow tongue is cooked and served in vinegar ( lengua a la vinagreta ).  In the Czech Republic and in Poland, a pork tongue is considered a delicacy, and there are many ways of preparing it. In Eastern Slavic countries, pork and beef tongues are commonly consumed, boiled and garnished with horseradish or jellied; beef tongues fetch a significantly higher price and are considered more of a delicacy.  In Alaska, cow tongues are among the more common. Both cow and moose tongues are popular toppings on open-top-sandwiches in Norway, the latter usually amongst hunters."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6551", "text": "Tongues of seals and whales have been eaten, sometimes in large quantities, by sealers and whalers, and in various times and places have been sold for food on shore. [ 33 ] [ page\u00a0needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6552", "text": "This article incorporates text in the  public domain  from  page 1125  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6553", "text": "The  transverse folds of rectum  (or  Houston's valves  or  the valves of Houston ) are semi-lunar transverse folds of the   rectal  wall that protrude into the rectum, not the  anal canal  as that lies below the rectum. Their use seems to be to support the weight of  fecal matter , and prevent its urging toward the  anus , which would produce a strong urge to  defecate . Although the term rectum means straight, these transverse folds overlap each other during the empty state of the intestine to such an extent that, as Houston remarked, they require considerable maneuvering to conduct an instrument along the canal, as often occurs in  sigmoidoscopy  and  colonoscopy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6554", "text": "These folds are about 12\u00a0mm. in width and are composed of the circular muscle coat of the rectum. They are usually three in number; sometimes a fourth is found, and occasionally only two are present."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6555", "text": "Transverse folds were first described by Irish anatomist  John Houston , curator of the  Royal College of Surgeons in Ireland  Museum, in 1830. They appear to be peculiar to human physiology: Baur (1863) looked for Houston's valves in a number of mammals, including wolf, bear, rhinoceros, and several Old World primates, but found no evidence. They are formed very early during human development, and may be visible in embryos of as little as 55\u00a0mm in length (10 weeks of gestational age.) [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6556", "text": "This article incorporates text in the  public domain  from  page 1183  of\u00a0the 20th edition of   Gray's Anatomy   (1918)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6557", "text": "Ure2 , or Ure2p, is a  yeast  protein encoded by a  gene  known as  URE2  (systematic designation  YNL229C ).  The Ure2 protein can also form a yeast  prion  known as [URE3]. [ 1 ]  When Ura2p is expressed at high levels in yeast, it will readily convert from its native  protein conformation  into an aggregate known as an  amyloid . [URE3], along with  [PSI+] , were both determined by Wickner (1994) to meet the genetic definition of a yeast prion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6558", "text": "The gene prefix \"URE\" stands for ureidosuccinate transport, as the Ure2 protein in its native state is responsible for repressing nitrogen  catabolism  of  glutamine  by controlling the GLN3  transcription factor . Gln3p is retained in the cytoplasm by Ure2p when a preferred nitrogen source like ammonium sulfate is present in the growth media, but enters the nucleus when the cells are shifted to a nonpreferred source of nitrogen such as proline. [ 2 ]  Ure2 protein also plays a role in responding to  oxidative stress . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6559", "text": "Ure2p is a protein composed of 354  amino acids  and has a  molecular weight  of 40,226. Its gene,  URE2 , been mapped to chromosome XIV, 5  map units  from  KEX2 . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6560", "text": "Uroguanylin  is a 16  amino acid   peptide  that is secreted by  enterochromaffin cells  in the  duodenum  and proximal  small intestine . Guanylin acts as an  agonist  of the  guanylyl cyclase  receptor  guanylate cyclase 2C  (GC-C), and regulates  electrolyte  and  water  transport in  intestinal  and  renal   epithelia . By agonizing this guanylyl cyclase receptor, uroguanylin and guanylin cause intestinal secretion of chloride and bicarbonate to dramatically increase; this process is helped by the second messenger  cGMP . [ 1 ]  Its sequence is H-Asn-Asp-Asp-Cys(1)-Glu-Leu-Cys(2)-Val-Asn-Val-Ala-Cys(1)-Thr-Gly-Cys(2)-Leu-OH."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6561", "text": "In humans, the uroguanylin peptide is encoded by the  GUCA2B   gene . [ 2 ] [ 3 ]  Uroguanylin may be involved in appetite and perceptions of 'fullness' after eating meals, as suggested by a study into mice. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6562", "text": "This  biochemistry  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6563", "text": "The  appendix  ( pl. :  appendices  or  appendixes ; also  vermiform appendix ;   cecal  (or  caecal ,  c\u00e6cal )  appendix ;  vermix ; or  vermiform process ) is a finger-like, blind-ended tube connected to the  cecum , from which it  develops in the embryo ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6564", "text": "The cecum is a pouch-like structure of the  large intestine , located at the junction of the  small  and the large intestines. The term \" vermiform \" comes from  Latin  and means \"worm-shaped\". The appendix was once considered a  vestigial organ , but this view has changed since the early 2000s. [ 1 ] [ 2 ]  Research suggests that the appendix may serve an important purpose as a reservoir for beneficial  gut bacteria ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6565", "text": "The human appendix averages 9\u00a0cm (3.5\u00a0in) in length, ranging from 5 to 35\u00a0cm (2.0 to 13.8\u00a0in). The diameter of the appendix is 6\u00a0mm (0.24\u00a0in), and more than 6\u00a0mm (0.24\u00a0in) is considered a thickened or inflamed appendix. The longest appendix ever removed was 26\u00a0cm (10\u00a0in) long. [ 3 ]  The appendix is usually located in the lower right  quadrant  of the  abdomen , near the right  hip bone . The base of the appendix is located 2\u00a0cm (0.79\u00a0in) beneath the  ileocecal valve  that separates the large intestine from the small intestine. Its position within the abdomen corresponds to a point on the surface known as  McBurney's point ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6566", "text": "The appendix is connected to the  mesentery  in the lower region of the  ileum , by a short region of the  mesocolon  known as the  mesoappendix . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6567", "text": "Some identical twins\u2014known as  mirror image twins \u2014can have a  mirror-imaged anatomy , a  congenital condition  with the appendix located in the lower left quadrant of the abdomen instead of the lower right. [ 5 ] [ 6 ]   Intestinal malrotation  may also cause displacement of the appendix to the left side."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6568", "text": "While the base of the appendix is typically located 2\u00a0cm (0.79\u00a0in) below the  ileocecal valve , the tip of the appendix can be variably located\u2014in the  pelvis , outside the  peritoneum  or behind the cecum. [ 7 ]  The prevalence of the different positions varies amongst populations with the retrocecal position being most common in  Ghana  and  Sudan , with 67.3% and 58.3% occurrence respectively, in comparison to  Iran  and  Bosnia  where the pelvic position is most common, with 55.8% and 57.7% occurrence respectively. [ 8 ] [ 9 ] [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6569", "text": "In very rare cases, the appendix may not be present at all ( laparotomies  for suspected appendicitis have given a frequency of 1 in 100,000). [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6570", "text": "Sometimes there is a semi-circular fold of  mucous membrane  at the opening of the appendix. This  valve of the vermiform appendix  is also called  Gerlach's  valve. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6571", "text": "Although it has been long accepted that the immune tissue surrounding the appendix and elsewhere in the gut\u2014called  gut-associated lymphoid tissue \u2014carries out a number of important functions, explanations were lacking for the distinctive shape of the appendix and its apparent lack of specific importance and function as judged by an absence of side effects following  its removal . [ 13 ]  Therefore, the notion that the appendix is only  vestigial  became widely held."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6572", "text": "William Parker, Randy Bollinger, and colleagues at  Duke University  proposed in 2007 that the appendix serves as a haven for useful  bacteria  when illness flushes the bacteria from the rest of the intestines. [ 14 ] [ 15 ]  This proposition is based on an understanding that emerged by the early 2000s of how the immune system supports the growth of beneficial  intestinal bacteria , [ 16 ] [ 17 ]  in combination with many well-known features of the appendix, including its architecture, its location just below the normal one-way flow of food and germs in the large intestine, and its association with copious amounts of immune tissue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6573", "text": "Research performed at  Winthrop\u2013University Hospital  showed that individuals without an appendix were four times as likely to have a recurrence of  Clostridioides difficile  colitis . [ 18 ]  The appendix, therefore, may act as a \"safe house\" for beneficial bacteria. [ 14 ]  This reservoir of bacteria could then serve to repopulate the  gut flora  in the  digestive system  following a bout of  dysentery  or  cholera  or to boost it following a milder gastrointestinal illness. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6574", "text": "The appendix has been identified as an important component of mammalian  mucosal immune function , particularly  B cell -mediated immune responses and  extrathymically  derived  T cells . This structure helps in the proper movement and removal of waste matter in the digestive system, contains lymphatic vessels that regulate pathogens, and lastly, might even produce early defences that prevent deadly diseases. Additionally, it is thought that this may provide more immune defences from invading pathogens and getting the lymphatic system's B and T cells to fight the viruses and bacteria that infect that portion of the bowel and training them so that immune responses are targeted and more able to reliably and less dangerously fight off pathogens. [ 19 ]  In addition, there are different immune cells called  innate lymphoid cells  that function in the gut in order to help the appendix maintain digestive health. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6575", "text": "Research also shows a positive correlation between the existence of the appendix and the concentration of cecal lymphoid tissue, which supports the suggestion that not only does the appendix evolve as a complex with the cecum but also has major immune benefits. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6576", "text": "Common  diseases  of the appendix (in humans) are  appendicitis  and  carcinoid  tumors (appendiceal carcinoid). [ 22 ]   Appendix cancer  accounts for about 1 in 200 of all gastrointestinal malignancies. In rare cases,  adenomas  are also present. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6577", "text": "Appendicitis  is a condition characterized by  inflammation  of the appendix. Pain often begins in the center of the abdomen, corresponding to the appendix's development as part of the embryonic  midgut . This pain is typically a dull, poorly localized,  visceral  pain. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6578", "text": "As the inflammation progresses, the pain begins to localize more clearly to the right lower quadrant, as the  peritoneum  becomes inflamed. This peritoneal inflammation, or  peritonitis , results in  rebound tenderness  (pain upon removal of pressure rather than application of pressure). In particular, it presents at  McBurney's point , 1/3 of the way along a line drawn from the  anterior superior iliac spine  to the  umbilicus . Typically, point (skin) pain is not present until the  parietal peritoneum  is inflamed, as well. Fever and an immune system response are also characteristic of appendicitis. [ 24 ]  Other signs and symptoms may include  nausea  and vomiting, low-grade fever that may get worse,  constipation  or  diarrhea , abdominal bloating, or  flatulence . [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6579", "text": "Appendicitis usually requires the removal of the inflamed appendix, in an  appendectomy  either by  laparotomy  or  laparoscopy . Untreated, the appendix may rupture, leading to  peritonitis , followed by  shock , and, if still untreated, death. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6580", "text": "The surgical removal of the appendix is called an  appendectomy . This removal is normally performed as an emergency procedure when the patient is suffering from  acute  appendicitis. In the absence of surgical facilities,  intravenous   antibiotics  are used to delay or avoid the onset of  sepsis . In some cases, the appendicitis resolves completely; more often, an inflammatory mass forms around the appendix. This is a relative  contraindication  to surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6581", "text": "The appendix is also used for the construction of an efferent urinary conduit, in an operation known as the  Mitrofanoff procedure , [ 26 ]  in people with a  neurogenic bladder ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6582", "text": "The appendix is also used as a means to access the colon in children with paralysed bowels or major rectal sphincter problems. The appendix is brought out to the skin surface and the child/parent can then attach a catheter and easily wash out the colon (via normal defaecation) using an appropriate solution. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6583", "text": "Charles Darwin  suggested that the appendix was mainly used by earlier hominids for digesting fibrous vegetation, then evolved to take on a new purpose over time. The very long cecum of some herbivorous animals, such as in the  horse  or the  koala , appears to support this hypothesis. The koala's cecum enables it to host bacteria that specifically help to break down cellulose. Human ancestors may have also relied upon this system when they lived on a diet rich in foliage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6584", "text": "As people began to eat more easily digested foods, they may have become less reliant on cellulose-rich plants for energy. As the cecum became less necessary for digestion, mutations that were previously deleterious (and would have hindered evolutionary progress) were no longer important, so the mutations survived. It is suggested that these  alleles  became more frequent and the cecum continued to shrink. After millions of years, the once-necessary cecum degraded to be the appendix of modern humans. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6585", "text": "Dr. Heather F. Smith of  Midwestern University  and colleagues explained:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6586", "text": "Recently ... improved understanding of gut immunity has merged with current thinking in biological and medical science, pointing to an apparent function of the mammalian cecal appendix as a safe-house for symbiotic gut microbes, preserving the flora during times of gastrointestinal infection in societies without modern medicine. This function is potentially a selective force for the evolution and maintenance of the appendix.\nThree morphotypes of cecal-appendices can be described among mammals based primarily on the shape of the cecum: a distinct appendix branching from a rounded or sac-like cecum (as in many primate species), an appendix located at the apex of a long and voluminous cecum (as in the rabbit, greater glider and Cape dune mole rat), and an appendix in the absence of a pronounced cecum (as in the wombat). In addition, long narrow appendix-like structures are found in mammals that either lack an apparent cecum (as in monotremes) or lack a distinct junction between the cecum and appendix-like structure (as in the koala). A cecal appendix has evolved independently at least twice, and apparently represents yet another example of convergence in morphology between Australian marsupials and placentals in the rest of the world. Although the appendix has apparently been lost by numerous species, it has also been maintained for more than 80 million years in at least one clade. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6587", "text": "In a 2013 paper, the appendix was found to have independently evolved in different animals at least 32 times (and perhaps as many as 38 times) and to have been lost no more than six times over the course of history. [ 30 ]  A more recent study using similar methods on an updated database yielded similar, though less spectacular results, with at least 29 gains and at the most 12 losses (all of which were ambiguous), and this is still significantly asymmetrical. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6588", "text": "This suggests that the cecal appendix has a selective advantage in many situations and argues strongly against its vestigial nature. Given that this organ may have a selective advantage in numerous situations, it appears to be associated with greater maximal longevity, for a given body mass. [ 32 ]  For example, in a 2023 study, the protective functions conferred against diarrhea were observed in young primates. [ 33 ]  This complex evolutionary history of the appendix, along with a great heterogeneity in its evolutionary rate in various taxa, suggests that it is a recurrent trait. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6589", "text": "Such a function may be useful in a culture lacking modern sanitation and healthcare practice, where  diarrhea  may be prevalent. Current  epidemiological  data on the cause of death in developing countries collected by the  World Health Organization  in 2001 show that acute diarrhea is now the fourth leading cause of disease-related death in developing countries (data summarized by the  Bill and Melinda Gates Foundation ). Two of the other leading causes of death are expected to have exerted limited or no selection pressure. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6590", "text": "Zonulin  (haptoglobin 2 precursor) [ 1 ]  is a  protein  that increases the permeability of  tight junctions  between  cells  of the wall of the  digestive tract . [ 2 ]  It was discovered in 2000 by  Alessio Fasano  and his team at the  University of Maryland School of Medicine . As the mammalian analogue of  zonula occludens toxin , secreted by  cholera  pathogen  Vibrio cholerae , zonulin has been implicated in the pathogenesis of  coeliac disease  and  diabetes mellitus type 1 . [ 3 ]   Type 2 diabetic  patients have shown increased zonulin. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6591", "text": "Gliadin  (a glycoprotein present in  gluten ) activates zonulin signaling irrespective of the genetic expression of autoimmunity, leading to increased  intestinal permeability  of macromolecules. [ 3 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6592", "text": "Zonula occludens toxin is being studied as an adjuvant to improve absorption of drugs and vaccines. [ 6 ]  In 2014 a zonulin  receptor antagonist ,  larazotide acetate  (formerly known as AT-1001), completed a  phase 2b  clinical trial. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6593", "text": "Elie Abadie  ( Arabic :  \u0627\u064a\u0644\u064a \u0639\u0628\u0627\u062f\u064a ) is Senior Rabbi in the  Association of Gulf Jewish Communities  and Senior Rabbi in Residence of the  Jewish Council of the Emirates  (JCE). [ 1 ] [ 2 ] [ 3 ]  He is the former Director of the Jacob E. Safra Institute of Sephardic Studies at  Yeshiva University , with an area of interest on the topics of  Sephardic Judaism , history, philosophy, and comparative traditional law. He is a member of the board of the  American Sephardi Federation  and the World Sephardic Educational Center, and co-president of  Justice for Jews from Arab Countries . He is a former member of the Board and an Officer of the  Rabbinical Council of America  (RCA), the Treasurer/Vice-president of the  New York Board of Rabbis , and co-chair of the Sadat Congressional Gold Medal Committee. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6594", "text": "Abadie's parents were forced to flee  Aleppo, Syria , where his family had lived for millennia, under government pressure. [ 6 ]  Abadie explained his parents' flight from Syria:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6595", "text": "\u201cMy parents lived right next to the  synagogue . They saw people enter the synagogue, pillage it, torched it, took out the  Torah scrolls  and holy books and burnt them. My parents escaped from their home through the backdoor as people tried to get into my parents\u2019 house. They left and never returned.\u201d [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6596", "text": "Abadie was born in  Beirut , Lebanon in 1960. The Abadie family moved to  Mexico City  in 1971 after the  Palestinian Liberation Organization  relocated its headquarters from  Jordan  to Lebanon. They lived in Lebanon with no citizenship, as registered refugees, with identity documents reading \"stateless.\" Abadie's father, had his picture posted on walls around Beirut claiming he was a  Zionist leader , prompting his family's emigration. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6597", "text": "After moving to the United States in 1979 to attend Yeshiva University, he earned his  B.A . in  Health Sciences  in 1983, B.S.C. in 1984 in  Bible Studies , Hebrew Teacher's diploma in 1985, and a master's degree in  Jewish Philosophy  in 1986 from  Bernard Revel Graduate School of Yeshiva University . Abadie received his ordination in 1986 from  Rabbi Isaac Elchanan Theological Seminary . He attended  SUNY Downstate Medical Center , where he graduated in 1990 with an M.D. degree. He did his residency in  Internal Medicine , and later his fellowship in gastroenterology at  Maimonides Medical Center  where he finished in 1995. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6598", "text": "Abadie became a rabbi at  Congregation Beit Edmond  in 2001. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6599", "text": "He was the founding rabbi of Shaare Mizrah-Manhattan East Synagogue, the Head of School of the  Sephardic Academy of Manhattan , and the Spiritual Leader of the Moise Safra Community Center in Manhattan. From 2003 to 2017 he was the founding Rabbi and Spiritual Leader of the  Edmond J. Safra Synagogue  in New York City (now Congregation Beit Edmond), one of the largest Sephardic synagogues in New York City. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6600", "text": "He is currently the President of  JJAC  ( Justice for Jews from Arab Countries ) and a member of the governing council of the  World Zionist Organization  (WZO). He is the founder of the  Sephardic Academy of Manhattan  and served as the Director of the Jacob E. Safra Institute of Sephardic Studies, at  Yeshiva University  and college professor of Sephardic Judaism, history, philosophy, and comparative traditional law. [ 12 ] [ 13 ] [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6601", "text": "In November 2020, after the signing of the  Abraham Accords , which normalized relations between the  UAE  and  Israel , Abadie moved to  Dubai  to become the country's Senior Rabbi. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6602", "text": "In 2021, Abadie issued an official condemnation of the  Houthis  for imprisoning a Yemenite Jew,  Levi Salem Marhabi , for helping smuggle a group of  Jews  into  Israel ; dubbing it as a  crime against humanity . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6603", "text": "Abadie's native language is  Arabic  and is fluent in six languages. He is also a part-time  gastroenterologist. [ 7 ]  Abadie has received the  Orden Del Merito Civil , the highest civil decoration in  Spain . He has been married to Elise Eichler for over 36 years. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6604", "text": "Ken Croitoru  is a Canadian  gastroenterologist  who works at  Mount Sinai Hospital in Toronto , a scientist at the  Lunenfeld-Tanenbaum Research Institute , and a professor in the Department of Medicine at the  University of Toronto . He is best known for his leadership of the Genetic, Environmental, Microbial (GEM) Project, a comprehensive research initiative aiming to understand the triggers of  Crohn's disease . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6605", "text": "Croitoru is a 1981 graduate of  McGill University Faculty of Medicine and Health Sciences . [ 3 ]   He did post-doctoral training with  John Bienenstock  at  McMaster University Medical School . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6606", "text": "Croitoru is a gastroenterologist at Mount Sinai Hospital, and also serves as a scientist at the Lunenfeld-Tanenbaum Research Institute. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6607", "text": "Croitoru is the lead investigator and architect of the GEM Project, which was launched in 2008. The project's purpose is to uncover the potential triggers of Crohn's disease by monitoring first-degree relatives of Crohn's patients. These individuals do not have the disease themselves but are at a higher risk of developing it. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6608", "text": "Under Croitoru's guidance, the GEM Project has made significant strides in Crohn's disease research. For instance, the team has discovered indications of barrier dysfunction, also known as \"leaky gut,\" occurring before the onset of the disease. The researchers also identified specific bacteria that appear to be significantly different in people who develop the disease compared to those who do not. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6609", "text": "The work of the GEM Project, under the leadership of Croitoru, has significantly advanced the understanding of Crohn's disease and has the potential to improve prevention and treatment strategies. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6610", "text": "Croitoru is a Tier 1  Canada Research Chair  in Inflammatory bowel diseases. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6611", "text": "Melita Alison Gordon   CMG   FRCP  is a  gastroenterologist  who works on invasive gut pathogens and tropical  gastrointestinal disease . She leads the  Malawi Liverpool Wellcome Trust  Salmonella and Enterics Group. Gordon was awarded the  British Society of Gastroenterology  Sir Francis Avery Jones Research Medal in 2011."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6612", "text": "Gordon completed her undergraduate studies at the  University of Cambridge . She completed her clinical qualifications at the  University of Oxford  and eventually specialised in  internal medicine   Queen's University Belfast . She has since worked in  Zambia ,  Sheffield  and  Liverpool . [ 1 ]  In 1993 she was awarded the  Liverpool School of Tropical Medicine  Blacklock medal. [ 2 ]  In 1997 she was appointed a  Wellcome Trust  Clinical Fellow and Lecturer. [ 3 ]  She moved to  Malawi  in 1997, where she lived until 2005 and was part of the  Malawi Liverpool Wellcome Trust . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6613", "text": "In 2008 Gordon was made an NHS  Higher Education Funding Council for England  Clinical Fellow at the  University of Liverpool .  Her early work was the first to show how  Salmonella  becomes a lethal disease for  HIV-positive people . [ 5 ]  She was promoted to Reader in 2012 and Professor in 2015. In 2015 she returned to  Malawi  where she leads the  Malawi Liverpool Wellcome Trust  Salmonella and Enterics Group. [ 6 ]  Gordon's research focuses on the development of vaccinations to protect against invasive bloodstream diseases caused by two groups of  Salmonellae ;  typhoid fever  and  Invasive Non-Typhoidal Salmonellosis  (iNTS). [ 7 ]  Gordon is committed to identifying novel vaccinations that can protect children in Africa from bacterial disease."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6614", "text": "iNTS is a rare bacterial disease that is caused by extraintestinal infection of certain  serotypes  of  Salmonella . iNTS kills around 80,000 people each year. It is more likely to occur in patients with  HIV infection  or  malaria  and the majority of people who suffer from iNTS are in  Sub-Saharan Africa . [ 8 ]  In 2011 Gordon was awarded the  British Society of Gastroenterology  Sir Francis Avery Jones Research Medal and in 2012 the Shire Awards for Gastrointestinal Excellence prize for Excellence in Gastroenterology. [ 9 ]  She became Director of the  World Gastroenterology Organisation  Blantyre Training Center in 2016. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6615", "text": "In 2018 Gordon led Africa's launch of the new  typhoid conjugate vaccine , and successfully vaccinated 24,000 children in  Malawi  in the first six months. [ 11 ]  The first child, Golden Kondowe, received the first vaccination in Ndirande,  Blantyre . [ 12 ] [ 13 ]  The Typhoid Vaccine Acceleration Consortium (TyVAC) study was funded by the  Bill & Melinda Gates Foundation  and was the result of twenty years of research of  Salmonella  in  Malawi . [ 11 ] [ 14 ]  The vaccine, which contains the Vi antigen  [ 15 ]  (a part of the Salmonella Typhi bacterium that helps it cause disease), is expected to protect against typhoid and other infections. [ 16 ] [ 17 ]  She works with local scientists, health workers and the Malawi Ministry of Health. [ 11 ]  The vaccine was shown to protect 81% of children from becoming infected with  typhoid fever . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6616", "text": "Gordon and the  University of Liverpool  Centre for Global Vaccine Research were awarded a multi-million pound research grant to establish the  Horizon 2020  Vacci-iNTS consortium. [ 18 ]  The consortium looks to develop new vaccines and research the financial and social impact of iNTS on communities in Africa impacted by the disease. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6617", "text": "In 2019 Gordon was made a  National Institute for Health Research  Global Research Professor. [ 19 ]  Her research has been supported by the  Bill & Melinda Gates Foundation ,  Medical Research Council ,  Wellcome Trust ,  British Society of Gastroenterology  and  Department for Business, Energy and Industrial Strategy . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6618", "text": "Her publications include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6619", "text": "Gordon is married to Stephen Gordon, former Director of the  Malawi Liverpool Wellcome Trust  Programme in Malawi. [ 21 ] [ 22 ] [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6620", "text": "In the  2024 King's Birthday Honours , she was appointed  Companion of the Order of St Michael and St George  (CMG) \"for services to global health\". [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6621", "text": "Bana Jabri  is a French gastroenterologist and immunologist of Syrian and Armenian descent. She is the Sarah and Harold Lincoln Thompson Professor in the Department of Medicine at the  University of Chicago . She researches inflammatory diseases of the intestine, including  celiac disease . She is an elected fellow of the  Association of American Physicians ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6622", "text": "Bana Jabri was born in Syria; her father was Syrian and her mother was Armenian. She moved to Germany when she was two years old and to France when she was twelve. [ 1 ] \nShe attended  Paris Diderot University , graduating in 1986 with a bachelor's degree in  biochemistry . She graduated from the  Pasteur Institute  in 1991 with her  Doctor of Medicine , followed by a residency at  Assistance Publique \u2013 H\u00f4pitaux de Paris , [ 2 ]  which is when she had her first child. [ 1 ]  She then completed a fellowship at the US  National Institutes of Health . She returned to Paris Diderot University for a PhD in immunology, graduating in 1996. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6623", "text": "In 1994, she accepted a position as an assistant professor in the department of  pediatric gastroenterology  at  Necker\u2013Enfants Malades Hospital , remaining through 1998. In 1999, she worked at  Princeton University  as a staff researcher, becoming a research scientist the following year. She accepted a position at the  University of Chicago  in 2002 as an assistant professor; she was promoted in 2005 to associate professor and in 2011 to full professor. In 2006, she became the co-director of its Digestive Disease Research Core Center and in 2011 she was made the director of research for its Celiac Disease Center. [ 3 ]  In 2018 she received a named professorship, becoming the Sara and Harold Lincoln Thompson Professor. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6624", "text": "In 2009, she became the first researcher in the US to win the William K. Warren, Jr. Prize for Excellence in Celiac Disease Research. [ 5 ]  In 2017 she received the Lloyd Mayer Prize in  Mucosal Immunology . [ 4 ]  She is also an elected member of the  Association of American Physicians  and a recipient of the Llewellyn John and Harriet Manchester Quantrell Award for Excellence in Undergraduate Education. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6625", "text": "Khursheed Nowrojee Jeejeebhoy  (born August 26, 1935) was a gastroenterologist at the  Toronto General Hospital ,  St. Michael's Hospital ,  Unity Health Toronto  and professor of medicine, nutrition and physiology at the  University of Toronto , best known for his pioneering work in the development of  parenteral nutrition ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6626", "text": "Jeejeebhoy was born to an  Indian Parsi family  in  Rangoon ,  Burma  on August 26, 1935, Nowrojee Jeejeebhoy and Gulbanoo Nowrojee (Tarapore) Jeejeebhoy. [ 1 ]  The family was evacuated to  India  by air in a  DC-3  ahead of advancing Japanese forces during the  Japanese invasion of Burma . His father joined the  Indian Army , and his maternal grandfather Pheroze Khurshetjee Tarapore was recalled to service after he had retired as an officer in the  Indian Medical Service . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6627", "text": "Due to  World War II  and his family's flight to India as refugees, Jeejeebhoy's schooling was initially very checkered. After his family fled to India, they lived a nomadic life and whether or not he attended school depended on where his father was stationed. However, his maternal grandmother Rattan Tarapore, a medical doctor trained at  JJ Hospital Medical School  in  Bombay , home schooled him. At age 15 he entered  Nirmala College  in  Delhi  and studied  economics  and  political science . At age 17, upon hearing of the excellence of  Christian Medical College Vellore  he applied for one of the ten spots available to students not sponsored by a Christian Mission. Entrance was by competitive written exam and interview. He was the first one called to fill one of the ten spots. He convocated in February 1959, capturing nine of ten gold medals. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6628", "text": "His graduate medical training was in  London . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6629", "text": "He is married and had three children."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6630", "text": "This biography related to medicine in Canada is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6631", "text": "Orestes Manousos  ( Greek :  \u039f\u03c1\u03ad\u03c3\u03c4\u03b7\u03c2 \u039c\u03b1\u03bd\u03bf\u03cd\u03c3\u03bf\u03c2 , 15 May 1931 \u2013 21 June 2021), was a Greek  gastroenterologist  and Professor of Medicine at the  University of Crete . He was Director of the First Gastroenterology Clinic of the  Evangelismos Hospital  (1977\u20131985), President of the Hellenic Society of Gastroenterology (1981\u20131982), founding member and first President of the Mediterranean Medical Society (1989), founding member and first President of the Hellenic Society for the Study of  Helicobacter Pylori  (1996)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6632", "text": "Orestes Manousos published a large number of clinical and research papers on digestive diseases in international medical journals. [ 1 ] [ 2 ] [ 3 ] [ 4 ] [ 5 ] [ 6 ] [ 7 ] [ 8 ] [ 9 ] [ 10 ]  He also wrote three medical textbooks,  Introduction to Clinical Medicine  with Professor Theodoros Mountokalakis,  The Immunology of Enteropathies  with Professor Ioanna Economidou, and  Colitis and... \"Colitis\" , which had a significant impact on the Greek gastroenterological community. After his retirement in 1998, he wrote several books on Cretan history and folklore as well as a historical novel."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6633", "text": "Orestes Manousos was born in 1931 in the  Cretan  village of  Anogeia . His father was Nikolaos Manousos, a local doctor with significant activity and recognition during  World War II , and his mother was Irini Kefalogianni, sister of Kostas Kefalogiannis, a local war hero of the  Greek resistance ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6634", "text": "Orestes Manousos attended the Heraklion High School and studied medicine at the  University of Thessaloniki . In 1959, after completing his military service in the Air Force, he left for England for postgraduate studies in London ( Central Middlesex  and  St Marks Hospitals ) and Oxford ( Radcliffe Infirmary ). He stayed in the UK for the next six years, gaining specialties in  internal medicine  (1961) and  gastroenterology  (1965). In 1964 his research into  diverticular disease  was acknowledged with the degree of Doctor of Philosophy (Ph.D.) from the  University of Oxford . [ 11 ]  His professors were Sidney Truelove, Sir Francis Avery Jones,  Leslie Witts , and John Lennard-Jones."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6635", "text": "After his return to Greece, he worked initially at  Evangelismos Hospital  and at the University Clinic of Hippocrateon Private Hospital, under the guidance of Professor George Merikas. In the following years, he became head of the Department of Pathology at the Columbia Clinic of Evangelismos, chaired by Cushman Haagensen, a professor at  Columbia University College  in New York."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6636", "text": "In 1973 he was elected Lecturer of the Faculty of Medicine of the  University of Athens  and from 1977 to 1985 he was Director of the first Gastroenterology Clinic of Evangelismos Hospital."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6637", "text": "His work on immunology of the digestive tract, in collaboration with Professor Ioanna Economidou was important. In particular, their work on \u03b1-heavy chain disease and Mediterranean Lymphoma was of global impact. [ 3 ] [ 8 ] [ 9 ] [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6638", "text": "He organized an important and unique for his era, endoscopic department at the Evangelismos Hospital and played a leading role in the Hellenic Society of Gastroenterology, of which he was president in 1981 and 1982. He was also President of the 8th Panhellenic Congress of Gastroenterology, which was held with great success in Heraklion, Crete."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6639", "text": "In 1985 he was elected Professor of Gastroenterology at the Medical School of the  University of Crete  and during the period 1990\u20131998, he was Director of the Gastroenterology Clinic of the University Hospital of Heraklion. He was an important pioneer in the first difficult steps of both the Medical University of Crete and the University Hospital of Heraklion. In 2003 he was awarded Professor Emeritus of the Faculty of Medicine of the University of Crete."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6640", "text": "In his spare time, Orestes Manousos played chess with his friends, read detective novels, took walks at the foothills of  Mount Hymettus , and spent time with his family. In 1955, when he was 24 years old, he married Mary Papastefanakis. In the 66 years of their marriage, they had five children and four grandchildren."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6641", "text": "In 2015 he was diagnosed with  Alzheimer's disease . He died in 2021. [ 14 ] [ 15 ] [ 16 ]  In November 2022, in honor of his work and contribution, the University Hospital of Heraklion renamed the hospital's Gastroenterology Clinic to \"Orestes Manousos Gastroenterology Clinic\". [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6642", "text": "This template is used to identify a  gastroenterology  stub. It uses {{ asbox }}, which is a meta-template designed to ease the process of creating and maintaining stub templates."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6643", "text": "Typing  {{Gastroenterology-stub}}  produces the message shown at the beginning, and adds the article to the following category:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6644", "text": "This is a  stub template . A brief explanation of these templates follows; for full details please consult  Wikipedia:Stub ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6645", "text": "A stub is an article containing only a few sentences of text which is too short to provide encyclopedic coverage of a subject."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6646", "text": "Further information can be found at:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6647", "text": "New stub templates and categories (collectively \"stub types\") should not be created without prior proposal at  Wikipedia:WikiProject Stub sorting/Proposals . This allows for the proper coordination of all stub types across Wikipedia, and for the checking of any new stub type for possible problems prior to its creation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6648", "text": "Brainerd diarrhea  is a sudden-onset watery, explosive  diarrhea  that lasts for months and does not respond to  antibiotics ; the cause of Brainerd diarrhea is unknown.  Brainerd diarrhea was first described in  Brainerd, Minnesota  in 1983. [ 1 ] \nIt has been associated with the consumption of  raw milk [ 1 ]  and untreated water. [ 2 ] [ 3 ]   Of the ten  outbreaks  reported since 1983, nine have been in the  U.S.   The characteristics of each outbreak have been similar to that caused by an  infectious agent ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6649", "text": "Although a comparatively large outbreak (117 patients) occurred in 1996 in  Fannin County, Texas , [ 4 ]  the largest outbreak (122 patients) was the original one in Brainerd, MN.  There have been no secondary cases reported in any of the outbreaks, suggesting that the\n causative agent  cannot be  passed  from person to person, but boiling water appears to inactivate the Brainerd agent.  Although there is no treatment available, the disease does appear to resolve itself, although this process takes months if not years. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6650", "text": "In  surgical pathology ,  strawberry gallbladder , more formally  cholesterolosis of the gallbladder  and  gallbladder cholesterolosis , is a change in the  gallbladder  wall due to excess  cholesterol . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6651", "text": "The name  strawberry gallbladder  comes from the typically stippled appearance of the  mucosal  surface on  gross examination , which resembles a  strawberry . Cholesterolosis results from abnormal deposits of cholesterol esters in macrophages within the lamina propria ( foam cells ) and in mucosal epithelium. The gallbladder may be affected in a patchy localized form or in a diffuse form. The diffuse form macroscopically appears as a bright red mucosa with yellow mottling (due to lipid), hence the term  strawberry  gallbladder. \nIt is not tied to  cholelithiasis  ( gallstones ) or  cholecystitis  ( inflammation  of the gallbladder). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6652", "text": "De Garengeot's hernia  is a rare subtype of an incarcerated  femoral hernia . This eponym may be used to describe the incarceration of the  vermiform appendix  within a  femoral hernia . [ 1 ]  This mechanism is contrasted with the Amyand hernia, in which the appendix protrudes through an inguinal hernia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6653", "text": "Akopian and Alexander, named this  hernia  after the 18th century Parisian surgeon Rene Jacques Croissant de Garengeot. He is quoted in the surgical literature as the first to describe this hernia in 1731. Although the surgeon's full last name is Croissant de Garengeot, for linguistic convenience it has been suggested to abbreviate this eponym to \"de Garengeot\". De Garengeot's first-described patient developed tenderness and a bulge in her right upper thigh after lifting 24 lb of bread. The bulge was unable to be reduced, after which surgery was conducted and a femoral hernia was discovered. The hernia was reduced back into the peritoneal cavity and the patient made an adequate recovery in 6 weeks. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6654", "text": "Similar as with the situation of an  Amyand's hernia , the true nature of the incarcerated tissue is rarely diagnosed preoperatively. Patients present clinically similar to other incarcerated femoral herniae. Treatment consists of an  appendectomy  and hernia repair. Laparoscopic options are described. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6655", "text": "De Garengeot hernia are most commonly seen in females and patients between 60 and 90 years of age. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6656", "text": "Diagnosis of De Garengeot hernia is most commonly made at the time of surgery, but some are diagnosed pre-operatively by CT scan, ultrasound, or MRI. If De Garengeot hernia is suspected based on general clinical signs of abdominal tenderness or bulging, CT scan is recommended. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6657", "text": "A individualized treatment approach is required based on the severity of the hernia and the surgeon's skill level and experience. Since the condition is rare, there have not been documented randomized control trials. De Garengeot hernias can be treated with closed reduction, laparoscopic repair, appendectomy, and open repair. [ 4 ]  Mesh placement can be considered based on severity of the hernia. The most common route of surgical management was through a groin incision, and appendectomy was performed in 98.5% of patients. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6658", "text": "Prevention of De Garengeot hernia involves measures that prevent hernias generally, such as maintaining a healthy weight, avoiding tight-fitting clothes, avoiding heavy straining when using the restroom, and avoiding improper heavy lifting."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6659", "text": "Factitious diarrhea  is a condition in which a person deliberately produces  diarrhea , most commonly by surreptitious  laxative  abuse ( laxative abuse syndrome )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6660", "text": "These people tend to have persistent and unexplained watery diarrhea that is high in volume and frequency and, despite extensive evaluation, the cause may remain unknown. Many cases may mimic  inflammatory bowel disease  or  malabsorption syndromes . [ 1 ]   Bowel movements  are generally about 10 to 20 a day and may be especially associated with nocturnal movements. Factitious diarrhea is most often seen in people of high  socioeconomic  status and many are employed in the medical field."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6661", "text": "Melanosis coli  is a frequent find in long-standing factitious diarrhea. [ 2 ] [ 3 ]  It demonstrates  hyperpigmentation  of the  colon  with white  lymph nodes  showing through on  colonoscopy . An alternative means of diagnosis is by detecting  pigment  in  macrophages  of the  lamina propria ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6662", "text": "Gastric pacing  is the process where a  pacemaker  is placed external to the  stomach , [ 1 ]  and leads penetrate the  gastric tissue  to ensure that an adequate current is running through the cells. It is used as a treatment for  gastroparesis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6663", "text": "The  gastroileal reflex  is one of the three extrinsic reflexes of the  gastrointestinal tract , the other two being the  gastrocolic reflex  and the  enterogastric reflex . The gastroileal reflex is stimulated by the presence of food in the stomach and gastric peristalsis. Initiation of the reflex causes peristalsis in the ileum and the opening of the ileocecal valve (which allows the emptying of the ileal contents into the large intestine, or colon). [ 1 ]  This in turn stimulates colonic peristalsis and an urge to defecate."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6664", "text": "High-resolution manometry  ( HRM ) is a  gastrointestinal motility   diagnostic system  that measures  intraluminal pressure activity  in the  gastrointestinal tract  using a series of closely spaced  pressure sensors . For a  manometry  system to be classified as \"high-resolution\" as opposed to \"conventional\", the pressure sensors need to be spaced at most 1\u00a0cm apart. [ 1 ] [ 2 ]  Two dominant  pressure transduction  technologies are used:  solid state pressure sensors  and  water perfused pressure sensors . [ 2 ] [ 3 ]  Each pressure transduction technology has its own inherent advantages and disadvantages. HRM systems also require advanced  computer hardware  and  software  to store and analyze the manometry data. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6665", "text": "The  Journal of Pediatric Gastroenterology and Nutrition  is a monthly  peer-reviewed   medical journal  covering research on  digestive diseases  and nutrition in children. It is published by   Lippincott Williams & Wilkins  and was established in 1982. [ 1 ]  It is an official journal of the  European Society for Paediatric Gastroenterology, Hepatology and Nutrition  and the  North American Society for Pediatric Gastroenterology, Hepatology and Nutrition . [ 2 ]  The journal provides a forum for original papers and reviews dealing with pediatric gastroenterology and nutrition, including normal and abnormal functions of the alimentary tract and its associated organs, including the salivary glands, pancreas, gallbladder, and liver. Particular emphasis is on development and its relation to infant and childhood nutrition [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6666", "text": "This article about a  pediatrics   journal  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6667", "text": "See tips for writing articles about academic journals . Further suggestions might be found on the article's  talk page ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6668", "text": "Umbilical cord ulceration and intestinal atresia  is a rare [ 1 ]   congenital  disease that leads to  intestinal atresia , umbilical cord ulceration and severe intrauterine  haemorrhage . Only 15 cases have so far been reported, [ 2 ]  though newer studies are beginning to conclude that this disease has a higher incidence rate than has been previously reported. [ 3 ]  A particular study has given intestinal atresia and umbilical cord ulceration a clear link after 5 such cases were reported at the time of publication. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6669", "text": "This article about a disorder arising in the  perinatal  period is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6670", "text": "Endoscopic image of diverticulosis, taken by myself, and released with permission of patient under GFDL --  Samir       (the scope)   \u0927\u0930\u094d\u092e    16:36, 2 May 2006 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6671", "text": "GFDL with disclaimers \n GNU Free Documentation License with  disclaimers \n //en.wikipedia.org/wiki/Wikipedia:Text_of_the_GNU_Free_Documentation_License"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6672", "text": "This licensing tag was added to this file as part of the GFDL  licensing update ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6673", "text": "Any user may perform this transfer; refer to  Wikipedia:Moving files to Commons  for details."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6674", "text": "If this file has problems with  attribution ,  copyright , or is otherwise  ineligible  for Commons, then  remove  this tag and  DO NOT  transfer it; repeat violators may be  blocked  from editing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6675", "text": "Endoscopic image of patient with  eosinophilic esophagitis  showing multiple rings and linear furrows.  Signed release into public domain from patient. --  Samir  08:37, 8 October 2007 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6676", "text": "GFDL \n GNU Free Documentation License \n //en.wikipedia.org/wiki/Wikipedia:Text_of_the_GNU_Free_Documentation_License"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6677", "text": "Fluoroscopic image of multiple  common bile duct   stones  seen at the time of  ERCP  and  duodenoscope assisted cholangiopancreatography  (DACP).  The stone was impacted in the distal common bile duct and was crushed with intracorporeal  lithotripsy .  Released into public domain on permission of patient/substitute decision maker. --  Samir   \u0927\u0930\u094d\u092e  06:13, 19 January 2007 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6678", "text": "Fluoroscopic image of two  metal biliary stents  in the  common bile duct .  The large black tube across the image is the duodenoscope.  Released into public domain on written permission of patient --  Samir   \u0927\u0930\u094d\u092e  06:52, 19 January 2007 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6679", "text": "Endoscopic picture of gastric ulcer with visible vessel.  Reproduced with permission of patient. --  Samir     (the scope)   \u0927\u0930\u094d\u092e    00:45, 5 May 2006 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6680", "text": "Isolated gastric varices seen on retroflexion of the  gastroscope .  The picture was placed into the public domain on the permission of the patient.  --  Samir   \u0927\u0930\u094d\u092e  04:53, 17 May 2006 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6681", "text": "Endoscopic image of  glycogenic acanthosis , placed under GFDL with permission of patient --  Samir   \u0927\u0930\u094d\u092e  05:53, 17 May 2006 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6682", "text": "Endoscopic  still of  common bile duct stone  impacted at  ampulla of Vater .  Released into public domain on permission of patient. --  Samir   \u0927\u0930\u094d\u092e  07:20, 15 August 2006 (UTC)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6683", "text": "Colonoscopic  image of  ulcer  seen bleeding after  polypectomy , closed with an  endoclip ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6684", "text": "c:Template:PD-medical"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6685", "text": "The person who associated a work with this deed has dedicated the work to the  public domain  by waiving all of his or her rights to the work worldwide under copyright law, including all related and neighboring rights, to the extent allowed by law. You can copy, modify, distribute and perform the work, even for commercial purposes, all without asking permission.\n https://creativecommons.org/publicdomain/zero/1.0/deed.en \n CC0 \n Creative Commons Zero, Public Domain Dedication \n false"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6686", "text": "The  American College of Gastroenterology  ( ACG ) is a  Bethesda ,  Maryland \u2013based  medical association  of  gastroenterologists ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6687", "text": "The association was founded in 1932 [ 1 ]  and holds annual meetings and regional postgraduate  continuing education  courses, establishes  research grants , and publishes  The American Journal of Gastroenterology ,   Clinical and Translational Gastroenterology  and  The ACG Case Reports Journal . More than 20,000 physicians from 86 countries are members of the ACG.  The ACG provides its members with scientific information on  digestive health  and the  etiology ,  symptomatology  and treatment of  GI disorders . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6688", "text": "The current president (2024\u201325) is Amy S. Oxentenko, MD, FACG. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6689", "text": "The  American Gastroenterological Association  ( AGA ) is a  medical association  of  gastroenterologists . Approximately 16,000  scientists  and  physicians  are members of the organization."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6690", "text": "The American Gastroenterological Association is a professional association for gastroenterologists. The AGA was founded in 1897 and has grown to include 16,000 members worldwide who are involved in all aspects of the science, practice, and advancement of  gastroenterology . [ 1 ]  The AGA Institute administers the practice, research and educational programs of the organization. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6691", "text": "The AGA, a  501(c)(6)  organization, administers all membership and public policy activities, while the AGA Institute, a  501(c)(3)  organization, runs the organization's practice, research, and educational programs. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6692", "text": "On a monthly basis, the AGA Institute publishes two journals,  Gastroenterology  and  Clinical Gastroenterology and Hepatology . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6693", "text": "The organization's annual meeting is Digestive Disease Week, which is held each May and is the largest international gathering of physicians, researchers and academics in the fields of  Gastroenterology ,  Hepatology ,  Endoscopy  and  Gastrointestinal surgery . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6694", "text": "The  AGA Research Foundation provides digestive disease research grants on behalf of the AGA Institute [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6695", "text": "The American Society for Gastrointestinal Endoscopy  ( ASGE ) is a  professional organization  of  physicians  dedicated to improving  endoscopy . The ASGE is made up largely of  gastroenterologists  from the  United States . Included in its membership are endoscopists from other medical specialties as well as from other countries. ASGE publishes the  medical journal   Gastrointestinal Endoscopy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6696", "text": "\"The core purpose of the American Society for Gastrointestinal Endoscopy is to be the leader in advancing and promoting excellence in gastrointestinal endoscopy.\" [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6697", "text": "American Society for Gastrointestinal Endoscopy was founded on December 30, 1941. [ 3 ] [ 4 ]  Established as the American Gastroscopic Society, the organization changed its name in 1961 to the \"American Society for Gastrointestinal Endoscopy.\" [ 5 ]  As of 2017, the budget for ASGE was about $17.8 million. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6698", "text": "American Society for Gastrointestinal Endoscopy sponsors grants for research in gastroenterology and endoscopy. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6699", "text": "The  British Society of Gastroenterology  ( BSG ) is a British professional organisation of  gastroenterologists , surgeons, pathologists, radiologists, scientists, nurses, dietitians and others amongst its members, which number over 4,000. It was founded in 1937, [ 1 ]  and is a registered charity. Its offices are in  Regent's Park ,  London . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6700", "text": "The society is  an organisation focused on the promotion of gastroenterology within the United Kingdom . [ 3 ]  It is involved with the training of gastroenterologists in the  United Kingdom , and with  original research  into gastroenterology. The society also produces information for patients with gastrointestinal diseases. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6701", "text": "The society publishes the  medical journals   Gut ,  BMJ Open Gastroenterology  and  Frontline Gastroenterology . [ 5 ] [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6702", "text": "It produces  clinical practice guidelines  and various other documents relevant to the field of gastroenterology including diseases of the  gastrointestinal tract ,  liver ,  pancreas  and  biliary tract , and the disciplines of gastrointestinal  endoscopy ,  nutrition ,  pathology  and  gastrointestinal surgery . [ 8 ] [ 9 ] [ 10 ] [ 11 ] [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6703", "text": "The society holds an Annual General Meeting during which original research, updates and reviews in gastroenterology and hepatology are presented.  Named lectures include the Sir  Arthur Hurst  lecture and the Sir  Francis Avery Jones  BSG Research medallist."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6704", "text": "Recent presidents have been  Hermon Dowling  (1996\u20131997),  Chris Hawkey  (2010),  Jon Rhodes  (2011\u201312),  Ian Gilmore  (2013\u201314),  Ian Forgacs  (2014\u201316),  Martin Lombard  (2016\u201318),  Cathryn Edwards  (2018\u201320), Alastair McKinlay (2020-22), and Andy Veitch (2022-24).  The current president is Professor Colin Rees. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6705", "text": "The British Society of Gastroenterology is a National Society Member of the  United European Gastroenterology ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6706", "text": "51\u00b031\u203230.76\u2033N   0\u00b08\u203242.45\u2033W \ufeff / \ufeff 51.5252111\u00b0N 0.1451250\u00b0W \ufeff /  51.5252111; -0.1451250"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6707", "text": "The Canadian Association of Gastroenterology  (CAG) was founded in 1962 to promote the  study  of the  digestive tract  in  health  and disease, including  liver disease . The Association is built on broad principles and includes individuals of different disciplines ( physicians ,  surgeons ,  paediatricians ,  radiologists ,  basic scientists ). Today, the Association comprises more than 1,100 members. CAG members are actively involved in research, education and patient care in all areas of digestive health and disease, contributing to the  economic  and social health of all Canadians.  The  Canadian Digestive Health Foundation  is the  foundation  of the CAG."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6708", "text": "The  Journal of the Canadian Association of Gastroenterology  is a  peer-reviewed   medical journal  dealing with topics in  gastroenterology  and in  liver disease . It was established in 2018 as the official journal of the Canadian Association of Gastroenterology. [ 1 ]  The journal is published by  Oxford University Press . The  editor-in-chief  is Eric Benchimol ( University of Toronto ). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6709", "text": "Crohn's & Colitis UK  (formerly  NACC ) is a UK  charity  dedicated to  Crohn's disease ,  ulcerative colitis , and other forms of  inflammatory bowel disease  (IBD). It was founded in 1979 as the  National Association for Colitis and Crohn's Disease ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6710", "text": "Crohn's & Colitis UK brings together people of all ages who have Crohn's or colitis, their families, and the health professionals involved in their care. These two illnesses are both forms of  Iinflammatory bowel disease  (IBD) and they affect over 500,000 people in the UK."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6711", "text": "Crohn's & Colitis UK provides information and support to enable people to manage their conditions. They work with the UK health sector to improve diagnosis, treatment and management of IBD. They fund  research  to increase knowledge of the causes and the best treatments for Crohn's and colitis, and they campaign for greater awareness, better services and more support for Crohn's and colitis patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6712", "text": "This article about a UK medical organisation, hospital, or association is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6713", "text": "Guts UK , formerly known as the  Digestive Disorders Foundation , is a British medical  research   charity  dedicated to the research of  digestive disorders . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6714", "text": "In 1970, the Council of the  British Society of Gastroenterology  first considered founding a charity to promote research in this speciality. A steering group, chaired by their President at the time, Dr Nelson Coghill, compiled facts and figures which established the importance of digestive disorders as a national health problem. Using this evidence as a basis for appeal, a Digestive Disorders Trust Fund was established."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6715", "text": "Dr Thomas Hunt, a founder member of the British Society of Gastroenterology, agreed to launch the new charity. [ 3 ]  He succeeded in attracting prominent lay and professional support. By 1974 its funds were sufficient to award the first research fellowship and to inaugurate the charity as a Foundation with Hunt as its first President. On his death in 1980, Sir Francis Avery Jones took over the presidency for the next 12 years. Important landmarks during this time were the appointment of the first full-time director, expansion of research support and the development of the successful patient information programme."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6716", "text": "This article about a charitable organisation in the United Kingdom is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6717", "text": "The  United European Gastroenterology  ( UEG ) is a  non-profit organisation  combining European societies concerned with  digestive health ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6718", "text": "Founded in 1992 United European Gastroenterology (UEG) is the leading non-profit organisation for excellence in digestive health in  Europe  and beyond with its headquarters in Vienna."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6719", "text": "We improve the prevention and care of digestive diseases in Europe through providing top tier education, supporting research and advancing clinical standards. As Europe\u2019s home and umbrella for multidisciplinary  gastroenterology , we unite over 50,000 engaged professionals from national and specialist societies, individual digestive health experts and related scientists from all fields and career stages."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6720", "text": "UEG unites 17 Specialist Member Societies and 50 National Societies working in the broad area of digestive health, constantly adapting to the changing requirements of scientific research and health care."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6721", "text": "Following our mission and a dedicated  strategic plan , the overall leadership and strategic direction of UEG rests with the Council. The committees and task forces enable interested volunteers to play an active role in shaping current and future UEG initiatives and form the operating body of the organisation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6722", "text": "Member Societies are represented in the Meeting of Members that elects or appoints UEG Council members. Each Specialist Member Society has the opportunity to send one representative to UEG\u2019s committees."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6723", "text": "All officers of UEG, regardless of position, provide their effort and time on a complete voluntary basis, and therefore make UEG a non-profit organisation concerned solely with the well-being of patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6724", "text": "UEG is a Regional Affiliate Association of the  World Gastroenterology Organisation . UEG is a member of the  European Medicines Agency , the Biomedical Alliance in Europe, the AC Forum, the Optimal Nutritional Care for All, and Pancreatic Cancer Europe."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6725", "text": "Presidents  of UEG:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6726", "text": "The House of European Gastroenterology (HEG) is UEG's home and offers a meeting point and communication hub to the European gastroenterological community. The HEG is situated in the heart of  Vienna , near the  Rathaus  (City Hall) in a 19th-century building."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6727", "text": "UEG Week [ 8 ]  is the largest congress  of its kind in  Europe  and is held once a year. It has been running since 1992 and now attracts more than 10,000 people from around the world. It features the latest advances in clinical management and  research in the field of digestive health. A two-day Postgraduate Teaching Programme is also held on occasion of UEG Week. The programme provides continuing medical education for  gastroenterologists  in training and practice."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6728", "text": "UEG provides educational online and face-to-face courses, a podcast and webinars in the field of digestive health."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6729", "text": "Additionally  Gutflix , UEG's interactive and personalised GI learning platform, provides all educational content in one place. Gutflix includes UEG Week recordings, online courses, clinical practice guidelines, webinars, \"Mistakes in...\" articles, podcasts, webinars and more."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6730", "text": "UEG aims to act as a united voice of European  gastroenterology  in the  Institutions of the European Union  and the  governments  of the member states in order to promote digestive health in  Europe . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6731", "text": "UEG offers fellowships, awards and grants in the following fields and categories: Fellowships and awards for researchers under the age of 40, a prize for researchers having achieved the highest level of international recognition, an award honouring outstanding contributions to digestive health and UEG, national as well as international scholarship awards, prizes for best abstracts, an award to recognise the first named author of the best original scientific research published in UEG Journal and travel grants. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6732", "text": "Focuses on providing coverage of both translational as well as clinical studies from different fields of gastroenterology. The latest impact factor ranking indicates that the UEG Journal has already established itself as an authoritative, high quality and trusted journal in the field. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6733", "text": "UEG's latest pan-European study on digestive health where the burden of digestive diseases and associated research gaps are highlighted. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6734", "text": "The  World Gastroenterology Organisation  ( WGO ) is an international federation of over 100 national GI societies and 4 regional associations of gastroenterology representing over 50,000 individual members."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6735", "text": "WGO is focused on \"the improvement of standards in gastroenterology training and education on a global scale.\" [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6736", "text": "The association was founded in 1935 and incorporated in 1958.  The WGO was originally known as the Organisation Mondiale de Gastroenterologie (OMGE) and was renamed the World Gastroenterology Organisation in 2006. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6737", "text": "Its activities include educational initiatives such as  Training Centers ,  Train the Trainers Workshops , public awareness campaigns such as  World Digestive Health Day [ 3 ]  and  Global Guidelines  which cascade, providing viable solutions which are adaptable to varying resource levels around the world, as well as a quadrennial World Congress of Gastroenterology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6738", "text": "The WGO Foundation was incorporated in 2007 and is dedicated to raising funds to support the ongoing WGO education initiatives and activities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6739", "text": "Georges Broh\u00e9e (1887\u20131957), a Belgian surgeon who promoted modern gastroenterology, is largely responsible for the origin of the WGO, in particular by founding the Belgian Society of Gastroenterology in 1928 and by organizing the first International Congress of Gastroenterology in Brussels in 1935.  In May 1958 the first World Congress of Gastroenterology was held in Washington DC, where Georges Broh\u00e9e\u2019s continuing efforts culminated in the constitution of the \"Organisation Mondiale de Gastro-ent\u00e9rologie\" (OMGE) on May 29, 1958."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6740", "text": "Dr H.L. Bockus was the organisation\u2019s first President.  His vision was to enhance standards of education and training in gastroenterology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6741", "text": "Developed nations  were the initial focus of the organization, however today the WGO embraces a global approach with a special emphasis on  developing regions [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6742", "text": "General management of the WGO is conducted by a Governing Council.  Acting through the Governing Council, the organisation is empowered to undertake those activities necessary to fulfill the goals and mission of the WGO."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6743", "text": "The Executive Committee oversees various program and consists of  the President, Vice President, Past President, Secretary General, and Treasurer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6744", "text": "A General Assembly reviews and approves the work of the Governing Council and attends to other business (including the World Congress venue).  The General Assembly is composed of representatives from all WGO Member Societies and regional associations.  Each WGO Member Society has one vote in the General Assembly. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6745", "text": "WGO has a number of committees including: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6746", "text": "The elections and renewal of the WGO officers and committees takes place on the occasion of the General Assembly, which is held during the quadrennial World Congress of Gastroenterology. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6747", "text": "There are currently 20 WGO Training Centers: [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6748", "text": "Each guideline is translated into six languages including English, French, Spanish, Portuguese, Russian and Mandarin Chinese."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6749", "text": "Guidelines with cascades:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6750", "text": "Guidelines with cascades in development:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6751", "text": "The WGO celebrates World Digestive Health Day (WDHD) every May 29, initiating a worldwide public health campaign through its national societies and 50,000 individual members.  Each year, WDHD focuses upon a particular digestive disorder and seeks to increase general public awareness of prevention and therapy.  WDHD themes have included: [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6752", "text": "In 2008, the WGO, together with Danone, launched a global campaign to improve digestive health, titled \" Optimum Health and Nutrition .\"  The campaign is part of a three-year partnership between WGO and Danone to \" help raise awareness of digestive disorders and the importance of maintaining good digestive health .\" [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6753", "text": "The WGO Foundation  was established in 2007 to raise financial support to develop and sustain the World  Gastroenterology  Organisation's global training and education programs.  These programs focus primarily on developing, low-resource countries and aim to meet the increasing demand for digestive disorder prevention and treatment worldwide. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6754", "text": "To raise financial support to develop and sustain WGO's global training and education programs, especially in developing and low-resource countries. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6755", "text": "The WGO Foundation has fund raising activities including Initiating fund raising campaigns:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6756", "text": "Colorectal surgery  is a field in medicine dealing with disorders of the  rectum ,  anus , and  colon . [ 1 ]  The field is also known as  proctology , but this term is now used infrequently within medicine and is most often employed to identify practices relating to the anus and rectum in particular. [ clarification needed ]  The word  proctology  is derived from the  Greek  words  \u03c0\u03c1\u03c9\u03ba\u03c4\u03cc\u03c2   proktos , meaning \"anus\" or \"hindparts\", and  -\u03bb\u03bf\u03b3\u03af\u03b1   -logia , meaning \"science\" or \"study\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6757", "text": "Physicians specializing in this field of medicine are called colorectal surgeons or proctologists. In the United States, to become colorectal surgeons, surgical doctors have to complete a general surgery residency as well as a colorectal surgery fellowship, upon which they are eligible to be certified in their field of expertise by the  American Board of Colon and Rectal Surgery  or the  American Osteopathic Board of Proctology . In other countries,  certification  to practice proctology is given to surgeons at the end of a 2\u20133 year subspecialty  residency  by the country's board of surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6758", "text": "Colorectal surgical disorders include: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6759", "text": "Surgical forms of treatment for these conditions include:  colectomy , ileo/colostomy,  polypectomy ,  strictureplasty , hemorrhoidectomy (in severe cases of  hemorrhoids ), minimally invasive surgery, anoplasty, and more depending on the condition the patient has. Diagnostic procedures, such as a  colonoscopy , are very important in colorectal surgery, as they can tell the physician what type of diagnosis should be given and what procedure should be done to correct the condition. Other diagnostic procedures used by colorectal surgeons include:  proctoscopy ,  defecating proctography ,  sigmoidoscopy .   In recent times, the  laparoscopic  method of surgery has seen a surge of popularity, due to its lower risks, decreased recovery time, and smaller, more precise incisions achieved by using laparoscopic instruments. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6760", "text": "Mechanical bowel preparation (MBP) is a procedure lacking evidence in literature, [ 4 ]  wherein fecal matter is expelled from the bowel lumen prior to surgery, most commonly by using  sodium phosphate . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6761", "text": "Shafi Ahmed  is a chief surgeon, teacher,  futurist , innovator, professor and entrepreneur. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6762", "text": "Ahmed lives in London. He is married to Farzana Hussain, a  general practitioner , with whom he has two children. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6763", "text": "He was born on 26 January 1969 in  Sylhet District ,  East Pakistan  (now  Bangladesh ), and came to the United Kingdom as a child. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6764", "text": "Ahmed attended Chadwell Heath High School (now  Chadwell Heath Academy ) before attending the Redbridge technical college."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6765", "text": "From 1988 to 1993, he studied medicine at  King's College Hospital  School of Medicine. As the elected President of the Medical and Dental Society, he helped introduce medical ethics into the curriculum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6766", "text": "During his surgical training in London, he undertook a period of research at The  Royal London Hospital  and the  Queen Mary University of London . In 2010, he obtained a PhD with a thesis entitled \"The role of microarray profiling in predicting outcome in patients with colorectal cancer\". [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6767", "text": "Ahmed has been awarded four honorary PhDs (Honoris Causa) from Udabol University Bolivia, SIISDET Colombia, the University of Peru of Science and Informatics and EXIBED, Spain. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6768", "text": "In 2017, he was appointed as an honorary professor at The  University of Bradford  and awarded an Honorary Doctorate of Medicine in 2019. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6769", "text": "In 2020 he was awarded the Spinoza Honorary professorship at the  University of Amsterdam . [ 6 ] [ non-primary source needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6770", "text": "Ahmed is a specialist advisor to the Abu Dhabi Ministry of Health to help deliver innovation and  digital health . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6771", "text": "Ahmed works in the Academic Centre of Surgery and has established  minimally invasive   colorectal surgery  at the  Royal London Hospital ,  Barts Health NHS Trust . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6772", "text": "His main clinical interest is  colorectal cancer , and he performs surgery for primary and recurrent disease as well as multi-visceral resections."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6773", "text": "He has pioneered single incision  laparoscopic  colorectal surgery (virtual scarless surgery) and also works with liver surgeons to perform simultaneous laparoscopic liver and  bowel resections  for cancer. His other clinical interest is advanced stage 3/4  endometriosis , performing laparoscopic surgery with  gynaecologists . This has led to the development and recognition of a national centre for endometriosis. In addition, he has specialist experience in complex abdominal wall  hernias  and reconstruction. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6774", "text": "From 2010 to 2015, Ahmed was the lead clinician and multi-disciplinary team lead for colorectal cancer at Barts Health NHS Trust. He was also a CQC specialist advisor in general surgery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6775", "text": "Ahmed was the Associate Dean for Barts and the London undergraduate medical students at  The Royal London Hospital  from 2010 to 2019 and was the lead for surgery. He was programme director for core surgical trainees for North East London 2012\u20132013 and Tutor in Surgery for the Royal London Hospital 2011\u20132013. He teaches innovation and digital transformation for surgeons at  Harvard Medical School  and  Imperial College London . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6776", "text": "He is the civilian advisor for the  British Armed forces  for general surgery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6777", "text": "From 2013 to 2019, Ahmed was elected to the council of the  Royal College of Surgeons of England . [ 10 ]  He had numerous roles and led the International Surgical Training Programme. He was part of the Cancer 2020, 5 Year Forward View Taskforce 2015. [ 11 ]  He is a member of the court of examiners and is an international convenor of the MRCS for Bangladesh. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6778", "text": "In 2007, Ahmed was appointed as a Consultant General, Laparoscopic and Colorectal surgeon to  The Royal London Hospital  and  St Bartholomew's Hospital ,  Barts Health NHS Trust ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6779", "text": "He was chosen to curate the  NHS  Twitter account from 27 February 2017 to 3 March 2017 and tweeted the world's first live operation via this account."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6780", "text": "He was the clinical lead for surgery at the  NHS Nightingale  Hospital at Excel London during the COVID-19 pandemic in 2020."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6781", "text": "Ahmed performed a live cancer operation at  The Royal London Hospital  on Channel 5 for the series  Operation Live  in 2018."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6782", "text": "Ahmed is the module lead for an innovative new course at Barts and the London Medical School which aims to teach the third year medical students about future medicine and how to generate ideas to improve clinical care. [ 13 ] [ 1 ]  The students are taught by  digital health  innovators and those involved in Medtech from the UK and US."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6783", "text": "Ahmed has been working on new technologies to enhance surgical education globally. His online videos have been watched hundreds of thousands of times, earning him the accolade of the most-watched surgeon in human history. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6784", "text": "He aims to teach surgery and surgical processes to thousands of students at a time using VR technology. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6785", "text": "Ahmed's company Virtual Medics developed the use of  wearable technology  in education and clinical practice. This has allowed the development of a web-placed platform to stream live and interactive teaching."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6786", "text": "In May 2014, using  Google Glass , he performed and streamed a live operation to 14 thousand students across 132 countries and 1100 cities. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6787", "text": "Ahmed is the co-founder of Medical Realities, a group offering surgical training products, specialising in virtual reality, augmented reality and  serious games . [ 17 ]  Through Medical Realities, he aims to provide tutorials in a modular format to teaching hospitals around the world. This will be made accessible to students and surgical trainees."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6788", "text": "On 14 April 2016, in collaboration with  Barts Health , Medical Realities and Mativision, he performed the world's first virtual reality operation recorded and streamed live in  360 degrees . [ 8 ] [ 17 ] [ 18 ] [ 19 ]  This was viewed by 55,000 people in 140 countries and 4000 cities and reached 4.6 million people on Twitter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6789", "text": "This event was covered worldwide on over 400 newspaper/online articles and  BBC Click , Sky News, ARD German, TRT News, South American NTN,  ABC News ,  Aljazeera , and Press TV. [ 20 ] [ 21 ] [ 22 ] [ 23 ]  His work has been featured on  Wired ,  The Guardian ,  The Telegraph , ABC News,  CNET ,  The Verge ,  Huffington Post , and Tech China. [ 24 ] [ 25 ] [ 26 ] [ 27 ] [ 16 ] [ 28 ] [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6790", "text": "On 9 December 2016, he performed the world's first live operation using Snapchat Spectacles where he trained 200 medical students and surgical trainees, which was covered by  Time  magazine, and  BBC . [ 31 ] [ 32 ] [ 33 ]  The operation has been viewed over 100,000 times. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6791", "text": "He is a non-executive director of Medic creations, GPDQ and Imera. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6792", "text": "He is the chair of the GIANT (Global Innovation and New Technologies) Health Event in London and also the chair of the Webit Health conference in Sofia, Bulgaria, which showcases startups, innovation, technology and entrepreneurship. [ 36 ] [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6793", "text": "Ahmed is a three time  TEDx  speaker and four times Wired Health and international  keynote speaker , and a member of the faculty at Exponential Medicine,  Singularity University ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6794", "text": "On 15 March 2017, Ahmed delivered the Cantor Technology Lecture at the  University of Bradford  and also delivered the public lecture to open the Digital Health Enterprise Zone. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6795", "text": "He is Vice-President of Proshanti, a local charity community project to set up a health programme in Bangladesh, He is an advisor to Beani Bazaar Cancer Hospital, Bangladesh. [ 48 ]  He also teaches and trains surgeons in Dhaka, Bangladesh where he is the Dean for education at Rahetid, a postgraduate surgical training centre. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6796", "text": "The  American Board of Colon and Rectal Surgery  ( ABCRS ) is a member of the  American Board of Medical Specialties  that issues certificates for practitioners of  Colorectal surgery ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6797", "text": "The board was established in 1934 as the American Board of Proctology. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6798", "text": "The  American Osteopathic Board of Proctology  ( AOBPR ) is an organization that provides  board certification  to qualified  Doctors of Osteopathic Medicine  (D.O.) who specialize in the medical and surgical treatment of disorders of the  anus ,  colon , and  rectum  of the  gastrointestinal tract  ( proctologists ). The board is one of 18  medical specialty  certifying boards of the  American Osteopathic Association Bureau of Osteopathic Specialists  approved by the  American Osteopathic Association  (AOA), [ 3 ]  and was established in 1941. [ 1 ]  As of April 2011, there were 25 osteopathic proctologists certified by the AOBPR. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6799", "text": "To become board certified in proctology, candidates must have completed an AOA-approved  residency  in proctology and one year of practice as a licensed proctologist. [ 5 ]   Additionally, candidates must have successfully completed the required oral and written examinations. Since 2004, board certified osteopathic proctologists must renew their certification every ten years to avoid expiration of their board certified status. [ 6 ]  Physicians certified by the AOBPR are known as fellows of the American Osteopathic College of Proctology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6800", "text": "Anal dysplasia  is a pre-cancerous condition which occurs when the lining of the  anal canal  undergoes abnormal changes. It can be classified as  low grade squamous intraepithelial lesions  (LSIL) and high-grade squamous intraepithelial lesions (HSIL). [ 1 ]  \nMost cases are not associated with symptoms, but people may notice lumps in and around the  anus . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6801", "text": "Anal dysplasia is most commonly linked to  human papillomavirus  (HPV), a usually  sexually-transmitted infection . [ 3 ]  HPV is the most common  sexually transmitted infection  in the United States [ 4 ]  while  genital herpes  ( HSV ) was the most common sexually transmitted infection globally. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6802", "text": "This  oncology  article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6803", "text": "Anal fistula  is a chronic  abnormal communication  between the  anal canal  and the perianal skin. [ 1 ]  An anal fistula can be described as a narrow tunnel with its internal opening in the anal canal and its external opening in the skin near the anus. [ 2 ]  Anal fistulae commonly occur in people with a history of  anal abscesses . They can form when anal abscesses do not heal properly. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6804", "text": "Anal fistulae originate from the  anal glands , which are located between the  internal  and  external anal sphincter  and drain into the  anal canal . [ 4 ]  If the outlet of these glands becomes blocked, an  abscess  can form which can eventually extend to the skin surface. The tract formed by this process is a fistula. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6805", "text": "Abscesses can recur if the fistula seals over, allowing the accumulation of  pus . It can then extend to the surface again \u2013 repeating the process. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6806", "text": "Anal fistulae  per se  do not generally harm, but can be very painful, and can be irritating because of the drainage of pus (it is also possible for formed stools to be passed through the fistula). Additionally, recurrent abscesses may lead to significant short term morbidity from pain and, importantly, create a starting point for systemic infection. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6807", "text": "Treatment, in the form of surgery, is considered essential to allow drainage and prevent infection. Repair of the fistula itself is considered an elective procedure which many patients opt for due to the discomfort and inconvenience associated with an actively draining fistula. [ 5 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6808", "text": "Anal fistulae can present with the following symptoms: [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6809", "text": "Diagnosis is by examination, either in an  outpatient  setting or under  anaesthesia  (referred to as  EUA  or Examination Under Anaesthesia). The fistula may be explored by using a fistula probe (a narrow instrument). In this way, it may be possible to find both openings. The examination can be an  anoscopy . Diagnosis may be aided by performing a fistulogram, proctoscopy and/or sigmoidoscopy.\nPossible findings:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6810", "text": "Depending on their relationship with the  internal  and  external sphincter  muscles, fistulae are classified into five types:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6811", "text": "Other conditions in which infected perianal \"holes\" or openings may include  pilonidal cyst ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6812", "text": "There are several stages to treating an anal fistula:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6813", "text": "Definitive treatment of a fistula aims to stop it recurring.  Treatment depends on where the fistula lies, and which parts of the  internal  and  external anal sphincters  it crosses. However, treatment is challenging as complete eradication of the anal sphincters may lead to continence impairment, but failure to excise the affected areas results in recurrence. Those already treated for recurring anal fistula are at higher risk to experience re-recurrence of the disease.  [1]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6814", "text": "The VAAFT procedure is done in two phases, diagnostic and operative. Before the procedure, the patient is given a spinal or general anaesthetic and is placed in the lithotomy position (legs in stirrups with the perineum at the edge of the table).  In the diagnostic phase, the fistuloscope is inserted into the fistula to locate the internal opening in the anus and to identify any secondary tracts or abscess cavities. The anal canal is held open using a speculum and irrigation solution is used to give a clear view of the fistula tract. Light from the fistuloscope can be seen from inside the anal canal at the location of the internal opening of the fistula, which helps to locate the internal opening.  In the operative phase of the procedure, the fistula tract is cleaned and the internal opening of the fistula is sealed. To do this, the surgeon uses the unipolar electrode, under video guidance, to cauterise material in the fistula tract. Necrotic material is removed at the same time using the fistula brush and forceps, as well as by continuous irrigation. The surgeon then closes the internal opening from inside the anal canal using stitches and staples."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6815", "text": "Some people will have an active  infection  when they present with a fistula, and this requires clearing up before definitive treatment can be decided."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6816", "text": "Antibiotics  can be used as with other infections, but the best way of healing infection is to prevent the buildup of pus in the fistula, which leads to abscess formation.  This can be done with a  seton ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6817", "text": "A literature review published in 2018 showed an incidence as high as 21 people per 100,000. \"Anal fistulas are 2\u20136 times more prevalent in males than females, with the condition occurring most frequently in patients in their 30s and 40s.\" [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6818", "text": "Anal stricture  or  anal stenosis  is a narrowing of the anal canal. [ 1 ]  It can be caused by a number of surgical procedures including:  hemorrhoid  removal and following  anorectal wart  treatment. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6819", "text": "Anorectal anomalies  are congenital malformations of the  anus  and  rectum . [ 1 ]  One anal anomaly,  imperforate anus  has an estimated incidence of 1 in 5000 births. [ 2 ] [ 3 ]  It affects boys and girls with similar frequency. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6820", "text": "Examples of anorectal anomalies include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6821", "text": "Anorectal manometry  ( ARM ) is a  medical test  used to measure  pressures  in the  anus  and  rectum  and to assess their function. [ 1 ] [ 2 ]  The test is performed by inserting a  catheter , that contains a probe embedded with pressure sensors, through the anus and into the rectum. [ 3 ]  Patients may be asked to perform certain maneuvers, such as coughing or attempting to  defecate , to assess for pressure changes. [ 3 ]  Anorectal manometry is a safe [ 4 ]  and low risk [ 3 ]  procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6822", "text": "From 2014 to 2018, the international anorectal physiology working group (IAPWG) meet several times to develop consensus on  indications  for anorectal manometry. [ 5 ]  Their assessment concluded that anorectal manometry was indicated when used in assessment of  fecal incontinence ,  constipation , evacuation disorders (including  Hirschsprung's disease [ 6 ] ), functional anorectal pain and in the assessment of anorectal function  preoperatively  or after a traumatic  obstetric  injury. [ 5 ]  In addition to the indications outlined by the IAPWG, anorectal manometry has been used as a component of anorectal  biofeedback . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6823", "text": "Since its introduction in 2007,  high resolution  anorectal manometry (HR-ARM) has increasingly replaced conventional anorectal manometry as the standard. [ 7 ]  There has been increasing usage of high-definition (3D) anorectal manometry (HD-ARM) as well. [ 7 ]  Current advances in anorectal manometry include the development of  bedside  portable technology. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6824", "text": "After eliminating structural causes of  fecal incontinence  from the  differential diagnosis , anorectal manometry may be used to evaluate deficiencies in  sphincter  function or anorectal sensation. [ 4 ] [ 7 ]  An abnormal resting pressure or squeeze pressure may indicate problems with either the  internal anal sphincter  or the  external anal sphincter  respectively. [ 4 ]  Both increased and decreased anorectal sensation has also been detected in individuals with fecal incontinence. [ 6 ]  The use of HD-ARM can allow recognition of pressure asymmetry within the anorectum. [ 4 ]  Some patients with fecal incontinence benefit from muscle strength training which may make use of anorectal biofeedback. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6825", "text": "Anorectal manometry can be used in the diagnostic workup of individuals with  chronic constipation  without a known cause [ 8 ]  or with chronic constipation that has not improved on a trial of  laxatives  and/or  fiber . [ 9 ]  For example, on a  digital rectal exam , a physician may notice specific findings that point to  dyssynergic defecation , a cause of chronic constipation. [ 8 ]  In such instances, the physician may order an anorectal manometry study to verify their findings. [ 8 ]  Abnormal results, such as the presence of a  paradoxical  contraction of the anal sphincter muscles during  defecation  (i.e. the muscles are squeezing instead of relaxing), can also be used to guide treatment (e.g. anorectal  biofeedback ). [ 4 ] [ 8 ]  Other abnormal findings on manometry consistent with chronic constipation include an unsatisfactory generation of the propulsive  force  needed to defecate and a decreased movement of  pelvic floor  muscles. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6826", "text": "Anorectal manometry, especially HR-ARM and HD-ARM, has also been used to evaluate constipation due to structural causes such as a  rectocele , [ 2 ]  an  enterocele , or an intra-anal  intussusception . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6827", "text": "In infants and children, anorectal manometry may be used to assist in the diagnosis of  Hirschsprung's disease . [ 2 ]  The absence of the  rectoanal inhibitory reflex  (RAIR) is almost always  pathognomonic  for Hirschsprung's disease in this population. [ 6 ]  Anorectal manometry is not significantly less  sensitive and specific  when compared to the  gold standard  method of diagnosis, rectal suction  biopsy . [ 6 ]  In adults, the absence of the RAIR is less likely due to Hirschsprung's disease and may indicate the presence of  megarectum . [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6828", "text": "Functional anorectal pain includes disorders such as  levator ani syndrome ,  proctalgia fugax  and unspecified functional anorectal syndrome. [ 4 ]  Although diagnosis of these disorders is largely clinical, anorectal manometry may be used for further diagnostic assessment. [ 4 ]  For example, the degree of anal sphincter hypertension may be determined [ 7 ]  which may be useful information when treating functional anorectal pain with biofeedback therapy. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6829", "text": "The goal of anorectal  biofeedback  is to help patients improve  defecating  behaviors by providing patients with visual and verbal feedback. [ 10 ]  Visual feedback tools, such as anorectal manometry, are often used to aid patients in learning how to modify their behaviors. [ 10 ]  Patients may work on improving muscle strength, muscle relaxation or sensation during defecation. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6830", "text": "The effectiveness of anorectal biofeedback as a treatment remains an ongoing source of debate and research. A systemic review article [ 11 ]  concluded that although better than  placebo , there remained limited evidence demonstrating the effectiveness of anorectal biofeedback for chronic  idiopathic  constipation. [ 8 ]  In patients with  defecatory  disorders, including  dyssynergic defecation ,  pelvic floor  biofeedback therapy had been shown to be more effective than laxatives. [ 6 ] [ 9 ]  An American-European  Neurogastroenterology & Motility  task force (ANMS-ESNM) recommended the use of biofeedback in the short and long treatment of constipation with dyssynergic defecation and fecal incontinence. [ 10 ]  They did not recommend biofeedback treatment for constipation without dyssynergic defecation, nor in children with constipation. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6831", "text": "Types of anorectal manometry include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6832", "text": "HR-ARM and HD-ARM are newer methods that use multiple closely spaced sensors in the anus and rectum, compared to 3-6 widely spaced sensors used by non-HRM, to generate a more refined view. [ 3 ] [ 6 ]  An additional benefit to HR-ARM and HD-ARM is the increased ease in analyzing the results as pressure readings are displayed in both color and as a line plot. [ 3 ]  Accompanying the benefits shared by both high-resolution and high-definition methods, the HD-ARM method employs additional sensors placed circumferentially around the catheter allowing for closer interpretation of individual sensor pressure readings. [ 3 ]  In comparison to non-HRM, however, both of the newer methods utilize equipment that is more expensive and has a shorter  design life . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6833", "text": "The specifics of the equipment used for the procedure will ultimately depend on the type of manometry and the manufacturer of the device. Nonetheless, most share some common features: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6834", "text": "In 2019, the International Anorectal Physiology Working Group (IAPWG) released a standardized testing protocol for the use of anorectal manometry. [ 5 ]  One of the goals of this protocol was to standardize procedural techniques to better facilitate meaningful data sharing. [ 5 ]  This protocol is the most recent published guideline for anorectal manometry since the one published in 2002 [ 12 ]  which was not widely adopted. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6835", "text": "Fasting  is not a requirement for this procedure. [ 5 ]  Patients are  informed  as to how the procedure is performed, its benefits and risks. Risks include the possibility of developing discomfort, pain, minor bleeding, dizziness or a rare  perforation . [ 3 ] [ 13 ]  In the testing room, the patient is placed on their left side with their knees bent. [ 5 ]  A  digital rectal exam  is then performed prior to the procedure to evaluate initial anatomy and function, check for stool, and to assess patient's understanding of the verbal instructions employed during the procedure. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6836", "text": "Anorectal manometry is often performed alongside a rectal sensory test (RST) and a balloon expulsion test (BET). [ 5 ]  The RST is performed after the manometry while the BET may be performed immediately prior to the manometry or subsequent to the RST. [ 5 ]  The total time to conduct all three tests is 15 to 20 minutes. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6837", "text": "This test takes approximately 10 minutes. [ 5 ]  With the use of a lubricant, an anorectal manometry catheter is introduced into the anus. [ 5 ]  The catheter is advanced until the base of the balloon is above the  anal canal  by 3\u20135\u00a0cm (1.2\u20132.0\u00a0in) and the most  distal  sensor is below the  anal verge . [ 5 ]  In order, the following maneuvers are then performed:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6838", "text": "During the rectal sensory test, air is placed into the catheter balloon and slowly inflated either continuously or step-wise. [ 5 ]  The patient is asked to verbalize when they first sense the balloon, when the urge to defecate is first present and when they can no longer tolerate the balloon. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6839", "text": "To perform the balloon expulsion test, a catheter with a balloon on its tip is introduced into the patient's anorectum. [ 5 ]  The balloon is then distended to 50ml with water. [ 5 ]  Patients are then instructed to transfer from lying on their side to sitting on a toilet. [ 5 ]  Next, patients are asked to push out the balloon as if they are defecating. [ 5 ]  The time it takes for the expulsion of the balloon is then recorded. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6840", "text": "The anal resting pressure is the recorded pressure within the anus during muscle relaxation. [ 6 ]  After insertion of the catheter, a short amount of time is allowed for the muscles to relax. Afterwards, pressures are recorded over 60 seconds. [ 5 ]  The  maximum  resting pressure is the highest pressure reached during this time period, while the  mean  resting pressure is the average pressure during this time period. In healthy individuals, women, especially older women, have an average lower anal resting pressures than men. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6841", "text": "The anal squeeze pressure is the recorded pressure within the anus during a voluntary contraction of the  external anal sphincter . [ 6 ]  Similar to resting pressures, squeeze pressures in healthy women are lower than healthy men. [ 6 ]  If using high-definition anorectal manometry, asymmetry in squeeze pressures can also be measured. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6842", "text": "During  defecation , the pressure in the anorectum should increase while the  external anal sphincter  should relax. If the pressure difference during defecation does not increase sufficiently, it may indicate poor propulsive force. [ 6 ] [ 14 ]  Additionally, inadequate relaxation of the sphincter during defecation is another abnormal finding. [ 6 ]  Another method to assess changes during defecation is to calculate an anorectal gradient (or defecation index) in one of two ways. [ 14 ]  The anorectal gradient is either calculated as a difference (rectal pressure - anal pressure) or as a  ratio  (rectal pressure / anal pressure). [ 14 ]  A positive difference or a ratio over 1 indicates normal findings. [ 14 ]  Abnormal findings on manometry does not definitively indicate illness as a significant number of healthy individuals have been found to have abnormal results. [ 6 ] [ 14 ]  Values recorded during a defecation trial are influenced by a number of factors including the degree of patient involvement in defecation efforts. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6843", "text": "In healthy individuals, in the process of defecating, the  internal anal sphincter  will  reflexively  relax. The lack of a  rectoanal inhibitory reflex  may indicate either the absence or the non-functionality of certain muscle or nerve structures involved in proper defecation. [ 3 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6844", "text": "Patients are assessed on their anorectal sensory perception via the inflation of a balloon. As the balloon is inflated, its volume is recorded at certain milestones: [ 5 ]  initial sensation of the equipment, start of the sensory urge to defecate and the point of maximum discomfort. [ 6 ] [ 3 ]  An increased level of sensation has been noted in disorders such as  fecal incontinence , while a decreased level of sensation has been seen in individuals with  dyssynergic defecation . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6845", "text": "As part of the 2020 IAPWG consensus manuscript, the group published the newly created London Classification for Disorders of Anorectal Function which aimed to standardize the interpretation of anorectal manometry findings. [ 5 ] [ 7 ]  The London Classification divided disorders into 4 parts:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6846", "text": "Under each part, there are a list of diagnosis that are made based on manometry findings. For example, under part 2 (Disorders of anal tone and contractility), listed manometric diagnoses include: anal hypotension, anal hypertension, anal hypercontractility and combined anal hypertension and hypercontractility. [ 7 ]  Findings are also divided into: major findings, minor findings and inconclusive findings. [ 7 ]  Major findings are findings that are not present in healthy patient such as rectoanal areflexia, [ 7 ]  Minor findings are findings that are more commonly found in patients with anorectal disease compared to healthy patients, while inconclusive findings are findings that may be present in both groups. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6847", "text": "Centers rely on published data sets from healthy volunteers to evaluate test findings. [ 4 ]  However, the lack of standardization in equipment usage and procedural protocol, can in certain cases, impact the ability to determine what may be considered normal or abnormal values. [ 4 ]  This is further complicated by the limited amount of data on the impact of different epidemiological characteristics (such as age or gender) on said values. [ 4 ]  For an individual patient, findings on anorectal manometry, alone, does not dictate management. [ 7 ]  In addition to correlating manometry findings with clinical findings, as part of a diagnostic or evaluatory workup, the use of anorectal manometry may be complemented with other diagnostic tests such as  endoanal ultrasound ,  defecography  or gut transit studies. [ 7 ]  High resolution anorectal manometry also experiences pressure drift, variable linear changes in pressure readings over time, that could impact the clinical value of manometry findings in some specific situations. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6848", "text": "An  anoscopy  is a  medical examination  using a small, rigid, tubular instrument called an anoscope (also called a  rectal speculum ).  This is inserted a few inches into the  anus  in order to evaluate problems of the  anal canal . Anoscopy is used to diagnose  hemorrhoids ,  anal fissures  (tears in the lining of the anus), and some  cancers . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6849", "text": "This test is usually done in a doctor's office. The patient is required to remove their underwear, and must either lie on their side on top of an examining table, with their knees bent up towards the chest, or bend forward over the table. The anoscope is 3 to 4\u00a0inches long and the width of an average-to-large bowel movement. The doctor will coat the anoscope with a lubricant and then gently push it into the anus and rectum. The doctor may ask the patient to \"bear down\" or push as if they were going to have a bowel movement, and then relax. This helps the doctor insert the anoscope more easily and identify any bulges along the lining of the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6850", "text": "By shining a light into this tube, the doctor will have a clear view of the lining of the lower rectum and anus. The anoscope is pulled out slowly once the test is finished."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6851", "text": "The patient will feel pressure during the examination, and the anoscope will make one feel as if they were about to have a bowel movement. This is normal, however, and many patients do not feel pain from anoscopy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6852", "text": "Anoscopy will permit  biopsies  to be taken, and is used when ligating prolapsed hemorrhoids. It is used in the treatment of warts produced by  HPV ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6853", "text": "The procedure is done on an outpatient basis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6854", "text": "A  cholecystoenterostomy  is a surgical procedure in which the  gall bladder  is joined to the  small intestine . It is performed in order to allow bile to pass from the  liver  to the  intestine  when the  common bile duct  is obstructed by an irremovable cause. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6855", "text": "A  cul-de-sac hernia  (also termed a  peritoneocele ) is a  herniation  of  peritoneal  folds into the  rectovaginal septum  (in females), [ 2 ]  or the  rectovesical septum  (in males). The herniated structure is the  recto-uterine pouch  (pouch of Douglas) in females, [ 2 ]  or the  rectovesical pouch  in males. The hernia descends below the proximal (upper) third of the vagina in females, [ 2 ]  or, according to another definition, below the pubococcygeal line (PCL). [ 3 ] [ note 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6856", "text": "According to a consensus statement by the USA, Australia and the UK, [ note 2 ]  a cul-de-sac hernia / peritoneocele is defined as \"a protrusion of the peritoneum between the rectum and vagina that does not contain any abdominal viscera\" (organs). [ 4 ]  An enterocele is defined as \"a protrusion of the peritoneum between the rectum and vagina containing the small intestine.\" [ 4 ]  A sigmoidocele is defined as \"a protrusion of the peritoneum between the rectum and vagina that contains the sigmoid colon.\" [ 4 ]  An omentocele is defined as \"a protrusion of the omentum between the rectum and the vagina.\" [ 4 ]  As such, peritoneocele, enterocele, sigmoidocele, and omentocele could be considered as types of cul-de-sac hernia. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6857", "text": "This hernia is so named because it is a herniation of the recto-uterine pouch (pouch of Douglas), which is also sometimes called the \"cul-de-sac\". This is the pocket formed by the reflection of the peritoneum from the rectum and the posterior wall of the uterus. The equivalent structure in males is the rectovesical pouch, which is the pocket formed by the reflections of the peritoneum from the rectum to the male bladder. In terms of pelvic organ prolapse, a cul-de-sac hernia is located in the posterior compartment of the pelvis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6858", "text": "A true cul-de-sac hernia contains only  omental  fat, and often  intraperitoneal liquid. [ 6 ]  If the hernia contains omentum, sometimes the term \"omentocele\" is used. [ 7 ]  If the cul-de-sac hernia contains loops of small bowel, the term  enterocele  is used. [ 2 ]  If it contains sigmoid colon, the term  sigmoidocele  is used. [ 2 ]  It has been suggested that the terms enterocele and sigmoidocele are inaccurate, since hernias are usually named according to location and not according to contents. [ 8 ]  However, the terms are in widespread use. [ 8 ]  As such, peritoneocele, enterocele, sigmoidocele, and omentocele could be considered as types of cul-de-sac hernia. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6859", "text": "Cul-de-sac hernias may be classified as rectal, septal, or vaginal depending on the structure they herniate into. Rectal cul-de-sac hernias herniate into an internal or external  rectal prolapse . Septal cul-de-sac hernias herniate into the recto-vaginal septum (rectovesical septum in males). Vaginal cul-de-sac hernias bulge into the vagina itself. Combinations of these types are also possible. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6860", "text": "Severity of the hernia may be classed as first degree if it is above the pubococcygeal line, second degree if it is below the pubococcygeal line but above the ischiococcygeal line, [ note 3 ]  or third degree if it is below the ischiococcygeal line. [ 9 ]  Severity may also be graded according the distance between the pubococcygeal line and the lowest point of the sac as follows: small (less than 3\u00a0cm), moderate (3\u20136\u00a0cm) or large (more than 6\u00a0cm). [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6861", "text": "Cul-de-sac hernias may also be classified as primary and secondary. Primary cul-de-sac hernias are associated with factors such as  multiparity , old age, lack of elasticity,  obesity ,  constipation , and increased abdominal pressure are present. [ 8 ]  Secondary cul-de-sac hernias are those which develop after gynecologic procedures, especially after vaginal hysterectomy. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6862", "text": "Another classification of cul-de-sac hernias is internal, meaning those that are only visible on defecography, or external, which are associated with a clinically visible rectocele or rectal prolapse. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6863", "text": "Symptoms are variable, and depend on the exact location and severity of the hernia. [ 10 ]  Possible symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6864", "text": "Cul-de-sac hernias are the most difficult to diagnose during physical examination, and to distinguish from anterior  rectocele  or enterocele. [ 2 ]  Furthermore, rectocele and cul-de-sac hernia may occur together. [ 3 ]  Combined vaginal and rectal digital palpation may be used (examiner's thumb in vagina, index finger in anal canal). [ 11 ]  The peritoneal sac containing omentum may be palpable between the thumb and index finger. [ 11 ]  The prolapse may be detectable at the upper posterior vaginal wall during  Valsalva's maneuver . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6865", "text": "Imaging which may be used to detect cul-de-sac hernia includes standard  defecography , magnetic resonance defecography and  dynamic transperineal ultrasound . [ 5 ]  Cul-de-sac hernias usually only appear on such imagining at the end of the simulated defecation, and require complete or near complete evacuation of the rectum before they are visible. [ 3 ]  This feature may distinguish cul-de-sac hernia from rectocele. [ 1 ]  However, a large rectocele that retains contrast medium may hide a cul-de-sac hernia. [ 3 ]  Cul-de-sac hernia (peritoneocele / omentocele) may appear on fluoroscopic defecography as an un-opacified mass which deforms the anterior border of the rectum and the posterior border of the vagina, with widening of the recto-vaginal space in between. [ 1 ]  On magnetic resonance defecography, the vagina and rectum may appear clearly \"splayed\" apart. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6866", "text": "Risk factors include prior  hysterectomy  and  urethropexy  because of the damage caused to the  rectovaginal fascia . [ 2 ]  Hysterectomy also increases the size of the pouch of Douglas. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6867", "text": "Defecography  (also known as proctography, defecating/defecation proctography, evacuating/evacuation proctography or dynamic rectal examination) is a type of medical  radiological  imaging in which the mechanics of a patient's  defecation  are visualized in real time using a  fluoroscope . [ 1 ]  The anatomy and function of the anorectum and  pelvic floor  can be dynamically studied at various stages during defecation. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6868", "text": "Defecating proctography was pioneered in 1945, during  World War II . The procedure gained popularity at this time in the midst of an outbreak of  whipworm , which is known to cause  rectal prolapse . [ 3 ]  It has since become used for diagnosis of various anorectal disorders, including  anismus  and other causes of  obstructed defecation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6869", "text": "It has fallen out of favor due to inadequate training in the technique. It is now only performed at a few institutions. Many radiology residents refer to the procedure as the \"Def Proc\", \"Defogram\", or \"Stool Finale\". [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6870", "text": "Defecography may be indicated for the following reasons:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6871", "text": "Specifically, defecography can differentiate between anterior and posterior  rectocele . [ 4 ]  Also, in external  rectal prolapse  that was not directly visualized during examination, this radiographic projection will demonstrate its presence."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6872", "text": "In females, pre-procedural preparation involves smearing a small amount of  barium   contrast agent  in the vagina, which will help to identify if anterior  rectocele ,  enterocele  or  sigmoidocele  is present."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6873", "text": "The technique itself involves the insertion of a  caulking gun  device into the rectum with a subsequent manual infusion of barium paste until there is adequate distension. The patient is then transferred to a portable plastic commode which is situated next to a fluoroscope which records the defecation. Positioning of the X-ray camera is of paramount importance as visualization of the buttocks, rectal vault, and lower pelvis is critical."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6874", "text": "Anatomical and physiological parameters that can be objectively measured by this investigation include: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6875", "text": "Conditions which may be demonstrated include: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6876", "text": "The rectum may be seen to prolapse, whether internally or externally. There can be difficulty differentiating between internal intussusception and a normal rectal fold. The thickness of the intussusception is half the width of the intussusception (the intussusception is a doubled over layer of rectal wall). This is most likely to be seen during straining."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6877", "text": "Cinedefecography is a technique that is an evolution of defecography. The defecation cycle is recorded as a continuous series rather than individual still radiographs. [ 2 ]  More recent techniques involve the use of advanced, cross-sectional imaging modalities such as  magnetic resonance imaging . [ 6 ]  This is known as dynamic pelvic MRI, or MRI proctography. [ 2 ]  The MRI proctography also called MRI defecography is not as efficient as conventional X-ray defecography for some problems. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6878", "text": "Diseases of the Colon & Rectum  is a monthly  peer-reviewed   medical journal  covering  colorectal surgery . It was established in 1958 and is published by  Lippincott Williams and Wilkins  on behalf of the  American Society of Colon and Rectal Surgeons , of which it is the official journal. The  editor-in-chief  is Susan Galandiuk ( University of Louisville ). According to the  Journal Citation Reports , the journal has a 2016  impact factor  of 3.519. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6879", "text": "Endodermal sinus tumor  ( EST ) is a member of the  germ cell tumor  group of  cancers . [ 1 ]  It is the most common testicular tumor in children under three, [ 2 ]  and is also known as  infantile embryonal carcinoma . This age group has a very good prognosis. In contrast to the pure form typical of infants, adult endodermal sinus tumors are often found in combination with other kinds of germ cell tumor, particularly  teratoma  and  embryonal carcinoma . While pure teratoma is usually  benign , endodermal sinus tumor is  malignant ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6880", "text": "Causes for this cancer are poorly understood. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6881", "text": "The  histology  of EST is variable, but usually includes malignant endodermal cells. These cells secrete  alpha-fetoprotein  (AFP), which can be detected in tumor tissue,  serum ,  cerebrospinal fluid ,  urine  and, in the rare case of fetal EST, in  amniotic fluid . When there is incongruence between  biopsy  and AFP test results for EST, the result indicating presence of EST dictates treatment. [ 3 ]  This is because EST often occurs as small \"malignant foci\" within a larger tumor, usually  teratoma , and biopsy is a sampling method; biopsy of the tumor may reveal only teratoma, whereas elevated AFP reveals that EST is also present. GATA-4, a  transcription factor , also may be useful in the diagnosis of EST. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6882", "text": "Diagnosis of EST in  pregnant women  and in  infants  is complicated by the extremely high levels of AFP in those two groups. Tumor surveillance by monitoring AFP requires accurate correction for gestational age in pregnant women, and age in infants. In pregnant women, this can be achieved simply by testing  maternal serum AFP  rather than  tumor marker AFP . In infants, the tumor marker test is used, but must be interpreted using a reference table or graph of normal AFP in infants. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6883", "text": "EST can have a multitude of morphologic patterns including: reticular, endodermal sinus-like, microcystic, papillary, solid, glandular, alveolar, polyvesicular vitelline, enteric and hepatoid. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6884", "text": "Schiller\u2013Duval bodies  on  histology  are  pathognomonic  and seen in the context of the endodermal sinus-like pattern. Rarely, it can be found in the vagina. [ 6 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6885", "text": "Most treatments involve some combination of  surgery  and  chemotherapy . Treatment with  cisplatin ,  etoposide , and  bleomycin  has been described. [ 8 ]  Before modern chemotherapy, this type of neoplasm was highly lethal, but the prognosis has significantly improved since then. [ citation needed ]  When endodermal sinus tumors are treated promptly with surgery and chemotherapy, fatal outcomes are exceedingly rare. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6886", "text": "Germ cell tumor  ( GCT ) is a  neoplasm  derived from the  primordial germ cells . [ 1 ]  Germ-cell tumors can be  cancerous  or  benign . Germ cells normally occur inside the  gonads  ( ovary [ 2 ]  and  testis ).  GCTs that originate outside the gonads may be  birth defects  resulting from errors during  development  of the  embryo ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6887", "text": "GCTs are classified by their  histology , [ 4 ]  regardless of location in the body. However, as more information about the genetics of these tumors become available, they may be classified based on specific gene mutations that characterize specific tumors. [ 5 ]  They are broadly divided in two classes: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6888", "text": "The two classes reflect an important clinical difference. Compared with germinomatous tumors, nongerminomatous tumors tend to grow faster, have an earlier mean age at time of diagnosis (around 25 years versus 35 years, in the case of  testicular cancers ), and have a lower five-year survival rate.  The survival rate for germinomatous tumors is higher in part because these tumors are very sensitive to radiation, and they also respond well to chemotherapy.  The prognosis for nongerminomatous tumours has improved dramatically, however, due to the use of platinum-based chemotherapy regimens. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6889", "text": "Mixed germ cell tumors occur in many forms.  Among these, a common form is teratoma with endodermal sinus tumor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6890", "text": "Teratocarcinoma refers to a germ cell tumor that is a mixture of  teratoma  with  embryonal carcinoma , or with  choriocarcinoma , or with both. [ 9 ]   This kind of mixed germ cell tumor may be known simply as a teratoma with elements of embryonal carcinoma or choriocarcinoma, or simply by ignoring the teratoma component and referring only to its malignant component:  embryonal carcinoma and/or choriocarcinoma. They can present in the  anterior mediastinum . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6891", "text": "Some investigators suggest that this distribution arises as a consequence of abnormal migration of germ cells during embryogenesis. Others hypothesize a widespread distribution of germ cells to multiple sites during normal embryogenesis, with these cells conveying genetic information or providing regulatory functions at somatic sites. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6892", "text": "Extragonadal GCTs were thought initially to be isolated  metastases  from an undetected primary tumor in a  gonad , but many germ cell tumors are now known to be   congenital  and originate outside the gonads.  The most notable of these is  sacrococcygeal teratoma , the single most common tumor diagnosed in babies at birth. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6893", "text": "Of all anterior mediastinal tumors, 15\u201320% are GCTs of which about 50% are benign teratomas. [ 10 ]  Ovarian teratomas may be associated with  anti-NMDA receptor encephalitis . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6894", "text": "Despite their name, GCTs occur both within and outside the  ovary  and  testis . They are found in: [ citation needed ] }"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6895", "text": "In females, GCTs account for 30% of ovarian tumors, but only 1 to 3% of  ovarian cancers  in  North America . In younger women, they are more common, thus in patients under the age of 21, 60% of ovarian tumors are of the  germ-cell type , and up to one-third are  malignant . In males, GCTs of the testis occur typically after puberty and are malignant ( testicular cancer ).  In  neonates ,  infants , and  children  younger than 4 years, most are  sacrococcygeal teratomas . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6896", "text": "Males with  Klinefelter syndrome  have a 50 times greater risk of GSTs. [ 12 ]   In these persons, GSTs usually contain nonseminomatous elements, present at an earlier age, and seldom are gonadal in location. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6897", "text": "Women with benign GCTs such as  mature teratomas  (dermoid cysts) are cured by  ovarian cystectomy  or  oophorectomy . [ 13 ]  In general, all patients with malignant GCTs have the same staging surgery that is done for  epithelial ovarian cancer . [ 14 ]  If the patient is in her reproductive years, an alternative is unilateral  salpingoophorectomy , while the uterus, the ovary, and the fallopian tube on the opposite side can be left behind. This is not an option when the cancer is in both ovaries. If the patient has finished having children, the surgery involves complete staging, including salpingoophorectomy on both sides, as well as  hysterectomy . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6898", "text": "Patients with germ-cell cancer often need to be treated with combination  chemotherapy  for at least three cycles, but female patients with early-stage disease may not require this treatment. [ 15 ]  The  chemotherapy regimen  most commonly used in GCTs is called PEB (or BEP), and consists of  bleomycin ,  etoposide , and a  platinum-based antineoplastic  ( cisplatin ). [ 13 ]  Targeted treatments, such as immunotherapy, hormonal therapy and kinase inhibitors, are being evaluated for tumors that do not respond to chemotherapy. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6899", "text": "The 1997 International Germ Cell Consensus Classification [ 17 ]  is a tool for estimating the risk of relapse after treatment of malignant germ-cell tumor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6900", "text": "A small study of ovarian tumors in girls [ 18 ]  reports a correlation between  cystic  and benign tumors, and conversely, solid and malignant tumors.  Because the cystic extent of a tumor can be estimated by ultrasound, MRI, or CT scan before surgery, this permits selection of the most appropriate surgical plan to minimize risk of spillage of a malignant tumor. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6901", "text": "Access to appropriate treatment has a large effect on outcome.  A 1993 study of outcomes in Scotland found that for 454 men with nonseminomatous (nongerminomatous) GCTs diagnosed between 1975 and 1989, five-year survival increased over time and with earlier diagnosis.  Adjusting for these and other factors, survival was 60% higher for men treated in a cancer unit that treated the majority of these men,  though the unit treated more men with the worst prognosis. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6902", "text": "Choriocarcinoma  of the testicles has the worst prognosis of all germ-cell cancers. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6903", "text": "A  gonadoblastoma  is a complex  neoplasm  composed of a mixture of  gonadal  elements, [ 1 ]  such as large primordial  germ cells , immature  Sertoli cells  or  granulosa cells  of the  sex cord , and gonadal  stromal cells . Gonadoblastomas are by definition benign, but more than 50% have a co-existing  dysgerminoma  which is malignant, and an additional 10% have other more aggressive malignancies, and as such are often treated as malignant. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6904", "text": "Gonadoblastoma is most often associated with an abnormal chromosomal  karyotype , gonadal  dysgenesis , or the presence of a  Y chromosome  in over 90% of cases. Gonadoblastoma has been found in association with  androgen insensitivity syndrome ,  mixed gonadal dysgenesis  and  Turner syndrome , especially in the presence of Y chromosome-bearing cells. [ 3 ] [ 4 ]  Women with Turner syndrome whose karyotype includes a Y chromosome (as in 45,X/46,XY mosaicism) are at increased risk for gonadoblastoma. Because of the risk of gonadoblastoma, individuals with Turner syndrome with detectable Y chromosome material (Mosaic Turner syndrome) should have their gonads prophylactically removed. In a population-based study, the cumulative risk for women with Turner syndrome and Y chromosome material was 7.9 percent by age 25 years. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6905", "text": "Gonadoblastomas can contain elements of both germ cells and gonadal stroma. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6906", "text": "Formerly, gonadoblastoma was sometimes regarded as a subset of  dysgerminoma . In modern literature, it is sometimes considered to progress to dysgerminoma. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6907", "text": "Standard treatment would include surgical exploration via  laparotomy .  Laparoscopy  may be an option if the surgeon is particularly skilled in removing ovarian neoplasms via laparoscopy intact. If the diagnosis of gonadoblastoma is certain, a bilateral  salpingo-oophorectomy  (BSO) should be performed to remove both the primary tumor and the dysgenic contralateral ovary. If uninvolved, the  uterus  should be left intact. Modern reproductive endocrinology technology allows patients post BSO to achieve pregnancy via in-vitro fertilization ( IVF ) with a donor egg. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6908", "text": "Goodsall's rule  relates the external opening (in the perianal skin) of an  anal fistula  to its internal opening (in the anal canal). It states that if the perianal skin opening is posterior to the transverse anal line, the fistulous tract will open into the anal canal in the midline posteriorly, sometimes taking a curvilinear course. A perianal skin opening anterior to the transverse anal line (within 3cm radius) is usually associated with a radial fistulous tract but if it's beyond the 3 cm radius it will take a curvilinear course and open in the midline posterioly. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6909", "text": "Or in more direct terms, it means that anterior-opening fistulas tend to follow a simple, direct course if it is within the 3cm radius, beyond which it takes a curving path and opens in poster midline. The posterior-opening fistulas may follow a devious, curving path with some even being horseshoe-shaped before opening in the posterior midline. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6910", "text": "Fistulas  can be described as  anterior or posterior  relating to a line drawn in the  coronal plane  across the  anus , the so-called transverse anal line. Anterior fistulas will have a direct track into the anal canal. Posterior fistulas will have a curved track with their external opening lying in the posterior midline of the  anal canal . An exception to the rule are anterior fistulas lying more than 3.75\u00a0cm from the anus, which may have a curved track (similar to posterior fistulas) that opens into the posterior midline of the anal canal."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6911", "text": "According to a study on patients undergoing operations for cryptoglandular anal fistulas, 92.9% of fistulas within 1.5\u00a0cm followed the Goodsall rule, whereas only 47.4% followed it beyond 3.6\u00a0cm. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6912", "text": "In situations where there are multiple anal fistulae, the course would be similar to that of posterior-opening fistulae because of branching and communication between these openings. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6913", "text": "The investigation of choice for anal fistulas is  magnetic resonance imaging  (MRI). Fistulograms can be used to demonstrate the track of the fistula."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6914", "text": "Goodsall's rule is named after  David Henry Goodsall  who described it in 1900."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6915", "text": "An  imperforate anus  or  anorectal malformations  ( ARMs ) are  birth defects  in which the  rectum  is malformed. ARMs are a spectrum of different congenital anomalies which vary from fairly minor  lesions  to complex anomalies. [ 1 ]  The cause of ARMs is unknown; the genetic basis of these anomalies is very complex because of their anatomical variability. In 8% of patients, genetic factors are clearly associated with ARMs. [ 2 ]   Anorectal malformation  in  Currarino syndrome  represents the only association for which the gene  HLXB9  has been identified. [ clarification needed ] [ 1 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6916", "text": "There are other forms of anorectal malformations though imperforate anus is most common. Other variants include  cloacal malformation , rectal atresia, rectal stenosis, and anterior ectopic anus. [ 4 ] [ 5 ]  This form is more commonly seen in females and presents with constipation. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6917", "text": "There are several forms of imperforate anus and anorectal malformations. The new classification is in relation of the type of associated  fistula . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6918", "text": "The Wingspread classification was in low and high anomalies: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6919", "text": "Imperforate anus is usually present along with other birth defects\u2014 spinal  problems,  heart  problems,  tracheoesophageal fistula ,  esophageal atresia ,  renal  anomalies and  limb  anomalies are among the possibilities, collectively being called the  VACTERL association . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6920", "text": "Imperforate anus is associated with an increased incidence of some other specific anomalies as well, together being called the  VACTERL association . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6921", "text": "Other entities associated with an imperforate anus are trisomies 18 and 21, the  cat-eye syndrome  (partial  trisomy  or  tetrasomy  of a maternally derived  chromosome 22 ),  Baller\u2013Gerold syndrome ,  Currarino syndrome ,  caudal regression syndrome ,  FG syndrome ,  Johanson\u2013Blizzard syndrome ,  McKusick\u2013Kaufman syndrome ,  Pallister\u2013Hall syndrome ,  short rib\u2013polydactyly syndrome type 1 ,  Townes\u2013Brocks syndrome ,  13q deletion syndrome ,  urorectal septum malformation sequence  and the  OEIS complex  ( omphalocele ,  exstrophy  of the  cloaca , imperforate anus, spinal defects). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6922", "text": "When an infant is born with an anorectal malformation, it is usually detected quickly as it is a very obvious defect. Doctors will then determine the type of birth defect the child was born with and whether or not there are any associated malformations. Determining the presence of any associated defects during the newborn period in order to treat them early may avoid further  sequelae . There are two main categories of anorectal malformations: those that require a protective  colostomy  and those that do not. The decision to open a colostomy is usually taken within the first 24 hours of birth. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6923", "text": "Sonography  can be used to determine the type of imperforate anus. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6924", "text": "Imperforate anus usually requires immediate  surgery  to open a passage for  feces  unless a  fistula  can be relied on until corrective surgery takes place. Depending on the severity of the imperforate, it is treated either with a perineal  anoplasty [ 10 ]  or with a  colostomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6925", "text": "While many surgical techniques to definitively repair anorectal malformations have been described, the posterior sagittal approach (PSARP) has become the most popular. It involves dissection of the perineum without entry into the abdomen and 90% of defects in boys can be repaired this way. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6926", "text": "With a high lesion, many children have problems controlling bowel function and most also become  constipated . With a low lesion, children generally have good bowel control, but they may still become constipated. For children who have a poor outcome for continence and constipation from the initial surgery, further surgery to better establish the angle between the anus and the rectum may improve continence and, for those with a large rectum, surgery to remove that dilated segment may significantly improve the bowel control for the patient.  An antegrade enema mechanism can be established by joining the appendix to the skin (Malone stoma); however, establishing more normal anatomy is the priority. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6927", "text": "Imperforate anus has an estimated incidence of 1 in 5,000 births. [ 11 ] [ 12 ]  It affects boys and girls with similar frequency. [ 13 ]   However, imperforate anus will present as the low version 90% of the time in females and 50% of the time in males."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6928", "text": "Imperforate anus is an occasional complication of  sacrococcygeal teratoma . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6929", "text": "7th-century  Byzantine  physician  Paulus Aegineta  described a surgical treatment for imperforate anus for the first time. [ 15 ]  10th-century  Persian  physician  Haly Abbas  was the first to highlight preserving the  sphincter muscles  throughout the surgery and the prevention of strictures with a  stent . [ 15 ]  He has reported the use of wine for wound care in this surgery. Some reports of children surviving this surgery are available from the early  medieval Islamic era . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6930", "text": "A  keyhole defect  is a term used in medicine and in the  forensic sciences  to refer to the shape of an anomalous feature or traumatic lesion caused by a  gunshot wound ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6931", "text": "A keyhole defect is characteristic of a type of entrance wound caused by a bullet striking the surface of a flat bone (typically the  cranium ) at a shallow angle. [ 1 ]  The defect is characterized by a rounded portion with a clean margin where the bullet first perforates bone, and a wider area with external beveling on the opposite end.  The keyhole entrance wound can thus indicate the trajectory of the bullet at the time of impact."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6932", "text": "In  proctology , a keyhole defect may refer to a groove in the  anal canal  wall, which can occur after posterior midline  fissurectomy  or  fistulotomy  (surgical operations involving the anal canal), or with lateral internal anal sphincter defects. The keyhole defect is associated with minor degrees of  fecal incontinence , allowing seepage of liquid stool or mucus. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6933", "text": "LIFT technique  is the novel modified approach through the  intersphincteric  plane for the treatment of  fistula-in-ano , known as LIFT (ligation of intersphincteric fistula tract) procedure. LIFT procedure is based on secure closure of the internal opening and removal of infected  cryptoglandular  tissue through the intersphincteric approach. Essential steps of the procedure include, incision at the intersphincteric groove, identification of the intersphincteric tract, ligation of intersphincteric tract close to the internal opening and removal of intersphincteric tract, scraping out all  granulation tissue  in the rest of the fistulous tract, and suturing of the defect at the external sphincter muscle. [ 1 ] \nThe procedure was developed by Thai colorectal surgeon, Arun Rojanasakul, Colorectal Division Department of Surgery,  Chulalongkorn University  in  Bangkok, Thailand . The first report of preliminary healing result from the procedure were 94% in 2007  [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6934", "text": "In 1993 Matos et al. described a technique of total anal sphincter preservation in high fistula in ano, which is based on the concept of excision of intersphincteric anal gland infection through the intersphincteric approach. [ 3 ]  This novel technique was also documented in Corman\u2019s textbook of colon and rectal surgery. [ 4 ]  However, the technique was not widely adopted. [ 5 ] \nBetween 2004 and 2005 there was a personal experience in the similar technique by group of surgeons. That technique included coring out the intersphinteric fistula tract from the external opening to the external sphincter, excision of the intersphincteric fistula tract and suture of the internal sphincter defect through the intersphincteric plane. The outcome in 20 patients was disappointing with only 9 (45%) successes. Surgeons proposed that the reasons for the unfavorable outcome include dissection in the intersphincteric plane damaging blood supply to the internal opening area, and suturing delicate ischemic areas with increased risk of suture break-down. Surgeons thought that ligation of the intersphincteric tract close to the internal opening might solve the problem. Surgeons noticed that during intersphincteric plane dissection if the internal sphincter was damaged and the anal mucosa breached, failure was common despite meticulous repair. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6935", "text": "Researchers of the procedure agree that the LIFT technique may cause some injury to internal sphincter, but theoretically LIFT causes less trauma of the internal sphincter than the other fistula operations.  Matos et al. reported the technique of excision of the whole fistula tract plus primary repair, with intersphincteric plane approach for excision of the fistula tract and suturing of the internal anal sphincter defect, in 1993. [ 3 ]  However, Rojanasakul reported the ligation of intersphincteric fistula tract in 2007 with apparent satisfactory results probably due to secured closure of the internal opening. [ 2 ]  This represents a significant change from the originally described technique with improved outcomes . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6936", "text": "Low anterior resection syndrome  is a  complication  of  lower anterior resection , a type of surgery performed to remove the  rectum , typically for  rectal cancer . It is characterized by changes to bowel function that affect quality of life, and includes symptoms such as  fecal incontinence , incomplete defecation or the sensation of incomplete defecation ( rectal tenesmus ), changes in stool frequency or consistency, unpredictable bowel function, and painful defecation ( dyschezia ). [ 1 ]  Treatment options include symptom management, such as use of  enemas , or surgical management, such as creation of a  colostomy . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6937", "text": "Low anterior resection syndrome falls into two groups. Fecal urgency,  incontinence , and increased frequency make up the first.  Constipation , a sense of incomplete evacuation, and trouble emptying the bowels are included in the second category. Some patients describe characteristics from both groups, either switching back and forth between the two patterns or going through both at once. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6938", "text": "Low anterior resection syndrome emerges after rectal resection. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6939", "text": "The two factors that negatively affect patients' bowel function after lower anterior resection are low tumor height and  radiation , either pre- or post-operative. Additionally linked to worse bowel function are  stomas  that are temporary in nature and those that have been in place for an extended length of time. This, however, is probably a reflection of the height of the tumor and potential surgical complications, which may also have a deleterious effect on bowel function. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6940", "text": "Multiple factors likely contribute to low anterior resection syndrome. During intersphincteric resection, the  internal anal sphincter  may sustain direct structural damage that leads to fecal  incontinence , or secondary damage from the insertion of an anastomotic device through the  anus  during low anterior resection. [ 6 ]  In particular, if the surgical approach reaches the posterolateral side of the  prostate  (in men), where both the  sympathetic  and  parasympathetic   nerve fibers  enter the rectal wall, damage to the  internal anal sphincter 's nerve supply may also result in dysfunction. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6941", "text": "When performing a low anterior resection, the conjoint longitudinal muscle may also sustain damage during the surgical dissection of the intersphincteric space. [ 3 ]  Furthermore, in order to achieve a sufficient horizontal marginanally, the  rectococcygeus muscle  is frequently divided, which impairs the muscle's functionality. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6942", "text": "A decrease in the maximum allowable rectal volume following low anterior resection and an increase in the false urge to urinate can result from poor compliance brought on by rectal volume loss. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6943", "text": "The extrinsic  spinal cord  nerves that mediate the rectoanal inhibitory reflex may also be injured during a low anterior resection, resulting in intestinal dysfunction. [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6944", "text": "Low anterior resection syndrome can be assessed using two patient questionnaires that have been validated. [ 3 ]  After sphincter-preserving surgery, the 18-item validated  Memorial Sloan Kettering Cancer Center  Bowel Function Instrument (MSKCC-BFI) can be used to assess bowel function. It was developed in 2004. [ 12 ]  A 5-item validated questionnaire called the LARS score was developed in 2012 by Emmertsen et al. in a Danish population as a second scoring system to evaluate bowel function following sphincter-preserving surgery for rectal cancer. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6945", "text": "Anorectal manometry  objectively assesses anal sphincter function and rectal capacity by recording resting pressure, maximum squeezing pressure, rectoanal inhibitory reflex, rectal capacity, and compliance with a balloon catheter and pressure sensor. Although it can be used to direct and track the effectiveness of therapy,  anorectal manometry  is not necessary for the diagnosis of low anterior resection syndrome. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6946", "text": "Endoscopic rectal ultrasound  is a useful tool for evaluating the  pelvic floor  and sphincter complex structure. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6947", "text": "Fecoflowmetry is a valuable technique for evaluating anorectal motor function following surgery. It works by tracking changes in flow against time and analyzing the fecal flow rate, which is the result of rectal detrusor action against anorectal outlet resistance. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6948", "text": "The foundation of\u00a0treatment for low anterior resection syndrome is conservative therapy, including pelvic floor rehabilitation,\u00a0 colonic irrigation , or minimally invasive procedures, such as spinal nerve stimulation. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6949", "text": "For the short-term treatment of a single symptom, certain patients should be treated with loperamide or  antibiotics  like neomicine or  rifaximin  (in the event of proximal expansion of native gut microbes or  small-intestinal bacterial overgrowth  shown with the  lactulose  breath test). [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6950", "text": "Although  bile acid sequestrants  like  colesevelam  and  5-HT3 antagonists  like  ramosetron  have shown intriguing early results, more research is still needed. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6951", "text": "Transanal irrigation is an inexpensive and successful treatment for the high frequency of defecations and incontinence linked to low anterior resection syndrome. [ 18 ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6952", "text": "Sacral nerve stimulation  (SNS) is associated with improved fecal incontinence and deferred defecation among individuals with normal as well as impaired sphincters, as well as in patients with low anterior resection syndrome. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6953", "text": "When  fecal incontinence  becomes unmanageable, surgery may be a viable treatment option. When all other forms of treatment have been exhausted, a  stoma  should be taken into consideration. Sphincteric substitution and other advanced surgical techniques ought to be reserved for a very select group of patients. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6954", "text": "These procedures aim to inject  bio-compatible  material ( perianal injectable bulking agents , also termed  sphincter bulking agents [ 1 ]  or  biomaterial injectables ) [ 2 ]  into the walls of the anal canal, in order to bulk out these tissues. This may bring the walls of the anal canal into tighter contact, raising the resting pressure, creating more of a barrier to the loss of stool, and thereby reducing  fecal incontinence . This procedure has many advantages over more invasive surgery, since there are rarely any serious complications. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6955", "text": "Originally, injectable bulking agents were used to treat  stress urinary incontinence  in females. [ 4 ]  The procedure aimed to bulk out the tissues of the neck of the bladder, and it was successful. [ 5 ]  The technique was first used for FI in 1993 by an Egyptian surgeon. [ 6 ]  He used  polytetrafluroethylene  (PTFE/polytef/Teflon) paste injected into the submucosal layer of anal canal. [ 5 ] [ 4 ]  Later publications described autologous transplantation of fat from the abdominal wall or the buttock. [ 5 ] [ 4 ]  After about the year 2000, many different materials started to be used as well as variations of the technique. Some of these materials were concurrently being used to treat urinary incontinence. The latest development of this technique is the  implantable bulking agents  \"Gatekeeper\" and \"Sphinkeeper\". [ 4 ]  These are not injectable materials but rather implants which expand after placement. [ 7 ]  As such, they are termed \"self-expandable prostheses\", and the term \"non-self-expandable prostheses\" is used to refer to older injectable materials. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6956", "text": "The exact methods of this procedure are not standardized and vary considerably, [ 8 ] [ 9 ]  for example the exact number and locations of the injections and the volume of the injected material. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6957", "text": "Before the operation, antibiotic prophylaxis may be given. [ 10 ]  The rectum is prepared with a phosphate enema at least 2 hours before the procedure. [ 10 ]  The procedure can be carried out under  local anesthetic  on an  out patient  basis, or with  caudal epidural anesthesia , [ 8 ]  or with  intravenous sedation , or under  general anesthesia . [ 3 ]   Ultrasound  guidance may be used during the injections, which is sometimes reported as being more effective than the surgeon simply  palpating  (feeling) and looking where to inject."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6958", "text": "The site of the bulking material can be inter-sphincteric (in the space between the IAS and the EAS), submucosal injections (under the mucosal layer, usually just above the dentate line), or within the IAS itself. [ 3 ] [ 4 ]  Injection of the material can be by the different routes: transanal route, trans-sphincteric, intersphincteric, perianal route (going through the muscle complex) or transcutaneous route. [ 3 ]  As such, there are several different variations of injection location and route: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6959", "text": "The perianal injection route (intersphincteric or transsphincteric) gives better results than the transanal route according to one review. [ 3 ]  Submucosal implant location may have a higher risk of erosion and sepsis. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6960", "text": "Many different materials have been used as perianal injectable bulking agents. [ 11 ]  The ideal injectable or implantable material would be biocompatible, non-migratory, non- allergenic , non- carcinogenic  and non-immunogenic (and therefore induce a minimal inflammatory and fibrotic reaction). [ 5 ] [ 4 ] [ 10 ]  The material should also be easy to inject. The particles should be greater than 80 \u03bcm in diameter in order to prevent migration away from the injection site. On the other hand, materials with particles small enough to be used in small caliber needles may be desirable, in order to leave a smaller needle track, which may reduce the chance of leakage of the material via the needle track. Alternatively, some materials are shape-retaining porous hydrogels with no particles. [ 5 ]  The ideal material should produce an improvement in continence not only in the short term, but in the long term, and repeated procedures should not be necessary. [ 4 ]  Technically, most materials are particles suspended in a carrier (excipient) solution, which is usually a biodegradable gel. [ 12 ] [ 10 ]  It is not known which of the available materials is the best. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6961", "text": "This was the original material used as a bulking agent, first used to treat urinary incontinence in 1964, and then about 20 years later it was the first material used as a bulking agent to treat FI.  Polytef paste is  polytetrafluoroethylene ,  glycerin  and  polysorbide . The particles are mostly very small in size (4\u201340-\u03bcm). Research in animals has shown that these particles migrate and may be found in lymph nodes, lungs, kidneys, spleen and brain. [ 5 ]  If the material mostly migrates away, any benefit will be temporary, and there are safety concerns that it could lead to the formation of foreign body  granulomas  and the development of  sarcoma . [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6962", "text": "This variation of the procedure uses the patient's own fat cells, and therefore is non-allergenic and non-immunogenic. [ 5 ]  The fat cells are taken from the abdominal wall by suction. Then they are purified and put into a saline solution before injection. [ 10 ]  When used in other fields such as urology or facial surgery, autologous fat transplants have very rarely been reported to cause  fat embolism  and  stroke . [ 4 ]  This material is also subject to rapid digestion and migration. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6963", "text": "This is a silicone biomaterial, marketed as \"PTQ\" or \"Bioplastique\". It is polydimethylsiloxane elastomer particles suspended in a biocompatible carrier hydrogel of  poly-N-vinyl-pyrrolidone  (povidone). Significantly more publications exist which investigate this material compared to the other materials, [ 4 ]  and it has been the most widely used bulking material used for FI. [ 10 ]  Publications used inter-sphincteric or  within IAS injection sites via the trans-sphincteric route. [ 4 ]  The particles are in the range 100\u2013450 \u03bcm with smaller particles in the gel. Therefore there is a possibility of migration and granuloma formation. There are also concerns about a link between autoimmune diseases and silicone. The bulking agent is very viscous which makes it difficult to inject. [ 5 ]  After injection there is irregular collagen deposition around and inside the implant. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6964", "text": "After PTQ, this material has most scientific publications. Publications described using it via the transmucosal or trans-sphincteric routes, with the end location of the material being the submucosa. It is composed of carbon-coated zirconium beads (pyrolytic carbon-coated beads) in a water-based carrier gel containing  \u03b2-glucan . [ 4 ]  Pyrolytic carbon is not biologically reactive and does not undergo degradation. It is used in various medical devices including heart valves. The particle size of Durasphere is in the range 212-500 \u03bcm, [ 5 ]  which is approximately 3 times the migration threshold of 80 \u03bcm. [ 10 ]  However, one report of the material as used in urology showed significant migration to local and distant lymph nodes. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6965", "text": "This is a newer material which became more popular after 2011. [ 2 ]  It is marketed as NASHA Dx, Zuidex, or Solesta. [ 4 ]  As of 2022, NASHA Dx is the only material approved in the US by the U.S. Food and Drug Administration (FDA). [ 8 ]  This material is composed of crosslinked dextranomer (dextran) microspheres and non-animal stabilized sodium hyaluronate (NASHA) in phosphate-buffered 0.9%  sodium chloride  solution. [ 4 ]  The particles are 120 \u03bcm in diameter. The material is non-allergenic, non-immunogenic and non-migratory. After injection, the hyaluronic acid is degraded, and soft tissue fibrosis forms with ingrowth of fibroblasts, inflammatory cells, blood vessels and collagen. This means that even though the particles undergo degradation, the bulking effects may persist. [ 5 ]  There are several publications which report the use of this material. They used submucosal injection site via the transmucosal route. [ 4 ]  Uncertainty about indications, cost, and durability of the material in the long term stopped widespread adoption of this material. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6966", "text": "Marketed as \"Coaptite\", this is spherical particles of calcium hydroxylapatite ceramic suspended in a sodium carboxylmethylcellulose, glycerine and water carrier gel. [ 4 ]  This is a synthetic version of a compound that is a normal component of bones and teeth. It is non-antigenic and noninflammatory. The particle size is in the range 75\u2013125 \u03bcm and therefore should avoid migration away from the implant site.  Once in place, the particles are enmeshed in a non-encapsulated stable soft collagen matrix. This matrix maintains volume even after the solid particles have been degraded and resorbed. The material is radio-opaque (and therefore will be visible on x-rays). It has been used in dental and orthopedic reconstructive surgery, and for replacement heart valves. In the field of plastic surgery, it is termed Radiance FNTM. [ 5 ]  As of 2022 only one publication exists. The material was used in submucosal injection site via transsphincteric route. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6967", "text": "GAX (glutaraldehyde cross-linked) collagen is purified collagen from cow skin, marketed as Contigen. [ 5 ] [ 4 ]  Enzymes are used to remove  telopeptides , which reduces the antigenicity (the degree to which the body's immune cells will be able to recognize the material as a foreign body). About 5% of patients will have an immune reaction to this material, therefore allergy testing is carried out before the final procedure. There is also a concern about disease transmission. [ 5 ]  This material contains 95% collagen Type I and 1-5% of collagen Type III. [ 10 ]  Chemical cross-linking with glutaraldehyde is intended to stop the degradation of the material by collagenases. [ 5 ]  The carrier solution is physiological saline with phosphate. [ 10 ]  The material does not seem to be associated with formation of granulomas or migration, however it is subject to degradation over time. [ 5 ]  In publications is has been used with submucosal injection site via transmucosal route. [ 4 ]  This material has not achieved widespread use. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6968", "text": "Cross-linked porcine dermal collagen matrix (collagen from pig skin) has been used, marketed as Permacol. [ 5 ]  It consists of large particles of cross-linked porcine dermal collagen. [ 10 ]  It has been used for urinary incontinence and for facial contour augmentation, as well as for FI. It is biocompatible, non-allergenic and has improved durability due to revascularization and cell ingrowth following injection. [ 5 ]  In several publications where the material was used for FI, submucosal or intersphincteric injection site was used, via the transmucosal or intersphincteric routes. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6969", "text": "Marketed as Bulkamid, this material is a synthetic non-particulate hydrogel composed of water and cross-linked polyacrylamide (2.5%). [ 4 ]  The size of the molecules is large which makes it resistant to migration. Since it is a non particulate homogeneous hydrogel, it is thought to retain elasticity and does not lead to hard tissue fibrosis or cause other significant reaction in the surrounding tissues. [ 5 ] [ 10 ]  It is non-resorbable and non allergenic. In plastic surgery it is marketed as Aquamid. [ 5 ]  In one publication where it was used for FI, intersphincteric injection site was used via the intersphincteric route. [ 4 ]  This material has not achieved widespread use. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6970", "text": "ALTA injection is somewhat different to the other materials because it is a sclerosant (i.e. it is a type causes  sclerosis , or hardening of tissue). Therefore, it may be technically classified as a type of  sclerotherapy . This injectable material has been used for treatment of grade III to IV prolapsed internal  hemorrhoids , where it gives effects similar to  hemorrhoidectomy . It has also been used for treatment of  rectal prolapse  and  rectocele . [ 8 ]  The material causes a local inflammatory reaction, followed by sclerosis and retraction of tissues. This results in a chronic granulomatous inflammatory process and persistent  fibrosis . When used to treat rectal prolapse or mucosal prolapse, it is injected into a wider area (not just into the hemorrhoid cushions, but also into parts of the rectal mucosa), leading to thickening and toughening of the anal canal and rectal wall. This has been shown to increase the maximal resting pressure of the anal canal. Therefore, the result is thought to be similar to other injectable bulking agents, although it is claimed that there is no risk of dissipation and no need for repeated procedures. ALTA has the advantage that it may be used to treat related anorectal conditions which would be contraindications for other injectable bulking agents. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6971", "text": "8% ethylene vinyl alcohol co-polymer in dimethyl sulfoxide solution has been used. For FI it is marketed as Onyx34, and for gastroesophageal reflux disease it is marketed as Enteryx. [ 5 ] [ 4 ]  After injection, it forms a spongy solid mass via solidification of the hydrophobic copolymer. This occurs because the co-polymer is hydrophic, and the solvent is dissolved away upon contact with tissues. In one publication inter-sphincteric injection site was used via the inter-sphincteric route. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6972", "text": "Mesenchymal stem cells  (MSC) and  muscle-derived stem cells  (MDSC) have been used in urology to treat urinary incontinence.  Fibroblasts  in a collagen carrier were injected into the submucosa of the urethra, and  myoblasts  were injected into the urethral sphincter. The procedure was reported as being successful in most cases. [ 5 ]  Injection of MSCs may lead to engrafting and forming multinucleated myotubes, which helps to regeneration after injury. [ 10 ]  In theory, use of stem cells removes the problems of reabsorption and migration of the bulking material. [ 5 ]  There is similar research which aims to regenerate muscles and repair tissues by  cell therapy  to treat injuries of the external anal sphincter. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6973", "text": "The \"Gatekeeper\" and \"Sphinkeeper\" are related procedures. They are self-expandable prostheses which are implanted into the inter-sphincteric space of the anal canal using an applicator gun. [ 8 ] [ 2 ]  Gatekeeper is a solid  polyacrylonitrile  (hyexpan) cylinder which expands to approximately 720% original size within 24 hours after the implantation. [ 10 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6974", "text": "One review of 23 publications involved a total of 889 patients reported an overall rate of complications of 18%. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6975", "text": "Reported complications are mostly minor, and include: bleeding, perianal pain / discomfort (which may rarely be persistent), leakage of injected material, infection / abscess (which rarely may require drainage), mucosal erosion,  obstructed defecation , hypersensitivity reaction, hematoma, diarrhea,  pruritus ani ,  dermatitis , and bowel urgency (sudden strong urge to defecate). [ 3 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6976", "text": "A landmark randomized placebo control trial on NASHA Dx was published in 2011 in the Lancet. [ 13 ]  136 were given real injections and 70\npatients were given shame (fake) injections. 80% of the patients had no improvement 1 month after the procedure, and were given a second injection. [ 14 ]  After 6 months, 52% of patients who received real injections had improved symptoms. [ 15 ]  However, the patients who received fake injections reported over 30% improvement in symptoms, suggesting that patient psychology (i.e. the  placebo effect ) may be in part responsible for any positive results. [ 16 ]  6% of patients who received real injections were fully continent after 6 months. [ 14 ]  After publication of this study, the material was approved by the FDA in the USA in 2012. [ 14 ]  The material was aggressively marketed, and became popular for a time because of its potential as an in office treatment with low risks compared to other surgical options. [ 2 ]  However uncertainty about indications, cost, and long term durability stopped widespread adoption. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6977", "text": "A  Cochrane  systematic review of the efficacy of this type of treatment for FI was updated in 2013. The review included 5 randomized trials, which in total was 382 patients. 4 of the trials were assessed as uncertain or high risk of bias. [ 11 ]  Another commentator drew attention to the fact that all existing research on these procedures was driven by the companies who also marketed the treatments, and therefore the studies are indeed at high risk of bias. [ 16 ]  Another author in 2008 raised concern that 2 randomized placebo controlled trials had been conducted, but their results remained unpublished for unknown reasons. [ 9 ]  None of the studies in the Cochrane review reported long term follow up after 3, 6 or 12 months post procedure. Another problem with some of the trials is that they were too small. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6978", "text": "The Cochrane review found that most trials reported short term improvement following the procedure, regardless of which material was used. In some studies in the control groups, even placebo (sham) injections and saline injections lead to patients reporting improvement. One trial showed that dextranomer (NASHA Dx) was more effective six months after the procedure compared to placebo for just over half of patients. Another study showed that PTQ has some advantages and was safer than Durasphere in the short term. The authors concluded that due to the small amount of research available and its methodological weaknesses, further conclusions could not be made, especially regarding the long term effectiveness of the procedure. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6979", "text": "Another review which aimed to focus on the long term impact of the procedure included 889 patients across 23 studies. It reported a pooled improvement rate in measures of incontinence of 39.5%, on average 2 years after the procedure. [ 3 ]  In some cases there was no improvement after the procedure, and the injections needed to be repeated in up to 34% of cases. [ 3 ]  There can also be worsening of symptoms after an initial improvement period. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6980", "text": "A randomized trial by Dehli  et al . compared perianal injectable bulking agents to sphincter training and biofeedback, and found the former to be superior. Both methods lead to an improvement of FI, but comparisons of  St Mark's scores  between the groups showed no difference between treatments. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6981", "text": "Anal manometry  is sometimes used to investigate changes in the anal canal before and after the procedure. Usually mean anal resting pressure and mean anal squeeze pressure are the parameters used. [ 3 ]  Improvements in these measurements are often, but not always reported up to 3\u201312 months after the procedure. These improvements are not always maintained after 12 months. [ 3 ]  The length of the anal canal has also been reported to increase following the procedure. [ 3 ]  In one report, dextranomer did not increase anal resting or squeeze pressures. [ 15 ]  In the same study, dextranomer injections were found to be no different to  biofeedback . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6982", "text": "There is limited research available on this topic, and these publications are mostly of poor quality. [ 11 ]  Apart from the available research, most of the claims of benefit of these procedures is anecdotal. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6983", "text": "One author criticized these procedures, stating that simply narrowing the anal canal was an instinctive and na\u00efve solution which does not consider the complex pathopysiological mechanisms of FI. [ 16 ]  They suggested that these treatments are in theory suitable only for passive and minor forms of FI. [ 16 ]  Concerns have been raised about migration of the particles (in the case of Durasphere) away from the site of injection, or the total resorption of the material (in the case of hyaluronic acid and hydroxyl coaptite). [ 16 ]  Most research suggests that the positive effects of most of the bulking agents seem to reduce after 6 to 12 months. [ 8 ]  Endoanal ultrasound has sometimes been used to assess the presence of the material at follow up. At 6 months the material has been reported as missing or migrated in 18.4% of cases, at 3 years or more in 20.2% of cases. [ 3 ]  NASHA Dx and ALTA injection may have longer lasting effects, with most patients still having improvement after 3 years. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6984", "text": "The  pinworm  ( species   Enterobius vermicularis ), also known as  threadworm  (in the United Kingdom, Australia and New Zealand) or  seatworm , is a  parasitic worm .  It is a  nematode  (roundworm) and a common  intestinal parasite  or  helminth , especially in humans. [ 7 ]  The medical condition associated with pinworm infestation is known as  pinworm infection  ( enterobiasis ) [ 8 ]  (a type of  helminthiasis ) or less precisely as oxyuriasis in reference to the  family   Oxyuridae . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6985", "text": "Other than human,  Enterobius vermicularis  were reported from  bonnet macaque . [ 10 ]  Other species seen in  primates  include  Enterobius buckleyi  in  Orangutan [ 11 ]  and  Enterobius anthropopitheci  in  chimpanzee .   Enterobius vermicularis  is common in human children and transmitted via the faecal-oral route. Humans are the only natural host of   Enterobius vermicularis . [ 12 ]   Enterobius gregorii , another human species is morphologically indistinguishable from  Enterobius vermicularis  except the  spicule  size. [ 13 ]  Throughout this article, the word \"pinworm\" refers to  Enterobius . In British usage, however, pinworm refers to  Strongyloides , while  Enterobius  is called threadworm. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6986", "text": "The pinworm (genus  Enterobius ) is a type of  roundworm  (nematode), and three species of pinworm have been identified with certainty. [ 15 ]  Humans are hosts only to  Enterobius vermicularis  (formerly  Oxyurias vermicularis ). [ 16 ]   Chimpanzees  are host to  Enterobius anthropopitheci , which is  morphologically  distinguishable from the human pinworm. [ 5 ]  Hugot (1983) claims another species affects humans,  Enterobius gregorii , which is supposedly a  sister species  of  E. vermicularis , and has a slightly smaller  spicule  (i.e., sexual organ). [ 17 ]  Its existence is controversial, however; Totkova et al. (2003) consider the evidence to be insufficient, [ 6 ]  and Hasegawa et al. (2006) contend that  E. gregorii  is a younger stage of  E. vermicularis . [ 4 ] [ 5 ]  Regardless of its status as a distinct species,  E. gregorii  is considered clinically identical to  E. vermicularis . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6987", "text": "The adult female has a sharply pointed  posterior  end, is 8 to 13\u00a0mm long, and 0.5\u00a0mm thick. [ 18 ]  The adult male is considerably smaller, measuring 2 to 5\u00a0mm long and 0.2\u00a0mm thick, and has a curved posterior end. [ 18 ]  The eggs are  translucent [ 18 ]  and have a surface that adheres to objects. [ 19 ]  The eggs measure 50 to 60  \u03bcm  by 20 to 30 \u03bcm, and have a thick shell flattened on one side. [ 18 ]  The small size and colourlessness of the eggs make them invisible to the naked eye, except in barely visible clumps of thousands of eggs. Eggs may contain a developing  embryo  or a fully developed pinworm  larva . [ 18 ]  The larvae grow to 140\u2013150 \u03bcm in length. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6988", "text": "The entire life cycle, from egg to adult, takes place in the  human gastrointestinal tract  of a single host, [ 18 ] [ 19 ]  from about 2\u20134 weeks [ 20 ]  or about 4\u20138 weeks. [ 21 ]   E. vermicularis  molts four times; the first two within the egg before hatching and two before becoming an adult worm. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6989", "text": "Although infection often occurs via  ingestion  of embryonated eggs by inadequate hand washing or nail biting, inhalation followed by swallowing of airborne eggs may occur rarely. [ 19 ] [ 21 ]  The eggs hatch in the  duodenum  (i.e., first part of the  small intestine ). [ 23 ]  The emerging pinworm  larvae  grow rapidly to a size of 140 to 150 \u03bcm, [ 20 ]  and migrate through the small intestine towards the  colon . [ 19 ]  During this migration, they  moult  twice and become adults. [ 19 ] [ 21 ]  Females survive for 5 to 13 weeks, and males about 7 weeks. [ 19 ]  The male and female pinworms mate in the  ileum  (i.e., last part of the small intestine), [ 19 ]  whereafter the male pinworms usually die, [ 23 ]  and are passed out with stool. [ 24 ]  The gravid female pinworms settle in the  ileum ,  caecum  (i.e., beginning of the  large intestine ),  appendix  and  ascending colon , [ 19 ]  where they attach themselves to the  mucosa [ 21 ]  and ingest colonic contents. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6990", "text": "Almost the entire body of a  gravid  female becomes filled with eggs. [ 23 ]  The estimations of the number of eggs in a gravid female pinworm range from about 11,000 [ 19 ]  to 16,000. [ 21 ]  The egg-laying process begins about five weeks after initial ingestion of pinworm eggs by the human host. [ 19 ]  The gravid female pinworms migrate through the colon towards the  rectum  at a rate of 12 to 14\u00a0cm per hour. [ 19 ]  They emerge from the  anus , and while moving on the skin near the anus, the female pinworms deposit eggs either through (1) contracting and expelling the eggs, (2) dying and then disintegrating, or (3) bodily rupture due to the host scratching the worm. [ 23 ]  After depositing the eggs, the female becomes  opaque  and dies. [ 24 ]  The female emerges from the anus to obtain the oxygen necessary for the maturation of the eggs. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6991", "text": "E. vermicularis  causes the medical condition  pinworm infection  also known as  enterobiasis , whose primary symptom is  itching  in the anal area. [ 26 ]  Extraintestinal disease is rare and most commonly involves the female reproductive tract, [ 27 ]  but spleen abscess has also been reported. [ 28 ]  Enterobius vermicularis infections are found to be correlated with stunting and lower mean  I.Q.  among prepubescent children. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6992", "text": "The pinworm has a worldwide distribution, [ 25 ]  and is the cause of the most common  helminthiasis  ( parasitic worm  infection) in the United States, western Europe, and Oceania. [ 21 ]  In the United States, a study by the  Center of Disease Control  reported an overall  incidence rate  of 11.4% among children. [ 21 ]  Pinworms are particularly common in children, with  prevalence rates  in this age group having been reported as high as 61% in India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark. [ 21 ]   Finger sucking  has been shown to increase both incidence and relapse rates, [ 21 ]  and  nail biting  has been similarly associated. [ 31 ]  Because it spreads from host to host through  contamination , pinworms are common among people living in close contact, and tends to occur in all people within a household. [ 25 ]  The prevalence of pinworms is not associated with gender, [ 25 ]  nor with any particular social class,  race , or culture. [ 21 ]  Pinworms are an exception to the tenet that intestinal parasites are uncommon in affluent communities. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6993", "text": "A fossilized nematode egg was detected in 240 million-year-old fossil dung, [ 32 ]  showing that parasitic pinworms already infested pre-mammalian  cynodonts . The earliest known instance of the pinworms associated with humans is evidenced by pinworm eggs found in human  coprolites   carbon dated  to 7837 BC found in western  Utah . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6994", "text": "Pinworm infection  ( threadworm infection  in the UK), also known as  enterobiasis , is a  human parasitic disease  caused by the  pinworm ,  Enterobius vermicularis . [ 3 ]  The most common symptom is  pruritus ani , or  itching  in the  anal  area. [ 1 ]   The period of time from swallowing eggs to the appearance of new eggs around the anus is 4 to 8 weeks. [ 2 ]  Some people who are infected do not have symptoms. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6995", "text": "The disease is spread between people by pinworm eggs. [ 1 ]  The eggs initially occur around the anus and can survive for up to three weeks in the environment. [ 1 ]  They may be swallowed following contamination of the hands, food, or other articles. [ 1 ]  Those at risk are those who go to school, live in a health care institution or prison, or take care of people who are infected. [ 1 ]  Other animals do not spread the disease. [ 1 ]  Diagnosis is by seeing the worms which are about one  centimetre  long or the eggs under a  microscope . [ 1 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6996", "text": "Treatment is typically with two doses of the medications  mebendazole ,  pyrantel pamoate , or  albendazole  two weeks apart. [ 4 ]  Everyone who lives with or takes care of an infected person should be treated at the same time. [ 1 ]  Washing personal items in hot water after each dose of medication is recommended. [ 1 ]  Good  handwashing , daily bathing in the morning, and daily changing of  underwear  can help prevent reinfection. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6997", "text": "Pinworm infections commonly occur in all parts of the world. [ 1 ] [ 5 ]  They are the most common type of worm infection in  Western Europe ,  Northern Europe  and the  United States . [ 5 ]  School-aged children are the most commonly infected. [ 1 ]  In the United States about 20% of children will develop pinworm at some point. [ 3 ]  Infection rates among high-risk groups may be as high as 50%. [ 2 ]  It is not considered a serious disease. [ 5 ]  Pinworms are believed to have affected humans throughout history. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6998", "text": "One-third of individuals with pinworm infection are totally  asymptomatic . [ 8 ]  The main symptoms are  itching in and around the anus  and  perineum . [ 8 ] [ 9 ] [ 10 ]  The itching occurs mainly during the night, [ 9 ] [ 11 ]  and is caused by the female pinworms migrating to lay eggs around the anus. [ 12 ] [ 10 ]  Both the migrating females and the clumps of eggs are irritating, as well as the sticky substance that is produced by the worms when the eggs are laid. [ 11 ] [ 13 ]  The intensity of the itching varies, and it can be described as  tickling , crawling sensations, or even acute  pain . [ 14 ]  The itching leads to continuously scratching the area around the anus, which can further result in tearing of the skin and complications such as  secondary bacterial infections , including  bacterial   skin inflammation , and  hair follicle inflammation . [ 9 ] [ 10 ] [ 14 ]  General symptoms are  trouble sleeping , and  restlessness . [ 9 ]  A considerable proportion of children experience loss of appetite,  weight loss ,  irritability , emotional instability, and  bed wetting . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_6999", "text": "Pinworms cannot damage the skin, [ 15 ]  and they do not normally migrate through  tissues . [ 10 ]  However, they may move onto the  vulva  and into the  vagina , from there moving to the  external orifice of the uterus , and onwards to the  uterine cavity ,  fallopian tubes ,  ovaries , and  peritoneal cavity . [ 15 ]  This can cause  inflammation of the vulva and vagina . [ 9 ] [ 10 ]  This causes  vaginal discharge  and  itchiness of the vulva . [ 9 ]  The pinworms can also enter the  urethra , and presumably, they carry intestinal bacteria with them. [ 15 ]  According to Gutierrez (2000), a statistically significant correlation between pinworm infection and  urinary tract infections  has been shown; [ 15 ]  however, Burkhart & Burkhart (2005) maintain that the incidence of pinworms as a cause of urinary tract infections remains unknown. [ 8 ]  One report indicated that 36% of young girls with a  urinary tract infection  also had pinworms. [ 8 ]   Painful urination  has been associated with pinworm infection. Sometimes, pinworms can be stopped before reaching the vaginal area  [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7000", "text": "The relationship between pinworm infestation and  appendicitis  (a condition in which the appendix becomes inflamed and filled with pus, causing pain) has been researched, but there is a lack of clear consensus on the matter: While Guti\u00e9rrez maintains that there exists a consensus that pinworms do not produce the inflammatory reaction, [ 16 ]  Cook (1994) states that it is controversial whether pinworms are causatively related to acute  appendicitis , [ 14 ]  and Burkhart & Burkhart (2004) state that pinworm infection causes symptoms of appendicitis to surface. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7001", "text": "The cause of a pinworm infection is the worm  Enterobius vermicularis .  The entire lifecycle \u2013 from egg to adult \u2013 takes place in the  human gastrointestinal tract  of a single human host. [ 12 ] [ 17 ]  This process is two to eight weeks. [ 18 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7002", "text": "Pinworm infection spreads through human-to-human  transmission , by swallowing infectious pinworm eggs. [ 18 ] [ 19 ]  The eggs are hardy and can remain infectious in a moist environment for up to three weeks, [ 11 ] [ 18 ]  though in a warm dry environment they usually last only 1\u20132 days. [ 20 ]  They do not tolerate heat well, but can survive in low temperatures: at \u22128 degrees Celsius (18\u00a0\u00b0F), two-thirds of the eggs are still viable after 18 hours. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7003", "text": "After the eggs have been initially deposited near the anus, they are readily transmitted to other surfaces through  contamination . [ 19 ]  The surface of the eggs is sticky when laid, [ 12 ] [ 11 ]  and the eggs are readily transmitted from their initial deposit near the anus to fingernails, hands, night-clothing and bed linen. [ 9 ]  From here, eggs are further transmitted to food, water, furniture, toys, bathroom  fixtures  and other objects. [ 12 ] [ 18 ] [ 19 ]  Household pets often carry the eggs in their fur, while not actually being infected. [ 21 ]  Dust containing eggs can become airborne and widely dispersed when dislodged from surfaces, for instance when shaking out bed clothes and linen. [ 11 ] [ 18 ] [ 21 ]  Consequently, the eggs can enter the mouth and nose through inhalation, and be swallowed later. [ 9 ] [ 11 ] [ 18 ] [ 19 ]  Although pinworms do not strictly multiply inside the body of their human host, [ 9 ]  some of the pinworm larvae may hatch on the anal  mucosa , and migrate up the  bowel  and back into the  gastrointestinal tract  of the original host. [ 9 ] [ 18 ]  This process is called  retroinfection . [ 11 ] [ 18 ]  According to Burkhart (2005), when this retroinfection occurs, it leads to a heavy  parasitic  load and ensures that the pinworm infestation continues. [ 18 ]  This statement is contradictory to a statement by Caldwell, who contends that retroinfection is rare and not clinically significant. [ 11 ]  Despite the limited, 13-week lifespan of individual pinworms, [ 12 ]   autoinfection  (infection from the original host to itself), either through the anus-to-mouth route or through retroinfection, causes the pinworms to inhabit the same host indefinitely. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7004", "text": "The life cycle begins with eggs being  ingested . [ 12 ]  The eggs hatch in the  duodenum  (first part of the  small intestine ). [ 19 ]  The emerging pinworm  larvae  grow rapidly to a size of 140 to 150 micrometres, [ 9 ]  and migrate through the small intestine towards the  colon . [ 12 ]  During this migration they  moult  twice and become adults. [ 12 ] [ 18 ]  Females survive for 5 to 13 weeks, and males about 7 weeks. [ 12 ]  The male and female pinworms mate in the  ileum  (last part of the small intestine), [ 12 ]  whereafter the male pinworms usually die, [ 19 ]  and are passed out with stool. [ 11 ]  The gravid female pinworms settle in the  ileum ,  caecum  (beginning of the  large intestine ),  appendix  and  ascending colon , [ 12 ]  where they attach themselves to the  mucosa [ 18 ]  and ingest colonic contents. [ 10 ]  Almost the entire body of a gravid female becomes filled with eggs. [ 19 ]  The estimations of the number of eggs in a gravid female pinworm ranges from about 11,000 [ 12 ]  to 16,000. [ 18 ]  The egg-laying process begins approximately five weeks after initial ingestion of pinworm eggs by the human host. [ 12 ]  The gravid female pinworms migrate through the  colon  towards the  rectum  at a rate of 12 to 14 centimetres per hour. [ 12 ]  They emerge from the  anus , and while moving on the skin near the anus, the female pinworms deposit eggs either through contracting and expelling the eggs, dying and then disintegrating, or bodily rupture due to the host scratching the worm. [ 19 ]  After depositing the eggs, the female becomes opaque and dies. [ 11 ]  The reason the female emerges from the anus is to obtain the oxygen necessary for the maturation of the eggs. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7005", "text": "Diagnosis relies on finding the eggs or the adult pinworms. [ 19 ]  Individual eggs are invisible to the naked eye, but they can be seen using a low-power  microscope . [ 21 ]  On the other hand, the light-yellowish thread-like adult pinworms are clearly visually detectable, usually during the night when they move near the anus, or on toilet paper. [ 8 ] [ 14 ] [ 21 ]  Shining a flashlight on the infected individual's anus about one hour after they fall asleep is one form of detection and may show worms crawling out of the anus. [ 22 ]  Another form of detection is the use of transparent  adhesive tape  (e.g.  Scotch Tape ) applied on the anal area which will pick up deposited eggs, and diagnosis can be made by examining the tape with a microscope. [ 16 ] [ 21 ]  This test is most successful if done every morning for several days, because the females do not lay eggs every day, and the number of eggs varies. [ 21 ]  A third method of diagnosis is examining a sample from under their fingernails under a microscope as itching around the anal area is common and therefore they may have collected some eggs under their nails as a result. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7006", "text": "Pinworms do not lay eggs in the  feces , [ 21 ]  but sometimes eggs are deposited in the intestine. [ 19 ]  As such, routine examination of fecal material gives a positive diagnosis in only 5 to 15% of infected subjects, [ 14 ]  and is therefore of little practical diagnostic use. [ 9 ]  In a heavy infection, female pinworms may adhere to  stools  that pass out through the anus, and they may thus be detected on the surface on the stool. [ 14 ] [ 19 ]  Adult pinworms are occasionally seen during  colonoscopy . [ 14 ]  On a microscopic level, pinworms have an identifying feature of  alae  (i.e., protruding ridges) running the length of the worm. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7007", "text": "Pinworm infection cannot be totally prevented under most circumstances. [ 25 ]  This is due to the prevalence of the parasite and the ease of transmission through soiled night clothes, airborne eggs, contaminated furniture, toys and other objects. [ 19 ]  Infection may occur in the highest strata of society, where hygiene and  nutritional  status are typically high. [ 26 ]  The stigma associated with pinworm infection is hence considered a possible over-emphasis. [ 26 ]   Counselling  is sometimes needed for upset parents who have discovered their children are infected, as they may not realize how prevalent the infection is. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7008", "text": "Preventive action revolves around  personal hygiene  and the cleanliness of the living quarters. [ 26 ]  The  rate  of reinfection can be reduced through hygienic measures, and this is recommended especially in recurring cases. [ 21 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7009", "text": "The main measures are keeping fingernails short, and washing and scrubbing hands and fingers carefully, especially after  defecation  and before meals. [ 26 ] [ 27 ]  Showering every morning is also highly recommended to wash off any eggs that may be still lying on the skin. [ 28 ]  Under ideal conditions, bed covers, sleeping garments, and hand towels should be changed daily [ 26 ]  and clothes and linens should be washed in hot water and then be placed in a hot dryer in order to kill off any eggs. [ 28 ]  Children can wear gloves while asleep, and the bedroom floor should be kept clean. [ 26 ]  Regular disinfection of kitchen and bathroom surfaces will help to prevent spread as well. [ 29 ]  Food should be covered to limit contamination with dust-borne parasite eggs. [ 26 ]  It is not recommended to shake clothes and bed linen as the eggs may detach and spread [ 26 ]  or to share clothes and towels. Nail biting and sucking on fingers is also discouraged."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7010", "text": "Medication  is the primary treatment for pinworm infection. [ 26 ]  However, reinfection is frequent regardless of the medication used. [ 8 ]  Total elimination of the parasite in a household may require repeated doses of medication for up to a year or more. [ 9 ]  Because the drugs kill the adult pinworms, but not the eggs, the first retreatment is recommended in two weeks. [ 21 ]  Also, if one household member spreads the eggs to another, it will be a matter of two or three weeks before those eggs become adult worms and thus amenable to treatment. [ 27 ]   Asymptomatic  infections, often in small children, can serve as reservoirs of infection, and therefore the entire household should be treated regardless of whether or not symptoms are present. [ 9 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7011", "text": "The  benzimidazole  compounds  albendazole  ( brand names  e.g.,  Albenza ,  Eskazole ,  Zentel  and  Andazol ) and  mebendazole  ( brand names  e.g.,  Ovex ,  Vermox ,  Antiox  and  Pripsen ) are the most effective. [ 26 ]  They work by inhibiting the  microtubule  function in the pinworm adults, causing  glycogen  depletion, [ 26 ]  thereby effectively starving the parasite. [ 27 ]  A single 100 milligram dose of  mebendazole  with one repetition after two weeks, is considered the safest, and is usually effective with cure rate of 96%. [ 8 ] [ 26 ]  Mebendazole has no serious  side effects , although  abdominal pain  and  diarrhea  have been reported. [ 26 ]   Pyrantel pamoate  (also called pyrantel embonate,  brand names  e.g.,  Reese's Pinworm Medicine ,  Pin-X ,  Combantrin ,  Anthel ,  Helmintox , and  Helmex ) kills adult pinworms through  neuromuscular blockade , [ 27 ]  and is considered as effective as the  benzimidazole  compounds and is used as a second-line medication. [ 9 ]  Pyrantel pamoate is available over the counter and does not require a prescription. Pinworms located in the  genitourinary system  (in this case, female genital area) may require other drug treatments. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7012", "text": "The available data on mebendazole, albendazole, and pyrantel pamoate use in pregnancy is limited and they are all assigned to  pregnancy category  level C. Treatment of a pinworm infection during pregnancy is only recommended for patients with significant symptoms that may be causing adverse effects to the pregnant woman such as loss of sleep and weight loss. [ 30 ] [ 31 ]  Pyrantel pamoate is the treatment of choice in pregnancy but should be used only after consultation with a health care practitioner rather than self-treatment. [ 30 ]  Treatment should be avoided in the first trimester, and if possible done in the third trimester. [ 32 ] [ 31 ]  If the pregnant woman is asymptomatic, then they should be treated after the baby is delivered. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7013", "text": "Mebendazole has less than 10% of the oral dose absorbed into systemic circulation with a clinically insignificant amount of drug excreted in breastmilk, and therefore treatment should not be withheld during breastfeeding. [ 31 ]  There is limited data on the use of pyrantel pamoate and albendazole in breastfeeding but  WHO  also classifies them as compatible with breastfeeding. This is due to the drugs acting mainly in the intestinal system of the mother with only a very small amount of drug being absorbed into the systemic circulation. [ 31 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7014", "text": "Pinworm infection occurs worldwide, [ 10 ]  and is the most common  helminth  (i.e., parasitic worm) infection in the United States and Western Europe. [ 18 ]  In the United States, a study by the  Center of Disease Control  reported an overall  incidence rate  of 11.4% among people of all ages. [ 18 ]  Pinworms are particularly common in children with approximately 30% of children being infected and most commonly seen in children between 7 and 11 years old. [ 34 ]  The  prevalence rates  in children having been reported as high as 61% in India, 50% in England, 39% in Thailand, 37% in Sweden, and 29% in Denmark. [ 18 ]   Finger sucking  has been shown to increase both incidence and relapse rates, [ 18 ]  and  nail biting  has been similarly associated. [ 14 ]  Because it spreads from host to host through  contamination , enterobiasis is common among people living in close contact, and tends to occur in all people within a household. [ 10 ]  The prevalence of pinworms is not associated with gender, [ 10 ]  nor with any particular  social class ,  race , or culture. [ 18 ]  Pinworms are an exception to the tenet that intestinal parasites are uncommon in affluent communities. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7015", "text": "The earliest known instance of pinworms is evidenced by pinworm eggs found in  coprolite ,  carbon dated  to 7837 BC at western  Utah . [ 12 ]  Pinworm infection is not classified as a  neglected tropical disease  unlike many other parasitic worm infections. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7016", "text": "Garlic  has been used as a treatment in the ancient cultures of China, India, Egypt, and Greece. [ 36 ]   Hippocrates  mentioned garlic as a remedy against intestinal parasites. [ 37 ]  German botanist  Adam Lonicer  also recommended garlic against parasitic worms. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7017", "text": "Proctoscopy , or  rectoscopy , is a common medical procedure in which an instrument called a proctoscope (also known as a  rectoscope , although the latter may be a bit longer) is used to examine the  anal cavity ,  rectum , or  sigmoid colon . A proctoscope is a short, straight, rigid, hollow metal tube, and usually has a small light bulb mounted at the end. It is approximately 15\u00a0cm (5\u00a0inches) long, while a rectoscope is approximately 25\u00a0cm (10\u00a0inches) long. [ 1 ]  During proctoscopy, the proctoscope is lubricated and inserted into the  rectum , and then the  obturator  is removed, allowing an unobstructed view of the interior of the rectal cavity. This procedure is normally done to inspect for  hemorrhoids  or rectal  polyps  and might be mildly uncomfortable as the proctoscope is inserted further into the rectum. Modern  fibre-optic  proctoscopes allow more extensive observation with less discomfort."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7018", "text": "A  proctoscope  is a hollow, tube-like  speculum  that is used for visual inspection of the rectum. [ 2 ] [ 3 ]  Both disposable and non-disposable proctoscopes are available for use. Out of these, the non-disposable Kelly's rectal speculum, [ 4 ]  named after the American gynecologist  Howard Atwood Kelly , is the most commonly used speculum for proctoscopy. Some proctoscopes have a light source for better visibility. The proctoscope is inserted into the  anal canal  with the patient in  Sims' position . Fibre optic proctoscopes are now available which cause less discomfort to the patient. \nThe proctoscope is used in the diagnosis of  hemorrhoids , carcinoma of anal canal or rectum and  rectal polyp . It is used therapeutically for  polypectomy  and rectal biopsy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7019", "text": "Disposable proctoscopes without light are also available.   The proctoscope also has a hollow channel through which other instruments may be inserted. For example, another instrument may be used to take a  biopsy  of a small amount of  tissue  for examination under a  microscope . Also, air may be injected through the proctoscope to help make viewing easier. Similar instruments, the  sigmoidoscope  and  colonoscope  may be used to visualize more proximal parts of the bowels."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7020", "text": "A  rectal prolapse  occurs when walls of the  rectum  have  prolapsed  to such a degree that they protrude out of the  anus  and are visible outside the body. [ 2 ]  However, most researchers agree that there are 3 to 5 different types of rectal prolapse, depending on whether the prolapsed section is visible externally, and whether the full or only partial thickness of the rectal wall is involved. [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7021", "text": "Rectal prolapse may occur without any symptoms, but depending upon the nature of the prolapse there may be  mucous discharge  (mucus coming from the anus),  rectal bleeding , degrees of  fecal incontinence , and  obstructed defecation  symptoms. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7022", "text": "Rectal prolapse is generally more common in elderly women, although it may occur at any age and in either sex. It is very rarely life-threatening, but the symptoms can be debilitating if left untreated. [ 5 ]  Most external prolapse cases can be treated successfully, often with a surgical procedure. Internal prolapses are traditionally harder to treat and surgery may not be suitable for many patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7023", "text": "The different kinds of rectal prolapse can be difficult to grasp, as different definitions are used and some recognize some subtypes and others do not. Essentially, rectal prolapses may be: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7024", "text": "External (complete) rectal prolapse  (rectal procidentia, full thickness rectal prolapse, overt rectal prolapse [ 6 ] ) is\na full thickness, circumferential, true intussusception of the rectal wall which protrudes from the anus and is visible externally. [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7025", "text": "Internal rectal intussusception  (occult rectal prolapse, internal procidentia) can be defined as a funnel shaped infolding of the upper rectal (or lower  sigmoid ) wall that can occur during  defecation . [ 9 ]  This infolding is perhaps best visualised as folding a sock inside out, [ 10 ]  creating \"a tube within a tube\". [ 11 ]  Another definition is \"where the rectum collapses but does not exit the anus\". [ 12 ]  Many sources differentiate between internal rectal intussusception and mucosal prolapse, implying that the former is a full thickness prolapse of rectal wall. However, a publication by the  American Society of Colon and Rectal Surgeons  stated that internal rectal intussusception involved the  mucosal  and  submucosal  layers separating from the underlying  muscularis mucosa  layer attachments, resulting in the separated portion of rectal lining \"sliding\" down. [ 5 ]  This may signify that authors use the terms internal rectal prolapse and internal mucosal prolapse to describe the same phenomena."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7026", "text": "Mucosal prolapse  (partial rectal mucosal prolapse) [ 13 ]  refers to prolapse of the loosening of the submucosal attachments to the muscularis propria of the distal rectummucosal layer of the rectal wall. Most sources define mucosal prolapse as an external, segmental prolapse which is easily confused with prolapsed (3rd or 4th degree)  hemorrhoids  (piles). [ 10 ]  However, both internal mucosal prolapse (see below) and circumferential mucosal prolapse are described by some. [ 13 ]  Others do not consider mucosal prolapse a true form of rectal prolapse. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7027", "text": "Internal mucosal prolapse  (rectal internal mucosal prolapse, RIMP) refers to prolapse of the mucosal layer of the rectal wall which does not protrude externally. There is some controversy surrounding this condition as to its relationship with hemorrhoidal disease, or whether it is a separate entity. [ 15 ]  The term \"mucosal hemorrhoidal prolapse\" is also used. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7028", "text": "Solitary rectal ulcer syndrome  (SRUS, solitary rectal ulcer, SRU) occurs with internal rectal intussusception and is part of the spectrum of rectal prolapse conditions. [ 5 ]  It describes  ulceration  of the rectal lining caused by repeated frictional damage as the internal intussusception is forced into the anal canal during straining. SRUS can be considered a consequence of internal intussusception, which can be demonstrated in 94% of cases."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7029", "text": "Mucosal prolapse syndrome  (MPS) is recognized by some. It includes solitary rectal ulcer syndrome, rectal prolapse, proctitis cystica profunda, and inflammatory polyps. [ 17 ] [ 18 ]  It is classified as a chronic benign inflammatory disorder."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7030", "text": "Rectal prolapse and internal rectal intussusception has been classified according to the size of the prolapsed section of rectum, a function of rectal mobility from the sacrum and infolding of the rectum. This classification also takes into account sphincter relaxation: [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7031", "text": "Rectal internal mucosal prolapse has been graded according to the level of descent of the intussusceptum, which was predictive of symptom severity: [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7032", "text": "The most widely used classification of internal rectal prolapse is according to the height on the rectal/sigmoid wall from which they originate and by whether the intussusceptum remains within the rectum or extends into the  anal canal . The height of intussusception from the anal canal is usually estimated by  defecography . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7033", "text": "Recto-rectal (high) intussusception  (intra-rectal intussusception) is where the intussusception starts in the rectum, does not protrude into the anal canal, but stays within the rectum. (i.e. the intussusceptum originates in the rectum and does not extend into the anal canal. The intussuscipiens includes rectal lumen distal to the intussusceptum only). These are usually intussusceptions that originate in the upper rectum or lower  sigmoid . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7034", "text": "Recto-anal (low) intussusception  (intra-anal intussusception) is where the intussusception starts in the rectum and protrudes into the anal canal (i.e. the intussusceptum originates in the rectum, and the intussuscipiens includes part of the anal canal)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7035", "text": "An Anatomico-Functional Classification of internal rectal intussusception has been described, [ 11 ]  with the argument that other factors apart from the height of intussusception above the anal canal appear to be important to predict symptomology. The parameters of this classification are anatomic descent, diameter of intussuscepted bowel, associated rectal hyposensitivity and associated delayed colonic transit:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7036", "text": "Patients may have associated gynecological conditions which may require multidisciplinary management. [ 5 ]  History of  constipation  is important because some of the operations may worsen constipation. Fecal incontinence may also influence the choice of management."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7037", "text": "Rectal prolapse may be confused easily with prolapsing hemorrhoids. [ 5 ]  Mucosal prolapse also differs from prolapsing (3rd or 4th degree) hemorrhoids, where there is a segmental prolapse of the hemorrhoidal tissues at the 3, 7 and 11 o'clock positions. [ 13 ]  Mucosal prolapse can be differentiated from a full thickness external rectal prolapse (a complete rectal prolapse) by the orientation of the folds (furrows) in the prolapsed section. In full thickness rectal prolapse, these folds run circumferential.  In mucosal prolapse, these folds are radially. [ 10 ]  The folds in mucosal prolapse are usually associated with internal hemorrhoids. Furthermore, in rectal prolapse, there is a sulcus present between the prolapsed bowel and the anal verge, whereas in hemorrhoidal disease there is no sulcus. [ 3 ]  Prolapsed, incarcerated hemorrhoids are extremely painful, whereas as long as a rectal prolapse is not strangulated, it gives little pain and is easy to reduce. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7038", "text": "The prolapse may be obvious, or it may require straining and squatting to produce it. [ 5 ]  The anus is usually patulous, (loose, open) and has reduced resting and squeeze pressures. [ 5 ]  Sometimes it is necessary to observe the patient while they strain on a toilet to see the prolapse happen [ 21 ]  (the perineum can be seen with a mirror or by placing an endoscope in the bowl of the toilet). [ 10 ]  A phosphate enema may need to be used to induce straining. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7039", "text": "The perianal skin may be macerated (softening and whitening of skin that is kept constantly wet) and show  excoriation . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7040", "text": "These may reveal congestion and  edema  (swelling) of the distal rectal mucosa, [ 21 ]  and in 10-15% of cases there may be a solitary rectal ulcer on the anterior rectal wall. [ 5 ]  Localized inflammation or ulceration can be biopsied and may lead to a diagnosis of SRUS or colitis cystica profunda. [ 5 ]  Rarely, a  neoplasm  (tumour) may form on the leading edge of the intussusceptum. In addition, patients are frequently elderly and therefore have increased incidence of  colorectal cancer . Full length colonoscopy is usually carried out in adults prior to any surgical intervention. [ 5 ]  These investigations may be used with contrast media ( barium enema ) which may show the associated mucosal abnormalities. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7041", "text": "This investigation is used to diagnose internal intussusception, or demonstrate a suspected external prolapse that could not be produced during the examination. [ 3 ]  It is usually not necessary with obvious external rectal prolapse. [ 10 ]   Defecography  may demonstrate associated conditions like  cystocele , vaginal vault prolapse or  enterocele . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7042", "text": "Colonic transit studies  may be used to rule out  colonic inertia  if there is a history of severe constipation. [ 3 ] [ 5 ]  Continent prolapse patients with slow transit constipation, and who are fit for surgery may benefit from subtotal colectomy with rectopexy. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7043", "text": "This investigation objectively documents the functional status of the sphincters. However, the clinical significance of the findings are disputed by some. [ 10 ]  It may be used to assess for pelvic floor dyssenergia, [ 5 ]  ( anismus  is a contraindication for certain surgeries, e.g. STARR), and these patients may benefit from post-operative  biofeedback  therapy. Decreased squeeze and resting pressures are usually the findings, and this may predate the development of the prolapse. [ 5 ]  Resting tone is usually preserved in patients with mucosal prolapse. [ 21 ]  In patients with reduced resting pressure, levatorplasty may be combined with prolapse repair to further improve continence. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7044", "text": "It may be used to evaluate incontinence, but there is disagreement about what relevance the results may show, as rarely do they mandate a change of surgical plan. [ 5 ]  There may be denervation of striated musculature on the electromyogram. [ 21 ]  Increased nerve conduction periods (nerve damage), this may be significant in predicting post-operative incontinence. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7045", "text": "Rectal prolapse is a \"falling down\" of the rectum so that it is visible externally. The appearance is of a reddened, proboscis-like object through the anal sphincters. Patients find the condition embarrassing. [ 10 ]  The symptoms can be socially debilitating without treatment, [ 5 ]  but it is rarely life-threatening. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7046", "text": "The true incidence of rectal prolapse is unknown, but it is thought to be uncommon. As most affected people are elderly, the condition is generally under-reported. [ 22 ]  It may occur at any age, even in children, [ 23 ]  but there is peak onset in the fourth and seventh decades. [ 3 ]  Women over 50 are six times more likely to develop rectal prolapse than men. It is rare in men over 45 and in women under 20. [ 21 ]  When males are affected, they tend to be young and report significant bowel function symptoms, especially  obstructed defecation , [ 5 ]  or have a predisposing disorder (e.g., congenital  anal atresia ). [ 10 ]  When children are affected, they are usually under the age of 3."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7047", "text": "35% of women with rectal prolapse have never had children, [ 5 ]  suggesting that pregnancy and labor are not significant factors. Anatomical differences such as the wider pelvic outlet in females may explain the skewed gender distribution. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7048", "text": "Associated conditions, especially in younger patients include autism, developmental delay syndromes, and psychiatric conditions requiring several medications. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7049", "text": "Signs and symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7050", "text": "Initially, the mass may protrude through the anal canal only during defecation and straining, and spontaneously return afterwards. Later, the mass may have to be pushed back in following defecation. This may progress to a chronically prolapsed and severe condition, defined as spontaneous prolapse that is difficult to keep inside, and occurs with walking, prolonged standing, [ 5 ]  coughing or sneezing ( Valsalva  maneuvers). [ 3 ]  A chronically prolapsed rectal tissue may undergo pathological changes such as thickening, ulceration and bleeding. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7051", "text": "If the prolapse becomes trapped externally outside the anal sphincters, it may become strangulated and there is a risk of perforation. [ 21 ]   This may require an urgent surgical operation if the prolapse cannot be manually reduced. [ 5 ]  Applying granulated sugar on the exposed rectal tissue can reduce the  edema  (swelling) and facilitate this. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7052", "text": "The precise cause is unknown, [ 3 ] [ 10 ] [ 9 ]  and has been much debated. [ 5 ]  In 1912 Moschcowitz proposed that rectal prolapse was a sliding hernia through a pelvic  fascial  defect. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7053", "text": "This theory was based on the observation that rectal prolapse patients have a mobile and unsupported pelvic floor, and a hernia sac of peritoneum from the Pouch of Douglas and rectal wall can be seen. [ 5 ]   Other adjacent structures can sometimes be seen in addition to the rectal prolapse. [ 5 ]  Although a  pouch of Douglas   hernia , originating in the cul de sac of Douglas, may protrude from the anus (via the anterior rectal wall), [ 21 ]  this is a different situation from rectal prolapse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7054", "text": "Shortly after the invention of  defecography , In 1968 Broden and Snellman used  cinedefecography  to show that rectal prolapse begins as a circumferential intussusception of the rectum, [ 3 ] [ 10 ]  which slowly increases over time. [ 21 ]  The leading edge of the intussusceptum may be located at 6\u20138\u00a0cm or at 15\u201318\u00a0cm from the  anal verge . [ 21 ]  This proved an older theory from the 18th century by  John Hunter  and  Albrecht von Haller  that this condition is essentially a full-thickness rectal intussusception, beginning about 3 inches above the  dentate line  and protruding externally. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7055", "text": "Since most patients with rectal prolapse have a long history of constipation, [ 10 ]  it is thought that prolonged, excessive and repetitive straining during defecation may predispose to rectal prolapse. [ 3 ] [ 9 ] [ 21 ] [ 24 ] [ 25 ] [ 26 ]  Since rectal prolapse itself causes functional obstruction, more straining may result from a small prolapse, with increasing damage to the anatomy. [ 9 ]  This excessive straining may be due to predisposing pelvic floor dysfunction (e.g.  obstructed defecation ) and anatomical factors: [ 10 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7056", "text": "Some authors question whether these abnormalities are the cause, or secondary to the prolapse. [ 3 ]  Other predisposing factors/associated conditions include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7057", "text": "The association with uterine prolapse (10-25%) and cystocele (35%) may suggest that there is some underlying abnormality of the pelvic floor that affects multiple pelvic organs. [ 3 ]  Proximal bilateral pudendal neuropathy has been demonstrated in patients with rectal prolapse who have fecal incontinence. [ 5 ]  This finding was shown to be absent in healthy subjects, and may be the cause of denervation-related atrophy of the external anal sphincter. Some authors suggest that  pudendal nerve  damage is the cause for pelvic floor and anal sphincter weakening, and may be the underlying cause of a spectrum of pelvic floor disorders. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7058", "text": "Sphincter function in rectal prolapse is almost always reduced. [ 3 ]  This may be the result of direct sphincter injury by chronic stretching of the prolapsing rectum. Alternatively, the intussuscepting rectum may lead to chronic stimulation of the rectoanal inhibitory reflex (RAIR - contraction of the external anal sphincter in response to stool in the rectum). The RAIR was shown to be absent or blunted. Squeeze (maximum voluntary contraction) pressures may be affected as well as the resting tone. This is most likely a denervation injury to the external anal sphincter. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7059", "text": "The assumed mechanism of  fecal incontinence  in rectal prolapse is by the chronic stretch and trauma to the anal sphincters and the presence of a direct conduit (the intussusceptum) connecting rectum to the external environment which is not guarded by the sphincters. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7060", "text": "The assumed mechanism of obstructed defecation is by disruption to the rectum and anal canal's ability to contract and fully evacuate rectal contents. The intussusceptum itself may mechanically obstruct the rectoanal  lumen , creating a blockage that straining, anismus and colonic dysmotility exacerbate. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7061", "text": "Some believe that internal rectal intussusception represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. However, internal intussusception rarely progresses to external rectal prolapse. [ 30 ]  The factors that result in a patient progressing from internal intussusception to a full thickness rectal prolapse remain unknown. [ 5 ]  Defecography studies demonstrated that degrees of internal intussusception are present in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7062", "text": "Surgery is thought to be the only option to potentially cure a complete rectal prolapse. [ 7 ]  For people with medical problems that make them unfit for surgery, and those who have minimal symptoms, conservative measures may be beneficial. Dietary adjustments, including increasing dietary fiber may be beneficial to reduce constipation, and thereby reduce straining. [ 7 ]  A bulk forming agent (e.g.  psyllium ) or stool softener can also reduce constipation. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7063", "text": "Surgery is often required to prevent further damage to the anal sphincters. The goals of surgery are to restore the normal anatomy and to minimize symptoms. There is no globally agreed consensus as to which procedures are more effective, [ 7 ]  and there have been over 50 different operations described. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7064", "text": "Surgical approaches in rectal prolapse can be either perineal or abdominal. A perineal approach (or trans-perineal) refers to surgical access to the rectum and sigmoid colon via an incision around the anus and  perineum  (the area between the genitals and the anus). [ 32 ]  Abdominal approach (trans-abdominal approach) involves the surgeon cutting into the  abdomen  and gaining surgical access to the  pelvic cavity . Procedures for rectal prolapse may involve fixation of the bowel (rectopexy), or resection (a portion removed), or both. [ 7 ]  Trans-anal (endo-anal) procedures are also described where access to the internal rectum is gained through the anus itself."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7065", "text": "Abdominal procedures are associated with lower risk of postoperative recurrence of the prolapse, compared with perineal procedures (6.1% vs 16.3% in patients who are younger than 65 years of age at the time of surgery). [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7066", "text": "The abdominal approach carries a small risk of impotence in males (e.g. 1-2% in abdominal rectopexy). [ 10 ]  Abdominal operations may be open or  laparoscopic  (keyhole surgery). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7067", "text": "Laparoscopic procedures \nRecovery time following laparoscopic surgery is shorter and less painful than following traditional abdominal surgery. [ 32 ]  Instead of opening the pelvic cavity with a wide incision (laparotomy), a laparoscope (a thin, lighted tube) and surgical instruments are inserted into the pelvic cavity via small incisions. [ 32 ]  Rectopexy and anterior resection have been performed laparoscopically with good results."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7068", "text": "The perineal approach generally results in less post-operative pain and complications, and a reduced length of hospital stay. These procedures generally carry a higher recurrence rate and poorer functional outcome. [ 5 ]  The perineal procedures include perineal rectosigmoidectomy and Delorme repair. [ 3 ]  Elderly, or other medically high-risk patients are usually treated by perineal procedures, [ 3 ]   as they can be performed under a  regional anesthetic , or even  local anesthetic  with  intravenous sedation , thus avoid the risks of a  general anesthetic . [ 10 ]  Alternatively, perineal procedures may be selected to reduce risk of nerve damage, for example in young male patients for whom sexual dysfunction may be a major concern. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7069", "text": "Perineal rectosigmoidectomy"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7070", "text": "The goal of Perineal rectosigmoidectomy is to resect or remove the redundant bowel. This is done through the perineum. The lower rectum is anchored to the sacrum through fibrosis in order to prevent future prolapse. [ 7 ]  The full thickness of the rectal wall is incised at a level just above the dentate line. Redundant rectal and sigmoid wall is removed and the new edge of colon is reconnected (anastomosed) with the anal canal with stitches or staples. [ 10 ]  This procedure may be combined with levatorplasty, to tighten the pelvic muscles. [ 7 ]  A combined a perineal proctosigmoidectomy with anterior levatorplasty is also called an Altemeier procedure. [ 3 ]  Levatorplasty is performed to correct levator diastasis which is commonly associated with rectal prolapse. [ 3 ]  Perineal rectosigmoidectomy was first introduced by Mikulicz in 1899, and it remained the preferred treatment in Europe for many years. [ 3 ]  It was Popularized by Altemeier. [ 10 ]  The procedure is simple, safe and effective. [ 3 ]  Continence levatorplasty may enhance restoration of continence (2/3 of patients). [ 3 ]  Complications occur in less than 10% of cases, and include pelvic bleeding, pelvic abscess and anastomotic dehiscence (splitting apart of the stitches inside), bleeding or leak at a dehiscence [ 3 ]  Mortality is low. [ 10 ]  Recurrence rates are higher than for abdominal repair, [ 3 ]  16-30%, but more recent studies give lower recurrence rates. [ 3 ]  Additional levatorplasty can reduce recurrence rates to 7%. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7071", "text": "Delorme Procedure"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7072", "text": "This is a modification of the perineal rectosigmoidectomy, differing in that only the mucosa and submucosa are excised from the prolapsed segment, rather than full thickness resection. [ 10 ]  The prolapse is exposed if it is not already present, and the mucosal and submucosal layers are stripped from the redundant length of bowel. The muscle layer that is left is plicated (folded) and placed as a buttress above the pelvic floor. [ 7 ]  The edges of the mucosal are then stitched back together. \"Mucosal proctectomy\" was first discussed by Delorme in 1900, [ 10 ]  now it is becoming more popular again as it has low morbidity and avoids an abdominal incision, while effectively repairing the prolapse. [ 3 ]  The procedure is ideally suited to those patients with full-thickness prolapse limited to partial circumference (e.g., anterior wall) or less-extensive prolapse (perineal rectosigmoidectomy may be difficult in this situation). [ 3 ] [ 10 ]  Fecal incontinence is improved following surgery (40%\u201375% of patients). [ 5 ] [ 10 ]  Post operatively, both mean resting and squeeze pressures were increased. [ 5 ]  Constipation is improved in 50% of cases, [ 5 ]  but often urgency and tenesmus are created. Complications, including infection, urinary retention, bleeding,  anastomotic  dehiscence (opening of the stitched edges inside),  rectal stricture  (narrowing of the gut lumen), diarrhea, and fecal impaction occur in 6-32% of cases. [ 5 ] [ 10 ]  Mortality occurs in 0\u20132.5% cases. [ 10 ]  There is a higher recurrence rate than abdominal approaches (7-26% cases). [ 5 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7073", "text": "Anal encirclement (Thirsch procedure)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7074", "text": "This procedure can be carried out under  local anaesthetic . After reduction of the prolapse, a subcutaneous suture (a stitch under the skin) or other material is placed encircling the anus, which is then made taut to prevent further prolapse. [ 7 ]  Placing silver wire around the anus first described by Thiersch in 1891. [ 10 ]  Materials used include nylon, silk, silastic rods, silicone, Marlex mesh, Mersilene mesh, fascia, tendon, and Dacron. [ 10 ]  This operation does not correct the prolapse itself, it merely supplements the anal sphincter, narrowing the anal canal with the aim of preventing the prolapse from becoming external, meaning it remains in the rectum. [ 10 ]  This goal is achieved in 54-100% cases. Complications include breakage of the encirclement material, fecal impaction, sepsis, and erosion into the skin or anal canal. Recurrence rates are higher than the other perineal procedures. This procedure is most often used for people who have a severe condition or who have a high risk of adverse effects from general anesthetic, [ 7 ]  and who may not tolerate other perineal procedures."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7075", "text": "Internal rectal intussusception  (rectal intussusception, internal intussusception, internal rectal prolapse, occult rectal prolapse, internal rectal  procidentia  and rectal invagination) is a medical condition defined as a funnel shaped infolding of the  rectal  wall that can occur during  defecation . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7076", "text": "This phenomenon was first described in the late 1960s when  defecography  was first developed and became widespread. [ 5 ]  Degrees of internal intussusception have been demonstrated in 40% of asymptomatic subjects, raising the possibility that it represents a normal variant in some, and may predispose patients to develop symptoms, or exacerbate other problems. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7077", "text": "Internal intussusception may be  asymptomatic , but common symptoms include: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7078", "text": "Recto-rectal  intussusceptions may be  asymptomatic , apart from mild obstructed defecation. \"interrupted defaecation\" in the morning is thought by some to be characteristic. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7079", "text": "Recto-anal  intussusceptions commonly give more severe symptoms of straining, incomplete evacuation, need for digital evacuation of stool, need for support of the  perineum  during defecation, urgency, frequency or intermittent  fecal incontinence . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7080", "text": "It has been observed that intussusceptions of thickness \u22653\u00a0mm, and those that appear to cause obstruction to rectal evacuation may give clinical symptoms. [ 36 ] [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7081", "text": "There are two schools of thought regarding the nature of internal intussusception, viz: whether it is a primary phenomenon, or secondary to (a consequence of) another condition."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7082", "text": "Some believe that it represents the initial form of a progressive spectrum of disorders the extreme of which is external rectal prolapse. The intermediary stages would be gradually increasing sizes of intussusception. The folding section of rectum can cause repeated trauma to the mucosa, and can cause  solitary rectal ulcer syndrome . [ 10 ]  However, internal intussusception rarely progress to external rectal prolapse. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7083", "text": "Others argue that the majority of patients appear to have rectal intussusception as a consequence of obstructed defecation rather than a cause, [ 38 ] [ 39 ]  possibly related to excessive straining in patients with obstructed defecation. [ 36 ]  Patients with other causes of obstructed defecation ( outlet obstruction ) like  anismus  also tend to have higher incidence of internal intussusception.  Enteroceles  are coexistent in 11% of patients with internal intussusception. [ 40 ]  Symptoms of internal intussusception overlap with those of  rectocele , indeed the 2 conditions can occur together. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7084", "text": "Patients with  solitary rectal ulcer syndrome  combined with internal intussusception (as 94% of SRUS patients have) were shown to have altered rectal wall biomechanics compared to patients with internal intussusception alone. [ 42 ]  The presumed mechanism of the  obstructed defecation  is by telescoping of the intussusceptum, occluding the rectal lumen during attempted defecation. [ 36 ]  One study analysed resected rectal wall specimens in patients with obstructed defecation associated with rectal intussusception undergoing  stapled trans-anal rectal resection . They reported abnormalities of the  enteric nervous system  and  estrogen receptors . [ 43 ]  One study concluded that intussusception of the  anterior  rectal wall shares the same cause as  rectocele , namely deficient recto-vaginal ligamentous support. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7085", "text": "The following conditions occur more commonly in patients with internal rectal intussusception than in the general population:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7086", "text": "Unlike external rectal prolapse, internal rectal intussusception is not visible externally, but it may still be diagnosed by  digital rectal examination , while the patient strains as if to defecate. [ 11 ]  Imaging such as a  defecating proctogram [ 47 ]  or dynamic MRI defecography can demonstrate the abnormal folding of the rectal wall. Some have advocated the use of anorectal physiology testing ( anorectal manometry ). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7087", "text": "Nonsurgical measures to treat internal intussusception include pelvic floor retraining, [ 48 ]  a  bulking agent  (e.g.  psyllium ),  suppositories  or  enemas  to relieve constipation and straining. [ 21 ]  If there is  incontinence  ( fecal leakage  or more severe FI), or paradoxical contraction of the pelvic floor ( anismus ), then biofeedback retraining is indicated. [ 49 ]  Some researchers advise that internal intussusception be managed conservatively, compared to external rectal prolapse which usually requires surgery. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7088", "text": "As with external rectal prolapse, there are a great many different surgical interventions described. Generally, a section of rectal wall can be  resected  (removed), or the rectum can be fixed (rectopexy) to its original position against the  sacral vertebrae , or a combination of both methods. Surgery for internal rectal prolapse can be via the abdominal approach or the transanal approach. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7089", "text": "It is clear that there is a wide spectrum of symptom severity, meaning that some patients may benefit from surgery and others may not. Many procedures receive conflicting reports of success, leading to a lack of any consensus about the best way to manage this problem. [ 49 ]  Relapse of the intussusception after treatment is a problem. Two of the most commonly employed procedures are discussed below."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7090", "text": "This procedure aims to \"[correct] the descent of the posterior and middle pelvic compartments combined with reinforcement of the rectovaginal septum\". [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7091", "text": "Rectopexy has been shown to improve anal incontinence ( fecal leakage ) in patients with rectal intussusception. [ 52 ]  The operation has been shown to have low recurrence rate (around 5%). [ 53 ]  It also improves obstructed defecation symptoms. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7092", "text": "Complications include constipation, which is reduced if the technique does not use posterior rectal mobilization (freeing the rectum from its attached back surface). [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7093", "text": "The advantage of the laparoscopic approach is decreased healing time and less complications. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7094", "text": "This operation aims to \"remove the anorectal mucosa circumferentially and reinforce the anterior anorectal junction wall with the use of a circular stapler\". [ 45 ] [ 46 ]  In contrast to other methods, STARR does not correct the descent of the rectum, it removes the redundant tissue. [ 51 ]  The technique was developed from a similar stapling procedure for prolapsing  hemorrhoids . Since, specialized circular staplers have been developed for use in external rectal prolapse and internal rectal intussusception. [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7095", "text": "Complications, sometimes serious, have been reported following STARR, [ 57 ] [ 58 ] [ 59 ] [ 60 ] [ 61 ]   but the procedure is now considered safe and effective. [ 60 ]  STARR is   contraindicated  in patients with weak sphincters (fecal incontinence and urgency are a possible complication) and with  anismus  (paradoxical contraction of the pelvic floor during attempted defecation). [ 60 ]  The operation has been shown to improve rectal sensitivity and decrease rectal volume, the reason thought to create urgency. [ 51 ]  90% of patients do not report urgency 12 months after the operation. The anal sphincter may also be stretched during the operation. STARR was compared with biofeedback and found to be more effective at reducing symptoms and improving quality of life. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7096", "text": "Rectal mucosal prolapse  (mucosal prolapse, anal mucosal prolapse) is a sub-type of rectal prolapse, and refers to abnormal descent of the  rectal   mucosa  through the  anus . [ 21 ]  It is different to an internal intussusception (occult prolapse) or a complete rectal prolapse (external prolapse, procidentia) because these conditions involve the full thickness of the rectal wall, rather than only the mucosa (lining). [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7097", "text": "Mucosal prolapse is a different condition to prolapsing (3rd or 4th degree)  hemorrhoids , [ 13 ]  although they may look similar."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7098", "text": "Rectal mucosal prolapse can be a cause of  obstructed defecation  (outlet obstruction). [ 9 ]  and rectal malodor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7099", "text": "Symptom severity increases with the size of the prolapse, and whether it spontaneously reduces after defecation, requires manual reduction by the patient, or becomes irreducible. The symptoms are identical to advanced hemorrhoidal disease, [ 13 ]  and include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7100", "text": "The condition, along with complete rectal prolapse and  internal rectal intussusception , is thought to be related to chronic straining during  defecation  and  constipation ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7101", "text": "Mucosal prolapse occurs when the results from loosening of the submucosal attachments (between the mucosal layer and the  muscularis propria ) of the  distal   rectum . [ 3 ]  The section of prolapsed rectal mucosa can become ulcerated, leading to bleeding."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7102", "text": "Mucosal prolapse can be differentiated from a full thickness external rectal prolapse (a complete rectal prolapse) by the orientation of the folds (furrows) in the prolapsed section. In full thickness rectal prolapse, these folds run circumferential. In mucosal prolapse, these folds are radially. [ 10 ]  The folds in mucosal prolapse are usually associated with internal hemorrhoids. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7103", "text": "EUA  (examination under anesthesia) of anorectum and banding of the mucosa with rubber bands."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7104", "text": "Solitary rectal ulcer syndrome  (SRUS, SRU), is a disorder of the  rectum  and  anal canal , caused by straining and increased pressure during  defecation . This increased pressure causes the anterior portion of the rectal lining to be forced into the anal canal (an  internal rectal intussusception ). The lining of the rectum is repeatedly damaged by this friction, resulting in  ulceration . SRUS can therefore be considered to be a consequence of internal intussusception (a sub type of rectal prolapse), which can be demonstrated in 94% of cases. It may be  asymptomatic , but it can cause  rectal pain ,  rectal bleeding ,  rectal malodor , incomplete evacuation and  obstructed defecation  (rectal outlet obstruction)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7105", "text": "Symptoms include: [ 18 ] [ 21 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7106", "text": "The condition is thought to be uncommon. It usually occurs in young adults, but children can be affected too. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7107", "text": "The essential cause of SRUS is thought to be related to too much straining during defecation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7108", "text": "Overactivity of the anal sphincter during defecation causes the patient to require more effort to expel stool. This pressure is produced by the modified valsalva manovoure (attempted forced exhalation against a closed glottis, resulting in increased abdominal and intra-rectal pressure). Patiest with SRUS were shown to have higher intra-rectal pressures when straining than healthy controls. [ 65 ]  SRUS is also associated with prolonged and incomplete evacuation of stool. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7109", "text": "More effort is required because of concomitant  anismus , or non-relaxation/paradoxical contraction of  puborectalis  (which should normally relax during defecation). [ 67 ]  The increased pressure forces the anterior rectal lining against the contracted puborectalis and frequently the lining prolapses into the anal canal during straining and then returns to its normal position afterwards."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7110", "text": "The repeated trapping of the lining can cause the tissue to become swollen and congested. Ulceration is thought to be caused by resulting poor blood supply ( ischemia ), combined with repeated frictional trauma from the prolapsing lining, and exposure to increased pressure are thought to cause ulceration. Trauma from hard stools may also contribute."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7111", "text": "The site of the ulcer is typically on the  anterior  wall of the  rectal ampulla , about 7\u201310\u00a0cm from the anus. However, the area may of ulceration may be closer to the anus, deeper inside, or on the lateral or posterior rectal walls. The name \"solitary\" can be misleading since there may be more than one ulcer present. Furthermore, there is a \"preulcerative phase\" where there is no ulcer at all. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7112", "text": "Pathological specimens of sections of rectal wall taken from SRUS patients show thickening and replacement of muscle with fibrous tissue and excess collagen. [ 69 ]  Rarely, SRUS can present as polyps in the rectum. [ 70 ] [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7113", "text": "SRUS is therefore associated and with internal, and more rarely, external rectal prolapse. [ 66 ]  Some believe that SRUS represents a spectrum of different diseases with different causes. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7114", "text": "Another condition associated with internal intussusception is  colitis cystica profunda  (also known as CCP, or proctitis cystica profunda), which is  cystica profunda  in the rectum. Cystica profunda is characterized by formation of  mucin   cysts  in the muscle layers of the gut lining, and it can occur anywhere along the gastrointestinal tract. When it occurs in the rectum, some believe to be an interchangeable diagnosis with SRUS since the  histologic  features of the conditions overlap. [ 73 ] [ 74 ]  Indeed, CCP is managed identically to SRUS. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7115", "text": "Electromyography may show  pudendal nerve  motor latency. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7116", "text": "Complications are uncommon, but include massive rectal bleeding, ulceration into the prostate gland or formation of a  stricture . [ 76 ] [ 77 ] [ 78 ]  Very rarely, cancer can arise on the section of prolapsed rectal lining. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7117", "text": "SRUS is commonly misdiagnosed, and the diagnosis is not made for 5\u20137 years. [ 64 ]  Clinicians may not be familiar with the condition, and treat for Inflammatory bowel disease, or simple constipation. [ 79 ] [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7118", "text": "The thickened lining or ulceration can also be mistaken for types of cancer. [ 81 ] [ 82 ] [ 83 ] [ 84 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7119", "text": "The differential diagnosis of SRUS (and CCP) includes: [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7120", "text": "Defecography ,  sigmoidoscopy ,  transrectal  ultrasound , mucosal  biopsy , anorectal  manometry  and  electromyography  have all been used to diagnose and study SRUS. [ 18 ] [ 67 ]  Some recommend biopsy as essential for diagnosis since ulcerations may not always be present, and others state  defecography  as the investigation of choice to diagnose SRUS. [ 63 ] [ 74 ] [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7121", "text": "Although SRUS is not a medically serious disease, it can be the cause of significantly reduced  quality of life  for patients. It is difficult to treat, and treatment is aimed at minimizing symptoms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7122", "text": "Stopping straining during bowel movements, by use of  correct posture ,  dietary fiber  intake (possibly included bulk forming  laxatives  such as  psyllium ), stool softeners (e.g.  polyethylene glycol , [ 85 ] [ 86 ]  and  biofeedback  retraining to coordinate pelvic floor during defecation. [ 87 ] [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7123", "text": "Surgery may be considered, but only if non surgical treatment has failed and the symptoms are severe enough to warrant the intervention. Improvement with surgery is about 55-60%. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7124", "text": "Ulceration may persist even when symptoms resolve. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7125", "text": "A group of conditions known as  Mucosal prolapse syndrome  (MPS) has now been recognized. It includes SRUS, rectal prolapse, proctitis cystica profunda, and inflammatory polyps. [ 17 ] [ 18 ]  It is classified as a chronic benign inflammatory disorder. The unifying feature is varying degrees of rectal prolapse, whether internal intussusception (occult prolapse) or external prolapse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7126", "text": "Rectal prolapse affects less than 0.5% of the general population. [ 91 ]  It affects women more commonly, with a female to male ratio of 9:1. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7127", "text": "Rosebud pornography and prolapse pornography (or rosebudding or rectal prolapse pornography) is an anal sex practice that occurs in some extreme anal pornography wherein a pornographic actor or actress performs a rectal prolapse wherein the walls of the rectum slip out of the anus. Rectal prolapse is a serious medical condition that requires the attention of a medical professional. However, in rosebud pornography, it is performed deliberately. Michelle Lhooq, writing for VICE, argues that rosebudding is an example of producers making 'extreme' content due to the easy availability of free pornography on the internet. She also argues that rosebudding is a way for pornographic actors and actresses to distinguish themselves. [ 92 ]  Repeated rectal prolapses can cause bowel problems and anal leakage and therefore risk the health of pornographic actors or actresses who participate in them. [ 92 ]  Lhooq also argues that some who participate in this form of pornography are unaware of the consequences. [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7128", "text": "Prolapse refers to \"the falling down or slipping of a body part from its usual position or relations\". It is derived from the Latin  pro-  - \"forward\" +  labi  - \"to slide\".  \"Prolapse\" .  Merriam-Webster.com Dictionary . Merriam-Webster.   Prolapse  can refer to many different medical conditions other than rectal prolapse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7129", "text": "procidentia has a similar meaning to prolapse, referring to \"a sinking or prolapse of an organ or part\". It is derived from the Latin  procidere  - \"to fall forward\". [ 93 ]   Procidentia  usually refers to  uterine prolapse , but rectal procidentia can also be a synonym for rectal prolapse."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7130", "text": "Intussusception is defined as  invagination  (infolding), especially referring to \"the slipping of a length of intestine into an adjacent portion\". It is derived from the Latin  intus  - \"within\" and  susceptio  - \"action of undertaking\", from  suscipere  - \"to take up\".  \"Intussusception\" .  Merriam-Webster.com Dictionary . Merriam-Webster.  Rectal intussusception is not to be confused with other  intussusceptions  involving  colon  or  small intestine , which can sometimes be a medical emergency. Rectal intussusception by contrast is not life-threatening."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7131", "text": "Intussusceptum refers to the  proximal  section of rectal wall, which telescopes into the  lumen  of the  distal  section of  rectum  (termed the intussuscipiens). [ 10 ]  What results is 3 layers of rectal wall overlaid. From the lumen outwards, the first layer is the proximal wall of the intussusceptum, the middle is the wall of the intussusceptum folded back on itself, and the outer is the distal rectal wall, the intussuscipiens. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7132", "text": "A  rectal stricture  ( rectal stenosis ) [ 1 ]  is a chronic and abnormal narrowing or constriction of the  lumen  of the  rectum  which presents a partial or complete obstruction to the movement of bowel contents. A rectal stricture is located deeper inside the body compared to an  anal stricture . Sometimes other terms with wider meaning are used, such as  anorectal stricture ,  colorectal stricture  or  rectosigmoid stricture ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7133", "text": "Rectal stricture has been defined as the inability to pass a rigid  proctoscope  (12\u00a0mm diameter) or a rigid  sigmoidoscope  (19\u00a0mm diameter) through the affected cross-section of rectum. [ 1 ]  If the rectal stricture is accessible during digital rectal examination, a rectal stricture may be defined as narrowing to less than one-finger breadth. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7134", "text": "Anal strictures are usually located at the anal verge in a narrow band, but sometimes they involve the entire length of the anal canal. [ 1 ]  Surgeons and anatomists have different definitions of the anal canal. [ 3 ]  Surgically and clinically, the anal canal is usually defined as the zone from the anal verge to the anorectal ring (at the level of the external anal sphincter and the  puborectalis muscle ). The anorectal ring is easy to identify when patients are asked to squeeze during  digital rectal examination . [ 3 ]  Anatomically, the anal canal is defined as the zone from the anal verge to the dentate line ( pectinate line ). [ 3 ]  This is a line formed by the lower ends of the anal columns and represents the embryological junction between the  hindgut  and the  proctodeum . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7135", "text": "Both rectal stricture and  anal stricture  (anal stenosis) are types of colonic stricture. They both can also be more widely categorized as gastrointestinal strictures. However, rectal strictures behave differently to colonic strictures because of the proximity of the rectum to the anal canal and pelvic organs, and because of different blood supply. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7136", "text": "There may be no symptoms (clinically silent stricture), [ 4 ]  or only minor symptoms, but may get worse over time. [ 2 ]  On the other hand, acute  bowel obstruction  may develop as the first major sign of a stricture. This may be the case with malignant strictures, and the condition may be a medical emergency which requires urgent treatment in order to avoid serious complications such as  bowel perforation . [ 5 ]  When symptoms are caused, the term \"clinically relevant rectal stricture\" is used. [ 1 ]  Possible symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7137", "text": "The first step is exclusion of malignant causes. This may involve tissue  biopsy ,  endorectal ultrasound ,  computed tomography , and  magnetic resonance imaging . [ 1 ]  The next step is assessment of the stricture. The distance from the anal verge, the diameter of the narrowest point of the stricture, and the longitudinal length are ascertained. The degree of narrowing can be assessed with a water-soluble  contrast enema . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7138", "text": "Rectal strictures are usually classified as benign or malignant (associated with cancer)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7139", "text": "Benign rectal strictures can be further subcategorized as primary (caused by diseases) and secondary (caused by complication of surgery). Secondary strictures very often occur at the site of a previous surgical anastomosis. Primary strictures have various causes, including different inflammatory disease processes. Causes of benign strictures include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7140", "text": "Acute bowel obstruction is a common presenting manifestation of colorectal cancer which is locally advanced. [ 5 ]  Malignant strictures may also develop in the context of inflammatory bowel disease. Treatment for malignant strictures is ideally resection (surgical removal) with or without radiotherapy. If resection is not possible or not sensible, symptoms of the stricture may be palliated with radiotherapy, stents, or debulking. [ 1 ]  Possible malignant processes which may cause rectal stricture include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7141", "text": "The narrowing may be because of an intrinsic process occurring within the lumen of the rectum (luminal), within the wall of the rectum (mural), or it can be due to an extrinsic process that is compressing the rectum from the outside (extramural). [ 1 ] [ 8 ]  In the case of external compression of the bowel, the term pseudostricture may be used. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7142", "text": "According to one review of a total of 730 cases, those which formed after anastomosis represented 74% of all reported benign rectal strictures. [ 2 ]  The next most common cause of benign rectal stricture was inflammatory bowel disease, accounting for 20% of all cases. [ 2 ]  This means all other causes of rectal stricture are, by comparison, rare."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7143", "text": "Rectal stricture is reported to develop after colorectal resection at a rate of 3-30%. Such strictures mostly form after resection due to rectal cancer with colorectal or coloanal anastomosis. Stricture is also possible as a complication following resection because of diverticular disease. According to some reports, rectal strictures are more likely following stapled anastomosis compared to hand sutured anastomosis. [ 2 ]  However, a Cochrane review found no significant difference in the rate of rectal stricture between hand sewn and stapled  ileocolic anastomosis  (usually performed after right\u2010sided  colon cancer  and  Crohn's disease ). [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7144", "text": "Inflammatory bowel diseases (IBD) include Crohn\u2019s disease, which affects only the colon, and ulcerative colitis, which may affect any section of the gastrointestinal tract. The relapsing-remitting, chronic inflammation in the bowel wall non uncommonly leads to the development of colonic strictures, including rectal strictures. [ 6 ]  Rectal strictures are more common in Crohn's disease than in ulcerative colitis. [ 2 ]  There is a risk of malignancy developing at the site of stricture. Therefore, tissue biopsy of strictures is carried out in order to check for dysplasia or malignancy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7145", "text": "Stricture may occur following trauma such as caustic burns caused by chemical agents. [ 11 ] [ 12 ]  If they cause inflammation, chronic use of  suppositories  may cause rectal stricture, [ 2 ]  but overall this is a safe method of drug delivery. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7146", "text": "Thermal burns are possible if hot water enemas are attempted by patients or practitioners of alternative medicine in the belief that they will provide a stronger stimulus for evacuation of stool. [ 11 ]  The rectal mucosa is vulnerable to thermal burns in such cases because it is sensitive only to distension (stretching) and not to thermal stimuli. [ 11 ]  Usually a burn of the rectal wall heals after 2\u20133 weeks without permanent stricture. Such burns may be treated with bowel resting, antibiotics, stool softeners, liquid diet and steroid suppository to reduce inflammation. [ 11 ]  Sometimes thermal burns progress to chronic stricture. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7147", "text": "The rectum is very close to the prostate in males and the uterus and cervix in females, and therefore it frequently receives radiation during radiotherapy for cancers in the pelvic region.  Radiation proctitis  (chronic radiation enterocolitis) usually appears after several months of treatment, and is characterized by rectal bleeding or obstructed defecation secondary to the formation of strictures. [ 7 ]  Such rectal strictures are usually located in the proximal rectum, and are one of the most common features of late radiation damage. [ 14 ]  The mechanism of stricture formation is  obliterative endarteritis , lymphatic dilation, and tissue ischemia and necrosis. [ 7 ]  Then there is collagen deposition and fibrosis in the submucosal layer. [ 7 ]  They are often associated with a fistula. [ 14 ]  Post-irradiation strictures may cause symptoms such as diarrhea, tenesmus, narrow feces, abdominal pain, and vomiting. [ 7 ]  The risk of intestinal obstruction due to strictures in patients receiving radiotherapy in the pelvis is reported as 1\u201315%. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7148", "text": "Sexually transmitted infections  may sometimes cause rectal strictures in persons who engage in anoreceptive sex. [ 2 ]   Lymphogranuloma venereum  usually affects the genital mucosa. However, it may rarely present as the anorectal variant, termed \"lymphogranuloma venereum proctitis\". Lymph nodes are enlarged and suppurative (produce pus). The condition is similar to Crohn's disease with rectal stricture formation (eventually), bowel perforation and fistulae. [ 15 ]  In one report,  herpes simplex virus 2  was implicated as the cause of a rectal stricture. [ 2 ]  Rarely, rectal stricture may develop in  actinomycosis  infection. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7149", "text": "If a foreign body becomes stuck there is reactive inflammation and fibrosis, which eventually may lead to the formation of a stricture. [ 2 ]  In  endometriosis , if ectopic endometrial tissue is present in the rectal wall it may cause rectal stricture. [ 2 ]   Solitary rectal ulcer syndrome  may also sometimes be associated with rectal stricture. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7150", "text": "Rectal stricture may sometimes be a complication of surgical procedures other than anastomosis. For example, endoscopic submucosal dissection, which is a minimally invasive treatment for colorectal cancer, may rarely cause development of a rectal stricture. [ 2 ]  Other surgical procedures which may cause the development of a stricture include  ventral rectopexy , [ 8 ]   Delorme\u2019s procedure , [ 16 ]  and  hemorrhoidectomy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7151", "text": "How a rectal stricture is treated depends on the exact cause, the distance from the anal verge, the degree of narrowing, the severity of symptoms, and the health of the patient. [ 1 ]  Short strictures are more responsive to dilation. Longer strictures may require more significant surgical procedures. [ 1 ]  Generally, benign rectal strictures may not require treatment if they do not cause symptoms. [ 1 ]  For example, a non symptomatic stricture may be detected as an incidental finding during colonoscopy for an unrelated reason. [ 1 ]  Treatment options fall into 3 main categories: dilatation, stenting, or surgery. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7152", "text": "The treatment depends on the cause. For example, strictures caused by infections may respond well to  antibiotics . [ 2 ]  Use of  stool softeners ,  laxatives  and high fiber diet is a general measure for most strictures, and is also sometimes advised for prevention of recurrence of stricture even after treatment. [ 2 ]  Non surgical treatment may be combined with other procedures such as dilation.  Steroids  may be injected into the stricture. It is unknown exactly how the steroid helps to prevent recurrence of the stricture, but it may involve inhibition of collagen formation and cross-linking, and increase of collagen breakdown. In combination, this reduces contraction of scar tissue. [ 7 ]   TNF inhibitors  such as  infliximab  have also been injected into strictures endoscopically. However, this is not a common treatment. [ 6 ]  Healing of rectal strictures in inflammatory bowel disease with TNF inhibitor occurs in 59% of cases. [ 2 ]   Mitomycin C  has been used as a topical application, in combination with manual dilation. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7153", "text": "For rectal strictures which are mild and close to the anal verge (<6\u00a0cm), digital dilation (with fingers) or dilation with instruments is possible. [ 1 ]  Such instruments include Hagar's dilators, esophageal dilators, St Marks anal dilators, and bougie dilators. [ 16 ] [ 1 ] [ 2 ]  Sometimes the patient can be shown how to perform this dilation at home, but this is may be difficult for them, and rarely gives good long term results. [ 16 ]  Dilation with instruments by the surgeon may be performed under sedation or under general aesthesia for moderate strictures. [ 16 ]  This treatment is often the first to be attempted, and is successful about 50% of the time. [ 2 ]  Hegar dilators come in multiple sizes with different diameters. This enables progressive dilation over time which reduces the risk of bowel perforation. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7154", "text": "Balloon dilation is the most common method of mechanical dilation, [ 11 ]  and is also often considered the first line treatment. [ 2 ]  This treatment is simple, but repeat procedures may be needed. [ 11 ]  Balloon dilation may be combined with intralesional steroid injection. [ 7 ]  Injection of steroid seems to increase the effectiveness of balloon dilation, and increases the length of time before relapse. [ 7 ]  The success rate of balloon dilation for benign rectal strictures overall is about 78%. [ 2 ]  In rectal strictures in the context of Crohn's disease, the long-term success rate of balloon dilation is about 80%. However, it may be ineffective for very tight, fibrotic strictures. [ 17 ]  Fluoroscopic guidance can be used during the procedure to improve visualization. [ 2 ]  The risk of bowel perforation is about 1%. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7155", "text": "Surgical procedures are indicated if multiple other treatments have failed, or if the stricture involves a long section of bowel. [ 11 ]  Surgical procedures may be carried out by the transanal approach or via the transabdominal approach. [ 11 ]  Debulking of malignant strictures may be carried out with laser ablation or with argon beam plasma coagulation. [ 1 ]  Various procedures and methods have been used to surgically treat strictures, including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7156", "text": "Self-expandable metallic stents  (SEMS) are sometimes used, but they are usually considered not suitable for very low rectal strictures. [ 14 ]  However, this view is now challenged. [ 18 ]  Stents may be used as the definitive treatment of a stricture, or as a temporary measure to stabilize a patient with acute obstruction before another procedure is carried out. [ 11 ]  Stents are not commonly used for benign rectal strictures. [ 11 ]  Sometimes they are used when strictures are associated with malignancy. In such cases, use of a stent may avoid or delay the need for  colostomy . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7157", "text": "A  rectovestibular fistula , also referred to simply as a  vestibular fistula , is an anorectal  congenital disorder  where an abnormal connection ( fistula ) exists between the  rectum  and the  vulval vestibule  of the female genitalia."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7158", "text": "If the fistula occurs within the  hymen , it is known as a  rectovaginal fistula , a much rarer condition. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7159", "text": "If a colostomy is not performed immediately after birth, patients with rectovestibular fistulae may present later in life with complications including severe  constipation  and  megacolon  (abnormal dilation of the colon), requiring colostomy or further surgery. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7160", "text": "A rectovestibular fistula occurs when the  colon  or  rectum  deviates anteriorly. [ 1 ]  This leads to the formation of an abnormal connection between the rectum and the  vulval vestibule , immediately posterior to the  hymen , so that an  ectopic anus  opens into the  fourchette , or frenulum, of the  labia minora . [ 3 ]  A common wall is shared between the rectum and  vagina  above the site of the fistula. [ 2 ]  Although the opening of the rectum into the  anal canal  is shorter and narrower than normal, the rectum itself is completely normal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7161", "text": "The diagnosis of a rectovestibular fistula can be made in female newborns if the vulva is stained with  meconium  (the earliest form of  stool  in an infant). [ 3 ]  The opening of the  anus  may be difficult to see due to its small size and position, but it may be visible as a thickening of the median  perineal raphe  with an obvious anal dimple. [ 3 ] [ 2 ]  Patients with rectovestibular fistulae are commonly misdiagnosed with rectovaginal fistulae. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7162", "text": "Colostomy  is recommended by most surgeons, and has a good prognosis, with 90% of patients regaining normal bowel control. [ 4 ]  Since the rectal opening and  anal orifice  in a vestibular fistula tend to be short and narrow, a colostomy is usually performed to allow decompression of the bowel unless the orifice is wide enough to allow normal defecation. [ 2 ]  Colostomy is often followed by  posterior sagittal anorectoplasty  (PSARP), a surgical procedure to repair the anal orifice, at a later date. [ 4 ] [ 5 ]  Some surgeons prefer to perform an immediate PSARP without a colostomy first, while others perform neither a colostomy nor a PSARP and instead opt for a simple dilatation of the orifice to allow stool to pass and the bowel to decompress. [ 5 ]  It has been suggested that only experienced surgeons should perform repair without an initial colostomy. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7163", "text": "Rectovestibular fistula is the most common defect of the rectum and anal canal in females. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7164", "text": "Sigmoidocele  (also known as  pouch of Douglas  descent) is a medical condition in which a  herniation  of  peritoneum  containing loops of redundant  sigmoid colon  descends (prolapses) into the  rectouterine pouch  (in females), between the  rectum  and the  vagina . [ 1 ] [ 2 ]  This can obstruct the rectum and cause  obstructed defecation syndrome . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7165", "text": "Sigmoidocele may be internal if it is only detectable on  defecography , or external if it detectable without imaging and associated with a  rectocele  or  rectal prolapse . [ 2 ]  It is a type of posterior compartment prolapse. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7166", "text": "Sigmoidocele may be classified according to size relative to the pubococcygeal line. [ 2 ] [ note 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7167", "text": "The severity of sigmoidocele can be described with reference to the position of the lowest loop of the sigmoid relative to lines drawn on defecography:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7168", "text": "Sigmoidocele may not cause any symptoms. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7169", "text": "The phenomenon is caused by a weak section of   fascial supports  of the vagina (the uterosacral cardinal ligament complex and rectal vaginal septum), which allows a section of peritoneum containing the sigmoid colon to prolapse out of normal position and descend between the rectum and the vagina. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7170", "text": "The  mesentery  of the sigmoid colon (the structure which attaches the colon to the abdominal wall) is termed the mesosigmoid. This structure is very flexible, which means that the sigmoid colon is very mobile and may change position. During defecation it may be pushed down, eventually causing sigmoidocele. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7171", "text": "Sigmoidocele may be associated with  descending perineum syndrome . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7172", "text": "It is not possible to differentiate between a  rectocele  and a sigmoidocele on  vaginal examination .   Defecating proctography  will demonstrate a sigmoidocele during straining. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7173", "text": "Surgery is considered if there is a significant hernia combined with symptoms of obstructed defecation. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7174", "text": "Laparoscopic  ventral mesh rectopexy  has been used to correct sigmoidocele. [ 7 ]  This procedure involves inserting a mesh between the rectum and the vagina. The mesh is suspended from the sacral promontory without tension. This acts to support the recto-vaginal septum and elevate a deep pouch of Douglas. [ 7 ]  If there is prolapse of the middle compartment,  sacrocolpopexy  may be carried out to surgically correct all pelvic prolapse problems in the same procedure. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7175", "text": "Other treatment options are  anterior resection , [ 4 ]   sigmoidopexy  with rectocele repair, [ 4 ]  or  sigmoidectomy . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7176", "text": "Sigmoidocele normally occurs in females, and is uncommon. [ 1 ]  Sigmoidocele is detected about 4-5% of the time when defecography is carried out. [ 3 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7177", "text": "Solitary rectal ulcer syndrome  ( SRUS  or  SRU ) is a chronic disorder of the rectal  mucosa  (the lining of the rectum). [ 1 ]  Very often but not always it occurs in association with varying degrees of  rectal prolapse . The condition is thought to be caused by different factors, such as long term  constipation , straining during defecation, and  dyssynergic defecation  (anismus). Treatment is by normalization of bowel habits,  biofeedback , and other conservative measures. In more severe cases, various surgical procedures may be indicated. The condition is relatively rare, affecting approximately 1 in 100,000 people per year. It affects mainly adults aged 30\u201350. Females are affected slightly more often than males. The disorder can be confused clinically with  rectal cancer  or other conditions such as  inflammatory bowel disease , even when a  biopsy  is done. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7178", "text": "The signs and symptoms are variable, and in up to 25% of patients there may be no symptoms. [ 3 ]  The most common signs and symptoms are bleeding, which can vary from minor to severe, rectal prolapse and incomplete evacuation (35%-76% of cases). [ 4 ]  According to one report, constipation is present in about 55% of cases, but diarrhea is present in 20%\u201340% of cases. [ 1 ]  Reported symptoms are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7179", "text": "The exact cause is unclear and the condition is not fully understood. [ 3 ]  There are thought to be multiple factors which simultaneously cause the condition. [ 3 ]  Long term injury to the rectal mucosa and ischemic trauma are thought to be the main mechanisms. [ 5 ]  In a report of 36 patients with SRUS, the underlying cause was internal prolapse (intussusception) in 20 patients, external rectal prolapse in 14 patients, and dyssynergic defecation (anismus) in 2 patients. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7180", "text": "Self-digitation is when individuals with constipation resort to inserting a finger into the rectum in order to \"hook out\" fecal pellets or to apply pressure to an obstructing lesion (see:  obstructed defecation ). The rectal mucosa is fragile and vulnerable to trauma when such manoeuvres are performed chronically. It is thought that this self-induced trauma is one possible mechanism of SRUS. [ 1 ]  However, since sometimes the location of SRUS lesion(s) is much further than a finger could reach means that this cannot be the only cause. [ 5 ]  In constipation, the stools may be very hard and this is another possible mechanism of trauma. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7181", "text": "People with constipation or certain anatomical anomalies are more likely to end up using excessive straining during defecation attempts. [ 5 ]  Prolonged straining may cause direct trauma to the rectal mucosa. [ 5 ]  Most patients with SRUS have  dyssynergic defecation  (previously termed anismus). [ 8 ]  This is a failure of relaxation (or paradoxical contraction) of the  puborectalis muscle  during defecation attempts. This pelvic floor muscle is normally supposed to relax, thereby straightening the anorectal angle and allowing rectal contents to be evacuated. Dyssynergic defecation causes high pressure in the rectum and in the anal canal, [ 1 ]  which causes lengthening [ 1 ]  and compression of the rectal tissues, which in turn leads to ischema of the mucosa. [ 8 ]  There is also a shearing movement of the rectum against the pelvic floor muscles. [ 8 ]  In the long term this leads to repeated mucosal damage. [ 8 ]  Inappropriate contraction of puborectalis in the squatting position causes traumatic compression of the rectal wall against the anal canal. [ 5 ]  Also, it is reported that individuals with SRUS have not only increased pressure when squeezing, but also higher resting pressure compared to normal controls. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7182", "text": "SRUS is usually accompanied by prolapse (e.g. external prolapse or rectoanal intussusception/internal prolapse) or other pelvic-floor disorders. [ 1 ] [ 7 ]  This is association is common, but not always present. [ 9 ]  Some state that if SRUS is not treated, it would always tend to progress to rectal prolapse. [ 5 ]  The relationship of SRUS with  rectal prolapse  and rectal cystitis profunda is debated. [ 8 ]  Some see SRUS and prolapse as synonymous, while others see them as separate entities, [ 8 ]  and state that they do not share the same physiology. [ 6 ]  For example, the mucosal changes that occur with external rectal prolapse can be separated from the mucosal changes seen in SRUS. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7183", "text": "The excessive pressure caused by straining (i.e. dyssynergic defecation and constipation) may in the long term lead to development of the spectrum of rectal prolapse conditions (mucosal versus full-thickness prolapse, internal versus external rectal prolapse). [ 5 ]  These conditions create chronic vascular trauma (ischemia or hypoperfusion) in the rectal mucosa, [ 1 ]  which predisposes it to ulceration, [ 8 ]  and pressure necrosis. [ 4 ]  Even the initial small areas of an intussusception can lead to vascular injury and reduce blood supply to the region. [ 5 ]  This is the first stage of ulcer development. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7184", "text": "Psychological factors are also thought to be involved, since patients with SRUS sometimes have psychological disorders such as  obsessive-compulsive disorder . [ 1 ]  Also, some unknown factors may also be involved, such as hormonal factors related to pregnancy. [ 5 ]  Other possible factors are rectal hypersensitivity, [ 4 ]  and impaired rectal evacuation of stool. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7185", "text": "Diagnosis is difficult because of rarity of the condition and because of the variability of the symptoms and the histologic appearance. [ 1 ] [ 5 ]  The condition is sometimes misdiagnosed. [ 1 ]  Clinicians may not be familiar with the condition, and treat for  inflammatory bowel disease , or simple constipation. [ 10 ] [ 11 ]  Diagnosis may be delayed by many years as a result. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7186", "text": "The  differential diagnosis  is as follows:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7187", "text": "Investigations used in the diagnosis of SRUS include  defecography ,  endoanal ultrasound ,  colonoscopy  and histological examination of a  biopsy . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7188", "text": "The macroscopic appearance of SRUS is very variable. [ 8 ]  Indeed, the condition has been referred to as \u201cthe three-lies disease\u201d, [ 4 ]  because the name of the condition is sometimes misleading. In reality, there may be more than one lesion, which may not be  ulcerative , [ 12 ]  and the condition may appear in different parts of the gastrointestinal tract (i.e. other than the  rectum ). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7189", "text": "Classically, there is a solitary ulcer. But only 20% of patients have a single ulcer whereas in other cases there may be multiple lesions. [ 6 ]  The size of the ulcers is usually 0.5\u20134\u00a0cm. [ 5 ]  The lesion is most often located on the anterior (front) or lateral (side) rectal wall, centered on a rectal fold, [ 1 ]  usually 10\u00a0cm from the anal verge. [ 8 ]  Less commonly there may be ulcers in the  anal canal  or even in the  sigmoid colon . [ 5 ]  The nature of the tissue changes can vary from simple  erythema  (redness) /  hyperaemia  (increased blood flow) of the mucosa in 18% of cases, [ 1 ]  to a chronic-appearing, small, shallow ulcer with nodular margins and a white or sloughing base. [ 8 ] [ 1 ]  In up to 33% of cases there is no ulceration but instead one or more well-developed polyps or mass lesions. [ 8 ] [ 5 ]  There is usually mild  proctitis  (inflammation of the rectal mucosa) surrounding the ulcer. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7190", "text": "Conventional defecography or magnetic resonance defecography may be used. [ 1 ]  Between 50-100% of patients with SRUS will have abnormal defecography results. [ 5 ]  Defecography findings in SRUS may include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7191", "text": "Endoanal ultrasound  can determine the depth of the ulcer and the structure of the external and internal anal sphincters. [ 8 ]  Endoanal ultrasound findings in SRUS include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7192", "text": "As a diagnostic investigation, anorectal manometry can evaluate defecation function. It can highlight excessive and prolonged straining effort during defecation attempts, and also record any improvement in function before and after treatment interventions. [ 13 ]  It is uncommonly used to diagnose SRUS, although biofeedback is still commonly used as a treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7193", "text": "The histological appearance is as follows:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7194", "text": "If the biopsy includes polypoid lesions, there are villiform structures visible. [ 5 ]  Gland entrapment in the submucosa is sometimes seen, which is termed  colitis cystica profunda . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7195", "text": "Treatment of SRUS is difficult and there is a lack of evidence-based guidelines. [ 4 ]  The treatment is based on the pathophysiology of SRUS, [ 5 ]  and the main aim is restoration of a normal pattern of defecation. [ 1 ]  The exact treatment depends on the severity of the symptoms, the severity/type of SRUS, and whether rectal prolapse is present or absent. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7196", "text": "Conservative measures are the first line treatment for patients with no symptoms or only mild to moderate symptoms, and those who have no significant anatomical defect. [ 1 ]  Conservative measures by themselves may improve symptoms and prevent the condition getting worse. [ 1 ]  Where conservative measures fail, or with severe disease and symptoms, or with significant anatomical defects, surgical options may be indicated. [ 5 ] [ 1 ]  Improvement in symptoms does not always equate to healing of the ulcer as seen on endoscopy. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7197", "text": "Conservative management is focused on education of the patient and behavioral modification. Where indicated, conservative management may also involve treatment of psychological problems, [ 5 ]  and avoidance of anoreceptive sex (to prevent trauma to the rectum). [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7198", "text": "Biofeedback targets pelvic floor behaviors and enables a reprogramming of autonomic neurologic pathways associated with defecation. [ 8 ]  The treatment is particularly helpful for dyssynergic defecation (anismus). Research studies have shown that there is improved blood flow to the rectal mucosa after biofeedback therapy. [ 1 ]  The overall rate of complete resolution of both symptoms and ulceration varies at 50-75%. [ 8 ]  Stool frequency and straining effort decrease after this treatment. [ 1 ]  In about 56% of cases, biofeedback treatment stops rectal bleeding. [ 1 ]  Some patients are able to cease relying on digitation. [ 1 ]  Biofeedback is more effective in children with SRUS compared to adults. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7199", "text": "A randomized controlled study compared topical agents (dexamethasone, sucralfate and bismuth) with biofeedback. Overall, biofeedback gave 80% improvements in evacuation difficulty, need for digitation, sensation of incomplete evacuation, evacuation time, and appearance of mucosa on colonoscopy compared to the topical agents (50% improvement). [ 13 ]  However, the degree of long term improvement is not known. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7200", "text": "Several different topical treatments have been reported, with variable outcomes. [ 1 ]  These are substances applied directly to the ulcer, usually administered by enema. [ 8 ]  They may be helpful for short term management of acute symptoms in SRUS. [ 8 ]  They are thought to work by reducing inflammation and physically forming a barrier over the surface of the ulcer to protect it from irritants, thereby allowing it to heal. [ 4 ] [ 5 ]  However, the long term efficacy is unknown. According to a systematic review, 57% of SRUS patients who received medical treatment had resolution of ulceration. [ 4 ]  Topical agents which have been used for SRUS include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7201", "text": "According to one report, topical agents had an efficacy between 28 and 90%. Sucralfate had a 45-81% resolution rate compared to sulfasalazine (30-64%) and combination of other topical agents (20-79%). [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7202", "text": "Surgery may be indicated for severe cases of SRUS (either severe symptoms, severe ulceration, or significant associated anatomical defect such as prolapse), or when conservative measures fail. [ 8 ] [ 5 ]  Some authors state that most patients do not benefit from surgery. [ 5 ]  Overall, up to 33% of SRUS patients end up requiring surgery. [ 8 ]  A systematic review reported that SRUS improved in 77% of patients who underwent any type of surgery. [ 6 ]  However, recurrence of the condition later developed in 52% of cases. [ 6 ]  It has been suggested that any treatment which only addresses the ulcer without correcting the underlying causes will typically lead to recurrence. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7203", "text": "There are multiple different surgical procedures which have been reported for SRUS, [ 5 ]  including:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7204", "text": "Various local treatments for SRUS have been reported. According to one report, such measures have generally unfavorable results, and sometimes the ulcer returns deeper and larger than before the treatment. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7205", "text": "Excision (removal) of the ulcer and suturing the resulting defect with surrounding healthy mucosa has been reported. However, there may not be any long-term benefit. [ 8 ]  Ulcers in the upper part of the rectum may be accessible to local excision using a transanal minimally invasive approach (TAMIS). [ 8 ]  Excision with  neodymium yttrium-aluminium garnet laser  has also been reported. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7206", "text": "Rectopexy is a surgery for rectal prolapse. [ 3 ]  A newer version of the procedure is termed ventral mesh rectopexy, which has also been used for SRUS. [ 14 ]  It may be performed with or without anterior resection (removal of a portion of the front wall of the rectum). [ 9 ]  A mesh may be used to reinforce the anterior rectal wall. [ 8 ]  It can be done as an open procedure or with a laparoscopic abdominal approach. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7207", "text": "Some authors state rectopexy is suitable in highly select cases, [ 9 ]  while others say it is the procedure of choice, [ 7 ]  since it directly addresses the most likely cause. [ 8 ]  There is not much evidence for the use of laparoscopic ventral rectopexy to treat SRUS, [ 13 ]  but there is more evidence to support the its use compared to other surgical procedures. [ 8 ]  Approximately 55-83% of patients with SRUS get reduced symptoms after rectopexy, [ 8 ]  and these benefits appear to be long term. [ 3 ]  In one study, 11 people with SRUS underwent laparoscopic ventral rectopexy. All of the patients showed resolved symptoms and mucosal injury one year after the procedure. In the long term, 1 patient developed recurrence after 4 years, and the other 7 who were evaluated in the long term did not develop recurrence. [ 13 ]  Another study combined laparoscopic ventral rectopexy and biofeedback for 48 patients with SRUS. In all cases there was healing of the mucosa 3 months after the procedure. In 65% of cases there was improvement in symptoms of obstructed defecation and in 45% of cases there was improved quality of life. The rate of recurrence was 4-8% after an average follow up time of 33 months. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7208", "text": "The stapled transanal rectal resection (STARR) procedure has been used both as an alternative to ventral mesh rectopexy and as a secondary procedure when ventral mesh rectopexy failed to completely resolve the condition. [ 16 ]  In one study, STARR gave improvement in all cases where biofeedback had not worked. [ 13 ]  In comparison with ventral mesh rectopexy, STARR may result in higher rates of bowel  urgency , recurrence and other complications, some of which may be serious. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7209", "text": "The following \"last resort\" surgical procedures (which may have significant consequences) have been reported in severe, persistent or recurrent cases of SRUS:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7210", "text": "The condition is relatively rare, but the exact prevalence is not known. [ 3 ]  Prevalence has been estimated as 1 in 100,000 people per year. [ 3 ]  SRUS can occur at any age, but it is most common in adults aged between 30-50. [ 3 ]  Males and females are affected almost equally, [ 3 ]  or females slightly more. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7211", "text": "Misdiagnosis  as  inflammatory bowel disease  (IBD) or  rectal polyps  may hide the true prevalence of SRUS. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7212", "text": "Stapled hemorrhoidopexy  is a  surgical  procedure that involves the cutting and removal of anal hemorrhoidal vascular cushion, whose function is to help to seal stools and create continence. Procedure also removes abnormally enlarged  hemorrhoidal tissue , followed by the repositioning of the remaining hemorrhoidal tissue back to its normal anatomic position. Severe cases of hemorrhoidal prolapse will normally require surgery. Newer surgical procedures include  stapled transanal rectal resection  (STARR) and procedure for prolapse and hemorrhoids (PPH).  Both STARR and PPH are  contraindicated  in persons with either  enterocele  or  anismus . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7213", "text": "This procedure is for internal hemorrhoids only and not for external hemorrhoids or anal fissures. [ citation needed ]  During the procedure the external anal sphincter muscle is pulled in when the anal cushion is cut followed tight stapling with 2 rows of 28 staples so if external hemorrhoids are present they also get pulled in and get hidden inside and get tucked inside the anal canal and reappear when the staples fall after a few months when the external anal sphincter comes to its normal position."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7214", "text": "Previously a lot of surgeons thought that this procedure is for external hemorrhoids also as they disappear but instead they are hidden inside and fool the eye and reappear after the staples fall off. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7215", "text": "Hemorrhoids  are amongst the most common anal disorders. Patients may complain of bleeding,  prolapse , personal discomfort and minor  anal leakage . Where traditional non-surgical measures such as rest, suppositories and dietary advice fail to improve the condition, there is then a choice of further treatments. Opinion on the best management for patients varies considerably. While many treatments for hemorrhoids may be performed without  anesthetics , the lasting effect of these conservative therapies has been questioned. Many patients treated with  rubber band ligation  or injection  sclerotherapy  require multiple treatments and there is high recurrence rate following these procedures."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7216", "text": "Conventional hemorrhoidectomy provides permanent symptomatic relief for most patients, and effectively treats any external component of the hemorrhoids. However, the wounds created by the surgery are usually associated with considerable post-operative pain which necessitates a prolonged recovery period.  This can put a stress on a  general practitioner \u2019s resources, may alienate the patient and delays the patient's return to a full, normal lifestyle and the workplace. Because of this, surgeons will generally reserve formal  excision  for the most severe cases of prolapse, or for patients who have failed to respond to conventional treatments. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7217", "text": "Obstructed defecation  syndrome (ODS) can be caused by structural deformities in the rectum resulting in chronic constipation. STARR can treat ODS using minimally invasive methods. STARR is a surgical procedure developed by Antonio Longo, an Italian surgeon, that is performed through the anus, requires no external incisions, and leaves no visible scars. Using a surgical stapler, the procedure removes the excess tissue in the rectum, reducing the anatomical defects that can cause ODS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7218", "text": "In a study of 90 patients undergoing the STARR procedure, patients were hospitalized one to three days, experienced minimal postoperative pain after the procedure, and resumed employment or normal activity in 6 to 15 days. In this study, most ODS patients experienced a significant improvement in their ODS symptoms following STARR.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7219", "text": "PPH uses a circular stapler to reduce the degree of prolapse. The procedure avoids the need for wounds in the sensitive perianal area thus reducing post-operative pain considerably, and facilitates a speedier return to normal activities. This procedure is for internal hemorrhoids only and not for external hemorrhoids or anal fissures.\n [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7220", "text": "This procedure was first described by an Italian surgeon \u2013 Dr.  Antonio Longo , Department of Surgery, University of Palermo \u2013 in 1993 and since then has been widely adopted through Europe. This procedure avoids the need for wounds in the sensitive perianal area and, as a result, has the advantage of significantly reducing the patient's post operative pain. [ 2 ] [ 3 ] [ 4 ]  Follow-up on relief of symptoms indicate a similar success rate to that achieved by conventional haemorrhoidectomy. [ 2 ] [ 5 ]  Since PPH was first introduced it has been the subject of numerous clinical trials and in 2003 the National Institute of Clinical Evidence (NICE) in the UK issued full guidance on the procedure stating it was  safe and efficacious ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7221", "text": "PPH is generally indicated for the more severe cases of internal hemorrhoidal prolapse (3rd and 4th degree) where surgery would normally be indicated. It may also be indicated for patients with minor degree haemorrhoids who have failed to respond to conservative treatments.  The procedure may be contra-indicated when only one cushion is prolapsed or in severe cases of fibrotic piles which cannot be physically repositioned."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7222", "text": "In addition to correcting the symptoms associated with the prolapse, problems with bleeding from the piles are also resolved by this excision.  Although the cushions may be totally or partially preserved, the blood supply is interrupted or venous drainage is improved by the repositioning.  Any external component which remains will usually regress over a period of 3\u20136 months.  Prominent skin tags may, on occasion, be removed during the operation but this may increase the postoperative pain so is not routinely performed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7223", "text": "PPH employs a unique circular stapler which reduces the degree of prolapse by excising a circumferential strip of mucosa from the proximal anal canal.  This has the effect of pulling the hemorrhoidal cushions back up into their normal anatomical position.\nUsually, the patient will be under general anesthetic, but only for 20\u201330 minutes.  Many cases have been successfully performed under local or regional anesthesia and the procedure is suited to day case treatment.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7224", "text": "Due to the low level of post-operative pain and reduced analgesic use, patients will usually be discharged either the same day or on the day following surgery. Most patients can resume normal activities after a few days when they should be fit for work.  The first bowel motion is usually on day two and should not cause any great discomfort.  Staples may be passed from time to time during defecation.  This is normal and should not be a cause for concern. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7225", "text": "Since 2002 more than 100 articles have been published reporting complications during and after stapled hemorrhoidectomy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7226", "text": "Bleeding is the most common postoperative complication. Severe postoperative pain could be caused by dehiscence of the anastomosis or due to the fact that the anastomosis is too near to the linea dentata. [ citation needed ]  A rare complication stemming from PPH is intra- abdominal  bleeding. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7227", "text": "Many long-term complications have been described. Most of them are related to either an incorrect indication for surgery or technical errors. Several authors stated that although it seems to be an easy operation to perform, it should only be done by experienced surgeons. Severe complications leading to death have been described but are rare. Irreversible urge incontinence due to lesions of the sphincter muscle or a diminished rectal capacity due to resection of too much mucosa, are quite common complications if the procedure is not performed properly. Rectovaginal fistulas and anastomotic diverticula are very rare but possible."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7228", "text": "Argon plasma coagulation  ( APC ) is a medical  endoscopic  procedure used to  control bleeding  from certain lesions in the  gastrointestinal tract . It is administered during gastrointestinal  endoscopy  such as   esophagogastroduodenoscopy  or  colonoscopy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7229", "text": "APC involves the use of a jet of  ionized   argon  gas ( plasma ) directed through a probe passed through the  endoscope . The probe is placed at some distance from the bleeding lesion, and argon gas is emitted, then ionized by a high-voltage discharge (approx 6 kV ). [ 1 ]  High-frequency  electric current  is then conducted through the jet of gas, resulting in coagulation of the bleeding lesion. As no physical contact is made with the lesion, the procedure is safe if the bowel has been cleaned of colonic gases, [ 2 ] [ 3 ]  and can be used to treat bleeding in parts of the gastrointestinal tract with thin walls, such as the  cecum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7230", "text": "Assisted feeding , also called  hand feeding  or  oral feeding , is the action of a person feeding another person who cannot otherwise feed themselves. The term is used in the context of some medical issue or in response to a  disability , such as when a person living with  dementia  is no longer able to manage eating alone.\nThe person being fed must be able to eat by mouth, but lacks either the cognitive or physical ability to self-feed. Individuals who are born with a disability like cerebral palsy, or arthrogryposis multiplex congenita (AMC) may be unable to feed themselves. Also, those who acquire a disability due to an accident or a disease like amyotrophic lateral sclerosis (ALS) may require hand feeding because they may become unable to pick-up and bring food to their own mouth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7231", "text": "A feeding tube is a medical device used to provide nutrition to patients who cannot obtain nutrition by mouth, are unable to swallow safely, or need nutritional supplementation. [ 1 ]  Patients who are able to use assisted feeding should have that in preference to tube feeding whenever possible. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7232", "text": "Oral assisted feedings are preferable to  percutaneous feeding  in individuals with advanced dementia. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7233", "text": "In the United States a study reviewed a set of patients and found that the expenses to arrange assisted feeding for patients was higher than the cost of using a feeding tube. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7234", "text": "Balloon tamponade  is the use of  balloons  inserted into the  esophagus ,  stomach  or  uterus , and inflated to alleviate or stop  refractory  bleeding."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7235", "text": "Balloon tamponade is considered a bridge to more definitive treatment modalities, and is usually administered in the emergency department or in the  intensive-care unit  setting, due to the illness of patients and the complications of the procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7236", "text": "In the uterus, balloon tamponade can alleviate or stop  postpartum hemorrhage  (PPH). Inflating a  Sengstaken\u2013Blakemore tube  in the uterus successfully treats atonic postpartum hemorrhage refractory to medical management in approximately 80% of cases. [ 2 ]  Such procedure is relatively simple, inexpensive and has low surgical morbidity. [ 2 ]  A  Bakri balloon [ 3 ]  is a balloon tamponade specifically constructed for uterine postpartum hemorrhage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7237", "text": "The Bakri balloon tamponade (BBT), designed for postpartum hemorrhage, is an effective life-saving balloon. [ 4 ]  A recent study involving 50 cases was carried out by the department of Obstetrics and Gynecology at University Central Hospital in Helsinki, Finland. With an overall success rate of 86%, the authors concluded that the Bakri balloon tamponade is \"a simple, readily available, effective and safe procedure\" in the management of postpartum hemorrhage. The research also indicates that BBT is able to provide practitioners with \"time for other interventions or transportation from local hospital to tertiary centre\". The authors of the study recommend BBT be included in the PPH protocol. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7238", "text": "An alternative to the Bakri is the BT-Cath (balloon-tamponade catheter) which has an easy-fill system allowing single person inflation and saving time in the theatre setting. The BT-Cath is more pear-shaped and contours to the uterus more easily than the Bakri."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7239", "text": "A low-cost alternative is a condom balloon tamponade, a form of intrauterine tamponade, created from a catheter, a male latex condom, and a string to tie the condom to the catheter. The method was developed in Bangladesh in 2001 by  Sayeba Akhter  and has since been supported by health workers worldwide as an effective method to stop postpartum hemorrhage, particularly in low-resource settings. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7240", "text": "Biliary endoscopic sphincterotomy  is a procedure where the  sphincter of Oddi  and the segment of the  common bile duct  where it enters the  duodenum  are cannulated and then cut with a sphincterotome, a device that includes a wire which cuts with an electric current ( electrocautery ). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7241", "text": "This procedure was developed in both Germany and Japan and was first published in each nation in 1974. [ 2 ] [ 3 ]  It has become a very common technique, useful for treatment of a wide variety of conditions of the biliary system such as the evacuation of gallstones within the bile duct ( choledocholithiasis ), biliary or papillary strictures,  sphincter of Oddi dysfunction , bile leaks, and others. In addition, it is commonly performed during an  endoscopic retrograde cholangiopancreatography  (ERCP), and it may be used for facilitating diagnostic procedures such as transpapillary bile duct biopsy, papillary tumor biopsy, and insertion of a cholangioscope. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7242", "text": "Extraction of choledocholithiasis and/or intrahepatic stones:  choledocholithiasis is the presence of  gallstones  within the common bile duct. They can be either primary (formed within the duct) or secondary (entering the duct from the  gallbladder ). Biliary endoscopic sphincterotomy allows for opening of the sphincter of Oddi, allowing stones to be removed. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7243", "text": "Treatment of benign biliary/papillary strictures:  diseases such as  primary sclerosing cholangitis  can lead to fibrosis and stricture of the ducts of the  biliary tree . These strictures can cause  cholestasis  which can lead to  jaundice ,  pruritus ,  cholangitis , and gallstone formation. Biliary endoscopic sphincterotomy is sometimes used, with or without  stenting , to relieve the obstruction, but systematic reviews have not demonstrated consistent benefits. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7244", "text": "Treatment of sphincter of Oddi dysfunction:  this is a diagnosis of exclusion which encompasses a broad spectrum of hepatobiliary disorders including spasms, strictures, or inappropriate relaxation. Sphincterotomy appears to be safe and effective for the treatment of sphincter of Oddi dysfunction. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7245", "text": "Treatment of bile leaks:  leakage of bile into the abdominal cavity is a complication of  laparoscopic cholecystectomy . The purpose of biliary endoscopic sphincterotomy in the treatment of a bile leak is to reduce or eliminate the pressure gradient between the bile duct and the duodenum, encouraging transpapillary bile flow and allowing the leak to heal. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7246", "text": "Others:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7247", "text": "Bleeding/coagulopathy:   platelet count  and  international normalized ratio  (INR) should be checked before the procedure. Discontinuation of antiplatelet therapy or  anticoagulation  requires consideration of the risks of  hemorrhage  vs.  thrombosis  and management should be based on current guidelines. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7248", "text": "Sphincterotomes:  a sphincterotome (also called a papillotome) is a  catheter  with a cutting wire at its far end. They have various configurations based on cutting wire length, outer diameter, number of lumens, and presence of other features such as the ability to rotate. The sphincterotome is connected to an electrosurgical generator, allowing the cutting wire to function as a knife when an electrical current is applied. Additional lumens allow the addition of a  guidewire  and injection of radio-opaque contrast. They can be broadly categorized as pull-type, push-type, or needle-knife. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7249", "text": "Pull-type:  pull-type sphincterotomes consist of a steel cutting wire within a  Teflon  catheter. The wire exits the catheter approximately 3\u00a0cm before its distal end and re-enters the catheter approximately 3\u00a0mm from its tip. When tension is applied to the wire, the distal portion of the catheter becomes curved so that the exposed wire is brought upwards into contact with the biliary sphincter and  papilla , away from the catheter. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7250", "text": "Push-type:  push-type sphincterotomes have a similar design to pull-type, but instead tightening the wire pushes it out to form a bow oriented downwards. This is useful for patients with  Billroth II  anatomy. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7251", "text": "Needle-knife:  a needle-knife sphincterotome has a retractable cutting wire of 3 to 5\u00a0mm with a Teflon sheath. They are most often used for a pre-cut sphincterotomy when standard methods of cannulation fail. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7252", "text": "Standard sphincterotomy:  the sphincterotome is inserted into the bile duct. A  cholangiogram  is then used to evaluate any biliary abnormalities requiring further intervention. The papilla is then incised with the cutting wire by applying electrocautery. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7253", "text": "Pre-cut sphincterotomy:  pre-cut biliary endoscopic sphincterotomy refers to the techniques used to cut the papillary mucosa and biliary sphincter in order to expose the underlying bile duct and gain access to it when standard cannulation fails. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7254", "text": "Transpancreatic biliary sphincterotomy (septotomy):  when the guidewire is unintentionally inserted into the  main pancreatic duct  the sphincterotome is then placed in the pancreatic duct and used to cut the  septum  between the pancreatic duct and bile duct. It is then withdrawn and re-directed through the incision site into the bile duct with the guidewire. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7255", "text": "Needle knife papillotomy:  a needle knife sphincterotome is placed en face to the biliary papilla. An incision is then made stepwise, starting at the upper margin of the papillary orifice and extending towards the biliary sphincter, creating an incision to allow the bile duct to be cannulated. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7256", "text": "Needle knife fistulotomy:  a needle knife  fistulotomy  has two different technique which are used. For the first technique an incision is made a few millimeters above the opening to the duct and then extended upwards. The other option is to make an incision in the roof of the papilla and then extend it either up or down without cutting the papillary orifice itself. [ 1 ]  The rate of  pancreatitis  after ERCP was significantly lower after fistulotomy, compared to other precut techniques. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7257", "text": "Periampullary diverticulum:  periampullary diverticulum makes the procedure more difficult because it becomes harder to assess the incision. [ 10 ]  Needle-knife fistulotomy or pancreatic stent placement followed by precut sphincterotomy are two of several techniques that have been used to account for the increased difficulty. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7258", "text": "Surgically altered anatomy (Billroth II):  if a patient has undergone a partial  gastrectomy  with Billroth II anastomosis, the papilla may appear to be upside down from the perspective of the endoscope compared to normal. Cannulation may need to be performed in a reverse position with the bile duct oriented downwards. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7259", "text": "The reported overall incidence of complications associated with ERCP and biliary endoscopic sphincterotomy has ranged from 3 to 12 percent. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7260", "text": "Pancreatitis: \u00a0 biliary endoscopic sphincterotomy is not an independent risk factor for pancreatitis after ERCP. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7261", "text": "Bleeding:  immediate bleeding occurs during or immediately after biliary endoscopic sphincterotomy. It is seen in up to 30% of patients and self-limiting most of the time. Delayed bleeding occurs from a few hours up to 2 wk after the procedure. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7262", "text": "Perforation:  the incidence of sphincterotomy related  perforation , also named Type 2 duodenal perforation, is between 0% and 1.8%. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7263", "text": "Cholangitis/sepsis:  the incidence of cholangitis after biliary endoscopic sphincterotomy is between 1% and 3%. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7264", "text": "Late complications:  long-term complication vs of biliary endoscopic sphincterotomy include recurrent common bile duct stone, cholecystitis, cholangitis,  hepatic abscess , papillary stenosis and biliary stricture. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7265", "text": "Balloon Dilation:  balloon dilation is an alternative often used in patients with a coagulation disorder or if their anatomy makes a traditional sphincterotomy more difficult. Balloon dilation is associated with fewer long term complications owing to preservations of sphincter function. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7266", "text": "Diagnostic peritoneal lavage  ( DPL ) or  diagnostic peritoneal aspiration  ( DPA ) is a surgical diagnostic procedure to determine if there is free floating fluid (most often blood) in the  abdominal cavity . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7267", "text": "This procedure is performed when intra-abdominal bleeding ( hemoperitoneum ), usually secondary to trauma, is suspected. [ 2 ]  In a hemodynamically  unstable patient with high-risk mechanism of injury, peritoneal lavage is a means of rapidly diagnosing intra-abdominal injury requiring laparotomy, but has largely been replaced in trauma care by the use of a  focused assessment with sonography for trauma  (FAST scan) due to its repeatability, non-invasiveness and non-interference with subsequent  computed tomography  (CT scan). Abdominal CT and  contrast duodenography  may complement lavage in stable patients, but in an unstable or uncooperative persons, these studies are too time-consuming or require ill-advised sedation.  Magnetic resonance imaging  is extremely accurate for the anatomic definition of structural injury, but logistics limit its practical application in acute abdominal trauma. [ 3 ] [ 4 ] \nThe procedure was first described in 1965 by Hauser Root. [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7268", "text": "After the application of  local anesthesia , a vertical skin incision is made one third of the distance from the  umbilicus  to the  pubic symphysis .  The  linea alba  is divided and the  peritoneum  entered after it has been picked up to prevent bowel perforation. A catheter is inserted towards the pelvis and aspiration of material attempted using a syringe. If no blood is aspirated, 1 litre of warm 0.9% saline is infused and after a few (usually 5) minutes this is drained and sent for analysis. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7269", "text": "If any of the following are found then the DPL is positive and operative exploration is warranted: [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7270", "text": "Duodenal-Jejunal Bypass Liner , or  Gastric Bypass Stent [ 1 ] , Common brand names include  EndoBarrier , is an  implantable   medical device  in the form of a thin flexible 60\u00a0cm-long tube that creates a physical barrier between ingested food and the  duodenum / proximal jejunum . The duodenal-jejunal bypass liner prevents the interaction of food with enzymes and hormones in the proximal intestine to treat  type 2 diabetes  and  obesity . The duodenal-jejunal bypass liner is delivered  endoscopically  and has been tested on the morbidly obese (those with a  body mass index  [BMI] greater than 40) as well as obese patients with a BMI less than 40, particularly those with difficult-to-manage type 2 diabetes. Despite a handful of serious adverse events such as gastrointestinal bleeding, abdominal pain, and device migration \u2014 all resolved with device removal \u2014 initial clinical trials have produced promising results in the treatment's ability to improve weight loss and  glucose homeostasis  outcomes. [ 2 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7271", "text": "The device is connected at one end to the beginning of the duodenum (first portion of the small intestine from the stomach) and at the other the mid-jejunum (the secondary stage of the small intestine). A  nitinol  anchor secures the bag at the duodenum, ensuring the liner doesn't migrate and that the  chyme  (the semifluid mass of partially digested food that exits the stomach) completely enters into the liner. This prevents the partially digested food from entering the first and initial part of the secondary stage of the small intestine, mimicking the effects of the  biliopancreatic portion  of  Roux en-Y gastric bypass  (RYGB) surgery. This reduces the amount of calories absorbed and causes bile and pancreatic fluids to be redistributed later in the mid-jejunum for reduced breakdown and absorption of the chyme. [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7272", "text": "Initial clinical research by Rubino  et al.  in 2006 produced two hypotheses for why duodenal-jejunal bypass is effective in improving glucose homeostasis. Their \"hindgut hypothesis\" claims that by expediting the delivery of chyme to the  distal intestine , the secretion of the gut hormone  GLP-1  and glucose-dependent insulin is more effectively promoted, improving glucose metabolism. The \"foregut hypothesis,\" on the other hand, states that by bypassing the duodenum and proximal jejunum (the initial parts of the small intestine), the inhibiting hormone  GIP  is secreted less, resulting in improved glucose tolerance. [ 5 ] [ 6 ]  As of 2015 [update] , those hypotheses continue to be tested, with Xiong  et al.  finding elements of both being involved. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7273", "text": "A specialized study of the product noted that the rate of adverse events could reach 84.4% of the 1,056 cases counted, with a moderate adverse event rate of 20.5% and a serious adverse event rate of 3.7%. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7274", "text": "Common adverse event, other than those related to surgery, were mainly implant rejections (e.g., abdominal pain, vomiting),  gastrointestinal bleeding , anchor displacement,  ulceration , and  perforation , as well as liner-related adverse events (e.g., obstruction, ectopia) and inflammatory conditions such as  pancreatitis ,  cholecystitis , and  cholangitis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7275", "text": "Severe adverse events includes perforation of the  esophagus ,  gastrointestinal hemorrhage , anchor tissue overgrowth, perforation of the duodenal bulb, hepatic abscess and acute pancreatitis, the majority (85%) of serious adverse events were directly or indirectly related to anchor."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7276", "text": "Endoscopic foreign body retrieval  refers to the removal of ingested objects from the  esophagus ,  stomach  and  duodenum  by  endoscopic  techniques.  It does not involve  surgery , but rather encompasses a variety of techniques employed through the  gastroscope  for grasping  foreign bodies , manipulating them, and removing them while protecting the esophagus and  trachea . [ 1 ]   It is of particular importance with children, [ 2 ]  people with  mental illness , [ 3 ]  and  prison  inmates [ 4 ]  as these groups have a high rate of foreign body ingestion."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7277", "text": "Commonly swallowed objects include  coins ,  buttons ,  batteries , and small bones (such as fish bones), [ 1 ]  but can include more complex objects, such as  eyeglasses , [ 5 ]   spoons , [ 6 ]  and  toothbrushes [ 5 ]  (see image)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7278", "text": "Some patients at risk for foreign body ingestion may not be able to give an accurate  medical history  of ingestion, either due to  age  or mental illness.  It is important that physicians treating these patients recognize the  symptoms  of esophageal foreign body impaction requiring urgent intervention. Most frequently, these include drooling and the inability to swallow  saliva , neck tenderness,  regurgitation  of food,  stridor  and  shortness of breath  if there is compression of the trachea. [ 1 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7279", "text": "There are several situations in which endoscopic techniques are not indicated, such as for small blunt objects less than 2.5\u00a0cm which have already passed into the stomach (as these usually do not obstruct anywhere else), when there is  perforation of the esophagus  or  mediastinitis  (inflammation of structures around the esophagus), and for  narcotic -containing bags or  condoms  that have been ingested, because of the risk of overdose if they are ruptured. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7280", "text": "Foreign bodies should be removed from the esophagus within 24 hours of ingestion because of a high risk of complication. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7281", "text": "Prior to undertaking endoscopy, attempts should be made to locate the foreign body with  x-rays  or other  non-invasive techniques . [ 1 ]   For radio-opaque objects, x-rays of the neck, chest and abdomen can be used to locate the foreign body and assist endoscopy. [ 9 ]   Alternative approaches, including the use of  metal detectors , have also been described. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7282", "text": "X-rays are also useful for identifying the type of foreign body ingested and complications of foreign body ingestion, including mediastinitis and perforation of the esophagus. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7283", "text": "Endoscopic  retrieval involves the use of a gastroscope or an optic fiber  charge-coupled device  camera. This instrument is shaped as a long tube, which is inserted through the  mouth  into the esophagus and stomach to identify the foreign body or bodies.  This procedure is typically performed under  conscious sedation .  Many techniques have been described to remove foreign bodies from the stomach and esophagus.  Usually the esophagus is protected with an overtube (a plastic tube of varying length), through which the gastroscope and retrieved objects are passed. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7284", "text": "Once the foreign body has been identified with the gastroscope, various devices can be passed through the gastroscope to grasp or manipulate the foreign body. Devices used include  forceps , which come in varying shapes, sizes and grips, [ 12 ]   snares , and oval loops that can be retracted from outside the gastroscope to  lasso  objects, [ 13 ]  as well as  Roth baskets  (mesh nets that can be closed to trap small objects), [ 14 ]  and   magnets  placed at the end of the scope or at the end of  orogastric tubes . [ 12 ] [ 15 ]  Some techniques have been described that use  foley catheters  to trap objects, or use two snares to orient foreign bodies. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7285", "text": "In  veterinary medicine  or when there is no endoscope available to extract  foreign bodies  economically without operation the  Hartmann alligator forceps  can be used. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7286", "text": "Endoscopic retrograde cholangiopancreatography  ( ERCP ) is a technique that combines the use of  endoscopy  and  fluoroscopy  to diagnose and treat certain problems of the  biliary  or  pancreatic ductal  systems. It is primarily performed by highly skilled and specialty trained gastroenterologists. Through the endoscope, the physician can see the inside of the  stomach  and  duodenum , and inject a  contrast medium  into the ducts in the biliary tree and/or  pancreas  so they can be seen on  radiographs ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7287", "text": "ERCP is used primarily to diagnose and treat conditions of the bile ducts and main pancreatic duct, [ 1 ]  including  gallstones , inflammatory strictures (scars), leaks (from trauma and surgery), and cancer.\nERCP can be performed for diagnostic and therapeutic reasons, although the development of safer and relatively non-invasive investigations such as  magnetic resonance cholangiopancreatography  (MRCP) and  endoscopic ultrasound  has meant that ERCP is now rarely performed without therapeutic intent. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7288", "text": "The following represent indications for ERCP, particularly if or when less invasive options are not adequate or definitive:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7289", "text": "ERCP may be indicated in the above diagnostic scenarios when any of the following are needed:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7290", "text": "Hypersensitivity to iodinated contrast medium or a history of iodinated contrast dye  anaphylaxis  is not a contraindication of ERCP, though it should be discussed with your health provider, and you should tell them you are allergic to iodine, as an alternative contrast iodine-free material (\"dye\") is then injected gently into the ducts (pancreatic or biliary) and x-rays are taken. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7291", "text": "The patient is sedated or anaesthetized. Then a flexible camera ( endoscope ) is inserted through the mouth, down the esophagus, into the stomach, through the  pylorus  into the  duodenum  where the  ampulla of Vater  (the union of the common bile duct and pancreatic duct) exists. The  sphincter of Oddi  is a muscular valve that controls the opening to the ampulla. The region can be directly visualized with the endoscopic camera while various procedures are performed. A plastic catheter or  cannula  is inserted through the ampulla, and radiocontrast is injected into the bile ducts and/or pancreatic duct.  Fluoroscopy  is used to look for blockages, or other lesions such as stones. [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7292", "text": "When needed, the sphincters of the ampulla and bile ducts can be enlarged by a cut (sphincterotomy) with an electrified wire called a sphincterotome for access into either so that gallstones may be removed or other therapy performed. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7293", "text": "Other procedures associated with ERCP include the trawling of the common bile duct with a basket or balloon to remove gallstones and the insertion of a plastic  stent  to assist the drainage of bile. [ 11 ]  Also, the pancreatic duct can be cannulated and stents be inserted."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7294", "text": "The pancreatic duct requires visualisation in cases of pancreatitis. Ultrasound is frequently the first investigation performed on admission; although it has little value in the diagnosis of pancreatitis or its complications. contrast-enhanced computed tomography (MD-CECT) is the most used imaging technique. However, magnetic resonance imaging (MRI) offers diagnostic capabilities similar to those of CT, with additional intrinsic advantages including lack of ionizing radiation and exquisite soft tissue characterization. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7295", "text": "In specific cases, other specialized or ancillary endoscopes may be used for ERCP. These include mother-baby and SpyGlass cholangioscopes (to help in diagnosis by directly visualizing the duct as opposed to only obtaining X-ray images [ 13 ] [ 14 ] [ 15 ] ) as well as balloon enteroscopes (e.g. in patients that have previously undergone  digestive system surgery  with post- Whipple  or  Roux-en-Y  surgical anatomy). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7296", "text": "One of the most frequent and feared complications after endoscopic retrograde cholangiopancreatography (ERCP) is post-ERCP pancreatitis (PEP). In previous studies, the incidence of PEP has been estimated at 3.5 to 5%. [ 17 ] [ 18 ]  According to Cotton et al., PEP is defined as a \"clinical pancreatitis with amylase at least three times the upper limit of normal at more than 24 hours after the procedure requiring hospital admission or prolongation of planned admission\". Grading of severity of PEP is mainly based on the length of hospital stay. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7297", "text": "Risk factors for developing PEP include technical matters related to the ERCP procedure and patient-specific ones. The technical factors include manipulation of and injection of contrast into the pancreatic duct, cannulation attempts lasting more than five minutes, and biliary balloon sphincter dilation; among patient-related factors are female gender, younger age, and Sphincter of Oddi dysfunction. [ citation needed ]  A systematic review of clinical trials concluded that a previous history of PEP or pancreatitis significantly increases the risk for PEP to 17.8% and to 5.5% respectively. [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7298", "text": "Intestinal perforation  is a risk of any gastroenterologic endoscopic procedure, and is an additional risk if a  sphincterotomy  is performed. As the second part of the duodenum is anatomically in a  retroperitoneal  location (that is, behind the peritoneal structures of the abdomen), perforations due to sphincterotomies are retroperitoneal. Sphincterotomy is also associated with a risk of bleeding. [ 22 ]  ERCP may provoke hemobilia from trauma to friable hilar tumors or a guide-wire penetrating the bile duct wall, creating a  biliary fistula . Delayed bleeding is a rare but potentially serious complication of sphincterotomy, particularly as many patients are discharged home within hours of ERCP."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7299", "text": "There is also a risk associated with the  contrast dye  in patients who are allergic to compounds containing  iodine , which can be very severe, even if the anaphylactoid reactions occur while you are in a hospital. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7300", "text": "Oversedation can result in dangerously low blood pressure, respiratory depression, nausea, and vomiting. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7301", "text": "Other complications (less than 1%) may include heart and lung problems, infection in the bile duct called  cholangitis , that can be life-threatening, and is regarded as a medical emergency. Using antibiotics before the procedure shows some benefits to prevent cholangitis and septicaemia. [ 25 ]  In rare cases, ERCP can cause fatal complications. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7302", "text": "Cases of hospital-acquired (i.e., nosocomial) infections with  carbapenem resistant enterobacteriaceae  linked to incompletely disinfected duodenoscopes have occurred in the U.S. since at least 2009 per the  Food and Drug Administration . [ 27 ]  Outbreaks were reported from  Virginia Mason Hospital  in Seattle in 2013,  UCLA Health System  Los Angeles in 2015, Chicago and Pittsburgh. [ 28 ]  The FDA issued a safety communication \"Design of ERCP Duodenoscopes May Impede Effective Cleaning\" in February 2015, [ 29 ]  which was updated in December 2015, [ 30 ]  and more recently in 2022 which recommended disposable components. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7303", "text": "Prevalence of vitamin K and vitamin D deficiency, [ 32 ]  as bile is to assist in the breakdown and absorption of fat in the intestinal tract; a relative deficiency of bile can lead to fat malabsorption and deficiencies of fat-soluble vitamins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7304", "text": "In  medicine ,  endoscopic sleeve gastroplasty  (ESG) is a minimally-invasive, non-surgical (incisionless), endoscopic weight loss procedure that is part of the  field of endoscopic bariatric therapies. To perform ESG, a physician sutures a patient\u2019s  stomach  into a narrower, smaller tube-like configuration. [ 1 ]  The result is a more restricted stomach that forces patients to feel fuller sooner, eating fewer calories, which facilitates  weight loss  . [ 2 ] [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7305", "text": "Early iterations of endoscopic gastric remodeling for weight loss included the endoluminal vertical gastroplasty, which attempted to mimic the restricted stomach configuration of the vertical sleeve gastrectomy. [ 5 ]  Around the same time, similar endoscopic remodeling along the stomach\u2019s larger curvature was performed through tissue acquisition with a suction-based device, though this was limited by suture loss. [ 6 ] [ 7 ]  In 2012, Dr. Christopher Thompson, a Harvard Medical School professor and later Co-founder of Bariendo, performed the first ESG case in humans. [ 8 ]  This was modified and tissue was acquired with a full-thickness suturing device, which has been the basis of the present ESG procedure. [ 9 ]   In July 2022, the creation of the ESG using the Apollo Overstitch device was authorized by the  United States Food and Drug Administration  for the treatment of  obesity  in patients with a  body mass index  between 30\u201350\u00a0kg/m 2 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7306", "text": "The ESG may be performed with slight variations by different physicians. It most commonly is performed using the Apollo ESG Device (formally Overstitch device). This device fits over a therapeutic double-channel  endoscope  to create a sutured row of stomach tissue. The tissue helix is advanced from the endoscope, put up against stomach tissue, and turned 2-4 rotations to access the gastric muscle layer. The helix is then retracted towards the scope, bringing the full-thickness acquired stomach tissue with it. Using the handle-operated needle driver, a needle attached to the suture wire is passed through the full-thickness tissue to the anchor exchange. This creates a full-thickness plication of stomach tissue. The needle is then passed back from the anchor exchange to the needle driver, and the process is repeated, threading the suture wire through each bite of stomach tissue. When enough full-thickness bites have been taken for a suture row, a cinch is passed through the scope over the suture. Typically, sutures are placed starting at the border of the  antrum  and  gastric body  at the  incisura , then placed proximally up to the border of the  gastric body  and  fundus . Each row of sutures can be a straight line or one of the variety of suture patterns reported in the literature, such as the \u201cM,\u201d \u201cZ,\u201d and \u201cU\u201d pattern as well as other novel patterns; nonetheless, to date, no suture pattern has been proven to be superior for weight loss. [ 10 ] [ 11 ] [ 12 ] [ 13 ]  Regardless of suture pattern, creation of the ESG focuses on tissue imbrication along the greater curvature of the stomach. The  fundus  is typically avoided due to the relatively thinner wall compared to the  gastric body  to avoid complications from the procedure. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7307", "text": "Accredited advanced  fellowship  training programs in ESG and other endoscopic bariatric therapies are currently rare, and competency in ESG is typically achieved through proctoring by experts after completion of an accredited gastroenterology or surgical training program. Studies have reported that efficiency with performance of ESG and improved weight loss outcomes occur after approximately 35-38 cases. [ 15 ] [ 16 ] [ 17 ]  Mastery was reported in one study to occur after 55 cases. [ 15 ]  While early performance of the ESG has traditionally been carried out in university-affiliated/academic centers, ESG has been shown to be feasible and safe when performed in the community setting. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7308", "text": "The primary measures of weight loss outcomes for endoscopic bariatric therapies include total body weight loss (percentage of pre-procedure weight lost by a certain time point) and excess weight loss (percentage of pre-procedure weight above ideal body weight that is lost by a certain time point). The Preservation and Incorporation of Valuable Endoscopic Innovation thresholds is an expert panel with gastroenterologists and surgeons from the  American Society for Gastrointestinal Endoscopy  and  The American Society for Metabolic and Bariatric Surgery , and in 2015, this panel recommended that any new endoscopic therapy for weight loss should have an excess weight loss exceeding 25% and a serious adverse event rate less than 5%. [ 19 ]  Total body weight loss thresholds were not defined but are generally considered meaningful in novel endoscopic bariatric therapies if exceeding 5%. [ 20 ] [ 21 ]  Multiple studies of ESG have shown that this therapy satisfies these criteria, as outlined below."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7309", "text": "The recently published MERIT study is the first and only  randomized controlled trial  of the ESG for treatment of obesity and included 209 adult subjects with class I and II obesity ( BMI  30\u201340\u00a0kg/m 2 ). [ 22 ]  It was conducted from Dec. 2017 to Jun. 2019, spanned nine centers in the United States, and comprised 85 adults in the ESG arm and 124 adults in the control arm (lifestyle modification only). Subjects in the ESG arm lost 13.6% of body weight and 49.2% of excess body weight at one year, compared to 0.8% total body weight loss and 3.2% excess weight loss in the control arm at the same time point."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7310", "text": "Prior to the MERIT study, numerous meta-analyses of studies on ESG report a total body weight loss of approximately 16% at one year. [ 23 ] [ 24 ] [ 25 ] [ 26 ] [ 27 ]  Excess weight loss was observed to be approximately 60% at one year. [ 23 ] [ 25 ] [ 27 ] [ 28 ]  Weight loss reported from high volume community practices that have both expertise in ESG and robust longitudinal aftercare programs with  dietitians  have shown even greater outcomes, with total body weight loss approaching 30% and excess weight loss of 66% at one year. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7311", "text": "Patient selection is an important consideration for any weight loss therapy. The present published literature shows either no influence or conflicting results for patient age, sex, starting weight/ BMI  on weight loss from ESG. Long-term after care programs have demonstrated benefit for sustained weight loss after ESG, with one study showing that patients who continued after care visits following ESG had 20.5% total body weight loss compared to 16.9% total body weight loss in those who dropped out of long-term follow up programs. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7312", "text": "There are over 200  obesity-related comorbidities , and it has been reported that achieving a total body weight loss of 10% has a significant impact of such conditions. [ 30 ]  Thus, the weight loss outcomes with ESG are unsurprisingly accompanied by an improvement in several  obesity-related comorbidities . Weight loss facilitated by ESG has been observed to bring about benefits in or even cure of  diabetes /insulin sensitivity, [ 31 ] [ 32 ] [ 33 ]   dyslipidemia , [ 31 ] [ 32 ]   blood pressure , [ 31 ]  and  fatty liver disease , [ 31 ] [ 33 ] [ 34 ]  as well as quality of life. [ 35 ] [ 36 ]  The MERIT study showed 80% of patients who underwent ESG had improvement in one or more comorbidities at one year. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7313", "text": "Mid-term durability from ESG appears promising. A total body weight loss of 17% and excess weight loss of between approximately 60-67% was observed to be sustained at 18\u201324 months. [ 23 ] [ 26 ] [ 28 ]  This was later confirmed in the multicenter, randomized controlled MERIT study, which observed that 68% of subjects who underwent an ESG maintained 25% or more of their excess weight loss at two years. [ 22 ]  \u00a0As a novel therapy, ESG presently lacks studies assessing long-term durability, though more data on this component of ESG are anticipated as more ESGs are performed over time. One recent study observed at 5 years from ESG that at least 10% total body weight loss was maintained in 90% of patients and at least 15% total body weight loss was maintained in 61% of patients. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7314", "text": "Mild to moderate gastrointestinal side effects (such as nausea, cramping, bloating, and abdominal discomfort) are common after ESG (reported in over 70% of patients), but these are predictable, temporary, and can be managed with medications. [ 25 ]  Most will resolve within one week after ESG. Due to the minimally invasive nature of ESG, serious complications are rare. These include pain or nausea requiring hospitalization (1.08%);  upper gastrointestinal tract bleeding  (0.56%);  peri-gastric leak or infected fluid collection  (0.48%);  pulmonary embolism  (0.06%);  perforation  (0.06%). [ 23 ]  Similar rates of serious adverse events were reported in the multicenter, randomized controlled MERIT study. [ 22 ]  No deaths have been observed in the published ESG literature."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7315", "text": "Mechanisms of weight loss from ESG remains an area of active study. There are at least two mechanisms of  peripheral appetite signaling  thought to be mediated by ESG: first, increased sense of fullness during a meal leading to meal termination, potentially a result of the intact gastric fundus that serves as a food reservoir and the restriction to gastric expansion (accommodation) during a meal; [ 2 ] [ 4 ]  and second, from delayed emptying of the stomach, which promotes a prolonged sensation of fullness after a meal. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7316", "text": "Unlike the surgical  sleeve gastrectomy , the ESG does not appear to affect central appetite signaling through the hunger hormone,  ghrelin . [ 29 ]  This is thought to be because the surgical sleeve removes the fundus, the primary site of ghrelin production, and the relatively thinner-walled fundus is avoided in the ESG for safety concerns. Furthermore, in cases where the fundus was sutured in ESG, this did not benefit weight loss outcomes. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7317", "text": "ESG can safely be combined with  weight loss medications  to improve weight loss or prevent weight regain after the procedure. The daily injectable medication  liraglutide  showed greater total body weight loss when combined with ESG compared to ESG alone at 7 months (approximately 25% vs 20% respectively). [ 14 ]  Similar results are anticipated with other  incretin  agents, such as  semaglutide  and  tirzepatide , though no studies have directly assessed these combinations."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7318", "text": "Weight regain after surgical sleeve gastrectomy has historically been managed with medications or a more invasive revisional surgery. [ 37 ] [ 38 ] [ 39 ] [ 40 ]  Recent data suggested that an ESG can safely be performed after the  surgical sleeve gastrectomy  (sometimes referred to as a \u201crevisional ESG\u201d), with total body weight loss of approximately 16-18% at 12 months. [ 41 ] [ 42 ]  While weight loss is not thought to be as robust as the initial weight loss surgery, the revisional ESG has an improved safety profile compared to a surgical revision and is therefore hypothesized to have greater patient acceptance. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7319", "text": "Laparoscopic  sleeve gastrectomy  (LSG) is one of the most common bariatric surgeries performed worldwide and shares a similar restricted stomach configuration with the ESG. However, it appears to operate with different weight loss mechanisms from the ESG, as it has been shown to reduce the hunger hormone  ghrelin , [ 29 ] [ 43 ]  as well as accelerate, rather than delay, stomach emptying. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7320", "text": "Large, prospective studies directly comparing LSG to ESG are lacking. Comparison of the two therapies has relied on retrospective analysis and findings are conflicting. In a recent propensity score-matched study, the difference in weight loss for LSG vs ESG was 9.7% at 1 year, 6.0% at 2 years, and 4.8% at 3 years in favor of LSG, though the authors described the ESG as  non-inferior  based on an  a priori  definition of non-inferiority as being within 10% total body weight loss of the surgical arm. [ 44 ]  Advantages of the ESG over LSG include lack of incisions, shorter length of stay (same-day-discharge vs 3 days in hospital); [ 29 ]  less  gastroesophageal reflux  (0-2% vs 15-31%); [ 36 ] [ 45 ]  and lower morbidity and overall adverse event rate (1.9% vs 14.5%), [ 45 ] [ 46 ]  though some studies have presented similar rates of adverse events between ESG and LSG. [ 47 ] [ 48 ]  Despite less weight loss, one study found that patients who had undergone ESG had the same degree of comorbidity resolution and had higher quality of life scores at 6 months compared to those who had undergone LSG. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7321", "text": "EndoStim Electrical Stimulation Therapy  is a form of anti-reflux  surgery , intended to assist in correcting a problem with the muscles at the bottom of the  esophagus  (the tube from the mouth to the stomach). Problems with these muscles allow  gastroesophageal reflux disease  (GERD) to happen. [ 1 ]  The procedure was developed by Endostim, based in  St. Louis ,  Missouri , and  Amsterdam ,  Netherlands . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7322", "text": "EndoStim therapy directly targets the weak  lower esophageal sphincter  (LES) muscle, without altering anatomy or using mechanical constraints. EndoStim's proprietary technology uses  functional electrical stimulation  (a type of  neuromodulation ) to restore esophageal function, thereby reducing GERD symptoms. Tiny pulses of electric current are delivered to the LES without causing any sensation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7323", "text": "The implantable pulse generator (IPG) and bipolar lead deliver therapy to the lower esophageal sphincter. The IPG is a small device similar to a  pacemaker  and is implanted under the skin of the  abdomen . The lead connects two electrodes from the IPG to the esophagus. Both the IPG and lead are placed  laparoscopically  through a short,  minimally-invasive procedure  under  general anesthesia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7324", "text": "The  implantation  procedure lasts approximately 40 minutes, and involves attaching two small electrodes from the lead to the lower esophagus. The lead is brought out into a small pocket located under the abdominal skin and connected to the stimulation device (IPG). Minimally-invasive procedures have been shown to dramatically reduce healing time as well as reduce procedure risk. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7325", "text": "The first  clinical study  using EndoStim technology was published in 2010, showing that in patients with GERD, electrical stimulation therapy significantly and consistently increased LES pressure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7326", "text": "An  open-label trial  conducted in Chile showed the procedure showed \u201csignificant and sustained improvement in GERD symptoms, esophageal pH, and reduction in  proton-pump inhibitor  (PPI) usage without any side effects\u201d in patients. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7327", "text": "Endostim therapy is currently not approved by the U.S.  Food and Drug Administration  (FDA)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7328", "text": "The procedure, however, received the  CE mark  allowing implants in Europe. [ 5 ] \nEndostim is carried out in Argentina, [ 6 ]  Chile, Colombia, Brazil, [ 7 ]  Hong Kong, India, [ 8 ]  Denmark, Germany, [ 9 ]  Netherlands and Switzerland."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7329", "text": "Esophageal dilation  or  oesophageal dilatation  (British English) is a therapeutic  endoscopic  procedure that enlarges the  lumen  of the  esophagus . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7330", "text": "It can be used to treat a number of medical conditions that result in narrowing of the esophageal lumen, or decrease motility in the distal esophagus.  These include the following:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7331", "text": "There are three major classes of dilators: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7332", "text": "Complications of esophageal dilatation include the following: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7333", "text": "A  gastrostomy  is the creation of an artificial external opening into the stomach for nutritional support or gastric decompression.\nTypically this would include an incision in the patient's  epigastrium  as part of a formal operation. When originally devised over a century ago the procedure was completed through open surgery using the Stamm technique. [ 1 ]  It can be performed through surgical approach,  percutaneous  approach by  interventional radiology ,  percutaneous endoscopic gastrostomy  (PEG) or  percutaneous ultrasound gastrostomy  (PUG). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7334", "text": "A gastrostomy may be required due to illness, trauma or disability impacting upon the ability to eat or swallow safely, or conditions causing increased nutritional requirement  [ 3 ]  and once formed (or for some techniques, during formation), a  gastrostomy tube  is inserted."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7335", "text": "The  Stamm gastrostomy  is an open technique, [ 4 ]  requiring an upper midline  laparotomy  and gastrotomy, with the catheter brought out in the left  hypochondrium . It was first devised in 1894 by the American Gastric Surgeon, Martin Stamm (1847\u20131918), who was educated greatly in surgery when he visited Germany. [ 5 ] [ circular reference ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7336", "text": "Over the last three decades less invasive approaches such as percutaneous endoscopic gastrostomy (PEG) and laparoscopic assisted Stamm gastrostomy [ 6 ]  have become increasingly popular. [ 7 ] [ 8 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7337", "text": "Conventional PEG involves inserting the primary feeding device through the mouth and extracting it through a small incision formed through the abdomen. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7338", "text": "Apparent benefits of PEG include shorter operative times and reduced financial cost. [ 11 ] [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7339", "text": "Severe complications for gastrostomy formation classify as Clavien-Dindo grade 3 and above, requiring surgical or radiological interventions with potential morbidity and mortality. [ 14 ] [ 15 ]  These complications may occur due to damage to surrounding structures intra-operatively, issues affecting the immature gastrostomy early post-operatively, or be secondary to device or site complications, including: adjacent bowel injury, gastrocolic fistulae, migration of gastrostomy to ribs, and failure for spontaneous closure when gastrostomy no longer needed (persistent gastrocutaneous fistula). [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7340", "text": "Impedance\u2013pH monitoring  is a technique used in the diagnosis of  gastroesophageal reflux disease  (GERD), by monitoring both  impedance  and  pH . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7341", "text": "Patients with ongoing symptoms while on  proton-pump inhibitor (PPI) therapy  are commonly diagnosed with impedance\u2013pH monitoring while continuing their medications. The impedance\u2013pH monitoring diagnostic test determines the frequency of reflux episodes and the time relationship of reflux episodes and symptoms. The impedance\u2013pH monitoring test determines if the patient's symptoms are related to  acid reflux , related to  nonacid reflux , or not related to reflux of any type. A positive GERD diagnosis is made if acid or nonacid reflux precedes symptoms in a statistically meaningful manner. Patients with a positive impedance\u2013pH monitoring test may benefit from acid-reduction therapy such as  fundoplication surgery  or  endoscopic  fundoplication techniques. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7342", "text": "Intraperitoneal injection  or  IP injection  is the injection of a substance into the  peritoneum  (body cavity). It is more often applied to non-human animals than to humans. In general, it is preferred when large amounts of blood replacement fluids are needed or when low blood pressure or other problems prevent the use of a suitable blood vessel for  intravenous injection . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7343", "text": "In humans, the method is widely used to administer  chemotherapy  drugs to treat some  cancers , particularly  ovarian cancer . Although controversial, intraperitoneal use in ovarian cancer has been recommended as a  standard of care . [ 1 ]  Fluids are injected intraperitoneally in infants, also used for  peritoneal dialysis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7344", "text": "Intraperitoneal injections are a way to administer therapeutics and drugs through a peritoneal route (body cavity). They are one of the few ways drugs can be administered through injection, and have uses in research involving animals, drug administration to treat ovarian cancers, and much more. Understanding when intraperitoneal injections can be utilized and in what applications is beneficial to advance current drug delivery methods and provide avenues for further research. The benefit of administering drugs intraperitoneally is the ability for the peritoneal cavity to absorb large amounts of a drug quickly. A disadvantage of using intraperitoneal injections is that they can have a large variability in effectiveness and misinjection. [ 2 ]  Intraperitoneal injections can be similar to oral administration in that hepatic metabolism could occur in both."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7345", "text": "There are few accounts of the use of intraperitoneal injections prior to 1970. One of the earliest recorded uses of IP injections involved the insemination of a guinea-pig in 1957. [ 3 ]  The study however did not find an increase in conception rate when compared to mating. In that same year, a study injected egg whites intraperitoneally into rats to study changes in \"droplet\" fractions in kidney cells. The study showed that the number of small droplets decreased after administration of the egg whites, indicating that they have been changed to large droplets. [ 4 ]  In 1964, a study delivered chemical agents such as acetic acid, bradykinin, and kaolin to mice intraperitoneally in order to study a \"squirming\" response. [ 5 ]  In 1967, the production of amnesia was studied through an injection of physostigmine. [ 6 ]  In 1968, melatonin was delivered to rats intraperitoneally in order to study how brain  serotonin  would be affected in the midbrain. [ 7 ]  In 1969, errors depending on a variety of techniques of administering IP injections were analyzed, and a 12% error in placement was found when using a one-man procedure versus a 1.2% error when using a two-man procedure. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7346", "text": "A good example of how intraperitoneal injections work is depicted through \"The distribution of salicylate in mouse tissues after intraperitoneal injection\" because it includes information on how a drug can travel to the blood, liver, brain, kidney, heart, spleen, diaphragm, and skeletal muscle once it has been injected intraperitoneally. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7347", "text": "These early uses of Intraperitoneal injections provide good examples of how the delivery method can be used, and provides a base for future studies on how to properly inject mice for research."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7348", "text": "Currently, there are a handful of drugs that are delivered through intraperitoneal injection for chemotherapy. They are mitomycin C, cisplatin, carboplatin, oxaliplatin, irinotecan, 5-fluorouracil, gemcitabine, paclitaxel, docetaxel, doxorubicin, premetrexed, and melphalan. [ 10 ]  There needs to be more research done to determine appropriate dosing and combinations of these drugs to advance intraperitoneal drug delivery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7349", "text": "There are few examples of the use of intraperitoneal injections in humans cited in literature because it is mainly used to study the effects of drugs in mice. The few examples that do exist pertain to the treatment of pancreatic/ovarian cancers and injections of other drugs in clinical trials. One study utilized IP injections to study pain in the abdomen after a hysterectomy when administering anesthetic continuously vs patient-controlled. [ 11 ]  The results depicted that ketobemidone consumption was significantly lower when patients controlled anesthetic through IP. This led to the patients being able to be discharged earlier than when anesthesia was administered continuously. These findings could be advanced by studying how the route of injection affects the organs in the peritoneal cavity."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7350", "text": "In another Phase I clinical trial, patients with ovarian cancer were injected intraperitoneally with dl1520 in order to study the effects of a replication-competent/-selective virus. [ 12 ]  The effects of this study were the onset of flu-like symptoms, emesis, and abdominal pain. The study overall defines appropriate doses and toxicity levels of dl1520 when injected intraperitoneally."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7351", "text": "One study attempted to diagnose  hepatic hydrothorax  with the use of injecting Sonazoid intraperitoneally. Sonazoid was utilized to aid with contrast-enhanced ultrasonography by enhancing the peritoneal and pleural cavities. [ 13 ]  This study demonstrates how intraperitoneal injections can be used to help diagnose diseases by providing direct access to the peritoneal cavity and affecting the organs in the cavity."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7352", "text": "In a case of a ruptured hepatocellular carcinoma, it was reported that the patient was treated successfully through the use of an intraperitoneal injection of OK-432, which is an immunomodulatory agent. [ 14 ]  The patient was a 51-year-old male who was hospitalized. The delivery of OK-432 occurred a total of four times in a span of one week. The results of this IP injection were the disappearance of the ascites associated with the rupture. This case is a good example of how IP injections can be used to deliver a drug that can help to treat or cure a medical diagnosis over the use of other routes of delivery. The results set a precedent of how other drugs may be delivered in this way to treat other similar medical issues after further research."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7353", "text": "In 2018, a patient with stage IV ovarian cancer and peritoneal metastases was injected intraperitoneally with 12g of mixed cannabinoid before later being hospitalized. [ 15 ]  The symptoms of this included impairment of cognitive and psychomotor abilities. Because of the injection of cannabis, the patient was predicted to have some level of THC in the blood from absorption. This case presents the question of how THC is absorbed in the peritoneal cavity. It also shows how easily substances are absorbed through the peritoneal cavity after an IP injection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7354", "text": "Overall, this section provides a few examples of the effects and uses of intraperitoneal injections in human patients. There are a variety of uses and possibilities for many more in the future with further research and approval."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7355", "text": "Intraperitoneal injections are the preferred method of administration in many experimental studies due to the quick onset of effects post injection. This allows researchers to observe the effects of a drug in a shorter period of time, and allows them to study the effects of drugs on multiple organs that are in the peritoneal cavity at once. In order to effectively administer drugs through IP injections, the stomach of the animal is exposed, and the injection is given in the lower abdomen. The most efficient method to inject small animals is a two-person method where one holds the rodent and the other person injects the rodent at about 10 to 20 degrees in mice and 20 to 45 degrees in rats. The holder retains the arms of the animal and tilts the head lower than the abdomen to create optimal space in the peritoneal cavity. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7356", "text": "There has been some debate on whether intraperitoneal injections are the best route of administration for experimental animal studies. It was concluded in a review article that utilizing IP injections to administer drugs to laboratory rodents in experimental studies is acceptable when being applied to proof-of-concept studies. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7357", "text": "A study was conducted to determine the best route of administration to transplant mesenchymal stem cells for colitis. This study compared intraperitoneal injections, intravenous injections, and anal injections. It was concluded that the intraperitoneal injection had the highest survival rate of 87.5%. [ 17 ]  This study shows how intraperitoneal injections can be more effective and beneficial than other traditional routes of administration."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7358", "text": "One article reviews the injection of sodium pentobarbital to euthanize rodents intraperitoneally. [ 2 ]  Killing the rodent through an intraperitoneal route was originally recommended over other routes such as inhalants because it was thought to be more efficient and ethical. The article overviews whether IP is the best option for euthanization based on evidence associated with welfare implications. It was concluded that there is evidence that IP may not be the best method of euthenasia due to possibilities of missinjection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7359", "text": "Another example of how intraperitoneal injections are used in studies involving rodents is the use of IP for micro-CT contrast enhanced detection of liver tumors. [ 18 ]   Contrast agents  were administered intraperitoneally instead of intravenously to avoid errors and challenges. It was determined that IP injections are a good option for Fenestra to quantify liver tumors in mice."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7360", "text": "An example of how intraperitoneal injections can be optimized is depicted in a study where IP injections are used to deliver anesthesia to mice. This study goes over the dosages, adverse effects, and more of using intraperitoneal injections of anesthesia. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7361", "text": "An example of when intraperitoneal injections are not ideal is given in a study where the best route of administration was determined for cancer biotherapy. [ 20 ]  It was concluded that IP administration should not be used over intravenous therapy due to high radiation absorption in the intestines. This shows an important limitation to the use of IP therapy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7362", "text": "The provided examples show a variety of uses for intraperitoneal injections in animals for in vitro studies. Some of the examples depict situations where IP injections are not ideal, while others prove the advantageous uses if this delivery method. Overall, many studies utilize IP injections to deliver therapeutics to lab animals due to the efficiency of the administration route."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7363", "text": "Lithotripsy  is a procedure involving the physical destruction of hardened masses like  kidney stones , [ 1 ]   bezoars [ 2 ]  or  gallstones , which may be done  non-invasively . The term is derived from the  Greek  words meaning \"breaking (or pulverizing) stones\" ( litho-  +  \u03c4\u03c1\u03af\u03c8\u03c9  [tripso])."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7364", "text": "Lithotripsy is a  non-invasive procedure  used to break up hardened masses like  kidney stones , [ 1 ]   bezoars [ 2 ]  or  gallstones ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7365", "text": "Commonly cited absolute contraindications to shock wave lithotripsy (SWL) include pregnancy,  coagulopathy  or use of  platelet aggregation inhibitors ,  aortic aneurysms , severe untreated  hypertension , and untreated urinary tract infections. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7366", "text": "Surgery was the only method to remove stones too large to pass until  French   surgeon  and  urologist   Jean Civiale  in 1832 invented a  surgical instrument  (the  lithotrite ) to crush stones inside the  urinary bladder  without having to open the  abdomen . To remove a calculus, Civiale inserted his instrument through the  urethra  and bored holes in the stone. Afterwards, he crushed it with the same instrument and aspirated the resulting fragments or let them flow normally with  urine . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7367", "text": "Lithotripsy replaced using lithotrites as the most common treatment beginning in the mid 1980s.  In extracorporeal shock wave lithotripsy (ESWL), external shockwaves are focused at the stone to pulverize it. [ 6 ]   Ureteroscopic  methods use a rigid or flexible scope to reach the stone and direct mechanical or light energy at it. Endoscopy can use lasers as well as other modes of energy delivery: ultrasound or electrohydraulics. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7368", "text": "ESWL was first used on kidney stones in 1980. It is also applied to gallstones and pancreatic stones. External shockwaves are focused and pulverize the stone which is located by imaging. The first shockwave lithotriptor approved for human use was the Dornier HM3 (human model 3) derived from a device used for testing aerospace parts. Second generation devices used  piezoelectricity  or  electromagnetism  generators. American Urological Association guidelines consider ESWL a potential primary treatment for stones between 4 mm and 2 cm. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7369", "text": "Electrohydraulic lithotripsy is an industrial technique for fragmenting rocks by using electrodes to create shockwaves. It was applied to bile duct stones in 1975. It can damage tissue and is mostly used in biliary tract specialty centers. Pneumatic mechanical devices have been used with endoscopes, commonly for large and hard stones. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7370", "text": "Laser lithotripsy  was introduced in the 1980s.  Pulsed dye lasers  emit 504 nm ( cyan -colored) light that is delivered to the stone by optical fibers through a scope.  Holmium:YAG  lasers were developed more recently and produce smaller fragments."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7371", "text": "Endovascular lithotripsy is an  angioplasty  procedure using a balloon internally fitted with an ultrasound generator. [ 8 ]  It can be used in the reduction of very calcified  coronary arteries , with or without the combined usage of  stents . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7372", "text": "A  liver support system  or  diachysis  is a type of  therapeutic device  to assist in performing the functions of the liver. Such systems focus either on removing the accumulating toxins ( liver dialysis ), or providing additional replacement of the  metabolic  functions of the liver through the inclusion of hepatocytes to the device ( bioartificial liver device ). A diachysis machine is used for acute care i.e. emergency care, as opposed to a  dialysis machine  which are typically used over the longer term. These systems are being trialed to help people with  acute liver failure  (ALF) or acute-on-chronic liver failure. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7373", "text": "The primary functions of the liver include removing toxic substances from the blood, manufacturing  blood proteins , storing energy in the form of  glycogen , and secreting  bile . The  hepatocytes  that perform these tasks can be killed or impaired by disease, resulting in  acute liver failure  (ALF) which can be seen in person with previously diseased liver or a healthy one."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7374", "text": "In hyperacute and acute liver failure, the clinical picture develops rapidly with progressive  encephalopathy  and  multiorgan dysfunction  such as  hyperdynamic circulation ,  coagulopathy ,  acute kidney injury  and  respiratory insufficiency , severe metabolic alterations, and  cerebral edema  that can lead to brain death. [ 2 ] [ 3 ]  In these cases the mortality without  liver transplantation  (LTx) ranges between 40-80%. [ 4 ] [ 5 ]  LTx is the only effective treatment for these patients although it requires a precise indication and timing to achieve good results. Nevertheless, due to the scarcity of organs to carry out liver transplantations, it is estimated that one third of patients with ALF die while waiting to be transplanted. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7375", "text": "On the other hand, a patient with a chronic hepatic disease can suffer acute decompensation of liver function following a precipitating event such as variceal bleeding,  sepsis  and excessive alcohol intake among others that can lead to a condition referred to as acute-on-chronic liver failure (ACLF)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7376", "text": "Both types of hepatic insufficiency, ALF and ACLF, can potentially be reversible and liver functionality can return to a level similar to that prior to the insult or precipitating event."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7377", "text": "LTx has shown an improvement in the prognosis and survival with severe cases of ALF. Nevertheless, cost and donor scarcity have prompted researchers to look for new supportive treatments that can act as \u201cbridge\u201d to the transplant procedure. By stabilizing the patient's clinical state, or by creating the right conditions that could allow the recovery of native liver functions, both detoxification and synthesis can improve, after an episode of ALF or ACLF. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7378", "text": "Three different types of supportive therapies have been developed: bio-artificial, artificial and hybrid liver support systems (Table 2)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7379", "text": "Extracorporeal liver assist device"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7380", "text": "Molecular adsorbent recirculating system"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7381", "text": "Bioartificial Liver Support System"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7382", "text": "Fractionated plasma separation and adsorption system"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7383", "text": "TECA-Hybrid Artificial Liver Support System"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7384", "text": "Radial Flow Bioreactor"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7385", "text": "Single-pass albumin dialysis"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7386", "text": "Modular Extracorporeal Liver Support"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7387", "text": "Bioartificial Liver"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7388", "text": "Selective plasma filtration therapy"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7389", "text": "Bioartificial liver devices  are experimental extracorporeal devices that use living cell lines to provide detoxification and synthesis support to the failing liver. Bio-artificial liver (BAL) Hepatassist 2000 uses porcine hepatocytes whereas ELAD system employs hepatocytes derived from human hepatoblastoma C3A cell lines. [ 19 ] [ 20 ]  Both techniques can produce, in fulminant hepatic failure (FHF), an improvement of hepatic encephalopathy grade and biochemical parameters. Potential side effects that have been documented include immunological issues (porcine endogenous retrovirus transmission), infectious complications, and tumor transmigration."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7390", "text": "Other biological hepatic systems are Bioartificial Liver Support (BLSS) and Radial Flow Bioreactor (RFB). Detoxification capacity of these systems is poor and therefore they must be used combined with other systems to mitigate this deficiency. Today, its use is limited to centers with high experience in their application. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7391", "text": "A  bioartificial liver device (BAL)  is an artificial  extracorporeal  liver support (ELS) system for an individual who is suffering from  acute liver failure  (ALF) or  acute-on-chronic liver failure  (ACLF). The fundamental difference between artificial and BAL systems lies in the inclusion of hepatocytes into the reactor, often operating alongside the purification circuits used in artificial ELS systems. The overall design varies between different BAL systems, but they largely follow the same basic structure, with patient blood or plasma flow through an artificial matrix housing hepatocytes. Plasma is often separated from the patient\u2019s blood to improve efficiency of the system, and the device can be connected to artificial liver dialysis devices in order to further increase the effectiveness of the device in filtration of toxins. The inclusion of functioning hepatocytes in the reactor allows the restoration of some of the synthetic functions that the patient\u2019s liver is lacking. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7392", "text": "The first bioartificial liver device was developed in 1993 by Dr. Achilles A. Demetriou at Cedars-Sinai Medical Center. The bioartificial liver helped an 18-year-old southern California woman survive without her own liver for 14 hours until she received a human liver using a 20-inch-long, 4-inch-wide plastic cylinder filled with cellulose fibers and pig liver cells. Blood was routed outside the patient's body and through the artificial liver before being returned to the body. [ 23 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7393", "text": "Dr. Kenneth Matsumara's work on the BAL led it to be named an invention of the year by  Time  magazine in 2001. [ 25 ]  Liver cells obtained from an animal were used instead of developing a piece of equipment for each function of the  liver . The structure and function of the first device also resembles that of today's BALs. Animal liver cells are suspended in a solution and a patient's blood is processed by a  semipermeable membrane  that allow toxins and blood proteins to pass but restricts an immunological response. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7394", "text": "Advancements in  bioengineering  techniques in the decade after Matsumara's work have led to improved membranes and hepatocyte attachment systems. [ 26 ]  Cell sources now include primary porcine hepatocytes, primary human hepatocytes, human hepatoblastoma (C3A),  immortalized human cell lines  and  stem cells . [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7395", "text": "The purpose of BAL-type devices is not to permanently replace  liver functions , but to serve as a supportive device, [ 27 ]  either allowing the liver to regenerate properly upon  acute liver failure , or to bridge the individual's liver functions until a  transplant  is possible."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7396", "text": "BALs are essentially  bioreactors , with embedded  hepatocytes  (liver  cells ) that perform the functions of a normal  liver . They process oxygenated  blood plasma , which is separated from the other  blood  constituents. [ 28 ]  Several types of BALs are being developed, including hollow fiber systems and flat membrane sheet systems. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7397", "text": "Various types of hepatocytes are used in these devices. Porcine hepatocytes are often used due to ease of acquisition and cost; however, they are relatively unstable and carry the risk of cross-species disease transmission. [ 30 ]  Primary human hepatocytes sourced from donor organs present several problems in their cost and difficulty to obtain, especially with the current lack in transplantable tissue. [ 30 ]  In addition, questions have been raised about tissue collected from patients transmitting malignancy or infection via the BAL device. Several lines of human hepatocytes are also used in BAL devices, including C3A and HepG2 tumour cell lines, but due to their origin from hepatomas, they possess the potential to pass on malignancy to the patient. [ 31 ]  There is ongoing research into the cultivation of new types of human hepatocytes capable of improved longevity and efficacy in a bioreactor over currently used cell types, that do not pose the risk of transfer of malignancy or infection, such as the HepZ cell line created by Werner  et al. . [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7398", "text": "Similar to  kidney dialysis , hollow fiber systems employ a hollow fiber cartridge. Hepatocytes are suspended in a gel solution such as  collagen , which is injected into a series of hollow fibers. In the case of collagen, the suspension is then gelled within the fibers, usually by a temperature change. The hepatocytes then contract the gel by their attachment to the collagen matrix, reducing the volume of the suspension and creating a flow space within the fibers. Nutrient media is circulated through the fibers to sustain the cells. During use, plasma is removed from the patients blood. The patient's plasma is fed into the space surrounding the fibers. The fibers, which are composed of a semi-permeable membrane, facilitate transfer of toxins, nutrients and other chemicals between the blood and the suspended cells. The membrane also keeps immune bodies, such as  immunoglobulins , from passing to the cells to prevent an immune system rejection. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7399", "text": "Currently, hollow-fibre bioreactors are the most commonly accepted design for clinical use due to their capillary-network allowing for easy perfusion of plasma across cell populations. [ 34 ]  However, these structures have their limitations, with convectional transport issues, nutritional gradients, non-uniform seeding, inefficient immobilisation of cells, and reduced hepatocyte growth restricting their effectiveness in BAL designs. [ 35 ]  Researchers are now investigating the use of cryogels to replace hollow-fibres as the cell carrier components in BAL systems."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7400", "text": "Cryogels  are super-macroporous three-dimensional polymers prepared at sub-zero temperatures, by the freezing of a solution of cryogel precursors and solvent. The pores develop during this freezing process \u2013 as the cryogel solution cools, the solvent begins to form crystals. This causes the concentration of the cryogel precursors in the solution to increase, initiating the cryogelation process and forming the polymer walls. As the cryogel warms, the solvent crystals thaw, leaving cavities that form the pores. [ 36 ]  Cryogel pores range in size from 10-100\u00a0\u03bcm in size, forming an interconnected network that mimics a capillary system with a very large surface area to volume ratio, supporting large numbers of immobilised cells. Convection mediated transport is also supported by cryogels, enabling even distribution of nutrients and metabolite elimination, overcoming some of the shortcomings of hollow-fibre systems. [ 35 ]  Cryogel scaffolds demonstrate good mechanical strength and biocompatibility without triggering an immune response, improving their potential for long-term inclusion in BAL devices or  in-vitro  use. [ 37 ]  Another advantage of cryogels is their flexibility for use in a variety of tasks, including separation and purification of substances, along with acting as extracellular matrix for cell growth and proliferation. Immobilisation of specific ligands onto cryogels enables adsorption of specific substances, supporting their use as treatment options for toxins, [ 38 ]  for separation of haemoglobin from blood, [ 39 ]  and as a localised and sustained method for drug delivery. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7401", "text": "Developing an effective bioartificial liver (BAL) remains a formidable challenge, as it necessitates the intricate optimization of cell colonization, biomaterial scaffold design, and BAL fluid dynamics. Expanding upon prior research indicating its potential as a blood perfusion device for detoxification, some studies have explored the application of Arg-Gly-Asp (RGD)-containingPoly(2-hydroxyethyl methacrylate) (pHEMA)-alginate cryogels as scaffolds for BAL. These cryogels, incorporating alginate to mitigate protein fouling and functionalized with an RGD-containing peptide to enhance hepatocyte adhesion, represent a promising avenue for BAL scaffold development. Methods for characterizing internal flow within the porous cryogel matrix such as Particle Image Velocimetry (PIV), enables visualization of flow dynamics. PIV analysis revealed the laminar flow characteristics within cryogel pores, prompting the design of a multi-layered bioreactor consisting of spaced cryogel discs to optimize blood/hepatocyte mass exchange. Compared to the column configuration, the stacked bioreactor demonstrated significantly elevated production of albumin and urea, alongside enhanced cell colonization and proliferation over time. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7402", "text": "Recent developments in bioartificial liver (BAL) using living liver cells have shown promising advancements in the field of liver support and regeneration. These developments focus on utilizing various cell sources, scaffold materials, and bioreactor designs to enhance the functionality and viability of BAL systems. Key advancements include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7403", "text": "Cell Sources: Researchers have explored different cell sources for BAL, including primary hepatocytes, stem cell-derived hepatocyte-like cells, and immortalized liver cell lines. Efforts have been made to optimize cell culture conditions to maintain cell viability and functionality within BAL systems."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7404", "text": "Scaffold Materials: Biomaterial scaffolds play a critical role in providing structural support and facilitating cell attachment and proliferation in BAL systems. Recent studies have investigated the use of natural and synthetic materials, such as hydrogels, alginate, and decellularized liver scaffolds, to create biomimetic environments conducive to liver cell growth and function."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7405", "text": "Bioreactor Designs: Innovative bioreactor designs have been developed to enhance the performance of BAL systems by optimizing mass transfer, fluid dynamics, and cell-matrix interactions. These designs include perfusion-based bioreactors, microfluidic devices, and three-dimensional (3D) bioprinted constructs, which aim to mimic the physiological microenvironment of the liver and promote liver cell function and survival."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7406", "text": "Functional Assessment: Advances in bioanalytical techniques have enabled researchers to assess the functionality of liver cells within BAL systems more accurately. These techniques include measuring the secretion of liver-specific biomarkers, such as albumin, urea, and bile acids, as well as evaluating metabolic activity, drug metabolism, and detoxification capacity."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7407", "text": "There have been numerous clinical studies involving hollow-fibre bioreactors. Overall, they show promise but do not provide statistically significant evidence supporting their effectiveness. This is generally due to inherent design limitations, causing convectional transport issues, nutritional gradients, non-uniform seeding, inefficient immobilisation of cells, and reduced hepatocyte growth. [ 35 ]  As of writing, no cryogel-based devices have entered clinical trials. However, laboratory results have been promising, [ 35 ] [ 41 ]  and hopefully trials will begin soon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7408", "text": "The  HepatAssist , developed at the Cedars-Sinai Medical Center, is a BAL device containing porcine hepatocytes within a hollow-fibre bioreactor. These semi-permeable fibres act as capillaries, allowing the perfusion of plasma through the device, and across the hepatocytes surrounding the fibres. The system incorporates a charcoal column to act as a filter, removing additional toxins from the plasma. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7409", "text": "Demetriou  et al. [ 42 ]  carried out a large, randomised, multicentre, controlled trial on the safety and efficacy of the HepatAssist device. 171 patients with ALF stemming from viral hepatitis, paracetamol overdose or other drug complications, primary non-function (PNF), or of indeterminate aetiology, were involved in the study and were randomly assigned to either the experimental or control groups. The study found that at the primary end-point 30-day post admission mark, there was an increased survival rate in BAL patients over control patients (71% vs 62%), but the difference was not significant. However, when patients with PNF are excluded from the results there is a 44% reduction in mortality for BAL treated patients, a statistically significant advantage. The investigators noted that exclusion of PNF patients is justifiable due to early retransplantation and lack of intercranial hypertension, so HepatAssist would give little benefit to this group. For the secondary end-point of time-to-death, in patients with ALF of known aetiology there was a significant difference between BAL and control groups, with BAL patients surviving for longer. There was no significant difference for patients of unknown aetiology, however."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7410", "text": "The conclusions of the study suggest that such a device has potentially significant importance when used as a treatment measure. While the overall findings were not statistically significant, when the aetiology of the patients was taken into account the BAL group gained a statistically significant reduction in mortality over the control group. This suggests that while the device may not be applicable to patients as an overall treatment for liver dysfunction, it can provide an advantage when the heterogeneity of patients is considered and is used with patients of specific aetiology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7411", "text": "The  Extracorporeal Liver Assist Device  (ELAD) is a human-cell based treatment system. A catheter removes blood from the patient, and an ultrafiltrate generator separates the plasma from the rest of the blood. This plasma is then run through a separate circuit containing cartridges filled with C3A cells, before being returned to the main circuit and re-entering the patient. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7412", "text": "Thompson  et al. [ 43 ]  performed a large open-label trial, measuring the effectiveness of ELAD on patients with severe alcoholic hepatitis resulting in ACLF. Their study involved patients screened at 40 sites across the US, UK, and Australia, and enrolled a total of 203 patients. Patients were then randomised into either ELAD (n=96) or standard medical care (n=107) groups, with even distribution for patients in terms of sex, MELD score, and bilirubin levels. Of the 96 patients in the ELAD group, 45 completed the full 120 hours of treatment \u2013 the rest were unable to complete the full regimen due to a variety of reasons, including withdrawal of consent or severe adverse events, though 37 completed >72 hours of treatment, with results showing minimal difference in mortality between those receiving either >72 hours or the full 120 hours of treatment. The study was unable to complete its goal, finding no statistically significant improvement in mortality rates for patients that received ELAD treatment over those receiving standard care at 28 and 91 days (76.0% versus 80.4% and 59.4% versus 61.7%, respectively). Biomarker measurements showed a significantly reduced level of bilirubin and alkaline phosphatase in ELAD patients, though neither improvement translated into increased survivability rates. Outcomes for patients with MELD score <28 showed trends towards improved survival on ELAD, whereas those with MELD >28 had decreased survivability on ELAD. These patients presented with raised creatinine from kidney failure, suggesting a reason why ELAD decreased survival chance over standard care. Unlike artificial ELS devices and HepatAssist, ELAD does not incorporate any filtration devices, such as charcoal columns and exchange resins. Therefore, it cannot replace the filtration capability of the kidneys and cannot compensate for multi-organ failure from more severe presentations of ACLF, resulting in increased mortality rates."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7413", "text": "While the results of the study cannot provide conclusive evidence to suggest that a BAL device like ELAD improves the outcome of severe ACLF, it does suggest that it can aid the survival of patients with a less severe form of the disease. In those patients with a MELD <28, beneficial effects were seen 2\u20133 weeks post treatment, suggesting that while C3A incorporating BAL devices are unable to provide short-term aid like artificial albumin filtration devices, they instead provide more long-term aid in recovery of the patient\u2019s liver. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7414", "text": "A randomized, phase 3 trial of the ELAD device in patients with severe alcoholic hepatitis failed to show benefit on overall survival and development was discontinued. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7415", "text": "Artificial liver support systems are aimed to temporarily replace native liver detoxification functions and they use  albumin  as scavenger molecule to clear the toxins involved in the physiopathology of the failing liver. Most of the toxins that accumulate in the plasma of patients with liver insufficiency are protein bound, and therefore conventional  renal dialysis  techniques, such as  hemofiltration ,  hemodialysis  or  hemodiafiltration  are not able to adequately eliminate them."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7416", "text": "Liver dialysis has shown promise for patients with  hepatorenal syndrome . It is similar to  hemodialysis  and based on the same principles, but hemodialysis does not remove toxins bound to  albumin  that accumulate in liver failure. Like a  bioartificial liver device , it is a form of artificial extracorporeal liver support. [ 45 ] [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7417", "text": "A critical issue of the clinical syndrome in  liver failure  is the accumulation of toxins not cleared by the failing  liver . Based on this hypothesis, the removal of  lipophilic , albumin-bound substances such as  bilirubin ,  bile acids , metabolites of  aromatic amino acids , medium-chain  fatty acids  and  cytokines  should be beneficial to the clinical course of a patient in liver failure. This led to the development of artificial filtration and absorption devices."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7418", "text": "Liver dialysis is performed by physicians and surgeons and specialized nurses with training in gastroenterological medicine and surgery, namely, in  hepatology , alongside their colleagues in the intensive or  critical care unit  and the transplantation department, which is responsible for procuring and implanting a new liver, or a part (lobe) of one, if and when it becomes available in time and the patient is eligible. Because of the need for these experts, as well as the relative newness of the procedure in certain areas, it is usually available only in larger hospitals, such as level I trauma center teaching hospitals connected with medical schools."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7419", "text": "Between the different albumin dialysis modalities, single pass albumin dialysis (SPAD) has shown some positive results at a very high cost; [ 47 ]  it has been proposed that lowering the concentration of albumin in the dialysate does not seem to affect the detoxification capability of the procedure. [ 48 ]  Nevertheless, the most widely used systems today are based on hemodialysis and adsorption. These systems use conventional dialysis methods with an albumin containing dialysate that is later regenerated by means of adsorption columns, filled with  activated charcoal  and  ion exchange  resins.\nAt present, there are two artificial extracorporeal liver support systems: the Molecular Adsorbents Recirculating System (MARS) from  Gambro  and Fractionated Plasma Separation and Adsorption (FPSA), commercialised as Prometheus (PROM) from  Fresenius Medical Care . Of the two therapies, MARS is the most frequently studied, and clinically used system to date."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7420", "text": "While the technique is in its infancy, the prognosis of patients with liver failure remains guarded. Liver dialysis is currently only considered to be a bridge to  transplantation  or liver regeneration (in the case of  acute liver failure ) [ 49 ] [ 50 ] [ 51 ]  and, unlike  kidney dialysis  (for  kidney failure ), cannot support a patient for an extended period of time (months to years)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7421", "text": "Artificial detoxification devices currently under clinical evaluation include the Single Pass Albumin Dialysis (SPAD), Molecular Adsorbent Recirculating System (MARS), Prometheus system, and Dialive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7422", "text": "Single pass albumin dialysis (SPAD) is a simple method of  albumin  dialysis using standard renal replacement therapy machines without an additional perfusion pump system: The patient's blood flows through a circuit with a high-flux hollow fiber hemodiafilter, identical to that used in the MARS system. The other side of this membrane is cleansed with an albumin solution in counter-directional flow, which is discarded after passing the filter. Hemodialysis can be performed in the first circuit via the same high-flux hollow fibers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7423", "text": "The  Molecular Adsorbents Recirculation System  (MARS) is the best known extracorporal liver dialysis system. It consists of two separate dialysis circuits. The first circuit consists of  human serum albumin , is in contact with the patient's blood through a semipermeable membrane and has two filters to clean the albumin after it has absorbed toxins from the patient's blood. The second circuit consists of a hemodialysis machine and is used to clean the albumin in the first circuit, before it is recirculated to the semipermeable membrane in contact with the patient's blood."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7424", "text": "SPAD, MARS and continuous veno-venous haemodiafiltration (CVVHDF) were compared  in vitro  with regard to detoxification capacity. [ 52 ]  SPAD and CVVHDF showed a significantly greater reduction of ammonia compared with MARS. No significant differences could be observed between SPAD, MARS and CVVHDF concerning other water-soluble substances. However, SPAD enabled a significantly greater  bilirubin  reduction than MARS. Bilirubin serves as an important marker substance for albumin-bound (non-water-soluble) substances. Concerning the reduction of  bile acids  no significant differences between SPAD and MARS were seen. It was concluded that the detoxification capacity of SPAD is similar or even higher when compared with the more sophisticated, more complex and hence more expensive MARS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7425", "text": "Albumin dialysis is a costly procedure: for a seven-hour treatment with MARS, approximately \u20ac300 for 600 mL  human serum albumin  solution (20%), \u20ac1740 for a MARS treatment kit, and \u20ac125 for disposables used by the dialysis machine have to be spent. The cost of this therapy adds up to approximately \u20ac2165. Performing SPAD according to the protocol by Sauer et al., however, requires 1000 mL of human albumin solution (20%) at a cost of \u20ac500. A high-flux dialyzer costing approximately \u20ac40 and the tubings (\u20ac125) must also be purchased. The overall costs of a SPAD treatment is approximately \u20ac656\u201430% of the costs of an equally efficient MARS therapy session. The expenditure for the MARS monitor necessary to operate the MARS disposables is not included in this calculation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7426", "text": "The  Prometheus  system ( Fresenius  Medical Care,  Bad Homburg , Germany) is a device based on the combination of  albumin   adsorption  with high-flux  hemodialysis  after selective filtration of the albumin fraction through a specific polysulfon filter (AlbuFlow). It has been studied [ 53 ]  in a group of eleven patients with  hepatorenal syndrome  (acute-on-chronic liver failure and accompanying kidney failure). The treatment for two consecutive days for more than four hours significantly improved serum levels of conjugated bilirubin, bile acids, ammonia, cholinesterase, creatinine, urea and blood pH. Prometheus was proven to be a safe supportive therapy for patients with liver failure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7427", "text": "Dialive (Yaqrit Limited, London, UK) incorporates albumin removal and replacement and, endotoxin removal. It is at \" Technology readiness level \" (TRL) 5, which means it is validated in the disease environment. [ 54 ] [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7428", "text": "MARS was developed by a group of researchers at the  University of Rostock  (Germany), in 1993 and later commercialized for its clinical use in 1999. [ 56 ]  The system is able to replace the detoxification function of the liver while minimizing the inconvenience and drawbacks of previously used devices. [ 57 ] [ 58 ] [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7429", "text": "In vivo  preliminary investigations indicated the ability of the system to effectively remove bilirubin, biliary salts, free fatty acids and tryptophan while important physiological proteins such as albumin, alpha-1-glicoproteine, alpha 1 antitrypsin, alpha-2-macroglobulin, transferrin, globulin tyrosine, and hormonal systems are unaffected. [ 60 ]  Also, MARS therapy in conjunction with CRRT/HDF can help clear cytokines acting as inflammatory and immunological mediators in hepatocellular damage, and therefore can create the right environment to favour hepatocellular regeneration and recovery of native liver function."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7430", "text": "MARS is an extracorporeal hemodialysis system composed of three different circuits: blood,  albumin  and low-flux dialysis. The blood circuit uses a double lumen  catheter  and a conventional hemodialysis device to pump the patient's blood into the MARS FLUX, a biocompatible polysulfone high-flux dialyser. With a membrane surface area of 2.1 m 2 , 100\u00a0nm of thickness and a cut-off of 50 KDa, the MARSFLUX is essential to retaining the albumin in the  dialysate . Blood is dialysed against a  human serum albumin  (HSA) dialysate solution that allows blood detoxification of both  water-soluble  and protein-bound toxins, by means of the presence of albumin in the dialysate (albumin dialysis). The albumin dialysate is then regenerated in a close loop in the MARS circuit by passing through the fibres of the low-flux diaFLUX filter, to clear water-soluble toxins and provide electrolyte/acid-base balance, by a standard dialysis fluid. Next, the albumin dialysate passes through two different adsorption columns; protein-bound substances are removed by the diaMARS AC250, containing activated charcoal and anionic substances are removed by the diaMARS IE250, filled with cholestyramine, an anion-exchange resin. The albumin solution is then ready to initiate another detoxifying cycle of the patient's blood that can be sustained until both adsorption columns are saturated, eliminating the need to continuously infuse albumin into the system during treatment (Fig. 1)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7431", "text": "A systematic review of the literature from 1999 to June 2011 was performed in the following databases:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7432", "text": "Hepatic encephalopathy  (HE) represents one of the more serious extrahepatic complications associated with liver dysfunction. [ 61 ] [ 62 ]  Neuro-psychiatric manifestations of HE affect consciousness and behaviour."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7433", "text": "Evidence suggests that HE develops as some neurotoxins and neuro active substances, produced after hepatocellular breakdown, accumulates in the brain as a consequence of a portosystemic shunt and the limited detoxification capability of the liver. Substances involved are ammonia, manganese, aromatic aminoacids, mercaptans, phenols, medium chain fatty acids, bilirubin, endogenous benzodiazepines, etc. \nThe relationship between ammonia neurotoxicity and HE was first described in animal studies by Pavlov et al. [ 63 ] \nSubsequently, several studies in either animals or humans have confirmed that, a ratio in ammonia concentration higher than 2 mM between the brain and blood stream, causes HE, and even a comatose state when the value is greater than 5 mM. Some investigators have also reported a decrease in serum ammonia following a MARS treatment (Table 3)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7434", "text": "Hours/patient"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7435", "text": "(\u03bcg/dL)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7436", "text": "Manganese and copper serum levels are increased in patients with either acute or acute on chronic liver failure. Nevertheless, only in those patients with chronic hepatic dysfunction, a bilateral magnetic resonance alteration on Globos Pallidus is observed, [ 68 ]  probably because this type of patients selectively shows higher cerebral membrane permeability.\nImbalance between aromatic and branched chain aminoacids (Fischer index), traditionally involved in HE genesis, [ 69 ] [ 70 ] [ 71 ]  can be normalized following a MARS treatment. The effects are noticeable even after 3 hours of treatment and this reduction in the Fisher index is accompanied with an improvement in the HE. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7437", "text": "Novelli G  et al. [ 73 ]  published their three years experience on MARS analyzing the impact of the treatment in the cerebral level for 63 patients reporting an improvement in Glasgow Coma Score (GCS) for all observed in all patients. In the last 22 patients, cerebral perfusion pressure was monitored by Doppler (mean flow velocity in middle cerebral artery), establishing a clear relationship between a clinical improvement (especially neurological) and an improvement in arterial cerebral perfusion. This study confirms other results showing similar increments in cerebral perfusion in patients treated with MARS. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7438", "text": "More recently, several studies have shown a significant improvement of HE in patients treated with MARS. In the studies by Heemann  et al. [ 74 ]  and Sen  et al. [ 75 ]  an improvement in HE was considered when encephalopathy grade was reduced by one or more grades vs. basal values; for Hassenein et al., in their randomized controlled trial, improvement was considered when a decrease of two grades was observed. [ 76 ]  In the latter, 70 patients with acute on chronic liver failure and encephalopathy grade III and IV were included. Likewise, Kramer et al. [ 77 ]  estimated an HE improvement when an improvement in peak N70 latency in electroencephalograms was observed.\nSen  et al. 44 observed a significant reduction in Child-Pugh Score (p<0,01) at 7 days following a MARS treatment, without any significant change in the controls. Nevertheless, when they looked at the Model for End-Stage Liver Disease Score (MELD), a significant reduction in both groups, MARS and controls, was recorded (p<0,01 y p<0,05, respectively).\nLikewise, in several case series, an improvement in HE grade with MARS therapy is also reported. [ 78 ] [ 79 ] [ 80 ] [ 81 ] [ 82 ] [ 83 ] [ 84 ] [ 85 ] [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7439", "text": "Hemodynamic instability is often associated with acute liver insufficiency, as a consequence of endogenous accumulation of vasoactive agents in the blood. This is characterized by a systemic vasodilatation, a decrease of systemic vascular resistance, arterial hypotension, and an increase of cardiac output that gives rise to a hyperdynamic circulation. \nDuring MARS therapy, systemic vascular resistance index and mean arterial pressure have been shown to increase and show improvement. [ 78 ] [ 80 ] [ 82 ] [ 87 ] [ 88 ] \nSchmidt et al. [ 89 ]  reported the treatment of 8 patients, diagnosed with acute hepatic failure, that were treated with MARS for 6 hours, and were compared with a control group of 5 patients to whom ice pads were applied to match the heat loss produced in the treatment group during the extracorporeal therapy. They analyzed hemodynamic parameters in both groups hourly. In the MARS group, a statistically significant increase of 46% on systemic vascular resistance was observed (1215 \u00b1 437 to 1778 \u00b1 710 dinas x s x cm \u22125  x m \u22122 ) compared with a 6% increase in the controls. Mean arterial pressure also increased (69 \u00b1 5 to 83 \u00b1 11 mmHg, p< 0.0001) in the MARS group, whereas no difference was observed in the controls. Cardiac output and heart rate also decreased in the MARS group as a consequence of an improvement in the hyperdynamic circulation. Therefore, it was shown that a statistically significant improvement was obtained with MARS when compared with the SMT."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7440", "text": "Catalina et al. [ 90 ]  have also evaluated systemic and hepatic hemodynamic changes produced by MARS therapy. In 4 patients with acute decompensation of chronic liver disease, they observed after MARS therapy, an attenuation of hyperdynamic circulation and a reduction in the portal pressure gradient was measured. Results are summarized in table 4."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7441", "text": "There are other studies also worth mentioning with similar results: Heemann  et al . [ 74 ]  and Par\u00e9s  et al . [ 91 ]  among others. Dethloff T  et al . [ 92 ]  concluded that there is a statistically significant improvement favourable to MARS in comparison with Prometheus system (Table 5)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7442", "text": "Hepatorenal syndrome is one of the more serious complications in patients with acute decompensation of cirrhosis and increased portal hypertension. It is characterized by hemodynamic changes in splanchnic, systemic and renal circulation. Splanchnic vasodilatation triggers the production of endogenous vasoactive substances that produce renal vasoconstriction and low glomerular filtration rate, leading to oliguria with a concomitant reduction in creatinine clearance. Renal insufficiency is always progressive with an inferior prognosis, [ 93 ] [ 94 ]  with survival at 1 and 2 months of 20 and 10% respectively."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7443", "text": "Pierre Versin [ 95 ]  is one of the pioneers in the study of hepatorenal syndrome in patients with liver impairment.\nGreat efforts have been made trying to improve the prognosis of this type of patient; however, few have solved the problem. Orthotopic liver transplantation is the only treatment that has shown to improve acute and chronic complications derived from severe liver insufficiency. Today it is possible to combine albumin dialysis with continuous veno-venous hemodialfiltration, which provides a greater expectation for these patients [ 96 ]  by optimization of their clinical status."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7444", "text": "MARS treatment lowers serum urea and creatinine levels improving their clearance, [ 88 ] [ 89 ] [ 90 ] [ 92 ]  and even favors resolution of hepatorenal syndrome. [ 74 ] [ 81 ] [ 82 ] [ 87 ] [ 97 ]  Results are confirmed in a randomized controlled trial published by Mitzner  et al. . [ 93 ]  in which 13 patients diagnosed with hepatorenal syndrome type I was treated with MARS therapy. Mean survival was 25,2\u00b134,6 days in the MARS group compared to 4,6\u00b11,8 days observed in the controls in whom hemodiafiltration and standard care (SMT) was applied. This resulted in a statistically significance difference in survival at 7 and 30 days (p<0.05). Authors concluded that MARS therapy, applied to liver failure patients (Child-Pugh C and UNOS 2A scores) who develop hepatorenal syndrome type I, prolonged survival compared to patients treated with SMT."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7445", "text": "Although mechanisms explaining previous findings are not yet fully understood, it has been reported that there was a decrease in plasma renin concentrations in patients diagnosed with acute on chronic liver failure with renal impairment that were treated with MARS.\nLikewise, other studies have suggested some efficacy for MARS in the treatment of hepatorenal syndrome. [ 98 ] [ 99 ] [ 100 ] \nHowever, other references have been published that do not show efficacy in the treatment of these types of patients with MARS therapy. Khuroo  et al. . [ 101 ]  published a meta-analysis based on 4 small RCT's and 2 non RCT's in patients diagnosed with ACLF, concluding that MARS therapy would not bring any significant increment in survival compared with SMT.\nAnother observational study in 6 patients with cirrhosis, refractory ascites and hepatorenal syndrome type I, not responding to vasoconstrictor therapy, showed no impact on hemodynamics following MARS therapy; however authors concluded that MARS therapy could effectively serve as bridge to liver transplantation. [ 83 ] [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7446", "text": "Total bilirubin was the only parameter analyzed in all trials that was always reduced in the groups of patients treated with MARS; Banayosy  et al. . [ 103 ]  measured bilirubin levels 14 days after since MARS therapy was terminated and observed a consistent, significant decrease not only for bilirubin but also for creatinine and urea (Table 6)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7447", "text": "4 sessions"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7448", "text": "Impact of MARS therapy on plasma biliary acids levels was evaluated in 3 studies. In the study from Stadbauer  et al. ., [ 105 ]  that was specifically addressing the topic, it is reported that MARS and Prometheus systems lower to the same extent biliary acids plasma concentration. Heemann  et al. . [ 74 ]  and Laleman  et al. . [ 88 ]  have also published a significant improvement for these organic ions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7449", "text": "Pruritus  is one of the most common clinical manifestations in cholestasis liver diseases and one of the most distressing symptoms in patients with chronic liver disease caused by  viral hepatitis C . Many hypotheses have been formulated to explain physio pathogenesis of such manifestation, including incremental plasma concentration of biliary acids, abnormalities in the  bile ducts , [ 106 ]  increased central  neurotransmitters  coupling  opioid receptors , [ 107 ] [ 108 ]  etc. Despite the number of historical drugs used, individually or combined (exchange resins, hydrophilic biliary acids, antihistamines, antibiotics, anticonvulsants, opioid antagonists), there are reported cases of intractable or refractory pruritus with a dramatic reduction in patients\u2019 quality of life (i.e. sleep disorders, depression, suicide attempts...). [ 109 ] [ 110 ]  Intractable  pruritus  can be an indication for liver transplantation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7450", "text": "The MARS indication for intractable pruritus is therapeutically an option that has shown to be beneficial for patients in desperate cases, although at high cost. [ 111 ] [ 112 ] [ 113 ] [ 114 ]  In several studies, it was confirmed that after MARS treatments, patients remain free from pruritus for a period of time ranging from 6 to 9 months. [ 114 ]  Nevertheless, some authors have concluded that besides the good results found in the literature, application of MARS therapy in refractory pruritus requires larger evidence. [ 112 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7451", "text": "Pharmacokinetics  and  pharmacodynamics  for a majority of drugs can be significantly be modified with liver failure, affecting the therapeutic approach and potential toxicity of the drugs. In these type of patients,  Child-Pugh score  represents a poor prognostic factor to assess the metabolic capacity of the failing liver."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7452", "text": "In patients with hepatic failure, drugs that are only metabolized in the liver, accumulate in the plasma right after they are administered, and therefore it is needed to modify drug dosing in both, concentration and time intervals, to lower the risk of toxicity. It is also necessary to adjust the dosing for those drugs that are exclusively metabolized by the liver, and have low affinity for prioteins and high distribution volume, such as  fluoroquinolones  ( Levofloxacin  and  Ciprofloxacin ). [ 115 ] [ 116 ] [ 117 ] [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7453", "text": "Extracorporeal detoxification with albumin dialysis increases the clearance of drugs that are bound to plasmatic proteins (Table 7)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7454", "text": "In the meta-analysis published by Khuroo  et al. . [ 101 ]  which included 4 randomized trials [ 74 ] [ 89 ] [ 93 ] [ 103 ]  an improvement in survival for the patients with liver failure treated with MARS, compared with SMT, was not observed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7455", "text": "However, neither in the extracorporeal liver support systems review by the  Cochrane [ 119 ]  (published in 2004), nor the meta-analysis by Kjaergard  et al. . [ 120 ]  was a significance difference in survival found for patients diagnosed with ALF treated with extracorporeal liver support systems.\nNevertheless, these reviews included all kind of liver support systems and used a heterogeneous type of publication (abstracts, clinical trials, cohort, etc.)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7456", "text": "There is literature showing favorable results in survival for patients diagnosed with ALF, and treated with MARS., In a randomized controlled trial, Salib\u00e0  et al. . [ 121 ]  studied the impact on survival of MARS therapy for patients with ALF, waiting on the liver transplant list. Forty-nine patients received SMT and 53 were treated with MARS. They observed that patients that received 3 or more MARS sessions showed a statistically significance increase in transplant-free survival compared with the others patients of the study. Notably, 75% of the patients underwent liver transplantation in the first 24 hours after inclusion in the waiting list, and besides the short exposure to MARS therapy, some patients showed a better survival trend compared to controls, when they were treated with MARS prior to the transplant."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7457", "text": "In a case-controlled study by Montejo  et al. . [ 104 ]  it was reported that MARS treatment do not decrease mortality directly; however, the treatment contributed to significantly improve survival in patients that were transplanted. In studies by Mitzner  et al. . [ 93 ]  and Heemann  et al. . [ 74 ]  they were able to show a significance statistical difference in 30-day survival for patients in the MARS group. However, El Banayosy  et al. . [ 103 ]  and Hassanein  et al. . [ 76 ]  noticed a non significant improvement in survival, probably because of the short number of patients included in the trials. In the majority of available MARS studies published with patients diagnosed with ALF, either transplanted or not, survival was greater in the MARS group with some variations according to the type of trial, ranging from 20-30%, [ 122 ] [ 123 ]  and 60-80%. [ 83 ] [ 124 ] [ 125 ] [ 126 ]  Data is summarized in Tables 8, 9 and 10."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7458", "text": "MARS (%)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7459", "text": "Controls"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7460", "text": "For patients diagnosed with acute on chronic liver failure and treated with MARS therapy, clinical trial results showed a not statistically significant reduction in mortality (odds ratio [OR] =0,78; confident interval [CI] =95%: 0,58 \u2013 1,03; p= 0,1059, Figure 3)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7461", "text": "A non-statistically significant reduction of mortality was shown in patients with ALF treated with MARS (OR = 0,75 [CI= 95%, 0,42 \u2013 1,35]; p= 0,3427). (Figure 4)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7462", "text": "Combined results yielded a non-significant reduction on mortality in patients treated with MARS therapy. However, the low number of patients included in each of the studies may be responsible for not being able to achieve enough statistical power to show differences between both treatment groups. Moreover, heterogeneity for the number of MARS sessions and severity of liver disease of the patients included, make it very difficult for the evaluation of MARS impact on survival."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7463", "text": "Recently, a meta-analysis on survival in patients treated with an extra-hepatic therapy has been published. [ 131 ]  Searching strategies yielded 74 clinical trials: 17 randomized controlled trials, 5 case control and 52 cohort studies. Eight studies were included in the meta-analysis: three addressing acute liver failure, one with MARS therapy [ 103 ]  and five addressing acute on chronic, being four MARS related. [ 74 ] [ 75 ] [ 76 ] [ 93 ]  Authors concluded that extra-hepatic detoxifying systems improve survival for acute liver insufficiency, whereas results for acute decompensation of chronic liver diseases suggested a non significant survival benefit. Also, due to an increased demand for liver transplantation together with an augmented risk of liver failure following large resections, development of detoxifying extrahepatic systems are necessary."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7464", "text": "Safety, defined as presence of adverse events, is evaluated in few trials. Adverse events in patients receiving MARS therapy are similar to those in the controls with the exception of thrombocytopenia and hemorrhage that seems to occur more frequently with the MARS system. [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7465", "text": "Heemann et al. [ 74 ]  reported two adverse events most probably MARS related: fever and sepsis, presumably originated at the catheter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7466", "text": "In the study by Hassanein  et al. , [ 76 ]  two patients in the MARS group abandoned the study owing to   hemodynamic instability, three patients required larger than average platelets transfusion and three more patients presented gastrointestinal bleeding."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7467", "text": "Laleman  et al. . [ 88 ]  detected one patient with thrombocytopenia in both the MARS and Prometheus treatment groups, and an additional patient with clotting of the dialysis circuit and hypotension, only in the Prometheus group."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7468", "text": "Kramer  et al. . (Biologic-DT) [ 77 ]  wrote about 3 cases with disseminated intravascular coagulation in the interventional group, two of them with fatal outcomes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7469", "text": "Mitzner  et al. . [ 93 ]  described, among patients treated with MARS, a thrombocytopenia case and a second patient with chronic hepatitis B, who underwent TIPS placement on day 44 after randomization and died on day 105 of multiorgan failure, as a consequence of complications related to the TIPS procedure."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7470", "text": "Montejo  et al. . [ 104 ]  showed that MARS is an easy technique, without serious adverse events related to the procedure, and also easy to implement in ICU settings that are used to renal extracorporeal therapies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7471", "text": "The MARS International Registry, with data from more than 500 patients (although sponsored by the manufacturer), shows that the adverse effects observed are similar to the control group. However, in these severely ill patients it is difficult to distinguish between complications of the disease itself and side effects attributable to the technique."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7472", "text": "Only three Studies addressing cost-effectivenenss of MARS therapy have been found.\nHassanein et al. [ 133 ]  analysed costs of randomized patients with ACLF receiving MARS therapy or standard medical care. They used the study published in 2001 by Kim et al. [ 134 ]  describing the impact of complications in hospitalization costs in patients diagnosed with alcoholic liver failure. Cost of 11 patients treated with standard medical care (SMT) were compared to those that received MARS, in addition to SMT (12 patients). In the MARS group, there was less in-hospital mortality and complications related to the disease, with a remarkable reduction in cost which compensated the MARS related expenditure (Table 11)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7473", "text": "n=12"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7474", "text": "n=11"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7475", "text": "There were 5 survivors in the control group, with a cost per patient of $35.904, whereas in the MARS group, 11 patients out of 12 survived with a cost per patient of $32.036 which represents a $4000 savings per patient in favors of the MARS group.\nHessel et al. [ 135 ]  published a 3-year follow-up of a cohort of 79 patients with ACLF, of whom 33 received MARS treatments and 46 received SMT. Survival was 67% for the MARS group and 63% for the controls, that was reduced to 58 and 35% respectively at one year follow-up, and then 52 and 17% at three years."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7476", "text": "Hospitalization costs for the MARS treated group were greater than that for the controls (\u20ac31,539 vs. \u20ac7,543) and similarly direct cost at 3-year follow-up (\u20ac8,493 vs. \u20ac5,194). Nevertheless, after adjusting mortality rate, the annual cost per patient was \u20ac12,092 for controls and \u20ac5,827 for MARS group; also in the latter, they found an incremental cost-effectiveness ratio of 31.448 \u20ac per life-year gained (LYG) and an incremental costs per QALY gained of 47171 \u20ac."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7477", "text": "Two years later, same authors published the results of 149 patients diagnosed with ACLF. [ 136 ]  There were 67 patients (44,9%) treated with MARS and 82 patients (55,1%) were allocated to receive SMT. Mean survival time was 692 days in the MARS group (33% at 3 years) and 453 days in the controls (15% at 3 years); the results were significant (p=0,022). Differences in average cost was \u20ac19,853 (95% IC: 13.308-25.429): 35.639 \u20ac for MARS patients and 15.804 \u20ac for the control group. Incremental cost per LYG was 29.985 \u20ac (95% IC: 9.441-321.761) and \u20ac43,040 (95% IC: 13.551-461.856) per quality-adjusted life years (QALY)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7478", "text": "Liver support systems, such as MARS, are very important to stabilize patients with acute or acute on chronic liver failure and avoid organ dysfunction, as well as a bridge-to-transplant. Although initial in-hospital costs are high, they are worth for the favorable outcome."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7479", "text": "Etiology:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7480", "text": "Goals of MARS Therapy"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7481", "text": "MARS Therapy Indication"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7482", "text": "Treatment Schedule:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7483", "text": "[ 147 ] [ 148 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7484", "text": "[ 149 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7485", "text": "[ 97 ] [ 137 ] [ 140 ] [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7486", "text": "Same contraindications as with any other extracorporeal treatment may be applied to MARS therapy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7487", "text": "Blood Flow"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7488", "text": "The trend is to use high flow rates, although it is determined by the technical specifications of the combined machine and catheters\u2019 size"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7489", "text": "Intermittent treatments:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7490", "text": "Continuous treatments:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7491", "text": "Dyalisate Flow Rate"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7492", "text": "Replacement Flow Rate"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7493", "text": "Heparin Anticoagulation"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7494", "text": "Similarly to CVVHD, it depends on previous patient's coagulation status. In many cases it will not be needed, unless the patient presents a PTT inferior to 160 seconds. In patients with normal values, a bolus of 5000 to 10000 IU of heparin could be administered at the commencement of the treatment, followed by a continuous perfusion, to keep PTT in ratios from 1,5 to 2,5 or 160 to 180 seconds."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7495", "text": "Monitoring"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7496", "text": "A biochemical analysis is recommended (liver and kidney profile, ionic, glucose) together with a hemogram at the end of first session and before starting the following one."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7497", "text": "Coagulation analysis must be also performed before starting the session to adjusting heparin dose."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7498", "text": "In case that medication susceptible to be eliminated by MARS is being administered, it is also recommended to monitor their levels in blood"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7499", "text": "End of the Session"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7500", "text": "and both catheter's lumens heparinized"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7501", "text": "Federal Drug Administration  (FDA) cleared, in a document dated on May 27, 2005, MARS therapy for the treatment of drug overdose and poisoning. The only requirement is that the drug or poison must be susceptible to be dialysed and removed by activated charcoal or anionic exchange resins."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7502", "text": "More recently, on December 17, 2012, MARS therapy has been cleared by the FDA for the treatment of  hepatic encephalopathy  due to a decompensation of a chronic liver disease. Clinical trials conducted with MARS treatment in HE patients having a decompensation of chronic liver disease demonstrated a transient effect from MARS treatments to significantly decrease their hepatic encephalopathy scores by at least 2 grades compared to standard medical therapy (SMT)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7503", "text": "The MARS is not indicated as a bridge to liver transplant. Safety and efficacy has not been demonstrated in controlled, randomized clinical trials."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7504", "text": "The effectiveness of the MARS device in patients that are sedated could not be established in clinical studies and therefore cannot be predicted in sedated patients"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7505", "text": "The  LiverNet  is a database dedicated to the liver diseases treated with the support of extracorporeal therapies. To date, the most currently used system is the Molecular Adsorbent Recirculating System (MARS), which is based on the selective removal of albumin bound molecules and toxins from the blood in patients with acute and acute-on-chronic liver failure. The purpose is to register prospectively all patients treated worldwide with the MARS system in order to:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7506", "text": "The liverNet is an eCRF database (www.livernet.net) using a SAS platform that allows major advantages for the centres including the automatic calculations of most liver rand ICU scoring systems, instant queries online, instant export of all patients included in the database of each centre to an Excel file for direct statistical analysis and finally instant online statistical analysis of selective data decided by the scientific committee. Therefore, the LiverNet is an important tool to progress in the knowledge of liver support therapies."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7507", "text": "The  Model for End-Stage Liver Disease , or  MELD , is a scoring system for assessing the severity of  chronic liver disease . It was initially developed to predict mortality within three months of surgery in patients who had undergone a  transjugular intrahepatic portosystemic shunt  (TIPS) procedure, [ 1 ]  and was subsequently found to be useful in determining prognosis and prioritizing for receipt of a  liver transplant . [ 2 ] [ 3 ]  This score is now used by the  United Network for Organ Sharing  (UNOS) and  Eurotransplant  for prioritizing allocation of  liver transplants  instead of the older  Child-Pugh score . [ 3 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7508", "text": "MELD uses the patient's values for serum  bilirubin , serum  creatinine , and the  international normalized ratio for prothrombin time (INR)  to predict survival. It is calculated according to the following formula: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7509", "text": "M \n E \n L \n D \n \n \n \n = \n \n d \n e \n f \n \n \n \n 3.78 \n \u00d7 \n ln \n \u2061 \n \n ( \n \n serum bilirubin (mg/dL) \n \n ) \n \n + \n 11.2 \n \u00d7 \n ln \n \u2061 \n ( \n \n INR \n \n ) \n + \n 9.57 \n \u00d7 \n ln \n \u2061 \n \n ( \n \n serum creatinine (mg/dL) \n \n ) \n \n + \n 6.43 \n \n \n {\\displaystyle \\mathrm {MELD} {\\overset {\\mathrm {def} }{=}}3.78\\times \\ln \\left({\\text{serum bilirubin (mg/dL)}}\\right)+11.2\\times \\ln({\\text{INR}})+9.57\\times \\ln \\left({\\text{serum creatinine (mg/dL)}}\\right)+6.43}"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7510", "text": "MELD scores are reported as whole numbers, so the result of the equation above is rounded."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7511", "text": "UNOS has made the following modifications to the score: [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7512", "text": "The etiology of liver disease was subsequently removed from the model because it posed difficulties such as how to categorize patients with multiple causes of liver disease. Modification of the MELD score by excluding etiology of liver disease did not significantly affect the model's accuracy in predicting three-month survival."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7513", "text": "Patients with a diagnosis of liver cancer will be assigned a MELD score based on how advanced the cancer is.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7514", "text": "In interpreting the MELD Score in hospitalized patients, the 3 month observed mortality (considering 3,437 adult liver transplant candidates with chronic liver disease who were added to\nthe OPTN waiting list at 2A or 2B status between November, 1999, and December, 2001) is: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7515", "text": "Applications of MELD score include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7516", "text": "MELD was originally developed at the  Mayo Clinic  by Dr. Patrick Kamath, and at that point was called the \"Mayo End-stage Liver Disease\" score. It was derived in a series of patients undergoing TIPS procedures. The original version also included a variable based on the underlying etiology (cause) of the liver disease. [ 1 ]  The score turned out to be predictive of prognosis in chronic liver disease in general, and\u2014with some modifications\u2014came to be applied as an objective tool in assigning need for a liver transplant. The etiology turned out to be relatively unimportant, and was also regarded as relatively subjective; it was therefore removed from the score. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7517", "text": "The successor of MELD, an advanced scoring system, made by collaboration between  Massachusetts General Hospital  and  IBM , called  MELD-Plus  was introduced in 2017. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7518", "text": "The  United Network for Organ Sharing  proposed that MELD-Na score (an extension of MELD) may better rank candidates based on their risk of pre-transplant mortality and is projected to save 50-60 lives total per year. [ 8 ]  Furthermore, a study published in the  New England Journal of Medicine  in 2008, estimated that using MELD-Na instead of MELD would save 90 lives for the period from 2005 to 2006. [ 9 ]  In his viewpoint published in June 2018, co-creator of  MELD-Plus , Uri Kartoun, suggested that \"...MELD-Plus, if incorporated into hospital systems, could save hundreds of patients every year in the United States alone.\" [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7519", "text": "Paracentesis  (from  Greek  \u03ba\u03b5\u03bd\u03c4\u03ac\u03c9, \"to pierce\") is a form of  body fluid sampling  procedure, generally referring to  peritoneocentesis  (also called  laparocentesis  or  abdominal paracentesis ) in which the  peritoneal cavity  is punctured by a needle to sample  peritoneal fluid . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7520", "text": "The procedure is used to remove fluid from the peritoneal cavity, particularly if this cannot be achieved with medication. The most common indication is  ascites  that has developed in people with  cirrhosis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7521", "text": "It is used for a number of reasons: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7522", "text": "The procedure is often performed in a doctor's office or an outpatient clinic. In an expert's hands, it is usually very safe, [ 4 ]  although there is a small risk of infection, excessive bleeding or perforating a loop of bowel. These last two risks can be minimized greatly with the use of ultrasound guidance. [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7523", "text": "The use of  ultrasound  has become the standard of care when preparing a patient for paracentesis. Confirmation of an ascitic effusion reduces the risks associated with a dry or blind tap of the abdomen. Anatomic landmarks, such as the midline  linea alba  approach, were traditionally used as reference points for needle insertion. Phased array or curvilinear ultrasound transducers are typically used in the hospital and outpatient setting to identify ascites in the abdominal cavity. Fluid within the abdominal cavity appears hypoechoic or anechoic (black) on ultrasound.  Morison's pouch  (hepatorenal recess) is a common starting location in concordance with ultrasound FAST ( focused assessment with sonography for trauma ) exam. Fluid collection can occur in a number of different locations and may be difficult to find, especially if the patient only exhibits a small volume of ascites. Measurement of the amount of fluid within the abdominal cavity is not necessary or very successful. Identification of sufficient fluid within the abdominal cavity for fluid analysis or to achieve a therapeutic benefit is all that is required to proceed to paracentesis. Ultrasound guidance of the paracentesis can also be used as an additional safety measure to ensure the needle stays within the ascitic fluid and avoidance of important vessels within the abdominal cavity. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7524", "text": "The patient is requested to urinate before the procedure; alternately, a  Foley catheter  is used to empty the bladder. The patient is positioned in the bed with the head elevated at 45\u201360 degrees to allow fluid to accumulate in lower abdomen. After cleaning the side of the abdomen with an antiseptic solution, the physician numbs a small area of skin and inserts a large-bore needle with a plastic sheath 2 to 5\u00a0cm (1 to 2\u00a0in) in length to reach the peritoneal (ascitic) fluid. The needle is removed, leaving the plastic sheath to allow drainage of the fluid. The fluid is drained by gravity, a syringe, or by connection to a vacuum bottle. Several litres of fluid may be drained during the procedure; however, if more than two litres are to be drained, it will usually be done over the course of several treatments. [ 6 ]  After the desired level of drainage is complete, the plastic sheath is removed and the puncture site bandaged. [ 6 ]  The plastic sheath can be left in place with a flow control valve and protective dressing if further treatments are expected to be necessary. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7525", "text": "If fluid drainage in  cirrhotic  ascites is more than 5 litres, patients may receive  intravenous   serum albumin  (25% albumin, 8\u00a0g/L) to prevent  hypotension  (low blood pressure). [ 7 ]  There has been debate as to whether albumin administration confers benefit, but a recent 2016  meta-analysis  concluded that it can reduce mortality after large-volume paracentesis significantly. [ 8 ]  However, for every end-point investigated, while albumin was favorable as compared to other agents (e.g., plasma expanders, vasoconstrictors), these were not statistically significant and the meta-analysis was limited by the quality of the studies\u2014two of which that were in fact unsuitable\u2014included in it. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7526", "text": "The procedure generally is not painful and does not require  sedation . The patient is usually discharged within several hours following post-procedure observation provided that blood pressure is otherwise normal and the patient experiences no dizziness. [ 1 ] [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7527", "text": "Paracentesis is known to be a safe procedure when ascitic fluid is readily visible, so complications are typically rare. Possible complications following or during the procedure involve infection, bleeding, the leakage ascitic of fluid, or  bowel perforation . [ 7 ] [ 5 ]  Of these, the most concerning in the immediate setting is bleeding within the peritoneal cavity. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7528", "text": "The z-tracking technique has held particular importance in performing paracentesis. A z-track is a technique that allows for decreased ascitic fluid leak following the paracentesis by displacing the needle tracks with respect to the  epidermis  and the  peritoneum . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7529", "text": "The  serum-ascites albumin gradient  can help determine the cause of the ascites. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7530", "text": "The color of the ascitic fluid can also be useful in analysis. Blood fluid can indicate trauma or  malignancy . A milky appearance of the fluid can indicate  lymphoma  or malignant peritoneal ascites. Cloudy or turbid fluid can indicate possible infection or inflammation within the peritoneal cavity. Straw or light yellow colored fluid indicates more plasma-like and benign causes of peritoneal ascites. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7531", "text": "The ascitic white blood cell count can help determine if the ascites is infected. A count of 250 neutrophils per ml or higher is considered diagnostic for spontaneous bacterial peritonitis. Cultures of the fluid can be taken, but the yield is approximately 40% (72\u201390% if  blood culture  bottles are used). Empiric antibiotics are typically started when  spontaneous bacterial peritonitis  is highly suspected. A third-generation cephalosporin is typically started in these cases to cover the most common organisms,  E. coli  and  Klebsiella , in SBP. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7532", "text": "Mild hematologic abnormalities do not increase the risk of bleeding. [ 12 ] [ 7 ]  The risk of bleeding may be increased if: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7533", "text": "Absolute contraindication is the acute abdomen that requires surgery."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7534", "text": "Relative contraindications are: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7535", "text": "Pediatric end-stage liver disease  ( PELD ) is a disease severity scoring system for children under 12 years of age. [ 1 ]  It is calculated from the patient's  albumin ,  bilirubin , and  international normalized ratio  (INR) together with the patient's age and degree of  growth failure . This score is also used by the  United Network for Organ Sharing  (UNOS) for prioritizing allocation of  liver transplants ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7536", "text": "PELD uses the patient's values for serum  bilirubin , serum  albumin , the  international normalized ratio for prothrombin time (INR) , whether the patient is less than 1 year old, and whether the patient has growth failure (<-2 standard deviation) to predict survival. It is calculated according to the following formula: [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7537", "text": "The PELD score calculated for any given patient is correlated to their prognosis and how likely they are to die within a certain time period. [ 3 ]  A higher score correlates with a more critical condition. Thus, liver donations are usually allocated by UNOS according to the PELD score to maximize the life-saving capability of each donated liver. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7538", "text": "Peritoneal dialysis  ( PD ) is a type of  dialysis  that uses the  peritoneum  in a person's  abdomen  as the membrane through which fluid and dissolved substances are exchanged with the  blood . [ 1 ] [ 2 ]  It is used to remove excess fluid, correct  electrolyte problems , and remove toxins in those with  kidney failure . [ 3 ]  Peritoneal dialysis has better outcomes than  hemodialysis  during the first two years. [ 4 ]  Other benefits include greater flexibility and better tolerability in those with significant  heart disease . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7539", "text": "Complications may include  infections within the abdomen ,  hernias ,  high blood sugar , bleeding in the abdomen, and blockage of the catheter. [ 3 ]  Peritoneal dialysis is not possible in those with significant prior  abdominal surgery  or  inflammatory bowel disease . [ 3 ]  It requires some degree of technical skill to be done properly. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7540", "text": "In peritoneal dialysis, a specific solution is introduced through a permanent tube in the lower abdomen and then removed. [ 3 ]  This may either occur at regular intervals throughout the day, known as continuous ambulatory peritoneal dialysis (CAPD), or at night with the assistance of a machine, known as automated peritoneal dialysis (APD) [ 3 ]  or continuous cycling peritoneal dialysis (CCPD). [ 5 ]  The solution is typically made of  sodium chloride ,  bicarbonate , and an  osmotic agent  such as  glucose . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7541", "text": "The solution used for peritoneal dialysis is on the  World Health Organization's List of Essential Medicines . [ 6 ] [ 7 ]  As of 2009, peritoneal dialysis was available in 12 of 53 African countries. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7542", "text": "Peritoneal dialysis is a method of  renal replacement therapy  for those needing maintenance therapy for late stage  chronic kidney disease  and is an alternative to the most common method  hemodialysis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7543", "text": "A common cause of  peritonitis  is touch contamination, e.g. insertion of catheter by un-sanitized hands, which potentially introduces bacteria to the abdomen; other causes include catheter complication, transplantation of bowel bacteria, and systemic infections. [ 9 ]  Most common type of PD-peritonitis infection (80%) are from bacterial sources. [ 9 ]  Infection rates are highly variable by region and within centers with estimated rates between 0.06 - 1.66 episodes per patient year. [ 10 ]  With recent technical advances peritonitis incidence has decreased over time. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7544", "text": "Antibiotics are needed if the source of infection is bacterial; there is no clear advantage for other frequently used treatments such as routine peritoneal lavage or use of  urokinase . [ 12 ]  The use of preventative nasal  mupirocin  is of unclear effect with respect to peritonitis. [ 13 ]  Of the three types of connection and fluid exchange systems (standard, twin-bag and y-set; the latter two involving two bags and only one connection to the catheter, the y-set uses a single y-shaped connection between the bags involving emptying, flushing out then filling the peritoneum through the same connection) the twin-bag and y-set systems were found superior to conventional systems at preventing peritonitis. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7545", "text": "The fluid used for dialysis uses  glucose  as a primary osmotic agent. According to a 2020 review published in the  American Journal of Nephrology , some studies suggest that the use of glucose increases the risk of  peritonitis , possibly as a result of impaired host defenses, vascular disease, or damage to the peritoneal membrane. [ 15 ]  The  acidity , high concentration and presence of  lactate  and products of the degradation of glucose in the solution (particularly the latter) may contribute to these health issues [ ambiguous ] .  Solutions that are  neutral , use  bicarbonate  instead of lactate and have few glucose degradation products may offer more health benefits though this has not yet been studied. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7546", "text": "The mortality rate of peritoneal dialysis related peritonitis is estimated to be 3-10%, with approximately 50% of cases resulting in hospitalization. [ 17 ]  Peritoneal fluid studies with a white blood cell count greater than 100 per \u03bcL and greater than 50% neutrophils strongly suggest peritonitis, with a definitive diagnosis based on culture of microorganisms from the peritoneal fluid. [ 17 ]  In order to avoid delaying treatment, a cloudy fluid in the dialysate fluid can be assumed to be due to peritonitis unless an alternative cause is identified. [ 17 ]  Peritonitis in those undergoing PD is usually due to  gram positive bacteria . [ 17 ]  Intraperitoneal antibiotics are preferred to  intravenous  as they have a greater effect at the area of infection, unless  sepsis  is present, in which case intravenous antibiotics are indicated. [ 17 ]  The peritoneal dialysis catheter may have to be removed if the infection does not resolve with antibiotics, and it is recommended that the PD catheter be removed in all cases of fungal peritonitis. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7547", "text": "The volume of dialysate removed as well as patient's weight are monitored. If more than 500ml of fluid are retained or a liter of fluid is lost across three consecutive treatments, the patient's physician is generally notified. [ citation needed ]   Excessive loss of fluid can result in  hypovolemic shock  or  hypotension  while excessive fluid retention can result in  hypertension  and  edema .  Also monitored is the color of the fluid removed:  normally it is pink-tinged for the initial four cycles and clear or pale yellow afterward.  The presence of pink or bloody effluent suggests bleeding inside the abdomen while feces indicates a  perforated bowel  and cloudy fluid suggests infection.  The patient may also experience pain or discomfort if the dialysate is too acidic, too cold or introduced too quickly, while diffuse pain with cloudy discharge may indicate an infection.  Severe pain in the  rectum  or  perineum  can be the result of an improperly placed catheter.  The dwell can also increase pressure on the  diaphragm  causing impaired breathing, and  constipation  can interfere with the ability of fluid to flow through the catheter. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7548", "text": "Long term use of PD is rarely associated with fibrosis of the peritoneum. [ 11 ]  A potentially fatal complication estimated to occur in roughly 2.5% of patients is  encapsulating peritoneal sclerosis , in which the bowels become obstructed due to the growth of a thick layer of  fibrin  within the peritoneum. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7549", "text": "Other complications include  low back pain  and  hernia  or leaking fluid due to high pressure within the abdomen. [ 20 ]   Hypertriglyceridemia  and  obesity  are also concerns due to the large volume of glucose in the fluid, which can add 500-1200  calories  to the diet per day. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7550", "text": "Best practices for peritoneal dialysis state that before peritoneal dialysis should be implemented, the person's understanding of the process and support systems should be assessed, with education on how to care for the catheter and to address any gaps in understanding that may exist.  The person should receive ongoing monitoring to ensure adequate dialysis, and be regularly assessed for complications. Finally, they should be educated on the importance of infection control and an appropriate medical regimen established with their cooperation. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7551", "text": "The abdomen is cleaned in preparation for surgery and a  catheter  is surgically inserted with one end in the abdomen and the other protruding from the skin. [ 23 ]  Catheters can also be inserted without a general anaesthetic by a physician using a needle, known as a medical insertion. Both methods have similar safety profiles. [ 24 ] [ 25 ]  Before each infusion the catheter must be cleaned, and flow into and out of the abdomen tested.  2-3 liters of dialysis fluid is introduced into the abdomen over the next ten to fifteen minutes. [ 18 ]   The total volume is referred to as a  dwell [ 26 ]  while the fluid itself is referred to as dialysate.  The dwell can be as much as 3 liters, and medication can also be added to the fluid immediately before infusion. [ 18 ]  The dwell remains in the abdomen and waste products diffuse across the peritoneum from the underlying blood vessels.  After a variable period of time depending on the treatment (usually 4\u20136 hours [ 18 ]  ), the fluid is removed and replaced with fresh fluid.  This can occur automatically while the patient is sleeping (automated peritoneal dialysis, APD), or during the day by keeping two litres of fluid in the abdomen at all times, exchanging the fluids four to six times per day (continuous ambulatory peritoneal dialysis, CAPD). [ 26 ] [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7552", "text": "The fluid used typically contains  sodium chloride ,  lactate  or  bicarbonate  and a high percentage of  glucose  to ensure  hyperosmolarity .  The amount of dialysis that occurs depends on the volume of the dwell, the regularity of the exchange and the concentration of the fluid. APD cycles between 3 and 10 dwells per night, while CAPD involves four dwells per day of 2-3 liters per dwell, with each remaining in the abdomen for 4\u20138 hours.  The viscera accounts for roughly four-fifths of the total surface area of the membrane, but the parietal peritoneum is the most important of the two portions for PD.  Two complementary models explain dialysis across the membrane - the three-pore model (in which molecules are exchanged across membranes which sieve molecules, either  proteins , electrolytes or water, based on the size of the pores) and the distributed model (which emphasizes the role of  capillaries  and the solution's ability to increase the number of active capillaries involved in PD).  The high concentration of glucose drives the filtration of fluid by osmosis (osmotic UF) from the peritoneal capillaries to the peritoneal cavity. Glucose diffuses rather rapidly from the dialysate to the blood (capillaries). After 4-6 h of the dwell, the glucose osmotic gradient usually becomes too low to allow for further osmotic UF. Therefore, the dialysate will now be reabsorbed from the peritoneal cavity to the capillaries by means of the plasma colloid osmotic pressure, which exceeds the colloid osmotic pressure in the peritoneum by approximately 18-20 mmHg (cf. the Starling mechanism). [ 28 ]  Lymphatic absorption will also to some extent contribute to the reabsorption of fluid from the peritoneal cavity to the plasma. Patients with a high water permeability (UF-coefficient) of the peritoneal membrane can have an increased reabsorption rate of fluid from the peritoneum by the end of the dwell. The ability to exchange small solutes and fluid in-between the peritoneum and the plasma can be classified as high (fast), low (slow) or intermediate.  High transporters tend to diffuse substances well (easily exchanging small molecules between blood and the dialysis fluid, with somewhat improved results with frequent, short-duration dwells such as with APD), while low transporters have a higher UF (due to the slower reabsorption of glucose from the peritoneal cavity, which results in somewhat better results with long-term, high-volume dwells), though in practice either type of transporter can generally be managed through the appropriate use of either APD or CAPD. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7553", "text": "Though there are several different shapes and sizes of catheters that can be used, different insertion sites, number of cuffs in the catheter and immobilization, there is no evidence to show any advantages in terms of morbidity, mortality or number of infections, though the quality of information is not yet sufficient to allow for firm conclusions. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7554", "text": "A  peritoneal equilibration test  may be done to assess a person for peritoneal dialysis by determining the characteristics of the peritoneal membrane mass transport characteristics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7555", "text": "Peritoneal dialysis can be improvised in conditions such as combat surgery or disaster relief using surgical catheters and dialysate made from routinely available medical solutions to provide temporary renal replacement for people with no other options. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7556", "text": "As of 2017, hemodialysis is the most widely available renal replacement modality found in 96% of countries whereas peritoneal dialysis (PD) is only available in 75% of countries. [ 11 ]  In 2016, the proportion of people receiving peritoneal dialysis (PD) was estimated at 11% with wide differences between different countries and regions. [ 32 ]  In Hong Kong and  Mexico , PD is more common than the world average, with Mexico conducting most of its dialysis through PD, while  Japan  and  Germany  have rates lower than the world average. [ 33 ]  Peritoneal dialysis first models, patients requiring renal replacement therapy are placed on PD first, and financial incentives for using PD are associated with increase uptake of PD in multiple countries. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7557", "text": "Hong Kong has the highest rate of PD use worldwide at 71.9% in 2014, while in Mainland China had 20% in 2014, 23% in Thailand during 2012, and 10-20% in Vietnam during 2011. [ 32 ]  Hong Kong had a PD-first model since 1985, Thailand began a PD-first model since 2008 which increased their levels of PD from <10%. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7558", "text": "Prevalence in of PD use was 9.7% in USA during 2013 and 16.3% in Canada during 2013. [ 32 ]  The lower PD rates in the USA are due to higher availability of large corporate owned hemodialysis centers. There have been recent increase in PD uptake in the USA due to changes to medicare reimbursement such as  bundled payment  for dialysis this incentivizes use of PD which is a less costly modality for dialysis. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7559", "text": "Overall, prevalence of PD use is 24.6% in Latin America during 2011. [ 32 ]  Within Latin America, hemodialysis has a higher growth rate in use compared to PD between 1994 - 2010. In 2010, the most prevalent use of PD were in Mexico 55.9% and El Salvador 67.6%. Between 2000 - 2010, Colombia's PD rate dropped from 54% to 31.3%. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7560", "text": "Peritoneal dialysis was first carried out in the 1920s; however, long-term use did not come into medical practice until the 1960s. [ 35 ]  The timeline was"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7561", "text": "Compared to hemodialysis, PD allows greater patient mobility, produces fewer swings in symptoms due to its continuous nature, and  phosphate  compounds are better removed, but large amounts of  albumin  are removed which requires constant monitoring of nutritional status. [ 11 ]   The costs of PD are generally lower than those of HD in most parts of the world, this cost advantage is most apparent in developed economies. [ 42 ]  There is insufficient research to adequately compare the risks and benefits between CAPD and APD; a  Cochrane Review  of three small  clinical trials  found no difference in clinically important outcomes (i.e.  morbidity  or  mortality ) for patients with  end stage renal disease , nor was there any advantage in preserving the functionality of the kidneys.  The results suggested APD may have psychosocial advantages for younger patients and those who are employed or pursuing an education. [ 43 ] [ needs update ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7562", "text": "PD may also be used for patients with  cardiac instability  as it does not result in rapid and significant alterations to body fluids, and for patients with  insulin -dependent  diabetes mellitus  due to the inability to control  blood sugar  levels through the catheter."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7563", "text": "The cost of dialysis treatment is related to how wealthy the country is. [ 8 ]  In the United States peritoneal dialysis costs the government about $53,400 per person per year. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7564", "text": "Rapid urease test , also known as the  CLO test  (Campylobacter-like organism test), is a  rapid diagnostic test  for diagnosis of  Helicobacter pylori . [ 1 ]  The basis of the test is the ability of  H. pylori  to secrete the  urease  enzyme, which catalyzes the conversion of  urea  to  ammonia  and  carbon dioxide ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7565", "text": "The test is performed at the time of  gastroscopy . A  biopsy  of mucosa is taken from the  antrum  of the  stomach , and is placed into a medium containing urea and an indicator such as  phenol red . The urease produced by  H. pylori  hydrolyzes urea to ammonia, which raises the  pH  of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7566", "text": "Among different kinds of rapid urease tests (liquid-based, gel-based, dry cool) there is a design type with single-layer sensitive element \u2014 a layer impregnated simultaneously with urea and an indicator composition. Such a design bears the risk of false-positive result due to the pH value of the gastric biopsy when it is placed on the sensitive element. Excessive salivation and alkaline bile reflux into the stomach can shift the pH value of the biopsy of the stomach towards alkaline. Drugs that reduce the acidity of the stomach, also contribute to false positive results resulting from the alkalization. In each of these cases, the pH of the biopsy will be shifted to the alkaline side. All of these factors may trigger a non-targeted coloration of the sensitive element in a single-layer rapid urease test. The indicator would change color not in the course of the enzymatic reaction, which then causes alkalization of the medium as a result of ammonia formation, but under the effect of the pH of the gastric biopsy. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7567", "text": "Selective urease tests differ from the single-layer rapid urease tests by their design and higher sensitivity and specificity. [ 3 ]  In contrast to single-layer rapid urease tests, selective urease tests have several layers, enabling separate enzymatic and indicator reactions. The sample is placed on the first layer impregnated with urea. Ammonia formed during the hydrolysis of urea by urease penetrates through a special selective membrane to the layer impregnated with the indicator composition. [ 4 ]  Accordingly, the color change occurs directly during the enzymatic reaction. This avoids the influence of the pH value of the sample (gastric biopsy) on the result of a selective urease test, which virtually eliminates the occurrence of false-positive results. If the pH value of the sample is shifted to the acidic side, for example, in the case of increased acidity of gastric juice, this also does not distort the result of the selective urease test. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7568", "text": "There is evidence to suggest that  H. pylori  moves proximal in the stomach in patients on therapy with  proton pump inhibitors [ citation needed ] , and, as such, samples from the  fundus  and  body  should be taken in these patients."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7569", "text": "Active gastrointestinal bleeding reduces accuracy of the test. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7570", "text": "The specificity and sensitivity of this test is high compared with  urea breath test [ citation needed ] . The test is often done as part of point-of-care diagnostics, to eliminate the time and expense required to detect  H. pylori  on  pathology  testing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7571", "text": "Sialoendoscopy  is a  minimally invasive technique  that allows for  salivary gland   surgery  for the safe and effective treatment of  obstructive salivary gland disorders  and other conditions of the salivary glands.  During sialoendoscopy a small  endoscope  is placed into the salivary glands through the  salivary ducts  that empty into the  mouth . The procedure is not exclusively diagnostic, but is interventional; thus, it can be used for the extraction of salivary stones, salivary duct lavage, dilatation of stenotic segments, or instillation of various medications such as corticosteroids or antibiotics. [ 1 ]  Thus, sialoendoscopy is an efficient yet simple mode of treatment for major salivary gland obstructions, strictures and  sialoliths  (salivary stones).  Depending on the obstruction, sialoendoscopy can be conducted under  local anesthesia  in an  outpatient  office or in the  operating room  under  general anesthesia ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7572", "text": "Salivary gland  stones  are one of the major causes of salivary gland infections (sialadenitis). These types of stones can be found in 1.2 percent of the general population. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7573", "text": "The second leading cause of salivary obstruction is from strictures and adhesions, which can happen from prior salivary gland infections, including childhood  infections  like  mumps . Most strictures could be seen in the  parotid duct  and mostly in the disease process of chronic recurrent sialadenitis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7574", "text": "Generally, the salivary duct opening needs to be either  dilated  or incised prior to introduction of the  endoscope .  Once the sialoendoscope is in place,  saline  is utilized to dilate the salivary duct and its branching.  [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7575", "text": "Once the endoscopes are introduced into  gland , the internal anatomy is explored either for  diagnosis  or for treatment of a specific disease entity.  The endoscope is introduced into the gland through its natural  orifice  in the mouth or by making a small incision in the duct opening.  These techniques for introduction are completely intraoral techniques."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7576", "text": "In the case of  strictures  or  adhesions , the following technique can be used as a treatment  modality . First the surgeon will make their diagnosis and find the exact location of the obstruction using a  sialogram .  Following this, the surgeon can use the endoscopic method. The first step in this is anesthetizing and laving the duct with 2 percent  lidocaine  and saline. If there is no improvement, the surgeon then can insert a  dilation balloon , which can be inflated up to 3\u00a0mm. The pressure created by the inflation can be sufficient to dilate most strictures. Another technique for dilating strictures is to expand the stricture region with grasping  forceps  used as a dilator. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7577", "text": "The ability to perform this technique is the result of the development of miniaturized endoscopic imaging tools.  The majority of sialoendoscopes that are currently in use are of the semirigid type. The semirigid endoscope allows for visualization of the diseased process, but the stiffness allows manipulation and navigation of the internal salivary anatomy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7578", "text": "Multiple types of micro instrumentation are available, including grasping forceps, biopsy forceps,  drills ,  needles ,  laser  fibers, and  lithotripters  (although the last is currently unavailable in the US pending  U.S. Food and Drug Administration  approval).  Multiple companies make various types of sialoendoscopes and instrumentation.  There are advantages and disadvantages to all of the systems and none are recommended over the other [ citation needed ] .  Different practitioners utilize different systems due to the experience and clinical training of the surgeon."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7579", "text": "Sleeve gastrectomy  or  vertical sleeve gastrectomy , is a  surgical weight-loss procedure , typically performed  laparoscopically , in which approximately 75 - 85% of the stomach is removed, [ 1 ] [ 2 ]  along the  greater curvature , [ 3 ]  which leaves a cylindrical, or \"sleeve\"-shaped stomach the size of a banana. [ 1 ] [ 2 ]  Weight loss is affected not only through the reduction of the organ's size, but by the removal of the portion of it that produces  ghrelin , the hormone that stimulates appetite. Patients can lose 50-70 percent of excess weight over the course of the two years that follow the surgery. [ 2 ]  The procedure is irreversible, [ 4 ]  though in some uncommon cases, patients can regain the lost weight, via resumption of poor dietary habits, or dilation of the stomach over time, which can require gastric sleeve revision surgery to either repair the sleeve or convert it to another type of weight loss method that may produce better results, such as a  gastric bypass  or  duodenal switch . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7580", "text": "A meta-analysis of 174,772 participants published in  The Lancet  in 2021 found that  bariatric surgery  was associated with 59% and 30% reduction in all-cause mortality among  obese  adults with and without  type 2 diabetes , respectively. This meta-analysis also found that median life-expectancy was 9.3 years longer for obese adults with diabetes who received bariatric surgery as compared to routine (non-surgical) care, whereas the life expectancy gain was 5.1 years longer for obese adults without diabetes. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7581", "text": "Sleeve gastrectomy was originally performed as a modification to another  bariatric  procedure, the  duodenal switch , and then later as the first part of a two-stage  gastric bypass  operation on extremely  obese  patients for whom the risk of performing gastric bypass surgery was deemed too large. The initial weight loss in these patients was so successful it began to be investigated as a stand-alone procedure. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7582", "text": "Sleeve gastrectomy is the most commonly performed bariatric surgery worldwide. [ 8 ] [ 9 ]  In many cases, sleeve gastrectomy is as effective as gastric bypass surgery, including improvements in glucose homeostasis before substantial weight loss has occurred. This weight-loss independent benefit is related to the decrease in gastric volume, changes in gut peptides, and expression of  genes involved in glucose absorption . [ 10 ] [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7583", "text": "The procedure involves a longitudinal resection of the stomach starting from the antrum at the point 5\u20136\u00a0cm from the pylorus and finishing at the fundus close to the cardia. [ 12 ]  The remaining gastric sleeve is calibrated with a  bougie . Most surgeons prefer to use a bougie between 36 and 40  Fr  with the procedure and the ideal approximate remaining size of the stomach after the procedure is about 150 mL. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7584", "text": "Endorsed by the International Federation for the Surgery of Obesity and Metabolic Disorders [ 14 ]  and the  American Society for Metabolic and Bariatric Surgery , [ 15 ]  sleeve gastrectomy is gaining popularity in children and adolescents. Studies by Alqahtani and colleagues have found that sleeve gastrectomy causes large weight loss in children and adolescents aged 5 to 21 years. [ 16 ]  Moreover, they compared weight loss with adults and found comparable weight loss. [ 17 ]  A study published in 2016 showed that growth progresses were unaffected after sleeve gastrectomy in children younger than 14 years of age. [ 18 ]   Depression  following the procedure has been noted in some individuals. Another side effect is  insomnia . After this surgery many people can only sleep when they take  melatonin  or sleeping medications. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7585", "text": "Sleeve gastrectomy may cause complications; some of them are listed below:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7586", "text": "Micsorare stomac/ gastric sleeve  - info related"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7587", "text": "Stretta  is a minimally invasive  endoscopic  procedure for the treatment of  gastroesophageal reflux disease  (GERD) that delivers  radiofrequency energy  in the form of  electromagnetic waves  through electrodes at the end of a  catheter  to the  lower esophageal sphincter  (LES) and the  gastric cardia  \u2013 the region of the stomach just below the LES. The energy heats the tissue, ultimately causing it to swell and stiffen; the way this works was not understood as of 2015, but it was thought that perhaps the heat causes local inflammation, collagen deposition and muscular thickening of the LES and that it may  disrupt the nerves  there. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7588", "text": "Its relative efficacy is controversial, with the  American College of Gastroenterology  recommending against its use in 2013, and in the same year the  Society of American Gastrointestinal and Endoscopic Surgeons  (SAGES) giving it a strong recommendation for people who refuse laparoscopic  Nissen fundoplication , which involves making incisions in the torso and wrapping part of the stomach around the base of the esophagus, and which is considered the gold standard for efficacy. [ 2 ] [ 3 ] [ 4 ]  In 2015 an  American Society for Gastrointestinal Endoscopy  guideline noted that the quality of evidence was low for Stretta and the other available endoscopic treatment for GERD ( transoral incisionless fundoplication ) and called for better research to be conducted; it suggested that endoscopic treatments for GERD be considered. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7589", "text": "The device for carrying out the procedure was originally developed by a company called Curon which obtained FDA approval for the device in 2000 but then went bankrupt in 2006; the device was brought back to market by Mederi Therapeutics in 2010. [ 2 ] [ 6 ]  The procedure costs between $3,000 and $4,000 as of 2004. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7590", "text": "An American Society of Gastrointestinal Endoscopy (ASGE) statement in June 2015 state that endoscopic antireflux therapy is a potential treatment based on the 2012 review. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7591", "text": "In 2015 three reviews were published discussing the relative safety and effectiveness of the procedure compared with other endoscopic procedures delivered through the mouth, drug treatment (generally  proton-pump inhibitors ), and fundoplication. [ 1 ] [ 2 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7592", "text": "One was a systematic review and meta-analysis of clinical trials conducted with Stretta, done in response to the 2013 SAGES review (which did not include meta-analysis). [ 2 ]  This review found that quality of studies that had been conducted was generally poor, and that compared with sham therapy (used a placebo for medical device clinical trials), the procedure did not change time spent at a pH less than 4, did not increase lower esophageal sphincter pressure (LESP), did not allow people to stop treatment with proton-pump inhibitors, and did not improve health-related quality of life. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7593", "text": "Another of the 2015 reviews was a narrative  literature review , noted its long history of use, and found the procedure safe and effective, and noted that the procedure complemented drug treatment and fundoplication, providing a useful option. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7594", "text": "The other 2015 review was a narrative literature review was more tentative, noting the long safety record but only willing to state that the procedure \"may be effective in reducing symptom burden and quality of life scores up to 8 years post-intervention. However, there does not appear to be any sustained improvement in objective outcomes and there is no evidence that Stretta results in improved outcomes as compared to surgical intervention. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7595", "text": "A more recent study published in 2020 [ 9 ]  evaluated 25 patients post Stretta Procedure  and the results concluded significant improvement in reflux symptoms and quality of life, lowering Heartburn Score (DeMeester score) [ 10 ]  from 3.7 in women and 4.0 in men to 1.6\u00b11 (p = 0.05) in women and 1.68\u00b11.19 (p = 0.05) in men."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7596", "text": "A 2012 systematic review and meta-analysis upon which the 2013 SAGES review had relied, had found that it improves GERD symptoms. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7597", "text": "Therapeutic endoscopy  is the medical term for an endoscopic procedure during which treatment is carried out via the endoscope. This contrasts with  diagnostic endoscopy , where the aim of the procedure is purely to visualize a part of the  gastrointestinal ,  respiratory  or  urinary tract  in order to aid  diagnosis . In practice, a procedure which starts as a diagnostic endoscopy may become a therapeutic endoscopy depending on the findings, such as in cases of upper  gastrointestinal bleeding , or the finding of  polyps  during  colonoscopy ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7598", "text": "A number of different techniques have been developed to allow treatment to be carried out endoscopically, to treat disorders such as  bleeding ,  strictures  and polyps."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7599", "text": "Endoscopic injection of bleeding peptic ulcers with  adrenaline  has been practised since the 1970s, [ 1 ]  endoscopic heater probes have been used since the 1980s, [ 2 ]  and  Argon plasma coagulation  has been used since the 1990s. More recently, adrenaline injection tends to be combined with either heater probe coagulation or argon plasma coagulation to minimize the chance of an ulcer rebleeding. The disadvantage of this treatment is a low risk of  perforation  of the gastric wall and a low risk of peritonitis. [ 3 ]  Combined therapy may work better than epinephrine alone. However, there is no evidence that one kind of treatment is more effective than the other. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7600", "text": "Injection  sclerotherapy  has been used to treat  oesophageal varices  since the 1960s. [ 4 ]  A sheathed needle is passed through a channel in the endoscope, unsheathed and pushed into a varix. A sclerosing agent, such as  ethanolamine  or  absolute alcohol , is then injected into the varix to cause scarring and constriction of the varix with the aim of obliterating the varix (or varices). This technique has now largely been superseded by variceal band ligation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7601", "text": "Sclerotherapy has also been used in the treatment of gastric varices since the late 1980s. [ 5 ]  In this case Histoacryl glue ( cyanoacrylate ) is commonly used as the sclerosant. [ 6 ]  This technique is favoured over band ligation because the position of the varices in the stomach, most often in the gastric  fundus , makes the placing of bands very difficult."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7602", "text": "Argon plasma coagulation (APC) has been used to provide tissue coagulation and haemostasis since the early part of the 1990s. [ 7 ]  A stream of argon gas is passed through an endoscopic catheter; this is then ionized at the tip of the catheter by an electric current. The tip of the catheter is held close to the tissue to be treated, and the current arcs across to the tissue causing a superficial (2\u20133 mm) burn. The lack of contact between the catheter and the tissue stops the tendency of the catheter to stick to the tissue, reducing unwanted tissue damage. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7603", "text": "Its principal use is in providing haemostasis in gastrointestinal bleeding;  angiodysplasia ,  GAVE , [ 9 ]  bleeding  malignant tumours  and bleeding  peptic ulcers  can all be treated. Trials have also been carried out to assess its use in eradicating Barrett\u2019s oesophagus, but have found that relapse is common. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7604", "text": "Dilatation of  benign oesophageal strictures  using semi-rigid bougies existed long before the advent of flexible endoscopes. [ 11 ]  Since that time oesophageal dilatation has been carried out using either bougies or endoscopic balloons, and can be used to treat benign oesophageal strictures and  achalasia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7605", "text": "Initially, bougies were used to dilate benign strictures of the oesophagus. These could be passed alongside the endoscope, allowing visualisation of the bougie passing through the stricture, [ 12 ]  but the technique of passing a guidewire through the stricture endoscopically, then removing the endoscope and passing the bougie over the guidewire was more commonly used. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7606", "text": "More recently, balloon dilatation of the oesophageal strictures has become more common. It is thought that this technique carries a lower complication rate than the use of bougies, and since endoscopy balloons are single use items there are no concerns about equipment sterilization. [ 11 ]  In addition to oesophageal dilatation, endoscopic balloons can also be used to dilate pyloric strictures. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7607", "text": "Endoscopic polypectomy has been carried out since the early 1970s by both endoscopic snare removal and fulguration of polyps with hot biopsy forceps. [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7608", "text": "Oesophageal varices have been treated by band ligation since the late 1980s. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7609", "text": "Expandable mesh stents can be deployed in the oesophagus at endoscopy, primarily in patients with inoperable oesophageal cancer which is causing  dysphagia . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7610", "text": "Plastic stents can also be used to relieve obstruction of the  common bile duct  at  ERCP . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7611", "text": "A method for inserting a feeding gastrostomy tube without the need for surgery was first described in 1980. [ 20 ]   This endoscopic technique is of particular use as many patients who require feeding tubes (such as after patients with swallowing difficulties after a  stroke ) are at high risk for complications from  anaesthesia  and  surgery ; the endoscopic technique usually requires mild sedation only. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7612", "text": "Foreign bodies commonly impact in the lower oesophagus, and removal of these by pushing them into the stomach has been practised since the Middle Ages. [ 11 ]  Foreign body retrieval, using forceps and magnets, has been practised since the time of rigid oesophagoscopy and  bronchoscopy . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7613", "text": "A number of techniques are being developed for the endoscopic treatment of  gastro-oesophageal reflux disease  as an alternative to laparoscopic  Nissen fundoplication . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7614", "text": "Endoscopic circumferential radiofrequency ablation is being developed in an effort to obviate long-term endoscopic surveillance in patients with Barrett's oesophagus, and to reduce the risk of development of oesophageal carcinoma. Previous techniques, such as Argon plasma coagulation, have been unsuccessful because of incomplete removal of the Barrett's mucosa and therefore relapse of part of the treated area. [ 10 ]  Newer techniques using circumferential radiofrequency ablation, which allows larger areas of the oesophagus to be treated at one time giving a more uniform area of treatment, are showing more promising short-term results. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7615", "text": "Early trials are under way to evaluate an endoscopic technique for gastric stapling, a type of  bariatric surgery , which aims to induce long-term weight loss in  morbidly obese  patients. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7616", "text": "Transoral incisionless fundoplication  ( TIF ) is an endoscope treatment designed to relieve symptoms of  gastroesophageal reflux disease  (GERD). The TIF procedure, similar to  Nissen fundoplication , alleviates GERD symptoms by wrapping a portion of the stomach around the esophagus. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7617", "text": "The TIF procedure, unlike laparoscopic fundoplication, does not require surgical incisions. Instead a surgical device (called the EsophyX) is inserted into the mouth, passed through the throat, and into the stomach. An  endoscope  is utilized to perform the procedure. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7618", "text": "A minority of individuals who undergo the TIF procedure also require a  hiatal hernia  repair operation. [ 3 ]  The procedure is performed while the person is under general anesthesia [ 4 ]  and is typically an outpatient procedure. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7619", "text": "Transoral incisionless fundoplication may improve symptoms in  gastroesophageal reflux disease , at least in the short term. [ 5 ]   Benefits from the TIF procedure may last for up to 6 years. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7620", "text": "The risk of severe complications is 2.4%. [ 7 ]  About 1 in 30 people have major complications from the procedure. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7621", "text": "The device utilized to perform the procedure, called EsophyX, was developed by EndoGastric Solutions. The first TIF procedure utilizing the device was performed in 2005. [ 8 ]   The device received European Union CE mark in 2006 and United States Food and Drug Administration issued initial 510(k) clearance in 2007. [ 2 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7622", "text": "In February 2015, the  American Medical Association 's CPT Editorial Panel reviewed whether to create a new category 1  current procedural terminology  (CPT) code for the TIF procedure. In January 2016, a unique code for the transoral incisionless fundoplication procedure was created and implemented. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7623", "text": "As of 2016, more than 17,000 TIF procedures had been performed. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7624", "text": "In July 2016,  Health Care Service Corporation  (HCSC) became the first United States health insurance company to add the TIF procedure to their medical coverage policy. HSCS added the TIF procedure to their health insurance policy at the recommendation of both the  American Gastroenterological Association  (AGA) and  The Society of American Gastrointestinal and Endoscopic Surgeons  (SAGES). [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7625", "text": "The TIF procedure is not the ideal GERD solution for all people. Other medical and endoscopic treatments to alleviate GERD symptoms include:  Stretta procedure [ 12 ]  and  proton-pump inhibitors (PPIs) . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7626", "text": "The  United Kingdom Model for End-Stage Liver Disease  or  UKELD  is a  medical  scoring system used to predict the prognosis of patients with  chronic liver disease . It is used in the  United Kingdom  to help determine the need for  liver transplantation . [ 1 ]  It was developed from the  MELD  score, incorporating the  serum sodium  level. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7627", "text": "The UKELD score is calculated from the patient's  INR , serum  creatinine , serum  bilirubin  and serum sodium, according to the formula: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7628", "text": "( \n 5.395 \n \u00d7 \n ln \n \u2061 \n I \n N \n R \n ) \n + \n ( \n 1.485 \n \u00d7 \n ln \n \u2061 \n c \n r \n e \n a \n t \n i \n n \n i \n n \n e \n ) \n + \n ( \n 3.13 \n \u00d7 \n ln \n \u2061 \n b \n i \n l \n i \n r \n u \n b \n i \n n \n ) \n \u2212 \n ( \n 81.565 \n \u00d7 \n ln \n \u2061 \n N \n a \n ) \n + \n 435 \n \n \n {\\displaystyle (5.395\\times \\ln INR)+(1.485\\times \\ln creatinine)+(3.13\\times \\ln bilirubin)-(81.565\\times \\ln Na)+435}"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7629", "text": "Higher UKELD scores equate to higher one-year mortality risk. A UKELD score of 49 indicates a 9% one-year risk of mortality, and is the minimum score required to be added to the liver transplant waiting list in the U.K. [ 1 ]  A UKELD score of 60 indicates a 50% chance of one-year survival. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7630", "text": "The UKELD score was developed in 2008 to aid in the selection of patients for liver transplantation in the U.K. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7631", "text": "The  urea breath test  is a rapid  diagnostic  procedure used to identify  infections  by  Helicobacter pylori , a spiral  bacterium  implicated in  gastritis ,  gastric ulcer , and  peptic ulcer  disease. It is based upon the ability of  H. pylori  to convert  urea  to ammonia and carbon dioxide. Urea breath tests are recommended in leading society guidelines as a preferred non-invasive choice for detecting  H. pylori   before and after treatment. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7632", "text": "Patients swallow  urea  labelled with an uncommon  isotope , either  radioactive   carbon-14  (nowadays preferred in many countries) or non-radioactive  carbon-13 . In the subsequent 10\u201330 minutes, the detection of isotope-labelled  carbon dioxide  in exhaled breath indicates that the urea was split; this indicates that  urease  (the  enzyme  that   H. pylori  uses to  metabolize  urea to produce  ammonia ) is present in the  stomach , and hence that   H. pylori  bacteria are present."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7633", "text": "For the two different forms of urea, different instrumentation is required. Carbon-14 is normally measured by  scintillation , whereas carbon-13 can be detected by  isotope ratio mass spectrometry  or simpler by  nondispersive infrared (NDIR) spectrometry . For each of these methods, a baseline breath sample is required before taking the isotope-labeled urea, for comparison with the post-urea sample, with a 15- to 30-minute duration between them. Samples may be sent to a reference laboratory for analysis. Alternatively, NDIR spectrometry can be performed by a table-top instrument as an office-based test, and results are provided immediately within minutes. [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7634", "text": "The difference between the pre- and post urea measurements is used to determine infection. This value is compared to a cut-off value. Results below the value are assumed to be negative, those above positive. The cut-off value itself is determined by comparing the results of patients with two or more different detection methods. The value is chosen that gives the best combination of  sensitivity  and  specificity . Both carbon-14 and carbon-13 urea breath tests have high sensitivity and specificity, though the carbon-13 test is preferred in certain populations due to its non-radioactive nature. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7635", "text": "The test measures active  H. pylori  infection. If antibiotics are depressing the amount of  H. pylori  present, or the stomach conditions are less acidic than normal, the amount of urease present will be lessened."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7636", "text": "Accordingly, the test should only be performed 14 days after stopping acid reducing medication ( proton pump inhibitors , PPI) or 28 days after stopping antibiotic treatment. Some clinicians believe that a reservoir of  H. pylori  in dental plaque can affect the result. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7637", "text": "The test is especially done accompanying an eradication therapy by antibiotics (to avoid overdosing) or to check the success of an ulcer operation. In both cases, immunological tests can give false positive results. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7638", "text": "Helicobacter pylori , previously known as  Campylobacter pylori , is a  gram-negative ,  flagellated ,  helical bacterium . Mutants can have a rod or curved rod shape that exhibits less  virulence . [ 1 ] [ 2 ]  Its  helical  body (from which the  genus  name  Helicobacter  derives) is thought to have evolved to penetrate the  mucous lining  of the  stomach , helped by its  flagella , and thereby establish infection. [ 3 ] [ 2 ]  The bacterium was first identified as the causal agent of  gastric ulcers  in 1983 by Australian  physician-scientists   Barry Marshall  and  Robin Warren . [ 4 ] [ 5 ]  In 2005, they were awarded the  Nobel Prize in Physiology or Medicine  for their discovery. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7639", "text": "Infection of the stomach with  H. pylori  is not the cause of illness itself: over half of the global population is infected, but most individuals are asymptomatic. [ 7 ] [ 8 ]  Persistent  colonization  with more virulent strains can induce a number of gastric and non-gastric disorders. [ 9 ]  Gastric disorders due to infection begin with  gastritis , or inflammation of the stomach lining. [ 10 ]  When infection is persistent, the prolonged inflammation will become  chronic gastritis . Initially, this will be non-atrophic gastritis, but the damage caused to the stomach lining can bring about the development of  atrophic gastritis  and ulcers within the stomach itself or the  duodenum  (the nearest part of the intestine). [ 10 ]  At this stage, the risk of developing  gastric cancer  is high. [ 11 ]  However, the development of a  duodenal ulcer  confers a comparatively lower risk of cancer. [ 12 ]   Helicobacter pylori  are  class 1 carcinogenic bacteria , and potential cancers include gastric  MALT lymphoma  and  gastric cancer . [ 10 ] [ 11 ]  Infection with  H. pylori  is responsible for an estimated 89% of all gastric cancers and is linked to the development of 5.5% of all cases cancers worldwide. [ 13 ] [ 14 ]   H. pylori  is the only bacterium known to cause cancer. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7640", "text": "Extragastric complications that have been linked to  H. pylori  include  anemia  due either to iron deficiency or  vitamin B12 deficiency ,  diabetes mellitus , cardiovascular illness, and certain neurological disorders. [ 16 ]  An inverse association has also been claimed with  H. pylori  having a positive protective effect against  asthma ,  esophageal cancer ,  inflammatory bowel disease  (including  gastroesophageal reflux disease  and  Crohn's disease ), and others. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7641", "text": "Some studies suggest that  H. pylori  plays an important role in the natural stomach ecology by influencing the type of bacteria that colonize the gastrointestinal tract. [ 17 ] [ 18 ]  Other studies suggest that non-pathogenic strains of  H. pylori  may beneficially normalize stomach acid secretion, and regulate appetite. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7642", "text": "In 2023, it was estimated that about two-thirds of the world's population was infected with  H. pylori , being more common in  developing countries . [ 20 ]  The prevalence has declined in many countries due to  eradication treatments  with antibiotics and  proton-pump inhibitors , and with increased  standards of living . [ 21 ] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7643", "text": "Helicobacter pylori  is a species of  gram-negative bacteria  in the  Helicobacter  genus. [ 23 ] \nAbout half the world's population is infected with  H. pylori  but only a few strains are  pathogenic .  H pylori  is a  helical bacterium  having a predominantly  helical shape , also often described as having a spiral or  S  shape. [ 24 ] [ 25 ]  Its helical shape is better suited for progressing through the viscous  mucosa lining of the stomach , and is maintained by a number of  enzymes  in the  cell wall's   peptidoglycan . [ 1 ]  The bacteria reach the less acidic mucosa by use of their  flagella . [ 26 ]  Three strains studied showed a variation in length from 2.8\u20133.3\u00a0\u03bcm but a fairly constant diameter of 0.55\u20130.58\u00a0\u03bcm. [ 24 ]   H. pylori  can convert from a helical to an inactive  coccoid  form that can evade the immune system, and that may possibly become viable, known as  viable but nonculturable  (VBNC). [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7644", "text": "Helicobacter pylori  is  microaerophilic  \u2013 that is, it requires  oxygen , but at lower concentration than in the  atmosphere . It contains a  hydrogenase  that can produce energy by oxidizing molecular  hydrogen  (H 2 ) made by  intestinal bacteria . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7645", "text": "H.\u00a0pylori  can be demonstrated in tissue by  Gram stain ,  Giemsa stain ,  H&E stain ,  Warthin-Starry silver stain ,  acridine orange stain , and  phase-contrast microscopy . It is capable of forming  biofilms . Biofilms help to hinder the action of antibiotics and can contribute to treatment failure. [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7646", "text": "To successfully colonize its host,  H. pylori  uses many different  virulence factors  including  oxidase ,  catalase , and  urease . [ 32 ]  Urease is the most abundant protein, its expression representing about 10% of the total protein weight. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7647", "text": "H.\u00a0pylori  possesses five major  outer membrane protein  families. [ 32 ]  The largest family includes known and putative  adhesins . The other four families are  porins , iron transporters,  flagellum -associated proteins, and proteins of unknown function. Like other typical gram-negative bacteria, the outer membrane of  H.\u00a0pylori  consists of  phospholipids  and  lipopolysaccharide  (LPS). The  O-antigen  of LPS may be  fucosylated  and mimic  Lewis blood group antigens  found on the gastric epithelium. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7648", "text": "Helicobacter pylori  consists of a large diversity of strains, and hundreds of  genomes  have been completely  sequenced . [ 34 ] [ 35 ] [ 36 ]  The genome of the strain  26695  consists of about 1.7\u00a0million  base pairs , with some 1,576\u00a0genes. [ 37 ] [ 38 ]  The  pan-genome , that is the combined set of 30\u00a0sequenced strains, encodes 2,239\u00a0protein families ( orthologous groups  OGs). [ 39 ]  Among them, 1,248\u00a0OGs are conserved in all the 30\u00a0strains, and represent the  universal core . The remaining 991\u00a0OGs correspond to the  accessory genome  in which 277\u00a0OGs are unique to one strain. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7649", "text": "There are eleven  restriction modification systems  in the genome of  H. pylori . [ 38 ]  This is an unusually high number providing a  defence against bacteriophages . [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7650", "text": "Single-cell transcriptomics  using  single-cell RNA-Seq  gave the complete  transcriptome  of  H. pylori  which was published in 2010. This analysis of its  transcription  confirmed the known acid induction of major  virulence  loci, including the urease (ure) operon and the Cag  pathogenicity island  (PAI). [ 41 ]  A total of 1,907\u00a0 transcription start sites  337\u00a0primary  operons , and 126\u00a0additional suboperons, and 66\u00a0mono cistrons  were identified. Until 2010, only about 55\u00a0transcription start sites (TSSs) were known in this species. 27% of the primary TSSs are also antisense TSSs, indicating that \u2013 similar to  E.\u00a0coli  \u2013  antisense transcription  occurs across the entire  H.\u00a0pylori  genome. At least one antisense TSS is associated with about 46% of all  open reading frames , including many  housekeeping genes . [ 41 ]  About 50% of the  5 \u2032  UTRs  (leader sequences) are 20\u201340\u00a0nucleotides (nt) in length and support the AAGGag motif located about 6\u00a0nt (median distance) upstream of start codons as the consensus  Shine\u2013Dalgarno sequence  in  H.\u00a0pylori . [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7651", "text": "The  proteome  of  H. pylori  has been systematically analyzed and more than 70% of its  proteins  have been detected by  mass spectrometry , and other methods. About 50% of the proteome has been quantified, informing of the number of protein copies in a typical cell. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7652", "text": "Studies of the  interactome  have identified more than 3000  protein-protein interactions . This has provided information of how proteins interact with each other, either in stable  protein complexes  or in more dynamic, transient interactions, which can help to identify the functions of the protein. This in turn helps researchers to find out what the function of uncharacterized proteins is, e.g. when an uncharacterized protein interacts with several proteins of the  ribosome  (that is, it is likely also involved in ribosome function). About a third of all ~1,500 proteins in  H. pylori  remain uncharacterized and their function is largely unknown. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7653", "text": "An infection with  Helicobacter pylori  can either have no symptoms even when lasting a lifetime, or can harm the stomach and duodenal  linings  by  inflammatory responses  induced by several mechanisms associated with a number of  virulence factors .  Colonization  can initially cause  H. pylori induced gastritis , an  inflammation of the stomach lining  that became a listed disease in  ICD11 . [ 44 ] [ 45 ] [ 46 ]  This will progress to  chronic gastritis  if left untreated. Chronic gastritis may lead to  atrophy  of the stomach lining, and the development of  peptic ulcers  (gastric or duodenal). These changes may be seen as stages in the development of  gastric cancer , known as  Correa's cascade . [ 47 ] [ 48 ]  Extragastric complications that have been linked to  H. pylori  include  anemia  due either to iron-deficiency or vitamin B12 deficiency, diabetes mellitus, cardiovascular, and certain neurological disorders. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7654", "text": "Peptic ulcers are a consequence of inflammation that allows stomach acid and the digestive enzyme  pepsin  to overwhelm the protective mechanisms of the  mucous membranes . The location of colonization of  H.\u00a0pylori , which affects the location of the ulcer, depends on the acidity of the stomach. [ 49 ]  In people producing large amounts of acid,  H.\u00a0pylori  colonizes near the  pyloric antrum  (exit to the duodenum) to avoid the acid-secreting  parietal cells  at the  fundus  (near the entrance to the stomach). [ 32 ]   G cells  express relatively high levels of  PD-L1  that protects these cells from  H. pylori -induced immune destruction. [ 50 ]  In people producing normal or reduced amounts of acid,  H.\u00a0pylori  can also colonize the rest of the stomach."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7655", "text": "The inflammatory response caused by bacteria colonizing near the pyloric antrum induces G cells in the antrum to secrete the hormone  gastrin , which travels through the bloodstream to parietal cells in the fundus. [ 51 ]  Gastrin stimulates the parietal cells to secrete more acid into the stomach lumen, and over time increases the number of parietal cells, as well. [ 52 ]  The increased acid load damages the duodenum, which may eventually lead to the formation of ulcers."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7656", "text": "Helicobacter pylori  is a class I  carcinogen , and potential cancers include gastric  mucosa-associated lymphoid tissue  (MALT)  lymphomas  and  gastric cancer . [ 10 ] [ 11 ] [ 53 ]  Less commonly,  diffuse large B-cell lymphoma  of the stomach is a risk. [ 54 ]  Infection with  H. pylori  is responsible for around 89 per cent of all gastric cancers, and is linked to the development of 5.5 per cent of all cases of cancer worldwide. [ 13 ] [ 14 ]  Although the data varies between different countries, overall about 1% to 3% of people infected with  Helicobacter pylori  develop gastric cancer in their lifetime compared to 0.13% of individuals who have had no  H.\u00a0pylori  infection. [ 55 ] [ 32 ]   H.\u00a0pylori -induced gastric cancer is the third highest cause of worldwide cancer mortality as of 2018. [ 56 ]  Because of the usual lack of symptoms, when gastric cancer is finally diagnosed it is often fairly advanced. More than half of gastric cancer patients have lymph node metastasis when they are initially diagnosed. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7657", "text": "Chronic inflammation that is a feature of cancer development is characterized by infiltration of  neutrophils  and  macrophages  to the gastric epithelium, which favors the accumulation of  pro-inflammatory cytokines ,  reactive oxygen species  (ROS) and  reactive nitrogen species  (RNS) that cause  DNA damage . [ 58 ]  The  oxidative DNA damage  and levels of  oxidative stress  can be indicated by a biomarker,  8-oxo-dG . [ 58 ] [ 59 ]  Other damage to DNA includes  double-strand breaks . [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7658", "text": "Small  gastric  and  colorectal polyps  are  adenomas  that are more commonly found in association with the mucosal damage induced by  H. pylori  gastritis. [ 61 ] [ 62 ]  Larger polyps can in time become cancerous. [ 63 ] [ 61 ]  A modest association of  H. pylori  has been made with the development of  colorectal cancers , but as of 2020 causality had yet to be proved. [ 64 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7659", "text": "Most people infected with  H.\u00a0pylori  never experience any symptoms or complications, but will have a 10% to 20% risk of developing  peptic ulcers  or a 0.5% to 2% risk of stomach cancer. [ 8 ] [ 65 ]   H. pylori induced gastritis  may present as acute gastritis with  stomach ache ,  nausea , and ongoing  dyspepsia  (indigestion) that is sometimes accompanied by depression and anxiety. [ 8 ] [ 66 ]  Where the gastritis develops into chronic gastritis, or an ulcer, the symptoms are the same and can include  indigestion , stomach or abdominal pains, nausea,  bloating ,  belching , feeling hunger in the morning, feeling full too soon, and sometimes  vomiting , heartburn, bad breath, and weight loss. [ 67 ] [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7660", "text": "Complications of an ulcer can cause severe signs and symptoms such as black or tarry stool indicative of  bleeding  into the stomach or duodenum; blood - either red or coffee-ground colored in vomit; persistent sharp or severe abdominal pain; dizziness, and a fast heartbeat. [ 67 ] [ 68 ]  Bleeding is the most common complication. In cases caused by  H. pylori  there was a greater need for  hemostasis  often requiring gastric resection. [ 69 ]  Prolonged bleeding may cause anemia leading to weakness and fatigue. Inflammation of the pyloric antrum, which connects the stomach to the duodenum, is more likely to lead to duodenal ulcers, while inflammation of the  corpus  may lead to a gastric ulcer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7661", "text": "Stomach cancer  can cause nausea, vomiting, diarrhoea, constipation, and unexplained weight loss. [ 70 ]   Gastric polyps  are  adenomas  that are usually asymptomatic and benign, but may be the cause of dyspepsia, heartburn, bleeding from the stomach, and, rarely, gastric outlet obstruction. [ 61 ] [ 71 ]  Larger polyps may have  become cancerous . [ 61 ] \n Colorectal polyps  may be the cause of rectal bleeding, anemia, constipation, diarrhea, weight loss, and abdominal pain. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7662", "text": "Virulence factors  help a pathogen to evade the immune response of the host, and to successfully  colonize . The many virulence factors of  H. pylori  include its flagella, the production of urease, adhesins,  serine protease   HtrA  (high temperature requirement A), and the major  exotoxins   CagA  and  VacA . [ 30 ] [ 73 ]  The presence of VacA and CagA are associated with more  advanced outcomes . [ 74 ]  CagA is an oncoprotein associated with the development of gastric cancer. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7663", "text": "H.\u00a0pylori  infection is associated with  epigenetically  reduced efficiency of the  DNA repair  machinery, which favors the accumulation of mutations and genomic instability as well as gastric carcinogenesis. [ 75 ]  It has been shown that expression of two DNA repair proteins,  ERCC1  and  PMS2 , was severely reduced once  H.\u00a0pylori  infection had progressed to cause  dyspepsia . [ 76 ]  Dyspepsia occurs in about 20% of infected individuals. [ 77 ]  Epigenetically reduced protein expression of DNA repair proteins  MLH1 ,  MGMT  and  MRE11  are also evident. Reduced DNA repair in the presence of increased DNA damage increases carcinogenic mutations and is likely a significant cause of gastric carcinogenesis. [ 59 ] [ 78 ] [ 79 ]  These  epigenetic alterations  are due to  H.\u00a0pylori -induced  methylation of CpG sites in promoters of genes [ 78 ]  and  H.\u00a0pylori -induced altered expression of multiple  microRNAs . [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7664", "text": "Two related mechanisms by which  H.\u00a0pylori  could promote cancer have been proposed. One mechanism involves the enhanced production of  free radicals  near  H.\u00a0pylori  and an increased rate of host cell  mutation . The other proposed mechanism has been called a \"perigenetic pathway\", [ 80 ]  and involves enhancement of the transformed host cell phenotype by means of alterations in cell proteins, such as  adhesion  proteins.  H.\u00a0pylori  has been proposed to induce inflammation and locally high levels of  tumor necrosis factor  (TNF), also known as tumor necrosis factor alpha (TNF\u03b1)), and/or  interleukin 6  (IL-6). [ 81 ]  According to the proposed perigenetic mechanism, inflammation-associated signaling molecules, such as TNF, can alter gastric epithelial cell adhesion and lead to the dispersion and migration of mutated epithelial cells without the need for additional mutations in  tumor suppressor genes , such as genes that code for cell adhesion proteins. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7665", "text": "The first virulence factor of  Helicobacter pylori  that enables colonization is its  flagellum . [ 83 ]   H. pylori  has from two to seven flagella at  the same polar location  which gives it a high motility. The flagellar filaments are about 3\u00a0\u03bcm long, and composed of two copolymerized  flagellins , FlaA and FlaB, coded by the genes  flaA , and  flaB . [ 26 ] [ 73 ]  The minor flagellin FlaB is located in the proximal region and the major flagellin FlaA makes up the rest of the flagellum. [ 84 ]  The flagella are sheathed in a continuation of the bacterial outer membrane which gives protection against the gastric acidity. The sheath is also the location of the origin of the outer membrane vesicles that gives protection to the bacterium from bacteriophages. [ 84 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7666", "text": "Flagella motility is provided by the  proton motive force  provided by urease-driven hydrolysis allowing  chemotactic movements  towards the less acidic  pH  gradient in the mucosa. [ 30 ]  The mucus layer is about 300  \u03bcm  thick, and the helical shape of  H. pylori  aided by its flagella helps it to burrow through  this layer where it colonises a narrow region of about 25 \u03bcm closest to the epithelial cell layer, where the pH is near to neutral. They further colonise the  gastric pits  and live in the  gastric glands . [ 1 ] [ 84 ] [ 85 ]  Occasionally the bacteria are found inside the epithelial cells themselves. [ 86 ]  The use of  quorum sensing  by the bacteria enables the formation of a biofilm which furthers persistent colonisation. In the layers of the biofilm,  H. pylori  can escape from the actions of antibiotics, and also be protected from host-immune responses. [ 87 ] [ 88 ]  In the biofilm,  H. pylori  can change the flagella to become adhesive structures. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7667", "text": "In addition to using  chemotaxis  to avoid areas of high acidity (low pH),  H.\u00a0pylori  also produces large amounts of  urease , an  enzyme  which breaks down the  urea  present in the stomach to produce  ammonia  and  bicarbonate , which are released into the bacterial cytosol and the surrounding environment, creating a neutral area. [ 90 ]  The decreased acidity (higher pH) changes the mucus layer from a gel-like state to a more viscous state that makes it easier for the flagella to move the bacteria through the mucosa and attach to the gastric epithelial cells. [ 90 ]   Helicobacter pylori  is one of the few known types of bacterium that has a  urea cycle  which is uniquely configured in the bacterium. [ 91 ]  10% of the cell is of  nitrogen , a balance that needs to be maintained. Any excess is stored in urea excreted in the urea cycle. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7668", "text": "A final stage enzyme in the urea cycle is  arginase , an enzyme that is crucial to the pathogenesis of  H. pylori . Arginase produces  ornithine  and urea, which the enzyme urease breaks down into carbonic acid and ammonia. Urease is the bacterium\u2019s most abundant protein, accounting for 10\u201315% of the bacterium's total protein content. Its expression is not only required for establishing initial colonization in the breakdown of urea to carbonic acid and ammonia, but is also essential for maintaining chronic infection. [ 92 ] [ 65 ]  Ammonia reduces stomach acidity, allowing the bacteria to become locally established. Arginase promotes the persistence of infection by consuming arginine; arginine is used by macrophages to produce nitric oxide, which has a strong antimicrobial effect. [ 91 ] [ 93 ]  The ammonia produced to regulate  pH  is toxic to epithelial cells. [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7669", "text": "H. pylori  must make attachment with the epithelial cells to prevent its being swept away with the constant movement and renewal of the mucus. To give them this adhesion,  bacterial outer membrane proteins  as virulence factors called  adhesins  are produced. [ 95 ]  BabA (blood group antigen binding adhesin) is most important during initial colonization, and SabA (sialic acid binding adhesin) is important in persistence. BabA attaches to glycans and mucins in the epithelium. [ 95 ]  BabA (coded for by the  babA2  gene) also binds to the  Lewis b antigen  displayed on the surface of the epithelial cells. [ 96 ]  Adherence via BabA is acid sensitive and can be fully reversed by a decreased pH. It has been proposed that BabA's acid responsiveness enables adherence while also allowing an effective escape from an unfavorable environment such as a low pH that is harmful to the organism. [ 97 ]  SabA (coded for by the  sabA  gene) binds to increased levels of  sialyl-Lewis  X  antigen expressed on gastric mucosa. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7670", "text": "The outer membrane contains  cholesterol glucoside , a sterol glucoside that  H. pylori   glycosylates  from the  cholesterol  in the gastric gland cells, and inserts it into its outer membrane. [ 99 ]  This cholesterol glucoside is important for membrane stability, morphology and immune evasion, and is rarely found in other bacteria. [ 100 ] [ 101 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7671", "text": "The enzyme responsible for this is  cholesteryl \u03b1-glucosyltransferase  (\u03b1CgT or Cgt), encoded by the  HP0421  gene. [ 102 ]  A major effect of the depletion of host cholesterol by Cgt is to disrupt cholesterol-rich  lipid rafts  in the epithelial cells. Lipid rafts are involved in cell signalling and their disruption causes a reduction in the immune inflammatory response, particularly by reducing  interferon gamma . [ 103 ]  Cgt is also secreted by the type IV secretion system, and is secreted in a selective way so that gastric niches where the pathogen can thrive are created. [ 102 ]  Its lack has been shown to give vulnerability from environmental stress to bacteria, and also to disrupt CagA-mediated interactions. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7672", "text": "Colonization induces an intense anti-inflammatory response as a first-line immune system defence. Phagocytic leukocytes and monocytes infiltrate the site of infection, and antibodies are produced. [ 104 ]   H. pylori  is able to adhere to the surface of the phagocytes and impede their action. This is responded to by the phagocyte in the generation and release of oxygen metabolites into the surrounding space.  H. pylori  can survive this response by the activity of  catalase  at its attachment to the phagocytic cell surface. Catalase decomposes hydrogen peroxide into water and oxygen, protecting the bacteria from toxicity. Catalase has been shown to almost completely inhibit the phagocytic oxidative response. [ 104 ]  It is coded for by the gene  katA . [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7673", "text": "TNF-inducing protein alpha (Tip\u03b1) is a carcinogenic protein encoded by  HP0596  unique to  H. pylori  that induces the expression of  tumor necrosis factor . [ 82 ] [ 106 ]  Tip\u03b1 enters gastric cancer cells where it binds to cell surface  nucleolin , and induces the expression of  vimentin . Vimentin is important in the  epithelial\u2013mesenchymal transition  associated with the progression of tumors. [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7674", "text": "CagA  (cytotoxin-associated antigen A) is a major  virulence factor  for  H.\u00a0pylori , an  oncoprotein  that is encoded by the  cagA  gene. Bacterial strains with the  cagA  gene are associated with the ability to cause ulcers, MALT lymphomas, and gastric cancer. [ 108 ] [ 109 ]  The  cagA  gene codes for a relatively long (1186- amino acid ) protein. The  cag   pathogenicity island  (PAI) has about 30 genes, part of which code for a complex  type IV secretion system  (T4SS or TFSS). The low  GC-content  of the  cag  PAI relative to the rest of the  Helicobacter  genome suggests the island was acquired by  horizontal transfer  from another bacterial species. [ 38 ]  The  serine protease   HtrA  also plays a major role in the pathogenesis of  H.\u00a0pylori . The HtrA protein enables the bacterium to transmigrate across the host cells' epithelium, and is also needed for the translocation of CagA. [ 110 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7675", "text": "The virulence of  H.\u00a0pylori  may be increased by genes of the  cag  pathogenicity island; about 50\u201370% of  H.\u00a0pylori  strains in Western countries carry it. [ 111 ]  Western people infected with strains carrying the  cag  PAI have a stronger inflammatory response in the stomach and are at a greater risk of developing peptic ulcers or stomach cancer than those infected with strains lacking the island. [ 32 ]  Following attachment of  H.\u00a0pylori  to stomach epithelial cells, the type IV secretion system expressed by the  cag  PAI \"injects\" the  inflammation -inducing agent, peptidoglycan, from their own  cell walls  into the epithelial cells. The injected peptidoglycan is recognized by the cytoplasmic  pattern recognition receptor  (immune sensor) Nod1, which then stimulates expression of  cytokines  that promote inflammation. [ 112 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7676", "text": "The type-IV  secretion  apparatus also injects the  cag  PAI-encoded protein CagA into the stomach's epithelial cells, where it disrupts the  cytoskeleton , adherence to adjacent cells, intracellular signaling,  cell polarity , and other cellular activities. [ 113 ]  Once inside the cell, the CagA protein is  phosphorylated  on  tyrosine residues  by a host cell membrane-associated  tyrosine kinase  (TK). CagA then allosterically activates  protein tyrosine phosphatase / protooncogene   Shp2 . [ 114 ] \nThese proteins are directly toxic to cells lining the stomach and signal strongly to the immune system that an invasion is under way. As a result of the bacterial presence, neutrophils and macrophages set up residence in the tissue to fight the bacteria assault. [ 115 ]  Pathogenic strains of  H.\u00a0pylori  have been shown to activate the  epidermal growth factor receptor  (EGFR), a  membrane protein  with a TK  domain . Activation of the EGFR by  H.\u00a0pylori  is associated with altered  signal transduction  and  gene expression  in host epithelial cells that may contribute to pathogenesis. A  C-terminal  region of the CagA protein (amino acids 873\u20131002) has also been suggested to be able to regulate host cell  gene transcription , independent of protein tyrosine phosphorylation. [ 109 ]  A great deal of diversity exists between strains of  H.\u00a0pylori , and the strain that infects a person can predict the outcome."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7677", "text": "VacA  (vacuolating cytotoxin autotransporter) is another major virulence factor encoded by the  vacA  gene. [ 116 ]  All strains of  H. pylori  carry this gene but there is much diversity, and only 50% produce the encoded cytotoxin. [ 92 ] [ 33 ]  The four main subtypes of  vacA  are  s1/m1, s1/m2, s2/m1,  and  s2/m2 .  s1/m1  and  s1/m2  are known to cause an increased risk of gastric cancer. [ 117 ]  VacA is an oligomeric protein complex that causes a progressive vacuolation in the epithelial cells leading to their death. [ 118 ]  The vacuolation has also been associated with promoting intracellular reservoirs of  H. pylori  by disrupting the calcium channel cell membrane  TRPML1 . [ 119 ]  VacA has been shown to increase the levels of  COX2 , an up-regulation that increases the production of a  prostaglandin  indicating a strong host cell inflammatory response. [ 118 ] [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7678", "text": "About 4% of the genome encodes for  outer membrane proteins  that can be grouped into five families. [ 121 ]  The largest family includes  bacterial adhesins . The other four families are  porins , iron transporters,  flagellum -associated proteins, and proteins of unknown function. Like other typical gram-negative bacteria, the outer membrane of  H.\u00a0pylori  consists of  phospholipids  and  lipopolysaccharide  (LPS). The  O-antigen  of LPS may be  fucosylated  and mimic  Lewis blood group antigens  found on the gastric epithelium. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7679", "text": "H. pylori  forms blebs from the outer membrane that pinch off as  outer membrane vesicles  to provide an alternative delivery system for virulence factors including CagA. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7680", "text": "A  Helicobacter   cysteine-rich protein  HcpA is known to trigger an immune response, causing inflammation. [ 122 ]  \nA  Helicobacter pylori  virulence factor  DupA  is associated with the development of duodenal ulcers. [ 123 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7681", "text": "The need for survival has led to the development of different mechanisms of tolerance that enable the persistence of  H. pylori . [ 124 ]  These mechanisms can also help to overcome the effects of antibiotics. [ 124 ]   H. pylori  has to not only survive the harsh gastric acidity but also the sweeping of mucus by continuous  peristalsis , and  phagocytic  attack accompanied by the release of  reactive oxygen species . [ 125 ]   All organisms encode genetic programs for response to stressful conditions including those that cause DNA damage. [ 126 ]  Stress conditions activate bacterial response mechanisms that are regulated by proteins expressed by  regulator genes . [ 124 ]  The  oxidative stress  can induce potentially lethal mutagenic  DNA adducts  in its genome. Surviving this  DNA damage  is supported by  transformation -mediated  recombinational repair , that contributes to successful colonization. [ 127 ] [ 128 ]   H.\u00a0pylori  is naturally competent for transformation. While many organisms are competent only under certain environmental conditions, such as starvation,  H.\u00a0pylori  is competent throughout logarithmic growth. [ 126 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7682", "text": "Transformation  (the transfer of DNA from one bacterial cell to another through the intervening medium) appears to be part of an adaptation for  DNA repair . [ 126 ]   Homologous recombination  is required for repairing  double-strand breaks  (DSBs). The AddAB helicase-nuclease complex resects DSBs and loads  RecA  onto single-strand DNA (ssDNA), which then mediates strand exchange, leading to homologous recombination and repair. The requirement of RecA plus AddAB for efficient gastric colonization suggests that  H.\u00a0pylori  is either exposed to double-strand DNA damage that must be repaired or requires some other recombination-mediated event. In particular, natural transformation is increased by DNA damage in  H.\u00a0pylori , and a connection exists between the DNA damage response and DNA uptake in  H.\u00a0pylori . [ 126 ]   This natural competence contributes to the persistence of  H.\u00a0pylori .  H. pylori  has much greater rates of recombination and mutation than other bacteria. [ 3 ]   Genetically different strains can be found in the same host, and also in different regions of the stomach. [ 129 ]  An overall response to multiple stressors can result from an interaction of the mechanisms. [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7683", "text": "RuvABC  proteins are essential to the process of recombinational repair, since they resolve intermediates in this process termed  Holliday junctions .  H.\u00a0pylori  mutants that are defective in RuvC have increased sensitivity to DNA-damaging agents and to oxidative stress, exhibit reduced survival within macrophages, and are unable to establish successful infection in a mouse model. [ 130 ]  Similarly, RecN protein plays an important role in DSB repair. [ 131 ]  An  H.\u00a0pylori  recN mutant displays an attenuated ability to colonize mouse stomachs, highlighting the importance of recombinational DNA repair in survival of  H.\u00a0pylori  within its host. [ 131 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7684", "text": "An effective sustained colonization response is the formation of a  biofilm .\nHaving first adhered to cellular surfaces, the bacteria produce and secrete  extracellular polymeric substance  (EPS). EPS consists largely of  biopolymers  and provides the framework for the biofilm structure. [ 90 ]   H. pylori  helps the biofilm formation by altering its flagella into adhesive structures that provide adhesion between the cells. [ 89 ]  Layers of aggregated bacteria as microcolonies accumulate to thicken the biofilm."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7685", "text": "The matrix of EPS prevents the entry of antibiotics and immune cells, and provides protection from heat and competition from other microorganisms. [ 90 ]  Channels form between the cells in the biofilm matrix allowing the transport of nutrients, enzymes, metabolites, and waste. [ 90 ]  Cells in the deep layers may be nutritionally deprived and enter into the coccoid dormant-like state. [ 132 ] [ 133 ]  By changing the shape of the bacterium to a coccoid form, the exposure of  LPS  (targeted by antibiotics) becomes limited, and so evades detection by the immune system. [ 134 ]  It has also been shown that the  cag  pathogenicity island remains intact in the coccoid form. [ 134 ]  Some of these antibiotic resistant cells may remain in the host as  persister cells . Following eradication, the persister cells can cause a recurrence of the infection. [ 132 ] [ 133 ]  Bacteria can detach from the biofilm to relocate and colonize elsewhere in the stomach to form other biofilms. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7686", "text": "Colonization with  H.\u00a0pylori  does not always lead to disease, but is associated with a number of  stomach diseases . [ 32 ]  Testing is recommended in cases of  peptic ulcer disease  or low-grade gastric  MALT lymphoma ; after  endoscopic  resection of early  gastric cancer ; for first-degree relatives with gastric cancer, and in certain cases of indigestion. Other indications that prompt testing for  H. pylori  include long term  aspirin  or other  non-steroidal anti-inflammatory  use, unexplained  iron deficiency anemia , or in cases of  immune thrombocytopenic purpura . [ 135 ]  Several methods of testing exist, both invasive and non-invasive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7687", "text": "Non-invasive tests for  H.\u00a0pylori  infection include  serological tests  for  antibodies ,  stool tests , and  urea breath tests . Carbon urea breath tests include the use of  carbon-13 , or a radioactive  carbon-14  producing a labelled carbon dioxide that can be detected in the breath. [ 136 ]  Carbon urea breath tests have a high  sensitivity and specificity  for the diagnosis of  H. pylori . [ 136 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7688", "text": "Proton-pump inhibitors and antibiotics should be discontinued for at least 30 days prior to testing for  H. pylori  infection or eradication, as both agents inhibit  H. pylori  growth and may lead to false negative results. [ 135 ]  Testing to confirm eradication is recommended 30 days or more after completion of treatment for  H. pylori  infection.  H. pylori  breath testing or stool antigen testing are both reasonable tests to confirm eradication. [ 135 ]   H. pylori  serologic testing, including  IgG antibodies , are not recommended as a test of eradication as they may remain elevated for years after successful treatment of infection. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7689", "text": "An endoscopic biopsy is an invasive means to test for  H.\u00a0pylori  infection. Low-level infections can be missed by biopsy, so multiple samples are recommended. The most accurate method for detecting  H.\u00a0pylori  infection is with a  histological  examination from two sites after endoscopic  biopsy , combined with either a  rapid urease test  or microbial culture. [ 137 ]  Generally, repeating endoscopy is not recommended to confirm  H. pylori  eradication, unless there are specific indications to repeat the procedure. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7690", "text": "Helicobacter pylori  is contagious, and is  transmitted  through direct contact either with  saliva  (oral-oral) or  feces  ( fecal\u2013oral route ), but mainly through the oral\u2013oral route. [ 8 ]  Consistent with these transmission routes, the bacteria have been isolated from  feces ,  saliva , and  dental plaque . [ 138 ]   H.\u00a0pylori  may also be transmitted by consuming contaminated food or water. [ 139 ]  Transmission occurs mainly within families in developed nations, but also from the broader community in developing countries. [ 140 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7691", "text": "To prevent the development of  H. pylori -related diseases when infection is suspected, antibiotic-based therapy regimens are recommended to  eradicate the bacteria . [ 46 ]  When successful the disease progression is halted. First line therapy is recommended if low-grade gastric MALT lymphoma is diagnosed, regardless of evidence of  H. pylori . However, if a severe condition of atrophic gastritis with gastric lesions is reached antibiotic-based treatment regimens are not advised since such lesions are often not reversible and will progress to gastric cancer. [ 46 ]  If the cancer is managed to be treated it is advised that an eradication program be followed to prevent a recurrence of infection, or reduce a recurrence of the cancer, known as metachronous. [ 46 ] [ 141 ] [ 142 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7692", "text": "Due to  H.\u00a0pylori 's  role as a major cause of certain diseases (particularly cancers) and its consistently increasing  resistance to antibiotic therapy , there is an obvious need for alternative treatments. [ 143 ]  A vaccine targeted towards the development of gastric cancer, including MALT lymphoma, would also prevent the development of gastric ulcers. [ 5 ]  A vaccine that would be prophylactic for use in children, and one that would be therapeutic later are the main goals. Challenges to this are the extreme genomic diversity shown by  H. pylori  and complex host-immune responses. [ 143 ] [ 144 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7693", "text": "Previous studies in the Netherlands and in the US have shown that such a prophylactic vaccine programme would be ultimately cost-effective. [ 145 ] [ 146 ]  However, as of late 2019 there have been no advanced vaccine candidates and only one vaccine in a Phase I clinical trial.  Furthermore, development of a vaccine against  H.\u00a0pylori  has not been a priority of major pharmaceutical companies. [ 147 ]  A key target for potential therapy is the  proton-gated urea channel , since the secretion of urease enables the survival of the bacterium. [ 148 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7694", "text": "The 2022 Maastricht Consensus Report recognised  H. pylori  gastritis as  Helicobacter pylori induced gastritis , and has been included in  ICD11 . [ 44 ] [ 45 ] [ 46 ]  Initially the infection tends to be superficial, localised to the upper mucosal layers of the stomach. [ 149 ]  The intensity of chronic inflammation is related to the cytotoxicity of the  H. pylori  strain. A greater cytotoxicity will result in the change from a non-atrophic gastritis to an atrophic gastritis, with the loss of  mucous glands . This condition is a prequel to the development of peptic ulcers and gastric adenocarcinoma. [ 149 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7695", "text": "Eradication of  H. pylori  is recommended to treat the infection, including when advanced to  peptic ulcer disease .  The recommendations for first-line treatment is a quadruple therapy consisting of a  proton-pump inhibitor ,  amoxicillin ,  clarithromycin , and  metronidazole . Prior to treatment, testing is recommended to identify any pre-existing antibiotic resistances. A high rate of resistance to metronidazole has been observed. In areas of known clarithromycin resistance, the first-line therapy is changed to a  bismuth  based regimen including  tetracycline  and metronidazole for 14 days. If one of these courses of treatment fails, it is suggested to use the alternative. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7696", "text": "Treatment failure may typically be attributed to antibiotic resistance, or inadequate acid suppression from proton-pump inhibitors. [ 150 ]  Following clinical trials, the use of the  potassium-competitive acid blocker   vonoprazan , which has a greater acid suppressive action, was approved for use in the US in 2022. [ 151 ] [ 150 ]  Its recommended use is in combination with amoxicillin, with or without clarithromycin. It has been shown to have a faster action and can be used with or without food. [ 150 ]  Successful eradication regimens have revolutionised the treatment of peptic ulcers. [ 152 ] [ 153 ]  Eradication of  H. pylori  is also associated with a subsequent decreased risk of duodenal or gastric ulcer recurrence. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7697", "text": "Plant extracts  and  probiotic  foods are being increasingly used as  add-ons  to usual treatments. Probiotic yogurts containing  lactic acid bacteria   Bifidobacteria  and  Lactobacillus  exert a suppressive effect on  H.\u00a0pylori  infection, and their use has been shown to improve the rates of eradication. [ 14 ]  Some commensal intestinal bacteria as part of the  gut microbiota  produce  butyrate  that acts as a  prebiotic  and enhances the mucosal immune barrier. Their use as probiotics may help balance the gut dysbiosis that accompanies antibiotic use. [ 154 ]  Some probiotic strains have been shown to have bactericidal and bacteriostatic activity against  H. pylori , and also help to balance the gut dysbiosis. [ 155 ] [ 134 ]  Antibiotics have a negative impact on gastrointestinal microbiota and cause nausea, diarrhea, and  sickness  for which probiotics can alleviate. [ 134 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7698", "text": "Increasing  antibiotic resistance  is the main cause of initial treatment failure. Factors linked to resistance include mutations,  efflux pumps , and the formation of  biofilms . [ 156 ] [ 157 ]  One of the main  antibiotics  used in eradication therapies is  clarithromycin , but clarithromycin-resistant strains have become well-established and the use of alternative antibiotics needs to be considered. Fortunately, non-invasive stool tests for clarithromycin have become available that allow selection of patients that are likely to respond to the therapy. [ 158 ]  Multidrug resistance has also increased. [ 157 ]  Additional rounds of antibiotics or other therapies may be used. [ 159 ] [ 160 ] [ 161 ]   Next generation sequencing  is looked to for identifying initial specific antibiotic resistances that will help in targeting more effective treatment. [ 162 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7699", "text": "In 2018, the  WHO  listed  H. pylori  as a high priority pathogen for the research and  discovery of new drugs  and treatments. [ 163 ]  The increasing antibiotic resistance encountered has spurred interest in developing alternative therapies using a number of plant compounds. [ 164 ] [ 165 ]  Plant compounds have fewer side effects than synthetic drugs. Most plant extracts contain a complex mix of components that may not act on their own as antimicrobials but can work together with antibiotics to enhance treatment and work towards overcoming resistance. [ 164 ]  Plant compounds have a different mechanism of action that has proved useful in fighting antimicrobial resistance. For example, various compounds can act by inhibiting enzymes such as urease, and weakening adhesions to the mucous membrane. [ 166 ]  Sulfur-containing compounds from plants with high concentrations of polysulfides,  coumarins , and  terpenes  have all been shown to be effective against  H. pylori . [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7700", "text": "H. pylori  is found in saliva and  dental plaque . Its transmission is known to include oral-oral, suggesting that the dental plaque biofilm may act as a reservoir for the bacteria. Periodontal therapy or  scaling and root planing  has therefore been suggested as an additional treatment to enhance eradication rates, but more research is needed. [ 139 ] [ 167 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7701", "text": "Helicobacter pylori  is a risk factor for  gastric adenocarcinomas . [ 168 ]  Treatment is highly aggressive, with even localized disease being treated sequentially with chemotherapy and radiotherapy before surgical resection. [ 169 ]  Since this cancer, once developed, is independent of  H.\u00a0pylori  infection, eradication regimens are not used. [ 170 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7702", "text": "MALT lymphomas  are  malignancies  of  mucosa-associated lymphoid tissue . Early gastric MALTomas due to  H. pylori  may be successfully treated (70\u201395% of cases) with one or more  eradication programs . [ 14 ]  Some 50\u201380% of patients who experience eradication of the pathogen develop a remission and long-term clinical control of their lymphoma within 3\u201328\u00a0months.  Radiation therapy  to the stomach and surrounding (i.e. peri-gastric) lymph nodes has also been used to successfully treat these localized cases. Patients with non-localized (i.e. systemic Ann Arbor stage\u00a0III and IV) disease who are free of symptoms have been treated with  watchful waiting  or, if symptomatic, with the  immunotherapy  drug  rituximab  (given for 4\u00a0weeks) combined with the  chemotherapy  drug  chlorambucil  for 6\u201312\u00a0months; 58% of these patients attain a 58% progression-free survival rate at 5\u00a0years. Frail stage III/IV patients have been successfully treated with rituximab or the chemotherapy drug  cyclophosphamide  alone. [ 171 ]  Antibiotic-proton pump inhibitor eradication therapy and localized radiation therapy have been used successfully to treat H.\u00a0pylori-positive MALT lymphomas of the rectum; however radiation therapy has given slightly better results and therefore been suggested to be the disease's preferred treatment. [ 172 ]  However, the generally recognized treatment of choice for patients with systemic involvement uses various chemotherapy drugs often combined with rituximab."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7703", "text": "A MALT lymphoma may rarely transform into a more aggressive  diffuse large B-cell lymphoma  (DLBCL). [ 173 ]  Where this is associated with  H. pylori  infection, the DLBCL is less aggressive and more amenable to treatment. [ 174 ] [ 175 ] [ 176 ]  When limited to the stomach, they have sometimes been successfully treated with  H. pylori  eradication programs. [ 54 ] [ 175 ] [ 177 ] [ 176 ]  If unresponsive or showing a deterioration, a more conventional chemotherapy ( CHOP ), immunotherapy, or local radiotherapy can be considered, and any of these or a combination have successfully treated these more advanced types. [ 175 ] [ 176 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7704", "text": "Helicobacter pylori  colonizes the stomach for decades in most people, and induces chronic gastritis, a long-lasting inflammation of the stomach. In most \ncases symptoms are never experienced but about 10\u201320% of those infected will ultimately develop gastric and duodenal ulcers, and have a possible 1\u20132% lifetime risk of gastric cancer. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7705", "text": "H. pylori  thrives in a high salt diet, which is seen as an environmental risk factor for its association with gastric cancer. A diet high in salt enhances colonization, increases inflammation, increases the expression of  H. pylori  virulence factors, and intensifies chronic gastritis. [ 178 ] [ 179 ]  Paradoxically, extracts of  kimchi , a salted probiotic food, has been found to have a preventive effect on  H. pylori \u2013associated gastric  carcinogenesis . [ 180 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7706", "text": "In the absence of treatment,  H.\u00a0pylori  infection usually persists for life. [ 181 ]  Infection may disappear in the elderly as the stomach's mucosa becomes increasingly atrophic and inhospitable to colonization. Some studies in young children up to two years of age have shown that infection can be transient in this age group. [ 182 ] [ 183 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7707", "text": "It is possible for  H.\u00a0pylori  to re-establish in a person after eradication. This recurrence can be caused by the original strain ( recrudescence ), or be caused by a different strain ( reinfection ). A 2017 meta-analysis showed that the global per-person annual rates of recurrence, reinfection, and recrudescence is 4.3%, 3.1%, and 2.2% respectively. It is unclear what the main risk factors are. [ 184 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7708", "text": "Mounting evidence suggests  H.\u00a0pylori  has an important role in protection from some diseases. [ 16 ]  The incidence of  acid reflux disease ,  Barrett's esophagus , and  esophageal cancer  have been rising dramatically at the same time as  H.\u00a0pylori ' s presence decreases. [ 185 ]  In 1996,  Martin J. Blaser  advanced the hypothesis that  H.\u00a0pylori  has a beneficial effect by regulating the acidity of the stomach contents. [ 51 ] [ 185 ]  The hypothesis is not universally accepted, as several  randomized controlled trials  failed to demonstrate worsening of acid reflux disease symptoms following eradication of  H.\u00a0pylori . [ 186 ] [ 187 ]  Nevertheless, Blaser has reasserted his view that  H.\u00a0pylori  is a member of the normal  gastric microbiota . [ 17 ]  He postulates that the changes in gastric physiology caused by the loss of  H.\u00a0pylori  account for the recent increase in incidence of several diseases, including  type 2 diabetes ,  obesity , and asthma. [ 17 ] [ 188 ]  His group has recently shown that  H.\u00a0pylori  colonization is associated with a lower  incidence  of childhood asthma. [ 189 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7709", "text": "In 2023, it was estimated that about two-thirds of the world's population were infected with  H.\u00a0pylori  infection, being more common in  developing countries . [ 20 ]   H. pylori  infection is more prevalent in South America, Sub-Saharan Africa, and the Middle East. [ 153 ]  The global prevalence declined markedly in the decade following 2010, with a particular reduction in Africa. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7710", "text": "The age when someone acquires this bacterium seems to influence the pathologic outcome of the infection. People infected at an early age are likely to develop more intense inflammation that may be followed by atrophic gastritis with a higher subsequent risk of gastric ulcer, gastric cancer, or both. Acquisition at an older age brings different gastric changes more likely to lead to duodenal ulcer. [ 181 ]  Infections are usually acquired in early childhood in all countries. [ 32 ]  However, the infection rate of children in developing nations is higher than in  industrialized nations , probably due to poor sanitary conditions, perhaps combined with lower antibiotics usage for unrelated pathologies. In developed nations, it is currently uncommon to find infected children, but the percentage of infected people increases with age. The higher prevalence among the elderly reflects higher infection rates incurred in childhood. [ 32 ]  In the United States, prevalence appears higher in  African-American  and  Hispanic  populations, most likely due to socioeconomic factors. [ 190 ] [ 191 ]  The lower rate of infection in the West is largely attributed to higher hygiene standards and widespread use of antibiotics. Despite high rates of infection in certain areas of the world, the overall frequency of  H.\u00a0pylori  infection is declining. [ 192 ]  However, antibiotic resistance is appearing in  H.\u00a0pylori ; many metronidazole- and clarithromycin-resistant strains are found in most parts of the world. [ 193 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7711", "text": "Helicobacter pylori   migrated out of Africa  along with its human host around 60,000\u00a0years ago. [ 194 ]  Research has shown that  genetic diversity  in  H.\u00a0pylori , like that of its host, decreases with geographic distance from  East Africa . Using the genetic diversity data, researchers have created simulations that indicate the bacteria seem to have spread from East Africa around 58,000\u00a0years ago. Their results indicate modern humans were already infected by  H.\u00a0pylori  before their migrations out of Africa, and it has remained associated with human hosts since that time. [ 195 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7712", "text": "H.\u00a0pylori  was first discovered in the stomachs of patients with gastritis and  ulcers  in 1982 by  Barry Marshall  and  Robin Warren  of  Perth, Western Australia . At the time, the conventional thinking was that no bacterium could live in the acid environment of the human stomach. In recognition of their discovery, Marshall and Warren were awarded the 2005\u00a0 Nobel Prize in Physiology or Medicine . [ 196 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7713", "text": "Before the research of Marshall and Warren, German scientists found spiral-shaped  bacteria  in the lining of the human stomach in 1875, but they were unable to  culture  them, and the results were eventually forgotten. [ 185 ]  The Italian researcher  Giulio Bizzozero  described similarly shaped bacteria living in the acidic environment of the stomach of dogs in 1893. [ 197 ]  Professor  Walery Jaworski  of the  Jagiellonian University  in  Krak\u00f3w  investigated sediments of gastric washings obtained by  lavage  from humans in 1899. Among some rod-like bacteria, he also found bacteria with a characteristic spiral shape, which he called  Vibrio rugula . He was the first to suggest a possible role of this organism in the pathogenesis of gastric diseases. His work was included in the  Handbook of Gastric Diseases , but it had little impact, as it was published only in Polish. [ 198 ]  Several small studies conducted in the early 20th century demonstrated the presence of curved rods in the stomachs of many people with peptic ulcers and stomach cancers. [ 199 ]  Interest in the bacteria waned, however, when an American study published in 1954 failed to observe the bacteria in 1180 stomach biopsies. [ 200 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7714", "text": "Interest in understanding the role of bacteria in stomach diseases was rekindled in the 1970s, with the visualization of bacteria in the stomachs of people with gastric ulcers. [ 201 ]  The bacteria had also been observed in 1979, by Robin Warren, who researched it further with Barry Marshall from 1981. After unsuccessful attempts at culturing the bacteria from the stomach, they finally succeeded in visualizing colonies in 1982, when they unintentionally left their  Petri dishes  incubating for five days over the  Easter  weekend. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by bacterial infection and not by  stress  or  spicy food , as had been assumed before. [ 202 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7715", "text": "Some skepticism was expressed initially, but within a few years multiple research groups had verified the association of  H.\u00a0pylori  with gastritis and, to a lesser extent, ulcers. [ 203 ]  To demonstrate  H.\u00a0pylori  caused gastritis and was not merely a bystander, Marshall drank a beaker of  H.\u00a0pylori  culture. He became ill with nausea and vomiting several days later. An endoscopy 10\u00a0days after inoculation revealed signs of gastritis and the presence of  H.\u00a0pylori . These results suggested  H.\u00a0pylori  was the causative agent. Marshall and Warren went on to demonstrate antibiotics are effective in the treatment of many cases of gastritis. In 1994, the  National Institutes of Health  stated most recurrent duodenal and gastric ulcers were caused by  H.\u00a0pylori , and recommended antibiotics be included in the treatment regimen. [ 204 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7716", "text": "The bacterium was initially named  Campylobacter pyloridis , then renamed  C.\u00a0pylori  in 1987 ( pylori  being the  genitive  of  pylorus , the circular opening leading from the stomach into the duodenum, from the  Ancient Greek  word  \u03c0\u03c5\u03bb\u03c9\u03c1\u03cc\u03c2 , which means  gatekeeper [ 205 ] ). [ 206 ]  When  16S ribosomal RNA   gene sequencing  and other research showed in 1989 that the bacterium did not belong in the genus  Campylobacter , it was placed in its own  genus ,  Helicobacter  from the Ancient Greek  \u03ad\u03bb\u03b9\u03be  ( h\u011blix ) \"spiral\" or \"coil\". [ 205 ] [ 207 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7717", "text": "In October 1987, a group of experts met in Copenhagen to found the European Helicobacter Study Group (EHSG), an international multidisciplinary research group and the only institution focused on  H.\u00a0pylori . [ 208 ]  The Group is involved with the Annual International Workshop on Helicobacter and Related Bacteria, [ 209 ]  (renamed as the European Helicobacter and Microbiota Study Group [ 210 ] ), the Maastricht Consensus Reports (European Consensus on the management of  H.\u00a0pylori ), [ 211 ] [ 212 ] [ 213 ] [ 214 ]  and other educational and research projects, including two international long-term projects:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7718", "text": "Results from  in vitro  studies suggest that  fatty acids , mainly  polyunsaturated fatty acids , have a bactericidal effect against  H.\u00a0pylori , but their  in vivo  effects have not been proven. [ 218 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7719", "text": "The antibiotic resistance provided by biofilms has generated much research into targeting the mechanisms of  quorum sensing  used in the formation of biofilms. [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7720", "text": "A suitable vaccine for  H. pylori , either prophylactic or therapeutic, is an ongoing research aim. [ 8 ]  The  Murdoch Children's Research Institute  is working at developing a vaccine that instead of specifically targeting the bacteria, aims to inhibit the inflammation caused that leads to the associated diseases. [ 147 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7721", "text": "Gastric organoids  can be used as models for the study of  H. pylori  pathogenesis. [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7722", "text": "Bismuth subcitrate potassium  is a  bismuth  salt used in combination with antibiotics and a  proton pump inhibitor  for the treatment of  Helicobacter pylori  infections. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7723", "text": "A fixed-dose combination with the antibiotics  metronidazole  and  tetracycline  is sold under the trade name  Pylera . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7724", "text": "A known side effect of bismuth salts is harmless and reversible darkening of tongue and stool by formation of bismuth  sulfite . [ 3 ]  Other side effects of bismuth containing combination therapies are often difficult to assign to a specific component. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7725", "text": "Bismuth absorption is increased by  ranitidine  and  omeprazole . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7726", "text": "The mechanism of action of bismuth is not known. It has been reasoned to interfere with the function of the bacterial  cell membrane ,  protein  and  cell wall  synthesis, the enzyme  urease ,  cell adhesion ,  ATP synthesis , and iron transport mechanisms. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7727", "text": "Bismuth subcitrate potassium is a salt of  bismuth  (Bi 3+ ),  potassium  (K + ) and  citrate  ( C 6 H 4 O 4\u2212 7 ) in a  molar  ratio of about 1:5:2, with 3 moles of water. It contains about 25.6% ( mass percent ) bismuth, which is the active  moiety , and 22.9% potassium. [ 3 ] [ 4 ]  Other sources give somewhat different ratios of the constituents."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7728", "text": "The drug combination  bismuth subcitrate/metronidazole/tetracycline  (trade name  Pylera ) is used for the treatment of  peptic ulcer  with an infection by the bacterium  Helicobacter pylori . [ 1 ]  It is taken  by mouth . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7729", "text": "It is available as a  generic medication . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7730", "text": "This combination is used together with  omeprazole  as a 'quadruple therapy' for the  eradication of  H. pylori  and for preventing  peptic ulcers  that are caused by this bacterium. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7731", "text": "The drug must not be taken by pregnant women, because tetracycline is known to cause tooth and bone defects in unborn children. It is also contraindicated in breastfeeding women, children up to 12 years of age, and by patients with impaired liver or renal (kidney) function, because no studies in such persons have been conducted. Tetracycline is also likely to be harmful in liver patients. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7732", "text": "Common side effects include diarrhea, nausea and  dysgeusia  (distortion of the sense of taste), especially a metallic taste. These effects are known from the drug's components as well as from other antibiotics. A very rare but dangerous reaction is  Stevens\u2013Johnson syndrome , a life-threatening condition affecting the skin, which has also been described under metronidazole and tetracycline as separate drugs. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7733", "text": "Metronidazole in combination with alcohol causes severe reactions such as vomiting and flushes in many patients. Tetracycline resorption is reduced by dairy products,  antacids  and other products containing  calcium ,  magnesium ,  aluminium  as well as  iron . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7734", "text": "Bismuth subcitrate potassium is a salt of  bismuth  (Bi 3+ ),  potassium  (K + ) and  citrate  (C 6 H 5 O 7 3\u2212 ), containing about 25.6% ( mass percent ) bismuth, which is the active  moiety , and 22.9% potassium. Tetracycline is contained as the  hydrochloride , and metronidazole as the pure substance. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7735", "text": "In molecular biology,  CagZ  is a  protein  produced by  Helicobacter pylori  ( Campylobacter pylori ). It is a 23 kDa protein consisting of a single compact L-shaped domain, composed of seven  alpha-helices  that run  antiparallel  to each other. 70% of the amino acids are in  alpha-helix  conformation and no  beta-sheet  is present. CagZ is essential for the translocation of the  pathogenic  protein CagA into host  cells . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7736", "text": "Helicobacter pylori  eradication protocols  is a standard name for all treatment protocols for  peptic ulcers  and  gastritis  in the presence of  Helicobacter pylori  infection. The primary goal of the treatment is not only temporary relief of symptoms but also total elimination of  H. pylori  infection. Patients with active duodenal or gastric ulcers and those with a prior  ulcer  history should be tested for  H. pylori . Appropriate therapy should be given for eradication. Patients with  MALT lymphoma  should also be tested and treated for  H. pylori  since eradication of this infection can induce remission in many patients when the  tumor  is limited to the stomach. Several consensus conferences, including the Maastricht Consensus Report, recommend testing and treating several other groups of patients but there is limited evidence of benefit. This includes patients diagnosed with gastric  adenocarcinoma  (especially those with early-stage disease), patients found to have  atrophic gastritis  or intestinal metaplasia, as well as first-degree relatives of patients with gastric adenocarcinoma since the relatives themselves are at increased risk of gastric cancer partly due to the intrafamilial transmission of  H. pylori . To date, it remains controversial whether to test and treat all patients with  functional dyspepsia ,  gastroesophageal reflux disease , or other non-GI disorders as well as asymptomatic individuals. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7737", "text": "The success of  H. pylori  cure depends on the type and duration of therapy, patient compliance and bacterial factors such as  antibiotic resistance . Patients most often fail to respond to initial  H. pylori  eradication therapy because of noncompliance or antibiotic resistance. Patients should be queried about any side effects, missed doses, and completion of therapy. As culture with antibiotic sensitivities is not routinely performed when a  H. pylori  infection is diagnosed, it is generally recommended that different antibiotics be given at higher doses for 14 days. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7738", "text": "Achieving optimal eradication of  H. pylori  has proven difficult. Combination regimens that use two or three antibiotics with a  proton pump inhibitor  and/or  bismuth  are required to achieve adequate rates of eradication and to reduce the number of failures due to antibiotic resistance. In the United States, up to 50% of strains are resistant to metronidazole and 13% are resistant to clarithromycin. At present, experts disagree on the optimal regimen. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7739", "text": "In areas of low  clarithromycin  resistance, including the United States, a 14-day course of \"triple therapy\" with an oral proton pump inhibitor, clarithromycin 500 mg, and  amoxicillin  1 g (or, if  penicillin  allergic,  metronidazole  500 mg), all given twice daily for 14 days, is recommended for first-line therapy.  This regimen can achieve rates of eradication in up to 70% of cases. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7740", "text": "A 14-day course of \"quadruple therapy\" with a proton pump inhibitor, bismuth,  tetracycline , and  metronidazole  or  tinidazole  is a more complicated but also more effective regimen. In a 2011 randomized, controlled trial, the per protocol eradication rates were 93% with quadruple therapy and 70% with triple therapy. Bismuth-based quadruple therapy is recommended as first line therapy for patients in areas with high clarithromycin resistance (> 20%), in patients who have previously been treated with a macrolide antibiotic, or as second-line therapy for patients whose infection persists after an initial course of triple therapy. Several studies reported eradication rates of > 90% using a 10-day sequential regimen consisting of four drugs: a proton pump inhibitor and amoxicillin for 5 days, followed by a proton pump inhibitor, clarithromycin, and tinidazole for 5 days. However, subsequent studies confirmed equivalent or superior efficacy when all four drugs were given concomitantly for 10 days (non-bismuth quadruple therapy). [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7741", "text": "Sequential therapy is a newer approach that combines a 5-day course of a \"dual therapy\" using a proton pump inhibitor in combination with amoxicillin, with a sequential second 5-day course of the standard \"triple therapy\". [ 3 ]  High-dose dual therapy has comparable efficacy with bismuth-containing quadruple therapy, with fewer adverse effects and higher compliance. [ 7 ]  Although initial studies promisingly reported higher eradication rates, [ 3 ]  there is no superiority compared to the other therapies except in the presence of clarithromycin resistant organisms. In regions of high clarithromycin resistance, there is a high rate of eradication with a 14-day quadruple therapy consisting of a proton pump inhibitor, amoxicillin, clarithromycin, and  nitroimidazole ; still, the latter not available in the United States. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7742", "text": "A number of other eradication regimens have been proposed. In the Table below they are compared to with standard regimes."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7743", "text": "Recent meta-analyses have proposed two adjuvant therapies which may help in the eradication of  H. pylori . Periodontal therapy or what is known as  scaling and root planing  and  probiotics  both need further studies to confirm their adjuvant role. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7744", "text": "A 2016 systematic review has found that periodontal therapy (the use of mouthwash, tooth brushing, and manual removal of dental plaques) may have a role as an added treatment for short- and long-term follow up. For these results to be confirmed with regards eradication and non-recurrence, larger studies need to be carried out. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7745", "text": "Some studies have recently evaluated the role of the yeast  Saccharomyces boulardii  as a coadjutant in the eradication of  H. pylori  and in the prevention of the secondary effects of  antibiotic  therapy such as  antibiotic-associated diarrhea . A meta-analysis showed that supplementation with  S. boulardii  significantly increased the  H. pylori  eradication rate and reduced the risk of overall  H. pylori  therapy-related adverse effects. [ 12 ]  In a cohort of patients in Korea who received  S. boulardii  for 4 weeks during and after a 1-week course of standard triple therapy, eradication rates were 10% higher than for those who did not receive the supplement. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7746", "text": "Other studies in which  Bifidobacterium  spp.  and  Lactobacillus acidophilus  have been administered revealed no significant difference in eradication rates in patients who were infected with strains susceptible to both antibiotics and who were treated with standard triple therapy. Further studies will be necessary to clarify the exact role of the  probiotics  in the eradication treatment. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7747", "text": "One of the first \"eradication protocols\", if not the first, was used by  J. Robin Warren  and  Barry Marshall . Barry Marshall treated his own  gastritis , which developed following intentional ingestion of  H. pylori   culture . He used  bismuth  salt and  metronidazole . This treatment effectively cured his gastritis and eliminated the  H. pylori  infection.  This is not the current eradication protocol. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7748", "text": "One of the first \"modern\" eradication protocols was a one-week triple therapy, which the Sydney gastroenterologist  Thomas Borody  formulated in 1987. [ 14 ]  As of 2006, a standard triple therapy is  amoxicillin ,  clarithromycin , and a  proton pump inhibitor  such as  omeprazole , [ 15 ]   lansoprazole ,  pantoprazole , or  esomeprazole . Protocols with metronidazole were also in use. [ 15 ] \nAn example of a fixed-dose combination is PantoPac, containing pantoprazole, clarithromycin, and amoxicillin. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7749", "text": "Giving  acetylcysteine  before antibiotic treatment was effective in overcoming  H. pylori  antibiotic resistance in a study with 40 patients who had at least four eradication failures in their history. The researchers believe it works by inhibiting the formation of  biofilm . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7750", "text": "Whereas the conventional  proton pump inhibitor -based triple therapy is effective, there is research in using longer acid suppression therapies, in particular, using  potassium competitive acid blocker  triple and dual therapy. In particular,  vonoprazan  is approved by the  US Food and Drug Administration  (FDA) for H. pylori eradication. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7751", "text": "helicoCARE direct  is a  Helicobacter pylori  whole-blood  antibody test  that was introduced worldwide in 2006. It is manufactured by  CARE diagnostica . It is an  immunochromatographic  test which detects the presence of  antibodies  against  H. pylori  in whole-blood samples. This test is suitable for screening large populations for  peptic ulcer  disease. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7752", "text": "Omeprazole/amoxicillin/rifabutin , sold under the brand name  Talicia , is a  fixed-dose combination  medication used for the treatment of  Helicobacter pylori  infection. [ 1 ]  It is taken  by mouth . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7753", "text": "It was approved for medical use in the United States in November 2019. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7754", "text": "This systemic  antibiotic -related article is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7755", "text": "Rifasutenizol  is an  investigational new drug  developed by TenNor Therapeutics, primarily aimed at treating  Helicobacter pylori  infections. [ 1 ]  It is a novel multi-targeting small molecule that functions as a bacterial DNA-directed  RNA polymerase  inhibitor. [ 2 ]  This drug has been granted  Qualified Infectious Disease Product  and  Fast Track designations  by the  U.S. FDA . [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7756", "text": "This is a  timeline of the events relating to the discovery that peptic ulcer disease and some cancers are caused by  H. pylori . In 2005,  Barry Marshall  and  Robin Warren  were awarded the  Nobel Prize in Physiology or Medicine  for their discovery that  peptic ulcer disease  (PUD) was primarily caused by  Helicobacter pylori , a  bacterium  with affinity for acidic environments, such as the  stomach . As a result, PUD that is associated with  H. pylori  is currently treated with  antibiotics  used to eradicate the infection. For decades prior to their discovery, it was widely believed that PUD was caused by excess  acid  in the  stomach . During this time, acid control was the primary method of treatment for PUD, to only partial success. Among other effects, it is now known that acid suppression alters the stomach milieu to make it less amenable to  H. pylori  infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7757", "text": "Before the 1950s, there were many microbiological descriptions of bacteria in the stomach and in gastric acid secretions, lending credence to both the infective theory and the hyperacidity theory as being causes of peptic ulcer disease. A single study, conducted in 1954, did not find evidence of bacteria on biopsies of the stomach stained traditionally; this effectively established the acid theory as  dogma . This paradigm was altered when Warren and Marshall effectively proved  Koch's postulates  for causation of PUD by  H. pylori  through a series of experiments in the 1980s; however, an extensive effort was required to convince the medical community of the relevance of their work. Now, all major gastrointestinal societies agree that  H. pylori  is the primary nondrug cause of PUD worldwide, and advocate its eradication as essential to treatment of gastric and duodenal ulcers. Additionally,  H. pylori  has been associated with  lymphomas  and  adenocarcinomas  of the stomach, and has been classified by the  World Health Organization  as a  carcinogen . Advances in  molecular biology  in the late 20th century led to the sequencing of the  H. pylori  genome, resulting in a better understanding of  virulence factors  responsible for its colonization and infection, on the DNA level."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7758", "text": "Ascariasis  is a disease caused by the parasitic  roundworm   Ascaris lumbricoides . [ 1 ]  Infections have no symptoms in more than 85% of cases, especially if the number of worms is small. [ 1 ]  Symptoms increase with the number of worms present and may include  shortness of breath  and fever at the beginning of the disease. [ 1 ]  These may be followed by symptoms of abdominal swelling, abdominal pain, and  diarrhea . [ 1 ]  Children are most commonly affected, and in this age group the infection may also cause poor weight gain,  malnutrition , and learning problems. [ 1 ] [ 2 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7759", "text": "Infection occurs by ingesting food or drink contaminated with  Ascaris  eggs from feces. [ 2 ]  The eggs hatch in the  intestines , the larvae burrow through the gut wall, and migrate to the lungs via the blood. [ 2 ]  There they break into the  alveoli  and pass up the  trachea , where they are coughed up and may be swallowed. [ 2 ]  The larvae then pass through the stomach a second time into the intestine, where they become adult worms. [ 2 ]  It is a type of  soil-transmitted helminthiasis  and part of a group of diseases called  helminthiases . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7760", "text": "Prevention is by improved  sanitation , which includes improving access to toilets and proper disposal of  feces . [ 1 ] [ 7 ]  Handwashing with soap appears protective. [ 8 ]  In areas where more than 20% of the population is affected, treating everyone at regular intervals is recommended. [ 1 ]  Reoccurring infections are common. [ 2 ] [ 9 ]  There is no  vaccine . [ 2 ]  Treatments recommended by the  World Health Organization  are the medications  albendazole ,  mebendazole ,  levamisole , or  pyrantel pamoate . [ 2 ]  Other effective agents include  tribendimidine  and  nitazoxanide . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7761", "text": "About 0.8 to 1.2 billion people globally have ascariasis, with the most heavily affected populations being in  sub-Saharan Africa ,  Latin America , and Asia. [ 1 ] [ 10 ] [ 11 ]  This makes ascariasis the most common form of  soil-transmitted helminthiasis . [ 10 ]  As of 2010 it caused about 2,700 deaths a year, down from 3,400 in 1990. [ 12 ]  Another type of  Ascaris  infects pigs. [ 1 ]  Ascariasis is classified as a  neglected tropical disease . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7762", "text": "In populations where  worm infections  are widespread, it is common to find that most people are infected by a small number of worms, while a small number of people are heavily infected. This is characteristic of many types of worm infections. [ 1 ] [ 13 ]  Those people who are infected with only a small number of worms usually have no symptoms. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7763", "text": "As larval stages travel through the body, they may cause visceral damage,  peritonitis  and  inflammation , enlargement of the  liver  or  spleen , and an  inflammation of the lungs . Pulmonary manifestations take place during larval migration and may present as  Loeffler's syndrome , a transient respiratory illness associated with blood eosinophilia and pulmonary infiltrates with radiographic shadowing. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7764", "text": "The worms can occasionally cause intestinal blockage when large numbers get tangled into a bolus or they may migrate from the small intestine, which may require surgery. [ 17 ]  More than 796  A. lumbricoides  worms weighing up to 550\u00a0g (19\u00a0oz) were recovered at autopsy from a two-year-old South African girl. The worms had caused torsion and gangrene of the  ileum , which was interpreted as the cause of death. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7765", "text": "The worms lack teeth. However, they can rarely cause bowel perforations by inducing  volvulus  and closed-loop obstruction. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7766", "text": "Bowel obstruction  may occur in up to 0.2 per 1000 per year. [ 1 ]  A worm may block the  ampulla of Vater , or go into the  main pancreatic duct , resulting in acute  pancreatitis  with raised serum levels of  amylase  and  lipase . Occasionally, a worm can travel through the biliary tree and even into the  gallbladder , causing acute  cholangitis  or acute  cholecystitis . [ 19 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7767", "text": "Ascariasis may result in  allergies  to shrimp and  dustmites  due to the shared  antigen ,  tropomyosin ; this has not been confirmed in the laboratory. [ 20 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7768", "text": "The worms in the intestine may cause  malabsorption  and  anorexia , which contribute to  malnutrition . [ 22 ]  The malabsorption may be due to a loss of brush border enzymes, erosion and flattening of the villi, and inflammation of the  lamina propria . [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7769", "text": "Ascaris  have an aversion to some general anesthetics and may exit the body, sometimes through the mouth, when an infected individual is put under  general anesthesia . [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7770", "text": "The source of infection is from objects contaminated with fecal matter containing eggs. [ 2 ]  Ingestion of infective eggs from soil contaminated with human feces or contaminated vegetables and water is the primary route of infection. Infectious eggs may occur on objects such as hands, money, and furniture. [ 2 ]  Transmission from human to human by direct contact is impossible. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7771", "text": "Transmission comes through municipal recycled wastewater into crop fields. This is quite common in emerging industrial economies and poses serious risks for local crop sales and exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow  Balkan  vegetable exports. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7772", "text": "The number of  ova  (eggs) in  sewage  or in crops that were irrigated with raw or partially treated sewage, is a measure of the degree of ascariasis incidence. [ citation needed ]  For example:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7773", "text": "The first appearance of eggs in stools is 60\u201370 days. In larval ascariasis, symptoms occur 4\u201316 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever, and observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during the migration of the larvae. There are generally few or no symptoms. A  bolus  of worms may obstruct the intestine; migrating larvae may cause  pneumonitis  and  eosinophilia . Adult worms have a lifespan of 1\u20132 years which means that individuals may be infected all their lives as worms die and new worms are acquired. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7774", "text": "Eggs can survive potentially for 15 years and a single worm may produce 200,000 eggs a day. [ 2 ]  They maintain their position by swimming against the intestinal flow. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7775", "text": "Ascaris  takes most of its nutrients from the partially digested host food in the intestine. There is some evidence that it can secrete  enzyme inhibitors , presumably to protect itself from digestion by the hosts' enzymes. Children are often more severely affected. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7776", "text": "Most  diagnoses  are made by identifying the appearance of the  worm  or eggs in feces. Due to the large quantity of eggs laid, diagnosis can generally be made using only one or two  fecal smears . [ 31 ] \nThe diagnosis is usually incidental when the host passes a worm in the stool or vomit. The eggs can be seen in a smear of fresh feces examined on a glass slide under a microscope and there are various techniques to concentrate them first or increase their visibility, such as the ether sedimentation method or the  Kato technique . The eggs have a characteristic shape: they are oval with a thick, mamillated shell (covered with rounded mounds or lumps), measuring  35\u201350 micrometer in diameter and 40\u201370 in length. During pulmonary disease, larvae may be found in fluids aspirated from the lungs. White blood cell counts may demonstrate peripheral  eosinophilia ; this is common in many parasitic infections and is not specific to ascariasis. On X-ray, 15\u201335\u00a0cm long filling defects, sometimes with a whirled appearance (bolus of worms). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7777", "text": "Prevention is by improved access to sanitation which includes the use of properly functioning and clean toilets by all community members as one important aspect. [ 1 ]  Handwashing with soap may be protective; however, there is no evidence it affects the severity of the disease. [ 8 ]  Eliminating the use of untreated human faeces as  fertilizer  is also important. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7778", "text": "In areas where more than 20% of the population is affected treating everyone is recommended. [ 1 ]  This has a cost of about 2 to 3 cents per person per treatment. [ 1 ]  This is known as  mass drug administration  and is often carried out among school-age children. [ 32 ]  For this purpose, broad-spectrum  benzimidazoles  such as  mebendazole  and  albendazole  are the drugs of choice recommended by  WHO . [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7779", "text": "Medications that are used to kill roundworms are called  ascaricides . Those recommended by the World Health Organization for ascariasis are:  albendazole ,  mebendazole ,  levamisole  and  pyrantel pamoate . [ 2 ]  Single-dose of albendazole, mebendazole, and  ivermectin  are effective against ascariasis. They are effective at removing parasites and eggs from the intestines. [ 34 ]  Other effective agents include  tribendimidine  and  nitazoxanide . [ 2 ]  Pyrantel pamoate may induce intestinal obstruction in a heavy worm load. Albendazole is contraindicated during pregnancy and children under two years of age.  Thiabendazole  may cause migration of the worm into the  esophagus , so it is usually combined with  piperazine . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7780", "text": "Piperazine is a flaccid paralyzing agent that blocks the response of  Ascaris  muscle to acetylcholine, which immobilizes the worm. It prevents migration when treatment is accomplished with weak drugs such as thiabendazole. If used by itself, it causes the worm to be passed out in the feces and may be used when worms have caused blockage of the intestine or the biliary duct. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7781", "text": "Corticosteroids  can treat some of the symptoms, such as inflammation. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7782", "text": "In some cases with severe infestation, the worms may cause  bowel obstruction , requiring emergency surgery. [ 38 ]  The bowel obstruction may be due to the number of worms in the bowel or  twisting of the bowel . [ 38 ]  During the surgery the worms may be manually removed. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7783", "text": "It is rare for infections to be life-threatening. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7784", "text": "Ascariasis is  common  in tropical regions as well as subtropical and regions that lack proper sanitation. It is rare to find traces of the infection in developed or urban regions. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7785", "text": "Roughly 0.8\u20131.3 billion individuals are infected with this intestinal worm, primarily in Africa and Asia. [ 1 ] [ 2 ] [ 11 ]  About 120 to 220 million of these cases are symptomatic. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7786", "text": "As of 2010, ascariasis caused about 2,700 directly attributable deaths, down from 3,400 in 1990. [ 12 ]  The indirectly attributable deaths due to the malnutrition link may be much higher. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7787", "text": "Mouse and pig animal models are used to study  Ascaris  infection. [ 40 ] [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7788", "text": "Ascariasis is more common in young animals than mature ones, with signs including unthriftiness, potbelly, rough hair coat, and slow growth. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7789", "text": "In pigs, the infection is caused by  Ascaris suum .  It is characterized by poor weight gain, leading to financial losses for the farmer. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7790", "text": "In horses and other equines, the equine roundworm is  Parascaris equorum . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7791", "text": "Kings of England Richard III [ 43 ]  and Henry VIII [ 44 ]  both had ascariasis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7792", "text": "Blastocystosis  refers to a medical condition caused by infection with  Blastocystis .   Blastocystis  is a protozoal, single-celled parasite that inhabits the gastrointestinal tracts of humans and other animals.  Many different types of  Blastocystis  exist, and they can infect humans, farm animals, birds, rodents, amphibians, reptiles, fish, and even cockroaches. Blastocystosis has been found to be a possible risk factor for development of  irritable bowel syndrome . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7793", "text": "Researchers have published conflicting reports concerning whether  Blastocystis  causes symptoms in humans, with one of the earliest reports in 1916. [ 2 ]   The incidence of reports associated with symptoms began to increase in 1984, [ 3 ]  with physicians from Saudi Arabia reporting symptoms in humans [ 4 ]  and US physicians reporting symptoms in individuals with travel to less developed countries. [ 5 ]   A lively debate ensued in the early 1990s, with some physicians objecting to publication of reports that  Blastocystis  caused disease. [ 6 ] [ 7 ] [ 8 ] [ 9 ]   Some researchers believe the debate has been resolved by finding of multiple species of  Blastocystis  that can infect humans, with some causing symptoms and others being harmless (see Genetics and Symptoms). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7794", "text": "A few of most commonly reported symptoms are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7795", "text": "Some less commonly reported symptoms include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7796", "text": "Researchers have sought to develop models to understand the variety of symptoms seen in humans.  Some patients do not have symptoms, while others report severe diarrhea and fatigue. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7797", "text": "A number of researchers have investigated the possibility that some species of  Blastocystis  are more virulent than others. An Italian researcher reported differences in the protein profiles of isolates associated with chronic and acute infection. [ 19 ]   A research team from Malaysia reported that isolates from symptomatic patients produced large amoeboid forms that were not present in isolates from asymptomatic patients. [ 20 ]   The development of a classification system for  Blastocystis  in 2007 produced a series of studies investigating this possibility. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7798", "text": "The studies that followed generally found that no specific \"pathogenic\" or nonpathogenic species of  Blastocystis  exists. [ 21 ] [ 22 ]  One study investigated the subtypes found in patients with irritable bowel syndrome (IBS),  inflammatory bowel disease  (IBD), and chronic diarrhea, and found the subtypes in these diseases were similar (subtypes 2 and 3), and have also been found in asymptomatic carriers. The researchers concluded that host factors, such as age and genetics, may play the dominant role in determining the symptoms seen in the disease. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7799", "text": "Blastocystis colonisation is positively associated with  IBS  and is a possible risk factor for developing IBS. [ 1 ]  A study of IBS patients in the Middle East showed a \"significantly increased\" immune reaction in IBS patients to  Blastocystis , even when the organism could not be identified in stool samples. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7800", "text": "The following reports have linked  Blastocystis  infection to  inflammatory bowel disease :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7801", "text": "Humans contract  Blastocystis  infection by drinking water or eating food contaminated with  feces  from an infected human or animal. [ 29 ]   Blastocystis  infection can be spread from animals to humans, from humans to other humans, from humans to animals, and from animals to animals. [ 30 ] [ 31 ]  Risk factors for infection have been reported as following:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7802", "text": "Research studies have suggested the following items are  not  risk factors for contracting  Blastocystis  infection:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7803", "text": "Pathogenesis refers to the mechanism by which an organism causes disease.  The following disease-causing mechanisms have been reported in studies of  Blastocystis  infection:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7804", "text": "Diagnosis is performed by determining if the infection is present, and then making a decision as to whether the infection is responsible for the symptoms.  Diagnostic methods in clinical use have been reported to be of poor quality and more reliable methods have been reported in research papers. [ 30 ] [ 59 ] [ 60 ] [ 61 ] [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7805", "text": "For identification of infection, the only method clinically available in most areas is the ova and parasite (O&P) exam, which identifies the presence of the organism by microscopic examination of a chemically preserved stool specimen.  This method is sometimes called direct microscopy.  In the United States, pathologists are required to report the presence of  Blastocystis  when found during an O&P exam, so a special test does not have to be ordered. Direct microscopy is inexpensive, as the same test can identify a variety of gastrointestinal infections, such as  Giardia ,  Entamoeba histolytica , and  Cryptosporidium .  However, one laboratory director noted that pathologists using conventional microscopes failed to identify many  Blastocystis  infections, and indicated the necessity for special microscopic equipment for identification. [ 9 ]   The following table shows the sensitivity of Direct Microscopy in detecting  Blastocystis  when compared to stool culture, a more sensitive technique.  Stool culture was considered by some researchers to be the most reliable technique, but a recent study found stool culture only detected 83% of individuals infected when compared to  polymerase chain reaction  (PCR) testing. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7806", "text": "Reasons given for the failure of Direct Microscopy include: (1) Variable Shedding: The quantity of  Blastocystis  organisms varies substantially from day to day in infected humans and animals; [ 63 ]   (2) Appearance: Some forms of  Blastocystis  resemble fat cells or white blood cells, [ 62 ]  making it difficult to distinguish the organism from other cells in the stool sample; (3) Large number of morphological forms:  Blastocystis  cells can assume a variety of shapes, some have been described in detail only recently, so it is possible that additional forms exist but have not been identified. [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7807", "text": "Several methods have been cited in literature for determination of the significance of the finding of  Blastocystis :"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7808", "text": "The following diagnostic methods are not routinely available to patients.  Researchers have reported that they are more reliable at detecting infection, and in some cases can provide the physician with information to help determine whether  Blastocystis  infection is the cause of the patient's symptoms: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7809", "text": "Serum antibody testing : A 1993 research study performed by the  NIH  with United States patients suggested that it was possible to distinguish symptomatic and asymptomatic infection with  Blastocystis  using serum antibody testing. [ 67 ]   The study used blood samples to measure the patient's immune reaction to chemicals present on the surface of the  Blastocystis  cell.  It found that patients diagnosed with symptomatic  Blastocystis  infection exhibited a much higher immune response than controls who had  Blastocystis  infection but no symptoms.  The study was repeated in 2003 at  Ain Shams University  in Egypt with Egyptian patients with equivalent results. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7810", "text": "Fecal antibody testing : A 2003 study at Ain Shams University in Egypt indicated that patients symptomatically infected could be distinguished with a fecal antibody test. [ 59 ]  The study compared patients diagnosed with symptomatic  Blastocystis  infection to controls who had  Blastocystis  infection but no symptoms.  In the group with symptoms, IgA antibodies to  Blastocystis  were detected in fecal specimens that were not present in the healthy control group."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7811", "text": "Stool culture :  Culturing has been shown to be a more reliable method of identifying infection.  In 2006, researchers reported the ability to distinguish between disease causing and non-disease causing isolates of  Blastocystis  using stool culture. [ 68 ]   Blastocystis  cultured from patients who were sick and diagnosed with  Blastocystis  infection produced large, highly adhesive amoeboid forms in culture.  These cells were absent in  Blastocystis  cultures from healthy controls.  Subsequent genetic analysis showed the  Blastocystis  from healthy controls was genetically distinct from that found in patients with symptoms.  Protozoal culture is unavailable in most countries due to the cost and lack of trained staff able to perform protozoal culture."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7812", "text": "Genetic analysis of isolates : Researchers have used techniques which allow the DNA of  Blastocystis  to be isolated from fecal specimens. [ 30 ] [ 62 ]  This method has been reported to be more reliable at detecting  Blastocystis  in symptomatic patients than stool culture. [ 62 ]   This method also allows the species group of  Blastocystis  to be identified.  Research is continuing into which species groups are associated with symptomatic (see Genetics and Symptoms) blastocystosis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7813", "text": "Immuno-fluorescence (IFA) stain : An IFA stain causes  Blastocystis  cells to glow when viewed under a microscope, making the diagnostic method more reliable.  IFA stains are in use for  Giardia  and  Cryptosporidium  for both diagnostic purposes and water quality testing.  A 1991 paper from the  NIH  described the laboratory development of one such stain. [ 3 ]    However, no company currently offers this stain commercially. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7814", "text": "Reports conflict regarding whether  Blastocystis  causes disease in humans. These reports resulted in a brief debate in medical journals in the early 1990s between some physicians in the United States who believed that  Blastocystis  was harmless, and physicians in the United States and overseas who believed it could cause disease. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7815", "text": "At the time, it was common practice to identify all  Blastocystis  from humans as  Blastocystis hominis , while  Blastocystis  from animals was identified differently (e.g.  Blastocystis ratti  from rats).  Research performed since then has shown that the concept of  Blastocystis hominis  as a unique species of  Blastocystis  infecting humans is not supported by microbiological findings.  Although one species group associated with primates was found, it was also discovered that humans can acquire infection from any one of nine species groups of  Blastocystis  which are also carried by cattle, pigs, rodents, chickens, pheasants, monkeys, dogs, and other animals. [ 30 ] [ 31 ] [ 69 ]  Research has suggested that some types produce few or no symptoms, while others produce illness and intestinal inflammation. [ 68 ] [ 20 ]   Researchers have suggested conflicting reports may be due to the practice of naming all  Blastocystis  from humans  Blastocystis hominis [ 31 ]  and have proposed discontinuing the use of that term. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7816", "text": "A standard naming system for  Blastocystis  organisms from humans and animals has been proposed which names  Blastocystis  isolates according to the genetic identity of the  Blastocystis  organism rather than the host. [ 31 ]   The naming system used identifies all isolates as  Blastocystis  sp. subtype  nn  where nn is a number from 1 to 9 indicating the species group of the  Blastocystis  organism.  The identification of the species can not be performed with a microscope at this time, because the different species look alike.  Identification requires equipment for genetic analysis that is common in microbiology laboratories, but not available to most physicians.  Some new scientific papers have begun using the standard naming system. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7817", "text": "There is a lack of scientific study to support the efficacy of any particular treatment. [ 71 ]  An additional review published in 2009 made a similar conclusion, noting that because the diagnostics in use have been unreliable, it has been impossible to determine whether a drug has eradicated the infection, or just made the patient feel better. [ 72 ]   Historical reports, such as one from 1916, note difficulty associated with eradication of  Blastocystis  from patients, describing it as \"an infection that is hard to get rid of.\" [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7818", "text": "A 1999  in vitro  study from Pakistan found 40% of isolates are resistant to common antiprotozoal drugs. [ 73 ]  A study of isolates from patients diagnosed with IBS found 40% of isolates resistant to  metronidazole  and 32% resistant to  furazolidone . [ 74 ]  Drugs reported in studies to be effective in eradicating  Blastocystis  infection have included  metronidazole , [ 4 ] [ 75 ]   trimethoprim , [ 76 ]   TMP-SMX  (only trimethoprim is active with  sulphamethoxazole  demonstrating no activity), [ 75 ] [ 76 ]   tetracycline , [ 76 ]   doxycycline ,  nitazoxanide , [ 77 ]   pentamidine , [ 78 ]   paromomycin [ 79 ]  and  iodoquinol . [ 80 ]  Iodoquinol has been found to be less effective in practice than in-vitro. [ 81 ] [ 82 ]   Miconazole  and  quinacrine  have been reported as effective agents against  Blastocystis  growth in-vitro. [ 76 ] [ 83 ]   Rifaximin , [ 84 ]  and  albendazole  have shown promise as has  ivermectin  which demonstrated high effectiveness against blastocystis hominis isolates in an in vitro study. [ 85 ]  There is also evidence that the probiotic yeast  Saccharomyces boulardii , [ 79 ]  and the plant  Mallotus oppositifolius [ 86 ]  may be effective against  Blastocystis  infections."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7819", "text": "Physicians have described the successful use of a variety of discontinued antiprotozoals in treatment of  Blastocystis  infection.   Emetine  was reported as successful in cases in early 20th century with British soldiers who contracted  Blastocystis  infection while serving in Egypt. [ 2 ]   In vitro  testing showed  emetine  was more effective than  metronidazole  or  furazolidone . [ 87 ]  Emetine is available in the United States through special arrangement with the  Center for Disease Control .  Clioquinol  (Entero-vioform) was noted as successful in treatment of  Blastocystis  infection but removed from the market following an adverse event in Japan. [ 3 ]   Stovarsol  and Narsenol, two arsenic-based antiprotozoals, were reported to be effective against the infection. [ 3 ]  Carbarsone was available as an anti-infective compound in the United States as late as 1991, and was suggested as a possible treatment. [ 3 ]  The reduction in the availability of antiprotozoal drugs has been noted as a complicating factor in treatment of other protozoal infections. [ 88 ]   For example, in  Australia , production of  diloxanide furoate  ended in 2003,  paromomycin  is available under special access provisions, and the availability of  iodoquinol  is limited. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7820", "text": "Like other protozoal infections, the prevalence of  Blastocystis  infection varies depending on the area investigated and the population selected.  A number of different species groups of  Blastocystis  infect humans, [ 69 ]  with some being reported to cause disease while others do not. [ 68 ] [ 20 ]   To date, surveys have not distinguished between different types of  Blastocystis   in humans, so the significance of findings may be difficult to evaluate.  Developing countries have been reported to have higher incidences, but recent studies suggest that symptomatic infection with  Blastocystis  may be prevalent in certain industrialized countries, as well. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7821", "text": "Experimental infection in immunocompetent and immunocompromised mice has produced intestinal inflammation, altered bowel habits, lethargy, and death. [ 26 ] [ 27 ] [ 28 ]   Chronic diarrhea has been reported in non-human higher primates. [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7822", "text": "While many enteric protists are the subject of research,  Blastocystis  is unusual in that basic questions concerning how it should be diagnosed and treated and how it causes disease remain unsettled.  The following groups have ongoing research programs directed at these questions:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7823", "text": "Singh"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7824", "text": "treatment"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7825", "text": "Botulism  is a rare and potentially fatal  illness  caused by  botulinum toxin , which is produced by the bacterium  Clostridium botulinum . The disease begins with weakness, blurred vision,  feeling tired , and trouble speaking. This may then be followed by weakness of the arms, chest muscles, and legs. Vomiting, swelling of the abdomen, and diarrhea may also occur. The disease does not usually affect  consciousness  or cause a  fever ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7826", "text": "Botulism can occur in several ways. The  bacterial spores  which cause it are common in both soil and water and are very resistant. They produce the  botulinum toxin  when exposed to low oxygen levels and certain temperatures. Foodborne botulism happens when food containing the toxin is eaten. Infant botulism instead happens when the bacterium develops in the  intestines  and releases the toxin. This typically only occurs in children less than one year old, as protective mechanisms against development of the bacterium develop after that age. Wound botulism is found most often among those who  inject street drugs . In this situation, spores enter a wound, and in the absence of oxygen, release the toxin. The disease is not passed directly between people. Its diagnosis is confirmed by finding the toxin or bacteria in the person in question."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7827", "text": "Prevention is primarily by proper food preparation. The toxin, though not the spores, is destroyed by heating it to more than 85\u00a0\u00b0C (185\u00a0\u00b0F) for longer than five minutes. The clostridial spores can be destroyed in an autoclave with moist heat (120\u00b0C/ 250\u00b0F for at least 15 minutes) or dry heat (160\u00b0C for 2 hours) or by irradiation. The spores of group I strains are inactivated by heating at 121\u00b0C (250\u00b0F) for 3 minutes during commercial canning. Spores of group II strains are less heat-resistant, and they are often damaged by 90\u00b0C (194\u00b0F) for 10 minutes, 85\u00b0C for 52 minutes, or 80\u00b0C for 270 minutes; however, these treatments may not be sufficient in some foods. [ 1 ]   Honey  can contain the organism, and for this reason, honey should not be fed to children under 12 months. Treatment is with an  antitoxin . In those who lose their ability to breathe on their own,  mechanical ventilation  may be necessary for months.  Antibiotics  may be used for wound botulism. Death occurs in 5 to 10% of people. Botulism also affects many other animals. The word is from  Latin   botulus , meaning 'sausage'."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7828", "text": "The muscle weakness of botulism characteristically starts in the muscles supplied by the  cranial nerves \u2014a group of twelve nerves that control  eye movements , the  facial muscles  and the muscles controlling  chewing  and  swallowing .  Double vision ,  drooping of both eyelids , loss of facial expression and swallowing problems may therefore occur. In addition to affecting the  voluntary muscles , it can also cause  disruptions in the autonomic nervous system . This is experienced as  a dry mouth and throat  (due to decreased production of saliva),  postural hypotension  (decreased blood pressure on standing, with resultant lightheadedness and risk of blackouts), and eventually  constipation  (due to decreased  forward movement of intestinal contents ). [ 2 ]  Some of the toxins (B and E) also precipitate  nausea ,  vomiting , [ 2 ]  and  difficulty with talking . The weakness then spreads to the arms (starting in the shoulders and proceeding to the forearms) and legs (again from the thighs down to the feet). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7829", "text": "Severe botulism leads to reduced movement of the  muscles of respiration , and hence problems with  gas exchange . This may be experienced as  dyspnea  (difficulty breathing), but when severe can lead to  respiratory failure , due to the buildup of unexhaled  carbon dioxide  and its resultant depressant effect on the brain. This may lead to respiratory compromise and death if untreated. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7830", "text": "Clinicians frequently think of the symptoms of botulism in terms of a classic triad:  bulbar palsy  and descending paralysis, lack of fever, and clear senses and mental status (\"clear sensorium\"). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7831", "text": "Infant botulism (also referred to as  floppy baby syndrome ) was first recognized in 1976, and is the most common form of botulism in the United States. Infants are susceptible to infant botulism in the first year of life, with more than 90% of cases occurring in infants younger than six months. [ 4 ]  Infant botulism results from the ingestion of the  C. botulinum  spores, and subsequent colonization of the small intestine. The infant gut may be colonized when the composition of the  intestinal microflora  (normal flora) is insufficient to competitively inhibit the growth of  C. botulinum  and levels of bile acids (which normally inhibit  clostridial  growth) are lower than later in life. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7832", "text": "The growth of the spores releases  botulinum toxin , which is then absorbed into the bloodstream and taken throughout the body, causing paralysis by blocking the release of  acetylcholine  at the  neuromuscular junction . Typical symptoms of infant botulism include constipation, lethargy, weakness, difficulty feeding, and an altered cry, often progressing to a complete descending  flaccid paralysis . Although constipation is usually the first symptom of infant botulism, it is commonly overlooked. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7833", "text": "Honey  is a known dietary reservoir of  C. botulinum  spores and has been linked to infant botulism. For this reason, honey is not recommended for infants less than one year of age. [ 5 ]  Most cases of infant botulism, however, are thought to be caused by acquiring the spores from the natural environment.  Clostridium botulinum  is a ubiquitous soil-dwelling bacterium. Many infant botulism patients have been demonstrated to live near a construction site or an area of soil disturbance. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7834", "text": "Infant botulism has been reported in 49 of 50 US states (all save for Rhode Island), [ 4 ]  and cases have been recognized in 26 countries on five continents. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7835", "text": "Infant botulism has no long-term side effects. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7836", "text": "Botulism can result in death due to  respiratory  failure. However, in the past 50 years, the proportion of patients with botulism who die has fallen from about 50% to 7% due to improved supportive care. A patient with severe botulism may require  mechanical ventilation  (breathing support through a ventilator) as well as intensive medical and nursing care, sometimes for several months. The person may require rehabilitation therapy after leaving the hospital. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7837", "text": "Clostridium botulinum  is an  anaerobic ,  Gram-positive , spore-forming rod.  Botulinum toxin  is one of the most powerful known toxins: about one  microgram  is lethal to humans when inhaled. [ 10 ]  It acts by blocking  nerve  function ( neuromuscular blockade ) through inhibition of the excitatory  neurotransmitter   acetylcholine 's release from the  presynaptic  membrane of  neuromuscular junctions  in the  somatic nervous system . This causes paralysis. Advanced botulism can cause  respiratory failure  by paralysing the muscles of the chest; this can progress to  respiratory arrest . [ 11 ]  Furthermore, acetylcholine release from the presynaptic membranes of  muscarinic  nerve synapses is blocked. This can lead to a variety of autonomic signs and symptoms described above. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7838", "text": "In all cases, illness is caused by the botulinum toxin which the bacterium  C. botulinum  produces in anaerobic conditions and not by the bacterium itself. The pattern of damage occurs because the toxin affects nerves that fire (depolarize) at a higher frequency first. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7839", "text": "Mechanisms of entry into the human body for botulinum toxin are described below. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7840", "text": "The most common form in Western countries is infant botulism. This occurs in infants who are  colonized  with the bacterium in the small intestine during the early stages of their lives. The bacterium then produces the toxin, which is absorbed into the bloodstream. The consumption of  honey  during the first year of life has been identified as a risk factor for infant botulism; it is a factor in a fifth of all cases. [ 2 ]  The adult form of infant botulism is termed  adult intestinal toxemia , and is exceedingly rare. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7841", "text": "Toxin that is produced by the bacterium in containers of food that have been improperly preserved is the most common cause of food-borne botulism. Fish that has been pickled without the salinity or acidity of brine that contains  acetic acid  and high  sodium  levels, as well as smoked fish stored at too high a temperature, presents a risk, as does improperly canned food. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7842", "text": "Food-borne botulism results from contaminated food in which  C. botulinum  spores have been allowed to germinate in low-oxygen conditions. This typically occurs in improperly prepared home-canned food substances and fermented dishes without adequate salt or acidity. [ 13 ]  Given that multiple people often consume food from the same source, it is common for more than a single person to be affected simultaneously. Symptoms usually appear 12\u201336 hours after eating, but can also appear within 6 hours to 10 days. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7843", "text": "No withdrawal periods have been established for cows affected by Botulism. Lactating cows injected with various doses of Botulinum toxin C have not resulted in detectable Botulinum  neurotoxin  in milk produced. [ 15 ]  Using  mouse bioassays  and  immunostick ELISA tests , botulinum toxin was detected in whole blood and serum but not in milk samples, suggesting that botulinum type C toxin does not enter milk in detectable concentrations. [ 16 ]  Cooking and pasteurization denatures botulinum toxin but does not necessarily eliminate spores. Botulinum spores or toxins can find their way into the dairy production chain from the environment. [ 17 ]  Despite the low risk of milk and meat contamination, the protocol for fatal bovine botulism cases appears to be incineration of carcasses and withholding any potentially contaminated milk from human consumption. It is also advised that raw milk from affected cows should not be consumed by humans or fed to calves. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7844", "text": "There have been several reports of botulism from pruno wine made of food scraps in prison. [ 19 ] [ 20 ] [ 21 ]  In a Mississippi prison in 2016, prisoners illegally brewed alcohol that led to 31 cases of botulism. The research study done on these cases found the symptoms of mild botulism matched the symptoms severe botulism though the outcomes and progression of the disease were different. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7845", "text": "Wound botulism results from the contamination of a wound with the bacteria, which then secrete the toxin into the bloodstream. This has become more common in  intravenous drug users  since the 1990s, especially people using  black tar heroin  and those  injecting heroin into the skin  rather than the veins. [ 2 ]  Wound botulism can also come from a minor wound that is not properly cleaned out; the skin grows over the wound thus trapping the spore in an anaerobic environment and creating botulism. One example was a person who cut their ankle while using a weed eater; as the wound healed over, it trapped a blade of grass and spec of soil under the skin that lead to severe botulism requiring hospitalization and rehabilitation for months. Wound botulism accounts for 29% of cases. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7846", "text": "Isolated cases of botulism have been described after  inhalation  by laboratory workers. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7847", "text": "Symptoms of botulism may occur away from the injection site of  botulinum toxin . [ 24 ]  This may include loss of strength, blurred vision, change of voice, or trouble breathing which can result in death. [ 24 ]  Onset can be hours to weeks after an injection. [ 24 ]  This generally only occurs with inappropriate strengths of botulinum toxin for cosmetic use or due to the larger doses used to treat movement disorders. [ 2 ]  However, there are cases where an off-label use of botulinum toxin resulted in severe botulism and death. [ 25 ]  Following a 2008 review the FDA added these concerns as a  boxed warning . [ 26 ]  An international grassroots effort led by NeverTox to assemble the people experiencing Iatrogenic Botulism Poisoning (IBP) and provide education and emotional support serves 39,000 people through a Facebook group who are suffering from adverse events from botulinum toxin injections.  [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7848", "text": "Prior to the boxed warning labels that included a disclaimer that botulinum toxin injections could cause botulism, there were a series of lawsuits against the pharmaceutical firms that manufactured injectable botulinum toxin. A Hollywood producer's wife brought a lawsuit after experiencing debilitating adverse events from migraine treatment.  [ 28 ]  A lawsuit on behalf of a 3-year-old boy who was permanently disabled by a botulinum toxin injection was settled in court during the trial.  [ 29 ]  The family of a 7-year-old boy treated with botulinum toxin injections for leg spasms sued after the boy almost died. [ 30 ]  Several families of people who died after treatments with botulinum toxin injections brought lawsuits. [ 31 ]   [ 32 ]   [ 33 ] [ 34 ]  One lawsuit prevailed for the plaintiff who was awarded compensation of $18 million; the plaintiff was a physician who was diagnosed with botulism by thirteen neurologists at the NIH. [ 35 ]  Deposition video from that lawsuit quotes a pharmaceutical executive stating that \"Botox doesn't cause botulism.\" [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7849", "text": "The toxin is the protein  botulinum toxin  produced under anaerobic conditions (where there is no oxygen) [ 37 ]  by the bacterium  Clostridium botulinum . [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7850", "text": "Clostridium botulinum  is a large anaerobic Gram-positive bacillus that forms subterminal  endospores . [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7851", "text": "There are eight serological varieties of the bacterium denoted by the letters A to H. The toxin from all of these acts in the same way and produces similar symptoms: the motor nerve endings are prevented from releasing acetylcholine, causing flaccid paralysis and symptoms of blurred vision, ptosis, nausea, vomiting, diarrhea or constipation, cramps, and respiratory difficulty. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7852", "text": "Botulinum toxin is broken into eight neurotoxins (labeled as types A, B, C [C1, C2], D, E, F, and G), which are  antigenically  and  serologically  distinct but structurally similar. Human botulism is caused mainly by types A, B, E, and (rarely) F. Types C and D cause toxicity only in other animals. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7853", "text": "In October 2013, scientists released news of the discovery of type H, the first new botulism neurotoxin found in forty years. However, further studies showed type H to be a chimeric toxin composed of parts of types F and A (FA). [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7854", "text": "Some types produce a characteristic putrefactive smell and digest meat (types A and some of B and F); these are said to be  proteolytic ; type E and some types of B, C, D and F are nonproteolytic and can go undetected because there is no strong odor associated with them. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7855", "text": "When the bacteria are under stress, they develop spores, which are inert. Their natural habitats are in the soil, in the silt that comprises the bottom sediment of streams, lakes, and coastal waters and ocean, while some types are natural inhabitants of the intestinal tracts of mammals (e.g., horses, cattle, humans), and are present in their excreta. The spores can survive in their inert form for many years. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7856", "text": "Toxin is produced by the bacteria when environmental conditions are favourable for the spores to replicate and grow, but the gene that encodes for the toxin protein is actually carried by a virus or  phage  that infects the bacteria. Little is known about the natural factors that control phage infection and replication within the bacteria. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7857", "text": "The spores require warm temperatures, a protein source, an anaerobic environment, and moisture in order to become active and produce toxin. In the wild, decomposing vegetation and invertebrates combined with warm temperatures can provide ideal conditions for the botulism bacteria to activate and produce toxin that may affect feeding birds and other animals. Spores are not killed by boiling, but botulism is uncommon because special, rarely obtained conditions are necessary for botulinum toxin production from C. botulinum spores, including an anaerobic, low-salt, low-acid, low-sugar environment at ambient temperatures. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7858", "text": "Botulinum inhibits the release within the nervous system of  acetylcholine , a neurotransmitter, responsible for communication between motor neurons and muscle cells. All forms of botulism lead to  paralysis  that typically starts with the muscles of the face and then spreads towards the limbs. [ 2 ]  In severe forms, botulism leads to paralysis of the breathing muscles and causes  respiratory failure . In light of this life-threatening complication, all suspected cases of botulism are treated as  medical emergencies , and public health officials are usually involved to identify the source and take steps to prevent further cases from occurring. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7859", "text": "Botulinum toxin A and E specifically cleave the SNAP-25, whereas serotype B, D, F and G cut synaptobrevin. Serotype C cleaves both SNAP-25 and syntaxin. This causes blockade of neurotransmitter  acetylcholine  release, [ 45 ]  ultimately leading to paralysis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7860", "text": "For botulism in babies, diagnosis should be made on signs and symptoms. Confirmation of the diagnosis is made by testing of a  stool  or  enema  specimen with the mouse  bioassay ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7861", "text": "In people whose history and physical examination suggest botulism, these clues are often not enough to allow a diagnosis. Other diseases such as  Guillain\u2013Barr\u00e9 syndrome ,  stroke , and  myasthenia gravis  can appear similar to botulism, and special tests may be needed to exclude these other conditions. These tests may include a  brain scan ,  cerebrospinal fluid  examination, nerve conduction test ( electromyography , or EMG), and an  edrophonium  chloride (Tensilon) test for  myasthenia gravis . A definite diagnosis can be made if botulinum toxin is identified in the food, stomach or intestinal contents, vomit or feces. The toxin is occasionally found in the blood in  peracute  cases. Botulinum toxin can be detected by a variety of techniques, including  enzyme-linked immunosorbent assays  (ELISAs),  electrochemiluminescent  (ECL) tests and mouse inoculation or feeding trials. The toxins can be typed with neutralization tests in mice. In toxicoinfectious botulism, the organism can be cultured from tissues. On egg yolk medium, toxin-producing colonies usually display surface iridescence that extends beyond the colony. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7862", "text": "Although the vegetative form of the bacteria is destroyed by boiling, [ 47 ] [ 48 ]  the spore itself is not killed by the temperatures reached with normal sea-level-pressure boiling, leaving it free to grow and again produce the toxin when conditions are right. [ 49 ] [ 50 ] [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7863", "text": "A recommended prevention measure for infant botulism is to avoid giving honey to infants less than 12 months of age, as botulinum spores are often present. In older children and adults the normal intestinal bacteria suppress development of  C. botulinum . [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7864", "text": "While commercially canned goods are required to undergo a \"botulinum cook\" in a pressure cooker at 121\u00a0\u00b0C (250\u00a0\u00b0F) for 3 minutes, [ citation needed ]  and thus rarely cause botulism, there have been notable exceptions. Two were the 1978 Alaskan salmon outbreak and the 2007  Castleberry's Food Company  outbreak. Foodborne botulism is the rarest form, accounting for only around 15% of cases (US) [ 53 ]  and has more frequently resulted from  home-canned  foods with low acid content, such as  carrot juice ,  asparagus , green  beans ,  beets , and  corn . However, outbreaks of botulism have resulted from more unusual sources. In July 2002, fourteen  Alaskans  ate  muktuk  ( whale meat ) from a  beached whale , and eight of them developed symptoms of botulism, two of them requiring  mechanical ventilation . [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7865", "text": "Other, much rarer sources of infection (about every decade in the US [ 53 ] ) include  garlic  or herbs [ 55 ]  stored covered in  oil  without  acidification , [ 56 ]   chili peppers , [ 53 ]  improperly handled baked potatoes wrapped in  aluminum  foil, [ 53 ]  tomatoes, [ 53 ]  and home-canned or  fermented fish ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7866", "text": "When canning or preserving food at home, attention should be paid to hygiene, pressure, temperature, refrigeration and storage. When making home preserves, only acidic fruit such as apples, pears, stone fruits and berries should be used. Tropical fruit and tomatoes are low in acidity and must have some acidity added before they are canned. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7867", "text": "Low-acid foods have pH values higher than 4.6. They include red meats, seafood, poultry, milk, and all fresh vegetables except for most tomatoes. Most mixtures of low-acid and acid foods also have pH values above 4.6 unless their recipes include enough lemon juice, citric acid, or vinegar to make them acidic. Acid foods have a pH of 4.6 or lower. They include fruits, pickles, sauerkraut, jams, jellies, marmalades, and fruit butters. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7868", "text": "Although tomatoes usually are considered an acid food, some are now known to have pH values slightly above 4.6. Figs also have pH values slightly above 4.6. Therefore, if they are to be canned as acid foods, these products must be acidified to a pH of 4.6 or lower with lemon juice or citric acid. Properly acidified tomatoes and figs are acid foods and can be safely processed in a boiling-water canner. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7869", "text": "Oils infused with fresh garlic or herbs should be acidified and refrigerated. Potatoes which have been baked while wrapped in aluminum foil should be kept hot until served or refrigerated. Because the botulism toxin is destroyed by high temperatures, home-canned foods are best boiled for 10 minutes before eating. [ 59 ]  Metal cans containing food in which bacteria are growing may bulge outwards due to gas production from bacterial growth or the food inside may be foamy or have a bad odor; cans with any of these signs should be discarded. [ 60 ] [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7870", "text": "Any container of food which has been heat-treated and then assumed to be airtight which shows signs of not being so, e.g., metal cans with pinprick holes from rust or mechanical damage, should be discarded. Contamination of a canned food solely with  C. botulinum  may not cause any visual defects to the container, such as bulging. Only assurance of sufficient thermal processing during production, and absence of a route for subsequent contamination, should be used as indicators of food safety."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7871", "text": "The addition of  nitrites  and  nitrates  to processed meats such as ham, bacon, and sausages reduces growth and toxin production of  C. botulinum . [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7872", "text": "Vaccines  are under development, but they have side effects. [ 64 ] [ clarification needed ]  As of 2017 work to develop a better vaccine was being carried out, but the US FDA had not approved any vaccine against botulism. [ 65 ] [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7873", "text": "Botulism is generally treated with botulism  antitoxin  and supportive care. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7874", "text": "Supportive care for botulism includes monitoring of respiratory function. Respiratory failure due to  paralysis  may require  mechanical ventilation  for 2 to 8 weeks, plus intensive medical and nursing care. After this time, paralysis generally improves as new  neuromuscular connections  are formed. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7875", "text": "In some abdominal cases, physicians may try to remove contaminated food still in the digestive tract by inducing vomiting or using  enemas . Wounds should be treated, usually surgically, to remove the source of the toxin-producing bacteria. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7876", "text": "Botulinum antitoxin consists of  antibodies  that neutralize botulinum toxin in the  circulatory system  by  passive immunization . [ 69 ]  This prevents additional toxin from binding to the neuromuscular junction, but does not reverse any already inflicted paralysis. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7877", "text": "In adults, a trivalent antitoxin containing antibodies raised against botulinum toxin types A, B, and E is used most commonly; however, a  heptavalent botulism antitoxin  has also been developed and was approved by the U.S.  FDA  in 2013. [ 11 ] [ 70 ]  In infants, horse-derived antitoxin is sometimes avoided for fear of infants developing  serum sickness  or lasting  hypersensitivity  to horse-derived proteins. [ 71 ]  To avoid this, a human-derived antitoxin has been developed and approved by the U.S. FDA in 2003 for the treatment of infant botulism. [ 72 ]  This human-derived antitoxin has been shown to be both safe and effective for the treatment of infant botulism. [ 72 ] [ 73 ]  However, the danger of equine-derived antitoxin to infants has not been clearly established, and one study showed the equine-derived antitoxin to be both safe and effective for the treatment of infant botulism. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7878", "text": "Trivalent (A,B,E) botulinum antitoxin is derived from equine sources utilizing whole  antibodies  (Fab and Fc portions). In the United States, this antitoxin is available from the local health department via the  CDC . The second antitoxin,  heptavalent (A,B,C,D,E,F,G) botulinum antitoxin , is derived from \"despeciated\" equine  IgG  antibodies which have had the Fc portion cleaved off leaving the F(ab')2 portions. This less immunogenic antitoxin is effective against all known strains of botulism where not contraindicated. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7879", "text": "The paralysis caused by botulism can persist for two to eight weeks, during which supportive care and ventilation may be necessary to keep the patient alive. [ 67 ]  Botulism can be fatal in five to ten percent of people who are affected. [ 64 ]  However, if left untreated, botulism is fatal in 40 to 50 percent of cases. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7880", "text": "Infant botulism typically has no long-term side effects but can be complicated by treatment-associated adverse events. The  case fatality  rate is less than two percent for hospitalized babies. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7881", "text": "Globally, botulism is fairly rare, [ 64 ]  with approximately 1,000 identified cases yearly. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7882", "text": "In the United States an average of 145 cases are reported each year. Of these, roughly 65% are infant botulism, 20% are wound botulism, and 15% are foodborne. [ 77 ]  Infant botulism is predominantly sporadic and not associated with epidemics, but great geographic variability exists. From 1974 to 1996, for example, 47% of all infant botulism cases reported in the U.S. occurred in California. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7883", "text": "Between 1990 and 2000, the  Centers for Disease Control and Prevention  reported 263 individual foodborne cases from 160 botulism events in the United States with a case-fatality rate of 4%. Thirty-nine percent (103 cases and 58 events) occurred in Alaska, all of which were attributable to traditional Alaskan aboriginal foods. In the lower 49 states, home-canned food was implicated in 70 events (~69%) with canned asparagus being the most frequent cause. Two restaurant-associated outbreaks affected 25 people. The median number of cases per year was 23 (range 17\u201343), the median number of events per year was 14 (range 9\u201324). The highest incidence rates occurred in Alaska, Idaho, Washington, and Oregon. All other states had an incidence rate of 1 case per ten million people or less. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7884", "text": "The number of cases of food borne and infant botulism has changed little in recent years, but wound botulism has increased because of the use of  black tar heroin , especially in  California . [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7885", "text": "All data regarding botulism antitoxin releases and laboratory confirmation of cases in the US are recorded annually by the Centers for Disease Control and Prevention and published on their website. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7886", "text": "The largest recorded outbreak of foodborne botulism in the United Kingdom occurred in June 1989. A total of 27 patients were affected; one patient died. Twenty-five of the patients had eaten one brand of hazelnut yogurt in the week before the onset of symptoms. Control measures included the cessation of all yogurt production by the implicated producer, the withdrawal of the firm's yogurts from sale, the recall of cans of the hazelnut conserve, and advice to the general public to avoid the consumption of all hazelnut yogurts. [ 86 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7887", "text": "From 1958 to 1983 there were 986 outbreaks of botulism in China involving 4,377 people with 548 deaths. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7888", "text": "After the  Chinese Communist Revolution  in 1949, a mysterious plague (named  Qapqal disease ) was noticed to be affecting several  Sibe villages  in  Qapqal Xibe Autonomous County . It was endemic with distinctive epidemic patterns, yet the underlying cause remained unknown for a long period of time. [ 88 ]  It caused a number of deaths and forced some people to leave the place. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7889", "text": "In 1958, a team of experts were sent to the area by the Ministry of Health to investigate the cases. The epidemic survey conducted proved that the disease was primarily type A botulism, [ 90 ]  with several cases of type B. [ 88 ]  The team also discovered that the source of the botulinum was local fermented grain and beans, as well as a raw meat food called  mi song hu hu . [ 89 ]  They promoted the improvement of fermentation techniques among local residents, and thus eliminated the disease."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7890", "text": "From 1985 to 2005 there were outbreaks causing 91 confirmed cases of foodborne botulism in  Canada , 85% of which were in  Inuit  communities, especially  Nunavik , as well as   First Nations  of the coast of  British Columbia , following consumption of traditionally prepared marine mammal and fish products. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7891", "text": "In 2017, there were 70 cases of botulism with 8 deaths in Ukraine. The previous year there were 115 cases with 12 deaths. Most cases were the result of dried fish, a common local  drinking snack . [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7892", "text": "In 2020, several cases of botulism were reported in  Vietnam . All of them were related to a product containing contaminated vegetarian  p\u00e2t\u00e9 . Some patients were put on life support. [ 93 ] [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7893", "text": "Botulism can occur in many  vertebrates  and  invertebrates . Botulism has been reported in such species as rats, mice, chicken, frogs, toads, goldfish,  aplysia , squid, crayfish,  drosophila  and leeches. [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7894", "text": "Death from botulism is common in waterfowl; an estimated 10,000 to 100,000 birds die of botulism annually. The disease is commonly called \"limberneck\". In some large outbreaks, a million or more birds may die. Ducks appear to be affected most often. An  enzootic  form of duck botulism in the Western US and Canada is known as \"western duck sickness\". [ 96 ]  Botulism also affects commercially raised poultry. In chickens, the mortality rate varies from a few birds to 40% of the flock."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7895", "text": "Botulism seems to be relatively uncommon in domestic mammals; however, in some parts of the world, epidemics with up to 65% mortality are seen in cattle. The prognosis is poor in large animals that are recumbent."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7896", "text": "In cattle, the symptoms may include drooling, restlessness, incoordination, urine retention,  dysphagia , and sternal recumbency. Laterally recumbent animals are usually very close to death. In sheep, the symptoms may include drooling, a serous nasal discharge, stiffness, and incoordination. Abdominal respiration may be observed and the tail may switch on the side. As the disease progresses, the limbs may become paralyzed and death may occur. Phosphorus-deficient cattle, especially in southern Africa, are inclined to ingest bones and carrion containing clostridial toxins and consequently develop  lame sickness  or  lamsiekte ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7897", "text": "The clinical signs in horses are similar to cattle. The muscle paralysis is progressive; it usually begins at the hindquarters and gradually moves to the front limbs, neck, and head. Death generally occurs 24 to 72 hours after initial symptoms and results from respiratory paralysis. Some foals are found dead without other clinical signs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7898", "text": "Clostridium botulinum  type C toxin has been incriminated as the cause of  grass sickness , a condition in horses which occurs in rainy and hot summers in  Northern Europe . The main symptom is  pharynx  paralysis. [ 97 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7899", "text": "Domestic dogs  may develop systemic toxemia after consuming  C. botulinum  type C exotoxin or spores within bird carcasses or other infected meat [ 98 ]  but are generally resistant to the more severe effects of  C. botulinum  type C. Symptoms include flaccid muscle paralysis, which can lead to death due to cardiac and respiratory arrest. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7900", "text": "Pigs are relatively resistant to botulism. Reported symptoms include anorexia, refusal to drink, vomiting, pupillary dilation, and muscle paralysis. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7901", "text": "In poultry and wild birds,  flaccid paralysis  is usually seen in the legs, wings, neck and eyelids. Broiler chickens with the toxicoinfectious form may also have diarrhea with excess  urates ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7902", "text": "One of the main routes of exposure for botulism is through the consumption of food contaminated with  C. botulinum . Food-borne botulism can be prevented in domestic animals through careful inspection of the feed, purchasing high quality feed from reliable sources, and ensuring proper storage. Poultry litter and animal carcasses are places in which  C. botulinum  spores are able to germinate so it is advised to avoid spreading poultry litter or any carcass containing materials on fields producing feed materials due to their potential for supporting  C. botulinum  growth. [ 101 ]  Additionally, water sources should be checked for dead or dying animals, and fields should be checked for animal remains prior to mowing for hay or silage. Correcting any dietary deficiencies can also prevent animals from consuming contaminated materials such as bones or carcasses. [ 102 ]  Raw materials used for silage or feed mixed on site should be checked for any sign of mold or rotten appearance. Acidification of animal feed can reduce, but will not eliminate, the risk of toxin formation, especially in carcasses that remain whole. [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7903", "text": "Vaccines have been developed for use in animals to prevent botulism. The availability and approval of these vaccines varies depending on the location, with places experiencing more cases generally having more vaccines available and routine vaccination is more common. [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7904", "text": "A variety of vaccines have been developed for the prevention of botulism in livestock. Most initial vaccinations require multiple doses at intervals from 2\u20136 weeks, however, some newer vaccines require only one shot. This mainly depends on the type of vaccine and manufacturers recommendations. All vaccines require annual boosters to maintain immunity. Many of these vaccines can be used on multiple species including cattle, sheep, and goats with some labeled for use in horses and mules as well as separate vaccines for mink. Additionally, vaccination during an outbreak is as beneficial as therapeutic treatment in cattle, and this method is also used in horses and pheasants. [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7905", "text": "The use of region specific toxoids to immunize animals has been shown to be effective. Toxoid types C and D used to immunize cattle is a useful vaccination method in South Africa and Australia. Toxoid has also been shown to be an appropriate method of immunizing minks and pheasants. In endemic areas, for example Kentucky, vaccination with type B toxoid appears to be effective. [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7906", "text": "Based on CIA research in  Fort Detrick  on  biological warfare ,  anthrax  and botulism were widely regarded as the two most effective options. [ 104 ]  During the 1950s, a highly lethal strain was discovered during the biological warfare program. [ 104 ]  The  CIA  continued to hold 5 grams of  Clostridium botulinum , even after  Nixon's ban on biological warfare  in 1969. [ 104 ]  During the  Gulf War , when the United States were concerned with a potential biowarfare attack, the efforts around botulism turned to prevention. [ 104 ]  However, the only way to make antitoxin in America until the 1990s was by drawing antibodies from a single horse named  First Flight , raising much concern from Pentagon health officials. [ 104 ] [ 105 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7907", "text": "Iraq has historically possessed many types of germs, including botulism. [ 104 ]  The  American Type Culture Collection  sold 5 variants of botulinum to the  University of Baghdad  in May 1986. [ 104 ]  1991 CIA reports also show Iraqis filled shells, warheads, and bombs with biological agents like botulinum (though none have been deployed). [ 104 ]  The Iraqi air force used the code name \"tea\" to refer to botulinum, and it was also referred to as bioweapon \"A.\" [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7908", "text": "A Japanese cult called  Aum Shinrikyo  created laboratories that produced biological weapons, specifically botulinum,  anthrax , and  Q fever . [ 104 ]  From 1990 to 1995, the cult staged numerous unsuccessful bioterrorism attacks on civilians. [ 104 ]  They sprayed botulinum toxin from a truck in downtown Tokyo and in the Narita airport, but there are no reported cases of botulism as a result. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7909", "text": "Capillaria philippinensis  is a  parasitic   nematode  which causes  intestinal capillariasis .  This sometimes fatal disease was first discovered in Northern  Luzon , Philippines, in 1964.  Cases have also been reported from China, Egypt, Indonesia, Iran, Japan, Korea, Lao PDR, Taiwan and Thailand. [ 1 ]   Cases diagnosed in Italy and Spain were believed to be acquired abroad, with one case possibly contracted in Colombia. [ 2 ]  The natural life cycle of  C. philippinensis  is believed to involve fish as  intermediate hosts , and fish-eating birds as definitive hosts.  Humans acquire  C. philippinensis  by eating small species of infested fish whole and raw."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7910", "text": "Between the first case reported in 1964 and the end of 1967, more than 1000 cases were documented in and around Northern Luzon particularly at Tagudin, Ilocos Sur, including 77 deaths.   Witch doctors  were hired by the locals to  exorcise  the curse placed on them by the river god, which they believed was responsible for this sudden disaster. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7911", "text": "In 1968, the cause was identified as  Capillaria philippinensis . [ 4 ]   Adult  C. philippinensis  are very small, with males measuring 1.5\u20133.9\u00a0mm long and 23\u201328\u00a0\u03bcm maximum width, while adult females are 2.3\u20135.3\u00a0mm long and 29\u201347\u00a0\u03bcm maximum width.  Eggs measure 36\u201345\u00a0\u03bcm long and 20\u00a0\u03bcm wide, and are described as peanut-shaped with a striated shell."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7912", "text": "This species has been transferred to the genus  Aonchotheca , as  Aonchotheca philippinensis , [ 5 ]  and to the genus  Paracapillaria , as  Paracapillaria philippinensis . [ 6 ]  However, this species is almost universally referred to as  Capillaria philippinensis  in the current medical literature."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7913", "text": "The complete life cycle of  C. philippinensis  has been demonstrated in experimental studies, and may be either indirect (involving an intermediate host) or direct (complete in one host). [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7914", "text": "While the natural host range is not known, experimental infestations of several fishes, including  Cyprinus carpio ,  Puntius gonionotus ,  Rasbora borapetensis ,  Eleotris melanosoma ,  Ambassis  commersoni  and  Apogon  sp., with  C. philippinensis  eggs yielded infective larvae.  Experimental infestations with larvae of several birds, including  Amaurornis phoenicurus ,  Ardeola bacchus ,  Nycticorax nycticorax ,  Bubulcus ibis ,  Ixobrychus sinensis ,  Gallinula chloropus , and  Rostratula benghalensis , yielded mature adults."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7915", "text": "Direct life cycle.  Researchers also found that feeding just a few dozen larvae from the intestines of fish to Mongolian gerbils ( Meriones unguiculatus ) or monkeys ( Macaca  sp.) led to infestations with thousands of adult worms through \" autoinfection \".  Autoinfection is when the offspring produced by adults can reinfest the same host, allowing the infestation to multiply within a single host animal.  Both  oviparous  (egg-laying) and larviparous (giving birth to active larvae) adult female  C. philippinensis  were found in Mongolian gerbils and some birds. The experimentally infested monkeys never developed any clinical symptoms, even during prolonged, active infestations. Of several rodents tested, only Mongolian gerbils developed severe symptoms due to infestation and died."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7916", "text": "Although  C. philippinensis  infections are rare, it can serve as an indicator that one is being exposed to raw or undercooked fish. Early diagnosis of the parasite is beneficial so the number of worms in an infected person would not increase. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7917", "text": "This parasite can be diagnosed by taking a tissue  biopsy  from the small intestine or by examining stool samples through a microscope. [ 9 ]   In a heavily infected person, it is best to examine their feces because it will show an abundance of adult worms and eggs. When looking at the eggs of  C. philippinensis , one must be able to distinguish it from the eggs of  Trichuris trichiura .  C. philippinensis  eggs have nonprotruding polar plugs and are slightly smaller than  T. trichiura  eggs. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7918", "text": "C. philippinensis  infections should be treated with 200\u00a0mg of mebendazole. This drug is taken twice a day for 20 days or until all symptoms subside and there are no longer eggs present in the stool samples of the patient. Another drug that may be used is albendazole 400\u00a0mg, which is taken orally every day for at least 10 days. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7919", "text": "Clostridioides difficile  infection [ 5 ]  ( CDI  or  C-diff ), also known as  Clostridium difficile  infection , is a symptomatic  infection  due to the  spore -forming bacterium  Clostridioides difficile . [ 6 ]  Symptoms include watery  diarrhea , fever, nausea, and  abdominal pain . [ 1 ]  It makes up about 20% of cases of  antibiotic-associated diarrhea . [ 1 ]   Antibiotics can contribute to detrimental changes in  gut microbiota ; specifically, they decrease short-chain fatty acid absorption which results in osmotic, or watery, diarrhea. [ 7 ]  Complications may include  pseudomembranous colitis ,  toxic megacolon ,  perforation of the colon , and  sepsis . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7920", "text": "Clostridioides difficile  infection is spread by bacterial spores found within  feces . [ 1 ]  Surfaces may become contaminated with the spores with further spread occurring via the hands of healthcare workers. [ 1 ]  Risk factors for infection include  antibiotic  or  proton pump inhibitor  use, hospitalization, hypoalbuminemia, [ 8 ]  other health problems, and older age. [ 1 ]  Diagnosis is by  stool culture  or testing for the bacteria's  DNA  or  toxins . [ 1 ]  If a person tests positive but has no symptoms, the condition is known as  C. difficile   colonization  rather than an infection. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7921", "text": "Prevention efforts include  terminal room cleaning  in hospitals, limiting antibiotic use, and  handwashing  campaigns in hospitals. [ 2 ]   Alcohol based hand sanitizer  does not appear effective. [ 2 ]  Discontinuation of antibiotics may result in resolution of symptoms within three days in about 20% of those infected. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7922", "text": "The antibiotics  metronidazole ,  vancomycin , or  fidaxomicin , will cure the infection. [ 1 ] [ 3 ]  Retesting after treatment, as long as the symptoms have resolved, is not recommended, as a person may often remain colonized. [ 1 ]  Recurrences have been reported in up to 25% of people. [ 9 ]  Some tentative evidence indicates  fecal microbiota transplantation  and  probiotics  may decrease the risk of recurrence. [ 2 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7923", "text": "C. difficile  infections occur in all areas of the world. [ 11 ]  About 453,000 cases occurred in the United States in 2011, resulting in 29,000 deaths. [ 2 ] [ 4 ]  Global rates of disease increased between 2001 and 2016. [ 2 ] [ 11 ]   C. difficile  infections occur more often in women than men. [ 2 ]  The bacterium was discovered in 1935 and found to be disease-causing in 1978. [ 11 ]  Attributable costs for  Clostridioides difficile  infection in hospitalized adults range from\n$4500 to $15,000. [ 12 ]  In the United States,  healthcare-associated infections  increase the cost of care by US$1.5 billion each year. [ 13 ]  Although  C. difficile  is a common healthcare-associated infection, at most 30% of infections are transmitted within hospitals. [ 14 ]  The majority of infections are acquired outside of hospitals, where medications and a recent history of diarrheal illnesses (e.g.  laxative abuse  or food poisoning due to  salmonellosis ) are thought to drive the risk of colonization. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7924", "text": "Signs and symptoms of CDI range from mild diarrhea to severe life-threatening  inflammation of the colon . [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7925", "text": "In adults, a  clinical prediction rule  found the best  signs  to be significant diarrhea (\"new onset of more than three partially formed or watery stools per 24-hour period\"), recent antibiotic exposure, abdominal pain, fever (up to 40.5\u00a0\u00b0C or 105\u00a0\u00b0F), and a distinctive foul odor to the stool resembling horse manure. [ 17 ]  In a hospital population, prior antibiotic treatment plus diarrhea or abdominal pain had a  sensitivity  of 86% and a  specificity  of 45%. [ 18 ]  In this study with a prevalence of positive cytotoxin assays of 14%, the  positive predictive value  was 18% and the  negative predictive value  was 94%. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7926", "text": "In children, the most prevalent symptom of a CDI is watery diarrhea with at least three bowel movements a day for two or more days, which may be accompanied by fever, loss of appetite, nausea, and/or abdominal pain. [ 19 ]  Those with a severe infection also may develop serious inflammation of the colon and have little or no diarrhea. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7927", "text": "Infection with  C. difficile   bacteria  is responsible for  C. difficile  diarrhea."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7928", "text": "Clostridia are  anaerobic   motile   bacteria , ubiquitous in nature, and especially prevalent in soil. Under the microscope, they appear as long, irregular (often drumstick- or spindle-shaped) cells with a bulge at their terminal ends. Under  gram staining ,  C. difficile  cells are  gram-positive  and show optimum growth on  blood agar  at human body temperatures in the absence of  oxygen . When stressed, the bacteria produce  spores  that are able to tolerate extreme conditions that the active bacteria cannot tolerate. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7929", "text": "C. difficile  may colonize the human  colon  without symptom; approximately 2\u20135% of the adult population are carriers, although it varies considerably with  demographics . [ 20 ]  The risk of colonization has been linked to a history of unrelated diarrheal illnesses (e.g. laxative abuse and  food poisoning  due to Salmonellosis or  Vibrio cholerae  infection). [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7930", "text": "Pathogenic  C. difficile  strains produce multiple  toxins . [ 21 ]  The most well-characterized are  enterotoxin  ( Clostridium difficile  toxin A ) and  cytotoxin  ( Clostridium difficile  toxin B ), both of which may produce  diarrhea  and  inflammation  in infected people, although their relative contributions have been debated. [ 20 ]  Toxins A and B are glucosyltransferases that target and inactivate the  Rho family of GTPases . Toxin B (cytotoxin) induces  actin  depolymerization by a mechanism correlated with a decrease in the  ADP-ribosylation  of the low molecular mass GTP-binding Rho proteins. [ 22 ]  Another toxin,  binary toxin , also has been described, but its role in disease is not fully understood. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7931", "text": "Antibiotic treatment of CDIs may be difficult, due both to  antibiotic resistance  and physiological factors of the bacteria (spore formation, protective effects of the pseudomembrane). [ 20 ]  The emergence of a new and highly toxic strain of  C. difficile  that is resistant to  fluoroquinolone  antibiotics such as  ciprofloxacin  and  levofloxacin , said to be causing geographically dispersed outbreaks in North America, was reported in 2005. [ 24 ]  The U.S.  Centers for Disease Control and Prevention   in Atlanta warned of the emergence of an epidemic strain with increased virulence, antibiotic resistance, or both. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7932", "text": "C. difficile  is transmitted from person to person by the  fecal-oral route . The organism forms heat-resistant spores that are not killed by alcohol-based hand cleansers or routine surface cleaning. Thus, these spores survive in clinical environments for long periods. Because of this, the bacteria may be cultured from almost any surface. Once spores are ingested, their acid-resistance allows them to pass through the stomach unscathed. Upon exposure to  bile acids , they germinate and multiply into vegetative cells in the colon.  The presence of the bile acid  deoxycholic acid  in the intestinal environment can promote induction of  C. difficle   biofilm  formation. [ 26 ]  People without a history of gastrointestinal disturbances due to antibiotic use or diarrheal illness are less likely to become colonized by  C. difficile . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7933", "text": "In 2005, molecular analysis led to the identification of the  C. difficile  strain type characterized as group BI by  restriction endonuclease  analysis, as North American pulse-field-type NAP1 by  pulsed-field gel electrophoresis   and as  ribotype  027; the differing terminology reflects the predominant techniques used for epidemiological typing. This strain is referred to as  C. difficile  BI/NAP1/027. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7934", "text": "C. difficile  colitis is associated most strongly with the use of these antibiotics:  fluoroquinolones ,  cephalosporins , and  clindamycin . [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7935", "text": "Some research suggests the routine  use of antibiotics in the raising of livestock  is contributing to outbreaks of bacterial infections such as  C. difficile . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7936", "text": "People are most often  infected in hospitals ,  nursing homes , [ 30 ]  or other medical institutions, although infection outside medical settings is increasing. Individuals can develop the infection if they touch objects or surfaces that are contaminated with feces and then touch their mouth or mucous membranes. Healthcare workers could possibly spread the bacteria or contaminate surfaces through hand contact. [ 31 ]  The rate of  C. difficile  acquisition is estimated to be 13% in those with hospital stays of up to two weeks, and 50% with stays longer than four weeks. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7937", "text": "Long-term hospitalization or residence in a nursing home within the previous year are independent risk factors for increased  colonization . [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7938", "text": "Increasing rates of community-acquired CDI are associated with the use of medication to suppress  gastric acid  production:  H2-receptor antagonists  increased the risk 1.5-fold, and  proton pump inhibitors  by 1.7 with once-daily use and 2.4 with more than once-daily use. [ 34 ] [ 35 ]  Increased risk in recurrent CDI is also found with gastric acid repression use in observational studies, with a rate of 22.1%, compared to patients without gastric acid repression has a rate of 17.3% of recurrent CDI. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7939", "text": "People with a recent history of diarrheal illness are at increased risk of becoming colonized by  C. difficile  when exposed to spores, including laxative abuse and gastrointestinal pathogens. [ 15 ]   Disturbances that increase intestinal motility are thought to transiently elevate the concentration of available dietary sugars, allowing  C. difficile  to proliferate and gain a foothold in the gut. [ 37 ]  Although not all colonization events lead to disease, asymptomatic carriers remain colonized for years at a time. [ 15 ]  During this time, the abundance of  C. difficile  varies considerably day-to-day, causing periods of increased shedding that could substantially contribute to community-acquired infection rates. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7940", "text": "As a result of suppression of healthy bacteria, via a loss of bacterial food source, prolonged use of an  elemental diet  increases the risk of developing  C. difficile  infection. [ 38 ]  Low serum albumin levels is a risk factor for the development of  C. difficile  infection and when infected for severe disease. [ 39 ] [ 40 ]  The protective effects of serum albumin may be related to the capability of this protein to bind  C. difficile  toxin A and toxin B, thus impairing entry into enterocytes. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7941", "text": "Chronic kidney disease  (CKD) has been identified as a risk factor in the development of a  C. difficile  infection. [ 41 ] [ 42 ]  Patients with CKD have a higher risk of both initial and recurring infection, as well as a higher chance of severe infection, than those without CKD. [ 43 ]  Patients with Inflammatory Bowel Disease are also at higher risk for infection and a recent study suggests they may have intermittent  C. difficile  infection masked by IBD symptoms, and testing should be considered in patients with changes in disease activity. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7942", "text": "The use of systemic antibiotics, including broad-spectrum penicillins/cephalosporins, fluoroquinolones, and clindamycin, causes the normal microbiota of the bowel to be altered. In particular, when the  antibiotic  kills off other competing bacteria in the intestine, any bacteria remaining will have less competition for space and nutrients. The net effect is to permit more extensive growth than normal of certain bacteria.  C. difficile  is one such type of bacterium. In addition to proliferating in the bowel,  C. difficile  also produces  toxins . Without either toxin A or toxin B,  C. difficile  may colonize the gut, but is unlikely to cause pseudomembranous colitis. [ 45 ]  The colitis associated with severe infection is part of an inflammatory reaction, with the \"pseudomembrane\" formed by a viscous collection of inflammatory cells,  fibrin , and necrotic cells. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7943", "text": "Prior to the advent of tests to detect  C. difficile  toxins, the diagnosis most often was made by  colonoscopy  or  sigmoidoscopy . The appearance of \"pseudomembranes\" on the mucosa of the  colon  or  rectum  is highly suggestive, but not diagnostic of the condition. [ 46 ]  The pseudomembranes are composed of an exudate made of inflammatory debris,  white blood cells . Although colonoscopy and sigmoidoscopy are still employed, now stool testing for the presence of  C. difficile  toxins is frequently the first-line diagnostic approach. Usually, only two toxins are tested for\u2014toxin A and toxin B\u2014but the organism produces several others. This test is not 100% accurate, with a considerable false-negative rate even with repeat testing. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7944", "text": "CDI may be classified in non-severe CDI, severe CDI and fulminant CDI depending on creatinine and white blood count parameters. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7945", "text": "C. difficile  toxins have a  cytopathic  effect in cell culture, and neutralization of any effect observed with specific antisera is the practical  gold standard  for studies investigating new CDI diagnostic techniques. [ 20 ]  Toxigenic culture, in which organisms are cultured on selective media and tested for toxin production, remains the gold standard and is the most sensitive and specific test, although it is slow and labor-intensive. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7946", "text": "Assessment of the A and B toxins by enzyme-linked immunosorbent assay ( ELISA ) for toxin A or B (or both) has a  sensitivity  of 63\u201399% and a  specificity  of 93\u2013100%, depending on detection assays. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7947", "text": "Previously, experts recommended sending as many as three stool samples to rule out disease if initial tests are negative, but evidence suggests repeated testing during the same episode of diarrhea is of limited value and should be discouraged. [ 50 ]   C. difficile  toxin should clear from the stool of somebody previously infected if treatment is effective. Many hospitals only test for the prevalent toxin A. Strains that express only the B toxin are now present in many hospitals, however, so testing for both toxins should occur. [ 51 ] [ 52 ]  Not testing for both may contribute to a delay in obtaining laboratory results, which is often the cause of prolonged illness and poor outcomes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7948", "text": "Stool  leukocyte  measurements and stool  lactoferrin  levels also have been proposed as diagnostic tests, but may have limited diagnostic accuracy. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7949", "text": "Testing of stool samples by  real-time polymerase chain reaction  is able to detect  C. difficile  about 93% of the time and when positive is incorrectly positive about 3% of the time. [ 54 ]  This is more accurate than cytotoxigenic culture or cell cytotoxicity assay. [ 54 ]  Another benefit is that the result can be achieved within three hours. [ 54 ]  Drawbacks include a higher cost and the fact that the test only looks for the gene for the toxin and not the toxin itself. [ 54 ]  The latter means that if the test is used without confirmation, overdiagnosis may occur. [ 54 ]  Repeat testing may be misleading, and testing specimens more than once every seven days in people without new symptoms is highly unlikely to yield useful information. [ 55 ]  The screening specificity is relatively low because of the high number of false positive cases from asymptomatic infection. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7950", "text": "Self containment by housing people in private rooms is important to prevent the spread of  C. difficile . [ 56 ]  Contact precautions are an important part of preventing the spread of \u00a0C. difficile. C. difficile does not often occur in people who are not taking antibiotics so limiting use of antibiotics decreases the risk. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7951", "text": "The most effective method for preventing CDI is proper  antibiotic  prescribing. In the hospital setting, where CDI is most common, most people who develop CDI are exposed to antibiotics. Although proper antibiotic prescribing is highly recommended, about 50% is considered inappropriate. This is consistent whether in the hospital, clinic, community, or academic setting. A decrease in CDI by limiting antibiotics or by limiting unnecessary prescriptions in general, both in an outbreak and non-outbreak setting has been demonstrated to be most strongly associated with reduced CDI. Further, reactions to medication may be severe: CDI infections were the most common contributor to adverse drug events seen in U.S. hospitals in 2011. [ 58 ]  In some regions of the UK, reduced used of  fluoroquinolone  antibiotics seems to lead to reduced rates of CDI. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7952", "text": "Some evidence indicates  probiotics  may be useful to prevent infection and recurrence. [ 60 ] [ 61 ]  Treatment with  Saccharomyces boulardii  in those who are not immunocompromised with  C. difficile  also may be useful. [ 62 ] [ 63 ]  Initially, in 2010, the  Infectious Diseases Society of America  recommended against their use due to the risk of complications. [ 60 ] [ 62 ]  Subsequent reviews, however, did not find an increase in adverse effects with treatment, [ 61 ]  and overall treatment appears safe and moderately effective in preventing C. difficile-associated diarrhea. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7953", "text": "One study in particular found that there does appear to be a \"protective effect\" of probiotics, specifically reducing the risk of antibiotic-associated diarrhea (AAD) by 51% in 3,631 outpatients, but it is important to note that the types of infections in the subjects were not specified. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7954", "text": "Rigorous infection protocols are required to minimize this risk of transmission. [ 66 ]  Infection control measures, such as wearing gloves and noncritical medical devices used for a single person with CDI, are effective at prevention. [ 67 ]  This works by limiting the spread of  C. difficile  in the hospital setting. In addition, washing with soap and water will wash away the spores from contaminated hands, but alcohol-based hand rubs are ineffective. [ 68 ]  These precautions should remain in place among those in hospital for at least 2 days after the diarrhea has stopped. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7955", "text": "Bleach wipes containing 0.55%  sodium hypochlorite  have been shown to kill the spores and prevent transmission. [ 70 ]  Installing lidded toilets and closing the lid prior to flushing also reduces the risk of contamination. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7956", "text": "Those who have CDIs should be in rooms with other people with CDIs or by themselves when in hospital. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7957", "text": "Common hospital  disinfectants  are ineffective against  C. difficile  spores, and may promote spore formation, but various  oxidants    (e.g 1% sodium  hypochlorite  solution) rapidly destroy spores. [ 72 ]   Hydrogen peroxide vapor  (HPV) systems used to sterilize a room after treatment is completed have been shown to reduce infection rates and to reduce risk of infection to others. The incidence of CDI was reduced by 53% [ 73 ]  or 42% [ 74 ]  through use of HPV. Ultraviolet cleaning devices, and housekeeping staff especially dedicated to disinfecting the rooms of people with  C. difficile  after discharge may be effective. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7958", "text": "Carrying  C. difficile  without symptoms is common. Treatment in those without symptoms is controversial. In general, mild cases do not require specific treatment. [ 3 ] [ 20 ]   Oral rehydration therapy  is useful in treating dehydration associated with the diarrhea. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7959", "text": "Several different antibiotics are used for  C. difficile , with the available agents being more or less equally effective. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7960", "text": "Vancomycin  or  fidaxomicin  by mouth are the typically recommended for mild, moderate, and severe infections. [ 77 ]  They are also the first-line treatment for pregnant women, especially since metronidazole may cause birth defects. [ 78 ]  Typical vancomycin 125\u00a0mg is taken four times a day by mouth for 10 days. [ 78 ] [ 48 ]  Fidaxomicin is taken at 200\u00a0mg twice daily for 10 days. [ 48 ]  It may also be given rectally if the person develops an  ileus . [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7961", "text": "Fidaxomicin is tolerated as well as vancomycin, [ 79 ]  and may have a lower risk of recurrence. [ 76 ]  Fidaxomicin has been found to be as effective as vancomycin in those with mild to moderate disease, and it may be better than vancomycin in those with severe disease. [ 3 ] [ 80 ]  Fidaxomicin may be used in those who have recurrent infections and have not responded to other antibiotics. [ 80 ]   Metronidazole  (500\u00a0mg 3 times daily for 10 days [ 48 ] ) by mouth is recommended as an alternative treatment only for  C. difficile  infections when the affected person is  allergic  to first-line treatments, is unable to tolerate them, or has financial difficulties preventing them from accessing them. [ 77 ] [ 81 ]  In fulminant disease vancomycin by mouth and intravenous metronidazole are commonly used together. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7962", "text": "Medications used to slow or stop  diarrhea , such as  loperamide , may only be used after initiating the treatment. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7963", "text": "Cholestyramine , an  ion-exchange resin , is effective in binding both toxin A and B, slowing bowel motility, and helping prevent dehydration. [ 82 ]  Cholestyramine is recommended with vancomycin. A last-resort treatment in those who are immunosuppressed is  intravenous immunoglobulin . [ 82 ]  Monoclonal antibodies against  C. difficile  toxin A  and  C. difficile  toxin B  are approved to prevent recurrence of  C. difficile  infection including  bezlotoxumab . [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7964", "text": "Evidence to support the use of probiotics in the treatment of active disease is insufficient. [ 62 ] [ 84 ] [ 85 ] [ 86 ]  Researchers have recently begun taking a mechanical approach to fecal-derived products. It is known that certain microbes with 7\u03b1-dehydroxylase activity can metabolize primary to secondary bile acids, which inhibit C. difficile. Thus, incorporating such microbes into therapeutic products such as probiotics may be protective, although more pre-clinical investigations are needed. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7965", "text": "Fecal microbiota transplant , also known as a stool transplant, is roughly 85% to 90% effective in those for whom antibiotics have not worked. [ 88 ] [ 89 ] [ 90 ]  It involves infusion of the microbiota acquired from the feces of a healthy donor to reverse the bacterial imbalance responsible for the recurring nature of the infection. [ 91 ]  The procedure replenishes the normal colonic microbiota that had been wiped out by antibiotics, and re-establishes resistance to colonization by  Clostridioides difficile . [ 92 ]  Side effects, at least initially, are few. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7966", "text": "Fecal microbiota, live  (Rebyota) was approved for medical use in the United States in November 2022. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7967", "text": "Fecal microbiota spores, live  (Vowst) was approved for medical use in the United States in April 2023. [ 94 ] [ 95 ]  It is the first fecal microbiota product that is taken  by mouth . [ 94 ]  A 2023 review article discusses the beneficial effects of fecal microbiota transplantation in recurrent  Clostridioides difficile  infection  [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7968", "text": "In those with severe  C. difficile  colitis,  colectomy  may improve the outcomes. [ 97 ]  Specific criteria may be used to determine who will benefit most from surgery. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7969", "text": "Recurrent CDI occurs in 20 to 30% of the patients, with increasing rates of recurrence with each subsequent episode. [ 99 ]  In clinical settings, it is virtually impossible to distinguish a recurrence that develops as a relapse of CDI with the same strain of  C. difficile  versus reinfection that is the result of a new strain. [ citation needed ]  However, in laboratory settings paired isolates can be differentiated using  Whole-Genome Sequencing  or  Multilocus Variable-Number Tandem-Repeat Analysis . [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7970", "text": "Several treatment options exist for recurrent  C. difficile  infection. For the first episode of recurrent  C. difficile  infection, the 2017 IDSA guidelines recommend oral vancomycin at a dose of 125\u00a0mg four times daily for 10 days if metronidazole was used for the initial episode. If oral vancomycin was used for the initial episode, then a prolonged oral vancomycin pulse dose of 125\u00a0mg four times daily for 10\u201314 days followed by a taper (twice daily for one week, then every two to three days for 2\u20138 weeks) or fidaxomicin 200\u00a0mg twice daily for 10 days. For a second recurrent episode, the IDSA recommends options including the aforementioned oral vancomycin pulse dose followed by the prolonged taper; oral vancomycin 125\u00a0mg four times daily for 10 days followed by  rifaximin  400\u00a0mg three times daily for 20 days; fidaxomicin 200\u00a0mg twice daily for 10 days, or a fecal microbiota transplant. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7971", "text": "For patients with C. diff infections that fail to be resolved with traditional antibiotic regimens, fecal microbiome transplants boasts an average cure rate of >90%. [ 101 ]  In a review of 317 patients, it was shown to lead to resolution in 92% of the persistent and recurrent disease cases. [ 102 ]  It is clear that restoration of gut flora is paramount in the struggle against recurrent CDI. With effective antibiotic therapy, C. difficile can be reduced and natural colonization resistance can develop over time as the natural microbial community recovers. Reinfection or recurrence may occur before this process is complete. Fecal microbiota transplant may expedite this recovery by directly replacing the missing microbial community members. [ 103 ]  However, human-derived fecal matter is difficult to standardize and has multiple potential risks, including the transfer of infectious material and long-term consequences of inoculating the gut with a foreign fecal material. As a result, further research is necessary to study the long term effective outcomes of FMT. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7972", "text": "After a first treatment with metronidazole or vancomycin,  C. difficile  recurs in about 20% of people. This increases to 40% and 60% with subsequent recurrences. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7973", "text": "C. difficile  diarrhea is estimated to occur in eight of 100,000 people each year. [ 105 ]  Among those who are admitted to hospital, it occurs in between four and eight people per 1,000. [ 105 ]  In 2011, it resulted in about half a million infections and 29,000 deaths in the United States. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7974", "text": "Due in part to the emergence of a  fluoroquinolone -resistant strain,  C. difficile -related deaths increased 400% between 2000 and 2007 in the United States. [ 106 ]  According to the CDC, \" C. difficile \u00a0has become the most common microbial cause of healthcare-associated infections in U.S. hospitals and costs up to $4.8 billion each year in excess health care costs for acute care facilities alone.\" [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7975", "text": "Ivan C. Hall and Elizabeth O'Toole first named the bacterium  Bacillus difficilis  in 1935, choosing its specific epithet because it was resistant to early attempts at isolation and grew very slowly in culture. [ 104 ] [ 108 ]   Andr\u00e9 Romain Pr\u00e9vot  subsequently transferred it to  Clostridium ,  binomen  Clostridium difficile . [ 109 ] [ 110 ]  Its combination was later changed to  Clostridioides difficile  after being transferred to the new genus  Clostridioides . [ 111 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7976", "text": "Pseudomembranous colitis first was described as a complication of  C. difficile  infection in 1978, [ 112 ]  when a toxin was isolated from people with pseudomembranous colitis and  Koch's postulates  were met."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7977", "text": "The genus name is from the  Greek   kl\u014dst\u0113r  ( \u03ba\u03bb\u03c9\u03c3\u03c4\u03ae\u03c1 ), \"spindle\", [ 131 ]  and the specific name is from  Latin   difficile , neuter singular form of  difficilis  \"difficult, obstinate\", [ 132 ]   chosen  in reference to  fastidiousness  upon culturing."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7978", "text": "Regarding the pronunciation of the current and former genus assignments,  Clostridioides  is  / k l \u0252 \u02cc s t r \u026a d i \u02c8 \u0254\u026a d i s /  and  Clostridium  is  / k l \u0252 \u02c8 s t r \u026a d i \u0259m / . Both genera still have species assigned to them, but this species is now classified in the former. Via the norms of  binomial nomenclature , it is understood that the former binomial name of this species is now an alias. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7979", "text": "Regarding the specific name,  / d \u026a \u02c8 f \u026a s \u026a l i / [ 133 ]  is the traditional norm, reflecting how medical English usually pronounces naturalized New Latin words (which in turn largely reflects  traditional English pronunciation of Latin ), although a restored pronunciation of  / d \u026a \u02c8 f \u026a k \u026a l e\u026a /  is also sometimes used (the  classical Latin  pronunciation is reconstructed as  [klo\u02d0s\u02c8tr\u026ad\u026a.\u0169\u02d0   d\u026af\u02c8f\u026ak\u026al\u025b] ). The specific name is also commonly pronounced  / \u02cc d i\u02d0 f i \u02c8 s i\u02d0 l / , as though it were French, which from a  prescriptive  viewpoint is a \"mispronunciation\" [ 133 ]  but from a  linguistically descriptive  viewpoint cannot be described as erroneous because it is so widely used among health care professionals; it can be described as \"the non-preferred variant\" from the viewpoint of sticking most regularly to New Latin in  binomial nomenclature , which is also a valid viewpoint, although New Latin specific names contain such a wide array of extra-Latin roots (including surnames and jocular references) that extra-Latin pronunciation is involved anyway (as seen, for example, with  Ba humbugi ,  Spongiforma squarepantsii , and hundreds of others). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7980", "text": "Colitis  is swelling or  inflammation  of the large intestine ( colon ). [ 1 ]  Colitis may be  acute  and self-limited or  long-term . It broadly fits into the category of  digestive diseases ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7981", "text": "In a medical context, the label  colitis  (without qualification) is used if:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7982", "text": "The  signs  and  symptoms  of colitis are quite variable and dependent on the cause of the given colitis and factors that modify its course and severity. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7983", "text": "Common symptoms of colitis may include: mild to severe  abdominal pains  and  tenderness  (depending on the stage of the disease), persistent  hemorrhagic   diarrhea  with pus either present or absent in the  stools ,  fecal incontinence ,  flatulence ,  fatigue ,  loss of appetite  and unexplained  weight loss . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7984", "text": "More severe symptoms may include:  shortness of breath , a fast or  irregular heartbeat  and  fever . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7985", "text": "Other less common or rare  non-specific symptoms  that may accompany colitis include:  arthritis ,  mouth ulcers , painful, red and swollen skin and irritated,  bloodshot eyes . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7986", "text": "Signs seen on  colonoscopy  include: colonic mucosal  erythema  (redness of the colon's inner surface),  ulcerations  and  hemorrhage . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7987", "text": "Symptoms suggestive of colitis are worked-up by obtaining the  medical history , a physical examination and laboratory tests ( CBC ,  electrolytes , stool culture and sensitivity, stool ova and parasites et cetera).  Additional tests may include medical imaging (e.g. abdominal  computed tomography ,  abdominal X-rays ) and an examination with a camera inserted into the rectum ( sigmoidoscopy ,  colonoscopy ). [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7988", "text": "An important investigation in the assessment of colitis is biopsy for  histopathology . A very small piece of tissue (usually about 2mm) is removed from the bowel mucosa during endoscopy and examined under the microscope by a histopathologist. A biopsy report generally does not state the diagnosis, but should state any presence of chronic colitis, give an indication of disease activity, as well as state the presence of any epithelial damage (erosions and ulcerations). [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7989", "text": "Histopathology findings generally associated with chronic colitis include: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7990", "text": "Other findings include basal plasmacytosis and mucin depletion. [ 6 ] \nHistopathology findings generally associated with active colitis include: [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7991", "text": "There are many types of colitis. They are usually classified by the cause."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7992", "text": "Types of colitis include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7993", "text": "A subtype of infectious colitis is  Clostridioides difficile  colitis , [ 8 ]  which is informally abbreviated as \"C-diff colitis\". It classically forms  pseudomembranes  and is often referred to as pseudomembranous colitis, which is its (nonspecific)  histomorphologic  description."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7994", "text": "Enterohemorrhagic  colitis may be caused by  Shiga toxin  in  Shigella dysenteriae  or  Shigatoxigenic group  of  Escherichia coli  (STEC), which includes  serotype   O157:H7  and other enterohemorrhagic  E. coli . [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7995", "text": "Parasitic  infections, like those caused by  Entamoeba histolytica , can also cause colitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7996", "text": "Indeterminate colitis  is the classification for colitis that has features of both  Crohn's disease  and  ulcerative colitis . [ 10 ]   Indeterminate colitis' behaviour is usually closer to ulcerative colitis than Crohn's disease. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7997", "text": "Treatment for this condition can include medications such as steroids and dietary changes.\u00a0 In some instances, hospitalization and surgery may be required. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7998", "text": "Moreover, several studies recently have found significant relationship between colitis and  dairy allergy  (including: cow milk, cow milk UHT and casein), [ 13 ] [ 14 ] [ 15 ]  suggesting some patients may benefit from an  elimination diet ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_7999", "text": "The use of oral  probiotic  supplements to modify the composition and behavior of the microbiome has been considered as a possible therapy for both induction and maintenance of remission in people with Crohn's disease and ulcerative colitis. A Cochrane review in 2020 did not find clear evidence of improved remission likelihood, nor lower adverse events, in people with Crohn's disease, following probiotic treatment. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8000", "text": "For ulcerative colitis, there is low-certainty evidence that probiotic supplements may increase the probability of clinical remission. [ 17 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects. [ 17 ]  Although there was no clear evidence of greater remission when probiotic supplements were compared with  5\u2010aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy. [ 17 ]  Whereas in people who are already in remission, it is unclear whether probiotics help to prevent future relapse, either as a monotherapy or  combination therapy . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8001", "text": "One study reported successfully treating experimental colitis in mice with  mesenchymal stem cells . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8002", "text": "Additional research was conducted by Huang  et al.  that analyzed specific genes and biological markers that are associated with the risk of colon cancer development in patients with colitis. The results showed a correlation between certain biomarkers and the development of disease. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8003", "text": "Colitis is common in parts of the world where  helminthic  colonisation is rare, and uncommon in those areas where most people carry worms.  Infections  with helminths may alter the autoimmune response that causes the disease. Early trials of  Trichuris suis  ova (TSO) showed promising results when used in people with IBD [ 21 ] [ 22 ] [ 23 ] [ 24 ]  but later trials failed at Phase 2, and most were eventually discontinued. [ 25 ]  However, the phase 2 trials had used a different formulation of TSO from the one that had been used in the earlier studies that had shown positive outcomes. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8004", "text": "Colorectal cancer  ( CRC ), also known as  bowel cancer ,  colon cancer , or  rectal cancer , is the development of  cancer  from the  colon  or  rectum  (parts of the  large intestine ). [ 5 ]  Signs and symptoms may include  blood in the stool , a change in  bowel movements , weight loss, abdominal pain and fatigue. [ 9 ]  Most colorectal cancers are due to lifestyle factors and genetic disorders. [ 2 ] [ 3 ]  Risk factors include diet,  obesity , smoking, and lack of  physical activity . [ 2 ]  Dietary factors that increase the risk include  red meat ,  processed meat , and  alcohol . [ 2 ] [ 4 ]  Another risk factor is  inflammatory bowel disease , which includes  Crohn's disease  and  ulcerative colitis . [ 2 ]  Some of the inherited genetic disorders that can cause colorectal cancer include  familial adenomatous polyposis  and  hereditary non-polyposis colon cancer ; however, these represent less than 5% of cases. [ 2 ] [ 3 ]  It typically starts as a  benign tumor , often in the form of a  polyp , which over time becomes  cancerous . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8005", "text": "Colorectal cancer may be diagnosed by  obtaining a sample  of the colon during a  sigmoidoscopy  or  colonoscopy . [ 1 ]  This is then followed by  medical imaging  to determine whether the disease has spread. [ 5 ]   Screening  is effective for preventing and decreasing deaths from colorectal cancer. [ 10 ]  Screening, by one of a number of methods, is recommended starting from the age of 45 to 75. It was recommended starting at age 50 but it was changed to 45 due to increasing numbers of colon cancers. [ 10 ] [ 11 ]  During colonoscopy, small polyps may be removed if found. [ 2 ]  If a large polyp or tumor is found, a  biopsy  may be performed to check if it is cancerous.  Aspirin  and other  non-steroidal anti-inflammatory drugs  decrease the risk of pain during polyp excision. [ 2 ] [ 12 ]  Their general use is not recommended for this purpose, however, due to side effects. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8006", "text": "Treatments used for colorectal cancer may include some combination of surgery,  radiation therapy ,  chemotherapy , and  targeted therapy . [ 5 ]  Cancers that are confined within the wall of the colon may be curable with surgery, while  cancer that has spread widely  is usually not curable, with management being directed towards improving  quality of life  and symptoms. [ 5 ]  The  five-year survival rate  in the United States was around 65% in 2014. [ 6 ]  The individual likelihood of survival depends on how advanced the cancer is, whether or not all the cancer can be removed with surgery, and the person's overall health. [ 1 ]  Globally, colorectal cancer is the third most common type of cancer, making up about 10% of all cases. [ 14 ]  In 2018, there were 1.09 million new cases and 551,000 deaths from the disease. [ 8 ]  It is more common in  developed countries , where more than 65% of cases are found. [ 2 ]  It is less common in women than men. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8007", "text": "The signs and symptoms of colorectal cancer depend on the location of the  tumor  in the  bowel , and whether it has spread elsewhere in the body ( metastasis ). The classic warning signs include: worsening  constipation , blood in the  stool , decrease in stool caliber (thickness), loss of appetite, loss of weight, and  nausea  or  vomiting  in someone over 50 years old. [ 15 ]  Around 50% of people who have colorectal cancer do not report any symptoms. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8008", "text": "Rectal bleeding  or  anemia  are high-risk symptoms in people over the age of 50. [ 17 ]  Weight loss and changes in a person's bowel habit are typically only concerning if they are associated with rectal bleeding. [ 17 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8009", "text": "75\u201395% of colorectal cancer cases occur in people with little or no genetic risk. [ 19 ] [ 20 ]  Risk factors include older age, male sex, [ 20 ]  high intake of fat,  sugar ,  alcohol ,  red meat ,  processed meats ,  obesity ,  smoking , and a lack of  physical exercise . [ 19 ] [ 21 ]  The Rectal Cancer Survival Calculator developed by the  MD Anderson Cancer Center  additionally considers race to be a risk factor; however, there are equity issues concerning whether this might lead to inequity in clinical decision making. [ 22 ] [ 23 ]  Approximately 10% of cases are linked to insufficient activity. [ 24 ]  The risk from alcohol appears to increase at greater than one drink per day. [ 25 ]  Drinking five glasses of water a day is linked to a decrease in the risk of colorectal cancer and  adenomatous  polyps. [ 26 ]   Streptococcus gallolyticus  is associated with colorectal cancer. [ 27 ]  Some strains of  Streptococcus bovis/Streptococcus equinus  complex are consumed by millions of people daily and thus may be safe. [ 28 ]  25 to 80% of people with  Streptococcus bovis/gallolyticus  bacteremia have concomitant colorectal tumors. [ 29 ]  Seroprevalence of  Streptococcus bovis/gallolyticus  is considered as a candidate practical marker for the early prediction of an underlying bowel lesion at high risk population. [ 29 ]  It has been suggested that the presence of antibodies to  Streptococcus bovis/gallolyticus  antigens or the antigens themselves in the bloodstream may act as markers for the carcinogenesis in the colon. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8010", "text": "Pathogenic  Escherichia coli  may increase the risk of colorectal cancer by producing the  genotoxic   metabolite ,  colibactin . [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8011", "text": "People with  inflammatory bowel disease  ( ulcerative colitis  and  Crohn's disease ) are at increased risk of colon cancer. [ 31 ] [ 32 ]  The risk increases the longer a person has the disease, and the worse the severity of inflammation. [ 33 ]  In these high risk groups, both prevention with  aspirin  and regular  colonoscopies  are recommended. [ 34 ]   Endoscopic  surveillance in this high-risk population may reduce the development of colorectal cancer through early diagnosis and may also reduce the chances of dying from colon cancer. [ 34 ]  People with inflammatory bowel disease account for less than 2% of colon cancer cases yearly. [ 33 ]  In those with Crohn's disease, 2% get colorectal cancer after 10\u00a0years, 8% after 20\u00a0years, and 18% after\u00a030 years. [ 33 ]  In people who have ulcerative colitis, approximately 16% develop either a  cancer precursor  or cancer of the colon over 30\u00a0years. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8012", "text": "Those with a family history in two or more  first-degree relatives  (such as a parent or sibling) have a two to threefold greater risk of disease, and this group accounts for about 20% of all cases. A number of genetic syndromes are also associated with higher rates of colorectal cancer. The most common of these is  hereditary nonpolyposis colorectal cancer  (HNPCC, or Lynch syndrome) which is present in about 3% of people with colorectal cancer. [ 20 ]  Other syndromes that are strongly associated with colorectal cancer include  Gardner syndrome  and  familial adenomatous polyposis  (FAP). [ 35 ]  For people with these syndromes, cancer almost always occurs and makes up 1% of the cancer cases. [ 36 ]  A total  proctocolectomy  may be recommended for people with FAP as a preventive measure due to the high risk of malignancy. Colectomy, removal of the colon, may not suffice as a preventive measure because of the high risk of rectal cancer if the rectum remains. [ 37 ]  The most common polyposis syndrome affecting the colon is  serrated polyposis syndrome , [ 38 ]  which is associated with a 25-40% risk of CRC. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8013", "text": "Mutations in the pair of genes ( POLE  and  POLD1 ) have been associated with familial colon cancer. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8014", "text": "Most deaths due to colon cancer are associated with metastatic disease. A gene that appears to contribute to the potential for metastatic disease, metastasis associated in colon cancer 1 ( MACC1 ), has been isolated. [ 41 ]  It is a  transcriptional  factor that influences the expression of  hepatocyte growth factor . This gene is associated with the proliferation, invasion, and scattering of colon cancer cells in  cell culture , and tumor growth and metastasis in mice. MACC1 may be a potential target for cancer intervention, but this possibility needs to be confirmed with clinical studies. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8015", "text": "Epigenetic  factors, such as abnormal  DNA methylation  of  tumor suppressor  promoters, play a role in the development of colorectal cancer. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8016", "text": "Ashkenazi Jews  have a 6% higher risk rate of getting  adenomas  and then colon cancer due to mutations in the  APC gene  being more common. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8017", "text": "Colorectal cancer is a disease originating from the  epithelial cells  lining the colon or rectum of the  gastrointestinal tract , most frequently as a result of genetic mutations in the  Wnt signaling pathway  that increases signaling activity. [ 45 ]  The Wnt signaling pathway normally plays an important role for normal function of these cells including maintaining this lining. Mutations can be  inherited  or  acquired , and most probably occur in the  intestinal crypt   stem cell . [ 46 ] [ 47 ] [ 48 ]  The most commonly mutated gene in all colorectal cancer is the  APC  gene, which produces the APC protein. [ 45 ]  The APC protein prevents the accumulation of  \u03b2-catenin  protein. Without APC,  \u03b2-catenin  accumulates to high levels and translocates (moves) into the  nucleus , binds to DNA, and activates the  transcription  of proto- oncogenes . These genes are normally important for stem cell renewal and differentiation, but when inappropriately expressed at high levels, they can cause cancer. [ 45 ]  While APC is mutated in most colon cancers, some cancers have increased \u03b2-catenin because of mutations in \u03b2-catenin (CTNNB1) that block its own breakdown, or have mutations in other genes with function similar to APC such as  AXIN1 ,  AXIN2 ,  TCF7L2 , or  NKD1 . [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8018", "text": "Beyond the defects in the  Wnt signaling pathway , other mutations must occur for the cell to become cancerous. The  p53  protein, produced by the  TP53  gene, normally monitors  cell division  and induces their  programmed death  if they have Wnt pathway defects. Eventually, a  cell line  acquires a mutation in the  TP53  gene and transforms the tissue from a  benign epithelial tumor  into an invasive  epithelial cell cancer . Sometimes the gene encoding p53 is not mutated, but another protective protein named  BAX  is mutated instead. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8019", "text": "Other proteins responsible for programmed cell death that are commonly deactivated in colorectal cancers are  TGF-\u03b2  and DCC ( Deleted in Colorectal Cancer ). TGF-\u03b2 has a deactivating mutation in at least half of colorectal cancers. Sometimes TGF-\u03b2 is not deactivated, but a downstream protein named  SMAD  is deactivated. [ 49 ]  DCC commonly has a deleted segment of a chromosome in colorectal cancer. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8020", "text": "Approximately 70% of all  human genes  are expressed in colorectal cancer, with just over 1% of having increased expression in colorectal cancer compared to other forms of cancer. [ 51 ]  Some genes are  oncogenes : they are overexpressed in colorectal cancer. For example, genes encoding the proteins  KRAS ,  RAF , and  PI3K , which normally stimulate the  cell to divide  in response to growth factors, can acquire mutations that result in over-activation of cell proliferation. The chronological order of mutations is sometimes important. If a previous APC mutation occurred, a primary KRAS mutation often progresses to cancer rather than a self-limiting  hyperplastic  or borderline lesion. [ 52 ]   PTEN , a tumor suppressor, normally inhibits PI3K, but can sometimes become mutated and deactivated. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8021", "text": "Comprehensive,  genome -scale analysis has revealed that colorectal carcinomas can be categorized into hypermutated and non-hypermutated tumor types. [ 53 ]  In addition to the oncogenic and inactivating mutations described for the genes above, non-hypermutated samples also contain mutated  CTNNB1 ,  FAM123B ,  SOX9 ,  ATM , and  ARID1A . Progressing through a distinct set of genetic events, hypermutated tumors display mutated forms of  ACVR2A ,  TGFBR2 ,  MSH3 ,  MSH6 , SLC9A9,  TCF7L2 , and  BRAF . The common theme among these genes, across both tumor types, is their involvement in Wnt and TGF-\u03b2 signaling pathways, which results in increased activity of  MYC , a central player in colorectal cancer. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8022", "text": "Mismatch repair  (MMR) deficient tumours are characterized by a relatively high number of poly-nucleotide  tandem repeats . [ 54 ]  This is caused by a deficiency in MMR proteins \u2013 which are typically caused by  epigenetic  silencing and or inherited mutations ( e.g. ,  Lynch syndrome ). [ 55 ]  15 to 18 percent of colorectal cancer tumours have MMR deficiencies, with 3 percent developing due to Lynch syndrome. [ 56 ]  The role of the mismatch repair system is to protect the integrity of the genetic material within cells ( i.e. , error detecting and correcting). [ 55 ]  Consequently, a deficiency in MMR proteins may lead to an inability to detect and repair genetic damage, allowing for further cancer-causing mutations to occur and colorectal cancer to progress. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8023", "text": "The polyp to cancer progression sequence is the classical model of colorectal cancer  pathogenesis . [ 57 ]  In this  adenoma-carcinoma sequence , [ 58 ]  normal epithelial cells progress to  dysplastic  cells such as  adenomas , and then to carcinoma, by a process of progressive genetic mutation. [ 59 ]  Central to the polyp to CRC sequence are gene mutations, epigenetic alterations, and local inflammatory changes. [ 57 ]  The polyp to CRC sequence can be used as an underlying framework to illustrate how specific molecular changes lead to various cancer subtypes. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8024", "text": "The term \"field cancerization\" was first used in 1953 to describe an area or \"field\" of epithelium that has been preconditioned (by what were largely unknown processes at the time) to predispose it towards development of cancer. [ 60 ]  Since then, the terms \"field cancerization\", \"field carcinogenesis\", \"field defect\", and \" field effect \" have been used to describe pre-malignant or pre-neoplastic tissue in which new cancers are likely to arise. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8025", "text": "Field defects are important in progression to colon cancer. [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8026", "text": "However, as pointed out by Rubin, \"The vast majority of studies in cancer research has been done on well-defined tumors  in vivo , or on discrete neoplastic foci  in vitro . Yet there is evidence that more than 80% of the somatic mutations found in mutator phenotype human colorectal tumors occur before the onset of terminal clonal expansion.\" [ 64 ] [ 65 ]  Similarly, Vogelstein et al. [ 66 ]  pointed out that more than half of somatic mutations identified in tumors occurred in a pre-neoplastic phase (in a field defect), during growth of apparently normal cells. Likewise, epigenetic alterations present in tumors may have occurred in pre-neoplastic field defects. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8027", "text": "An expanded view of field effect has been termed \"etiologic field effect\", which encompasses not only molecular and pathologic changes in pre-neoplastic cells but also influences of exogenous environmental factors and molecular changes in the local  microenvironment  on neoplastic evolution from tumor initiation to death. [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8028", "text": "Epigenetic  alterations are much more frequent in colon cancer than genetic (mutational) alterations. As described by Vogelstein et al., [ 66 ]  an average cancer of the colon has only 1 or 2 oncogene mutations and 1 to 5 tumor suppressor mutations (together designated \"driver mutations\"), with about 60 further \"passenger\" mutations. The oncogenes and tumor suppressor genes are well studied and are described above under  Pathogenesis . [ 69 ] [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8029", "text": "In addition to epigenetic alteration of expression of miRNAs, other common types of epigenetic alterations in cancers that change gene expression levels include direct hypermethylation or hypomethylation of CpG islands of protein-encoding genes and alterations in histones and chromosomal architecture that influence gene expression. [ 71 ]  As an example, 147 hypermethylations and 27 hypomethylations of protein coding genes were frequently associated with colorectal cancers. Of the hypermethylated genes, 10 were hypermethylated in 100% of colon cancers, and many others were hypermethylated in more than 50% of colon cancers. [ 72 ]  In addition, 11 hypermethylations and 96 hypomethylations of miRNAs were also associated with colorectal cancers. [ 72 ]  Abnormal (aberrant)  methylation  occurs as a normal consequence of normal aging and the risk of colorectal cancer increases as a person gets older. [ 73 ]  The source and trigger of this age-related methylation is unknown. [ 73 ] [ 74 ]  Approximately half of the genes that show age-related methylation changes are the same genes that have been identified to be involved in the development of colorectal cancer. [ 73 ]  These findings may suggest a reason for age being associated with the increased risk of developing colorectal cancer. [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8030", "text": "Epigenetic reductions of DNA repair enzyme expression may likely lead to the genomic and epigenomic instability characteristic of cancer. [ 75 ] [ 76 ] [ 67 ]  As summarized in the articles  Carcinogenesis  and  Neoplasm , for sporadic cancers in general, a deficiency in DNA repair is occasionally due to a mutation in a DNA repair gene, but is much more frequently due to epigenetic alterations that reduce or silence expression of DNA repair genes. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8031", "text": "Epigenetic alterations involved in the development of colorectal cancer may affect a person's response to chemotherapy. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8032", "text": "Consensus molecular subtypes (CMS) classification of colorectal cancer was first introduced in 2015. CMS classification so far has been considered the most robust classification system available for CRC that has a clear biological interpretability and the basis for future clinical stratification and subtype-based targeted interventions. [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8033", "text": "A novel Epigenome-based Classification (EpiC) of colorectal cancer was proposed in 2021 introducing 4 enhancer subtypes in people with CRC. Chromatin states using 6 histone marks are characterized to identify EpiC subtypes. A combinatorial therapeutic approach based on the previously introduced consensus molecular subtypes (CMSs) and EpiCs could significantly enhance current treatment strategies. [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8034", "text": "Colorectal cancer diagnosis is performed by sampling of areas of the colon suspicious for possible tumor development, typically during colonoscopy or sigmoidoscopy, depending on the location of the lesion. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8035", "text": "A colorectal cancer is sometimes initially discovered on  CT scan . [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8036", "text": "Presence of  metastases  is determined by a  CT scan  of the chest, abdomen and pelvis. [ 20 ]  Other potential imaging tests such as  PET  and  MRI  may be used in certain cases. [ 20 ]  MRI is particularly useful to determine local stage of the tumor and to plan the optimal surgical approach. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8037", "text": "MRI is also performed after completion of neoadjuvant chemoradiotherapy to identify patients who achieve complete response. Patients with complete response on both MRI and endoscopy may not require surgical resection and can avoid unnecessary surgical morbidity and complications. [ 82 ]  Patients selected for non-surgical treatment of rectal cancer should have periodic MRI scans, receive physical examinations, and undergo endoscopy procedures to detect any tumor re-growth which can occur in a minority of these patients. When local recurrence occurs, periodic follow up can detect it when it is still small and curable with salvage surgery. In addition, MRI tumor regression grades can be assigned after chemoradiotherapy which correlate with patients' long-term survival outcomes. [ 83 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8038", "text": "The  histopathologic  characteristics of the  tumor  are reported from the analysis of tissue taken from a biopsy or surgery. A pathology report contains a description of the microscopical characteristics of the tumor tissue, including both tumor cells and how the tumor invades into healthy tissues and finally if the tumor appears to be completely removed. The most common form of colon cancer is  adenocarcinoma , constituting between 95% [ 85 ]  and 98% [ 86 ]  of all cases of colorectal cancer. Other, rarer types include  lymphoma , adenosquamous and  squamous cell carcinoma . Some subtypes are more aggressive. [ 87 ]   Immunohistochemistry  may be used in uncertain cases. [ 88 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8039", "text": "Staging  of the cancer is based on both radiological and pathological findings. As with most other forms of cancer, tumor staging is based on the  TNM system  which considers how much the initial tumor has spread and the presence of metastases in lymph nodes and more distant organs. [ 20 ]  The AJCC 8th edition was published in 2018. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8040", "text": "It has been estimated that about half of colorectal cancer cases are due to lifestyle factors, and about a quarter of all cases are preventable. [ 90 ]  Increasing surveillance, engaging in physical activity, consuming a diet high in fiber, quitting smoking and limiting alcohol consumption decrease the risk. [ 91 ] [ 92 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8041", "text": "Lifestyle risk factors with strong evidence include lack of exercise, cigarette smoking, alcohol, and obesity. [ 93 ] [ 94 ] [ 95 ]  The risk of colon cancer can be reduced by maintaining a normal body weight through a combination of sufficient exercise and eating a  healthy diet . [ 96 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8042", "text": "Current research consistently links eating more red meat and processed meat to a higher risk of the disease. [ 97 ]  Starting in the 1970s, dietary recommendations to prevent colorectal cancer often included increasing the consumption of  whole grains , fruits and vegetables, and reducing the intake of  red meat  and  processed meats . This was based on animal studies and retrospective observational studies. However, large scale prospective studies have failed to demonstrate a significant protective effect, and due to the multiple causes of cancer and the complexity of studying correlations between diet and health, it is uncertain whether any specific dietary interventions will have significant protective effects. [ 98 ] :\u200a432\u2013433\u200a [ 99 ] :\u200a125\u2013126\u200a  In 2018 the  National Cancer Institute  stated that \"There is no reliable evidence that a diet started in adulthood that is low in fat and meat and high in fiber, fruits, and vegetables reduces the risk of CRC by a clinically important degree.\" [ 93 ] [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8043", "text": "Consuming alcoholic drinks and consuming processed meat both increase the risk of colorectal cancer. [ 101 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8044", "text": "The 2014 World Health Organization cancer report noted that it has been hypothesized that dietary fiber might help prevent colorectal cancer, but that most studies at the time had not yet studied the correlation. [ 99 ]  A 2019 review, however, found evidence of benefit from dietary fiber and whole grains. [ 102 ]  The  World Cancer Research Fund  listed the benefit of fiber for prevention of colorectal cancer as \"probable\" as of 2017. [ 103 ]  A 2022  umbrella review  says there is \"convincing evidence\" for that association. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8045", "text": "Higher physical activity is recommended. [ 21 ] [ 105 ]   Physical exercise  is associated with a modest reduction in colon but not rectal cancer risk. [ 106 ] [ 107 ]  High levels of physical activity reduce the risk of colon cancer by about 21%. [ 108 ]   Sitting  regularly for prolonged periods is associated with higher mortality from colon cancer. Regular exercise does not negate the risk but does lower it. [ 109 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8046", "text": "Aspirin  and  celecoxib  appear to decrease the risk of colorectal cancer in those at high risk. [ 110 ] [ 111 ]  Aspirin is recommended in those who are 50 to 60 years old, do not have an increased risk of bleeding, and are at risk for cardiovascular disease to prevent colorectal cancer. [ 112 ]  It is not recommended in those at average risk. [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8047", "text": "There is tentative evidence for  calcium  supplementation, but it is not sufficient to make a recommendation. [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8048", "text": "Adequate  Vitamin D  intake and blood levels are associated with a lower risk of colon cancer. [ 115 ] [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8049", "text": "As more than 80% of colorectal cancers arise from  adenomatous polyps , screening for this cancer is effective for both early detection and for prevention. [ 20 ] [ 117 ]  Diagnosis of cases of colorectal cancer through screening tends to occur 2\u20133 years before diagnosis of cases with symptoms. [ 20 ]  Any polyps that are detected can be removed, usually by  colonoscopy  or  sigmoidoscopy , and thus prevent them from turning into cancer. Screening has the potential to reduce colorectal cancer deaths by 60%. [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8050", "text": "The three main screening tests are colonoscopy,  fecal occult blood  testing, and  flexible sigmoidoscopy . Of the three, only sigmoidoscopy cannot screen the  right side of the colon  where 42% of cancers are found. [ 119 ]  Flexible sigmoidoscopy, however, has the best evidence for decreasing the risk of death from any cause. [ 120 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8051", "text": "Fecal occult blood testing (FOBT) of the stool is typically recommended every two years and can be either  guaiac-based  or  immunochemical . [ 20 ]  If abnormal FOBT results are found, participants are typically referred for a follow-up colonoscopy examination. When done once every 1\u20132 years, FOBT screening reduces colorectal cancer deaths by 16% and among those participating in screening, colorectal cancer deaths can be reduced up to 23%, although it has not been proven to reduce all-cause mortality. [ 121 ]  Immunochemical tests are accurate and do not require dietary or medication changes before testing. [ 122 ]  However, research in the UK has found that for these immunochemical tests, the threshold for further investigation is set at a point that may miss more than half of bowel cancer cases. The research suggests that the  NHS England's  Bowel Cancer Screening Programme could make better use of the test's ability to provide the exact concentration of blood in faeces (rather than only whether it is above or below a cutoff level). [ 123 ] [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8052", "text": "Other options include  virtual colonoscopy  and stool DNA screening testing (FIT-DNA). Virtual colonoscopy via a  CT scan  appears as good as standard colonoscopy for detecting cancers and large adenomas but is expensive, associated with radiation exposure, and cannot remove any detected abnormal growths as standard colonoscopy can. [ 20 ]  Stool DNA screening test looks for  biomarkers  associated with colorectal cancer and precancerous lesions, including altered  DNA  and  blood hemoglobin . A positive result should be followed by  colonoscopy . FIT-DNA has more false positives than FIT and thus results in more adverse effects. [ 10 ]  Further study is required as of 2016 to determine whether a three-year screening interval is correct. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8053", "text": "In the United States, screening is typically recommended between ages 50 and 75\u00a0years. [ 10 ] [ 125 ]  The  American Cancer Society  recommends starting at the age of 45. [ 126 ]  For those between 76 and 85 years old, the decision to screen should be individualized. [ 10 ]  For those at high risk, screenings usually begin at around 40. [ 20 ] [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8054", "text": "Several screening methods are recommended including stool-based tests every 2 years,  sigmoidoscopy  every 10 years with  fecal immunochemical testing  every two years, and  colonoscopy  every 10 years. [ 125 ]  It is unclear which of these two methods is better. [ 128 ]  Colonoscopy may find more cancers in the first part of the colon, but is associated with greater cost and more complications. [ 128 ]  For people with average risk who have had a high-quality colonoscopy with normal results, the  American Gastroenterological Association  does not recommend any type of screening in the 10 years following the colonoscopy. [ 129 ] [ 130 ]  For people over 75 or those with a life expectancy of less than 10\u00a0years, screening is not recommended. [ 131 ]  It takes about 10 years after screening for one out of a 1000 people to benefit. [ 132 ]  The USPSTF list seven potential strategies for screening, with the most important thing being that at least one of these strategies is appropriately used. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8055", "text": "In Canada, among those 50 to 75 years old at normal risk, fecal immunochemical testing or FOBT is recommended every two years or sigmoidoscopy every 10 years. [ 133 ]  Colonoscopy is less preferred. [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8056", "text": "Some countries have national colorectal screening programs which offer FOBT screening for all adults within a certain age group, typically starting between ages 50 and 60. Examples of countries with organised screening include the United Kingdom, [ 134 ]  Australia, [ 135 ]  the Netherlands, [ 136 ]  Hong Kong, and Taiwan. [ 137 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8057", "text": "The UK Bowel Cancer Screening Programme aims to find warning signs in people aged 60 to 74, by recommending a faecal immunochemical test (FIT) every two years. FIT measures blood in faeces, and people with levels above a certain threshold may have bowel tissue examined for signs of cancer. Growths having cancerous potential are removed. [ 138 ] [ 124 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8058", "text": "The treatment of colorectal cancer can be aimed at cure or palliation. The decision on which aim to adopt depends on various factors, including the person's health and preferences, as well as the stage of the tumor. [ 139 ]  Assessment in multidisciplinary teams is a critical part of determining whether the patient is suitable for surgery or not. [ 140 ]  When colorectal cancer is caught early, surgery can be curative. However, when it is detected at later stages (for which  metastases  are present), this is less likely and treatment is often directed at palliation, to relieve symptoms caused by the tumour and keep the person as comfortable as possible. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8059", "text": "At an early stage, colorectal cancer may be removed during a colonoscopy using one of several techniques, including  endoscopic mucosal resection  or  endoscopic submucosal dissection . [ 5 ]  Endoscopic resection is possible if there is low possibility of lymph node metastasis and the size and location of the tumor make en bloc resection possible. [ 141 ]  For people with localized cancer, the preferred treatment is complete surgical removal with adequate  margins , with the attempt of achieving a cure. The procedure of choice is a partial  colectomy  (or proctocolectomy for rectal lesions) where the affected part of the colon or rectum is removed along with parts of its  mesocolon  and  blood supply  to facilitate removal of draining  lymph nodes . This can be done either by an open  laparotomy  or  laparoscopically , depending on factors related to the individual person and lesion factors. [ 20 ]  The colon may then be reconnected or a person may have a  colostomy . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8060", "text": "If there are only a few metastases in the liver or lungs, these may also be removed.  Chemotherapy  may be used before surgery to shrink the cancer before attempting to remove it. The two most common sites of recurrence of colorectal cancer are the  liver  and  lungs . [ 20 ]  For  peritoneal carcinomatosis   cytoreductive surgery , sometimes in combination with  HIPEC  can be used in an attempt to remove the cancer. [ 142 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8061", "text": "In both cancer of the  colon  and  rectum ,  chemotherapy  may be used in addition to surgery in certain cases. The decision to add chemotherapy in management of colon and rectal cancer depends on the stage of the disease. [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8062", "text": "In Stage I colon cancer, no chemotherapy is offered, and surgery is the definitive treatment. The role of chemotherapy in Stage II colon cancer is debatable, and is usually not offered unless risk factors such as T4 tumor, undifferentiated tumor, vascular and perineural invasion or inadequate lymph node sampling is identified. [ 144 ]  It is also known that the people who carry abnormalities of the mismatch repair genes do not benefit from chemotherapy. For Stage III and Stage IV colon cancer, chemotherapy is an integral part of treatment. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8063", "text": "If cancer has spread to the  lymph nodes  or distant organs, which is the case with Stage III and Stage IV colon cancer respectively, adding chemotherapy agents  fluorouracil ,  capecitabine  or  oxaliplatin  increases life expectancy. If the lymph nodes do not contain cancer, the benefits of chemotherapy are controversial. If the cancer is widely metastatic or unresectable, treatment is then  palliative . Typically in this setting, a number of different chemotherapy medications may be used. [ 20 ]  Chemotherapy drugs for this condition may include  capecitabine ,  fluorouracil ,  irinotecan ,  oxaliplatin  and  UFT . [ 145 ]  The drugs capecitabine and fluorouracil are interchangeable, with capecitabine being an oral medication and fluorouracil being an intravenous medicine. Some specific  regimens  used for CRC are  CAPOX ,  FOLFOX ,  FOLFOXIRI , and  FOLFIRI . [ 146 ]  Antiangiogenic drugs such as  bevacizumab  are often added in first line therapy. [ 147 ]  Another class of drugs used in the second line setting are  epidermal growth factor receptor  inhibitors, of which the three FDA approved ones are  aflibercept ,  cetuximab  and  panitumumab . [ 148 ] [ 149 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8064", "text": "The primary difference in the approach to low stage rectal cancer is the incorporation of radiation therapy. Often, it is used in conjunction with chemotherapy in a  neoadjuvant  fashion to enable surgical resection, so that ultimately a  colostomy  is not required. However, it may not be possible in low lying tumors, in which case, a permanent colostomy may be required. Stage IV rectal cancer is treated similar to Stage IV colon cancer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8065", "text": "Stage IV colorectal cancer due to  peritoneal carcinomatosis  can be treated using  HIPEC  combined with cytoreductive surgery, in some people. [ 150 ] [ 151 ] [ 152 ]  Also, T4 colorectal cancer can be treated with HIPEC to avoid future relapses. [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8066", "text": "While a combination of  radiation  and chemotherapy may be useful for  rectal cancer , [ 20 ]  for some people requiring treatment, chemoradiotherapy can increase acute treatment-related toxicity, and has not been shown to improve survival rates compared to radiotherapy alone, although it is associated with less local recurrence. [ 142 ]  For squamous cell carcinoma of the anal canal, chemoradiation therapy (CRT) with 5-FU and mitomycin C is preferred over radiation alone, offering improved survival outcomes but with increased risks of  acute hematological toxicity . [ 154 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8067", "text": "The use of radiotherapy in colon cancer is not routine due to the sensitivity of the bowels to radiation. [ 155 ]  Radiation therapy's side effects (and occurrence rates) include acute (27%) and late (17%)  dermatological toxicities , acute (14%) and late (27%)  gastrointestinal toxicities , [ 154 ]  and late  pelvic radiation disease  (1-10%), e.g.,  irreversible lumbosacral plexopathy . [ 156 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8068", "text": "As with chemotherapy, radiotherapy can be used as a neoadjuvant for clinical stages T3 and T4 for rectal cancer. [ 157 ]  This results in downsizing or downstaging of the tumour, preparing it for surgical resection, and also decreases local recurrence rates. [ 157 ]  For locally advanced rectal cancer, neoadjuvant chemoradiotherapy has become the standard treatment. [ 158 ]  Additionally, when surgery is not possible radiation therapy has been suggested to be an effective treatment against CRC pulmonary metastases, which are developed by 10-15% of people with CRC. [ 159 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8069", "text": "Immunotherapy  with immune checkpoint inhibitors has been found to be useful for a type of colorectal cancer with  mismatch repair deficiency  and  microsatellite instability . [ 160 ] [ 161 ] [ 162 ]   Pembrolizumab  is approved for advanced CRC tumours that are MMR deficient and have failed usual treatments. [ 163 ]  Most people who do improve, however, still worsen after months or years. [ 161 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8070", "text": "On the other hand, in a prospective phase 2 study published in June 2022 in The New England Journal of Medicine, 12 patients with Deficient Mismatch Repair (dMMR) stage II or III rectal adenocarcinoma were administered single-agent  dostarlimab , an anti\u2013PD-1 monoclonal antibody, every three weeks for six months. After a median follow-up of 12 months (range, 6 to 25 months), all 12 patients had a complete clinical response with no evidence of tumor on MRI, 18F-fluorodeoxyglucose\u2013positron-emission tomography, endoscopic evaluation, digital rectal examination, or biopsy. Moreover, no patient in the trial needed chemoradiotherapy or surgery, and no patient reported adverse events of grade 3 or higher. However, although the results of this study are promising, the study is small and has uncertainties about long-term outcomes. [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8071", "text": "Palliative care  can be used at the same time as the cancer treatment and is recommended for any person who has advanced colon cancer or who has significant symptoms. [ 165 ] [ 166 ]  Involvement of palliative care may be beneficial to improve the quality of life for both the person and his or her family, by improving symptoms, anxiety and preventing admissions to the hospital. [ 167 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8072", "text": "In people with incurable colorectal cancer, palliative care can consist of procedures that relieve symptoms or complications from the cancer but do not attempt to cure the underlying cancer, thereby improving  quality of life . Surgical options may include non-curative surgical removal of some of the cancer tissue, bypassing part of the intestines, or stent placement. These procedures can be considered to improve symptoms and reduce complications such as bleeding from the tumor, abdominal pain and intestinal obstruction. [ 168 ]  Non-operative methods of symptomatic treatment include radiation therapy to decrease tumor size as well as pain medications. [ 169 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8073", "text": "In addition to medical intervention, a variety of psychosocial interventions have been implemented to address psychosocial concerns in the context of colorectal cancer. [ 170 ]  Depression and anxiety are highly prevalent in patients diagnosed with CRC, therefore psychosocial interventions can be helpful for alleviating psychological distress. [ 171 ] [ 172 ]  Many patients continue to experience symptoms of anxiety and depression following treatment, regardless of treatment outcome. [ 171 ] [ 173 ]  Societal stigmas associated with colorectal cancer present further psychosocial challenges for CRC patients and their families. [ 174 ] [ 175 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8074", "text": "Colorectal cancer patients have a 51% higher risk of experiencing depression than individuals without the disease. [ 172 ]  Additionally, CRC patients are at high risk of experiencing severe anxiety, low self-esteem, poor self-concept, and social anxiety. [ 171 ] [ 176 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8075", "text": "Regardless of treatment outcome, many CRC patients experience ongoing symptoms of anxiety, depression, and distress. [ 171 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8076", "text": "Survivorship of CRC can involve significant lifestyle adjustments. [ 175 ]  Postoperative afflictions may include stomas, bowel issues, incontinence, odor, and changes to sexual functioning. [ 175 ] [ 176 ]  These changes can result in distorted body image, social anxiety, depression, and distress\u2014all of which contribute to a poorer quality of life. [ 175 ] [ 177 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8077", "text": "Colorectal cancer is the second leading cause of cancer-related death worldwide. [ 178 ]  Transitioning into palliative care and contending with mortality can be a deeply distressing experience for a CRC patient and their loved ones."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8078", "text": "Colorectal cancer is highly stigmatized and can elicit feelings of disgust from  patients, healthcare professionals, family, intimate partners, and the general public. [ 174 ]  Patients with stomas are especially vulnerable to stigmatization due to unavoidable odors, gas, and unpleasant noises from stoma bags. [ 174 ]  Additionally, associated CRC risk factors like poor diet, alcohol consumption, and lack of physical activity prompt negative assumptions of blame and personal responsibility onto CRC patients. [ 175 ]  Judgement from others along with internalized self-blame and embarrassment can negatively affect self-esteem, sociability, and quality of life. [ 175 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8079", "text": "Face-to-face interventions such as clinician-patient talk therapy, body-mind-spirit practices, and support group sessions have been identified as most effective in reducing anxiety and depression in CRC patients. [ 170 ]  Additionally, journaling exercises and over-the-phone talk therapy sessions have been implemented. [ 170 ]  Though deemed less effective, these non-face-to-face interventions are economically inclusive and have been found to reduce both depression and anxiety in CRC patients. [ 170 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8080", "text": "The U.S.  National Comprehensive Cancer Network  and  American Society of Clinical Oncology  provide guidelines for the follow-up of colon cancer. [ 179 ] [ 180 ]  A  medical history  and  physical examination  are recommended every 3 to 6 months for 2 years, then every 6 months for 5 years.  Carcinoembryonic antigen  blood level measurements follow the same timing, but are only advised for people with T2 or greater lesions who are candidates for intervention. A  CT-scan  of the chest, abdomen and pelvis can be considered annually for the first 3 years for people who are at high risk of recurrence (for example, those who had poorly differentiated tumors or venous or lymphatic invasion) and are candidates for curative surgery (with the aim to cure). A  colonoscopy  can be done after 1 year, except if it could not be done during the initial staging because of an obstructing mass, in which case it should be performed after 3 to 6 months. If a villous polyp, a polyp >1 centimeter or high-grade dysplasia is found, it can be repeated after 3 years, then every 5 years. For other abnormalities, the colonoscopy can be repeated after 1 year. [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8081", "text": "Routine  PET  or  ultrasound scanning ,  chest X-rays ,  complete blood count  or  liver function tests  are not recommended. [ 179 ] [ 180 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8082", "text": "For people who have undergone curative surgery or adjuvant therapy (or both) to treat non-metastatic colorectal cancer, intense surveillance and close follow-up have not been shown to provide additional survival benefits. [ 181 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8083", "text": "Exercise may be recommended in the future as secondary therapy to cancer survivors. In epidemiological studies, exercise may decrease colorectal cancer-specific mortality and all-cause mortality. Results for the specific amounts of exercise needed to observe a benefit were conflicting. These differences may reflect differences in tumour biology and the expression of biomarkers. People with tumors that lacked  CTNNB1  expression (\u03b2-catenin), involved in  Wnt signalling pathway , required more than 18  Metabolic equivalent  (MET) hours per week, a measure of exercise, to observe a reduction in colorectal cancer mortality. The mechanism of how exercise benefits survival may be involved in immune surveillance and inflammation pathways. In clinical studies, a pro-inflammatory response was found in people with stage II-III colorectal cancer who underwent 2 weeks of moderate exercise after completing their primary therapy. Oxidative balance may be another possible mechanism for benefits observed. A significant decrease in 8-oxo-dG was found in the urine of people who underwent 2 weeks of moderate exercise after primary therapy. Other possible mechanisms may involve metabolic hormone and sex-steroid hormones, although these pathways may be involved in other types of cancers. [ 182 ] [ 183 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8084", "text": "Another potential biomarker may be  p27 . Survivors with tumors that expressed p27 and performed greater and equal to 18 MET hours per week were found to have reduced colorectal cancer mortality survival compared to those with less than 18 MET hours per week. Survivors without p27 expression who exercised were shown to have worse outcomes. The constitutive activation of  PI3K/AKT/mTOR pathway  may explain the loss of p27 and excess energy balance may up-regulate p27 to stop cancer cells from dividing. [ 183 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8085", "text": "Physical activity provides benefits to people with non-advanced colorectal cancer. Improvements in aerobic fitness, cancer-related fatigue and health-related quality of life have been reported in the short term. [ 184 ]  However, these improvements were not observed at the level of disease-related mental health, such as anxiety and depression. [ 184 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8086", "text": "Fewer than 600 genes are linked to outcomes in colorectal cancer. [ 51 ]  These include both unfavorable genes, where high expression is related to poor outcome, for example the  heat shock 70 kDa protein 1 (HSPA1A) , and favorable genes where high expression is associated with better survival, for example the  putative RNA-binding protein 3 (RBM3) . [ 51 ]  The prognosis is also correlated with a poor fidelity of the pre-mRNA splicing apparatus, and thus a high number of deviating alternative splicing. [ 185 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8087", "text": "The average five-year recurrence rate in people with  colon cancer  where surgery is successful is 5% for  stage  I cancers, 12% in stage II and 33% in stage III. However, depending on the number of risk factors it ranges from 9\u201322% in stage II and 17\u201344% in stage III. [ 186 ]  The average five-year recurrence rate in people with  rectal cancer  where surgery is successful is 9% for stage 0  (after pre-treatment)  cancers, 8% for stage I cancers, 18% in stage II and 34% in stage III. Depending on the number of risk factors (0-2) the risk for distant metastasis in  rectal cancer  ranges from 4-11% in stage 0, 6-12% in stage I, 11-28% in stage II and 15-43% in stage III. [ 187 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8088", "text": "The recurrence rates have decreased over the past decades as a result of improvements in the colorectal cancer management. [ 188 ]  The risk of recurrence after five years of surveillance remain very low. [ 189 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8089", "text": "In Europe the  five-year survival rate  for colorectal cancer is less than 60%. In the  developed world  about a third of people who get the disease die from it. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8090", "text": "Survival is directly related to detection and the type of cancer involved, but overall is poor for symptomatic cancers, as they are typically quite advanced. Survival rates for early stage detection are about five times that of late stage cancers. People with a tumor that has not breached the  muscularis mucosa  (TNM stage Tis, N0, M0) have a five-year survival rate of 100%, while those with invasive cancer of T1 (within the submucosal layer) or T2 (within the muscular layer) have an average five-year survival rate of approximately 90%. Those with a more invasive tumor yet without node involvement (T3-4, N0, M0) have an average five-year survival rate of approximately 70%. People with positive regional lymph nodes (any T, N1-3, M0) have an average five-year survival rate of approximately 40%, while those with distant metastases (any T, any N, M1) have a poor prognosis and the five year survival ranges from <5 percent to 31 percent. [ 190 ] [ 191 ] [ 192 ] [ 193 ] [ 194 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8091", "text": "Five-year overall survival (OS)  in rectal cancer after modern  preoperative treatment  and surgery was 90% for stage 0, 86% for stage I, 78% for stage II, and 67% for stage III according to a nationwide, population-based study. [ 187 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8092", "text": "Whilst the impact of colorectal cancer on those who survive varies greatly there will often be a need to adapt to both physical and psychological outcomes of the illness and its treatment. [ 195 ]  For example, it is common for people to experience incontinence, [ 196 ]  sexual dysfunction, [ 197 ]  problems with stoma care [ 198 ]  and fear of cancer recurrence [ 199 ]  after primary treatment has concluded."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8093", "text": "A qualitative systematic review published in 2021 highlighted that there are three main factors influencing adaptation to living with and beyond colorectal cancer: support mechanisms, severity of late effects of treatment and psychosocial adjustment. Therefore, it is essential that people are offered appropriate support to help them better adapt to life following treatment. [ 200 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8094", "text": "Globally more than 1\u00a0million people get colorectal cancer every year [ 20 ]  resulting in about 715,000 deaths as of 2010 up from 490,000 in 1990. [ 201 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8095", "text": "As of 2012 [update] , it is the second most common cause of cancer in women (9.2% of diagnoses) and the third most common in men (10.0%) [ 14 ] :\u200a16\u200a  with it being the fourth most common cause of cancer death after  lung ,  stomach , and  liver cancer . [ 202 ]  It is more common in developed than developing countries. [ 203 ]  Global incidence varies 10-fold, with highest rates in Australia, New Zealand, Europe and the US and lowest rates in Africa and South-Central Asia. [ 204 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8096", "text": "In 2022, the incidence of colorectal cancer in the United States was anticipated to be about 151,000 adults, including over 106,000 new cases of colon cancer (some 54,000 men and 52,000 women) and about 45,000 new cases of rectal cancer. [ 205 ]  Since the 1980s, the incidence of colorectal cancer decreased, dropping by about 2% annually from 2014 to 2018 in adults aged 50 and older, due mainly to improved screening. [ 205 ]  However, incidence of colorectal cancer has increased in individuals aged 25 to 50. In early 2023, the American Cancer Society (ACS) reported that 20% of diagnoses (of colon cancer) in 2019 were in patients under age 55, which is about double the rate in 1995, and rates of advanced disease increased by about 3% annually in people younger than 50. It predicted that, in 2023, an estimated 19,550 diagnoses and 3,750 deaths would be in people younger than 50. [ 206 ]  Colorectal cancer also disproportionately affects the Black community, where the rates are the highest of any racial/ethnic group in the US. African Americans are about 20% more likely to get colorectal cancer and about 40% more likely to die from it than most other groups. Black Americans often experience greater obstacles to cancer prevention, detection, treatment, and survival, including systemic racial disparities that are complex and go beyond the obvious connection to cancer."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8097", "text": "In the UK about 41,000 people a year get colon cancer making it the fourth most common type. [ 207 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8098", "text": "One in 19 men and one in 28 women in Australia will develop colorectal cancer before the age of 75; one in 10 men and one in 15 women will develop it by 85 years of age. [ 208 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8099", "text": "In   Papua New Guinea  and other Pacific Island States including the  Solomon Islands , colorectal cancer is a very rare cancer compared to lung, stomach, liver or breast cancer. It is estimated that 8 in 100,000 people are likely to develop colorectal cancer every year, while 24 in 100,000 women are likely to develop breast cancer. [ 209 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8100", "text": "A diagnosis of colorectal cancer in patients under 50 years of age is referred to as early-onset colorectal cancer (EOCC). [ 178 ] [ 210 ]  Instances of EOCC have increased over the last decade, specifically in patient populations aged 20 to 40 years old throughout North America, Europe, Australia, and China. [ 210 ] [ 211 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8101", "text": "The incidence of colorectal cancer in younger populations has increased over the last decade. [ 178 ] [ 210 ] [ 211 ]   While advancements in diagnostic procedure may have some impact, reduced likelihood of screening among these populations suggests detection bias is not a major contributor to this trend.  It is more likely that cohort effects are contributing. [ 211 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8102", "text": "The population experiencing the greatest rise in EOCC cases are men and women aged 20 to 29 years old, with incidence increasing by 7.9% per year between 2004 and 2016. [ 211 ]  Similarly, though less severe, men and women aged 30 to 39 experienced an increase in cases at a rate of 3.4% per year during that same time period. Despite these increases, the mortality rate for colorectal cancer has remained the same. [ 211 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8103", "text": "Risk factors associated with EOCC are akin to those of all colorectal cancer cases. [ 210 ]  Observed cohort-effects are likely the product of generational shifts in lifestyle and environmental factors. [ 178 ] [ 210 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8104", "text": "In 2018, the American Cancer Society modified their previous screening guideline for colorectal cancer from age 50 down to age 45 following the recognition of increasing cases of EOCC. [ 211 ]  Individuals under the age of 60 have been identified as most susceptible to non-participation in colorectal cancer screening. [ 212 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8105", "text": "Rectal cancer has been diagnosed in an Ancient Egyptian  mummy  who had lived in the  Dakhleh Oasis  during the  Ptolemaic period . [ 213 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8106", "text": "In the United States, March is  colorectal cancer awareness month . [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8107", "text": "Preliminary  in-vitro  evidence suggests  lactic acid bacteria  (e.g.,  lactobacilli ,  streptococci  or  lactococci ) may be protective against the development and progression of colorectal cancer through several mechanisms such as  antioxidant  activity,  immunomodulation , promoting  programmed cell death ,  antiproliferative effects , and  epigenetic  modification of cancer cells. [ 214 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8108", "text": "Constipation  is a  bowel  dysfunction that makes  bowel movements  infrequent or hard to pass. [ 2 ]  The  stool  is often hard and dry. [ 4 ]  Other symptoms may include abdominal pain, bloating, and feeling as if one has not completely passed the bowel movement. [ 3 ]  Complications from constipation may include  hemorrhoids ,  anal fissure  or  fecal impaction . [ 4 ]  The normal frequency of bowel movements in adults is between three per day and three per week. [ 4 ]  Babies often have three to four bowel movements per day while young children typically have two to three per day. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8109", "text": "Constipation has many causes. [ 4 ]  Common causes include slow movement of stool within the colon,  irritable bowel syndrome , and  pelvic floor  disorders. [ 4 ]  Underlying associated diseases include  hypothyroidism ,  diabetes ,  Parkinson's disease ,  celiac disease ,  non-celiac gluten sensitivity ,  vitamin B 12  deficiency ,  colon cancer ,  diverticulitis , and  inflammatory bowel disease . [ 4 ] [ 5 ] [ 6 ] [ 9 ] [ 10 ]  Medications associated with constipation include  opioids , certain  antacids ,  calcium channel blockers , and  anticholinergics . [ 4 ]  Of those taking  opioids  about 90% develop constipation. [ 11 ]  Constipation is more concerning when there is weight loss or  anemia ,  blood is present in the stool , there is a history of inflammatory bowel disease or colon cancer in a person's family, or it is of new onset in someone who is older. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8110", "text": "Treatment of constipation depends on the underlying cause and the duration that it has been present. [ 4 ]  Measures that may help include drinking enough fluids, eating more  fiber , consumption of  honey [ 13 ]  and  exercise . [ 4 ]  If this is not effective,  laxatives  of the  bulk-forming agent ,  osmotic agent ,  stool softener , or  lubricant type  may be recommended. [ 4 ]   Stimulant laxatives  are generally reserved for when other types are not effective. [ 4 ]  Other treatments may include  biofeedback  or in rare cases surgery. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8111", "text": "In the general population rates of constipation are 2\u201330 percent. [ 7 ]  Among elderly people living in a care home the rate of constipation is 50\u201375 percent. [ 11 ]  People in the United States spend more than  US$ 250 \u00a0 million  on medications for constipation a year. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8112", "text": "Constipation is a symptom, not a disease. Most commonly, constipation is thought of as infrequent bowel movements, usually fewer than 3 stools per week. [ 15 ] [ 16 ]  However, people may have other complaints as well including: [ 3 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8113", "text": "The  Rome III Criteria  are a set of symptoms that help standardize the diagnosis of constipation in various age groups. These criteria help physicians to better define constipation in a standardized manner."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8114", "text": "The causes of constipation can be divided into  congenital , primary, and secondary. [ 2 ]  The most common kind is primary and not life-threatening. [ 18 ]  It can also be divided by the age group affected such as children and adults."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8115", "text": "Primary or  functional constipation  is defined by ongoing symptoms for greater than six months not due to an underlying cause such as medication  side effects  or an underlying medical condition. [ 2 ] [ 19 ]  It is not associated with abdominal pain, thus distinguishing it from  irritable bowel syndrome . [ 2 ]  It is the most common kind of constipation, and is often multifactorial. [ 18 ] [ 20 ]  In adults, such primary causes include: dietary choices such as insufficient dietary fiber or fluid intake, or behavioral causes such as decreased  physical activity . In children, causes can include diets low in fiber and fluids, underlying medical conditions, and reluctance to go to the bathroom. [ 21 ]  In the elderly, common causes have been attributed to insufficient dietary fiber intake, inadequate fluid intake, decreased  physical activity , side effects of medications,  hypothyroidism , and obstruction by  colorectal cancer . [ 22 ]  Evidence to support these factors however is poor. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8116", "text": "Secondary causes include side effects of medications such as opiates, endocrine and metabolic disorders such as  hypothyroidism , and obstruction such as from  colorectal cancer [ 20 ]  or  ovarian cancer . [ 23 ]   Celiac disease  and  non-celiac gluten sensitivity  may also present with constipation. [ 5 ] [ 24 ] [ 6 ]  Cystocele can develop as a result of chronic constipation. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8117", "text": "Constipation can be caused or exacerbated by a low-fiber diet, low liquid intake, or dieting. [ 17 ] [ 26 ]  Dietary fiber helps to decrease colonic transport time, increases stool bulk but simultaneously softens stool. Therefore, diets low in fiber can lead to primary constipation. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8118", "text": "Many medications have constipation as a side effect. Some include (but are not limited to)  opioids ,  diuretics ,  antidepressants ,  antihistamines ,  antispasmodics ,  anticonvulsants ,  tricyclic antidepressants ,  antiarrythmics ,  beta-adrenoceptor antagonists ,  anti-diarrheals , 5-HT3 receptor antagonists such as  ondansetron , and aluminum  antacids . [ 17 ] [ 27 ]  Certain  calcium channel blockers  such as  nifedipine  and  verapamil  can cause severe constipation due to dysfunction of motility in the  rectosigmoid colon . [ 28 ]  Supplements such as calcium and iron supplements can also have constipation as a notable side effect. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8119", "text": "Metabolic and endocrine problems which may lead to constipation include:  pheochromocytoma ,  hypercalcemia ,  hypothyroidism ,  hyperparathyroidism ,  porphyria ,  chronic kidney disease ,  pan-hypopituitarism ,  diabetes mellitus , and  cystic fibrosis . [ 17 ] [ 18 ]  Constipation is also common in individuals with muscular and myotonic dystrophy. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8120", "text": "Systemic diseases  that may present with constipation include  celiac disease  and  systemic sclerosis . [ 5 ] [ 24 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8121", "text": "Constipation has a number of structural (mechanical, morphological, anatomical) causes, namely through creating space-occupying lesions within the colon that stop the passage of stool, such as  colorectal cancer ,  strictures ,  rectocoles ,  anal sphincter  damage or malformation and post-surgical changes. Extra-intestinal masses such as other malignancies can also lead to constipation from external compression. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8122", "text": "Constipation also has neurological causes, including  anismus ,  descending perineum syndrome ,  desmosis  and  Hirschsprung's disease . [ 7 ]  In infants, Hirschsprung's disease is the most common medical disorder associated with constipation. Anismus occurs in a small minority of persons with chronic constipation or obstructed defecation. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8123", "text": "Spinal cord lesions and neurological disorders such as  Parkinson's disease  and  pelvic floor dysfunction [ 18 ]  can also lead to constipation."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8124", "text": "Chagas disease  may cause constipation through the destruction of the  myenteric plexus . [ 34 ] [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8125", "text": "Voluntary withholding of the stool is a common cause of constipation. [ 17 ]  The choice to withhold can be due to factors such as fear of pain, fear of public restrooms, or laziness. [ 17 ]  When a child holds in the stool a combination of encouragement,  fluids ,  fiber , and  laxatives  may be useful to overcome the problem. [ 36 ]  Early intervention with withholding is important as this can lead to  anal fissures . [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8126", "text": "A number of diseases present at birth  can result in  constipation in children . They are as a group uncommon with Hirschsprung's disease (HD) being the most common. [ 38 ]  There are also congenital structural anomalies that can lead to constipation, including anterior displacement of the anus,  imperforate anus , strictures, and small left colon syndrome. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8127", "text": "The diagnosis is typically made based on a person's description of the symptoms. Bowel movements that are difficult to pass, very firm, or made up of small hard pellets (like those excreted by rabbits) qualify as constipation, even if they occur every day. Constipation is traditionally defined as three or fewer bowel movements per week. [ 15 ]  Other symptoms related to constipation can include bloating,  distension , abdominal pain, headaches, a feeling of fatigue and nervous exhaustion, or a sense of incomplete emptying. [ 40 ]  Although constipation may be a diagnosis, it is typically viewed as a symptom that requires evaluation to discern a cause."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8128", "text": "Distinguish between acute (days to weeks) or chronic (months to years) onset of constipation because this information changes the  differential diagnosis . This in the context of accompanied symptoms helps physicians discover the cause of constipation. People often describe their constipation as bowel movements that are difficult to pass, firm stool with lumpy or hard consistency, and excessive straining during bowel movements. Bloating, abdominal  distension , and abdominal pain often accompany constipation. [ 41 ]  Chronic constipation (symptoms present at least three days per month for more than three months) associated with abdominal discomfort is often diagnosed as irritable bowel syndrome (IBS) when no obvious cause is found. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8129", "text": "Poor dietary habits, previous abdominal surgeries, and certain medical conditions can contribute to constipation. Diseases associated with constipation include  hypothyroidism , certain types of  cancer , and  irritable bowel syndrome . Low fiber intake, inadequate amounts of fluids, poor ambulation or immobility, or medications can contribute to constipation. [ 17 ] [ 26 ]  Once the presence of constipation is identified based on a culmination of the symptoms described above, then the cause of constipation should be figured out."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8130", "text": "Separating non-life-threatening from serious causes may be partly based on symptoms. For example, colon cancer may be suspected if a person has a family history of colon cancer, fever, weight loss, and rectal bleeding. [ 15 ]  Other alarming signs and symptoms include family or personal history of inflammatory bowel disease, age of onset over 50, change in stool caliber, nausea, vomiting, and neurological symptoms like weakness, numbness and difficulty urinating. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8131", "text": "A physical examination should involve at least an abdominal exam and rectal exam. Abdominal exam may reveal an abdominal mass if there is significant stool burden and may reveal abdominal discomfort.  Rectal examination  gives an impression of the anal sphincter  tone  and whether the lower rectum contains any feces or not. Rectal examination also gives information on the consistency of the stool, the presence of hemorrhoids, blood and whether any  perineal  irregularities are present including skin tags, fissures, anal warts. [ 26 ] [ 17 ] [ 15 ]  Physical examination is done manually by a physician and is used to guide which diagnostic tests to order."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8132", "text": "Functional constipation is common and does not warrant diagnostic testing. Imaging and laboratory tests are typically recommended for those with alarm signs or symptoms. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8133", "text": "The laboratory tests performed depends on the suspected underlying cause of the constipation. Tests may include CBC ( complete blood count ), thyroid function tests, serum calcium, serum potassium, etc. [ 17 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8134", "text": "Abdominal X-rays  are generally only performed if bowel obstruction is suspected, may reveal extensive impacted fecal matter in the colon, and may confirm or rule out other causes of similar symptoms. [ 26 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8135", "text": "Colonoscopy may be performed if an abnormality in the colon like a tumor is suspected. [ 15 ]  Other tests rarely ordered include  anorectal manometry , anal sphincter electromyography, and  defecography . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8136", "text": "Colonic propagating pressure wave sequences (PSs) are responsible for discrete movements of the bowel contents and are vital for normal defecation. Deficiencies in PS frequency, amplitude, and extent of propagation are all implicated in severe defecatory dysfunction (SDD). Mechanisms that can normalize these aberrant motor patterns may help rectify the problem. Recently the novel therapy of  sacral nerve stimulation  (SNS) has been utilized for the treatment of severe constipation. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8137", "text": "The Rome III Criteria for functional constipation must include two or more of the following and present for the past three months, with symptoms starting for at least 6 months prior to diagnosis. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8138", "text": "Constipation is usually easier to prevent than to treat. Following the relief of constipation, maintenance with adequate exercise, fluid intake, and high-fiber diet is recommended. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8139", "text": "A limited number of cases require urgent medical intervention or will result in severe consequences. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8140", "text": "The treatment of constipation should focus on the underlying cause if known. The National Institute of Health and Care Excellence (NICE) break constipation in adults into two categories: chronic constipation of unknown cause, and constipation due to opiates. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8141", "text": "In chronic constipation of unknown cause, the main treatment involves the increased intake of water and fiber (either dietary or as supplements). [ 18 ]  The routine use of laxatives or enemas is discouraged, as having bowel movements may come to be dependent upon their use. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8142", "text": "Soluble fiber supplements such as  psyllium  are generally considered first-line treatment for chronic constipation, compared to insoluble fibers such as wheat bran. Side effects of fiber supplements include bloating, flatulence, diarrhea, and possible  malabsorption  of iron, calcium, and some medications. However, patients with opiate-induced constipation will likely not benefit from fiber supplements. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8143", "text": "If  laxatives  are used,  milk of magnesia  or  polyethylene glycol  are recommended as first-line agents due to their low cost and safety. [ 3 ]  Stimulants should only be used if this is not effective. [ 18 ]  In cases of chronic constipation, polyethylene glycol appears superior to  lactulose . [ 46 ]   Prokinetics  may be used to improve gastrointestinal motility. A number of new agents have shown positive outcomes in chronic constipation; these include  prucalopride [ 47 ]  and  lubiprostone . [ 48 ]   Cisapride  is widely available in third world countries, but has been withdrawn in most of the west. It has not been shown to have a benefit on constipation, while potentially causing cardiac arrhythmias and deaths. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8144", "text": "Enemas  can be used to provide a form of mechanical stimulation. A large volume or high enema [ 50 ]  can be given to cleanse as much of the colon as possible of feces, [ 51 ] [ 52 ]  and the solution administered commonly contains  castile soap  which irritates the colon's lining resulting in increased urgency to defecate. [ 53 ]  However, a low enema is generally useful only for stool in the rectum, not in the intestinal tract. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8145", "text": "Constipation that resists the above measures may require physical intervention such as manual disimpaction (the physical removal of impacted stool using the hands; see  fecal impaction )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8146", "text": "Regular  exercise  can help improve chronic constipation. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8147", "text": "In refractory cases, procedures can be performed to help relieve constipation.  Sacral nerve stimulation  has been demonstrated to be effective in a minority of cases.  Colectomy  with ileorectal  anastomosis  is another intervention performed only in patients known to have a slow colonic transit time and in whom a defecation disorder has either been treated or is not present. [ 3 ]  Because this is a major operation, side effects can include considerable abdominal pain, small bowel obstruction, and post-surgical infections. Furthermore, it has a very variable rate of success and is very case dependent. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8148", "text": "Complications that can arise from constipation include  hemorrhoids ,  anal fissures ,  rectal prolapse , and fecal impaction. [ 17 ] [ 26 ] [ 56 ] [ 57 ]  Straining to pass stool may lead to hemorrhoids. In later stages of constipation, the abdomen may become distended, hard and diffusely tender. Severe cases (\"fecal impaction\" or  malignant constipation ) may exhibit symptoms of bowel obstruction (nausea,  vomiting , tender abdomen) and  encopresis , where soft stool from the small intestine bypasses the mass of impacted fecal matter in the  colon ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8149", "text": "Constipation is the most common chronic gastrointestinal disorder in adults. Depending on the definition employed, it occurs in 2% to 20% of the population. [ 18 ] [ 58 ]  It is more common in women, the elderly and children. [ 58 ]  Specifically constipation with no known cause affects females more often affected than males. [ 59 ]  The reasons it occurs more frequently in the elderly is felt to be due to an increasing number of health problems as humans age and decreased physical activity. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8150", "text": "Since ancient times different societies have published medical opinions about how health care providers should respond to constipation in patients. [ 61 ]  In various times and places, doctors have made claims that constipation has all sorts of medical or social causes. [ 61 ]  Doctors in history have treated constipation in reasonable and unreasonable ways, including use of a  spatula mundani . [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8151", "text": "After the advent of the  germ theory of disease  then the idea of \"auto-intoxication\" entered popular Western thought in a fresh way. [ 61 ]   Enema  as a scientific medical treatment and  colon cleansing  as alternative medical treatment became more common in medical practice. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8152", "text": "Since the 1700s in the West there has been some popular thought that people with constipation have some moral failing with  gluttony  or  laziness . [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8153", "text": "Approximately 3% of children have constipation, with girls and boys being equally affected. [ 39 ]  With constipation accounting for approximately 5% of general pediatrician visits and 25% of pediatric gastroenterologist visits, the symptom carries a significant financial impact upon the healthcare system. [ 8 ]  While it is difficult to assess an exact age at which constipation most commonly arises, children frequently experience constipation in conjunction with life-changes. Examples include: toilet training, starting or transferring to a new school, and changes in diet. [ 8 ]  Especially in infants, changes in formula or transitioning from breast milk to formula can cause constipation. The majority of constipation cases are not tied to a medical disease, and treatment can be focused on simply relieving the symptoms. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8154", "text": "The six-week period after pregnancy is called the  postpartum  stage. [ 63 ]  During this time, women are at increased risk of being constipated. Multiple studies estimate the prevalence of constipation to be around 25% during the first 3 months. [ 64 ]  Constipation can cause discomfort for women, as they are still recovering from the delivery process especially if they have had a  perineal tear  or underwent an  episiotomy . [ 65 ]  Risk factors that increase the risk of constipation in this population include: [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8155", "text": "Hemorrhoids  are common in pregnancy and also may get exacerbated when constipated. Anything that can cause pain with stooling (hemorrhoids, perineal tear, episiotomy) can lead to constipation because patients may withhold from having a bowel movement so as to avoid pain. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8156", "text": "The pelvic floor muscles play an important role in helping pass a bowel movement. Injury to those muscles by some of the above risk factors (examples- delivering a large child, lengthy second stage of labor, forceps delivery) can result in constipation. [ 65 ]  Enemas may be administered during labor and these can also alter bowel movements in the days after giving birth. [ 63 ]  However, there is insufficient evidence to make conclusions about the effectiveness and safety of laxatives in this group of people. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8157", "text": "Diarrhea  ( American English ), also spelled  diarrhoea  or  diarrh\u0153a  ( British English ), is the condition of having at least three loose, liquid, or watery  bowel movements  in a day. [ 2 ]  It often lasts for a few days and can result in  dehydration  due to fluid loss. [ 2 ]  Signs of dehydration often begin with loss of the normal stretchiness of the skin and irritable behaviour. [ 2 ]  This can progress to decreased  urination ,  loss of skin color , a  fast heart rate , and a  decrease in responsiveness  as it becomes more severe. [ 2 ]  Loose but non-watery  stools  in babies who are exclusively  breastfed , however, are normal. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8158", "text": "The most common cause is an infection of the  intestines  due to a  virus ,  bacterium , or  parasite \u2014a condition also known as  gastroenteritis . [ 2 ]  These infections are often acquired from food or water that has been contaminated by  feces , or directly from another person who is infected. [ 2 ]  The three types of diarrhea are: short duration watery diarrhea, short duration bloody diarrhea, and persistent diarrhea (lasting more than two weeks, which can be either watery or bloody). [ 2 ]  The short duration watery diarrhea may be due to  cholera , although this is rare in the developed world. [ 2 ]  If blood is present, it is also known as  dysentery . [ 2 ]  A number of non-infectious causes can result in diarrhea. [ 5 ]  These include  lactose intolerance ,  irritable bowel syndrome ,  non-celiac gluten sensitivity ,  celiac disease ,  inflammatory bowel disease  such as  ulcerative colitis ,  hyperthyroidism ,  bile acid diarrhea , and a number of medications. [ 5 ] [ 6 ] [ 7 ]  In most cases,  stool cultures  to confirm the exact cause are not required. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8159", "text": "Diarrhea can be prevented by improved  sanitation , clean  drinking water , and  hand washing  with soap. [ 2 ]   Breastfeeding  for at least six months and  vaccination against rotavirus  is also recommended. [ 2 ]   Oral rehydration solution  (ORS)\u2014clean water with modest amounts of salts and  sugar \u2014is the treatment of choice. [ 2 ]   Zinc tablets  are also recommended. [ 2 ]  These treatments have been estimated to have saved 50 million children in the past 25 years. [ 1 ]  When people have diarrhea it is recommended that they continue to eat healthy food, and babies continue to be breastfed. [ 2 ]  If commercial ORS is not available, homemade solutions may be used. [ 9 ]  In those with severe dehydration,  intravenous fluids  may be required. [ 2 ]  Most cases, however, can be managed well with fluids by mouth. [ 10 ]   Antibiotics , while rarely used, may be recommended in a few cases such as those who have bloody diarrhea and a high fever, those with severe  diarrhea following travelling , and those who grow specific bacteria or parasites in their stool. [ 8 ]   Loperamide  may help decrease the number of bowel movements but is not recommended in those with severe disease. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8160", "text": "About 1.7 to 5\u00a0billion cases of diarrhea occur per year. [ 2 ] [ 5 ] [ 11 ]  It is most common in  developing countries , where young children get diarrhea on average three times a year. [ 2 ]  Total deaths from diarrhea are estimated at 1.53\u00a0million in 2019\u2014down from 2.9 million in 1990. [ 4 ]  In 2012, it was the second most common cause of  deaths in children  younger than five (0.76 million or 11%). [ 2 ] [ 12 ]  Frequent episodes of diarrhea are also a common cause of  malnutrition  and the most common cause in those younger than five years of age. [ 2 ]  Other long term problems that can result include  stunted growth  and poor intellectual development. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8161", "text": "The word diarrhea is from the  Ancient Greek   \u03b4\u03b9\u03ac\u03c1\u03c1\u03bf\u03b9\u03b1  from  \u03b4\u03b9\u03ac   dia  \"through\" and  \u1fe5\u03ad\u03c9   rheo  \"flow\"."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8162", "text": "Diarrhea  is the spelling in  American English , whereas  diarrhoea  is the spelling in  British English ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8163", "text": "Slang terms for the condition include \"the runs\", \"the squirts\" (or \"squits\" in Britain [ 13 ] ) and \"the trots\". [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8164", "text": "The word is often pronounced as  / \u02cc d a\u026a \u0259 \u02c8 r i\u02d0 \u0259 /   DY -\u0259- REE -\u0259 ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8165", "text": "Diarrhea is defined by the  World Health Organization  as having three or more loose or liquid  stools  per day, or as having more stools than is normal for that person. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8166", "text": "Acute diarrhea is defined as an abnormally frequent discharge of semisolid or fluid fecal matter from the bowel, lasting less than 14 days, by  World Gastroenterology Organization . [ 16 ]  Acute diarrhea that is watery may be known as AWD (Acute Watery Diarrhoea.) [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8167", "text": "Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage. The most common cause of this type of diarrhea is a  cholera toxin  that stimulates the secretion of  anions , especially  chloride  ions (Cl \u2013 ). Therefore, to maintain a charge balance in the  gastrointestinal tract , sodium (Na + ) is carried with it, along with water. In this type of diarrhea intestinal fluid secretion is  isotonic  with plasma even during fasting. [ 18 ] [ 19 ]  It continues even when there is no oral food intake."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8168", "text": "Osmotic diarrhea occurs when too much water is drawn into the bowels. If a person drinks solutions with excessive sugar or excessive salt, these can draw water from the body into the bowel and cause osmotic diarrhea. [ 20 ] [ 19 ]  Osmotic diarrhea can also result from maldigestion (e.g., pancreatic disease or  coeliac disease ) in which the nutrients are left in the  lumen  to pull in water. Or it can be caused by osmotic  laxatives  (which work to alleviate  constipation  by drawing water into the bowels). In healthy individuals, too much  magnesium ,  vitamin C  or undigested  lactose  can produce osmotic diarrhea and distention of the bowel. A person who has  lactose intolerance  can have difficulty absorbing lactose after an extraordinarily high intake of dairy products. In persons who have  fructose malabsorption , excess fructose intake can also cause diarrhea. High-fructose foods that also have a high glucose content are more absorbable and less likely to cause diarrhea.  Sugar alcohols  such as  sorbitol  (often found in sugar-free foods) are difficult for the body to absorb and, in large amounts, may lead to osmotic diarrhea. [ 18 ]  In most of these cases, osmotic diarrhea stops when the offending agent (e.g., milk or sorbitol) is stopped."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8169", "text": "Exudative diarrhea occurs with the presence of blood and pus in the stool. This occurs with  inflammatory bowel diseases , such as  Crohn's disease  or  ulcerative colitis , and other severe infections such as  E. coli  or other forms of food poisoning. [ 19 ] [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8170", "text": "Inflammatory diarrhea occurs when there is damage to the mucosal lining or brush border, which leads to a passive loss of protein-rich fluids and a decreased ability to absorb these lost fluids. Features of all three of the other types of diarrhea can be found in this type of diarrhea. [ 21 ]  It can be caused by bacterial infections, viral infections, parasitic infections, or autoimmune problems such as inflammatory bowel diseases. It can also be caused by tuberculosis, colon cancer, and enteritis. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8171", "text": "If there is blood visible in the stools, it is also known as  dysentery . The blood is a trace of an invasion of bowel tissue. Dysentery is a symptom of, among others,  Shigella ,  Entamoeba histolytica , and  Salmonella . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8172", "text": "Diarrheal disease may have a negative impact on both physical fitness and mental development. \"Early childhood malnutrition resulting from any cause reduces physical fitness and work productivity in adults\", [ 22 ]  and diarrhea is a primary cause of childhood malnutrition. [ 23 ]  Further, evidence suggests that diarrheal disease has significant impacts on mental development and health; it has been shown that, even when controlling for  helminth  infection and early breastfeeding, children who had experienced severe diarrhea had significantly lower scores on a series of tests of intelligence. [ 22 ] [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8173", "text": "Diarrhea can cause  electrolyte imbalances ,  kidney impairment ,  dehydration , and defective  immune system  responses. When oral drugs are administered, the efficiency of the drug is to produce a  therapeutic effect  and the lack of this effect may be due to the medication travelling too quickly through the digestive system, limiting the time that it can be absorbed. Clinicians try to treat the diarrheas by reducing the dosage of medication, changing the dosing schedule, discontinuation of the drug, and rehydration. The interventions to control the diarrhea are not often effective. Diarrhea can have a profound effect on the quality of life because fecal incontinence is one of the leading factors for placing older adults in  long term care facilities  (nursing homes). [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8174", "text": "In the latter stages of human digestion, ingested materials are inundated with water and digestive fluids such as  gastric acid ,  bile , and  digestive enzymes  in order to break them down into their nutrient components, which are then absorbed into the bloodstream via the  intestinal tract  in the small intestine. Prior to defecation, the large intestine reabsorbs the water and other digestive solvents in the waste product in order to maintain proper hydration and overall equilibrium. [ 25 ]  Diarrhea occurs when the large intestine is prevented, for any number of reasons, from sufficiently absorbing the water or other digestive fluids from fecal matter, resulting in a liquid, or \"loose\", bowel movement. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8175", "text": "Acute  diarrhea is most commonly due to viral  gastroenteritis  with  rotavirus , which accounts for 40% of cases in children under five. [ 1 ]  In  travelers , however,  bacterial infections  predominate. [ 27 ]  Various toxins such as  mushroom poisoning  and drugs can also cause acute diarrhea."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8176", "text": "Chronic diarrhea can be the part of the presentations of a number of chronic medical conditions affecting the intestine. Common causes include  ulcerative colitis ,  Crohn's disease ,  microscopic colitis ,  celiac disease ,  irritable bowel syndrome , and  bile acid malabsorption . [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8177", "text": "There are many causes of infectious diarrhea, which include  viruses ,  bacteria  and parasites. [ 29 ]  Infectious diarrhea is frequently referred to as  gastroenteritis . [ 30 ]   Norovirus  is the most common cause of viral diarrhea in adults, [ 31 ]  but  rotavirus  is the most common cause in children under five years old. [ 32 ]   Adenovirus  types 40 and 41, [ 33 ]  and  astroviruses  cause a significant number of infections. [ 34 ]   Shiga-toxin producing Escherichia coli , such as  E coli o157:h7 , are the most common cause of infectious bloody diarrhea in the United States. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8178", "text": "Campylobacter   spp.  are a common cause of bacterial diarrhea, but infections by  Salmonella  spp.,  Shigella  spp. and some strains of  Escherichia coli  are also a frequent cause. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8179", "text": "In the elderly, particularly those who have been treated with antibiotics for unrelated infections, a toxin produced by  Clostridioides difficile  often causes severe diarrhea. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8180", "text": "Parasites, particularly  protozoa  e.g.,  Cryptosporidium  spp.,  Giardia  spp.,  Entamoeba histolytica ,  Blastocystis  spp.,  Cyclospora cayetanensis , are frequently the cause of diarrhea that involves chronic infection. The broad-spectrum antiparasitic agent  nitazoxanide  has shown efficacy against many diarrhea-causing parasites. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8181", "text": "Other infectious agents, such as  parasites  or  bacterial  toxins, may exacerbate symptoms. [ 27 ]  In sanitary living conditions where there is ample food and a supply of clean water, an otherwise healthy person usually recovers from viral infections in a few days. However, for ill or  malnourished  individuals, diarrhea can lead to severe  dehydration  and can become life-threatening. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8182", "text": "Open defecation  is a leading cause of infectious diarrhea leading to death. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8183", "text": "Poverty is a good indicator of the rate of infectious diarrhea in a population. This association does not stem from poverty itself, but rather from the conditions under which impoverished people live. The absence of certain resources compromises the ability of the poor to defend themselves against infectious diarrhea. \"Poverty is associated with poor housing, crowding, dirt floors, lack of access to clean water or to sanitary disposal of fecal waste ( sanitation ), cohabitation with domestic animals that may carry human pathogens, and a lack of refrigerated storage for food, all of which increase the frequency of diarrhea \u00a0 ... Poverty also restricts the ability to provide age-appropriate, nutritionally balanced diets or to modify diets when diarrhea develops so as to mitigate and repair nutrient losses. The impact is exacerbated by the lack of adequate, available, and affordable medical care.\" [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8184", "text": "One of the most common causes of infectious diarrhea is a lack of clean water. Often, improper fecal disposal leads to contamination of groundwater. This can lead to widespread infection among a population, especially in the absence of water filtration or purification. Human feces contains a variety of potentially harmful human  pathogens . [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8185", "text": "Proper nutrition is important for health and functioning, including the prevention of infectious diarrhea. It is especially important to young children who do not have a fully developed immune system.  Zinc deficiency , a condition often found in children in  developing countries  can, even in mild cases, have a significant impact on the development and proper functioning of the human immune system. [ 43 ] [ 44 ]  Indeed, this relationship between zinc deficiency and reduced immune functioning corresponds with an increased severity of infectious diarrhea. Children who have lowered levels of zinc have a greater number of instances of diarrhea, severe diarrhea, and diarrhea associated with fever. [ 45 ]  Similarly,  vitamin A deficiency  can cause an increase in the severity of diarrheal episodes. However, there is some discrepancy when it comes to the impact of vitamin A deficiency on the rate of disease. While some argue that a relationship does not exist between the rate of disease and vitamin A status, [ 46 ]  others suggest an increase in the rate associated with deficiency. [ 47 ]  Given that estimates suggest 127 million preschool children worldwide are vitamin A deficient, this population has the potential for increased risk of disease contraction. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8186", "text": "Malabsorption  is the inability to absorb food fully, mostly from disorders in the small bowel, but also due to maldigestion from diseases of the  pancreas ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8187", "text": "Causes include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8188", "text": "The two overlapping types here are of unknown origin:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8189", "text": "Another possible cause of diarrhea is irritable bowel syndrome (IBS), which usually presents with abdominal discomfort relieved by  defecation  and unusual  stool  (diarrhea or  constipation ) for at least three days a week over the previous three months. [ 49 ]  Symptoms of diarrhea-predominant IBS can be managed through a combination of dietary changes, soluble fiber supplements and medications such as  loperamide  or  codeine . About 30% of patients with diarrhea-predominant IBS have  bile acid malabsorption  diagnosed with an abnormal  SeHCAT  test. [ 50 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8190", "text": "Diarrhea can be caused by other diseases and conditions, namely:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8191", "text": "Over 700 medications, such as  penicillin , are known to cause diarrhea. [ 53 ] [ 54 ]  The classes of medications that are known to cause diarrhea are laxatives, antacids, heartburn medications, antibiotics, anti-neoplastic drugs, anti-inflammatories as well as many dietary supplements. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8192", "text": "According to two researchers,  Nesse  and  Williams , diarrhea may function as an evolved expulsion defense mechanism. As a result, if it is stopped, there might be a delay in recovery. [ 56 ]  They cite in support of this argument research published in 1973 that found that treating  Shigella  with the anti-diarrhea drug (Co-phenotrope,  Lomotil ) caused people to stay  feverish  twice as long as those not so treated. The researchers indeed themselves observed that: \"Lomotil may be contraindicated in shigellosis. Diarrhea may represent a defense mechanism\". [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8193", "text": "The following types of diarrhea may indicate further investigation is needed:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8194", "text": "A severity score is used to aid diagnosis in children. [ 58 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8195", "text": "When diarrhea lasts for more than four weeks a number of further tests may be recommended including: [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8196", "text": "A 2019 guideline recommended that testing for ova and parasites was only needed in people who are at high risk though they recommend routine testing for  giardia . [ 60 ]   Erythrocyte sedimentation rate  (ESR) and  C-reactive protein  (CRP) were not recommended. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8197", "text": "Worldwide in 2004, approximately 2.5 billion cases of diarrhea occurred, which resulted in 1.5 million deaths among children under the age of five. [ 1 ]  Greater than half of these were in Africa and South Asia. [ 1 ]  This is down from a death rate of 4.5 million in 1980 for gastroenteritis. [ 62 ]  Diarrhea remains the second leading cause of  infant mortality  (16%) after  pneumonia  (17%) in this age group. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8198", "text": "The majority of such cases occur in the developing world, with over half of the recorded cases of childhood diarrhea occurring in  Africa  and  Asia , with 696 million and 1.2 billion cases, respectively, compared to only 480 million in the rest of the world. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8199", "text": "Infectious diarrhea resulted in about 0.7 million deaths in children under five years old in 2011 and 250 million lost school days. [ 64 ] [ 65 ]  In the Americas, diarrheal disease accounts for a total of 10% of deaths among children aged 1\u201359 months while in South East Asia, it accounts for 31.3% of deaths. [ 66 ]  It is estimated that around 21% of child mortalities in developing countries are due to diarrheal disease. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8200", "text": "The  World Health Organization  has reported that \"deaths due to diarrhoeal diseases have dropped by 45%, from sixth leading cause of death in 2000 to thirteenth in 2021.\" [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8201", "text": "Even though diarrhea is best known in humans, it affects many other species, notably among  primates . [ 69 ]  The  cecal appendix , when present, appears to afford some protection against diarrhea to young primates. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8202", "text": "Numerous studies have shown that improvements in drinking water and sanitation ( WASH ) lead to decreased risks of diarrhoea. [ 71 ]  Such improvements might include for example use of water filters, provision of high-quality  piped water  and  sewer  connections. [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8203", "text": "In institutions, communities, and households, interventions that promote  hand washing  with soap lead to significant reductions in the incidence of diarrhea. [ 72 ]  The same applies to preventing  open defecation  at a community-wide level and providing access to  improved sanitation . [ 64 ] [ 73 ]  This includes use of  toilets  and implementation of the entire  sanitation  chain connected to the toilets (collection, transport, disposal or reuse of  human excreta )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8204", "text": "There is limited evidence that safe disposal of child or adult feces can prevent diarrheal disease. [ 74 ] [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8205", "text": "Basic sanitation techniques can have a profound effect on the transmission of diarrheal disease. The implementation of hand washing using soap and water, for example, has been experimentally shown to reduce the incidence of disease by approximately 30\u201348%. [ 76 ] [ 77 ] [ 72 ]  Hand washing in developing countries, however, is compromised by poverty as acknowledged by the  CDC : \"Handwashing is integral to disease prevention in all parts of the world; however, access to soap and water is limited in a number of less developed countries. This lack of access is one of many challenges to proper hygiene in less developed countries.\" Solutions to this barrier require the implementation of educational programs that encourage sanitary behaviours. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8206", "text": "Given that water contamination is a major means of transmitting diarrheal disease, efforts to provide clean  water supply  and  improved sanitation  have the potential to dramatically cut the rate of disease incidence. In fact, it has been proposed that we might expect an 88% reduction in child mortality resulting from diarrheal disease as a result of improved water sanitation and hygiene. [ 42 ] [ 79 ]  Similarly, a meta-analysis of numerous studies on improving water supply and sanitation shows a 22\u201327% reduction in disease incidence, and a 21\u201330% reduction in mortality rate associated with diarrheal disease. [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8207", "text": "Chlorine treatment of water, for example, has been shown to reduce both the risk of diarrheal disease, and of contamination of stored water with diarrheal pathogens. [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8208", "text": "Immunization against the pathogens that cause diarrheal disease is a viable prevention strategy, however it does require targeting certain pathogens for vaccination. In the case of Rotavirus, which was responsible for around 6% of diarrheal episodes and 20% of diarrheal disease deaths in the children of developing countries, use of a Rotavirus vaccine in trials in 1985 yielded a slight (2\u20133%) decrease in total diarrheal disease incidence, while reducing overall mortality by 6\u201310%. Similarly, a Cholera vaccine showed a strong reduction in morbidity and mortality, though the overall impact of vaccination was minimal as Cholera is not one of the major causative pathogens of diarrheal disease. [ 82 ]  Since this time, more effective vaccines have been developed that have the potential to save many thousands of lives in developing nations, while reducing the overall cost of treatment, and the costs to society. [ 83 ] [ 84 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8209", "text": "Rotavirus vaccine  decreases the rates of diarrhea in a population. [ 1 ] [ 85 ]  New vaccines against rotavirus,  Shigella ,  Enterotoxigenic Escherichia coli (ETEC) , and cholera are under development, as well as other causes of infectious diarrhea. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8210", "text": "Dietary deficiencies in developing countries can be combated by promoting better eating practices. Zinc supplementation proved successful showing a significant decrease in the incidence of diarrheal disease compared to a control group. [ 86 ] [ 87 ]  The majority of the literature suggests that vitamin A supplementation is advantageous in reducing disease incidence. [ 88 ]  Development of a supplementation strategy should take into consideration the fact that vitamin A supplementation was less effective in reducing diarrhea incidence when compared to vitamin A and zinc supplementation, and that the latter strategy was estimated to be significantly more cost effective. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8211", "text": "Breastfeeding practices have been shown to have a dramatic effect on the incidence of diarrheal disease in poor populations. Studies across a number of developing nations have shown that those who receive  exclusive breastfeeding  during their first 6 months of life are better protected against infection with diarrheal diseases. [ 90 ]  One study in Brazil found that non-breastfed infants were 14 times more likely to die from diarrhea than exclusively breastfed infants. [ 91 ]  Exclusive breastfeeding is currently recommended for the first six months of an infant's life by the  WHO , [ 92 ] [ 93 ]  with continued breastfeeding until at least two years of age. [ 93 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8212", "text": "Probiotics  decrease the risk of diarrhea in those taking  antibiotics . [ 94 ]  Insecticide spraying may reduce fly numbers and the risk of diarrhea in children in a setting where there is seasonal variations in fly numbers throughout the year. [ 95 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8213", "text": "In many cases of diarrhea, replacing lost fluid and salts is the only treatment needed. This is usually by mouth \u2013  oral rehydration therapy  \u2013 or, in severe cases,  intravenously . [ 1 ]  Diet restrictions such as the  BRAT diet  are no longer recommended. [ 96 ]  Research does not support the limiting of milk to children as doing so has no effect on duration of diarrhea. [ 97 ]  To the contrary, WHO recommends that children with diarrhea continue to eat as sufficient nutrients are usually still absorbed to support continued growth and weight gain, and that continuing to eat also speeds up recovery of normal intestinal functioning. [ 20 ]  CDC recommends that children and adults with cholera also continue to eat. [ 98 ]  There is no evidence that early refeeding in children can cause an increase in inappropriate use of intravenous fluid, episodes of vomiting, and risk of having persistent diarrhea. [ 99 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8214", "text": "Medications such as  loperamide  (Imodium) and  bismuth subsalicylate  may be beneficial; however they may be  contraindicated  in certain situations. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8215", "text": "Oral rehydration solution (ORS)  (a slightly sweetened and salty water) can be used to prevent dehydration. Standard home solutions such as salted rice water, salted yogurt drinks, vegetable and chicken soups with salt can be given. Home solutions such as water in which cereal has been cooked, unsalted soup, green coconut water, weak tea (unsweetened), and unsweetened fresh fruit juices can have from half a teaspoon to full teaspoon of salt (from one-and-a-half to three grams) added per liter. Clean plain water can also be one of several fluids given. [ 20 ]  There are commercial solutions such as  Pedialyte , and relief agencies such as  UNICEF  widely distribute packets of salts and sugar. A WHO publication for physicians recommends a homemade ORS consisting of one liter water with one teaspoon salt (3 grams) and two tablespoons sugar (18 grams) added [ 20 ]  (approximately the \"taste of tears\" [ 101 ] ). Rehydration Project recommends adding the same amount of sugar but only one-half a teaspoon of salt, stating that this more dilute approach is less risky with very little loss of effectiveness. [ 102 ]  Both agree that drinks with too much sugar or salt can make dehydration worse. [ 20 ] [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8216", "text": "Appropriate amounts of supplemental zinc and potassium should be added if available. But the availability of these should not delay rehydration. As WHO points out, the most important thing is to begin preventing dehydration as early as possible. [ 20 ]  In another example of prompt ORS hopefully preventing dehydration, CDC recommends for the treatment of cholera continuing to give Oral Rehydration Solution during travel to medical treatment. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8217", "text": "Vomiting often occurs during the first hour or two of treatment with ORS, especially if a child drinks the solution too quickly, but this seldom prevents successful rehydration since most of the fluid is still absorbed. WHO recommends that if a child vomits, to wait five or ten minutes and then start to give the solution again more slowly. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8218", "text": "Drinks especially high in simple sugars, such as  soft drinks  and fruit juices, are not recommended in children under five as they may  increase  dehydration. A too rich solution in the gut draws water from the rest of the body, just as if the person were to drink sea water. [ 20 ] [ 103 ]  Plain water may be used if more specific and effective ORT preparations are unavailable or are not palatable. [ 103 ]  Additionally, a mix of both plain water and drinks perhaps too rich in sugar and salt can alternatively be given to the same person, with the goal of providing a medium amount of sodium overall. [ 20 ]  A  nasogastric tube  can be used in young children to administer fluids if warranted. [ 104 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8219", "text": "The WHO recommends a child with diarrhea continue to be fed. Continued feeding speeds the recovery of normal intestinal function. In contrast, children whose food is restricted have diarrhea of longer duration and recover intestinal function more slowly. The WHO states \"Food should  never  be withheld and the child's usual foods should  not  be diluted. Breastfeeding should  always  be continued.\" [ 20 ]  In the specific example of cholera, the CDC makes the same recommendation. [ 98 ]  Breast-fed infants with diarrhea often choose to breastfeed more, and should be encouraged to do so. [ 20 ]  In young children who are not breast-fed and live in the developed world, a lactose-free diet may be useful to speed recovery. [ 105 ] \nEating food containing  soluble fibre  may help, but insoluble fibre might make it worse. [ 106 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8220", "text": "Antidiarrheal  agents  can  be  classified  into  four  different groups: antimotility, antisecretory, adsorbent, and anti-infectious. [ 107 ]  While  antibiotics  are beneficial in certain types of acute diarrhea, they are usually not used except in specific situations. [ 108 ] [ 109 ]  There are concerns that antibiotics may increase the risk of  hemolytic uremic syndrome  in people infected with  Escherichia coli O157:H7 . [ 110 ]  In resource-poor countries, treatment with antibiotics may be beneficial. [ 109 ]  However, some bacteria are developing  antibiotic resistance , particularly  Shigella . [ 111 ]  Antibiotics can also cause diarrhea, and  antibiotic-associated diarrhea  is the most common adverse effect of treatment with general antibiotics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8221", "text": "While bismuth compounds ( Pepto-Bismol ) decreased the number of bowel movements in those with travelers' diarrhea, they do not decrease the length of illness. [ 112 ]  Anti-motility agents like  loperamide  are also effective at reducing the number of stools but not the duration of disease. [ 8 ]  These agents should be used only if bloody diarrhea is not present. [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8222", "text": "Diosmectite , a natural aluminomagnesium silicate clay, is effective in alleviating symptoms of acute diarrhea in children, [ 114 ]  and also has some effects in chronic functional diarrhea, radiation-induced diarrhea, and chemotherapy-induced diarrhea. [ 52 ]  Another absorbent agent used for the treatment of mild diarrhea is  kaopectate ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8223", "text": "Racecadotril  an antisecretory medication may be used to treat diarrhea in children and  adults. [ 107 ]  It has better tolerability than  loperamide , as it causes less  constipation  and  flatulence . [ 115 ]  However, it has little benefit in improving acute diarrhea in children. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8224", "text": "Bile acid sequestrants  such as  cholestyramine  can be effective in chronic diarrhea due to  bile acid malabsorption . Therapeutic trials of these drugs are indicated in chronic diarrhea if bile acid malabsorption cannot be diagnosed with a specific test, such as  SeHCAT  retention. [ 117 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8225", "text": "Zinc supplementation may benefit children over six months old with diarrhea in areas with high rates of malnourishment or zinc deficiency. [ 118 ]  This supports the World Health Organization guidelines for zinc, but not in the very young."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8226", "text": "A Cochrane Review from 2020 concludes that  probiotics  make little or no difference to people who have diarrhea lasting 2 days or longer and that there is no proof that they reduce its duration. [ 119 ]  The  probiotic   lactobacillus  can help prevent  antibiotic-associated diarrhea  in adults but possibly not children. [ 120 ]  For those with  lactose intolerance , taking digestive  enzymes  containing  lactase  when consuming dairy products often improves symptoms."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8227", "text": "Diverticulosis  is the condition of having multiple pouches ( diverticula ) in the  colon  that are not inflamed. These are outpockets of the colonic  mucosa  and submucosa through weaknesses of  muscle  layers in the colon wall. [ 1 ]  Diverticula do not cause symptoms in most people. [ 2 ]   Diverticular disease  occurs when diverticula become clinically inflamed, a condition known as  diverticulitis . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8228", "text": "Diverticula typically occur in the  sigmoid colon , which is commonplace for increased pressure. The left side of the colon is more commonly affected in the United States while the right side is more commonly affected in Asia. [ 4 ]  Diagnosis is often during routine  colonoscopy  or as an incidental finding during  CT scan . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8229", "text": "It is common in Western countries with about half of those over the age of 60 affected in Canada and the United States. [ 4 ]  Diverticula are uncommon before the age of 40, and increase in incidence beyond that age. [ 5 ]  Rates are lower in Africa; [ 4 ]  the reasons for this remain unclear but may involve the greater prevalence of a high  fiber  diet in contrast with the lower-fiber diet characteristic of many Western populations. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8230", "text": "Some people with diverticulosis complain of symptoms such as cramping, bloating, flatulence, and irregular defecation. However, it is unclear if these symptoms are attributable to the underlying diverticulosis or to coexistent  irritable bowel syndrome . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8231", "text": "Diverticular disease was found associated with a higher risk of left sided colon cancer. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8232", "text": "Diverticular disease can present with painless rectal bleeding as bright red blood per rectum. Diverticular bleeding is the most common cause of acute lower gastrointestinal bleeding. [ 9 ]  However, it is estimated that 80% of these cases are self-limiting and require no specific therapy. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8233", "text": "Infection of a diverticulum can result in  diverticulitis . A 2013 study [ 11 ]  found that it happens only about 4% of the time. That contradicts the prevailing thinking that 10% to 25% of people with diverticulosis go on to develop diverticulitis. Tears in the colon leading to bleeding or perforations may occur; intestinal obstruction may occur (constipation or diarrhea does not rule this possibility out); and  peritonitis ,  abscess  formation,  retroperitoneal   fibrosis ,  sepsis , and  fistula  formation are also possible occurrences.  Rarely, an  enterolith  may form. Infection of a diverticulum often occurs as a result of stool collecting in a diverticulum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8234", "text": "Diverticulitis is defined as diverticular disease with signs and symptoms of diverticular inflammation. Clinical features of acute diverticulitis include constant abdominal pain, localized abdominal tenderness in the left lower quadrant of the abdomen, nausea, vomiting, constipation or diarrhea, fever and  leukocytosis . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8235", "text": "Most people with colonic diverticulosis are unaware of this structural change. When symptoms do appear in a person over 40 years of age it is important to obtain medical advice and exclude more dangerous conditions such as cancer of the colon or rectum. [ 13 ] [ 14 ] [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8236", "text": "Segmental colitis associated with diverticulosis (SCAD) is a condition characterized by localized  inflammation  of the colon between diverticula (interdiverticular mucosa) while sparing the diverticular orifices. SCAD may lead to abdominal pain, especially in the left lower quadrant, intermittent rectal bleeding, and chronic diarrhea."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8237", "text": "The U.S.  National Institutes of Health  notes that, although the low-fiber theory of the cause of diverticulosis is the leading theory, it has not yet been proven. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8238", "text": "The predisposition to diverticulosis for specific individuals is likely explained by a genetic component, a theory that is supported by studies examining the rates of diverticulosis among twins. [ 1 ]   The  heritability  of diverticulosis is estimated to be approximately 40%. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8239", "text": "Another theory suggests the degeneration of  glial   neurons  in the  myenteric plexus  and the  interstitial cells of Cajal  lead to slowed intestinal movement and consequently fecal content exerts increased pressure on the colon wall resulting in the formation of diverticula. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8240", "text": "The precise mechanisms by which diverticula are formed are unknown. [ 1 ]  Multiple theories have been proposed including genetic susceptibility, diet, intestinal motility, changes in the  microbiome , and  inflammation . One leading theory suggests that diverticula form in weakened areas of the colon wall that are subjected to increased pressure. [ 1 ]  The strength of the colon wall is known to decrease with age. [ 1 ]  Previous theories proposed that impacted fecal matter and certain foods would get stuck in diverticula (thereby causing trauma), which caused  poor blood flow ,  death of the affected intestinal wall cells , and  intestinal perforation . [ 1 ]  Newer theories have called this paradigm into question. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8241", "text": "Diverticulosis is defined by the presence of multiple pouches (diverticula) in the colon. [ 22 ]  In people without symptoms, these are usually found incidentally during other investigations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8242", "text": "While a good history is often sufficient to form a diagnosis of diverticulosis or diverticulitis, it is important to confirm the diagnosis and rule out other pathology (notably  colorectal cancer ) and complications."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8243", "text": "It is important to note that both barium enema and colonoscopy are contraindicated during acute episodes of diverticulitis, as the barium may leak out into the abdominal cavity, and colonoscopy can cause perforations of the bowel wall."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8244", "text": "Many people with diverticulosis have minimal to no symptoms and do not require any specific treatment. Colonic stimulants should be avoided. Treatments, like some colon cleansers, that cause hard stools, constipation, and straining, are not recommended. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8245", "text": "A high-fiber diet and fiber supplements are advisable to prevent constipation. [ 23 ] [ 24 ]  The American Dietetic Association recommends 20\u201335\u00a0grams each day. Wheat bran has been shown to reduce intra colonic pressure. [ 25 ] [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8246", "text": "The US  National Institute of Diabetes and Digestive and Kidney Diseases  (NIDDK) says foods such as nuts, popcorn hulls, sunflower seeds, pumpkin seeds, caraway seeds, and sesame seeds have traditionally been labeled as problem foods for people with this condition; however, no scientific data exists to prove this hypothesis. The seeds in tomatoes, zucchini, cucumbers, strawberries, raspberries, and poppy seeds, are not considered harmful by the NIDDK. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8247", "text": "One study found that nuts and popcorn do not contribute positively or negatively to patients with diverticulosis or diverticular complications. [ 27 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8248", "text": "Complicated diverticulosis requires treatment of the complication. These complications are often grouped under a single diagnosis of  diverticulitis  and require skilled medical care of the infection, bleeding and perforation which may include intensive antibiotic treatment, intravenous fluids, and surgery. Complications are more common in patients who are taking  NSAIDs  or aspirin. As diverticulosis occurs in an older population such complications are serious events. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8249", "text": "The prevalence of diverticulosis progressively increases with age. Approximately 50% of people over the age of 60 and 70% of people over the age of 80 have diverticulosis. [ 1 ]  This disease is common in the U.S., Britain, Australia, Canada, and is uncommon in Asia and Africa. [ 5 ]  Large-mouth diverticula are associated with  scleroderma . Diverticular disease is more common in collagen disorders such as Ehlers\u2013Danlos syndrome. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8250", "text": "The modern emphasis on the value of fiber in the diet began with  Thomas L. Cleave . [ 30 ]  A strong case was made by Neil Painter [ 31 ]  and Adam Smith [ 32 ]  that a deficiency of dietary fiber is the cause of diverticular disease. They argued that the colonic muscles needed to contract strongly in order to transmit and expel the small stool associated with a fiber deficient diet.  The increased pressure within the segmented section of the bowel over years gave rise to herniation at the vulnerable point where blood vessels enter the colonic wall."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8251", "text": "\"The complications of diverticulosis cause considerable morbidity in the United States; health care expenditures for this disorder are estimated to be $2.5\u00a0billion per year.\" [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8252", "text": "Dysentery  ( UK :  / \u02c8 d \u026a s \u0259n t \u0259r i /   DISS -\u0259n-t\u0259r-ee , [ 7 ]   US :  / \u02c8 d \u026a s \u0259n t \u025br i /   DISS -\u0259n-terr-ee ), [ 8 ]  historically known as the  bloody flux , [ 9 ]  is a type of  gastroenteritis  that results in  bloody   diarrhea . [ 1 ] [ 10 ]  Other symptoms may include  fever , abdominal pain, and a  feeling of incomplete defecation . [ 2 ] [ 6 ] [ 11 ]  Complications may include  dehydration . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8253", "text": "The cause of dysentery is usually the bacteria from genus  Shigella , in which case it is known as  shigellosis , or the amoeba  Entamoeba histolytica ; then it is called  amoebiasis . [ 1 ]  Other causes may include certain chemicals, other bacteria, other protozoa, or  parasitic worms . [ 2 ]  It may spread between people. [ 4 ]  Risk factors include contamination of food and water with  feces  due to poor  sanitation . [ 6 ]  The underlying mechanism involves  inflammation  of the  intestine , especially of the  colon . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8254", "text": "Efforts to prevent dysentery include  hand washing  and  food safety  measures while traveling in countries of high risk. [ 4 ]  While the condition generally resolves on its own within a week, drinking sufficient fluids such as  oral rehydration solution  is important. [ 4 ]  Antibiotics such as  azithromycin  may be used to treat cases associated with travelling in the  developing world . [ 11 ]  While medications used to decrease diarrhea such as  loperamide  are not recommended on their own, they may be used together with antibiotics. [ 11 ] [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8255", "text": "Shigella  results in about 165 million cases of diarrhea and 1.1 million deaths a year with nearly all cases in the developing world. [ 5 ]  In areas with poor sanitation nearly half of cases of diarrhea are due to  Entamoeba histolytica . [ 6 ]   Entamoeba histolytica  affects millions of people and results in more than 55,000 deaths a year. [ 12 ]  It commonly occurs in less developed areas of Central and South America, Africa, and Asia. [ 12 ]  Dysentery has been described at least since the time of  Hippocrates . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8256", "text": "The most common form of dysentery is bacillary dysentery, which is typically a mild sickness, causing symptoms normally consisting of mild abdominal pains and frequent passage of loose stools or diarrhea. Symptoms normally present themselves after 1\u20133 days, and are usually no longer present after a week. The frequency of urges to defecate, the large volume of liquid feces ejected, and the presence of blood, mucus, or pus depends on the  pathogen  causing the disease. Temporary  lactose intolerance  can occur, as well. In some occasions, severe abdominal cramps,  fever ,  shock , and  delirium  can all be symptoms. [ 2 ] [ 14 ] [ 15 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8257", "text": "In extreme cases, people may pass more than one liter of fluid per hour. More often, individuals will complain of  diarrhea  with  blood , accompanied by extreme abdominal pain,  rectal pain  and a low-grade  fever . Rapid weight loss and  muscle aches  sometimes also accompany dysentery, while  nausea  and  vomiting  are rare."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8258", "text": "On rare occasions, the  amoebic parasite  will invade the body through the bloodstream and  spread beyond the intestines . In such cases, it may more seriously infect other organs such as the  brain ,  lungs , and most commonly the  liver . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8259", "text": "Dysentery results from  bacterial  or  parasitic  infections. Viruses do not generally cause the disease. [ 10 ]  These pathogens typically reach the  large intestine  after entering orally, through ingestion of contaminated food or water, oral contact with contaminated objects or hands, and so on. Each specific pathogen has its own mechanism or pathogenesis, but in general, the result is damage to the intestinal linings, leading to the  inflammatory immune responses . This can cause  elevated physical temperature , painful spasms of the intestinal muscles ( cramping ), swelling due to fluid leaking from capillaries of the intestine ( edema ) and further tissue damage by the body's immune cells and the chemicals, called  cytokines , which are released to fight the infection. The result can be impaired nutrient absorption, excessive water and mineral loss through the stools due to breakdown of the control mechanisms in the intestinal tissue that normally remove water from the stools, and in severe cases, the entry of pathogenic organisms into the bloodstream.  Anemia  may also arise due to the blood loss through diarrhea. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8260", "text": "Bacterial infections that cause bloody diarrhea are typically classified as being either invasive or toxogenic. Invasive species cause damage directly by invading into the mucosa. The toxogenic species do not invade, but cause cellular damage by secreting toxins, resulting in bloody diarrhea. This is also in contrast to toxins that cause watery diarrhea, which usually do not cause cellular damage, but rather they take over cellular machinery for a portion of life of the cell. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8261", "text": "Definitions of dysentery can vary by region and by medical specialty. The U. S. Centers for Disease Control and Prevention (CDC) limits its definition to \"diarrhea with visible blood\". [ 19 ]  Others define the term more broadly. [ 20 ]  These differences in definition must be taken into account when defining mechanisms. For example, using the CDC definition requires that intestinal tissue be so severely damaged that blood vessels have ruptured, allowing visible quantities of blood to be lost with defecation. Other definitions require less specific damage. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8262", "text": "Amoebiasis , also known as amoebic dysentery, is caused by an infection from the  amoeba   Entamoeba histolytica , [ 21 ]  which is found mainly in tropical areas. [ 22 ]  Proper treatment of the underlying infection of amoebic dysentery is important; insufficiently treated amoebiasis can lie dormant for years and subsequently lead to  severe, potentially fatal, complications . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8263", "text": "When amoebae inside the bowel of an infected person are ready to leave the body, they group together and form a shell that surrounds and protects them. This group of amoebae is known as a cyst, which is then passed out of the person's body in the feces and can survive outside the body. If hygiene standards are poor \u2013 for example, if the person does not dispose of the feces hygienically \u2013 then it can contaminate the surroundings, such as nearby food and water.\nIf another person then eats or drinks food or water that has been contaminated with feces containing the cyst, that person will also become infected with the amoebae. Amoebic dysentery is particularly common in parts of the world where human feces are used as fertilizer.\nAfter entering the person's body through the mouth, the cyst travels down into the stomach. The amoebae inside the cyst are protected from the stomach's digestive acid. From the stomach, the cyst travels to the intestines, where it breaks open and releases the amoebae, causing the infection. The amoebae can burrow into the walls of the intestines and cause small abscesses and ulcers to form. The cycle then begins again. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8264", "text": "Dysentery may also be caused by  shigellosis , an infection by  bacteria  of the genus  Shigella , and is then known as bacillary dysentery (or Marlow syndrome). The term  bacillary dysentery  etymologically might seem to refer to any dysentery caused by any  bacilliform  bacteria, but its meaning is restricted by convention to  Shigella  dysentery. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8265", "text": "Some strains of  Escherichia coli  cause bloody diarrhea. The typical culprits are  enterohemorrhagic  Escherichia coli , of which  O157:H7  is the best known. These types of  E. coli  also make Shiga toxin. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8266", "text": "A diagnosis may be made by taking a history and doing a brief examination. Dysentery should not be confused with  hematochezia , which is the passage of fresh blood through the anus, usually in or with stools. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8267", "text": "The mouth, skin, and lips may appear dry due to dehydration. Lower abdominal tenderness may also be present. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8268", "text": "Cultures  of  stool samples  are examined to identify the organism causing dysentery. Usually, several samples must be obtained due to the number of amoebae, which changes daily. [ 17 ]   Blood tests  can be used to measure abnormalities in the levels of essential  minerals and salts . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8269", "text": "Efforts to prevent dysentery include  hand washing  and  food safety  measures while traveling in areas of high risk. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8270", "text": "Although there is currently no vaccine that protects against  Shigella  infection, several are in development. [ 25 ] [ 26 ]  Vaccination may eventually become a part of the strategy to reduce the incidence and severity of diarrhea, particularly among children in low-resource settings. For example,  Shigella  is a longstanding World Health Organization (WHO) target for vaccine development, and sharp declines in age-specific diarrhea/dysentery attack rates for this pathogen indicate that natural immunity does develop following exposure; thus, vaccination to prevent this disease should be feasible. The development of vaccines against these types of infection has been hampered by technical constraints, insufficient support for coordination, and a lack of market forces for research and development. Most vaccine development efforts are taking place in the public sector or as research programs within biotechnology companies. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8271", "text": "Dysentery is managed by maintaining fluids using  oral rehydration therapy . [ 4 ]  If this treatment cannot be adequately maintained due to vomiting or the profuseness of diarrhea, hospital admission may be required for  intravenous  fluid replacement. In ideal situations, no antimicrobial therapy should be administered until microbiological microscopy and culture studies have established the specific infection involved. When laboratory services are not available, it may be necessary to administer a combination of drugs, including an  amoebicidal  drug to kill the  parasite , and an  antibiotic  to treat any associated bacterial infection. [ citation needed ]   Laudanum  (Deodorized Tincture of Opium)] may be used for severe pain and to combat severe diarrhea."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8272", "text": "If shigellosis is suspected and it is not too severe, letting it run its course may be reasonable \u2013 usually less than a week. If the case is severe, antibiotics such as  ciprofloxacin  or  TMP-SMX  may be useful. However, many strains of  Shigella  are becoming resistant to common antibiotics, and effective medications are often in short supply in developing countries. If necessary, a doctor may have to reserve antibiotics for those at highest risk for death, including young children, people over 50, and anyone suffering from dehydration or malnutrition. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8273", "text": "Amoebic dysentery is often treated with two antimicrobial drugs such as  metronidazole  and  paromomycin  or  iodoquinol . [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8274", "text": "With correct treatment, most cases of amoebic and bacterial dysentery subside within 10 days, and most individuals achieve a full recovery within two to four weeks after beginning proper treatment. If the disease is left untreated, the prognosis varies with the immune status of the individual patient and the severity of disease. Extreme dehydration can delay recovery and significantly raises the risk for serious complications including death. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8275", "text": "Insufficient data exists, but  Shigella  is estimated to have caused the death of 34,000 children under the age of five in 2013, and 40,000 deaths in people over five years of age. [ 25 ]  Amoebiasis infects over 50 million people each year, of whom 50,000 die (one per thousand). [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8276", "text": "Shigella evolved with the human expansion out of Africa 50,000 to 200,000 years ago. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8277", "text": "The seed, leaves, and bark of the  kapok  tree have been used in traditional medicines by indigenous peoples of the rainforest regions in the Americas, west-central Africa, and Southeast Asia in the treatment of this disease. [ 31 ] [ 32 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8278", "text": "In 1915, Australian  bacteriologist   Fannie Eleanor Williams  was serving as a medic in Greece with the  Australian Imperial Force , receiving casualties directly from  Gallipoli . In Gallipoli, dysentery was severely affecting soldiers and causing significant loss of manpower. Williams carried out  serological  investigations into dysentery, co-authoring several groundbreaking papers with Sir  Charles Martin , director of the  Lister Institute . [ 34 ]  The result of their work into dysentery was increased demand for specific  diagnostics  and curative sera. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8279", "text": "Bacillus subtilis  was marketed throughout America and Europe from 1946 as an immunostimulatory aid in the treatment of gut and urinary tract diseases such as rotavirus and  Shigella , [ 36 ]  but declined in popularity after the introduction of consumer antibiotics."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8280", "text": "Gastritis  is the  inflammation  of the  lining of the stomach . [ 1 ]  It may occur as a  short episode  or may be of a  long duration . [ 1 ]  There may be no symptoms but, when symptoms are present, the most common is upper  abdominal pain  (see  dyspepsia ). [ 1 ]  Other possible symptoms include  nausea  and  vomiting , bloating, loss of appetite and  heartburn . [ 1 ] [ 2 ]  Complications may include  stomach bleeding ,  stomach ulcers , and  stomach tumors . [ 1 ]  When due to  autoimmune problems ,  low red blood cells  due to not enough  vitamin B12  may occur, a condition known as  pernicious anemia . [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8281", "text": "Common causes include infection with  Helicobacter pylori  and use of nonsteroidal anti-inflammatory drugs ( NSAIDs ). [ 1 ]  When caused by  H. pylori  this is now termed  Helicobacter pylori  induced gastritis, and included as a listed disease in  ICD11 . [ 6 ] [ 7 ]  Less common causes include  alcohol ,  smoking ,  cocaine , severe illness,  autoimmune  problems,  radiation therapy  and  Crohn's disease . [ 1 ] [ 8 ]   Endoscopy , a type of  X-ray  known as an  upper gastrointestinal series , blood tests, and stool tests may help with diagnosis. [ 1 ]  Other conditions with similar symptoms include  inflammation of the pancreas ,  gallbladder problems , and  peptic ulcer disease . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8282", "text": "Prevention is by avoiding things that cause the disease. [ 4 ] [ examples needed ]  Treatment includes medications such as  antacids ,  H2 blockers , or  proton pump inhibitors . [ 1 ]  During an acute attack drinking  viscous lidocaine  may help. [ 9 ]  If gastritis is due to NSAIDs these may be stopped. [ 1 ]  If  H. pylori  is present it may be treated with a combination of  antibiotics  such as  amoxicillin  and  clarithromycin . [ 1 ]  For those with pernicious anemia, vitamin B12 supplements are recommended either by mouth or by injection. [ 3 ]  People are usually advised to avoid foods that bother them. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8283", "text": "Gastritis is believed to affect about half of people worldwide. [ 4 ]  In 2013 there were approximately 90 million new cases of the condition. [ 11 ]  As people get older the disease becomes more common. [ 4 ]  It, along with a similar condition in the first part of the  intestines  known as  duodenitis , resulted in 50,000 deaths in 2015. [ 5 ]   H. pylori  was first discovered in 1981 by  Barry Marshall  and  Robin Warren . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8284", "text": "Many people with gastritis experience no symptoms at all. However,  upper central   abdominal pain  is the most common symptom; the pain may be dull, vague, burning, aching, gnawing, sore, or sharp. [ 13 ]  Pain is usually located in the upper central portion of the  abdomen , [ 14 ]  but it may occur anywhere from the upper left portion of the abdomen around to the back."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8285", "text": "Other signs and symptoms may include the following: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8286", "text": "There are two categories of gastritis depending on the cause of the disease. There is erosive gastritis, for which the common causes are  stress ,  alcohol , some  drugs , such as  aspirin  and other nonsteroidal anti-inflammatory drugs  (NSAIDs) , and Crohn's disease.  And, there is non-erosive gastritis, for which the most common cause is a  Helicobacter pylori  infection.  [ 15 ] [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8287", "text": "Helicobacter pylori  colonizes the stomachs of more than half of the world's population, and the infection continues to play a key role in the pathogenesis of a number of gastroduodenal diseases. Colonization of the gastric mucosa with  Helicobacter pylori  results in the development of chronic gastritis in infected individuals and, in a subset of patients, chronic gastritis progresses to complications (e.g., ulcer disease,  stomach cancers , and some distinct extragastric disorders). [ 16 ]  Gastritis caused by  H. pylori  infection is termed  Helicobacter pylori  induced gastritis, and listed as a disease in  ICD11 . [ 6 ] [ 7 ]  More than 80% of individuals infected with the bacterium are  asymptomatic  and it has been postulated that it may play an important role in the natural stomach ecology. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8288", "text": "Gastritis may also develop after major surgery or traumatic injury (\" Cushing ulcer \"), burns (\" Curling ulcer \"), or severe infections. Gastritis may also occur in those who have had weight loss surgery resulting in the  banding  or reconstruction of the digestive tract. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8289", "text": "Evidence does not support a role for specific foods, including spicy foods and coffee, in the development of  peptic ulcers . [ 18 ]  People are usually advised to avoid foods that bother them. [ 10 ]  There is little specific advice on diet published by authoritative sources. The  National Health Service  of the  United Kingdom  advises avoiding spicy, acidic or fried foods which may irritate the stomach. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8290", "text": "Acute erosive gastritis typically involves discrete foci of surface necrosis due to damage to mucosal defenses. [ 20 ]  NSAIDs inhibit  cyclooxygenase-1 , or COX-1, an enzyme responsible for the biosynthesis of  eicosanoids  in the stomach, which increases the possibility of  peptic ulcers  forming. [ 21 ] [ 22 ] [ 23 ]   Also, NSAIDs, such as aspirin, reduce a substance that protects the stomach called  prostaglandin . These drugs used in a short period are not typically dangerous. However, regular use can lead to gastritis. [ 24 ]  Additionally, severe physiologic stress from sepsis, hypoxia, trauma, or surgery is also a common etiology for acute erosive gastritis, resulting in \" stress ulcers \". This form of gastritis can occur in more than 5% of hospitalized patients. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8291", "text": "Also, alcohol consumption does not cause chronic gastritis.  It does, however, erode the mucosal lining of the stomach; low doses of alcohol stimulate  hydrochloric acid  secretion. High doses of alcohol do not stimulate secretion of acid. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8292", "text": "Chronic gastritis refers to a wide range of problems of the gastric issues. [ 20 ]   The immune system makes proteins and antibodies that fight infections in the body to maintain a  homeostatic  condition.  In some disorders the body targets the stomach as if it were a foreign protein or pathogen; it makes antibodies against, severely damages, and may even destroy the stomach or its lining. [ 24 ]   In some cases bile, normally used to aid digestion in the small intestine, will enter through the  pyloric valve  of the stomach if it has been removed during surgery or does not work properly, also leading to gastritis.  Gastritis may also be caused by other medical conditions, including  HIV/AIDS ,  Crohn's disease , certain  connective tissue disorders , and  liver  or  kidney failure . Since 1992, chronic gastritis lesions are classified according to the Sydney system. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8293", "text": "Mucous gland  metaplasia , the reversible replacement of differentiated cells, occurs in the setting of severe damage of the gastric glands, which then waste away ( atrophic gastritis ) and are progressively replaced by mucous glands. Gastric ulcers may develop; it is unclear if they are the causes or the consequences.  Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics.  Intestinal metaplasia  is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits  dysplasia . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8294", "text": "Often, a diagnosis can be made based on  patients' description of their symptoms. Other methods which may be used to verify gastritis include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8295", "text": "The OLGA staging frame of chronic gastritis on histopathology. Atrophy is scored as the percentage of atrophic glands and scored on a four-tiered scale. No atrophy (0%) = score 0; mild atrophy (1\u201330%) = score 1; moderate atrophy (31\u201360%) = score 2; severe atrophy (>60%) = score 3. These scores (0\u20133) are used in the OLGA staging assessment in each 10 compartment: [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8296", "text": "Antacids  are a common treatment for mild to medium gastritis. [ 29 ]  When antacids do not provide enough relief, medications such as  H 2  blockers  and  proton-pump inhibitors  that help reduce the amount of acid are often prescribed. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8297", "text": "Cytoprotective agents are designed to help protect the tissues that line the stomach and small intestine. [ 31 ]  They include the medications  sucralfate  and  misoprostol . If  NSAIDs  are being taken regularly, one of these medications to protect the stomach may also be taken. Another cytoprotective agent is  bismuth subsalicylate . [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8298", "text": "Several regimens are used to treat  H. pylori  infection. Most use a combination of two  antibiotics  and a proton pump inhibitor. Sometimes bismuth is added to the regimen."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8299", "text": "In 1,000 A.D,  Avicenna  first gave the description of stomach cancer. In 1728, German physician  Georg Ernst Stahl  first coined the term \"gastritis\". Italian anatomical pathologist  Giovanni Battista Morgagni  further described the characteristics of gastric inflammation. He described the characteristics of erosive or ulcerative gastritis and erosive gastritis. Between 1808 and 1831, French physician  Fran\u00e7ois-Joseph-Victor Broussais  gathered information from the autopsies of dead French soldiers. He described chronic gastritis as \"Gastritide\" and erroneously believed that gastritis was the cause of  ascites ,  typhoid fever , and  meningitis . In 1854,  Charles Handfield Jones  and  Wilson Fox  described the microscopic changes of stomach inner lining in gastritis which existed in diffuse and segmental forms. In 1855,  Baron Carl von Rokitansky  first described  hypertrophic  gastritis. In 1859, British physician,  William Brinton  first described about  acute ,  subacute , and  chronic  gastritis. In 1870, Samuel Fenwick noted that  pernicious anemia  causes glandular  atrophy  in gastritis. German surgeon Georg Ernst Konjetzny noticed that both gastric ulcer and gastric cancer are the results of gastric inflammation.  Shields Warren  and Willam A. Meissner described the  intestinal metaplasia  of the stomach as a feature of chronic gastritis. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8300", "text": "Gastroenteritis , also known as  infectious diarrhea , is an  inflammation  of the  gastrointestinal tract  including the  stomach  and  intestine . [ 8 ]  Symptoms may include  diarrhea ,  vomiting , and  abdominal pain . [ 1 ]   Fever , lack of energy, and  dehydration  may also occur. [ 2 ] [ 3 ]  This typically lasts less than two weeks. [ 8 ]  Although it is not related to  influenza , in the U.S. and U.K., it is sometimes called the \" stomach flu \". [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8301", "text": "Gastroenteritis is usually caused by  viruses ; [ 4 ]  however, gut  bacteria ,  parasites , and  fungi  can also cause gastroenteritis. [ 2 ] [ 4 ]  In children,  rotavirus  is the most common cause of severe disease. [ 10 ]  In adults,  norovirus  and  Campylobacter  are common causes. [ 11 ] [ 12 ]  Eating improperly prepared food, drinking contaminated water or close contact with a person who is infected can  spread the disease . [ 2 ]  Treatment is generally the same with or without a definitive diagnosis, so testing to confirm is usually not needed. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8302", "text": "For young children in impoverished countries, prevention includes  hand washing  with soap, drinking  clean water ,  breastfeeding  babies instead of using  formula , [ 2 ]  and proper disposal of  human waste . The  rotavirus vaccine  is recommended as a prevention for children. [ 2 ] [ 10 ]  Treatment involves getting enough fluids. [ 2 ]  For mild or moderate cases, this can typically be achieved by drinking  oral rehydration solution  (a combination of water, salts and sugar). [ 2 ]  In those who are breastfed, continued breastfeeding is recommended. [ 2 ]  For more severe cases,  intravenous fluids  may be needed. [ 2 ]  Fluids may also be given by a  nasogastric tube . [ 13 ]   Zinc  supplementation is recommended in children. [ 2 ]   Antibiotics  are generally not needed. [ 14 ]  However, antibiotics are recommended for young children with a fever and bloody diarrhea. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8303", "text": "In 2015, there were two billion cases of gastroenteritis, resulting in 1.3\u00a0million deaths globally. [ 6 ] [ 7 ]  Children and those in the  developing world  are affected the most. [ 15 ]  In 2011, there were about 1.7\u00a0billion cases, resulting in about 700,000 deaths of children under the age of five. [ 16 ]  In the developing world, children less than two years of age frequently get six or more infections a year. [ 17 ]  It is less common in adults, partly due to the development of  immunity . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8304", "text": "Gastroenteritis usually involves both  diarrhea  and  vomiting . [ 18 ]  Sometimes, only one or the other is present. [ 1 ]  This may be accompanied by abdominal cramps. [ 1 ]  Signs and symptoms usually begin 12\u201372\u00a0hours after contracting the infectious agent. [ 15 ]  If due to a virus, the condition usually resolves within one week. [ 18 ]  Some viral infections also involve  fever , fatigue,  headache  and  muscle pain . [ 18 ]  If the  stool is bloody , the cause is less likely to be viral [ 18 ]  and more likely to be bacterial. [ 19 ]  Some bacterial infections cause severe abdominal pain and may persist for several weeks. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8305", "text": "Children infected with rotavirus usually make a full recovery within three to eight days. [ 20 ]  However, in poor countries treatment for severe infections is often out of reach and persistent diarrhea is common. [ 21 ]   Dehydration  is a common complication of  diarrhea . [ 22 ]  Severe dehydration in children may be recognized if the skin color and position returns slowly when pressed. [ 23 ]  This is called \"prolonged  capillary refill \" and \"poor  skin turgor \". [ 23 ]  Abnormal breathing is another sign of severe dehydration. [ 23 ]  Repeat infections are typically seen in areas with poor sanitation, and  malnutrition . [ 15 ]   Stunted growth  and long-term cognitive delays can result. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8306", "text": "Reactive arthritis  occurs in 1% of people following infections with  Campylobacter  species. [ 19 ]   Guillain\u2013Barr\u00e9 syndrome  occurs in 0.1%. [ 19 ]   Hemolytic uremic syndrome  (HUS) may occur due to infection with  Shiga toxin -producing  Escherichia coli  or  Shigella  species. [ 24 ]  HUS causes  low platelet counts ,  poor kidney function , and  low red blood cell count (due to their breakdown) . [ 24 ]  Children are more predisposed to getting HUS than adults. [ 17 ]  Some viral infections may produce  benign infantile seizures . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8307", "text": "Viruses  (particularly  rotavirus  (in children) and  norovirus  (in adults)) and the bacteria  Escherichia coli  and  Campylobacter  species are the primary causes of gastroenteritis. [ 15 ] [ 25 ]  There are, however, many other infectious agents that can cause this syndrome including  parasites  and  fungi . [ 17 ] [ 4 ]  Non-infectious causes are seen on occasion, but they are less likely than a viral or bacterial cause. [ 1 ]  Risk of infection is higher in children due to their lack of  immunity . [ 1 ]  Children are also at higher risk because they are less likely to practice good  hygiene  habits. [ 1 ]  Children living in areas without easy  access to water and soap  are especially vulnerable. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8308", "text": "Rotaviruses ,  noroviruses ,  adenoviruses , and  astroviruses  are known to cause viral gastroenteritis. [ 26 ]  Rotavirus is the most common cause of gastroenteritis in children, [ 25 ]  and produces similar rates in both the  developed  and  developing world . [ 20 ]  Viruses cause about 70% of episodes of infectious diarrhea in the pediatric age group. [ 13 ]  Rotavirus is a less common cause in adults due to acquired immunity. [ 27 ]  Norovirus is the cause in about 18% of all cases. [ 28 ]  Generally speaking, viral gastroenteritis accounts for 21\u201340% of the cases of infectious diarrhea in developed countries. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8309", "text": "Norovirus is the leading cause of gastroenteritis among adults in America accounting for about 90% of viral gastroenteritis outbreaks. [ 18 ]  These localized  epidemics  typically occur when groups of people spend time proximate to each other, such as on  cruise ships , [ 18 ]  in hospitals, or in restaurants. [ 1 ]  People may remain infectious even after their diarrhea has ended. [ 18 ]  Norovirus is the cause of about 10% of cases in children. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8310", "text": "In some countries,  Campylobacter jejuni  is the primary cause of bacterial gastroenteritis, with half of these cases associated with exposure to  poultry . [ 19 ]  In children, bacteria are the cause in about 15% of cases, with the most common types being  Escherichia coli ,  Salmonella ,  Shigella , and  Campylobacter  species. [ 13 ]  If food becomes contaminated with bacteria and remains at room temperature for several hours, the bacteria multiply and increase the risk of infection in those who consume the food. [ 17 ]  Some foods commonly associated with illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. [ 30 ]  In the developing world, especially sub-Saharan Africa and Asia,  cholera  is a common cause of gastroenteritis. This infection is usually transmitted by contaminated water or food. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8311", "text": "Toxigenic  Clostridioides difficile  is an important cause of diarrhea that occurs more often in the elderly. [ 17 ]  Infants can carry these bacteria without developing symptoms. [ 17 ]  It is a common cause of diarrhea in those who are hospitalized and is frequently associated with antibiotic use. [ 32 ]   Staphylococcus aureus  infectious diarrhea may also occur in those who have used antibiotics. [ 33 ]  Acute \" traveler's diarrhea \" is usually a type of bacterial gastroenteritis, while the persistent form is usually parasitic. [ 34 ]  Acid-suppressing medication appears to increase the risk of significant infection after exposure to several organisms, including  Clostridioides difficile ,  Salmonella , and  Campylobacter  species. [ 35 ]  The risk is greater in those taking  proton pump inhibitors  than with  H 2  antagonists . [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8312", "text": "A number of  parasites  can cause gastroenteritis. [ 13 ]   Giardia lamblia  is most common, but  Entamoeba histolytica ,  Cryptosporidium  spp., and other species have also been implicated. [ 13 ] [ 34 ]  As a group, these agents comprise about 10% of cases in children. [ 24 ] [ 34 ]   Giardia  occurs more commonly in the developing world, but this type of illness can occur nearly everywhere. [ 36 ]  It occurs more commonly in persons who have traveled to areas with high prevalence, children who attend  day care ,  men who have sex with men , and following  disasters . [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8313", "text": "Transmission may occur from drinking contaminated water or when people share personal objects. [ 15 ]  Water quality typically worsens during the rainy season and outbreaks are more common at this time. [ 15 ]  In  areas with four seasons , infections are more common in the winter. [ 17 ]  Worldwide,  bottle-feeding  of babies with improperly sanitized bottles is a significant cause. [ 15 ]  Transmission rates are also related to poor hygiene, (especially among children), [ 18 ]  in crowded households, [ 37 ]  and in those with poor nutritional status. [ 17 ]  Adults who have developed immunities might still carry certain organisms without exhibiting symptoms. [ 17 ]  Thus, adults can become  natural reservoirs  of certain diseases. [ 17 ]  While some agents (such as  Shigella ) only occur in  primates , others (such as  Giardia ) may occur in a wide variety of animals. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8314", "text": "There are a number of non-infectious causes of inflammation of the gastrointestinal tract. [ 1 ]  Some of the more common include medications (like  NSAIDs ), certain foods such as  lactose  (in those who are intolerant), and  gluten  (in those with  celiac disease ).  Crohn's disease  is also a non-infectious cause of (often severe) gastroenteritis. [ 1 ]  Disease secondary to  toxins  may also occur. Some food-related conditions associated with nausea, vomiting, and diarrhea include:  ciguatera poisoning  due to consumption of contaminated predatory fish,  scombroid  associated with the consumption of certain types of spoiled fish,  tetrodotoxin poisoning  from the consumption of  puffer fish  among others, and  botulism  typically due to improperly preserved food. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8315", "text": "In the United States, rates of emergency department use for noninfectious gastroenteritis dropped 30% from 2006 until 2011. Of the twenty most common conditions seen in the emergency department, rates of noninfectious gastroenteritis had the largest decrease in visits in that time period. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8316", "text": "Gastroenteritis is defined as  vomiting  or  diarrhea  due to inflammation of the  small  or  large bowel , often due to infection. [ 17 ]  The changes in the small bowel are typically noninflammatory, while the ones in the large bowel are inflammatory. [ 17 ]  The number of pathogens required to cause an infection varies from as few as one (for  Cryptosporidium ) to as many as 10 8  (for  Vibrio cholerae ). [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8317", "text": "Gastroenteritis is typically diagnosed clinically, based on a person's signs and symptoms. [ 18 ]  Determining the exact cause is usually not needed as it does not alter the management of the condition. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8318", "text": "However,  stool cultures  should be performed in those with blood in the stool, those who might have been exposed to  food poisoning , and those who have recently traveled to the developing world. [ 13 ]  It may also be appropriate in children younger than 5, old people, and those with poor immune function. [ 40 ]  Diagnostic testing may also be done for surveillance. [ 18 ]  As  hypoglycemia  occurs in approximately 10% of infants and young children, measuring serum  glucose  in this population is recommended. [ 23 ]   Electrolytes  and  kidney function  should also be checked when there is a concern about severe dehydration. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8319", "text": "A determination of whether or not the person has  dehydration  is an important part of the assessment, with dehydration typically divided into mild (3\u20135%), moderate (6\u20139%), and severe (\u226510%) cases. [ 1 ]  In children, the most accurate signs of moderate or severe dehydration are a prolonged  capillary refill , poor  skin turgor , and abnormal breathing. [ 23 ] [ 41 ]  Other useful findings (when used in combination) include sunken eyes, decreased activity, a lack of tears, and a dry mouth. [ 1 ]  A normal urinary output and oral fluid intake is reassuring. [ 23 ]  Laboratory testing is of little clinical benefit in determining the degree of dehydration. [ 1 ]  Thus the use of urine testing or ultrasounds is generally not needed. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8320", "text": "Other potential causes of signs and symptoms that mimic those seen in gastroenteritis that need to be ruled out include  appendicitis ,  volvulus ,  inflammatory bowel disease ,  urinary tract infections , and  diabetes mellitus . [ 13 ]   Pancreatic insufficiency ,  short bowel syndrome ,  Whipple's disease ,  coeliac disease , and  laxative  abuse should also be considered. [ 43 ]  The differential diagnosis can be complicated somewhat if the person exhibits  only  vomiting or diarrhea (rather than both). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8321", "text": "Appendicitis may present with vomiting, abdominal pain, and a small amount of diarrhea in up to 33% of cases. [ 1 ]  This is in contrast to the large amount of diarrhea that is typical of gastroenteritis. [ 1 ]   Infections of the lungs  or urinary tract in children may also cause vomiting or diarrhea. [ 1 ]  Classical  diabetic ketoacidosis  (DKA) presents with abdominal pain, nausea, and vomiting, but without diarrhea. [ 1 ]  One study found that 17% of children with DKA were initially diagnosed as having gastroenteritis. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8322", "text": "A supply of easily accessible uncontaminated water and good  sanitation  practices are important for reducing rates of infection and clinically significant gastroenteritis. [ 17 ]  Personal  hygiene  measures (such as  hand washing  with soap) have been found to decrease rates of gastroenteritis in both the developing and developed world by as much as 30%. [ 23 ]  Alcohol-based gels may also be effective. [ 23 ]  Food or drink that is thought to be contaminated should be avoided. [ 44 ] \n Breastfeeding  is important, especially in places with poor hygiene, as is improvement of hygiene generally. [ 15 ]  Breast milk reduces both the frequency of infections and their duration. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8323", "text": "Due to both its effectiveness and safety, in 2009 the World Health Organization recommended that the  rotavirus vaccine  be offered to all children globally. [ 25 ] [ 45 ]  Two commercial rotavirus vaccines exist and several more are in development. [ 45 ]  In Africa and Asia these vaccines reduced severe disease among infants [ 45 ]  and countries that have put in place national immunization programs have seen a decline in the rates and severity of disease. [ 46 ] [ 47 ]  This vaccine may also prevent illness in non-vaccinated children by reducing the number of circulating infections. [ 48 ]  Since 2000, the implementation of a rotavirus vaccination program in the United States has substantially decreased the number of cases of diarrhea by as much as 80 percent. [ 49 ] [ 50 ] [ 51 ]  The first dose of vaccine should be given to infants between 6 and 15 weeks of age. [ 25 ]  The  oral cholera vaccine  has been found to be 50\u201360% effective over two years. [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8324", "text": "There are a number of vaccines against gastroenteritis in development. For example, vaccines against  Shigella  and enterotoxigenic  Escherichia coli  (ETEC), which are two of the leading bacterial causes of gastroenteritis worldwide. [ 53 ] [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8325", "text": "Gastroenteritis is usually an acute and self-limiting disease that does not require medication. [ 22 ]  The preferred treatment in those with mild to moderate  dehydration  is  oral rehydration therapy  (ORT). [ 24 ]  For children at risk of dehydration from vomiting, taking a single dose of the  anti vomiting  medication  metoclopramide  or  ondansetron , may be helpful, [ 55 ]  and  butylscopolamine  is useful in treating  abdominal pain . [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8326", "text": "The primary treatment of gastroenteritis in both children and adults is  rehydration . This is preferably achieved by drinking rehydration solution, although  intravenous  delivery may be required if there is a  decreased level of consciousness  or if dehydration is severe. [ 57 ] [ 58 ]  Drinking replacement therapy products made with complex carbohydrates (i.e. those made from wheat or rice) may be superior to those based on simple sugars. [ 59 ]  Drinks especially high in simple sugars, such as  soft drinks  and fruit juices, are not recommended in children under five years of age as they may  increase  diarrhea. [ 22 ]  Plain water may be used if more specific ORT preparations are unavailable or the person is not willing to drink them. [ 22 ]  A  nasogastric tube  can be used in young children to administer fluids if warranted. [ 13 ]  In those who require intravenous fluids, one to four hours' worth is often sufficient. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8327", "text": "It is recommended that breast-fed infants continue to be nursed in the usual fashion,  and that formula-fed infants continue their formula immediately after rehydration with ORT. [ 61 ]  Lactose-free or lactose-reduced formulas usually are not necessary. [ 61 ]  Children should continue their usual diet during episodes of diarrhea with the exception that foods high in  simple sugars  should be avoided. [ 61 ]  The  BRAT diet  (bananas, rice, applesauce, toast and tea) is no longer recommended, as it contains insufficient nutrients and has no benefit over normal feeding. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8328", "text": "A Cochrane Review from 2020 concludes that  probiotics  make little or no difference to people who have diarrhea lasting 2 days or longer and that there is no proof that they reduce its duration. [ 62 ]  They may be useful in preventing and treating  antibiotic associated diarrhea . [ 63 ]  Fermented milk products (such as  yogurt ) are similarly beneficial. [ 64 ]   Zinc  supplementation appears to be effective in both treating and preventing diarrhea among children in the developing world. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8329", "text": "Antiemetic  medications may be helpful for treating vomiting in children.  Ondansetron  has some utility, with a single dose being associated with less need for intravenous fluids, fewer hospitalizations, and decreased vomiting. [ 55 ] [ 66 ] [ 67 ] [ 68 ]   Metoclopramide  might also be helpful. [ 68 ]  However, the use of ondansetron might possibly be linked to an increased rate of return to hospital in children. [ 69 ]  The intravenous preparation of ondansetron may be given orally if clinical judgment warrants. [ 70 ]   Dimenhydrinate , while reducing vomiting, does not appear to have a significant clinical benefit. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8330", "text": "Antibiotics are not usually used for gastroenteritis, although they are sometimes recommended if symptoms are particularly severe [ 71 ]  or if a susceptible bacterial cause is isolated or suspected. [ 72 ]  If antibiotics are to be employed, a  macrolide  (such as  azithromycin ) is preferred over a  fluoroquinolone  due to higher rates of resistance to the latter. [ 19 ]   Pseudomembranous colitis , usually caused by antibiotic use, is managed by discontinuing the causative agent and treating it with either  metronidazole  or  vancomycin . [ 73 ]  Bacteria and protozoans that are amenable to treatment include  Shigella [ 74 ]   Salmonella typhi , [ 75 ]  and  Giardia  species. [ 36 ]  In those with  Giardia  species or  Entamoeba histolytica ,  tinidazole  treatment is recommended and superior to metronidazole. [ 36 ] [ 76 ]  The  World Health Organization  (WHO) recommends the use of antibiotics in young children who have both bloody diarrhea and fever. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8331", "text": "Antimotility medication has a theoretical risk of causing complications, and although clinical experience has shown this to be unlikely, [ 43 ]  these drugs are discouraged in people with bloody diarrhea or diarrhea that is complicated by fever. [ 77 ]   Loperamide , an  opioid  analogue, is commonly used for the symptomatic treatment of diarrhea. [ 78 ]  Loperamide is not recommended in children, however, as it may cross the immature blood\u2013brain barrier and cause toxicity.  Bismuth subsalicylate , an insoluble complex of trivalent  bismuth  and salicylate, can be used in mild to moderate cases, [ 43 ]  but  salicylate toxicity  is theoretically possible. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8332", "text": "It is estimated that there were two billion cases of gastroenteritis that resulted in 1.3\u00a0million deaths globally in 2015. [ 6 ] [ 7 ]  Children and those in the  developing world  are most commonly affected. [ 15 ]  As of 2011, in those younger than five, there were about 1.7\u00a0billion cases resulting in 0.7\u00a0million deaths, [ 16 ]  with most of these occurring in the world's poorest nations. [ 17 ]  More than 450,000 of these fatalities are due to rotavirus in children under five years of age. [ 10 ] [ 79 ]   Cholera  causes about three to five million cases of disease and kills approximately 100,000 people yearly. [ 31 ]  In the developing world, children less than two years of age frequently get six or more infections a year that result in significant gastroenteritis. [ 17 ]  It is less common in adults, partly due to the development of acquired  immunity . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8333", "text": "In 1980, gastroenteritis from all causes caused 4.6\u00a0million deaths in children, with the majority occurring in the developing world. [ 73 ]  Death rates were reduced significantly (to approximately 1.5\u00a0million deaths annually) by 2000, largely due to the introduction and widespread use of  oral rehydration therapy . [ 80 ]  In the US, infections causing gastroenteritis are the second most common infection (after the  common cold ), and they result in between 200 and 375\u00a0million cases of acute diarrhea [ 17 ] [ 18 ]  and approximately ten thousand deaths annually, [ 17 ]  with 150 to 300 of these deaths in children less than five years of age. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8334", "text": "Gastroenteritis is associated with many colloquial names, including \" Montezuma's revenge \", \"Delhi belly\", \"la turista\", and \"back door sprint\", among others. [ 17 ]  It has played a role in many military campaigns and is believed to be the origin of the term \"no guts no glory\". [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8335", "text": "Gastroenteritis is the main reason for 3.7\u00a0million visits to physicians a year in the United States [ 1 ]  and 3\u00a0million visits in France. [ 81 ]  In the United States gastroenteritis as a whole is believed to result in costs of US$23\u00a0billion per year, [ 82 ]  with rotavirus alone resulting in estimated costs of US$1\u00a0billion a year. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8336", "text": "The first usage of \"gastroenteritis\" was in 1825. [ 83 ]  Before this time it was commonly known as  typhoid fever  or \"cholera morbus\", among others, or less specifically as \"griping of the guts\", \"surfeit\", \"flux\", \"colic\", \"bowel complaint\", or any one of several other archaic names for acute diarrhea. [ 84 ]  Cholera morbus is a historical term that was used to refer to gastroenteritis rather than specifically  cholera . [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8337", "text": "Many of the same agents cause gastroenteritis in cats and dogs as in humans. The most common organisms are  Campylobacter ,  Clostridioides difficile ,  Clostridium perfringens , and  Salmonella . [ 86 ]  A large number of toxic plants may also cause symptoms. [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8338", "text": "Some agents are more specific to a certain species.  Transmissible gastroenteritis coronavirus  (TGEV) occurs in pigs resulting in vomiting, diarrhea, and dehydration. [ 88 ]  It is believed to be introduced to pigs by wild birds and there is no specific treatment available. [ 89 ]  It is not transmissible to humans. [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8339", "text": "Giardia duodenalis , also known as  Giardia intestinalis  and  Giardia lamblia , is a  flagellated   parasitic   protozoan  microorganism of the genus  Giardia  that colonizes the  small intestine , causing a diarrheal condition known as  giardiasis . [ 1 ] [ 2 ] [ 3 ]  The parasite attaches to the  intestinal epithelium  by a ventral disc ( syn .  adhesive disc or sucker ), and  reproduces  via  binary fission . [ 4 ] [ 5 ]   G. duodenalis  is a non-invasive parasite, that does not spread to other parts of the  gastrointestinal tract , but remains confined to the  lumen  of the small intestine. [ 6 ] [ 7 ]  The parasite exists in two forms;  trophozoites  and  cysts . The microorganism can undergo encystation, transforming into a dormant  cyst  that enables it to survive outside of its  host . [ 8 ]   Giardia   trophozoites  are  anaerobic , and absorb their nutrients from the intestinal lumen. If the organism is  stained , its characteristic pattern resembles the familiar \" smiley face \" symbol. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8340", "text": "Chief pathways of human infection include ingestion of  untreated  drinking water (which is the most common method of transmission for this parasite), [ 3 ]  food, soil contaminated with human feces, and  sewage , a phenomenon particularly common in many  developing countries . [ 10 ] [ 3 ]  Contamination of natural waters also occurs in  watersheds  where intensive  grazing  occurs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8341", "text": "Giardia  infections occur worldwide. It is the most commonly identified intestinal parasite among children in day-care centers, hikers and  immunocompromised  patients. About 20,000 cases per year in the United States are reported. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8342", "text": "Almost half of those infected with giardiasis remain asymptomatic. For those who do experience symptoms, they usually appear 1 to 2 weeks after infection. Common symptoms include abdominal pain, nausea, and bloating, along with large, watery, foul-smelling, and greasy stools. Due to frequent loose stools, individuals with giardiasis often experience dehydration. [ 12 ]  It has also been shown that  G. intestinalis  damages the intestinal epithelium, which directly affects nutrient absorption. [ 5 ]  In severe cases, giardiasis can lead to chronic diarrhea, chronic fatigue syndrome and cognitive impairment in children. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8343", "text": "G. duodenalis  takes on two morphologically distinct forms during its lifecycle.  Trophozoites  are the replicative stage of the parasite, characterized by a pear-shaped,  motile ,  flagellated  cell that survives only in the small intestine of the host. [ 14 ]  The trophozoites do not penetrate host cells, but rather attaches to the intestinal epithelium cells to establish an infection. A cyst is the environmentally stable stage of the parasite, that facilitates transmission between hosts. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8344", "text": "The infection process in the host begins with the ingestion of cysts, which pass through the stomach into the first part of small intestine, or the  duodenum . Exposure to  digestive enzymes  and an acidic  pH  triggers excystation, where the cysts release trophozoites. [ 8 ]  Trophozoites swim through the intestinal mucus until they eventually adhere to the  intestinal epithelium  using their  ventral disc . [ 15 ] [ 14 ]  Adhered trophozoites can then feed, divide by  binary fission  and cause the disease. Trophozoites cause structural and functional damage to the host epithelial cells, impairing the intestine's ability to absorb nutrients effectively. [ 16 ]  Some trophozoites differentiate back into cysts under specific conditions, such as high organism density. [ 8 ]  As the trophozoites travel through the intestinal lumen to the  large intestine , the alkaline environment and the presence of  pancreatic proteases  trigger the encystation. Trophozoites develop into cysts through encystation, which involves specialized vesicles (ESVs) that facilitate the formation of the cyst wall. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8345", "text": "Cysts and trophozoites pass through the host's  large intestine  and are shed in the feces. [ 14 ]  Trophozoites cannot survive outside of the host, whereas cysts can remain viable in the external environment for several months. [ 17 ]  The cysts remain  dormant  until ingested by a host animal. When a new potential host ingests water or food contaminated with this feces, the cysts gain entry to the gastrointestinal tract of the new host, repeating the cycle. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8346", "text": "The trophozoite has an elaborate structure with two nuclei and four pairs of  flagella  which allow it to swim within the intestinal lumen of the host. It also has an adhesive disk on its  ventral  surface that is associated with the parasite's attachment to the intestinal epithelium. The adhesive disk is composed of  microtubules , and is found only in  Giardia . The parasite lacks  Golgi apparatus  and  mitochondria  but has  mitosomes , which probably evolved from mitochondria. [ 19 ]  The mitosome is a double-membraned organelle, that lacks the enzymatic components required for classic mitochondrial functions, such as ATP synthesis and lipid metabolism. However, they do contain certain mitochondrial genes associated with iron-sulfur complex biosynthesis, which suggests that this organism likely lost its mitochondria during evolution. [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8347", "text": "The cyst contains four nuclei,  axonemes , median bodies as well as the rigid cyst wall. Additionally, the cysts contain fragments of the adhesive disc within the cytoplasm. [ 8 ] [ 16 ]  The two-layered cyst wall protects the parasite against different environmental conditions such as chemical treatments. The metabolic activity of the cyst is significantly lower compared to that of the trophozoites, which allows the parasite to survive for longer periods in harsh conditions, such as in cold environments. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8348", "text": "G. duodenalis  is the most widespread intestinal parasite affecting humans. The parasite  Giardia duodenalis  can be found all over the world, in both developing and industrialized nations. However, it is most commonly found in tropical and temperate climates. [ 20 ]   Giardia duodenalis  is common around the world because the parasite resides in bodies of water; typically rivers, lakes, and recreational swimming pools. [ 21 ]  Giardiasis is more prevalent in  developing countries , where the sanitation and overall hygiene is poorer compared to  developed countries . [ 22 ]  In developed nations, giardiasis has a prevalence of 2%-5%, whereas in developing nations it is significantly higher, ranging from 20% to 30%. [ 23 ]  In the United States, it has been discovered that a majority of whom are infected by the  Giardia duodenalis  parasite tend to reside in more urban areas, and, patients who are infected are more likely to live in the Southern United States. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8349", "text": "G. duodenalis  causes an infection called giardiasis. This disease is the cause of both endemic and epidemic disease worldwide and is the most frequently identified intestinal parasite in the United States and Canada. An infected individual can excrete between 1 million and 1 billion cysts daily, and the  infectious dose  can be as low as 10 cysts. This makes Giardia extremely infectious."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8350", "text": "It is estimated to infect over 280 million people world every year [ 23 ] resulting over 500,000 deaths. The most affected demographic is children 0 to 4 years of age. Globally G.  duodenalis  is the most commonly identified protozoal intestinal parasite. [ 22 ]  Giardia has common seasonal patterns in the distribution of infection rates with highest peaks in the late summer to early fall. [ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8351", "text": "The cyst can survive for weeks to months in cold water, [ 17 ]  so the parasite can be present in contaminated wells and water systems, especially in stagnant water sources, such as naturally occurring ponds, storm-water storage systems, and even clean-looking mountain streams. Cysts can also be found on contaminated surfaces, soil and food. [ 26 ]  They may also occur in city reservoirs and persist after water treatment, as the cysts are resistant to conventional water-treatment methods, such as  chlorination  and  ozonolysis . [ 17 ]   Zoonotic  transmission is also possible, but is less frequent.  Giardia  infection is a concern for people camping in the wilderness or swimming in contaminated streams or lakes, especially the artificial lakes formed by  beaver  dams (hence the popular name for giardiasis, \"beaver fever\"). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8352", "text": "In addition to waterborne sources, Giardia infections are more commonly found in children compared to adults, this is believed to be due to  fecal-oral  transmission of the cysts. For example, in developed countries it affects approximately 2% of adults and 8% of children. In developing countries the prevalence rates reach 15% to 20% in children under 10 years old. [ 12 ]  Thus, there is a significant variation in infection rates based on geographical area. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8353", "text": "Those who work with children are also at risk of being infected, as are family members of infected individuals. 7% of children aged 1 to 3 years and 11% of infants and toddlers tested for admission to day-care centers were found to be infected. [ 22 ]  Not all  Giardia  infections are symptomatic, and many people can unknowingly serve as carriers of the parasite. Re- infection and chronic infections of the parasite can occur.  [ 23 ] [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8354", "text": "Giardia  infects humans, but is also one of the most common parasites infecting cats, dogs, and birds. Mammalian hosts also include dozens of species, [ 27 ]  including  cattle ,  sheep , [ 28 ]  and  goats . [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8355", "text": "Cats can be cured easily, and lambs usually simply lose weight, but in calves, the parasites can be fatal and often are not responsive to antibiotics or electrolytes. Carriers among calves can also be asymptomatic. This parasite is deadly for  chinchillas , so extra care must be taken by providing them with safe water. Dogs have a high infection rate, as 30% of the population under one year old are known to be infected in  kennels . The infection is more prevalent in puppies than in adult dogs. Infected dogs can be isolated and treated, or the entire pack at a kennel can be presumptively treated together. Kennels and areas used for exercise should be considered contaminated for at least one month after dogs show signs of infection, as cysts can survive in the environment for long periods of time. Prevention can be achieved by  quarantine  of infected dogs for at least 20 days and careful management and maintenance of a clean water supply. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8356", "text": "G. duodenalis  trophozoites are pear-shaped cells, 10 to 20  \u03bcm  long, 7 to 10 \u03bcm across, and 2 to 4 \u03bcm thick. [ 14 ] [ 15 ]  They are motile by way of four pairs of  flagella , which propel the trophozoites through the intestine. [ 15 ]  Notably, each  G. duodenalis  cell has two  nuclei , both of which actively  transcribe  genes. [ 14 ]  Adjacent to the nucleus,  G. duodenalis  cells have an  endoplasmic reticulum  that extends through much of the cell. [ 29 ]  Trophozoites about to differentiate into cysts also contain prominent vesicles termed  encystation-specific vesicles  that disappear once cyst wall construction begins. [ 29 ]  Unlike most other eukaryotes,  G. duodenalis  cells contain no visible  mitochondria , but instead contains a substantially reduced metabolic organelle known as a  mitosome . [ 15 ]  Additionally, cells appear to contain no  Golgi bodies , and instead the  secretory system  consists entirely of the endoplasmic reticulum and numerous vesicles dispersed throughout the cell, termed  peripheral vesicles . [ 29 ]  Peripheral vesicles are responsible both for taking up extracellular nutrients, and expelling waste outside the cell. [ 30 ]  Each cell also contains a pair of rigid structures called  median bodies  which make up part of the  G. lamblia   cytoskeleton . [ 14 ]  Trophozoites adhere to host epithelial cells via a specialized disk-shaped organelle called the  ventral disk . [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8357", "text": "Cysts are oval-shaped cells slightly smaller than trophozoites. [ 15 ]  They lack flagella, and are covered by a smooth, clear cyst wall. [ 15 ]  Each cyst contains four nuclei and fragments of the ventral disc. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8358", "text": "G. duodenalis  primarily generates its energy by breaking down  glucose  via  glycolysis , as well as the  arginine deiminase  pathway. It is unable to synthesize  nucleotides  on its own, instead salvaging them from its host. Synthesis of  iron\u2013sulfur clusters  is done in a double-membrane-bound compartment called the mitosome, which is likely a remnant of mitochondria. [ 19 ]  Each cell contains 25 to 100 mitosomes divided into two categories - peripheral mitosomes, which are scattered throughout the cell, and central mitosomes, which gather at the center of the cell for unknown reasons. [ 31 ]  As in mitochondria, proteins with a certain peptide signal sequence are trafficked to and imported into the mitosome. Unlike mitochondria, mitosomes have no genome of their own. All mitosomal genes are encoded by the  Giardia  nuclear genome. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8359", "text": "Giardia  and the other  diplomonads  are unique in their possession of two  cell nuclei  that are similar in appearance, DNA content,  transcription , and time of replication.  Giardia  is a  polyploid  organism, with at least four, and perhaps eight or more, copies of each of five chromosomes per organism. [ 32 ]  The genome has been sequenced and was published in 2007, although the sequence contains several gaps. The sequence is about 12 million base pairs and contains about 5000 protein-coding genes. [ 33 ]  The  GC-content  is 46%. Trophozoites have a  ploidy  of four and the ploidy of cysts is eight, which in turn raises the question of how  Giardia  maintains homogeneity between the chromosomes of the same and opposite nuclei. Modern sequencing technologies have been used to resequence different strains. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8360", "text": "Infections with  Giardia  are self-limited in immunocompetent individuals, while people with immunodeficiency disorders may develop chronic giardiasis. [ citation needed ]  During the infection different mechanisms from the  innate  and  adaptive  immune system are activated. The first physical barrier is the mucus layer where the organism interacts with epithelial, immune cells, and some antimicrobial peptides released by those cells as well as  nitric oxide  and  inflammatory cytokines  like  interleukin 6 .  TLR2  and  TLR4  also can be activated by  Giardia . [ 35 ]  The T-cell response in giardiasis includes  T helper cells  and  cytotoxic T cells , and the production of  IgA  by  B cells  also helps to eliminate the infection. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8361", "text": "Giardia  had been assumed to be primitively asexual and with no means of transferring DNA between nuclei. These assumptions made  explaining the remarkably low level of allelic heterozygosity (< 0.01%) in the genome isolate, WB, very difficult, but all those assumptions of asexuality are now in doubt, with population genetics providing evidence for recombination [ 37 ]  and the identification of meiotic genes, evidence for recombination among isolates and the evidence for exchange of genetic material between nuclei during the process of encystation. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8362", "text": "These findings on sexuality in  Giardia , above, have important implications for understanding the origin of sexual reproduction in eukaryotes.  Though sexual reproduction is widespread among extant eukaryotes,  until recently, sex seemed unlikely to be a primordial and fundamental feature of eukaryotes.  A probable reason for the view that sex may not be fundamental to eukaryotes was that sexual reproduction previously appeared to be lacking in certain human pathogenic single-celled eukaryotes (e.g.  Giardia ) that diverged from early ancestors in the eukaryotic lineage. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8363", "text": "In addition to the evidence cited above for recombination in  Giardia , Malik et al. [ 39 ]  reported that many meiosis specific genes occur in the  Giardia  genome, and further that homologs of these genes also occur in another unicellular eukaryote,  Trichomonas vaginalis .  Because these two species are descendants of lineages that are highly divergent among eukaryotes, Malik et al. [ 39 ]  suggested that these meiotic genes were present in a common ancestor of all eukaryotes.  Thus, on this view, the earliest ancestor of eukaryotes was likely capable of sexual reproduction.  Furthermore, Dacks and Roger [ 40 ]  proposed, based on phylogenetic analysis, that facultative sex was present in the common ancestor of all eukaryotes.  Bernstein et al. also reviewed evidence in support of this view. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8364", "text": "Eight genotype assemblages of  G. duodenalis  have been recognized to date (A-H). [ 27 ]  Genotyping of  G. duodenalis  isolated from various hosts has shown that assemblages A and B infect the largest range of host species, and appear to be the main (or possibly only)  G. duodenalis  assemblages that undeniably infect human subjects. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8365", "text": "Frances Gillin of the  University of California, San Diego , and her colleagues cultivated the entire lifecycle of this  parasite  in the laboratory, and identified biochemical cues in the host's digestive system that trigger  Giardia' s lifecycle transformations. [ 42 ] [ 43 ]  They also uncovered several ways in which the parasite evades the defenses of the infected organism. One of these is by altering the proteins on its surface, which confounds the ability of the infected animal's  immune system  to detect and combat the parasite (called  antigenic variation ). Gillin's work reveals why  Giardia  infections are extremely persistent and prone to recur. In addition, these insights into its biology and survival techniques may enable scientists to develop better strategies to understand, prevent, and treat  Giardia  infections. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8366", "text": "In December 2008,  Nature  published an article showing the discovery of an  RNA interference  mechanism that allows  Giardia  to switch variant-specific surface proteins to avoid host immune response. [ 44 ]  The discovery was made by the team working at the Biochemistry and Molecular Biology Laboratory, School of Medicine, Catholic University of Cordoba, Argentina, led by Dr. Hugo Lujan. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8367", "text": "The main congress about  Giardia  is the International Giardia and Cryptosporidium Conference. A summary of results presented at the most recent edition (2019, in  Rouen , France) is available. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8368", "text": "In 2022, a study conducted by Elisa Barroeta-Echegaray and colleagues concluded that  Giardia duodenalis  secretes  enolase  as a monomer during the interaction, or attachment, of trophozoites with intestinal epithelial cells. This interaction was shown to activate  plasminogen  and induce  necroptotic damage  in intestinal epithelial cells. The researchers demonstrated that blocking the enolase inhibited trophozoite attachment to intestinal epithelial cells. Furthermore, enolase was shown to enhance plasmin activity, leading to significant cell damage characterized by vacuolization and intercellular separation. Enolase also induced  necroptosis  in epithelial cells via  tumor necrosis factor \u03b1 (TNF-\u03b1)  and  apoptosis-inducing factor  (AIF), independent of  caspase-3  activity. These findings suggest that Giardia enolase is a critical  virulence factor  in host-pathogen interactions. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8369", "text": "The first likely description of  Giardia  was in 1681 by  Antonie van Leeuwenhoek , who in a letter to  Robert Hooke , described \"animalcules\" resembling  Giardia  trophozoites in his stool. [ 14 ] [ 46 ]  The next known description of  Giardia  wasn't until 1859, when Czech physician  Vil\u00e9m Lambl  published a description of the trophozoite stages he saw in the stool of a pediatric patient. Lambl termed the organism  Cercomonas intestinalis . [ 47 ]  In 1888,  Rapha\u00ebl Blanchard  renamed the parasite  Lamblia intestinalis  in Lambl's honor. [ 47 ]  In 1915,  Charles Stiles  renamed the organism  Giardia lamblia  in honor of both Lambl and Professor  Alfred Mathieu Giard  of Paris. [ 47 ] [ 48 ]  In 1921,  Charles E. Simon  published a detailed description of the parasite's morphology. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8370", "text": "Halzoun  ( Arabic :\u062d\u0644\u0632\u0648\u0646) is the local name of a  buccopharyngeal   infection  occurring in  Lebanon , probably caused by  pentastomida larvae  of  Linguatula serrata  (dog tongue worm) which wander into the  throat  of the human host after ingestion of infected raw liver or lymph nodes from sheep or goats. [ 1 ]  The word Halzoun means \" Snail \" in Arabic."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8371", "text": "Halzoun is considered to be a form of infection with  Fasciola , whereby ingestion of infected raw sheep and goat livers may result in the attachment of adult living worms by their suckers to the pharyngeal mucosa causing  edema  of the  soft palate ,  pharynx  and  larynx . This edema is accompanied by  dyspnea  (shortness of breath) and occasionally  asphyxia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8372", "text": "This article related to  parasites  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8373", "text": "Helminthiasis , also known as  worm infection , is any  macroparasitic  disease of humans and other animals in which a part of the body is infected with  parasitic   worms , known as  helminths . There are numerous species of these  parasites , which are broadly classified into  tapeworms ,  flukes , and  roundworms . They often live in the  gastrointestinal tract  of their  hosts , but they may also burrow into other  organs , where they induce physiological damage."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8374", "text": "Soil-transmitted helminthiasis  and  schistosomiasis  are the most important helminthiases, and are among the  neglected tropical diseases . [ 1 ]  These group of helminthiases have been targeted under the joint action of the world's leading  pharmaceutical companies  and  non-governmental organizations  through a project launched in 2012 called the  London Declaration on Neglected Tropical Diseases , which aimed to control or eradicate certain neglected tropical diseases by 2020. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8375", "text": "Helminthiasis has been found to result in poor birth outcome, poor cognitive development, poor school and work performance, poor socioeconomic development, and poverty. [ 3 ] [ 4 ]  Chronic illness,  malnutrition , and  anemia  are further examples of secondary effects. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8376", "text": "Soil-transmitted helminthiases are responsible for parasitic infections in as much as a quarter of the human population worldwide. [ 6 ]  One well-known example of soil-transmitted helminthiases is  ascariasis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8377", "text": "Of all the known helminth species, the most important helminths with respect to understanding their transmission pathways, their control, inactivation and enumeration in samples of human excreta from dried feces,  faecal sludge ,  wastewater , and  sewage sludge  are: [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8378", "text": "Helminthiases are classified as follows (the disease names end with \"-sis\" and the causative worms are in brackets):"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8379", "text": "The signs and symptoms of helminthiasis depend on a number of factors including: the site of the infestation within the body; the type of worm involved; the number of worms and their volume; the type of  damage  the infesting worms cause; and, the immunological response of the body. Where the burden of parasites in the body is light, there may be no symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8380", "text": "Certain worms may cause particular constellations of symptoms. For instance,  taeniasis  can lead to  seizures  due to  neurocysticercosis . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8381", "text": "In extreme cases of  intestinal  infestation, the mass and volume of the worms may cause the outer layers of the intestinal wall, such as the muscular layer, to tear. This may lead to  peritonitis ,  volvulus , and  gangrene  of the intestine. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8382", "text": "As pathogens in the body, helminths induce an  immune  response. Immune-mediated  inflammatory  changes occur in the skin,  lung ,  liver , intestine,  central nervous system , and eyes. Signs of the body's immune response may include  eosinophilia ,  edema , and  arthritis . [ 10 ]  An example of the immune response is the  hypersensitivity  reaction that may lead to  anaphylaxis . Another example is the migration of  Ascaris  larvae through the  bronchi  of the lungs causing  asthma . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8383", "text": "In humans,  T helper cells  and  eosinophils  respond to helminth infestation. It is well established that T helper 2 cells are the central players of protective immunity to helminths, [ 12 ]  while the roles for B cells and antibodies are context-dependent. [ 13 ]  Inflammation leads to encapsulation of egg deposits throughout the body. Helminths excrete into the intestine toxic substances after they feed. These substances then enter the circulatory and lymphatic systems of the host body. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8384", "text": "Chronic immune responses to helminthiasis may lead to increased susceptibility to  other infections  such as  tuberculosis ,  HIV , and  malaria . [ 14 ] [ 15 ] [ 16 ]  There is conflicting information about whether deworming reduces HIV progression and viral load and increases  CD4  counts in  antiretroviral  naive and experienced individuals, although the most recent Cochrane review found some evidence that this approach might have favorable effects. [ 17 ] [ 18 ]  Helminth infection also lowers the immune responses to vaccination for other diseases such as  BCG ,  measles , and  Hepatitis B . [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8385", "text": "Chronic helminthiasis may cause severe  morbidity . [ 20 ]  Helminthiasis has been found to result in poor birth outcome, poor cognitive development, poor school and work performance, decreased productivity, poor socioeconomic development, and poverty. [ 3 ] [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8386", "text": "Helminthiasis may cause chronic illness through malnutrition including  vitamin deficiencies ,  stunted growth ,  anemia , and  protein-energy malnutrition . Worms compete directly with their hosts for nutrients, but the magnitude of this effect is likely minimal as the nutritional requirements of worms is relatively small. [ 21 ] [ 22 ] [ 23 ]  In pigs and humans,  Ascaris  has been linked to  lactose intolerance  and  vitamin A ,  amino acid , and fat  malabsorption . [ 3 ]  Impaired nutrient uptake may result from direct damage to the intestinal mucosal wall or from more subtle changes such as chemical imbalances and changes in gut flora. [ 24 ]  Alternatively, the worms\u2019 release of  protease inhibitors  to defend against the body's digestive processes may impair the breakdown of other nutrients. [ 21 ] [ 23 ]  In addition, worm induced diarrhoea may shorten gut transit time, thus reducing absorption of nutrients. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8387", "text": "Malnutrition due to worms can give rise to  anorexia . [ 22 ]  A study of 459 children in  Zanzibar  revealed spontaneous increases in appetite after  deworming . [ 25 ]  Anorexia might be a result of the body's immune response and the stress of combating infection. [ 23 ]  Specifically, some of the  cytokines  released in the immune response to worm infestation have been linked to anorexia in animals. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8388", "text": "Helminths may cause  iron-deficiency anemia . This is most severe in heavy  hookworm infections , as  Necator americanus  and  Ancylostoma duodenale  feed directly on the blood of their hosts. Although the daily consumption of an individual worm (0.02\u20130.07 ml and 0.14\u20130.26 ml respectively) is small, the collective consumption under heavy infection can be clinically significant. [ 3 ] [ 23 ]  Intestinal  whipworm  may also cause anemia. Anemia has also been associated with reduced stamina for physical labor, a decline in the ability to learn new information, and apathy, irritability, and fatigue. [ 3 ]  A study of the effect of deworming and iron supplementation in 47 students from the  Democratic Republic of the Congo  found that the intervention improved cognitive function. [ 26 ]  Another study found that in 159  Jamaican  schoolchildren, deworming led to better auditory  short-term memory  and scanning and retrieval of  long-term memory  over a period of nine-weeks. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8389", "text": "Malnutrition due to helminths may affect cognitive function leading to low educational performance, decreased concentration and difficulty with abstract cognitive tasks. Iron deficiency in infants and preschoolers is associated with \"lower scores ... on tests of mental and motor development ... [as well as] increased fearfulness, inattentiveness, and decreased social responsiveness\". [ 21 ]  Studies in the Philippines and Indonesia found a significant correlation between helminthiasis and decreased memory and fluency. [ 28 ] [ 29 ]  Large parasite burdens, particularly severe hookworm infections, are also associated with  absenteeism , under-enrollment, and attrition in school children. [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8390", "text": "Helminths are transmitted to the  final host  in several ways. The most common infection is through  ingestion  of contaminated vegetables, drinking water, and raw or undercooked meat. Contaminated food may contain eggs of nematodes such as  Ascaris ,  Enterobius , and  Trichuris ; cestodes such as  Taenia ,  Hymenolepis , and  Echinococcus ; and trematodes such as  Fasciola . Raw or undercooked meats are the major sources of  Taenia  (pork, beef and venison),  Trichinella  (pork and bear),  Diphyllobothrium  (fish),  Clonorchis  (fish), and  Paragonimus  (crustaceans). Schistosomes and nematodes such as hookworms ( Ancylostoma  and  Necator ) and  Strongyloides  can penetrate the skin directly. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8391", "text": "The roundworm,  Dracunculus  has a complex mode of transmission: it is acquired from drinking infested water or eating frogs and fish that contain (had eaten) infected crustaceans ( copepods ); and can also be transmitted from infected pets (cats and dogs). [ 30 ]  Roundworms such as  Brugia ,  Wuchereria and   Onchocerca  are directly  transmitted by mosquitoes . [ 31 ] [ 32 ]  In the developing world, the use of contaminated water is a major risk factor for infection. [ 33 ]  Infection can also take place through the practice of  geophagy , which is not uncommon in parts of  sub-Saharan Africa . Soil is eaten, for example, by children or pregnant women to counteract a real or perceived deficiency of minerals in their diet. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8392", "text": "Specific helminths can be identified through  microscopic  examination of their eggs (ova) found in faecal samples. The number of eggs is measured in units of  eggs per gram . [ 35 ]  However, it does not quantify  mixed infections , and in practice, is inaccurate for quantifying the eggs of schistosomes and soil-transmitted helminths. [ 36 ]  Sophisticated tests such as  serological assays ,  antigen tests , and  molecular diagnosis  are also available; [ 35 ] [ 37 ]  however, they are time-consuming, expensive and not always reliable. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8393", "text": "Disrupting the cycle of the worm will prevent infestation and re-infestation. Prevention of infection can largely be achieved by addressing the issues of  WASH \u2014water,  sanitation  and  hygiene . [ 39 ] [ 40 ] [ 41 ]  The reduction of  open defecation  is particularly called for, [ 42 ] [ 43 ]  as is stopping the use of  human waste  as  fertilizer . [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8394", "text": "Further preventive measures include adherence to appropriate  food hygiene , wearing of shoes, regular  deworming  of pets, and the proper disposal of their feces. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8395", "text": "Scientists are also searching for a vaccine against helminths, such as a  hookworm vaccine . [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8396", "text": "Broad-spectrum  benzimidazoles  (such as  albendazole  and  mebendazole ) are the first line treatment of intestinal  roundworm  and  tapeworm  infections. Macrocyclic lactones (such as  ivermectin ) are effective against adult and migrating larval stages of nematodes.  Praziquantel  is the drug of choice for schistosomiasis, taeniasis, and most types of food-borne trematodiases.  Oxamniquine  is also widely used in mass deworming programmes.  Pyrantel  is commonly used for veterinary nematodiasis. [ 45 ] [ 46 ]   Artemisinins  and derivatives are proving to be candidates as drugs of choice for trematodiasis. [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8397", "text": "In  regions where helminthiasis is common , mass deworming treatments may be performed, particularly among school-age children, who are a high-risk group. [ 48 ] [ 49 ]  Most of these initiatives are undertaken by the  World Health Organization  (WHO) with positive outcomes in many regions. [ 50 ] [ 51 ]  Deworming programs can improve school attendance by 25 percent. [ 52 ]  Although deworming improves the health of an individual, outcomes from  mass deworming  campaigns, such as reduced deaths or increases in cognitive ability, nutritional benefits, physical growth, and performance, are uncertain or not apparent. [ 53 ] [ 54 ] [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8398", "text": "If complications of helminthiasis, such as  intestinal obstruction  occur, emergency surgery may be required. [ 9 ] [ 57 ]  Patients who require non-emergency surgery, for instance for removal of worms from the  biliary tree , can be pre-treated with the anthelmintic drug albendazole. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8399", "text": "Areas with the highest prevalence of helminthiasis are  tropical  and  subtropical  areas including sub-Saharan Africa, central and east Asia, and the Americas. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8400", "text": "Some types of helminthiases are classified as  neglected tropical diseases . [ 1 ] [ 58 ]  They include:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8401", "text": "The soil-transmitted helminths ( A. lumbricoides ,  T. trichiura ,  N. americanus ,  A. duodenale) ,  schistosomes , and  filarial worms  collectively infect more than a quarter of the human population worldwide at any one time, far surpassing HIV and malaria together. [ 35 ] [ 37 ]   Schistosomiasis  is the second most prevalent parasitic disease of humans after malaria. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8402", "text": "In 2014\u201315, the WHO estimated that approximately 2 billion people were infected with soil-transmitted helminthiases, [ 6 ]  249 million with schistosomiasis, [ 60 ]  56 million people with food-borne trematodiasis, [ 61 ]  120 million with lymphatic filariasis, [ 62 ]  37 million people with onchocerciasis, [ 63 ]  and 1 million people with echinococcosis. [ 64 ]  Another source estimated a much higher figure of 3.5 billion infected with one or more soil-transmitted helminths. [ 65 ] [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8403", "text": "In 2014, only 148 people were reported to have  dracunculiasis  because of a successful eradication campaign for that particular helminth, which is easier to eradicate than other helminths as it is transmitted only by drinking contaminated water. [ 67 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8404", "text": "Because of their high mobility and lower standards of hygiene, school-age children are particularly vulnerable to helminthiasis. [ 68 ]  Most children from developing nations will have at least one infestation. Multi-species infections are very common. [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8405", "text": "The most common intestinal parasites in the United States are  Enterobius vermicularis ,  Giardia lamblia ,  Ancylostoma duodenale ,  Necator americanus , and  Entamoeba histolytica . [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8406", "text": "In a developing country like Bangladesh, the most common species are round worm ( Ascaris lumbricoides ), whipworm (Tricurias tricuras) and hookworm\n(Ancylostoma duodenalis).  [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8407", "text": "Even in areas of high prevalence, the frequency and severity of infection is not uniform within communities or families. [ 72 ]  A small proportion of community members harbour the majority of worms, and this depends on age. The maximum worm burden is at five to ten years of age, declining rapidly thereafter. [ 73 ]  Individual predisposition to helminthiasis for people with the same sanitation infrastructure and hygiene behavior is thought to result from differing  immunocompetence ,  nutritional status , and  genetic factors . [ 72 ]  Because individuals are predisposed to a high or a low worm burden, the burden reacquired after successful treatment is proportional to that before treatment. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8408", "text": "It is estimated that intestinal nematode infections cause 5 million  disability-adjusted life years  (DALYS) to be lost, of which hookworm infections account for more than 3 million DALYS and ascaris infections more than 1 million. [ 74 ]  There are also signs of progress: The  Global Burden of Disease Study  published in 2015 estimates a 46 percent (59 percent when age standardised) reduction in  years lived with disability  (YLD) for the 13-year time period from 1990 to 2013 for all intestinal/nematode infections, and even a 74 percent (80 percent when age standardised) reduction in YLD from ascariasis. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8409", "text": "As many as 135,000 die annually from soil transmitted helminthiasis. [ 3 ] [ 37 ] [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8410", "text": "The 1990\u20132013  Global Burden of Disease Study  estimated 5,500 direct deaths from schistosomiasis, [ 77 ]  while more than 200,000 people were estimated in 2013 to die annually from causes related to schistosomiasis. [ 78 ]  Another 20 million have severe consequences from the disease. [ 79 ]  It is the most deadly of the neglected tropical diseases. [ 80 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8411", "text": "807 to 1,121 [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8412", "text": "604\u2013795 [ 81 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8413", "text": "576\u2013740 (hookworm in general) [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8414", "text": "(210 \"affected\" [ 90 ] )"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8415", "text": "200,000 indirect deaths from \"causes related to\" Schistosomiasis [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8416", "text": "(all types of  Taenia : 40 to 60 [ 94 ] )"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8417", "text": "Hookworm infection  is an infection by a type of  intestinal parasite  known as a  hookworm . [ 1 ] [ 5 ]  Initially, itching and a rash may occur at the site of infection. Those only affected by a few worms may show no symptoms. Those infected by many worms may experience  abdominal pain , diarrhea, weight loss, and  tiredness . The mental and physical development of children may be affected.  Anemia  may result. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8418", "text": "Two common hookworm infections in humans are  ancylostomiasis  and  necatoriasis , caused by the species  Ancylostoma duodenale  and  Necator americanus  respectively. Hookworm eggs are deposited in the stools of infected people. If these end up in the environment, they can hatch into  larvae  (immature worms), which can then penetrate the skin. One type can also be spread through contaminated food. Risk factors include walking  barefoot  in warm climates, where  sanitation  is poor. Diagnosis is by examination of a  stool sample  with a  microscope . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8419", "text": "The risk of infection can be reduced on an individual level by not walking barefoot in areas where the disease is common. At a population level, decreasing  outdoor defecation , not using raw feces as  fertilizer , and  mass deworming  are effective. [ 1 ]  Treatment is typically with the medications  albendazole  or  mebendazole  for one to three days.  Iron supplements  may be needed in those with anemia. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8420", "text": "Hookworms infected about 428 million people in 2015. [ 4 ]  Heavy infections can occur in both children and adults, but are less common in adults. [ 2 ]  They are rarely fatal. [ 6 ]  Hookworm infection is a  soil-transmitted helminthiasis  and classified as a  neglected tropical disease . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8421", "text": "No symptoms or signs are specific to hookworm infection, but they give rise to a combination of intestinal  inflammation  and progressive  iron-deficiency anemia  and  protein deficiency . Coughing, chest pain, wheezing, and fever sometimes result from severe infection. Epigastric pains, indigestion, nausea,  vomiting ,  constipation , and  diarrhea  can occur early or in later stages, as well, although gastrointestinal symptoms tend to improve with time. Signs of advanced severe infection are those of anemia and protein deficiency, including  emaciation ,  cardiac failure , and abdominal distension with  ascites . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8422", "text": "Larval  invasion of the  skin  (mostly in the Americas) can produce a skin disease called  cutaneous larva migrans  also known as creeping eruption. The hosts of these worms are not human and the larvae can only penetrate the upper five layers of the skin, where they give rise to intense, local  itching , usually on the foot or lower leg, known as  ground itch . This infection is due to larvae from the  A. braziliense  hookworm. The larvae migrate in tortuous tunnels between the  stratum basale  and  stratum corneum  of the skin, causing  serpiginous  vesicular  lesions . With the advancing movement of the larvae, the rear portions of the lesions become dry and crusty. The lesions are typically intensely itchy. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8423", "text": "The incubation period can vary between a few weeks to many months and is largely dependent on the number of hookworm parasites an individual is infected with. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8424", "text": "Hookworm infections in humans include  ancylostomiasis  and  necatoriasis . Ancylostomiasis is caused by  Ancylostoma duodenale ,  which is the more common type found in the  Middle East ,  North Africa ,  India , and (formerly) in  southern Europe . Necatoriasis is caused by  Necator americanus ,  the more common type in  the Americas ,  sub-Saharan Africa ,  Southeast Asia ,  China , and  Indonesia . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8425", "text": "Other animals such as  birds ,  dogs , and  cats  may also be affected.  A. tubaeforme  infects cats,  A. caninum  infects dogs, and  A. braziliense  and  Uncinaria stenocephala  infect both cats and dogs. Some of these infections can be  transmitted to humans . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8426", "text": "A. duodenale  worms are grayish-white or pinkish with the head slightly bent in relation to the rest of the body. This bend forms a definitive hook shape at the anterior end for which hookworms are named. They possess well-developed mouths with two pairs of teeth. While males measure approximately one centimeter by 0.5 millimeter, the females are often longer and stouter. Additionally, males can be distinguished from females based on the presence of a prominent posterior copulatory bursa. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8427", "text": "N. americanus  is very similar in morphology to  A. duodenale .  N. americanus  is generally smaller than  A. duodenale  with males usually 5 to 9\u00a0mm long and females about 1\u00a0cm long. Whereas  A. duodenale  possesses two pairs of teeth,  N. americanus  possesses a pair of cutting plates in the buccal capsule. Additionally, the hook shape is much more defined in  Necator  than in  Ancylostoma . [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8428", "text": "The hookworm thrives in warm soil where temperatures are over 18\u00a0\u00b0C (64\u00a0\u00b0F). They exist primarily in  sandy  or  loamy  soil and cannot live in  clay  or muck.  Rainfall  averages must be more than 1,000\u00a0mm (39\u00a0in) a year for them to survive. Only if these conditions exist can the eggs hatch. Infective larvae of  N. americanus  can survive at higher temperatures, whereas those of  A. duodenale  are better adapted to cooler climates. Generally, they live for only a few weeks at most under natural conditions and die almost immediately on exposure to direct sunlight or  desiccation . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8429", "text": "Infection of the host is by the larvae, not the eggs. While  A. duodenale  can be ingested, the usual method of infection is through the skin; this is commonly caused by walking  barefoot  through areas contaminated with fecal matter. The larvae can penetrate the skin of the foot, and once inside the body, they migrate through the  vascular system  to the  lungs , and from there up the  trachea , and are swallowed. They then pass down the  esophagus  and enter the digestive system, finishing their journey in the  intestine , where the larvae mature into adult worms. [ 12 ] [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8430", "text": "Once in the host gut,  Necator  tends to cause a prolonged infection, generally 1 to 5 years (many worms die within a year or two of infection), though some adult worms have been recorded to live for 15 years or more.  Ancylostoma  adults are short-lived, surviving on average for only about 6 months. However, the infection can be prolonged because dormant larvae can be \"recruited\" sequentially from tissue \"stores\" over many years, to replace expired adult worms. This can give rise to seasonal fluctuations in infection prevalence and intensity (apart from normal seasonal variations in transmission). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8431", "text": "They mate inside the host, females laying from 10,000 to 30,000 eggs per day and some 15 to 56 million eggs during their adult lifetimes, which pass out in feces. Because 5 to 7 weeks are needed for adult worms to mature, mate, and produce eggs, in the early stages of very heavy infection, acute symptoms might occur without any eggs being detected in the patient's feces. This can make diagnosis very difficult. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8432", "text": "N. americanus  and  A. duodenale  eggs can be found in warm, moist soil where they eventually hatch into first-stage larvae, or L1. L1, the feeding noninfective rhabditoform stage, will feed on soil microbes and eventually molt into second-stage larvae, L2, which is also in the rhabditoform stage. It will feed for about 7 days and then molt into the third-stage larvae, or L3. This is the filariform stage of the parasite, that is, the nonfeeding infective form of the larvae. The L3 larvae are extremely motile and seek higher ground to increase their chances of penetrating the skin of a human host. The L3 larvae can survive up to 2 weeks without finding a host. While  N. americanus  larvae only infect through penetration of the skin,  A. duodenale  can infect both through penetration and orally. After the L3 larvae have successfully entered the host, they then travel through the subcutaneous venules and lymphatic vessels of the human host. Eventually, the L3 larvae enter the lungs through the pulmonary capillaries and break out into the alveoli. They then travel up the trachea to be coughed and swallowed by the host. After being swallowed, the L3 larvae are then found in the small intestine, where they molt into the L4, or adult worm stage. The entire process from skin penetration to adult development takes about 5\u20139 weeks. The female adult worms release eggs ( N. americanus  about 9,000\u201310,000 eggs/day and  A. duodenale  25,000\u201330,000 eggs/day), which are passed in the feces of the human host. These eggs hatch in the environment within several days and the cycle starts anew. [ 12 ] [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8433", "text": "Hookworm infection is generally considered to be asymptomatic, but as Norman Stoll described in 1962, it is an extremely dangerous infection because its damage is \"silent and insidious.\" [ 16 ]  An individual may experience general symptoms soon after infection. Ground-itch, which is an allergic reaction at the site of parasitic penetration and entry, is common in patients infected with  N. americanus . [ 11 ]  Additionally, cough and  pneumonitis  may result as the larvae begin to break into the  alveoli  and travel up the trachea. Then once the larvae reach the small intestine of the host and begin to mature, the infected individual will experience diarrhea and other gastrointestinal discomfort. [ 11 ]  However, the \"silent and insidious\" symptoms referred to by Stoll are related to chronic, heavy-intensity hookworm infections. Major morbidity associated with hookworm infection is caused by intestinal blood loss, iron deficiency anemia, and protein malnutrition. [ 14 ]  They result mainly from adult hookworms in the small intestine ingesting blood, rupturing  erythrocytes , and degrading  hemoglobin  in the host. [ 12 ]  This long-term blood loss can manifest itself physically through facial and peripheral  edema ;  eosinophilia  and pica/ geophagy  caused by iron deficiency anemia are also experienced by some hookworm-infected patients. [ 11 ]  Recently, more attention has been given to other important outcomes of hookworm infection that play a large role in public health. It is now widely accepted that children who have chronic hookworm infection can experience growth retardation as well as intellectual and cognitive impairments. [ 12 ] [ 17 ]  Additionally, recent research has focused on the potential of adverse maternal-fetal outcomes when the mother is infected with hookworm during pregnancy. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8434", "text": "The disease was linked to nematode worms ( Ankylostoma duodenalis ) from one-third to half an inch long in the intestine chiefly through the labours of  Theodor Bilharz  and  Griesinger  in Egypt (1854). [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8435", "text": "The symptoms can be linked to inflammation in the gut stimulated by feeding hookworms, such as nausea, abdominal pain and intermittent diarrhea, and to progressive anemia in prolonged disease:  capricious  appetite,  pica / geophagy  (or dirt-eating), obstinate constipation followed by  diarrhea ,  palpitations , thready pulse, coldness of the skin, pallor of the mucous membranes, fatigue and weakness, shortness of breath and in cases running a fatal course,  dysentery ,  hemorrhages  and  edema . [ 18 ]  The worms suck  blood  and damage the  mucosa . However, the blood loss in the stools is not visibly apparent. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8436", "text": "Blood tests in early infection often show a rise in numbers of eosinophils, a type of white blood cell that is preferentially stimulated by worm infections in tissues (large numbers of eosinophils are also present in the local inflammatory response). Falling blood hemoglobin levels will be seen in cases of prolonged infection with anemia. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8437", "text": "In contrast to most intestinal  helminthiases , where the heaviest parasitic loads tend to occur in children, hookworm prevalence and intensity can be higher among adult males. The explanation for this is that hookworm infection tends to be occupational so that coworkers and other close groups maintain a high prevalence of infection among themselves by contaminating their work environment. However, in most endemic areas, adult women are the most severely affected by anemia, mainly because they have much higher physiological needs for iron (menstruation, repeated pregnancy). An interesting consequence of this in the case of  Ancylostoma duodenale  infection is translactational transmission of infection: the skin-invasive larvae of this species do not all immediately pass through the lungs and on into the gut, but spread around the body via the circulation, to become dormant inside muscle fibers. In a pregnant woman, after childbirth some or all of these larvae are stimulated to re-enter the circulation (presumably by sudden hormonal changes), then to pass into the mammary glands, so that the newborn baby can receive a large dose of infective larvae through its mother's milk. This accounts for otherwise inexplicable cases of very heavy, even fatal, hookworm infections in children a month or so of age, in places such as China, India, and northern Australia.\nAn identical phenomenon is much more commonly seen with  Ancylostoma caninum  infections in dogs, where the newborn pups can even die of hemorrhaging from their intestines caused by massive numbers of feeding hookworms. This also reflects the close evolutionary link between the human and canine parasites, which probably have a common ancestor dating back to when humans and dogs first started living closely together.\nFilariform larvae are the infective stage of the parasite: infection occurs when larvae in soil penetrate the skin, or when they are ingested through contaminated food and water following skin penetration. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8438", "text": "Diagnosis depends on finding characteristic worm eggs on microscopic examination of the stools, although this is not possible in early infection. Early signs of infection in most dogs include limbular limping and anal itching. The eggs are oval or elliptical, measuring 60 by 40\u00a0\u03bcm, colorless, not  bile  stained, and with a thin transparent  hyaline  shell membrane. When released by the worm in the intestine, the egg contains an unsegmented  ovum . During its passage down the intestine, the ovum develops and thus the eggs passed in feces have a segmented ovum, usually with 4 to 8  blastomeres .\nAs the eggs of both  Ancylostoma  and  Necator  (and most other hookworm species) are indistinguishable, to identify the genus, they must be cultured in the lab to allow larvae to hatch out. If the fecal sample is left for a day or more under tropical conditions, the larvae will have hatched out, so eggs might no longer be evident. In such a case, it is essential to distinguish hookworms from  Strongyloides  larvae, as infection with the latter has more serious implications and requires different management. The larvae of the two hookworm species can also be distinguished microscopically, although this would not be done routinely, but usually for research purposes. Adult worms are rarely seen (except via endoscopy, surgery or autopsy), but if found, would allow definitive identification of the species. Classification can be performed based on the length of the buccal cavity, the space between the oral opening and the esophagus: hookworm rhabditoform larvae have long buccal cavities whereas  Strongyloides  rhabditoform larvae have short buccal cavities. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8439", "text": "Recent research has focused on the development of DNA-based tools for diagnosis of infection, specific identification of hookworm, and analysis of genetic variability within hookworm populations. [ 19 ]  Because hookworm eggs are often indistinguishable from other parasitic eggs,  PCR  assays could serve as a molecular approach for accurate diagnosis of hookworm in the feces. [ 19 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8440", "text": "The infective larvae develop and survive in an environment of damp dirt, particularly sandy and loamy soil. They cannot survive in clay or muck. The main lines of precaution are those dictated by good  hygiene  behaviors:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8441", "text": "Moxidectin  is available in the United States as ( imidacloprid  + moxidectin) topical solution for dogs and cats. It utilizes moxidectin for control and prevention of roundworms, hookworms,  heartworms , and  whipworms ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8442", "text": "Most of these public health concerns have focused on children who are infected with hookworm. This focus on children is largely due to the large body of evidence that has demonstrated strong associations between hookworm infection and impaired learning, increased absences from school, and decreased future economic productivity. [ 12 ]  In 2001, the 54th World Health Assembly passed a resolution demanding member states to attain a minimum target of regular deworming of at least 75% of all at-risk school children by the year 2010. [ 21 ]  A 2008 World Health Organization publication reported on these efforts to treat at-risk school children. Some of the interesting statistics were as follows: 1) only 9 out of 130 endemic countries were able to reach the 75% target goal; and 2) less than 77 million school-aged children (of the total 878 million at risk) were reached, which means that only 8.78% of at-risk children are being treated for hookworm infection. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8443", "text": "School-based  mass deworming  programs have been the most popular strategy to address the issue of hookworm infection in children. School-based programs are extremely cost-effective as schools already have an available, extensive, and sustained infrastructure with a skilled workforce that has a close relationship with the community. [ 21 ]  With little training from a local health system, teachers can easily administer the drugs which often cost less than US$0.50 per child per year. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8444", "text": "Recently, many people have questioned if the school-based programs are necessarily the most effective approach. An important concern with school-based programs is that they often do not reach children who do not attend school, thus ignoring a large number of at-risk children. A 2008 study by Massa  et al.  continued the debate regarding school-based programs. They examined the effects of community-directed treatments versus school-based treatments in the Tanga Region of Tanzania. A major conclusion was that the mean infection intensity of hookworm was significantly lower in the villages employing the community-directed treatment approach than the school-based approach. The community-directed treatment model used in this specific study allowed villagers to take control of the child's treatment by having villagers select their own community drug distributors to administer the antihelminthic drugs. Additionally, villagers organized and implemented their own methods for distributing the drugs to all children. [ 24 ]  The positive results associated with this new model highlight the need for large-scale community involvement in deworming campaigns. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8445", "text": "Many mass deworming programs also combine their efforts with public health education. These health education programs often stress important preventative techniques such as: washing your hands before eating and staying away from water/areas contaminated by human feces. These programs may also stress that shoes must be worn, however, these come with their own health risks and may not be effective. [ 25 ]  Shoe wearing patterns in towns and villages across the globe are determined by cultural beliefs, and the levels of education within that society. The wearing of shoes will prevent the entry of hookworm infections from the surrounding soils into tender skin regions; such as areas between the toes. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8446", "text": "Historical examples, such as the hookworm campaigns in Mississippi and Florida from 1943 to 1947 have shown that the primary cause of hookworm infection is poor sanitation, which can be solved by building and maintaining  toilets . But while these may seem like simple tasks, they raise important public health challenges. Most infected populations are from poverty-stricken areas with very poor sanitation. Thus, it is most likely that at-risk children do not have access to  clean water  to  wash their hands  and live in environments with no proper sanitation infrastructure. Health education, therefore, must address preventive measures in ways that are both feasible and sustainable in the context of resource-limited settings. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8447", "text": "Evaluation of numerous public health interventions has generally shown that improvement in each individual component ordinarily attributed to poverty (for example, sanitation, health education, and underlying nutrition status) often has minimal impact on transmission. For example, one study found that the introduction of latrines into a resource-limited community only reduced the prevalence of hookworm infection by four percent. [ 27 ]  However, another study in Salvador, Brazil found that improved  drainage  and  sewerage  had a  significant impact  on the prevalence of hookworm infection but no impact at all on the intensity of hookworm infection. [ 28 ]  This seems to suggest that environmental control alone has a limited but incomplete effect on the transmission of hookworms. It is imperative, therefore, that more research is performed to understand the efficacy and sustainability of integrated programs that combine numerous preventive methods including education, sanitation, and treatment."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8448", "text": "The most common treatments for hookworm are  benzimidazoles , specifically  albendazole  and  mebendazole . BZAs kill adult worms by binding to the nematode's \u03b2- tubulin  and subsequently inhibiting  microtubule  polymerization within the parasite. [ 14 ]  In certain circumstances,  levamisole  and  pyrantel pamoate  may be used. [ 12 ]  A 2008 review found that the efficacy of single-dose treatments for hookworm infections were as follows: 72% for albendazole, 15% for mebendazole, and 31% for pyrantel pamoate. [ 29 ]  This substantiates prior claims that albendazole is much more effective than mebendazole for hookworm infections. Also of note is that the World Health Organization does recommend anthelmintic treatment in pregnant women after the first trimester. [ 14 ]  It is also recommended that if the patient also has anemia that  ferrous sulfate  (200\u00a0mg) be administered three times daily at the same time as anthelmintic treatment; this should be continued until hemoglobin values return to normal which could take up to 3 months. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8449", "text": "Hookworm infection can be treated with local  cryotherapy  when the hookworm is still in the skin. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8450", "text": "Albendazole is effective both in the intestinal stage and during the stage the parasite is still migrating under the skin. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8451", "text": "In the case of anemia,  iron  supplementation can cause relief symptoms of  iron-deficiency anemia . However, as red blood cell levels are restored, a shortage of other essentials such as  folic acid  or  vitamin B 12  may develop, so these might also be supplemented."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8452", "text": "During the 1910s, common treatments for hookworm included  thymol ,  2-naphthol ,  chloroform ,  gasoline , and  eucalyptus oil . [ 31 ]  By the 1940s, the treatment of choice used  tetrachloroethylene , [ 32 ]  given as 3 to 4 cc in the fasting state, followed by 30 to 45 g of  sodium sulfate . Tetrachloroethylene was reported to have a cure rate of 80 percent for Necator infections, but 25 percent in Ancylostoma infections, and often produced mild intoxication in the patient."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8453", "text": "Other important issues related to the treatment of hookworm are reinfection and drug resistance. It has been shown that reinfection after treatment can be extremely high. Some studies even show that 80% of pretreatment hookworm infection rates can be seen in treated communities within 30\u201336 months. [ 14 ]  While reinfection may occur, it is still recommended that regular treatments be conducted as it will minimize the occurrence of chronic outcomes. There are also increasing concerns about the issue of drug resistance. Drug resistance has appeared in front-line anthelmintics used for livestock nematodes. Generally, human nematodes are less likely to develop resistance due to longer reproducing times, less frequent treatment, and more targeted treatment. Nonetheless, the global community must be careful to maintain the effectiveness of current anthelmintic as no new anthelmintic drugs are in the late-stage development. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8454", "text": "It is estimated that between 576 and 740 million individuals are infected with hookworm. [ 33 ] [ 14 ]  Of these infected individuals, about 80 million are severely affected. [ 19 ]  The major cause of hookworm infection is  N. americanus  which is found in the Americas, sub-Saharan Africa, and Asia. [ 12 ]   A. duodenale  is found in more scattered focal environments, namely Europe and the Mediterranean. Most infected individuals are concentrated in sub-Saharan Africa and East Asia/the Pacific Islands with each region having estimates of 198 million and 149 million infected individuals, respectively. Other affected regions include: South Asia (50 million), Latin America and the Caribbean (50 million), South Asia (59 million), and Middle East/North Africa (10 million). [ 14 ]  A majority of these infected individuals live in poverty-stricken areas with poor sanitation. Hookworm infection is most concentrated among the world's poorest who live on less than $2 a day. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8455", "text": "While hookworm infection may not directly lead to mortality, its effects on morbidity demand immediate attention. When considering  disability-adjusted life years  (DALYs), neglected tropical diseases, including hookworm infection, rank among diarrheal diseases,  ischemic heart disease ,  malaria , and  tuberculosis  as one of the most important health problems of the developing world."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8456", "text": "It has been estimated that as many as 22.1 million  DALYs  have been lost due to hookworm infection. Recently, there has been increasing interest to address the public health concerns associated with hookworm infection. For example, the  Bill & Melinda Gates Foundation  recently donated US$34 million to fight Neglected Tropical Diseases including hookworm infection. [ 34 ]  Former US President Clinton also announced a mega-commitment at the Clinton Global Initiative (CGI) 2008 Annual Meeting to de-worm 10 million children. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8457", "text": "Many of the numbers regarding the prevalence of hookworm infection are estimates as there is no international surveillance mechanism currently in place to determine prevalence and global distribution. [ 12 ]  Some prevalence rates have been measured through survey data in endemic regions around the world. The following are some of the most recent findings on prevalence rates in regions endemic with hookworm."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8458", "text": "Darjeeling ,  Hooghly District ,  West Bengal , India  (Pal  et al.  2007) [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8459", "text": "Xiulongkan  Village,  Hainan Province , China  (Gandhi  et al.  2001) [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8460", "text": "H\u00f2a B\u00ecnh , Northwest Vietnam  (Verle  et al.  2003) [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8461", "text": "Minas Gerais , Brazil  (Fleming  et al.  2006) [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8462", "text": "KwaZulu-Natal , South Africa  (Mabaso  et al.  2004) [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8463", "text": "Lowndes County, Alabama ,  United States   [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8464", "text": "There have also been technological developments that may facilitate more accurate mapping of hookworm prevalence. Some researchers have begun to use geographical information systems (GIS) and  remote sensing  (RS) to examine helminth ecology and epidemiology. Brooker  et al.  utilized this technology to create helminth distribution maps of sub-Saharan Africa. By relating satellite-derived environmental data with prevalence data from school-based surveys, they were able to create detailed prevalence maps. The study focused on a wide range of helminths, but interesting conclusions about hookworm specifically were found. As compared to other helminths, hookworms can survive in much hotter conditions and were highly prevalent throughout the upper end of the thermal range. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8465", "text": "Improved molecular diagnostic tools are another technological advancement that could help improve existing prevalence statistics. Recent research has focused on the development of a DNA-based tool that can be used for diagnosis of infection, specific identification of hookworm, and analysis of genetic variability in hookworm populations. Again this can serve as a major tool for different public health measures against hookworm infection. Most research regarding diagnostic tools is now focused on the creation of a rapid and cost-effective assay for the specific diagnosis of hookworm infection. Many are hopeful that its development can be achieved within the next five years. [ when? ] [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8466", "text": "The symptoms now attributed to hookworm appear in  papyrus  papers of ancient  Egypt  ( c. \u20091500 BC ), described as a derangement characterized by anemia.  Avicenna , a Persian physician of the eleventh century, discovered the worm in several of his patients and related it to their disease. In later times, the condition was noticeably prevalent in the mining industry in  England ,  France ,  Germany ,  Belgium ,  North Queensland , and elsewhere. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8467", "text": "Italian physician  Angelo Dubini  was the modern-day discoverer of the worm in 1838 after an  autopsy  of a peasant woman. Dubini published details in 1843 and identified the species as  A. duodenale . [ 44 ]  Working in the Egyptian medical system in 1852 German physician  Theodor Bilharz , drawing upon the work of colleague  Wilhelm Griesinger , found these worms during autopsies and went a step further in linking them to local endemic occurrences of  chlorosis , which would probably be called  iron-deficiency anemia  today."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8468", "text": "A breakthrough came 25 years later following a  diarrhea  and  anemia  epidemic that took place among  Italian  workmen employed on the  Gotthard Rail Tunnel . [ 18 ]  In an 1880 paper, physicians  Camillo Bozzolo ,  Edoardo Perroncito , and  Luigi Pagliani  correctly hypothesized that hookworm was linked to the fact that workers had to defecate inside the 15\u00a0km tunnel, and that many wore worn-out shoes. [ 45 ]  The work environment often contained standing water, sometimes knee-deep, and the larvae were capable of surviving several weeks in the water, allowing them to infect many of the workers. In 1897, it was established that the skin was the principal avenue of infection and the  biological life cycle  of the hookworm was clarified."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8469", "text": "In 1899, American zoologist  Charles Wardell Stiles  identified progressive  pernicious anemia  seen in the southern United States as being caused by the hookworm  A. duodenale . Testing in the 1900s revealed very heavy infestations in school-age children. In  Puerto Rico , Dr. Bailey K. Ashford, a US Army physician, organized and conducted a parasite treatment campaign, which cured approximately 300,000 people (one-third of the Puerto Rican population) and reduced the death rate from this anemia by 90 percent during the years 1903\u201304."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8470", "text": "On October 26, 1909, the Rockefeller Sanitary Commission for the Eradication of Hookworm Disease was organized as a result of a gift of US$1 million from  John D. Rockefeller , Sr. The five-year program was a remarkable success and a great contribution to the United States' public health, instilling public education, medication, field work and modern government health departments in eleven southern states. [ 46 ] \nThe hookworm exhibit was a prominent part of the 1910 Mississippi State Fair."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8471", "text": "The commission found that an average of 40% of school-aged children were infected with hookworm. Areas with higher levels of hookworm infection prior to the eradication program experienced greater increases in school enrollment, attendance, and literacy after the intervention. Econometric studies have shown that this effect cannot be explained by a variety of alternative factors, including differential trends across areas, changing crop prices, shifts in certain educational and health policies, and the effect of malaria eradication. [ 47 ]  No significant contemporaneous results were found for adults who should have benefited less from the intervention owing to their substantially lower (prior) infection rates. The program nearly eradicated hookworm and would flourish afterward with new funding as the  Rockefeller Foundation   International Health Division . [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8472", "text": "The RF's hookworm campaign in Mexico showed how science and politics play a role in developing health policies. It brought together government officials, health officials, public health workers, Rockefeller officials, and the community. This campaign was launched to eradicate hookworms in Mexico. Although the campaign did not focus on long-term treatments, it did set the terms of the relationship between Mexico and the Rockefeller Foundation. The scientific knowledge behind this campaign helped shape public health policies, improved public health and built a strong relationship between US and Mexico. [ 49 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8473", "text": "In the 1920s, hookworm eradication reached the Caribbean and Latin America, where great mortality was reported among people in the  West Indies  towards the end of the 18th century, as well as through descriptions sent from  Brazil  and various other tropical and subtropical regions. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8474", "text": "Treatment in the early 20th century relied on the use of  Epsom salt  to reduce protective mucus, followed by  thymol  to kill the worms. [ 50 ] [ 31 ]  By the 1940s,  tetrachloroethylene  was the leading method. [ 32 ]  It was not until later in the mid-20th century when new organic drug compounds were developed. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8475", "text": "It is estimated that a third of all pregnant women in developing countries are infected with hookworm, 56% of all pregnant women in developing countries experience anemia, and 20% of all maternal deaths are either directly or indirectly related to anemia. Numbers like this have led to an increased interest in the topic of hookworm-related anemia during pregnancy. [ 52 ]  With the understanding that chronic hookworm infection can often lead to anemia, many people are now questioning if the treatment of hookworm could effect change in severe anemia rates and thus also on maternal and child health as well. Most evidence suggests that the contribution of hookworm to maternal anemia merits that all women of child-bearing age living in endemic areas be subject to periodic anthelmintic treatment. The World Health Organization even recommends that infected pregnant women be treated after their first trimester. [ 14 ]  Regardless of these suggestions, only Madagascar, Nepal, and Sri Lanka have added deworming to their antenatal care programs. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8476", "text": "This lack of deworming of pregnant women is explained by the fact that most individuals still fear that anthelmintic treatment will result in adverse birth outcomes. However, a 2006 study by Gyorkos et al. found that when comparing a group of pregnant women treated with mebendazole with a control placebo group, both illustrated rather similar rates of adverse birth outcomes. The treated group demonstrated 5.6% adverse birth outcomes, while the control group had 6.25% adverse birth outcomes. [ 52 ]  Furthermore, Larocque et al. illustrated that treatment for hookworm infection actually led to positive health results in the infant. This study concluded that treatment with mebendazole plus iron supplements during antenatal care significantly reduced the proportion of very low birth weight infants when compared to a placebo control group. [ 54 ]  Studies so far have validated recommendations to treat infected pregnant women for hookworm infection during pregnancy."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8477", "text": "A review found that a single dose of  antihelminthics  (anti-worm drugs) given in the second trimester of pregnancy \"may reduce maternal anaemia and worm prevalence when used in settings with a high prevalence of maternal helminthiasis\". [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8478", "text": "The intensity of hookworm infection as well as the species of hookworm have yet to be studied as they relate to hookworm-related anemia during pregnancy. Additionally, more research must be done in different regions of the world to see if trends noted in completed studies persist. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8479", "text": "Co-infection with hookworm and  Plasmodium falciparum  is common in Africa. [ 56 ]  Although exact numbers are unknown, preliminary analyses estimate that as many as a quarter of African schoolchildren (17.8\u201332.1 million children aged 5\u201314 years) may be coincidentally at-risk of both  P. falciparum  and hookworm. [ 57 ]  While original hypotheses stated that co-infection with multiple parasites would impair the host's immune response to a single parasite and increase susceptibility to clinical disease, studies have yielded contrasting results. For example, one study in Senegal showed that the risk of clinical malaria infection was increased in helminth-infected children in comparison to helminth-free children while other studies have failed to reproduce such results, [ 58 ]  and even among laboratory mouse experiments the effect of helminths on malaria is variable. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8480", "text": "Some hypotheses and studies suggest that helminth infections may protect against cerebral malaria due to the possible modulation of pro-inflammatory and anti-inflammatory cytokine responses. [ 60 ]  Furthermore, the mechanisms underlying this supposed increased susceptibility to disease are unknown. For example, helminth infections cause potent and highly polarized immune response characterized by increased  T-helper cell  type 2 (T h 2)  cytokine  and  Immunoglobulin E  (IgE) production. [ 61 ]  However, the effect of such responses on the human immune response is unknown. Additionally, both malaria and helminth infection can cause anemia, but the effect of co-infection and possible enhancement of anemia is poorly understood. [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8481", "text": "The  hygiene hypothesis  states that infants and children who lack exposure to infectious agents are more susceptible to allergic diseases via modulation of immune system development. The theory was first proposed by David P. Strachan who noted that  hay fever  and  eczema  were less common in children who belonged to large families. [ 62 ]  Since then, studies have noted the effect of gastrointestinal worms on the development of allergies in the developing world. For example, a study in Gambia found that the eradication of worms in some villages led to increased skin reactions to allergies among children. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8482", "text": "While annual or semi-annual mass antihelminthic administration is a critical aspect of any public health intervention, many have begun to realize how unsustainable it is due to aspects such as poverty, high rates of re-infection, and diminished efficacy of drugs with repeated use. Current research, therefore, has focused on the development of a vaccine that could be integrated into existing control programs. The goal of vaccine development is not necessarily to create a vaccine with sterilizing immunity or complete protection against immunity. A vaccine that reduces the likelihood of vaccinated individuals developing severe infections and thus reduced blood and nutrient levels could still have a significant impact on the high burden of disease throughout the world."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8483", "text": "Current research focuses on targeting two stages in the development of the worm: the larval stage and the adult stage. Research on larval antigens has focused on proteins that are members of the  pathogenesis-related protein  superfamily,  Ancylostoma  Secreted Proteins. [ 64 ]  Although they were first described in  Anyclostoma , these proteins have also been successfully isolated from the secreted product of  N. americanus .  N. americanus  ASP-2 (Na-ASP-2) is currently the leading larval-stage hookworm vaccine candidate. A randomized, double-blind, placebo-controlled study has already been performed; 36 healthy adults without a history of hookworm infection were given three intramuscular injections of three different concentrations of Na-ASP-2 and observed for six months after the final vaccination. [ 65 ]  The vaccine induced significant anti-Na-ASP-2 IgG and cellular immune responses. In addition, it was safe and produced no debilitating side effects. The vaccine is now in a phase one trial; healthy adult volunteers with documented evidence of previous infection in Brazil are being given the same  dose concentration  on the same schedule used in the initial study. [ 64 ]  If this study is successful, the next step would be to conduct a phase two trial to assess the rate and intensity of hookworm infection among vaccinated persons. Because the Na-ASP-2 vaccine only targets the larval stage, it is critical that all subjects enrolled in the study be treated with antihelminthic drugs to eliminate adult worms prior to vaccination."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8484", "text": "Adult hookworm antigens have also been identified as potential candidates for vaccines. When adult worms attach to the intestinal mucosa of the human host, erythrocytes are ruptured in the worm's digestive tract which causes the release of free hemoglobin which is subsequently degraded by a proteolytic cascade. Several of these proteins that are responsible for this proteolytic cascade are also essential for the worm's nutrition and survival. [ 66 ]  Therefore, a vaccine that could induce antibodies for these antigens could interfere with the hookworm's digestive pathway and impair the worm's survival. Three proteins have been identified: the aspartic protease-hemoglobinase APR-1, the cysteine protease-hemoglobinase CP-2, and a glutathione S-transferase. [ 67 ] [ 68 ] [ 69 ]  Vaccination with APR-1 and CP-2 led to reduced host blood loss and fecal egg counts in dogs. [ 67 ] [ 68 ]  With APR-1, vaccination even led to reduced worm burden. [ 67 ]  Research is currently stymied at the development of at least one of these antigens as a recombinant protein for testing in clinical trials."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8485", "text": "The term \"hookworm\" is sometimes used to refer to hookworm infection. [ 12 ]  A hookworm is a type of parasitic worm ( helminth )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8486", "text": "Intestinal capillariasis  is a disease in the group of  helminthiasis  diseases caused by the  nematode   Capillaria philippinensis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8487", "text": "Symptoms in infested humans include watery  diarrhea , abdominal pain,  edema , weight loss,  borborygmus  (stomach growling), and depressed levels of  potassium  and  albumin  in the blood.  In humans, the parasites damage the cells of the intestinal wall.  This damage interferes with the absorption of nutrients and the maintenance of a proper  electrolyte  balance.  Untreated  C. philippinensis  infestations are often fatal. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8488", "text": "Diagnosis usually involves finding the eggs and/or adults of  C. philippinensis  in stool samples. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8489", "text": "Prevention is as simple as avoiding eating small, whole, uncooked fish.  However, in  C. philippinensis   endemic  areas, such dietary habits are common and have been practiced for many generations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8490", "text": "Anthelmintics  such as  mebendazole  and  albendazole  have been reported to eliminate infestation of humans more effectively than  thiabendazole . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8491", "text": "Irritable bowel syndrome  ( IBS ) is a  functional gastrointestinal disorder  characterized by a group of symptoms that commonly include  abdominal pain , abdominal bloating and changes in the consistency of  bowel movements . [ 1 ]  These symptoms may occur over a long time, sometimes for years. [ 2 ]  IBS can negatively affect  quality of life  and may result in missed school or work or reduced productivity at work. [ 13 ]  Disorders such as  anxiety ,  major depression , and  myalgic encephalomyelitis/chronic fatigue syndrome  (ME/CFS) are common among people with IBS. [ 1 ] [ 14 ] [ note 1 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8492", "text": "The cause of IBS is not known but multiple factors have been proposed to lead to the condition. [ 2 ]  Theories include combinations of \" gut\u2013brain axis \" problems, alterations in  gut motility , visceral hypersensitivity, infections including  small intestinal bacterial overgrowth ,  neurotransmitters , genetic factors, and  food sensitivity . [ 2 ]  Onset may be triggered by a  stressful  life event, [ 16 ]  or an  intestinal infection . [ 17 ]  In the latter case, it is called  post-infectious irritable bowel syndrome . [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8493", "text": "Diagnosis is based on symptoms in the absence of worrisome features and once other potential conditions have been ruled out. [ 7 ]  Worrisome or \"alarm\" features include onset at greater than 50 years of age, weight loss,  blood in the stool , or a family history of  inflammatory bowel disease . [ 7 ]  Other conditions that may present similarly include  celiac disease ,  microscopic colitis , inflammatory bowel disease,  bile acid malabsorption , and  colon cancer . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8494", "text": "Treatment of IBS is carried out to improve symptoms. This may include dietary changes, medication,  probiotics , and  counseling . [ 9 ] [ 18 ]  Dietary measures include increasing  soluble fiber  intake, or a  diet low in fermentable oligosaccharides, disaccharides, monosaccharides, and polyols  (FODMAPs). The \"low FODMAP\" diet is meant for short to medium term use and is not intended as a life-long therapy. [ 7 ] [ 19 ] [ 20 ]  The medication  loperamide  may be used to help with diarrhea while  laxatives  may be used to help with constipation. [ 7 ]  There is strong clinical-trial evidence for the use of  antidepressants , often in lower doses than that used for depression or anxiety, even in patients without comorbid mood disorder.  Tricyclic antidepressants  such as  amitriptyline  or  nortriptyline  and medications from the  selective serotonin reuptake inhibitor  (SSRI) group may improve overall symptoms and reduce pain. [ 7 ]   Patient education  and a good  doctor\u2013patient relationship  are an important part of care. [ 7 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8495", "text": "About 10\u201315% of people in the  developed world  are believed to be affected by IBS. [ 1 ] [ 11 ]  The prevalence varies according to country (from 1.1% to 45.0%) and criteria used to define IBS; however the average global prevalence is 11.2%. [ 12 ]  It is more common in  South America  and less common in  Southeast Asia . [ 7 ]  In the  Western world , it is twice as common in women as men and typically occurs before age 45. [ 1 ]  However, women in  East Asia  are not more likely than their male counterparts to have IBS, indicating much lower rates among East Asian women. [ 22 ]  Similarly, men from South America, South Asia and Africa are just as likely to have IBS as women in those regions, if not more so. [ 23 ]  The condition appears to become less common with age. [ 7 ]  IBS does not affect life expectancy or lead to other serious diseases. [ 10 ]  The first description of the condition was in 1820, while the current term  irritable bowel syndrome  came into use in 1944. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8496", "text": "The primary symptoms of IBS are  abdominal pain  or discomfort in association with frequent diarrhea or constipation and a change in bowel habits. [ 25 ]  Symptoms usually are experienced as acute attacks that subside within one day, but recurrent attacks are likely. [ 26 ]  There may also be urgency for bowel movements, a feeling of incomplete evacuation ( tenesmus ) or bloating. [ 27 ]  In some cases, the symptoms are relieved by  bowel movements . [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8497", "text": "People with IBS, more commonly than others, have  gastroesophageal reflux , symptoms relating to the  genitourinary system ,  fibromyalgia ,  headache ,  backache , and psychiatric symptoms such as depression, sleep disorders, [ 28 ]  and  anxiety . [ 14 ] [ 27 ]  About a third of adults who have IBS also report  sexual dysfunction , typically in the form of a reduction in  libido . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8498", "text": "While the causes of IBS are still unknown, it is believed that the entire  gut\u2013brain axis  is affected. [ 30 ] [ 31 ]  Recent findings suggest that an allergy triggered peripheral immune mechanism may underlie the symptoms associated with abdominal pain in patients with irritable bowel syndrome. [ 32 ]  IBS is more prevalent in obese patients. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8499", "text": "People who are younger than 50, women, and those with a family history of the condition are more likely to develop IBS. [ 34 ]  Further risk factors are  anxiety ,  depression , and  stress . [ 35 ]  The risk of developing IBS increases six-fold after having a gastrointestinal infection ( gastroenteritis ). [ 34 ]  This is also called  post-infectious IBS . The risk of developing IBS following an infection is further increased in those who also had a prolonged fever during the illness. [ 36 ]  Antibiotic use also appears to increase the risk of developing IBS. [ 37 ]  Genetic defects in  innate immunity  and  epithelial  homeostasis increase the risk of developing both post-infectious as well as other forms of IBS. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8500", "text": "The role of the brain\u2013gut axis in IBS has been suggested since the 1990s [ 4 ]  and childhood physical and psychological abuse is often associated with the development of IBS. [ 6 ]  It is believed that psychological stress may trigger IBS in predisposed individuals. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8501", "text": "Given the high levels of anxiety experienced by people with IBS and the overlap with conditions such as  fibromyalgia  and  chronic fatigue syndrome , a potential explanation for IBS involves a disruption of the stress system. The stress response in the body involves the  hypothalamic\u2013pituitary\u2013adrenal axis  (HPA) and the  sympathetic nervous system , both of which have been shown to operate abnormally in people with IBS. Psychiatric illness or anxiety precedes IBS symptoms in two-thirds of people with IBS, and psychological traits predispose previously healthy people to developing IBS after gastroenteritis. [ 39 ] [ 40 ]  Individuals with IBS also report high rates of sleep disturbances such as trouble falling asleep and frequent arousal throughout the night. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8502", "text": "Approximately 10 percent of IBS cases are triggered by an acute  gastroenteritis  infection. [ 42 ]  The  CdtB toxin  is produced by bacteria causing gastroenteritis and the host may develop an  autoimmunity  when host antibodies to CdtB cross-react with  vinculin . [ 43 ]  Genetic defects relating to the  innate immune system  and epithelial barrier as well as high stress and anxiety levels appear to increase the risk of developing post-infectious IBS. Post-infectious IBS usually manifests itself as the diarrhea-predominant subtype. Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes increased  gut permeability  leading to  translocation  of the  commensal  bacteria across the  epithelial  barrier; this in turn can result in significant damage to local tissues, which can develop into chronic gut abnormalities in sensitive individuals. However, increased gut permeability is strongly associated with IBS regardless of whether IBS was initiated by an infection or not. [ 38 ]  A link between  small intestinal bacterial overgrowth  and  tropical sprue  has been proposed to be involved as a cause of post-infectious IBS. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8503", "text": "Small intestinal bacterial overgrowth  (SIBO) occurs with greater frequency in people who have been diagnosed with IBS compared to healthy controls. [ 45 ]  SIBO is most common in diarrhea-predominant IBS but also occurs in constipation-predominant IBS more frequently than healthy controls. Symptoms of SIBO include bloating, abdominal pain, diarrhea or constipation among others. IBS may be the result of the immune system interacting abnormally with gut microbiota resulting in an abnormal  cytokine  signalling profile. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8504", "text": "Certain bacteria are found in lower or higher abundance when compared with healthy individuals. Generally  Bacteroidota ,  Bacillota , and  Pseudomonadota  are increased and  Actinomycetota ,  Bifidobacteria , and  Lactobacillus  are decreased. Within the human gut, there are common phyla found. The most common is Bacillota. This includes  Lactobacillus , which is found to have a decrease in people with IBS, and  Streptococcus , which is shown to have an increase in abundance. Within this phylum, species in the class  Clostridia  are shown to have an increase, specifically  Ruminococcus  and  Dorea . The family  Lachnospiraceae  presents an increase in IBS-D patients. The second most common phylum is Bacteroidota. In people with IBS, the Bacteroidota phylum has been shown to have an overall decrease, but an increase in the genus  Bacteroides . IBS-D shows a decrease for the phylum Actinomycetota and an increase in Pseudomonadota, specifically in the family  Enterobacteriaceae . [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8505", "text": "Alterations of  gut microbiota  ( dysbiosis ) are associated with the intestinal manifestations of IBS, but also with the psychiatric morbidity that coexists in up to 80% of people with IBS. [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8506", "text": "Protozoal  infections can cause symptoms that mirror specific IBS subtypes, [ 51 ]  e.g., infection by certain substypes of  Blastocystis hominis  ( blastocystosis ). [ 52 ] [ 53 ]  Many people regard these organisms as incidental findings, and unrelated to symptoms of IBS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8507", "text": "Blastocystis and  Dientamoeba fragilis  colonisation occurs more commonly in IBS affected individuals but their role in the condition is unclear. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8508", "text": "Vitamin D deficiency  is more common in individuals affected by IBS. [ 55 ] [ 56 ]  Vitamin D is involved in regulating triggers for IBS including the gut microbiome, inflammatory processes and immune responses, as well as psychosocial factors. [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8509", "text": "SCN5A   mutations  are found in a small number of people who have IBS, particularly the constipation-predominant variant (IBS-C). [ 58 ] [ 59 ]  The resulting defect leads to disruption in bowel function, by affecting the  Nav1.5  channel, in smooth muscle of the colon and  pacemaker cells . [ 60 ] [ 61 ] [ 62 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8510", "text": "Genetic, environmental, and psychological factors seem to be important in the development of IBS. The condition also has a genetic component even though there is a predominant influence of environmental factors. [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8511", "text": "Dysregulated brain-gut axis, abnormal  serotonin / 5-hydroxytryptamine  (5-HT) metabolism, and high density of mucosal  nerve fibers  in the intestines have been implicated in the mechanisms of IBS. A number of  5-HT receptor  subtypes were involved in the IBS symptoms, including  5-HT 3 ,  5-HT 4 , and  5-HT 7  receptors. High levels of 5-HT 7  receptor-expressing mucosal nerve fibers were observed in the colon of IBS patients. A role of  5-HT7 receptor  in intestinal  hyperalgesia  was demonstrated in mouse models with  visceral hypersensitivity , of which a novel 5-HT 7  receptor antagonist administered by mouth reduced intestinal pain levels. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8512", "text": "Abnormalities occur in the gut flora of individuals who have IBS, such as reduced diversity, a decrease in bacteria belonging to the phylum  Bacteroidota , and an increase in those belonging to the phylum  Bacillota . [ 48 ]  The changes in gut flora are most profound in individuals who have diarrhoea-predominant IBS. Antibodies against common components (namely  flagellin ) of the commensal gut flora are a common occurrence in IBS affected individuals. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8513", "text": "Chronic low-grade inflammation commonly occurs in IBS affected individuals with abnormalities found including increased  enterochromaffin cells ,  intraepithelial lymphocytes , and  mast cells  resulting in chronic immune-mediated inflammation of the gut mucosa. [ 30 ] [ 66 ]  IBS has been reported in greater quantities in multigenerational families with IBS than in the regular population. [ 67 ]  It is believed that psychological stress can induce increased inflammation and thereby cause IBS to develop in predisposed individuals. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8514", "text": "No specific laboratory or imaging tests can diagnose irritable bowel syndrome. Diagnosis should be based on symptoms, the exclusion of worrisome features, and the performance of specific investigations to rule out organic diseases that may present similar symptoms. [ 7 ] [ 68 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8515", "text": "The recommendations for physicians are to minimize the use of medical investigations. [ 69 ]  The  Rome criteria  are typically used for diagnosis. They allow the diagnosis to be based only on symptoms, but no criteria based solely on symptoms is sufficiently accurate to diagnose IBS. [ 70 ] [ 71 ]  Worrisome features include onset at greater than 50 years of age, weight loss,  blood in the stool ,  iron-deficiency anemia , or a family history of  colon cancer ,  celiac disease , or  inflammatory bowel disease . [ 7 ]  The criteria for selecting tests and investigations also depends on the level of available medical resources. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8516", "text": "The Rome IV criteria for diagnosing IBS include recurrent abdominal pain, on average, at least one day/week in the last three months, associated with additional stool- or defecation-related criteria. [ 73 ]  The algorithm may include additional tests to guard against misdiagnosis of other diseases as IBS.  Such \"red flag\" symptoms that may indicate other diseases as well include weight loss, gastrointestinal bleeding, anemia, or nocturnal symptoms. However, red flag conditions may not always contribute to accuracy in diagnosis; for instance, as many as 31% of people with IBS have blood in their stool, many possibly from  hemorrhoidal  bleeding. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8517", "text": "Investigations are performed to exclude other conditions: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8518", "text": "Colon cancer ,  inflammatory bowel disease ,  thyroid  disorders ( hyperthyroidism  or  hypothyroidism ), and  giardiasis  can all feature abnormal defecation and abdominal pain. Less common causes of this symptom profile are  carcinoid syndrome ,  microscopic colitis ,  bacterial overgrowth , and  eosinophilic gastroenteritis ; IBS is, however, a common presentation, and testing for these conditions would yield low numbers of positive results, so it is considered difficult to justify the expense. [ 75 ]  Conditions that may present similarly include celiac disease,  bile acid malabsorption , colon cancer, and  dyssynergic defecation . [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8519", "text": "Ruling out parasitic infections,  lactose intolerance , small intestinal bacterial overgrowth, and celiac disease is recommended before a diagnosis of IBS is made. [ 68 ]  An  upper endoscopy  with  small bowel   biopsies  is necessary to identify the presence of celiac disease. [ 76 ]  An ileocolonoscopy with biopsies is useful to exclude  Crohn's disease  and  ulcerative colitis  (Inflammatory bowel disease). [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8520", "text": "Some people, managed for years for IBS, may have  non-celiac gluten sensitivity  (NCGS). [ 8 ]  Gastrointestinal symptoms of IBS are clinically indistinguishable from those of NCGS, but the presence of any of the following non-intestinal manifestations suggest a possible NCGS:  headache  or  migraine , \"foggy mind\",  chronic fatigue , [ 77 ]   fibromyalgia , [ 78 ] [ 79 ] [ 80 ]  joint and muscle pain, [ 77 ] [ 78 ] [ 81 ]  leg or arm  numbness , [ 77 ] [ 78 ] [ 81 ]   tingling  of the extremities, [ 77 ] [ 81 ]  dermatitis ( eczema  or  skin rash ), [ 77 ] [ 81 ]   atopic disorders , [ 77 ]   allergy  to one or more inhalants, foods or metals [ 77 ] [ 78 ]  (such as  mites ,  graminaceae ,  parietaria , cat or dog hair/dander,  shellfish , or  nickel [ 78 ] ),  depression , [ 77 ] [ 78 ] [ 81 ]   anxiety , [ 78 ]   anemia , [ 77 ] [ 81 ]   iron-deficiency anemia ,  folate deficiency ,  asthma ,  rhinitis ,  eating disorders , [ 78 ]   neuropsychiatric disorders  (such as  schizophrenia , [ 81 ] [ 82 ]   autism , [ 78 ] [ 81 ] [ 82 ]   peripheral neuropathy , [ 81 ] [ 82 ]   ataxia , [ 82 ]   attention deficit hyperactivity disorder [ 77 ] ) or  autoimmune diseases . [ 77 ]  An improvement with a  gluten-free diet  of immune-mediated symptoms, including autoimmune diseases, once having reasonably ruled out  celiac disease  and  wheat allergy , is another way to realize a differential diagnosis. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8521", "text": "People with IBS are at increased risk of being given inappropriate surgeries such as  appendectomy ,  cholecystectomy , and  hysterectomy  due to being misdiagnosed as other medical conditions. [ 83 ]  Some common examples of misdiagnosis include  infectious diseases ,  coeliac disease , [ 84 ]   Helicobacter pylori , [ 85 ] [ 86 ]   parasites  (non- protozoal ). [ 51 ] [ 87 ] [ 88 ]  The American College of Gastroenterology recommends all people with symptoms of IBS be tested for coeliac disease. [ 89 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8522", "text": "Bile acid malabsorption  is also sometimes missed in people with diarrhea-predominant IBS.  SeHCAT  tests suggest around 30% of people with D-IBS have this condition, and most respond to  bile acid sequestrants . [ 90 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8523", "text": "Several medical conditions, or  comorbidities , appear with greater frequency in people with IBS."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8524", "text": "IBS can be classified as  diarrhea -predominant (IBS-D),  constipation -predominant (IBS-C), with mixed/alternating stool pattern (IBS-M/IBS-A) or pain-predominant. [ 104 ]  In some individuals, IBS may have an acute onset and develop after an  infectious  illness characterized by two or more of: fever, vomiting, diarrhea, or positive  stool culture . This post-infective syndrome has consequently been termed \"post-infectious IBS\" (IBS-PI). [ 105 ] [ 106 ] [ 107 ] [ 108 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8525", "text": "A number of treatments have been found to be effective, including fiber,  talk therapy ,  antispasmodic  and  antidepressant  medication, and peppermint oil. [ 109 ] [ 110 ] [ 111 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8526", "text": "FODMAPs  are short-chain carbohydrates that are poorly absorbed in the small intestine. A 2018 systematic review found that although there is evidence of improved IBS symptoms with a  low-FODMAP diet , the evidence is of very low quality. [ 112 ]  Symptoms most likely to improve on this type of diet include urgency,  flatulence ,  bloating , [ 113 ]  abdominal pain, and altered stool output. One national guideline advises a low FODMAP diet for managing IBS when other dietary and lifestyle measures have been unsuccessful. [ 114 ]  The diet restricts various carbohydrates which are poorly absorbed in the  small intestine , as well as  fructose  and  lactose , which are similarly poorly absorbed in those with intolerances to them. Reduction of fructose and  fructan  has been shown to reduce IBS symptoms in a dose-dependent manner in people with  fructose malabsorption  and IBS. [ 115 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8527", "text": "FODMAPs are fermentable  oligo- ,  di- ,  monosaccharides  and  polyols , which are poorly absorbed in the small intestine and subsequently fermented by the bacteria in the distal small and proximal  large intestine . This is a normal phenomenon, common to everyone. The resultant production of gas potentially results in bloating and flatulence. [ 116 ]  Although FODMAPs can produce certain digestive discomfort in some people, not only do they not cause intestinal inflammation, but they help avoid it, because they produce beneficial alterations in the intestinal flora that contribute to maintaining the good health of the colon. [ 117 ] [ 118 ] [ 119 ]  FODMAPs are not the cause of irritable bowel syndrome nor other  functional gastrointestinal disorders , but rather a person develops symptoms when the underlying bowel response is exaggerated or abnormal. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8528", "text": "A  low-FODMAP diet  consists of restricting them from the diet. They are globally trimmed, rather than individually, which is more successful than for example restricting only fructose and fructans, which are also FODMAPs, as is recommended for those with fructose malabsorption. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8529", "text": "A low-FODMAP diet might help to improve short-term digestive symptoms in adults with irritable bowel syndrome, [ 120 ] [ 114 ] [ 121 ] [ 20 ]  but its long-term follow-up can have negative effects because it causes a detrimental impact on the  gut microbiota  and  metabolome . [ 122 ] [ 114 ] [ 20 ] [ 123 ]  It should only be used for short periods of time and under the advice of a specialist. [ 124 ]   A low-FODMAP diet is highly restrictive in various groups of nutrients and can be impractical to follow in the long-term. [ 125 ]  More studies are needed to assess the true impact of this diet on health. [ 114 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8530", "text": "In addition, the use of a low-FODMAP diet without verifying the diagnosis of IBS may result in misdiagnosis of other conditions such as celiac disease. [ 126 ]  Since the consumption of  gluten  is suppressed or reduced with a low-FODMAP diet, the improvement of the digestive symptoms with this diet may not be related to the withdrawal of the FODMAPs, but of gluten, indicating the presence of unrecognized celiac disease, avoiding its diagnosis and correct treatment, with the consequent risk of several serious health complications, including various types of cancer. [ 126 ] [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8531", "text": "Soluble  fiber  supplementation (e.g.,  psyllium/ispagula husk ) may be effective in improving symptoms. [ 19 ]  However soluble fiber does not appear to reduce pain. [ 128 ]  It acts as a bulking agent, and for many people with IBS-D, allows for a more consistent stool. For people with IBS-C, it seems to allow for a softer, moister, more easily passable stool. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8532", "text": "However, insoluble fiber (e.g.,  bran ) is not effective for IBS. [ 129 ] [ 130 ]  In some people, insoluble fiber supplementation may aggravate symptoms. [ 131 ] [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8533", "text": "Fiber might be beneficial in those who have a predominance of constipation. In people who have IBS-C, soluble fiber can reduce overall symptoms but will not reduce pain. The research supporting dietary fiber contains conflicting small studies complicated by the heterogeneity of types of fiber and doses used. [ 128 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8534", "text": "Physical activity  can have beneficial effects on irritable bowel syndrome. [ 133 ]  In light of this, the latest British Society of Gastroenterology guidelines on the management of IBS have stated that all patients with IBS should be advised to take regular exercise (strong recommendation, weak certainty evidence), [ 134 ]  whereas the  American College of Gastroenterology  guidelines have suggested with a lower certainty of evidence. [ 135 ]   Physical activity  could significantly improve people\u2019s adherence and, consequently, lead to a significant clinical benefit for symptoms of irritable bowel syndrome. [ 133 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8535", "text": "Medications that may be useful include antispasmodics such as  dicyclomine  and  antidepressants . [ 136 ]  Both H1- antihistamines  and  mast cell stabilizers  have shown efficacy in reducing pain associated with  visceral hypersensitivity  in IBS. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8536", "text": "A number of  5-HT3 antagonists  or 5-HT4 agonists were proposed clinically to treat diarrhea-predominant IBS and constipation-predominant IBS, respectively. However, severe side effects have resulted in its withdrawal by food and drug administration and are now prescribed under emergency investigational drug protocol. [ 137 ]  Other 5-HT receptor subtypes, such as  5-HT7 receptor , have yet to be developed."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8537", "text": "For people who do not adequately respond to dietary fiber, osmotic  laxatives  such as  polyethylene glycol ,  sorbitol , and  lactulose  can help avoid \"cathartic colon\" which has been associated with stimulant laxatives. [ 138 ]   Lubiprostone  is a gastrointestinal agent used for the treatment of constipation-predominant IBS. [ 139 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8538", "text": "The use of  antispasmodic  drugs (e.g.,  anticholinergics  such as  hyoscyamine  or  dicyclomine ) may help people who have cramps or diarrhea. A meta-analysis by the  Cochrane Collaboration  concludes that one out of seven people benefit from treatment with antispasmodics. [ 136 ]  Antispasmodics can be divided into two groups: neurotropics and musculotropics. Musculotropics, such as  mebeverine , act directly at the smooth muscle of the gastrointestinal tract, relieving spasm without affecting normal gut motility. [ citation needed ]  Since this action is not mediated by the autonomic nervous system, the usual anticholinergic side effects are absent. [ 140 ]  The antispasmodic  otilonium  may also be useful. [ 141 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8539", "text": "Proton-pump inhibitors  (PPIs) used to suppress stomach acid production may cause  small intestinal bacterial overgrowth  (SIBO) leading to IBS symptoms. [ 142 ]  Discontinuation of PPIs in selected individuals has been recommended as it may lead to an improvement or resolution of IBS symptoms. [ 143 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8540", "text": "Evidence is conflicting about the benefit of  antidepressants  in IBS. Some meta-analyses have found a benefit, while others have not. [ 144 ]  There is good evidence that low doses of  tricyclic antidepressants  (TCAs) can be effective for IBS. [ 136 ] [ 145 ]  With TCAs, about one in three people improve. [ 146 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8541", "text": "However, the evidence is less robust for the effectiveness of other antidepressant classes such as  selective serotonin reuptake inhibitor  antidepressants (SSRIs). Because of their serotonergic effect, SSRIs have been studied in IBS, especially for people who are constipation predominant. As of 2015, the evidence indicates that SSRIs do not help. [ 147 ]  Antidepressants are not effective for IBS in people with depression, possibly because lower doses of antidepressants than the doses used to treat depression are required for relief of IBS. [ 148 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8542", "text": "Magnesium aluminum silicates  and  alverine citrate  drugs can be effective for IBS. [ 149 ] [ 132 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8543", "text": "Rifaximin  may be useful as a treatment for IBS symptoms, including abdominal bloating and flatulence, although relief of  abdominal distension  is delayed. [ 3 ] [ 150 ]  It is especially useful where small intestinal bacterial overgrowth is involved. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8544", "text": "In individuals with IBS and low levels of  vitamin D , supplementation is recommended. Some evidence suggests that vitamin D supplementation may improve symptoms of IBS, but further research is needed before it can be recommended as a specific treatment for IBS. [ 55 ] [ 56 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8545", "text": "There is inconsistent evidence from studies with poor methodological quality that psychological therapies can be effective in the treatment of IBS. [ 148 ]  Preliminary research shows that psychotherapeutic interventions are correlated with reductions in both  autonomic nervous system  dysregulation and gastrointestinal symptoms. [ 41 ]  Reducing stress may also reduce the frequency and severity of IBS symptoms. Techniques that may be helpful include regular exercise, such as swimming, walking, or running. [ 151 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8546", "text": "Probiotics  can be beneficial in the treatment of IBS; taking 10 billion to 100 billion beneficial bacteria per day is recommended for beneficial results. However, further research is needed on individual strains of beneficial bacteria for more refined recommendations. [ 150 ] [ 152 ]  Probiotics have positive effects such as enhancing the  intestinal mucosal barrier , providing a physical barrier,  bacteriocin  production (resulting in reduced numbers of pathogenic and gas-producing bacteria), reducing intestinal permeability and bacterial translocation, and regulating the immune system both locally and systemically among other beneficial effects. [ 83 ]  Probiotics may also have positive effects on the  gut\u2013brain axis  by their positive effects countering the effects of stress on gut immunity and gut function. [ 153 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8547", "text": "A number of probiotics have been found to be effective, including  Lactobacillus plantarum , [ 83 ]  and  Bifidobacteria  infantis ; [ 154 ]  but one review found only  Bifidobacteria infantis  showed efficacy. [ 155 ]   B. infantis  may have effects beyond the gut via it causing a reduction of proinflammatory cytokine activity and elevation of blood  tryptophan  levels, which may cause an improvement in symptoms of depression. [ 156 ]  Some  yogurt  is made using probiotics that may help ease symptoms of IBS. [ 157 ]  A probiotic yeast called  Saccharomyces boulardii  has some evidence of effectiveness in the treatment of irritable bowel syndrome. [ 158 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8548", "text": "Certain probiotics have different effects on certain symptoms of IBS. For example,  Bifidobacterium breve ,  B. longum,  and  Lactobacillus acidophilus  have been found to alleviate abdominal pain.  B. breve, B. infantis, L. casei , or  L. plantarum  species alleviated  distension  symptoms.  B. breve, B. infantis, L. casei, L. plantarum, B. longum, L. acidophilus, L. bulgaricus , and  Streptococcus salivarius  ssp.  thermophilus  have all been found to affect flatulence levels. Most clinical studies show probiotics do not improve straining, sense of incomplete evacuation, stool consistency, fecal urgency, or stool frequency, although a few clinical studies did find some benefit of probiotic therapy. The evidence is conflicting for whether probiotics improve overall quality of life scores. [ 159 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8549", "text": "Probiotics may exert their beneficial effects on IBS symptoms via preserving the gut microbiota, normalisation of cytokine blood levels, improving the intestinal transit time, decreasing small intestine permeability, and by treating  small intestinal bacterial overgrowth  of fermenting bacteria. [ 159 ]  A  fecal transplant  does not appear useful as of 2019. [ 160 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8550", "text": "Peppermint oil  appears useful. [ 161 ]  In a meta-analysis it was found to be superior to placebo for improvement of IBS symptoms, at least in the short term. [ 111 ]  An earlier meta-analysis suggested the results of peppermint oil were tentative as the number of people studied was small and blinding of those receiving treatment was unclear. [ 109 ]  Safety during pregnancy has not been established, however, and caution is required not to chew or break the  enteric coating ; otherwise,  gastroesophageal reflux  may occur as a result of  lower esophageal sphincter  relaxation. Occasionally, nausea and perianal burning occur as side effects. [ 130 ]   Iberogast , a multi-herbal extract, was found to be superior in efficacy to placebo. [ 162 ]   A comprehensive meta-analysis using twelve random trials resulted that the use of peppermint oil is an effective therapy for adults with irritable bowel syndrome. [ 163 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8551", "text": "Research into  cannabinoids  as treatment for IBS is limited. GI propulsion, secretion, and inflammation in the gut are all modulated by the  ECS  (Endocannabinoid system), providing a rationale for cannabinoids as treatment candidates for IBS. [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8552", "text": "Only limited evidence exists for the effectiveness of other herbal remedies for IBS. As with all herbs, it is wise to be aware of possible drug interactions and adverse effects. [ 130 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8553", "text": "There are no benefits of  acupuncture  compared to placebo for IBS symptom severity or IBS-related quality of life. [ 165 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8554", "text": "The prevalence of IBS varies by country and by age range examined. The bar graph at right shows the percentage of the population reporting symptoms of IBS in studies from various geographic regions (see table below for references). The following table contains a list of studies performed in different countries that measured the prevalence of IBS and IBS-like symptoms:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8555", "text": "10.5% [ 169 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8556", "text": "Wilson, 2004"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8557", "text": "In  Western countries , women are around two to three times more likely to be diagnosed with IBS and four to five times more likely to seek specialty care for it than men. [ 174 ]  However, women in East Asian countries are not more likely than men to have irritable bowel syndrome, and there are conflicting reports about the female predominance of the disease in Africa and other parts of Asia. [ 175 ]  People diagnosed with IBS are usually younger than 45 years old. [ 1 ]  Studies of females with IBS show symptom severity often fluctuates with the menstrual cycle, suggesting hormonal differences may play a role. [ 176 ]  Endorsement of gender-related traits has been associated with quality of life and psychological adjustment in IBS. [ 177 ]  The increase in gastrointestinal symptoms during menses or early menopause may be related to declining or low estrogen and progesterone, suggesting that estrogen withdrawal may play a role in IBS. [ 178 ]  Gender differences in healthcare-seeking may also play a role. [ 179 ]  Gender differences in trait anxiety may contribute to lower pain thresholds in women, putting them at greater risk for a number of chronic pain disorders. [ 180 ]  Finally, sexual trauma is a major risk factor for IBS, as are other forms of abuse. [ 181 ]  Because women are at higher risk of sexual abuse than men, sex-related risk of abuse may contribute to the higher rate of IBS in women. [ 182 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8558", "text": "The concept of an \"irritable bowel\" was introduced by  P. W. Brown , first in  The Journal of the Kansas Medical Society  in 1947 [ 183 ]  and later in the  Rocky Mountain Medical Journal  in 1950. [ 184 ]   The term was used to categorize people who developed symptoms of diarrhea, abdominal pain, and constipation, but where no well-recognized infective cause could be found.  Early theories suggested the irritable bowel was caused by a psychosomatic or mental disorder. [ 185 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8559", "text": "The aggregate cost of irritable bowel syndrome in the United States has been estimated at $1.7\u201310 billion in direct medical costs, with an additional $20 billion in indirect costs, for a total of $21.7\u201330 billion. [ 13 ]  A study by a managed care company comparing medical costs for people with IBS to non-IBS controls identified a 49% annual increase in medical costs associated with a diagnosis of IBS. [ 186 ]  People with IBS incurred average annual direct costs of $5,049 and $406 in out-of-pocket expenses in 2007. [ 187 ]  A study of workers with IBS found that they reported a 34.6% loss in productivity, corresponding to 13.8 hours lost per 40 hour week. [ 188 ]  A study of employer-related health costs from a Fortune 100 company conducted with data from the 1990s found people with IBS incurred US$4527 in claims costs vs. $3276 for controls. [ 189 ]  A study on Medicaid costs conducted in 2003 by the  University of Georgia College of Pharmacy  and  Novartis  found IBS was associated in an increase of $962 in Medicaid costs in California, and $2191 in North Carolina.  People with IBS had higher costs for physician visits, outpatients visits, and prescription drugs.  The study suggested the costs associated with IBS were comparable to those found for people with asthma. [ 190 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8560", "text": "Individuals with IBS have been found to have decreased diversity and numbers of  Bacteroidota  microbiota. Preliminary research into the effectiveness of  fecal microbiota transplant  in the treatment of IBS has been very favourable with a 'cure' rate of between 36 percent and 60 percent with remission of core IBS symptoms persisting at 9 and 19 months follow up. [ 191 ] [ 192 ]  Treatment with probiotic strains of bacteria has shown to be effective, though not all strains of microorganisms confer the same benefit and adverse side effects have been documented in a minority of cases. [ 193 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8561", "text": "There is increasing evidence for the effectiveness of  mesalazine  (5-aminosalicylic acid) in the treatment of IBS. [ 194 ]  Mesalazine is a drug with  anti-inflammatory  properties that has been reported to significantly reduce immune mediated inflammation in the gut of IBS affected individuals with mesalazine therapy resulting in improved IBS symptoms as well as feelings of general wellness in IBS affected people. It has also been observed that mesalazine therapy helps to normalise the gut flora which is often abnormal in people who have IBS. The therapeutic benefits of mesalazine may be the result of improvements to the  epithelial  barrier function. [ 195 ]  Treatment based on \"abnormally\" high IgG antibodies cannot be recommended. [ 196 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8562", "text": "Differences in visceral sensitivity and intestinal physiology have been noted in IBS. Mucosal barrier reinforcement in response to oral 5-HTP was absent in IBS compared to controls. [ 197 ]  IBS/IBD individuals are less often  HLA  DQ2/8 positive than in upper functional gastrointestinal disease and healthy populations. [ 198 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8563", "text": "Efficacy of mast cell directed therapies in irritable bowel syndrome is an area of ongoing research. [ 199 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8564", "text": "A similar syndrome is found in rats ( Rattus  spp.). [ 200 ]  In rats a short-chain fatty acid receptor is involved, a  free fatty acid receptor 2  subtype \u2013   GPR43   \u2013 that is expressed in both  enteroendocrine cells  and  mucosal mast cells . [ 200 ]  These cells then respond in an exaggerated way to the IBS rat's own large quantity of  maldigestion  products. [ 200 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8565", "text": "Isosporiasis , also known as  cystoisosporiasis , is a human intestinal disease caused by the parasite  Cystoisospora belli  (previously known as  Isospora belli ). It is found worldwide, especially in tropical and subtropical areas. Infection often occurs in  immuno-compromised  individuals, notably  AIDS  patients, and outbreaks have been reported in institutionalized groups in the United States. The first documented case was in 1915. It is usually spread indirectly, normally through contaminated food or water (CDC.gov). [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8566", "text": "Infection causes acute, non-bloody  diarrhea  with crampy abdominal pain, which can last for weeks and result in  malabsorption  and weight loss. In immunodepressed patients, and in infants and children, the diarrhea can be severe.  Eosinophilia  may be present (differently from other protozoan infections). [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8567", "text": "The  coccidian  parasite  Cystoisospora belli  infects the  epithelial  cells of the small intestine, and is the least common of the three intestinal coccidia that infect humans ( Toxoplasma ,  Cryptosporidium , and  Cystoisospora ). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8568", "text": "People become infected by swallowing the mature parasite; this normally occurs through the ingestion of contaminated food or water. The infected host then produces an immature form  of the parasite in their feces, and when the parasite matures, it is capable of infecting its next host, via food or water containing the parasite. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8569", "text": "At time of excretion, the immature  oocyst  usually contains one  sporoblast  (more rarely two). In further maturation after excretion, the sporoblast divides in two, so the oocyst now contains two sporoblasts. The sporoblasts secrete a cyst wall, thus becoming sporocysts; and the sporocysts divide twice to produce four sporozoites each. Infection occurs by ingestion of sporocyst-containing oocysts: the sporocysts excyst in the small intestine and release their sporozoites, which invade the epithelial cells and initiate  schizogony . Upon rupture of the  schizonts , the  merozoites  are released, invade new  epithelial cells , and continue the cycle of asexual multiplication.  Trophozoites  develop into  schizonts  which contain multiple merozoites. After a minimum of one week, the sexual stage begins with the development of male and female gametocytes.  Fertilization  results in the development of oocysts that are excreted in the stool.  Cystoisospora belli  infects both humans and animals. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8570", "text": "Microscopic demonstration of the large typically shaped oocysts is the basis for diagnosis. Because the oocysts may be passed in small amounts and intermittently, repeated stool examinations and concentration procedures are recommended. If stool examinations are negative, examination of  duodenal  specimens by biopsy or string test (Enterotest) may be needed. The oocysts can be visualized on wet mounts by microscopy with bright-field, differential interference contrast (DIC), and  epifluorescence . They can also be stained by modified  acid-fast stain . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8571", "text": "Typical laboratory analyses include: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8572", "text": "Avoiding food or water that may be contaminated with stools can help prevent the infection of  Cystoisospora  (Isosporiasis). Good hand-washing, and personal-hygiene practices should be used as well. One should wash their hands with soap and warm water after using the toilet, changing diapers, and before handling food (CDC.gov). [ 1 ]  It is also important to teach children the importance of washing their hands, and how to properly wash their hands. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8573", "text": "The treatment of choice is  trimethoprim-sulfamethoxazole  (Bactrim). [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8574", "text": "While isosporiasis occurs throughout the world, it is more common in tropical and subtropical areas. Cystoisospora infections are more common in individuals with compromised immune systems, such as HIV or leukemia. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8575", "text": "Parasitic worms , also known as  helminths , [ 1 ]  are a  polyphyletic  group of large  macroparasites ; adults can generally be seen with the naked eye. Many are  intestinal worms  that are  soil-transmitted  and  infect  the  gastrointestinal tract . Other parasitic worms such as   schistosomes  reside in blood vessels."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8576", "text": "Some parasitic worms, including  leeches  and  monogeneans , are  ectoparasites \u00a0\u2013  thus, they are not classified as helminths, which are  endoparasites ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8577", "text": "Parasitic worms live in and feed in living  hosts . They receive  nourishment  and protection while disrupting their hosts' ability to absorb  nutrients . This can cause weakness and  disease  in the host, and poses a global health and economic problem. [ 2 ]  Parasitic worms cannot reproduce entirely within their host's body; they have a life cycle that includes some stages that need to take place outside of the host. [ 3 ]  Helminths are able to survive in their mammalian hosts for many years due to their ability to manipulate the host's  immune response  by secreting immunomodulatory products. [ 4 ]  All parasitic worms produce  eggs  during reproduction. These eggs have a strong shell that protects them against a range of environmental conditions. The eggs can therefore survive in the environment for many months or years."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8578", "text": "Many of the worms referred to as helminths are intestinal parasites. An infection by a helminth is known as  helminthiasis , helminth infection, or intestinal worm infection. There is a naming convention which applies to all helminths: the ending \"-asis\" (or in veterinary science: \"-osis\") is added at the end of the name of the worm to denote the infection with that particular worm. [ citation needed ]  For example,  Ascaris  is the name of a type of helminth, and  ascariasis  is the name of the infection caused by that helminth."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8579", "text": "Helminths are a group of organisms which share a similar form but are not necessarily  evolutionarily related . The term \"helminth\" is an artificial term. [ 5 ] [ 6 ]  There is no real consensus on the taxonomy (or groupings) of the helminths, particularly within the  nematodes . [ 7 ]  The term \"helminth\" contains a number of  phyla , many of which are completely unrelated. However, for practical considerations the term is currently used to describe four phyla with superficial similarities:  Annelida  (ringed or segmented worms),  Platyhelminthes  ( flatworms ),  Nematoda  (roundworms), and  Acanthocephala  (thorny-headed worms). [ 7 ]  The phylum  Platyhelminthes  includes two classes of worms of particular medical significance: the  cestodes  (tapeworms) and the  trematodes  (flukes and  blood flukes ), depending on whether or not they have segmented bodies. [ 1 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8580", "text": "There may be as many as 300,000 species of parasites affecting vertebrates, [ 9 ]  and as many as 300 affecting humans alone. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8581", "text": "Helminths of importance in the  sanitation  field are the human parasites, and are classified as  Nemathelminthes  (nematodes) and  Platyhelminthes , depending on whether they possess a round or flattened body, respectively. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8582", "text": "Ringworm  (dermatophytosis) is actually caused by various  fungi , and not by a parasitic worm. [ 11 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8583", "text": "The  lifetime  of adult worms varies tremendously from one species to another but is generally in the range of 1 to 8 years (see following table). This lifetime of several years is a result of their ability to manipulate the immune response of their hosts by secreting immunomodulatory products. [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8584", "text": "Helminths can be either hermaphroditic (having the sex organs of both sexes), like tapeworms and flukes (not including the blood fluke), or have their sexes differentiated, like the roundworms. [ 13 ]  All helminths produce eggs (also called ova) for reproduction. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8585", "text": "Generally, thousands or even hundreds of thousands of eggs are produced each time the female worm deposits its eggs - a process called  oviposition . There is a large variation in the number of eggs produced by different species of worm at one time; it varies in the range of 3,000 to 700,000. The frequency of egg deposition from an adult helminth is generally daily, and can occur up to six times per day for some  Taenia  species. Adult trematodes lay smaller numbers of eggs compared to cestodes or nematodes. However, the egg develops into a  miracidia  from which thousands of  cercariae , or swimming larvae, develop. This means that one egg may produce thousands of adult worms. [ 15 ]  Helminth eggs remain viable for 1\u20132 months in crops and for many months in soil, fresh water, and  sewage , or even for several years in  feces ,  fecal sludge  (historically called  night soil ), and  sewage sludge  \u2013 a period that is much longer compared to other microorganisms. [ 16 ] [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8586", "text": "Helminth eggs are resistant to various environmental conditions due to the composition of the egg shell. Each helminth egg species has 3 to 4 layers with different physical and chemical characteristics: [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8587", "text": "Larvae hatch from eggs, either inside or outside the host, depending on the type of helminth. For eggs in moist soil at optimal temperature and oxygen levels, the embryo develops into an infective larva after 2 to 4 weeks, named \"second-stage larva\". Once ingested by a host, this larva has the ability to get out of the egg, hatch in the small intestine and migrate to different organs. These infective larvae (or \"infective eggs\") may remain viable in soil for two years or longer. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8588", "text": "The process of larval maturation in the host can take from about two weeks up to four months, depending on the helminth species. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8589", "text": "The following table shows the principal morphological and reproductive distinctions for three helminth groups:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8590", "text": "Fasciola hepatica"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8591", "text": "Number of species"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8592", "text": "Registered > 25,000 [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8593", "text": "Hymenolepis nana"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8594", "text": "Taenia solium  / Taenia saginata"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8595", "text": "Ascaris lumbricoides"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8596", "text": "Hookworm"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8597", "text": "Trichuris trichiura"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8598", "text": "Some days (eggs can survive for months) [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8599", "text": "9\u201315 days [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8600", "text": "18 days to several weeks [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8601", "text": "1\u20132 days [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8602", "text": "15\u201330 days [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8603", "text": "After hatching, the larvae develop into cysticercoid, which can survive for years in an animal [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8604", "text": "5\u20137 weeks as  cercariae  in snails and longer periods in wet environments as encysted  metacercariae [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8605", "text": "10\u201314 days [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8606", "text": "5\u201310 days (after maturing can survive for weeks outside the host) [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8607", "text": "60\u201370 days (from hatching to mature state) [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8608", "text": "5\u20136 days [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8609", "text": "2 months (from cysticercoid to adult) [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8610", "text": "3\u20134 months [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8611", "text": "2\u20133 months [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8612", "text": "2\u20138 weeks [ 23 ]  (can become dormant for months)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8613", "text": "4\u20136 weeks"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8614", "text": "Several years [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8615", "text": "8\u201310 years [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8616", "text": "1\u20132 years [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8617", "text": "Several years [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8618", "text": "1 year [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8619", "text": "up to 6 times a day [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8620", "text": "daily [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8621", "text": "daily [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8622", "text": "daily [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8623", "text": "50,000-100,000 [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8624", "text": "200,000 [ 27 ] [ 22 ]  to 250,000 or more [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8625", "text": "5,000-10,000 [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8626", "text": "3,000-20,000 [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8627", "text": "Draft genomes for all categories of helminth have been sequenced in recent years and are available through the ParaSite sub-portal of  WormBase . [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8628", "text": "Parasitic worms have been used as a medical treatment for various diseases, particularly those involving an overactive  immune response . [ 31 ]  As  humans  have evolved with parasitic worms, proponents argue they are needed for a healthy immune system. [ 31 ]  Scientists are looking for a connection between the prevention and control of parasitic worms and the increase in  allergies  such as hay-fever in developed countries. [ 31 ]  Removal of parasitic worms from areas is correlated with an increase in autoimmune disorders in those areas. [ 32 ]  Parasitic worms may be able to damp down the immune system of their host, making it easier for them to live in the intestine without coming under attack. [ 31 ]  This may be one mechanism for their proposed medicinal effect. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8629", "text": "One study suggests a link between the rising rates of  metabolic syndrome  in the developed worlds and the largely successful efforts of Westerners to eliminate intestinal parasites.  The work suggests eosinophils (a type of white blood cell) in fat tissue play an important role in preventing insulin resistance by secreting interleukin 4, which in turn switches  macrophages  into \"alternative activation\".  Alternatively-activated macrophages are important to maintaining glucose homeostasis (i.e., blood sugar regulation).  Helminth infection causes an increase in eosinophils.  In the study, the authors fed rodents a high-fat diet to induce metabolic syndrome, and then injected them with helminths.  Helminth infestation improved the rodents' metabolism. [ 33 ]   The authors concluded:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8630", "text": "Although sparse in blood of persons in developed countries, eosinophils are often elevated in individuals in rural developing countries where intestinal parasitism is prevalent and metabolic syndrome rare.  We speculate that eosinophils may have evolved to optimize metabolic homeostasis during chronic infections by ubiquitous intestinal parasites\u2026. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8631", "text": "For medical purposes, the exact number of helminth eggs is less important and therefore most  diagnoses  are made simply by identifying the appearance of the  worm  or eggs in  feces . Due to the large quantity of eggs laid,  physicians  can  diagnose  using as few as one or two  fecal smears . [ citation needed ]  The  Kato technique  (also called the Kato-Katz technique) is a laboratory method for preparing human stool samples prior to searching for parasite eggs.  Eggs per gram  is a laboratory test that determines the number of eggs per gram of feces in patients suspected of having a parasitological infection, such as schistosomiasis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8632", "text": "Helminth eggs can reach the soil when polluted  wastewater ,  sewage sludge  or  human waste  are used as  fertilizer . Such soil is often characterized by moist and warm conditions. Therefore, the risk of using contaminated wastewater and sludge in agricultural fields is a real problem, especially in poor countries, where this practice is prevalent. [ 18 ] [ 34 ]  Helminth eggs are regarded as the main biological health risk when applying sewage sludge, fecal sludge or fecal matter on agricultural soils. [ 16 ]  The eggs are the infective stage of the helminths\u2019 life cycle for causing the disease  helminthiasis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8633", "text": "Due to this strong shell, helminth eggs or ova remain viable in soil, fresh water and sewage for many months. In feces, fecal sludge and sewage sludge they can even remain viable for several years. [ 16 ] [ 17 ]  Helminth eggs of concern in  wastewater  used for  irrigation  have a size between 20 and 90\u00a0\u03bcm and a relative density of 1.06\u20131.23. [ 18 ]   It is very difficult to inactivate helminth eggs, unless temperature is increased above 40\u00a0\u00b0C or moisture is reduced to less than 5%. [ 18 ]  Eggs that are no longer viable do not produce any larvae. In the case of  Ascaris lumbricoides  (giant roundworm), which has been considered the most resistant and common helminth type, fertilized eggs deposited in soil are resistant to desiccation but are, at this stage of development, very sensitive to environmental temperatures: The reproduction of a fertilized egg within the eggshell develops at an environmental soil temperature about 25\u00a0\u00b0C which is lower than the body temperature of the host (i.e., 37\u00a0\u00b0C for humans). [ 22 ]  However, development of the larvae in the egg stops at temperatures below 15.5\u00a0\u00b0C, and eggs cannot survive temperatures much above 38\u00a0\u00b0C. If the temperature is around 25\u00a0\u00b0C, the infectiousness occurs after nearly 10 days of incubation. [ 8 ] [ 35 ] [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8634", "text": "Processes that remove particles, such as sedimentation, filtration or  coagulation-flocculation  physically remove helminth eggs from wastewater (but do not inactivate them). [ 37 ] [ 38 ]  Therefore,  waste stabilization ponds  (lagoons), storage basins,  constructed wetlands , rapid filtration or  upflow anaerobic sludge blanket  (UASB) reactors can be used."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8635", "text": "Helminth ova cannot be inactivated with chlorine, UV light or ozone (in the latter case at least not with economical doses because >36\u00a0mg/L ozone are needed with 1 hour contact time). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8636", "text": "Helminth ova can be inactivated in  sewage sludge treatment  if the temperature is increased over 40\u00a0\u00b0C or moisture is reduced to less than 5%. [ 18 ]  Best results can be obtained when both of these conditions are met together for an extended period of time. [ 39 ]  Details about the contact time under these conditions and other related environmental factors are generally not well-defined for every type of helminth egg species. [ 8 ]  Helminth eggs are considered highly resistant biological structures. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8637", "text": "The eggs from  helminths  (parasitic worms) are a commonly used indicator organism to assess the safety of  sanitation  and  wastewater  reuse systems (such schemes are also called  reuse of human excreta ). [ 40 ] :\u200a55\u200a  This is because they are the most resistant  pathogens  of all types of pathogens (pathogens can be  viruses ,  bacteria ,  protozoa  and helminths). [ 41 ]  It means they are relatively hard to destroy through conventional treatment methods. They can survive for 10\u201312 months in tropical climates. [ 41 ]  These eggs are also called  ova  in the literature. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8638", "text": "Helminth eggs that are found in wastewater and sludge stem from soil-transmitted helminths (STHs) which include  Ascaris lumbricoides  (Ascaris),  Anclostoma duodenale ,  Necator americanus  (hookworm), and  Trichuris trichiura  (whipworm). [ 43 ]  Ascaris and whipworm that are identified in reusable wastewater systems can cause certain diseases and complications if ingested by humans and pigs. [ 44 ]  Hookworms will plant and hatch their larvae into the soil where they grow until maturity. Once the hookworm eggs are fully developed, they infect organisms by crawling through the organism\u2019s skin. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8639", "text": "The presence or absence of viable helminth eggs (\"viable\" meaning that a larva would be able to hatch from the egg) in a sample of dried fecal matter,  compost  or  fecal sludge  is often used to assess the efficiency of diverse wastewater and sludge treatment processes in terms of pathogen removal. [ 40 ] :\u200a55\u200a  In particular, the number of viable  Ascaris  eggs is often taken as an indicator for all helminth eggs in treatment processes as they are very common in many parts of the world and relatively easy to identify under the microscope. However, the exact inactivation characteristics may vary for different types of helminth eggs. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8640", "text": "For the purpose of setting treatment standards and reuse legislation, it is important to be able to determine the amount of helminth eggs in an environmental sample with some accuracy. The detection of viable helminth eggs in samples of wastewater, sludge or fresh feces (as a diagnostic tool for the infection  helminthiasis ) is not straight forward. In fact, many laboratories in developing countries lack the right equipment or skilled staff required to do so. An important step in the analytical methods is usually the concentration of the eggs in the sample, especially in the case of wastewater samples. A concentration step may not be required in samples of dried feces, e.g. samples collected from  urine-diverting dry toilets . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8641", "text": "Proctitis  or  anusitis  is an  inflammation  of the  anus  and the lining of the  rectum , affecting only the last 6\u00a0inches of the rectum."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8642", "text": "A common symptom is a continual urge to have a bowel movement\u2014the rectum could feel full or have constipation. Another is tenderness and mild irritation in the rectum and anal region. A serious symptom is pus and blood in the  discharge , accompanied by cramps and pain during the bowel movement. If there is severe bleeding,  anemia  can result, showing symptoms such as pale skin, irritability, weakness, dizziness, brittle nails, and shortness of breath. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8643", "text": "Symptoms are ineffectual straining to empty the bowels,  diarrhea ,  rectal bleeding  and possible discharge, a feeling of not having adequately emptied the bowels, involuntary spasms and cramping during bowel movements, left-sided abdominal pain, passage of mucus through the rectum, and anorectal pain."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8644", "text": "Gonorrhea   (Gonococcal proctitis)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8645", "text": "Chlamydia   (chlamydia proctitis)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8646", "text": "Herpes Simplex Virus 1 and 2   (herpes proctitis)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8647", "text": "Syphilis   (syphilitic proctitis)"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8648", "text": "Proctitis has many possible causes. It may occur idiopathically (idiopathic proctitis, that is, arising spontaneously or from an unknown cause). Other causes include damage by irradiation (for example in radiation therapy for  cervical cancer  and prostate cancer) or as a  sexually transmitted infection , as in  lymphogranuloma venereum  and  herpes proctitis . Studies suggest a celiac disease-associated \"proctitis\" can result from an intolerance to  gluten . [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8649", "text": "A common cause is engaging in  anal sex  with partner(s) infected with sexual transmitted diseases in  men who have sex with men . [ 3 ] [ 4 ]  Shared enema usage has been shown to facilitate the spread of  Lymphogranuloma venereum  proctitis. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8650", "text": "Doctors can diagnose proctitis by looking inside the rectum with a  proctoscope  or a  sigmoidoscope . A  biopsy  is taken, in which the doctor scrapes a tiny piece of tissue from the rectum, and this tissue is then examined by microscopy. The physician may also take a stool sample to test for infections or bacteria. If the physician suspects that the patient has Crohn's disease or ulcerative colitis, colonoscopy or barium  enema  X-rays are used to examine areas of the intestine."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8651", "text": "Treatment for proctitis varies depending on severity and the cause. For example, the physician may prescribe antibiotics for proctitis caused by bacterial infection. If the proctitis is caused by Crohn's disease or ulcerative colitis, the physician may prescribe the drug  5-aminosalicyclic acid  (5ASA) or  corticosteroids  applied directly to the area in enema or  suppository  form, or taken orally in pill form. Enema and suppository applications are usually more effective, but some patients may require a combination of oral and rectal applications."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8652", "text": "Another treatment available is that of fiber supplements such as  Metamucil .  Taken daily these may restore regularity and reduce pain associated with proctitis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8653", "text": "Chronic radiation proctitis is usually treated first-line with sucralfate enemas. These are non-invasive and are effective in diffuse, distal disease. Other treatments may include mesalamine suppositories, vitamin E, hyperbaric oxygen, or short chain fatty acid enemas; however these treatments are only supported by observational or anecdotal evidence."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8654", "text": "Reactive arthritis , previously known as  Reiter's syndrome , [ 1 ]  is a form of  inflammatory   arthritis [ 2 ]  that develops in response to an  infection  in another part of the body (cross-reactivity). Coming into contact with  bacteria  and developing an infection can trigger the disease. [ 3 ]  By the time a person presents with symptoms, the \"trigger\" infection has often been cured or is in  remission  in chronic cases, thus making determination of the initial cause difficult."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8655", "text": "The arthritis often is coupled with other characteristic symptoms; this was previously called  Reiter's syndrome ,  Reiter's disease  or  Reiter's arthritis .  The condition was renamed to reactive arthritis because of  Hans Reiter 's war crimes with the  Nazi Party ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8656", "text": "The manifestations of reactive arthritis include the following triad of symptoms: an inflammatory arthritis of large joints, inflammation of the eyes in the form of  conjunctivitis  or  uveitis , and  urethritis  in men or  cervicitis  in women. Arthritis occurring alone following sexual exposure or enteric infection is also known as reactive arthritis. Affected people may present with mucocutaneous lesions, as well as  psoriasis -like skin lesions such as  circinate balanitis , and  keratoderma blennorrhagicum .  Enthesitis  can involve the Achilles tendon resulting in heel pain. [ 4 ]  Not all affected persons have all the manifestations."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8657", "text": "The clinical pattern of reactive arthritis commonly consists of an  inflammation  of fewer than five joints which often includes the knee or  sacroiliac joint . The arthritis may be \"additive\" (more joints become inflamed in addition to the primarily affected one) or \"migratory\" (new joints become inflamed after the initially inflamed site has already improved). [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8658", "text": "Reactive arthritis is an  RF-seronegative ,  HLA-B27 -linked arthritis [ 7 ]  often precipitated by genitourinary or gastrointestinal  infections . The most common triggers are intestinal infections (with  Salmonella ,  Shigella  or  Campylobacter ) and sexually transmitted infections (with  Chlamydia trachomatis ); [ 8 ]  however, it also can happen after  group A streptococcal infections . [ 9 ] [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8659", "text": "It most commonly strikes individuals aged 20\u201340 years of age, is more common in men than in women, and more common in white than in black people. This is owing to the high frequency of the HLA-B27 gene in the white population. [ 11 ] [ 12 ]  It can occur in epidemic form. Patients with  HIV  have an increased risk of developing reactive arthritis as well."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8660", "text": "Numerous cases during World Wars I and II focused attention on the triad of arthritis, urethritis, and conjunctivitis (often with additional mucocutaneous lesions), which at that time was also referred to as  Fiessenger\u2013Leroy\u2013Reiter syndrome . [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8661", "text": "Reactive arthritis is associated with the  HLA-B27  gene on chromosome 6 and by the presence of  enthesitis  as the basic pathologic lesion [ 16 ]  and is triggered by a preceding  infection . The most common triggering infection in the US is a genital infection with  Chlamydia trachomatis . Other bacteria known to cause reactive arthritis which are more common worldwide are  Ureaplasma urealyticum ,  Salmonella  spp.,  Shigella  spp.,  Yersinia  spp., and  Campylobacter  spp. [ 17 ]  A bout of  food poisoning  or a  gastrointestinal  infection may also precede the disease (the last four  genera  of bacteria mentioned above are enteric bacteria). [ 18 ]   Shigella  is the most common organism causing reactive arthritis following diarrhea.  Chlamydia trachomatis  is the most common cause of reactive arthritis following urethritis.  Ureaplasma  and  mycoplasma  are rare causes. There is some circumstantial evidence for other organisms causing the disease, but the details are unclear. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8662", "text": "Reactive arthritis usually manifests about 1\u20133 weeks after a known infection. The mechanism of interaction between the infecting organism and the host is unknown. Synovial fluid cultures are negative, suggesting that reactive arthritis is caused either by an autoimmune response involving cross-reactivity of bacterial antigens with joint tissues or by bacterial antigens that have somehow become deposited in the joints. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8663", "text": "There are few clinical symptoms, but the clinical picture is dominated by arthritis in one or more joints, resulting in pain, swelling, redness, and heat sensation in the affected areas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8664", "text": "The  urethra ,  cervix  and the  throat  may be swabbed in an attempt to  culture  the causative organisms. Cultures may also be carried out on  urine  and  stool  samples or on fluid obtained by  arthrocentesis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8665", "text": "Tests for  C-reactive protein  and  erythrocyte sedimentation rate  are non-specific tests that can be done to corroborate the diagnosis of the syndrome.\nA blood test for the genetic marker  HLA-B27  may also be performed. About 75 percent of all the patients with reactive arthritis have this gene."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8666", "text": "Although there are no definitive criteria to diagnose the existence of reactive arthritis, the  American College of Rheumatology  has published  sensitivity and specificity  guidelines. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8667", "text": "The main goal of treatment is to identify and eradicate the underlying infectious source with the appropriate  antibiotics  if still present. Otherwise, treatment is symptomatic for each problem. Nonspecific urethritis may be treated with a short course of  tetracycline .  Analgesics , particularly  NSAIDs , are used.  Steroids ,  sulfasalazine  and  immunosuppressants  may be needed for patients with severe reactive symptoms that do not respond to any other treatment. Local  corticosteroids  are useful in the case of  iritis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8668", "text": "Reactive arthritis may be self-limiting, frequently recurring, chronic or progressive. Most patients have severe symptoms lasting a few weeks to six months. 15 to 50 percent of cases involve recurrent bouts of arthritis. Chronic arthritis or sacroiliitis occurs in 15\u201330 percent of cases. Repeated attacks over many years are common, and patients sometimes end up with chronic and disabling  arthritis ,  heart disease ,  amyloid  deposits,  ankylosing spondylitis ,  immunoglobulin A   nephropathy , cardiac conduction abnormalities, or  aortitis  with  aortic regurgitation . [ 20 ]  However, most people with reactive arthritis can expect to live  normal life spans  and maintain a near-normal lifestyle with modest adaptations to protect the involved organs."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8669", "text": "Because women may be underdiagnosed, the exact incidence of reactive arthritis is difficult to estimate. A few studies have been completed, though. In  Norway  between 1988 and 1990, the incidence was 4.6 cases per 100,000 for chlamydia-induced reactive arthritis and 5 cases per 100,000 for that induced by  enteric bacteria . [ 21 ]  In 1978 in  Finland , the annual incidence was found to be 43.6 per 100,000. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8670", "text": "When reactive arthritis appears in a triad that also includes ophthalmic and urogenital manifestations, the  eponym  \"Reiter's syndrome\" is often applied; [ citation needed ]  German physician  Hans Conrad Julius Reiter  described the condition in a soldier he treated during  World War I ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8671", "text": "A number of physicians have suggested that the eponym is undeserved. Reiter's  Nazi Party  affiliation, and in particular his involvement in forced human experimentation in the  Buchenwald concentration camp  (which, after his capture at the end of  World War II , resulted in his  prosecution in Nuremberg  as a  war criminal ), have come to overshadow his medical accomplishments. Furthermore, he was not the first physician to make associations between the arthritis and other symptoms\u2014the names arthritis urethritica, venereal arthritis and polyarteritis enterica had previously been applied\u2014and the full triad was described by another physician in the 19th century. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8672", "text": "The  Simple Clinical Colitis Activity Index  ( SCCAI ) is a diagnostic tool and questionnaire used to assess the severity of  symptoms  in people who suffer from  ulcerative colitis . It was created in 1998 and is still used to assess the severity of symptoms. [ 1 ]  It is also used for research purposes to determine the efficacy of various treatments aimed at relieving symptoms. [ 2 ]   The calculated score ranges from 0 to 19, where active disease is a score of 5 or higher. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8673", "text": "The score is determined by asking the person with colitis questions regarding: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8674", "text": "The  soil-transmitted helminths  (also called  geohelminths ) are a group of  intestinal parasites  belonging to the  phylum   Nematoda  that are transmitted primarily through contaminated soil. They are so called because they have a direct  life cycle  which requires no  intermediate hosts  or  vectors , and the  parasitic infection  occurs through  faecal  contamination of soil, foodstuffs and water supplies. The adult forms are essentially  parasites  of humans, causing  soil-transmitted helminthiasis  (STH), but also infect  domesticated   mammals . The  juveniles  are the infective forms and they undergo tissue-migratory stages during which they invade vital organs such as  lungs  and  liver . Thus the disease manifestations can be both local and systemic. The geohelminths together present an enormous infection burden on humanity, amounting to 135,000 deaths every year, and persistent infection of more than two billion people. [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8675", "text": "Soil-transmitted helminths are typically from the following  families  of  nematodes , namely: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8676", "text": "Soil-transmitted helminthiasis is a collective name for the diseases caused by ascaris, whipworm and hookworms in humans. It includes species-specific diseases such as [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8677", "text": "Soil-transmitted helminthiasis is classified as one of the  neglected tropical diseases  projected to be controlled/eradicated by 2020 through the  London Declaration on Neglected Tropical Diseases . [ 4 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8678", "text": "This is caused by  Strongyloides stercoralis . Even though the disease is principally a soil-transmitted helminthiasis, the infection being mediated through contaminated soil, it is however generally omitted in clinical practices and control programmes because of its (allegedly) relatively less significant influence on health and socio-economic conditions. Also it is not restricted to humans, as it is common in  pets . But there is an emerging hyperinfection syndrome caused by  S. stercoralis , which exhibits a high  mortality rate  (15% to 87%). [ 5 ] [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8679", "text": "Geohelminth infection is a major health problem particularly in  rural areas  of  developing countries  like  Subsaharan Africa ,  India  and other  Southeast Asian  countries. It is an important cause of  morbidity  in  school age  children who harbour the highest intensity of worm infestation. Some of the significant morbidity attributed to intestinal  helminthiasis  are  malnutrition ,  growth retardation ,  anaemia ,  vitamin A deficiency  and  impaired intellectual performance . [ 2 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8680", "text": "The World Health Organization is promoting the control of \u00a0soil transmitted helminthiasis with large scale, regular distribution of anthelminthics (albendazole or mebendazole) to the population groups more at risk of morbidity (children and women of reproductive age). The number of school-age children treated with PC has progressed steadily from less than 120 million in 2008 to over 450 million in 2018 and is in contiuous espansion. [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8681", "text": "Anguillula stercoralis   Bavay, 1876"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8682", "text": "Strongyloides stercoralis  is a  human pathogenic   parasitic   roundworm  causing the disease  strongyloidiasis . Its common name in the US is  threadworm . In the UK and Australia, however, the term  threadworm  can also refer to  nematodes  of the genus  Enterobius , otherwise known as  pinworms . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8683", "text": "The  Strongyloides stercoralis  nematode can parasitize humans. The adult parasitic stage lives in tunnels in the  mucosa  of the small  intestine . The genus  Strongyloides  contains 53 species, [ 3 ] [ 4 ]  and  S. stercoralis  is the  type species .  S. stercoralis  has been reported in other  mammals , including  cats  and  dogs . However, it seems that the species in dogs is typically not  S. stercoralis , but the related species  S. canis .  Non-human primates  are more commonly infected with  S. fuelleborni  and  S. cebus , although  S. stercoralis  has been reported in captive primates. Other species of  Strongyloides  that are naturally parasitic in humans, but with restricted distributions, are  S. fuelleborni fuelleborni  in  central Africa  and  S. fuelleborni kellyi  in  Papua New Guinea . [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8684", "text": "S. stercoralis  infection is associated with fecal contamination of soil or water. Hence, it is a very rare infection in developed economies. In developing countries, it is less prevalent in urban areas than in rural areas (where sanitation standards are poor).  S. stercoralis  can be found in areas with tropical and subtropical climates. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8685", "text": "Strongyloidiasis was first described in the 19th century in French soldiers returning home from expeditions in  Indochina . Today, the countries of the old Indochina ( Vietnam ,  Cambodia , and  Laos ) still have endemic strongyloidiasis, with the typical prevalences being 10% or less. Regions of  Japan  used to have endemic strongyloidiasis, but control programs have eliminated the disease. Strongyloidiasis appears to have a high prevalence in some areas of  Brazil  and  Central America . It is endemic in  Africa , but the prevalence is typically low (1% or less). Pockets have been reported from rural  Italy , but the current status is unknown. In the  Pacific islands , strongyloidiasis is rare, although some cases have been reported from  Fiji . In tropical  Australia , some rural and remote  Australian Aboriginal  communities have very high prevalences of strongyloidiasis. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8686", "text": "In some African countries (e.g.,  Congo ),  S. fuelleborni  was more common than  S. stercoralis  in parasite surveys from the 1970s, but the current status is unknown. In  Papua New Guinea ,  S. stercoralis  is endemic, but prevalence is low. However, in some areas, another species,  S. kellyi , [ 8 ]  is a very common parasite of children in the  New Guinea Highlands  and  Western Province . [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8687", "text": "Knowledge of the geographic distribution of strongyloidiasis is of significance to travelers who may acquire the parasite during their stays in endemic areas."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8688", "text": "Because strongyloidiasis could theoretically be transmittable through unsanitary bedclothes care must be taken never to use unclean hotel bed sheets in endemic areas. Using plastic slippers when showering may be very important when travelling in tropical regions."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8689", "text": "Estimates of the number of people infected vary with one estimate putting the figure at 370 million worldwide. [ 9 ] [ 10 ]  Local prevalence can exceed 40% in some tropical and subtropical countries. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8690", "text": "The life cycle of this parasite is more complex than that of most  nematodes , with its alternation between free-living and parasitic cycles, and its potential for autoinfection (the parasite has the ability to complete its life cycle without the involvement of another host) and multiplication within the  host . The parasitic cycle is  homogonic , while the free-living cycle is heterogonic. The heterogonic life cycle is advantageous to the parasite because it allows reproduction in the absence of a host."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8691", "text": "In the free-living cycle, the  rhabditiform   larvae  passed in the  stool  can either molt twice and become infective filariform larvae (direct development) or molt four times and become free-living adult males and females that mate and produce eggs from which rhabditiform larvae hatch. In the direct development, first-stage larvae (L1) transform into infective larvae (IL) via three molts. The indirect route results first in the development of free-living adults that mate; the female lays eggs, which hatch and then develop into IL. The direct route gives IL faster (three days) versus the indirect route (seven to 10 days). However, the indirect route results in an increase in the number of IL produced. Speed of development of IL is traded for increased numbers. The free-living males and females of  S. stercoralis  die after one generation; they do not persist in the soil. The latter, in turn, can either develop into a new generation of free-living adults or develop into infective  filariform  larvae. The filariform larvae penetrate the human host skin to initiate the parasitic cycle.\nUpon contact with contaminated soil, infectious larvae contained in the soil can penetrate the skin."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8692", "text": "Some of the larvae enter the superficial veins and are carried in the blood to the lungs, where they enter the  alveoli . They are then coughed up and swallowed into the gut, where they parasitise the intestinal mucosa of the  duodenum  and  jejunum . In the small intestine, they molt twice and become adult female worms. The females live threaded in the  epithelium  of the small intestine and, by  parthenogenesis , produce eggs, which yield rhabditiform larvae. Only females will reach reproductive adulthood in the intestine. Female strongyloids reproduce through parthenogenesis. The eggs hatch in the intestine and young larvae are then excreted in the feces. It takes about two weeks to reach egg development from the initial skin penetration. By this process,  S. stercoralis  can cause both respiratory and gastrointestinal symptoms. The worms also participate in autoinfection, in which the rhabditiform larvae become infective filariform larvae, which can penetrate either the intestinal mucosa (internal autoinfection) or the skin of the perianal area (external autoinfection); in either case, the filariform larvae may follow the previously described route, being carried successively to the lungs, the bronchial tree, the  pharynx , and the small intestine, where they mature into adults; or they may disseminate widely in the body. To date, occurrence of autoinfection in humans with helminthic infections is recognized only in  Strongyloides stercoralis  and  Capillaria philippinensis  infections. [ citation needed ]   In the case of  Strongyloides , autoinfection may explain the possibility of persistent infections for many years in persons not having been in an endemic area and of hyperinfections in immunodepressed individuals."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8693", "text": "Strongyloides  is thought to be attracted to humans via paired thermosensory neurons. [ 12 ]  While  S. stercoralis  is attracted to chemicals such as carbon dioxide or sodium chloride, these chemicals are not specific. Larvae have been thought to locate their hosts via chemicals in the skin, the predominant one being  urocanic acid , a  histidine  metabolite on the uppermost layer of skin that is removed by sweat or the daily skin-shedding cycle. [ 13 ]  Urocanic acid concentrations can achieve at least fivefold greater levels on the foot sole than any other part of the human body. [ 13 ] [ 14 ] [ verification needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8694", "text": "Dogs can act as a host for this parasite both in the wild and in the laboratory, but  transmission from dog to human  has been difficult to prove. Molecular genetic analyses have shown that there are two populations of this parasite in dogs, one of which (type B) is exclusive to dogs and a second (type A) that is common to dogs and humans. [ 15 ] [ 16 ]  These two genotypes may be separate species. The identity of the genes suggests that dog to human transmission may occur."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8695", "text": "Whereas males grow to only about 0.9\u00a0 mm  (0.04\u00a0 in ) in length, females can grow from 2.0 to 2.5\u00a0mm (0.08 to 0.10\u00a0in). Both sexes also possess a tiny buccal capsule and cylindrical esophagus without a posterior bulb. [ 17 ]  In the free-living stage, the esophagi of both sexes are rhabditiform. Males can be distinguished from females by two structures: the  spicules  and  gubernaculum ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8696", "text": "An unusual feature of  S. stercoralis  is autoinfection. Only one other species in the genus  Strongyloides ,  S. felis , has this trait. Autoinfection is the development of L1 into small infective larvae in the gut of the host. These autoinfective larvae penetrate the wall of the lower ileum or colon or the skin of the perianal region, enter the circulation again, travel to the lungs, and then to the small intestine, thus repeating the cycle. Autoinfection makes strongyloidiasis due to  S. stercoralis  an infection with several unusual features."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8697", "text": "Persistence of infection is the first of these important features. Because of autoinfection, humans have been known to still be infected up to 65 years after they were first exposed to the parasite (e.g.,  World War II  or  Vietnam War  veterans). Once a host is infected with  S. stercoralis , infection is lifelong unless effective treatment eliminates all adult parasites and migrating autoinfective larvae."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8698", "text": "Many people infected are asymptomatic at first. Symptoms include  dermatitis : swelling, itching,  larva currens , and mild hemorrhage at the site where the skin has been penetrated. Spontaneous scratch-like lesions may be seen on the face or elsewhere. If the parasite reaches the lungs, the chest may feel as if it is burning, and wheezing and coughing may result, along with pneumonia-like symptoms ( L\u00f6ffler's syndrome ). The intestines could eventually be invaded, leading to burning pain, tissue damage, sepsis, and ulcers. Stools may have yellow  mucus  with a recognizable smell. Chronic  diarrhea  can be a symptom. [ 18 ]  In severe cases, edema may result in obstruction of the intestinal tract, as well as loss of  peristaltic  contractions. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8699", "text": "Strongyloidiasis in immunocompetent individuals is usually an indolent disease. However, in immunocompromised individuals, it can cause a hyperinfective syndrome (also called disseminated strongyloidiasis) due to the reproductive capacity of the parasite inside the host. This hyperinfective syndrome can have a mortality rate close to 90% if disseminated. [ 20 ] [ 21 ] [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8700", "text": "Immunosuppressive drugs, especially corticosteroids and agents used for tissue transplantation, can increase the rate of autoinfection to the point where an overwhelming number of larvae migrate through the lungs, which in many cases can prove fatal. In addition, diseases such as  human T-lymphotropic virus 1 , which enhance the Th1 arm of the immune system and lessen the Th2 arm, increase the disease state. [ 21 ]  Another consequence of autoinfection is the autoinfective larvae can carry gut bacteria back into the body. About 50% of people with hyperinfection present with bacterial disease due to enteric bacteria. Also, a unique effect of autoinfective larvae is larva currens due to the rapid migration of the larvae through the skin. Larva currens appears as a red line that moves rapidly (more than 5\u00a0cm or 2\u00a0in per day), and then quickly disappears. It is pathognomonic for autoinfective larvae and can be used as a diagnostic criterion for strongyloidiasis due to  S. stercoralis ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8701", "text": "Locating juvenile larvae, either rhabditiform or filariform, in recent stool samples will confirm the presence of this parasite. [ 23 ]  Other techniques used include direct fecal smears, culturing fecal samples on  agar  plates, serodiagnosis through  ELISA , and duodenal fumigation. Still, diagnosis can be difficult because of the day-to-day variation in juvenile parasite load."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8702", "text": "Ideally, prevention, by improved sanitation (proper disposal of feces), practicing good hygiene (washing of hands), etc., is used before any drug regimen is administered."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8703", "text": "Ivermectin  is the drug of choice for treatment, due to its low side effect profile. [ 24 ]   Albendazole  is also effective in treating strongyloidiasis.  Mebendazole  has a much higher failure rate in clinical practice than albendazole or ivermectin. [ 25 ]  However, these drugs have little effect on the autoinfective larvae. Hence, repeat treatments with ivermectin or albendazole must be administered to kill newly matured parasites that have developed from the autoinfective larvae. This means a full treatment dose every two weeks until all larvae capable of maturing into adults have been extirpated. Follow-up stool samples, potential additional treatment, and blood tests are necessary to ensure a cure. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8704", "text": "This parasite depends on chemical cues to find a potential host. It uses sensor neurons of class AFD to identify cues excreted by the host. [ 27 ]  S. stercoralis  is attracted to nonspecific attractants of warmth, carbon dioxide, and sodium chloride. Urocanic acid, a component of skin secretions in mammals, is a major chemoattractant. Larvae of  S. stercoralis  are strongly attracted to this compound. [ 13 ]  This compound can be suppressed by metal ions, suggesting a possible strategy for preventing infection."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8705", "text": "Strongyloidiasis  is a  human parasitic disease  caused by the  nematode  called  Strongyloides stercoralis , or sometimes the closely related  S. f\u00fclleborni . These  helminths  belong to a group of  nematodes  called  roundworms . These intestinal worms can cause a number of symptoms in people, principally skin symptoms,  abdominal pain ,  diarrhea  and  weight loss , but also many other specific and vague symptoms in disseminated disease, and severe life-threatening conditions through hyperinfection. In some people, particularly those who require  corticosteroids  or other immunosuppressive medication,  Strongyloides  can cause a  hyperinfection syndrome  that can lead to death if untreated. The diagnosis is made by blood and stool tests. The medication  ivermectin  is widely used to treat strongyloidiasis."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8706", "text": "Strongyloidiasis is a type of  soil-transmitted helminthiasis . Low estimates postulate it to affect 30\u2013100\u00a0million people worldwide, [ 1 ]  mainly in tropical and subtropical countries, while higher estimates conservatively extrapolate that infection is upwards to or above 370 million people. [ 2 ]   It belongs to the group of  neglected tropical diseases , and worldwide efforts are aimed at eradicating the infection. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8707", "text": "Strongyloides  infection occurs in five forms. As the infection continues and the larvae mature, there may be respiratory symptoms ( L\u00f6ffler's syndrome ). The infection may then become chronic with mainly digestive symptoms. There may be respiratory, skin, and digestive symptoms of reinfection (when larvae migrate through the body) from the skin to the lungs and finally to the small intestine. Finally, the hyperinfection syndrome causes symptoms in many organ systems, including the  central nervous system . [ 4 ] [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8708", "text": "Frequently  asymptomatic .  Gastrointestinal system   symptoms  include abdominal  pain  and  diarrhea  and/or conversely  constipation .   Pulmonary  symptoms (including  L\u00f6ffler's syndrome ) can occur during pulmonary migration of the filariform larvae.   Pulmonary infiltrate  may be present through radiological investigation.   Dermatologic  manifestations include  urticarial   rashes  in the buttocks and waist areas as well as  larva currens . [ 6 ]   Eosinophilia  is generally present. Strongyloidiasis can become chronic and then become completely asymptomatic. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8709", "text": "Disseminated strongyloidiasis occurs when patients with chronic strongyloidiasis become  immunosuppressed . There is a distinction to be made between dissemination and hyperinfection. It is mainly a semantic distinction. There can be mild dissemination where the worm burden is relatively lower yet causes insidious symptoms, or extreme dissemination that the term hyperinfection is used to describe.  Thus hyperinfection of varying levels of severe dissemination may present with abdominal pain, distension,  shock , pulmonary and neurologic  complications ,  sepsis ,  haemorrhage ,  malabsorption , and depending on the combination, degree, number, and severity of symptoms, is potentially fatal.   The worms enter the bloodstream from the bowel wall, simultaneously allowing entry of bowel bacteria such as  Escherichia coli . This may cause symptoms such as  sepsis  (bloodstream infection), [ 7 ]  and the bacteria may spread to other organs where they may cause localized infection such as  meningitis . [ 8 ]   Dissemination without hyperinfection may present to a lesser degree the above and many other symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8710", "text": "Dissemination can occur many decades after the initial infection [ 9 ]  and has been associated with high dose  corticosteroids ,  organ transplant , any other instances and causes of immunosuppression,  HIV , [ 10 ] [ 11 ]  lepromatous  leprosy , tertiary  syphilis ,  aplastic anemia , malnutrition, advanced  tuberculosis  and  radiation poisoning . [ 12 ]   It is often recommended that patients being started on immunosuppression be screened for chronic strongyloidiasis; however, this is often impractical (screen tests are sometimes unavailable) and in developed countries, the prevalence of chronic strongyloidiasis is minimal, so screening is usually not cost-effective, except in endemic areas.  The reality of global travel and the need for modern advanced healthcare, even in the so-called \"developed world\", necessitates that in non-endemic areas there is easily accessible testing and screening for neglected tropical diseases such as strongyloidiasis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8711", "text": "There is not necessarily any eosinophilia in the disseminated disease. The absence of eosinophilia in an infection limited to the gastrointestinal tract may indicate a poor prognosis. [ 13 ]  Eosinophilia is often absent in disseminated infection. Steroids will also suppress eosinophilia while leading to dissemination and potential hyperinfection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8712", "text": "Escalated disseminated infections caused by immunosuppression can result in a wide variety and variable degree of disparate symptoms depending on the condition and other biological aspects of the individual, that may emulate other diseases or diagnoses. In addition to the many palpable gastrointestinal and varied other symptoms drastic  cachexia  amidst lassitude is often present, although severe disseminated infections can occur in individuals without weight loss regardless of  body mass index . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8713", "text": "Diagnosis  rests on the  microscopic  identification of larvae (rhabditiform and occasionally filariform) in the stool or  duodenal  fluid. Examination of many samples may be necessary, and not always sufficient, because direct stool examination is relatively  insensitive , with a single sample only able to detect larvae in about 25% of cases. [ 14 ]  It can take 4 weeks from initial infection to the passage of larvae in the stool. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8714", "text": "The stool can be examined in  wet mounts : [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8715", "text": "Culture techniques are the most sensitive, but are not routinely available in the West.  In the UK, culture is available at either of the Schools of Tropical Medicine in Liverpool or London. The direct examination must be done on a stool sample that is freshly collected and not allowed to cool down, because  hookworm  eggs hatch on cooling and the larvae are very difficult to distinguish from  Strongyloides . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8716", "text": "Finding  Strongyloides  in the stool is negative in up to 70% of tests. It is important to undergo frequent stool sampling and duodenal biopsy if a severe infection is suspected. The duodenal fluid can be examined using techniques such as the  Enterotest string  or duodenal aspiration. [ 15 ]   Larvae may be detected in  sputum  from patients with disseminated strongyloidiasis. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8717", "text": "Given the poor ability of stool examination to diagnose  Strongyloides , detecting  antibodies  by  ELISA  can be useful. [ 16 ]  Serology can cross-react with other parasites, remain positive for years after successful treatment or be falsely negative in immunocompromised patients. [ 14 ] [ 17 ]  Infected patients will also often have an elevated  eosinophil  count, with an average of absolute eosinophil count of 1000 in one series. [ 18 ]   Eosinophilia of a gastrointestinal infection may fluctuate in response to larval output, or may be permanently lacking in some disseminated infections. Hence lack of eosinophilia is not evidence of the absence of infection. The combination of clinical suspicion, a positive antibody, and peripheral eosinophilia can strongly suggest Stronglyoides infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8718", "text": "It would be useful to have significant advances in the sensitivity of the means of diagnosis, as it would also solve the challenging problem of proof of cure. If a definitive diagnosis is solved then it stands to reason that proof of cure becomes easily realizable. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8719", "text": "The consensus drug of choice for the treatment of uncomplicated strongyloidiasis is  ivermectin . However, even if it is considered the main drug of choice, recent studies have illustrated the challenges in ivermectin curing strongyloidiasis. [ 20 ]  Ivermectin does not kill the  Strongyloides  larvae, only the adult worms, therefore repeat dosing may be necessary to properly eradicate the infection. There is an auto-infective cycle of roughly two weeks during which ivermectin should be re-administered; however, additional dosing may still be necessary as it will not kill  Strongyloides  in the blood or larvae deep within the bowels or diverticula. [ 21 ]  Other drugs that can be effective are  albendazole  and  thiabendazole  (25\u00a0mg/kg twice daily for 5 days\u2014400\u00a0mg maximum (generally)). [ 11 ]   All patients who are at risk of disseminated strongyloidiasis should be treated. The optimal duration of treatment for patients with disseminated infections is not clear. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8720", "text": "Treatment of strongyloidiasis can be difficult and if ceasing treatment before being entirely cleared  Strongyloides  via the autoinfective cycle has been known to live in individuals for decades; [ 22 ]  even after initial or inadequate sustained treatment. Continued treatment, blood, and stool monitoring thus may be necessary even if symptoms temporarily resolve. As cited earlier, since some infections are insidiously asymptomatic, and relatively expensive bloodwork is often inconclusive via false-positives or false-negatives, [ 23 ]  just as stool samples can be unreliable in diagnoses, [ 24 ]  there is yet, unfortunately, no real gold standard for proof of cure, mirroring the lack of an efficient and reliable methodology of diagnosis. [ 4 ] [ 19 ] [ 25 ]  An objective eradication standard for strongyloidiasis is elusive given the high degree of suspicion needed to even begin treatment, the sometimes difficulty of the only definitive diagnostic criteria of detecting and isolating larvae or adult  Strongyloides , the importance of early diagnosis, particularly before steroid treatments, [ 26 ]  and the very wide variability and exclusion/inclusion of differing collections of diffuse symptoms. Disregarding mis-ascribing bonafide delusional parasitosis disorders, [ 27 ] [ 28 ] [ 29 ]  strongyloidiasis should be more well known among medical professionals and have serious consideration for broad educational campaigns in effected geographic locales both within the semi-tropical developed world and otherwise, as well as in the tropical developing world where, among many other neglected tropical diseases, it is endemic. [ 30 ] [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8721", "text": "Government programs are needed to help decontaminate endemic areas and to help affected populations from infection. [ 32 ]  Furthermore, progress is required in establishing financial support to facilitate and cover affordable medications for individuals in affected at-risk regions and communities to help continue treatments. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8722", "text": "There are conflicting reports on effective drug treatments. Ivermectin ineffectiveness and rising  drug resistance  have been documented. [ 34 ] [ 35 ]  Albendazole is noted by the  WHO  as being the least effective. [ 36 ]   Thiabendazole can have severe side effects and is unavailable in many countries. [ 37 ]  Major inroads are required to advance the development of successful medications and drug protocols for strongyloidiasis and other neglected tropical diseases. [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8723", "text": "Contagiousness via textiles, unlike  Enterobius vermicularis , is unfounded. As is, generally speaking, person-to-person contagiousness of asymptomatic and disseminated infection. It has rarely been transmitted through organ transplantation. [ 39 ]  Married  Vietnam War  veterans who were infected, yet never developed significant hyperinfection, lived for multiple decades with non-debilitating disseminated infection, without treatment, with wives who failed to ever contract infection. [ 40 ]   Contraction occurs overwhelmingly from skin exposure to any contaminated soil, contaminated potting soil, contaminated waters, lack of sanitation, or environmental factors as potential vectors. Nearly never to extraordinarily very rarely documented is a transmission from person to person (besides from infected male homosexual sex), other than closeness of contact to the productive coughing of a very ill hyperinfected individual. It has been shown possible to occur in that situation, or potentially other similar scenarios, it is speculated via pulmonary secretions of a direly hyperinfected individual. In which case treatment for others may be indicated, if deemed necessary by proximity, symptoms, precautions, probable exposures to the same vectors, or through screening of serology and stool samples, until infection is eradicated. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8724", "text": "Before administering steroids at least somewhat screening for infection in even remotely potentially susceptible individuals to prevent escalating the infection is advised. As not doing so in certain cohorts can have extremely high mortality rates from inadvertently caused hyperinfection via immunosuppression of application of certain steroids. Thus extreme caution with respect to  iatrogenic  risks is crucial to avoiding deaths or other adverse consequences in treatment, that of course prefigures a correct diagnosis. [ 42 ] [ 43 ]  People with high exposure to  Strongyloides stercoralis  may mitigate the risk of strongyloidiasis hyperinfection associated with corticosteroid treatment, with the presumptive use of ivermectin. Such hyperinfection has been a particular concern during the  COVID-19 pandemic  because of the use of corticosteroids to treat COVID-19. The CDC and other international bodies recommend the use of ivermectin for refugees from areas that have a risk of strongyloidiasis. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8725", "text": "During the 1940s, the treatment of choice was enteric-coated tablets of 60\u00a0mg  gentian violet , three times daily, for 16 days. [ 45 ]   The cure rate was reported to be only about 50 to 70 percent, requiring repeat courses.  It is possible the cure rate was even less than that published in the literature, due to the difficulty in positively diagnosing infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8726", "text": "Low estimates postulate it to affect 30\u2013100\u00a0million people worldwide, [ 1 ]  mainly in tropical and subtropical countries, while higher estimates conservatively extrapolate that infection is upwards to or above 370 million people. [ 2 ]   It belongs to the group of  neglected tropical diseases , and worldwide efforts are aimed at eradicating the infection. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8727", "text": "The disease was first recognized in 1876 by the  French  physician Louis Alexis Normand, working in the naval hospital in  Toulon ; he identified the adult worms and sent them to  Arthur Ren\u00e9 Jean Baptiste Bavay , affiliated with France's Superior Council on Health, who observed that these were the adult forms of the larvae found in the stool. In 1883 the  German  parasitologist  Rudolf Leuckart  made initial observations on the life cycle of the parasite, and Belgian physician Paul Van Durme (building on observations by the German parasitologist  Arthur Looss ) described the mode of infection through the skin. The German parasitologist  Friedrich F\u00fclleborn  described autoinfection and the way by which strongyloidiasis involves the intestine. Interest in the condition increased in the 1940s when it was discovered that those who had acquired the infection abroad and then received immunosuppression developed hyperinfestation syndrome. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8728", "text": "Travelers' diarrhea  ( TD ) is a stomach and intestinal infection. TD is defined as the passage of unformed  stool  (one or more by some definitions, three or more by others) while traveling. [ 2 ] [ 3 ]  It may be accompanied by abdominal cramps, nausea, fever, headache and bloating. [ 3 ]  Occasionally  dysentery  may occur. [ 5 ]  Most travelers recover within three to four days with little or no treatment. [ 3 ]  About 12% of people may have symptoms for a week. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8729", "text": "Bacteria  are responsible for more than half of cases, [ 3 ]  typically via  foodborne illness  and  waterborne diseases . The bacteria  enterotoxigenic  Escherichia coli  (ETEC) are typically the most common except in  Southeast Asia , where  Campylobacter  is more prominent. [ 2 ] [ 3 ]  About 10 to 20 percent of cases are due to  norovirus . [ 3 ]   Protozoa  such as  Giardia  may cause longer term disease. [ 3 ]  The risk is greatest in the first two weeks of travel and among young adults. [ 2 ]  People affected are more often from the  developed world . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8730", "text": "Recommendations for prevention include eating only properly cleaned and cooked food, drinking  bottled water , and frequent  hand washing . [ 4 ]  The  oral cholera vaccine , while effective for  cholera , is of questionable use for travelers'  diarrhea . [ 6 ]  Preventive  antibiotics  are generally discouraged. [ 3 ]  Primary treatment includes rehydration and replacing lost salts ( oral rehydration therapy ). [ 3 ] [ 4 ]  Antibiotics are recommended for significant or persistent symptoms, and can be taken with  loperamide  to decrease diarrhea. [ 3 ]  Hospitalization is required in less than 3 percent of cases. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8731", "text": "Estimates of the percentage of people affected range from 20 to 50 percent among travelers to the  developing world . [ 3 ]  TD is particularly common among people traveling to Asia (except for Japan and Singapore), the Middle East, Africa, Latin America, and Central and South America. [ 4 ] [ 7 ]  The risk is moderate in  Southern Europe , and Russia. [ 8 ]  TD has been linked to later  irritable bowel syndrome  and  Guillain\u2013Barr\u00e9 syndrome . [ 2 ] [ 3 ]  It has colloquially been known by a number of names, including \" Montezuma 's revenge,\" \u201c mummy  tummy\u201d [ 9 ]  and \" Delhi  belly\". [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8732", "text": "The onset of TD usually occurs within the first week of travel, but may occur at any time while traveling, and even after returning home, depending on the incubation period of the infectious agent. [ 11 ]  Bacterial TD typically begins abruptly, but  Cryptosporidium  may incubate for seven days, and  Giardia  for 14 days or more, before symptoms develop. Typically, a traveler experiences four to five loose or watery bowel movements each day. Other commonly associated symptoms are abdominal cramping, bloating, fever, and  malaise . Appetite may decrease significantly. [ 12 ]   Though unpleasant, most cases of TD are mild, and resolve in a few days without medical intervention. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8733", "text": "Blood or  mucus  in the diarrhea, significant abdominal pain, or high fever suggests a more serious cause, such as  cholera , characterized by a rapid onset of weakness and torrents of watery diarrhea with flecks of mucus (described as \"rice water\" stools). Medical care should be sought in such cases; dehydration is a serious consequence of cholera, and may trigger serious  sequelae \u2014including, in rare instances, death\u2014as rapidly as 24 hours after onset if not addressed promptly. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8734", "text": "Infectious agents  are the primary cause of travelers' diarrhea.  Bacterial enteropathogens  cause about 80% of cases.   Viruses  and  protozoans  account for most of the rest. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8735", "text": "The most common causative agent isolated in countries surveyed has been  enterotoxigenic  Escherichia coli  (ETEC). [ 12 ]  Enteroaggregative  E. coli  is increasingly recognized. [ 13 ]   Shigella   spp.  and  Salmonella  spp. are other common bacterial pathogens.   Campylobacter ,  Yersinia ,  Aeromonas , and  Plesiomonas  spp. are less frequently found. Mechanisms of action vary: some bacteria release  toxins  which bind to the intestinal wall and cause diarrhea; others damage the intestines themselves by their direct presence. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8736", "text": "Brachyspira pilosicoli  pathogen also appears to be responsible for many chronic intermittent watery diarrhea and is only diagnosed through colonic biopsies and microscopic discovery of a false brush border  [ 14 ]  on H&E or Warthin silver stain: its brush-border is stronger and longer that Brachyspira aalborgi's brush-border. It is unfortunately often not diagnosed as coproculture does not allow growth and 16S PCR panel primers do not match Brachyspira sequences. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8737", "text": "While viruses are associated with less than 20% of adult cases of travelers' diarrhea, they may be responsible for nearly 70% of cases in infants and children. Diarrhea due to viral agents is unaffected by antibiotic therapy, but is usually self-limited. [ 13 ]   Protozoans such as  Giardia lamblia ,  Cryptosporidium  and  Cyclospora cayetanensis  can also cause diarrhea. Pathogens commonly implicated in travelers' diarrhea appear in the table in this section. [ 13 ] [ 16 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8738", "text": "A subtype of travelers' diarrhea afflicting hikers and campers, sometimes known as  wilderness diarrhea , may have a somewhat different frequency of distribution of pathogens. [ 17 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8739", "text": "The primary source of infection is ingestion of  fecally  contaminated food or water. Attack rates are similar for men and women. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8740", "text": "The most important determinant of risk is the traveler's destination. High-risk destinations include  developing countries  in Latin America, Africa, the Middle East, and Asia. [ 12 ]  Among backpackers, additional risk factors include drinking untreated surface water and failure to maintain personal hygiene practices and clean cookware. [ 18 ]  Campsites often have very primitive (if any) sanitation facilities, making them potentially as dangerous as any developing country. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8741", "text": "Although travelers' diarrhea usually resolves within three to five days (mean duration: 3.6 days), in about 20% of cases, the illness is severe enough to require bedrest, and in 10%, the illness duration exceeds one week. [ 13 ]   For those prone to serious infections, such as   bacillary dysentery ,  amoebic dysentery , and  cholera , TD can occasionally be life-threatening. [ 13 ]   Others at higher-than-average risk include young adults,  immunosuppressed  persons, persons with  inflammatory bowel disease  or  diabetes , and those taking  H2 blockers  or  antacids . [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8742", "text": "Travelers often get diarrhea from eating and drinking foods and beverages that have no adverse effects on local residents. This is due to  immunity  that develops with constant, repeated exposure to pathogenic organisms. The extent and duration of exposure necessary to acquire immunity has not been determined; it may vary with each individual organism. A study among expatriates in Nepal suggests that immunity may take up to seven years to develop\u2014presumably in adults who avoid deliberate pathogen exposure. [ 19 ] \nConversely, immunity acquired by American students while living in Mexico disappeared, in one study, as quickly as eight weeks after cessation of exposure. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8743", "text": "Recommendations include avoidance of questionable foods and drinks, on the assumption that TD is fundamentally a  sanitation  failure, leading to bacterial contamination of drinking water and food. [ 12 ]  While the effectiveness of this strategy has been questioned, given that travelers have little or no control over sanitation in hotels and restaurants, and little evidence supports the contention that food vigilance reduces the risk of contracting TD, [ 21 ]  guidelines continue to recommend basic, common-sense precautions when making food and beverage choices: [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8744", "text": "If handled properly, thoroughly cooked fresh and packaged foods are usually safe. [ 12 ]  Raw or undercooked meat and seafood should be avoided.  Unpasteurized  milk, dairy products, mayonnaise, and pastry icing are associated with increased risk for TD, as are foods and beverages purchased from street vendors and other establishments where unhygienic conditions may be present. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8745", "text": "Although safe bottled water is now widely available in most remote destinations, travelers can treat their own water if necessary, or as an extra precaution. [ 13 ] \nTechniques include boiling, filtering, chemical treatment, and ultraviolet light; boiling is by far the most effective of these methods. [ 22 ]  Boiling rapidly kills all active bacteria, viruses, and protozoa. Prolonged boiling is usually unnecessary; most microorganisms are killed within seconds at water temperature above 55\u201370\u00a0\u00b0C (131\u2013158\u00a0\u00b0F). [ 23 ] [ 24 ]  The second-most effective method is to combine filtration and chemical disinfection. [ 25 ]   Filters eliminate most bacteria and protozoa, but not viruses. Chemical treatment with halogens\u2014chlorine bleach, tincture of iodine, or commercial tablets\u2014have low-to-moderate effectiveness against protozoa such as  Giardia , but work well against bacteria and viruses.\nUV light is effective against both viruses and cellular organisms, but only works in clear water, and it is ineffective unless manufacturer's instructions are carefully followed for maximum water depth/distance from UV source, and for dose/exposure time. Other claimed advantages include short treatment time, elimination of the need for boiling, no taste alteration, and decreased long-term cost compared with bottled water. The effectiveness of UV devices is reduced when water is muddy or turbid; as UV is a type of light, any suspended particles create shadows that hide microorganisms from UV exposure. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8746", "text": "Bismuth subsalicylate  four times daily reduces rates of travelers' diarrhea. [ 2 ] [ 27 ]  Though many travelers find a four-times-per-day regimen inconvenient, lower doses are not effective. [ 2 ] [ 27 ]  Potential side effects include black tongue, black stools, nausea, constipation, and  ringing in the ears . Bismuth subsalicylate should not be taken by those with  aspirin  allergy, kidney disease, or  gout , nor concurrently with certain antibiotics such as the  quinolones , and should not be taken continuously for more than three weeks. [ medical citation needed ]  Some countries do not recommend it due to the risk of rare but serious side effects. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8747", "text": "A  hyperimmune bovine colostrum  to be taken by mouth is marketed in Australia for prevention of ETEC-induced TD. As yet, no studies show efficacy under actual travel conditions. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8748", "text": "Though effective, antibiotics are not recommended for the prevention of TD in most situations because of the risk of allergy or adverse reactions to the antibiotics, and because intake of preventive antibiotics may decrease the effectiveness of such drugs should a serious infection develop subsequently. Antibiotics can also cause  vaginal yeast infections , or overgrowth of the bacterium  Clostridioides difficile , leading to  pseudomembranous colitis  and its associated severe, unrelenting diarrhea. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8749", "text": "Antibiotics may be warranted in special situations where benefits outweigh the above risks, such as immunocompromised travelers, chronic intestinal disorders, prior history of repeated disabling bouts of TD, or scenarios in which the onset of diarrhea might prove particularly troublesome. Options for prophylactic treatment include the  fluoroquinolone  antibiotics (such as  ciprofloxacin ),  azithromycin , and  trimethoprim/sulfamethoxazole , though the latter has proved less effective in recent years. [ 29 ]   Rifaximin  may also be useful. [ 27 ] [ 30 ]   Quinolone antibiotics may bind to metallic cations such as bismuth, and should not be taken concurrently with bismuth subsalicylate. Trimethoprim/sulfamethoxazole should not be taken by anyone with a history of  sulfa  allergy. [ medical citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8750", "text": "The  oral cholera vaccine , while effective for prevention of cholera, is of questionable use for prevention of TD. [ 6 ]  A 2008 review found tentative evidence of benefit. [ 31 ]  A 2015 review stated it may be reasonable for those at high risk of complications from TD. [ 3 ]  Several vaccine candidates targeting ETEC or  Shigella  are in various stages of development. [ 32 ] [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8751", "text": "One 2007 review found that  probiotics  may be safe and effective for prevention of TD, while another review found no benefit. [ 2 ]  A 2009 review confirmed that more study is needed, as the evidence to date is mixed. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8752", "text": "Most cases of TD are mild and resolve in a few days without treatment, but severe or protracted cases may result in significant fluid loss and dangerous  electrolytic imbalance . Dehydration due to diarrhea can also alter the effectiveness of medicinal and contraceptive drugs. Adequate fluid intake ( oral rehydration therapy ) is therefore a high priority. Commercial rehydration drinks [ 34 ]  are widely available; alternatively, purified water or other clear liquids are recommended, along with salty crackers or  oral rehydration salts  (available in stores and pharmacies in most countries) to replenish lost electrolytes. [ 12 ]  Carbonated water or soda, left open to allow dissipation of the carbonation, is useful when nothing else is available. [ 13 ]   In severe or protracted cases, the oversight of a medical professional is advised. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8753", "text": "If diarrhea becomes severe (typically defined as three or more loose stools in an eight-hour period), especially if associated with nausea, vomiting, abdominal cramps, fever, or blood in stools, medical treatment should be sought. Such patients may benefit from antimicrobial therapy. [ 12 ]   A 2000 literature review found that antibiotic treatment shortens the duration and severity of TD; most reported side effects were minor, or resolved on stopping the antibiotic. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8754", "text": "The antibiotic recommended varies based upon the destination of travel. [ 36 ]   Trimethoprim\u2013sulfamethoxazole  and  doxycycline  are no longer recommended because of high levels of resistance to these agents. [ 12 ]  Antibiotics are typically given for three to five days, but single doses of  azithromycin  or  levofloxacin  have been used. [ 37 ]   Rifaximin  and  rifamycin  are approved in the U.S. for treatment of TD caused by ETEC. [ 38 ] [ 39 ]  If diarrhea persists despite therapy, travelers should be evaluated for bacterial strains resistant to the prescribed antibiotic, possible viral or parasitic infections, [ 12 ]  bacterial or amoebic dysentery,  Giardia , helminths, or cholera. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8755", "text": "Antimotility drugs such as  loperamide  and  diphenoxylate  reduce the symptoms of diarrhea by slowing transit time in the gut. They may be taken to slow the frequency of stools, but not enough to stop bowel movements completely, which delays expulsion of the causative organisms from the intestines. [ 12 ]  They should be avoided in patients with fever, bloody diarrhea, and possible inflammatory diarrhea. [ 40 ]  Adverse reactions may include nausea, vomiting, abdominal pain, hives or rash, and loss of appetite. [ 41 ]  Antimotility agents should not, as a rule, be taken by children under age two. [ 42 ] [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8756", "text": "An estimated 10 million people\u201420 to 50% of international travelers\u2014develop TD each year. [ 12 ]   It is more common in the developing world, where rates exceed 60%, but has been reported in some form in virtually every travel destination in the world. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8757", "text": "Moctezuma's revenge  is a colloquial term for travelers' diarrhea contracted in Mexico. The name refers to  Moctezuma II  (1466\u20131520), the  Tlatoani  (ruler) of the  Aztec  civilization who was  overthrown  by the Spanish conquistador  Hern\u00e1n Cort\u00e9s  in the early 16th century, thereby bringing large portions of what is now Mexico and Central America under the rule of the  Spanish crown . The relevance being that Cort\u00e9s and his soldiers carried the  smallpox  virus, which Mexicans had never been exposed to. The resulting infection reduced the population of  Tenochtitlan  by 40 percent in 1520 alone. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8758", "text": "Wilderness diarrhea , also called wilderness-acquired diarrhea (WAD) or backcountry diarrhea, refers to diarrhea among backpackers, hikers, campers and other outdoor recreationalists in wilderness or backcountry situations, either at home or abroad. [ 17 ]   It is caused by the same fecal microorganisms as other forms of travelers' diarrhea, usually bacterial or viral. Since wilderness campsites seldom provide access to sanitation facilities, the infection risk is similar to that of any developing country. [ 18 ]   Water treatment, good hygiene, and dish washing have all been shown to reduce the incidence of WAD. [ 46 ] [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8759", "text": "This article incorporates  public domain material  from websites or documents of the  Centers for Disease Control and Prevention ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8760", "text": "Trichinosis , also known as  trichinellosis , is a  parasitic disease  caused by  roundworms  of the  Trichinella  genus. [ 1 ]  During the initial infection, invasion of the  intestines  can result in  diarrhea ,  abdominal pain , and  vomiting . [ 1 ]  Migration of  larvae  to muscle, which occurs about a week after being infected, can cause  swelling  of the face,  inflammation of the whites of the eyes ,  fever ,  muscle pains , and a  rash . [ 1 ]  Minor infection may be  without symptoms . [ 1 ]  Complications may include  inflammation of heart muscle ,  central nervous system  involvement, and  inflammation of the lungs . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8761", "text": "Trichinosis is mainly spread when undercooked meat containing  Trichinella   cysts  is eaten. [ 1 ]  In North America this is most often bear, but infection can also occur from pork, boar, and dog meat. [ 7 ]  Several  species  of  Trichinella  can cause disease, with  T. spiralis  being the most common. [ 1 ]  After the infected meat has been eaten, the larvae are released from their cysts in the stomach. [ 1 ]  They then invade the wall of the  small intestine , where they develop into adult worms. [ 1 ]  After one week, the females release new larvae that migrate to  voluntarily controlled muscles , where they form cysts. [ 1 ]  The diagnosis is usually based on symptoms and confirmed by finding specific  antibodies in the blood , or larvae on  tissue biopsy . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8762", "text": "The best way to prevent trichinosis is to fully cook meat. [ 3 ]  A  food thermometer  can verify that the temperature inside the meat is high enough. [ 3 ]  Infection is typically treated with antiparasitic medication such as  albendazole  or  mebendazole . [ 4 ]  Rapid treatment may kill adult worms and thereby stop further worsening of symptoms. [ 4 ]  Both medications are considered safe but have been associated with side effects such as  bone marrow suppression . [ 4 ]  Their use during pregnancy or in children under the age of 2 years is poorly studied but appears to be safe. [ 4 ]  Treatment with steroids is sometimes also required in severe cases. [ 4 ]  Without treatment, symptoms typically resolve within three months. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8763", "text": "Worldwide, about 10,000 infections occur a year. [ 6 ]  At least 55 countries including the United States, China, Argentina, and Russia have had recently documented cases. [ 5 ]  While the disease occurs in the tropics, it is less common there. [ 5 ]  Rates of trichinosis in the United States have decreased from about 400 cases per year in the 1940s to 20 or fewer per year in the 2000s. [ 6 ] [ 8 ]  The risk of death from infection is low. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8764", "text": "The great majority of trichinosis infections have either minor or no symptoms and no complications. [ 9 ]  The two main phases for the infection are enteral (affecting the intestines) and parenteral (outside the intestines). The symptoms vary depending on the phase, species of  Trichinella , the quantity of encysted larvae ingested, age, sex, and host immunity. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8765", "text": "A large burden of adult worms in the intestines promotes symptoms such as  nausea ,  heartburn ,  dyspepsia , and  diarrhea  from two to seven days after infection, while small worm burdens generally are asymptomatic.  Eosinophilia  presents early and increases rapidly. [ 11 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8766", "text": "The severity of symptoms caused by larval migration from the intestines depends on the number of larvae produced. As the larvae migrate through tissue and vessels, the body's inflammatory response results in  edema , muscle pain, fever, and weakness. A classic sign of trichinosis is  periorbital edema , swelling around the eyes, which may be caused by  vasculitis .  Splinter hemorrhage  in the nails is also a common symptom. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8767", "text": "They may very rarely cause enough damage to produce serious neurological deficits (such as  ataxia  or  respiratory paralysis ) from worms entering the  central nervous system  (CNS), which is compromised by trichinosis in 10\u201324% of reported cases of  cerebral venous sinus thrombosis , a very rare form of stroke (three or four cases per million annual incidence in adults). [ 13 ]  Trichinosis can be fatal depending on the severity of the infection; death can occur 4\u20136 weeks after the infection, [ 14 ]  and is usually caused by  myocarditis ,  encephalitis , or  pneumonia . [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8768", "text": "The classical agent is  T. spiralis  (found worldwide in many carnivorous and omnivorous animals, both domestic and  sylvatic  (wild), [ citation needed ]  but seven primarily sylvatic species of  Trichinella  also are now recognized:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8769", "text": "The typical lifecycle for  T. spiralis  involves humans, pigs, and rodents. A pig becomes infected when it eats infectious cysts in raw meat, often porcine  carrion  or a  rat  ( sylvatic cycle ). A human becomes infected by consuming raw or undercooked infected pork (domestic cycle). In the stomach, the  cysts  from infected undercooked meat are acted on by  pepsin  and  hydrochloric acid , which help release the larvae from the cysts into the  stomach . [ 10 ]  The larvae then migrate to the  small intestine , and burrow into the  intestinal mucosa , where they molt four times before becoming adults. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8770", "text": "Thirty to 34 hours after the cysts were originally ingested, the adults mate, and within five days produce larvae. [ 10 ]  Adult worms can only reproduce for a limited time because the  immune system  eventually expels them from the small intestine. [ 10 ]  The larvae then use their piercing mouthpart, called the \"stylet\", to pass through the  intestinal mucosa  and enter the  lymphatic vessels , and then enter the  bloodstream . [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8771", "text": "The larvae travel by  capillaries  to various organs, such as the  retina ,  myocardium , or  lymph nodes ; however, only larvae that migrate to  skeletal muscle  cells survive and  encyst . [ 14 ]  The larval host cell becomes a  nurse cell , in which the larva will be encapsulated, potentially for the life of the host, waiting for the host to be eaten. The development of a capillary network around the nurse cell completes encystation of the larva. Trichinosis is not soil-transmitted, as the  parasite  does not lay eggs, nor can it survive long outside a host. [ 5 ] [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8772", "text": "Diagnosis of trichinosis is confirmed by a combination of exposure history, clinical diagnosis, and laboratory testing. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8773", "text": "An epidemiological investigation can be done to determine a patient's exposure to raw infected meat. Often, an infection arises from home preparation of contaminated meat, in which case microscopy of the meat may be used to determine the infection. Exposure determination does not have to be directly from a laboratory-confirmed infected animal. Indirect exposure criteria include the consumption of products from a laboratory-confirmed infected animal or sharing of a common exposure with a laboratory-confirmed infected human. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8774", "text": "Clinical presentation of the common trichinosis symptoms may also suggest infection. These symptoms include eye puffiness,  splinter hemorrhage , nonspecific  gastroenteritis , and muscle pain. [ 14 ]  The case definition for trichinosis at the European Center for Disease Control states, \"at least three of the following six:  fever , muscle soreness and pain,  gastrointestinal symptoms , facial  edema ,  eosinophilia , and subconjunctival, subungual, and retinal  hemorrhages .\" [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8775", "text": "Blood tests and  microscopy  can be used to aid in the diagnosis of trichinosis. Blood tests include a complete blood count for eosinophilia,  creatine phosphokinase  activity, and various immunoassays such as  ELISA  for larval antigens. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8776", "text": "Laws and rules for food producers may improve food safety for consumers, such as the rules established by the  European Commission  for inspections, rodent control, and improved hygiene. [ 14 ]  A similar protocol exists in the United States, in the  USDA  guidelines for farms and slaughterhouse responsibilities in inspecting pork. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8777", "text": "Public education about the dangers of consuming raw and undercooked meat, especially pork, may reduce infection rates. Hunters are also an at-risk population due to their contact and consumption of wild game, including bears. As such, many states, such as New York, require the completion of a course in such matters before a hunting license can be obtained. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8778", "text": "Testing methods are available for both individual carcasses and monitoring of the herds. [ 24 ]  Artificial digestion method is usually used for the testing of individual carcasses, while the testing for specific antibodies is usually used for herd monitoring. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8779", "text": "Larvae may be killed by the heating or  irradiation  of raw meat. Freezing is normally only effective for  T. spiralis , since other species, such as  T. nativa , are freeze-resistant and can survive long-term freezing. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8780", "text": "Pork can be safely cooked to a slightly lower temperature, provided that the internal meat temperature is at least as hot for at least as long as listed in the  USDA  table below. [ 25 ]  Nonetheless, allowing a  margin of error  for variation in internal temperature within a particular cut of pork, which may have bones that affect temperature uniformity, is prudent. In addition, kitchen thermometers have measurement errors that must be considered. Pork may be cooked for significantly longer and at a higher uniform internal temperature than listed below to be safe. [ 26 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8781", "text": "[ 25 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8782", "text": "Unsafe and unreliable methods of cooking meat include the use of microwave ovens, curing, drying, and smoking, as these methods are difficult to standardize and control. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8783", "text": "Incidence of infection can be reduced by: [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8784", "text": "The US  Centers for Disease Control and Prevention  makes the following recommendation: \"Curing (salting), drying, smoking, or microwaving meat does not consistently kill infective worms.\" [ 27 ] \nHowever, under controlled commercial food processing conditions, some of these methods are considered effective by the USDA. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8785", "text": "The USDA Animal and Plant Health Inspection Service (APHIS) is responsible for the regulations concerning the importation of swine from foreign countries. The Foreign Origin Meat and Meat Products, Swine section covers swine meat (cooked, cured, dried, and fresh). APHIS developed the National Trichinae Certification Program; this is a voluntary \"preharvest\" program for U.S. swine producers \"that will provide documentation of swine management practices\" to reduce the incidence of  Trichinella  in swine. [ 29 ]  The CDC reports 0.013% of U.S. swine are infected with  Trichinella . [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8786", "text": "As with most diseases, early treatment is better and decreases the risk of developing the disease. If larvae do encyst in skeletal muscle cells, they can remain infectious for months to years. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8787", "text": "Early administration of  anthelmintics , such as  mebendazole  or  albendazole , decreases the likelihood of larval encystation, particularly if given within three days of infection. [ 12 ]  However, most cases are diagnosed after this time. [ 14 ]   In humans, mebendazole (200\u2013400\u00a0mg three times a day for three days) or albendazole (400\u00a0mg twice a day for 8\u201314 days) is given to treat trichinosis. [ 30 ]  These drugs prevent newly hatched larvae from developing, but should not be given to pregnant women or children under two years of age. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8788", "text": "Medical references from the 1940s described no specific treatment for trichinosis at the time, but intravenous injection of calcium salts was found to be useful in managing symptoms related to severe toxemia from the infection. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8789", "text": "After infection,  steroids , such as  prednisone , may be used to relieve muscle pain associated with larval migration. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8790", "text": "Researchers trying to develop a vaccine for  Trichinella  have tried using either \"larval extracts, excretory-secretory antigen, DNA, or recombinant antigen protein.\" [ 32 ]  Currently, no marketable vaccine is available for trichinosis, but experimental mouse studies have suggested possibilities."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8791", "text": "About 11 million humans are infected with  Trichinella ;  T. spiralis  is the species responsible for most of these infections. [ 36 ]  Infection was once very common, but this disease is now rare in the  developed world , but two known outbreaks occurred in 2015. In the first outbreak, around 40 people were infected in Liguria, Italy, during a New Year's Eve celebration. [ 37 ] [ 38 ]  The second outbreak in France was associated with pork sausages from  Corsica , which were eaten raw, affecting 14 people in total. [ 39 ] \nThe incidence of trichinosis in the U.S. has decreased dramatically in the past century from an average of 400 cases per year mid-20th century down to an annual average of 20 cases per year (2008\u201310). [ 8 ]  The number of cases has decreased because of legislation prohibiting the feeding of raw meat garbage to hogs, increased commercial and home freezing of pork, and the public awareness of the danger of eating raw or undercooked pork products. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8792", "text": "China reports around 10,000 cases every year and is the country with the highest number of cases. [ 14 ] [ dubious  \u2013  discuss ]  In China, between 1964 and 1998, over 20,000 people became infected with trichinosis, and more than 200 people died. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8793", "text": "Trichinosis is common in developing countries where meat fed to pigs is raw or undercooked, but infections also arise in developed countries in Europe where raw or undercooked pork, wild boar, and horse meat may be consumed as delicacies. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8794", "text": "In the  developing world , most infections are associated with undercooked pork. For example, in  Thailand , between 200 and 600 cases are reported annually around the  Thai New Year . This is mostly attributable to a particular delicacy,  larb , which calls for undercooked pork as part of the recipe. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8795", "text": "In parts of Eastern Europe, the  World Health Organization  reports, some swine herds have trichinosis infection rates above 50%, with correspondingly large numbers of human infections. [ 41 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8796", "text": "Historically, pork products were thought to have the most risk of infecting humans with  T. spiralis . However, a trichinosis surveillance conducted between 1997 and 2001 showed a higher percentage of cases caused by consumption of wild game (the sylvatic transmission cycle). This is thought to be due to the Federal Swine Health Protection Act (Public Law 96-468) that was passed by Congress in 1980. Before this act, swine were fed garbage that could potentially be infected by  T. spiralis . This act was put in place to prevent trichinella-contaminated food from being given to swine. Additionally, other requirements were put in place, such as rodent control, limiting commercial swine contact with wildlife, maintaining good hygiene, and removing dead pigs from pens immediately. [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8797", "text": "Between 2002 and 2007, 11 trichinosis cases were reported to the CDC each year on average in the United States, and 2008\u201310 averaged 20 cases per year; [ 8 ]  these were mostly the result of consuming undercooked game (sylvatic transmission) or home-reared pigs (domestic transmission). [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8798", "text": "The  kashrut  and  halal  dietary laws of  Judaism  and  Islam  prohibit eating pork. In the 19th century, when the association between trichinosis and undercooked pork was first established, this association was suggested to be the reason for the prohibition, reminiscent of the earlier opinion of medieval  Jewish  philosopher  Maimonides  that food forbidden by Jewish law was \"unwholesome\". This theory was controversial and eventually fell out of favor. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8799", "text": "The disappearance of the pathogen from domestic pigs has led to a relaxation of legislation and control efforts by veterinary public health systems. Trichinosis has lately been thought of as a re-emerging  zoonosis , supplemented by the increased distribution of meat products, political changes, a changing climate, and increasing  sylvatic  transmission. [ 44 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8800", "text": "Major sociopolitical changes can produce conditions that favor the resurgence of  Trichinella  infections in swine and, consequently, in humans. For instance, \"the overthrow of the social and political structures in the 1990s\" in Romania led to an increase in the incidence rate of trichinosis. [ 45 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8801", "text": "As early as 1835, trichinosis was known to have been caused by a parasite, but the mechanism of infection was unclear at the time. A decade later,  American  scientist  Joseph Leidy  pinpointed undercooked meat as the primary vector for the parasite, and two decades afterward, this hypothesis was fully accepted by the scientific community. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8802", "text": "The circumstances surrounding the first observation and identification of  T. spiralis  are controversial, due to a lack of records. In 1835,  James Paget , a first-year medical student, first observed the larval form of  T. spiralis , while witnessing an autopsy at St. Bartholomew\u2019s Hospital in London. Paget took a special interest in the presentation of muscle with white flecks, described as a \"sandy diaphragm\".  Although Paget is most likely the first person to have noticed and recorded these findings, the parasite was named and published in a report by his professor,  Richard Owen , who is now credited for the discovery of the  T. spiralis  larval form. [ 20 ] [ 47 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8803", "text": "A series of experiments conducted between 1850 and 1870 by the German researchers  Rudolf Virchow ,  Rudolf Leuckart , and  Friedrich Albert von Zenker , which involved feeding infected meat to a dog and performing the subsequent necropsy, led to the discovery of the lifecycle of  Trichinella . Through these experiments, Virchow was able to describe the development and infectivity of  T. spiralis . [ 48 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8804", "text": "The  International Commission on Trichinellosis  (ICT) was formed in Budapest in 1958. Its mission is to exchange information on the epidemiology, biology, pathophysiology, immunology, and clinical aspects of trichinosis in humans and animals. Prevention is a primary goal. Since the creation of the ICT, its members (more than 110 from 46 countries) have regularly gathered and worked together during meetings held every four years: the  International Conference on Trichinellosis . [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8805", "text": "Ascaris trichiura   Linnaeus, 1771"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8806", "text": "Trichuris trichiura ,  Trichocephalus trichiuris  or  whipworm , is a  parasitic   roundworm  (a type of  helminth ) that causes  trichuriasis  (a type of  helminthiasis  which is one of the  neglected tropical diseases ) when it infects a human  large intestine . It is commonly known as the  whipworm  which refers to the shape of the worm; it looks like a  whip  with wider \"handles\" at the posterior end. [ 2 ]  The helminth is also known to cause  rectal prolapse ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8807", "text": "The female  T. trichiura  produces 2,000\u201310,000 single-celled eggs per day. [ 3 ]  Eggs are deposited from human feces to soil where, after two to three weeks, they become embryonated and enter the \"infective\" stage. These embryonated infective eggs are ingested by hand-mouth or through  fomites  and hatch in the human  small intestine , exploiting the intestinal microflora as a stimulus to hatching. [ 4 ]  This is the location of growth and molting. The infective  larvae  penetrate the  villi  and continue to develop in the small intestine. The young worms move to the  caecum  and penetrate the  mucosa , and there they complete development as adult worms in the  large intestine . The life cycle from the time of ingestion of eggs to the development of mature worms takes approximately three months. During this time, there may be limited signs of infection in stool samples, due to a lack of egg production and shedding. The female  T. trichiura  begin to lay eggs after three months of maturity. Worms commonly live for about one year, [ 5 ]  during which time females can lay up to 20,000 eggs per day."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8808", "text": "Recent studies using genome-wide scanning revealed that two quantitative trait loci on  chromosome 9  and  chromosome 18  may be responsible for a genetic predisposition or susceptibility to infection of  T. trichiura  by some individuals. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8809", "text": "Trichuris trichiura  has a narrow anterior esophageal end and shorter and thicker posterior end. These pinkish-white worms are threaded through the  mucosa . They attach to the host through their slender anterior end and feed on tissue secretions instead of blood. Females are larger than males; approximately 35\u201350\u00a0mm long compared to 30\u201345\u00a0mm. [ 7 ]  The females have a bluntly round posterior end compared to their male counterparts with a coiled posterior end. Their characteristic eggs are barrel-shaped and brown, and have bipolar protuberances."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8810", "text": "Trichuriasis , also known as  whipworm infection,  occurs through ingestion of whipworm eggs and is more common in warmer climates. Whipworm eggs are passed in the feces of infected persons, and if an infected person  defecates outdoors  or if untreated human feces is used as fertilizer, eggs are deposited on soil where they can mature into an infective stage. [ 5 ]  Ingestion of these eggs \"can happen when hands or fingers that have contaminated dirt on them are put in the mouth or by consuming vegetables or fruits that have not been carefully cooked, washed or peeled.\" [ 5 ]  The eggs hatch in the small intestine, then move into the wall of the small intestine and develop. On reaching adulthood, the thinner end (the anterior of the worm) burrows into the large intestine, the thicker (posterior) end projecting into the  lumen , where it mates with nearby worms. The females can grow to 50\u00a0mm (2.0\u00a0in) long. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8811", "text": "Trichuris trichiura  can cause the serious disease Trichuris dysentery syndrome (TDS), with chronic dysentery, anemia, rectal prolapse, and poor growth. [ 8 ]  TDS is treated with  anthelminthics  as well as iron supplementation for anemia. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8812", "text": "Whipworm commonly infects patients also infected with  Giardia ,  Entamoeba histolytica ,  Ascaris lumbricoides , and  hookworms . [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8813", "text": "Trichuris trichiura  can be treated with a single dose of  albendazole . [ 11 ]  In Kenya, half of a group of children, 98% of whom had  Trichuris trichiura  with or without infections by other  soil-transmitted helminths , were given albendazole, while the other half of the children received placebos. It was found that the children who received the drug grew significantly better than the group of children who did not receive the treatment. [ 12 ]   Another treatment that can be used is  mebendazole , or  flubendazole . [ 13 ]  The medication interferes with the parasite\u2019s nutrient intake, which eventually leads to death."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8814", "text": "However, it has been shown that both albendazole and mebendazole have low cure rate for  Trichuris thrichiura  specifically, with treatments only achieving cure rates 30,7% for albendazole and 42,1% for mebendazole. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8815", "text": "There is a worldwide distribution of  Trichuris trichiura , with an estimated one billion human infections. [ 15 ] [ 16 ] [ 17 ] [ 8 ]  However, it is chiefly tropical, especially in Asia and, to a lesser degree, in Africa and South America. Within the United States, infection is rare overall but may be common in the rural Southeast, where 2.2 million people are thought to be infected. Poor hygiene is associated with  trichuriasis  as well as the consumption of shaded moist soil, or food that may have been fecally contaminated. Children are especially vulnerable to infection due to their high exposure risk. Eggs are infective about 2\u20133 weeks after they are deposited in the soil under proper conditions of warmth and moisture, hence its tropical distribution."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8816", "text": "A closely related species,  Trichuris suis , which typically infects pigs, is capable of infecting humans. This shows that the two species have very close evolutionary histories. However, morphology and developmental stages remain different, making them two separate species. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8817", "text": "WHO have since 2001 had a strategy for control of soil-transmitted helminths, including whipworms. This strategy entails treating at-risk individuals in the endemic areas. Risk groups for whipworm infections are children at preschool and school-aged children, people with specific high-risk jobs, women in reproductive and pregnant and breastfeeding women. The periodic treatment of the risk groups is done through either deworming campaigns or preventative chemotherapy. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8818", "text": "The  hygiene hypothesis  suggests that various immunological disorders that have been observed in humans only within the last 100 years, such as  Crohn's disease , or that have become more common during that period as hygienic practices have become more widespread, may result from a lack of exposure to parasitic worms ( helminths ) during childhood. The use of  Trichuris suis  ova (TSO, or pig whipworm eggs) by Weinstock, et al., as a therapy for treating Crohn's disease [ 20 ] [ 21 ] [ 22 ]  and to a lesser extent  ulcerative colitis [ 23 ]  are two examples that support this hypothesis. There is also anecdotal evidence that treatment of  inflammatory bowel disease  (IBD) with TSO decreases the incidence of  asthma , [ 24 ] [ self-published source? ]   allergy , [ 25 ]  and other inflammatory disorders. [ 26 ]  Some scientific evidence suggests that the course of  multiple sclerosis  may be very favorably altered by helminth infection; [ 27 ]  TSO is being studied as a treatment for this disease. [ 28 ] [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8819", "text": "Defecography"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8820", "text": "Caroline Pomeroy, PhD July 9th, 2019."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8821", "text": "Among untreated acute cases, 10% will shed bacteria for three months after the initial onset of symptoms, and 2\u20135% will become chronic typhoid carriers. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8822", "text": "Typhoid fever , also known simply as  typhoid , is a disease caused by  Salmonella enterica   serotype  Typhi bacteria, also called  Salmonella typhi . [ 2 ] [ 3 ]  Symptoms vary from mild to severe, and usually begin six to 30 days after exposure. [ 4 ] [ 5 ]  Often there is a gradual onset of a high  fever  over several days. [ 4 ]  This is commonly accompanied by weakness,  abdominal pain ,  constipation ,  headaches , and mild vomiting. [ 6 ] [ 5 ] [ 7 ]  Some people develop a skin rash with  rose colored spots . [ 5 ]  In severe cases, people may experience confusion. [ 7 ]  Without treatment, symptoms may last weeks or months. [ 5 ]   Diarrhea  may be severe, but is uncommon. [ 7 ]  Other people may carry it without being affected, but are still contagious. [ 8 ]  Typhoid fever is a type of  enteric  fever, along with  paratyphoid fever . [ 2 ]   Salmonella  enterica  Typhi is believed to infect and replicate only within humans. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8823", "text": "Typhoid is caused by the bacterium  Salmonella enterica  subsp.  enterica   serovar  Typhi growing in the  intestines ,  Peyer's patches ,  mesenteric lymph nodes ,  spleen ,  liver ,  gallbladder ,  bone marrow  and  blood . [ 5 ] [ 7 ]  Typhoid is spread by eating or drinking food or water contaminated with the  feces  of an infected person. [ 8 ]  Risk factors include limited access to clean drinking water and poor  sanitation . [ 2 ]  Those who have not yet been exposed to it and ingest contaminated drinking water or food are most at risk for developing symptoms. [ 7 ]  Only humans can be infected; there are no known animal reservoirs. [ 8 ]   Salmonella Typhi which causes typhoid fever is different than the other  Salmonella  bacteria that usually cause  salmonellosis , a common type of food poisoning. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8824", "text": "Diagnosis is performed by culturing and identifying  S. enterica typhi  from patient samples or  detecting an immune response to the pathogen from blood samples . [ 5 ] [ 2 ] [ 11 ]  Recently, new advances in large-scale data collection and analysis have allowed researchers to develop better diagnostics, such as detecting changing abundances of small molecules in the blood that may specifically indicate typhoid fever. [ 12 ]  Diagnostic tools in regions where typhoid is most prevalent are quite limited in their accuracy and specificity, and the time required for a proper diagnosis, the increasing spread of  antibiotic resistance , and the cost of testing are also hardships for under-resourced healthcare systems. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8825", "text": "A  typhoid vaccine  can prevent about 40\u201390% of cases during the first two years. [ 13 ]  The vaccine may have some effect for up to seven years. [ 2 ]  For those at high risk or people traveling to areas where it is common, vaccination is recommended. [ 8 ]  Other efforts to prevent it include providing clean  drinking water , good  sanitation , and  handwashing . [ 5 ] [ 8 ]  Until an infection is confirmed as cleared, the infected person should not prepare food for others. [ 5 ]  Typhoid is treated with  antibiotics  such as  azithromycin ,  fluoroquinolones , or  third-generation cephalosporins . [ 2 ]  Resistance to these antibiotics has been developing, which has made treatment more difficult. [ 2 ] [ 14 ] [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8826", "text": "In 2015, 12.5 million new typhoid cases were reported. [ 16 ]  The disease is most common in India. [ 2 ]  Children are most commonly affected. [ 2 ] [ 8 ]  Typhoid decreased in the  developed world  in the 1940s as a result of improved sanitation and the use of antibiotics. [ 8 ]  Every year about 400 cases are reported in the U.S. and an estimated 6,000 people have typhoid. [ 7 ] [ 17 ]  In 2015, it resulted in about 149,000 deaths worldwide \u2013 down from 181,000 in 1990. [ 18 ] [ 19 ]  Without treatment, the risk of death may be as high as 20%. [ 8 ]  With treatment, it is between 1% and 4%. [ 2 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8827", "text": "Typhus  is a different disease, caused by unrelated species of bacteria. [ 20 ]  Owing to their similar symptoms, they were not recognized as distinct diseases until the 1800s. \"Typhoid\" means \"resembling typhus\". [ 21 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8828", "text": "Classically, the progression of untreated typhoid fever has three distinct stages, each lasting about a week. Over the course of these stages, the patient becomes exhausted and emaciated. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8829", "text": "The  Gram-negative  bacterium that causes typhoid fever is  Salmonella enterica  subsp. enterica serovar Typhi. Based on the MLST subtyping scheme, the two main sequence types of the  S.  Typhi are ST1 and ST2, which are widespread globally. [ 25 ]  Global phylogeographical analysis showed dominance of a haplotype 58 (H58), which probably originated in India during the late 1980s and is now spreading through the world with  multi-drug resistance . [ 26 ]  A more detailed genotyping scheme was reported in 2016 and is now widely used. This scheme reclassified the nomenclature of H58 to genotype 4.3.1. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8830", "text": "Unlike other strains of  Salmonella , humans are the only known typhoid carriers. [ 28 ]   S. enterica  subsp. enterica serovar Typhi is spread by the  fecal-oral route  from people who are infected and from  asymptomatic carriers  of the bacterium. [ 28 ]  An asymptomatic human carrier is someone who is still excreting typhoid bacteria in stool a year after the acute stage of the infection. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8831", "text": "Diagnosis is made by any  blood ,  bone marrow , or  stool   cultures  and with the  Widal test  (demonstration of  antibodies  against  Salmonella   antigens   O-somatic  and  H-flagellar ). In epidemics and less wealthy countries, after excluding  malaria ,  dysentery , or  pneumonia , a therapeutic trial time with  chloramphenicol  is generally undertaken while awaiting the results of the Widal test and blood and stool cultures. [ 29 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8832", "text": "The  Widal  test is used to identify specific antibodies in the serum of people with typhoid by using antigen-antibody interactions. [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8833", "text": "In this test, the serum is mixed with a dead bacterial suspension of  Salmonella  with specific antigens. If the patient's serum contains antibodies against those antigens, they get attached to them, forming clumps. If clumping does not occur, the test is negative. The Widal test is time-consuming and prone to significant false positives. It may also be falsely negative in recently infected people. But unlike the Typhidot test, the Widal test quantifies the specimen with  titres . [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8834", "text": "Rapid diagnostic tests such as Tubex, Typhidot, and Test-It have shown moderate diagnostic accuracy. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8835", "text": "Typhidot is based on the presence of specific IgM and IgG antibodies to a specific 50 Kd  OMP antigen. This test is carried out on a cellulose nitrate membrane where a specific  S. typhi  outer membrane protein is attached as fixed test lines. It separately identifies IgM and IgG antibodies. IgM shows recent infection; IgG signifies remote infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8836", "text": "The sample pad of this kit contains colloidal gold-anti-human IgG or gold-anti-human IgM. If the sample contains IgG and IgM antibodies against those antigens, they will react and turn red. The typhidot test becomes positive within 2\u20133 days of infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8837", "text": "Two colored bands indicate a positive test. A single control band indicates a negative test. A single first fixed line or no band at all indicates an invalid test. Typhidot's biggest limitation is that it is not quantitative, just positive or negative. [ 33 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8838", "text": "The Tubex test contains two types of particles: brown magnetic particles coated with antigen and blue indicator particles coated with O9 antibody. During the test, if antibodies are present in the serum, they will attach to the brown magnetic particles and settle at the base, while the blue indicator particles remain in the solution, producing a blue color, which means the test is positive. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8839", "text": "If the serum does not have an antibody in it, the blue particles attach to the brown particles and settle at the bottom, producing a colorless solution, which means the test is negative. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8840", "text": "Sanitation and hygiene are important to prevent typhoid. It can spread only in environments where human feces can come into contact with food or drinking water. Careful food preparation and washing of hands are crucial to prevent typhoid. Industrialization contributed greatly to the elimination of typhoid fever, as it eliminated the public health hazards associated with having horse manure in public streets, which led to a large number of flies, [ 35 ]  which are  vectors  of many pathogens, including  Salmonella  spp. [ 36 ]  According to statistics from the U.S.  Centers for Disease Control and Prevention , the  chlorination  of drinking water has led to dramatic decreases in the transmission of typhoid fever. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8841", "text": "Two  typhoid vaccines  are licensed for use in the prevention of typhoid: [ 13 ]  the live, oral  Ty21a  vaccine (sold as Vivotif by  Crucell  Switzerland AG) and the injectable  typhoid polysaccharide vaccine  (sold as Typhim Vi by  Sanofi Pasteur  and Typherix by  GlaxoSmithKline ). Both are efficacious and recommended for travelers to areas where typhoid is endemic. Boosters are recommended every five years for the oral vaccine and every two years for the injectable form. [ 13 ]  An older, killed  whole-cell vaccine  is still used in countries where the newer preparations are not available, but this vaccine is no longer recommended for use because it has more side effects (mainly pain and inflammation at the site of the injection). [ 38 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8842", "text": "To help decrease rates of typhoid fever in  developing nations , the  World Health Organization  (WHO) endorsed the use of a vaccination program starting in 1999. Vaccination has proven effective at controlling outbreaks in high-incidence areas and is also very cost-effective: prices are normally less than US$1 per dose. Because the price is low, poverty-stricken communities are more willing to take advantage of the vaccinations. [ 39 ]  Although vaccination programs for typhoid have proven effective, they alone cannot eliminate typhoid fever. [ 39 ]  Combining vaccines with public health efforts is the only proven way to control this disease. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8843", "text": "Since the 1990s, the WHO has recommended two typhoid fever vaccines. The ViPS vaccine is given by injection and the Ty21a by capsules. Only people over age two are recommended to be vaccinated with the ViPS vaccine, and it requires a revaccination after 2\u20133 years, with a 55\u201372% efficacy. The Ty21a vaccine is recommended for people five and older, lasting 5\u20137 years with 51\u201367% efficacy. The two vaccines have proved safe and effective for epidemic disease control in multiple regions. [ 39 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8844", "text": "A version of the vaccine combined with a  hepatitis A  vaccine is also available. [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8845", "text": "Results of a phase 3 trial of typhoid  conjugate vaccine  (TCV) in December 2019 reported 81% fewer cases among children. [ 41 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8846", "text": "The rediscovery of  oral rehydration therapy  in the 1960s provided a simple way to prevent many of the deaths of  diarrheal  diseases in general. [ 43 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8847", "text": "Where resistance is uncommon, the treatment of choice is a  fluoroquinolone  such as  ciprofloxacin . [ 44 ] [ 45 ]  Otherwise, a third-generation cephalosporin such as  ceftriaxone  or  cefotaxime  is the first choice. [ 46 ] [ 47 ] [ 48 ] [ 49 ]   Cefixime  is a suitable oral alternative. [ 50 ] [ 51 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8848", "text": "Properly treated, typhoid fever is not fatal in most cases. Antibiotics such as  ampicillin , chloramphenicol,  trimethoprim-sulfamethoxazole ,  amoxicillin , and ciprofloxacin have been commonly used to treat it. [ 52 ]  Treatment with antibiotics reduces the case-fatality rate to about 1%. [ 53 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8849", "text": "Without treatment, some patients develop sustained fever, bradycardia, hepatosplenomegaly, abdominal symptoms, and occasionally pneumonia. In white-skinned patients, pink spots, which fade on pressure, appear on the skin of the trunk in up to 20% of cases. In the third week, untreated cases may develop gastrointestinal and cerebral complications, which may prove fatal in 10\u201320% of cases. The highest case fatality rates are reported in children under 4. Around 2\u20135% of those who contract typhoid fever become chronic carriers, as bacteria persist in the biliary tract after symptoms have resolved. [ 54 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8850", "text": "Surgery is usually indicated if  intestinal perforation  occurs. One study found a 30-day mortality rate of 9% (8/88), and surgical site infections at 67% (59/88), with the disease burden borne predominantly by low-resource countries. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8851", "text": "For surgical treatment, most surgeons prefer simple closure of the perforation with drainage of the  peritoneum . Small bowel  resection  is indicated for patients with multiple perforations. If antibiotic treatment fails to eradicate the  hepatobiliary  carriage, the  gallbladder  should be resected.  Cholecystectomy  is sometimes successful, especially in patients with  gallstones , but is not always successful in eradicating the carrier state because of persisting  hepatic  infection. [ 56 ] [ 57 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8852", "text": "As  resistance  to ampicillin, chloramphenicol, trimethoprim-sulfamethoxazole, and  streptomycin  is now common, these agents are no longer used as first-line treatment of typhoid fever. [ 58 ]  Typhoid resistant to these agents is known as multidrug-resistant typhoid. [ 59 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8853", "text": "Ciprofloxacin resistance is an increasing problem, especially in the  Indian subcontinent  and  Southeast Asia . Many centres are shifting from ciprofloxacin to  ceftriaxone  as the first line for treating suspected typhoid originating in South America, India, Pakistan, Bangladesh, Thailand, or Vietnam. Also, it has been suggested that  azithromycin  is better at treating resistant typhoid than both fluoroquinolone drugs and ceftriaxone. [ 45 ]  Azithromycin can be taken by mouth and is less expensive than ceftriaxone, which is given by injection. [ 60 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8854", "text": "A separate problem exists with laboratory testing for reduced susceptibility to ciprofloxacin; current recommendations are that isolates should be tested simultaneously against ciprofloxacin (CIP) and against  nalidixic acid  (NAL), that isolates sensitive to both CIP and NAL should be reported as \"sensitive to ciprofloxacin\", and that isolates sensitive to CIP but not to NAL should be reported as \"reduced sensitivity to ciprofloxacin\". But an analysis of 271 isolates found that around 18% of isolates with reduced susceptibility to  fluoroquinolones , the class to which CIP belongs ( MIC  0.125\u20131.0\u00a0mg/L), would not be detected by this method. [ 61 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8855", "text": "In 2000, typhoid fever caused an estimated 21.7 million illnesses and 217,000 deaths. [ 11 ]  It occurs most often in children and young adults between 5 and 19 years old. [ 62 ]  In 2013, it resulted in about 161,000 deaths \u2013 down from 181,000 in 1990. [ 19 ]  Infants, children, and adolescents in south-central and Southeast Asia have the highest rates of typhoid. [ 63 ]  Outbreaks are also often reported in sub-Saharan Africa and Southeast Asia. [ 64 ] [ 65 ] [ 66 ]  In 2000, more than 90% of morbidity and mortality due to typhoid fever occurred in Asia. [ 67 ]  In the U.S., about 400 cases occur each year, 75% of which are acquired while traveling internationally. [ 68 ] [ 69 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8856", "text": "Before the antibiotic era, the  case fatality rate  of typhoid fever was 10\u201320%. Today, with prompt treatment, it is less than 1%, [ 70 ]  but 3\u20135% of people who are infected develop a chronic infection in the gall bladder. [ 71 ]  Since  S. enterica  subsp. enterica serovar Typhi is human-restricted, these chronic carriers become the crucial reservoir, which can persist for decades for further spread of the disease, further complicating its identification and treatment. [ 57 ]  Lately, the study of  S. enterica  subsp. enterica serovar Typhi associated with a large outbreak and a carrier at the genome level provides new insight into the pathogenesis of the pathogen. [ 72 ] [ 73 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8857", "text": "In industrialized nations, water sanitation and food handling improvements have reduced the number of typhoid cases. [ 74 ]  Third world nations have the highest rates. These areas lack access to clean water, proper sanitation systems, and proper healthcare facilities. In these areas, such access to basic public-health needs is not expected in the near future. [ 75 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8858", "text": "In 2004\u20132005 an outbreak in the  Democratic Republic of Congo  resulted in more than 42,000 cases and 214 deaths. [ 62 ]  Since November 2016,  Pakistan  has had an outbreak of extensively  drug-resistant  (XDR) typhoid fever. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8859", "text": "In Europe, a report based on data for 2017 retrieved from The European Surveillance System (TESSy) on the distribution of confirmed typhoid and  paratyphoid fever  cases found that 22 EU/EEA countries reported a total of 1,098 cases, 90.9% of which were travel-related, mainly acquired during travel to  South Asia . [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8860", "text": "The  plague of Athens , during the  Peloponnesian War , was most likely an outbreak of typhoid fever. [ 82 ]  During the war,  Athenians  retreated into a walled-in city to escape attack from the  Spartans . This massive influx of humans into a concentrated space overwhelmed the water supply and waste infrastructure, likely leading to unsanitary conditions as fresh water became harder to obtain and waste became more difficult to collect and remove beyond the city walls. [ 82 ]  In 2006, examining the remains of a mass burial site from Athens from around the time of the plague (~430 B.C.) revealed that fragments of DNA similar to modern-day  S.  Typhi  DNA were detected, whereas  Yersinia pestis  (plague),  Rickettsia prowazekii  (typhus),  Mycobacterium tuberculosis ,  cowpox virus , and  Bartonella henselae  were not detected in any of the remains tested. [ 79 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8861", "text": "It is possible that the Roman emperor  Augustus Caesar  had either a liver abscess or typhoid fever, and survived by using ice baths and cold compresses as a means of treatment for his fever. [ 82 ]  There is a statue of the Greek physician,  Antonius Musa , [ 90 ]  who treated his fever. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8862", "text": "The French doctors  Pierre-Fidele Bretonneau  and  Pierre-Charles-Alexandre Louis  are credited with describing typhoid fever as a specific disease, unique from  typhus . Both doctors performed autopsies on individuals who died in Paris due to fever \u2013 and indicated that many had lesions on the  Peyer's patches  which correlated with distinct symptoms before death. [ 82 ]  British medics were skeptical of the differentiation between typhoid and typhus because both were endemic to Britain at that time. However, in France, only typhoid was present circulating in the population. [ 82 ]  Pierre-Charlles-Alexandre Louis also performed case studies and statistical analysis to demonstrate that typhoid was contagious \u2013 and that persons who already had the disease seemed to be protected. [ 82 ]  Afterward, several American doctors confirmed these findings, and then  Sir William Jenner  convinced any remaining skeptics that typhoid is a specific disease recognizable by lesions in the Peyer's patches by examining sixty-six autopsies from fever patients and concluding that the symptoms of headaches, diarrhea, rash spots, and abdominal pain were present only in patients who were found to have intestinal lesions after death; these observations solidified the association of the disease with the intestinal tract and gave the first clue to the route of transmission. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8863", "text": "In 1847  William Budd  learned of an epidemic of typhoid fever in Clifton, and identified that all 13 of 34 residents who had contracted the disease drew their drinking water from the same well. [ 82 ]  Notably, this observation was two years before  John Snow  first published an early version of his theory that contaminated water was the central conduit for transmitting  cholera . Budd later became health officer of  Bristol  ensured a clean water supply, and documented further evidence of typhoid as a water-borne illness throughout his career. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8864", "text": "Polish scientist  Tadeusz Browicz  described a short bacillus in the organs and feces of typhoid victims in 1874. [ 92 ]  Browicz was able to isolate and grow the bacilli but did not go as far as to insinuate or prove that they caused the disease. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8865", "text": "In April 1880, three months before Eberth's publication,  Edwin Klebs  described short and  filamentous  bacilli in the  Peyer's patches  in typhoid victims. [ 93 ]  The bacterium's role in disease was speculated but not confirmed. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8866", "text": "In 1880,  Karl Joseph Eberth  described a bacillus that he suspected was the cause of typhoid. [ 94 ] [ 95 ] [ 96 ]   Eberth is given credit for discovering the bacterium definitively by successfully isolating the same bacterium from 18 of 40 typhoid victims and failing to discover the bacterium present in any \"control\" victims of other diseases. [ 82 ]  In 1884, pathologist  Georg Theodor August Gaffky  (1850\u20131918) confirmed Eberth's findings. [ 97 ]  Gaffky isolated the same bacterium as Eberth from the spleen of a typhoid victim, and was able to grow the bacterium on solid media. [ 82 ]  The organism was given names such as Eberth's bacillus,  Eberthella  Typhi, and Gaffky-Eberth bacillus. [ 82 ]  Today, the bacillus that causes typhoid fever goes by the scientific name  Salmonella enterica  serovar Typhi. [ 98 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8867", "text": "Most developed countries had declining rates of typhoid fever throughout the first half of the 20th century due to vaccinations and advances in public sanitation and hygiene. In 1893 attempts were made to chlorinate the water supply in  Hamburg , Germany, and in 1897  Maidstone , England, was the first town to have its entire water supply chlorinated. [ 99 ]   In 1905, following an outbreak of typhoid fever, the City of  Lincoln, England , instituted permanent water chlorination. [ 100 ]   The first permanent disinfection of drinking water in the US was made in 1908 to the  Jersey City, New Jersey , water supply. Credit for the decision to build the chlorination system has been given to  John L. Leal . [ 101 ]  The  chlorination  facility was designed by  George W. Fuller . [ 102 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8868", "text": "Outbreaks in traveling military groups led to the creation of the Lyster bag in 1915: a bag with a faucet that can be hung from a tree or pole, filled with water, and comes with a chlorination tablet to drop into the water. [ 82 ]  The Lyster bag was essential for the survival of American soldiers in the  Vietnam War . [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8869", "text": "There were several occurrences of  milk delivery men  spreading typhoid fever throughout the communities they served. Although typhoid is not spread through milk itself, there were several examples of milk distributors in many locations watering their milk down with contaminated water, or cleaning the glass bottles the milk was placed in with contaminated water. [ 82 ] [ 85 ]   Boston  had two such cases around the turn of the 20th century. [ 85 ]  In 1899 there were 24 cases of typhoid traced to a single milkman, whose wife had died of typhoid fever a week before the outbreak. [ 85 ]  In 1908, J.J. Fallon, who was also a milkman, died of typhoid fever. [ 85 ]   Following his death and confirmation of the typhoid fever diagnosis, the city conducted an investigation of typhoid symptoms and cases along his route and found evidence of a significant outbreak. A month after the outbreak was first reported, the  Boston Globe  published a short statement declaring the outbreak over, stating \"[a]t Jamaica Plain there is a slight increase, the total being 272 cases. Throughout the city, there is a total of 348 cases.\" [ 85 ]  There was at least one death reported during this outbreak: Mrs. Sophia S. Engstrom, aged 46. [ 85 ]  Typhoid continued to ravage the  Jamaica Plain  neighborhood in particular throughout 1908, and several more people were reported dead due to typhoid fever, although these cases were not explicitly linked to the outbreak. [ 85 ]  The Jamaica Plain neighborhood at that time was home to many working-class and poor immigrants, mostly from  Ireland . [ 103 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8870", "text": "The most notorious carrier of typhoid fever, but by no means the most destructive, was  Mary Mallon , known as Typhoid Mary. [ 104 ] [ 87 ]  Although other cases of human-to-human spread of typhoid were known at the time, the concept of an asymptomatic carrier, who was able to transmit disease, had only been hypothesized and not yet identified or proven. [ 82 ]  Mary Mallon became the first known example of an  asymptomatic carrier  of an infectious disease, making typhoid fever the first known disease being transmissible through asymptomatic hosts. [ 82 ]  The cases and deaths caused by Mallon were mainly upper-class families in New York City. [ 82 ]  At the time of Mallon's tenure as a personal cook for upper-class families, New York City reported 3,000 to 4,500 cases of typhoid fever annually. [ 82 ]  In the summer of 1906 two daughters of a wealthy family and maids working in their home became ill with typhoid fever. [ 82 ]  After investigating their home water sources and ruling out water contamination, the family hired civil engineer  George Soper  to conduct an investigation of the possible source of typhoid fever in the home. [ 82 ]  Soper described himself as an \"epidemic fighter\". [ 82 ]  His investigation ruled out many sources of food, and led him to question if the cook the family hired just prior to their household outbreak, Mallon, was the source. [ 82 ]  Since she had already left and begun employment elsewhere, he proceeded to track her down in order to obtain a stool sample. [ 82 ]   When he was able to finally meet Mallon in person he described her by saying \"Mary had a good figure and might have been called athletic had she not been a little too heavy.\" [ 86 ]  In recounts of Soper's pursuit of Mallon, his only remorse appears to be that he was not given enough credit for his relentless pursuit and publication of her personal identifying information, stating that the media \"rob[s] me of whatever credit belongs to the discovery of the first typhoid fever carrier to be found in America.\" [ 86 ]  Ultimately, 51 cases and 3 deaths were suspected to be caused by Mallon. [ 105 ] [ 87 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8871", "text": "In 1924 the city of  Portland, Oregon , experienced an outbreak of typhoid fever, consisting of 26 cases and 5 deaths, all deaths due to intestinal  hemorrhage . [ 106 ]  All cases were concluded to be due to a single milk farm worker, who was shedding large amounts of the typhoid pathogen in his urine. [ 106 ]  Misidentification of the disease, due to inaccurate Widal test results, delayed identification of the carrier and proper treatment. [ 106 ]  Ultimately, it took four samplings of different secretions from all of the dairy workers in order to successfully identify the carrier. [ 106 ]  Upon discovery, the dairy worker was forcibly quarantined for seven weeks, and regular samples were taken, most of the time the stool samples yielding no typhoid and often the urine yielding the pathogen. [ 106 ]  The carrier was reported as being 72 years old and appearing in excellent health with no symptoms. [ 106 ]  Pharmaceutical treatment decreased the amount of bacteria secreted, however, the infection was never fully cleared from the urine, and the carrier was released \"under orders never again to engage in the handling of foods for human consumption.\" [ 106 ]  At the time of release, the authors noted \"for more than fifty years he has earned his living chiefly by milking cows and knows little of other forms of labor, it must be expected that the closest surveillance will be necessary to make certain that he does not again engage in this occupation.\" [ 106 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8872", "text": "Overall, in the early 20th century the medical profession began to identify disease carriers and evidence of transmission independent of water contamination. [ 82 ]  In a 1933  American Medical Association  publication, physicians' treatment of asymptomatic carriers is best summarized by the opening line \"Carriers of typhoid bacilli are a menace\". [ 107 ]  Within the same publication, the first official estimate of typhoid carriers is given: 2\u20135% of all typhoid patients, and distinguished between temporary carriers and chronic carriers. [ 107 ]  The authors further estimate that there are four to five chronic female carriers to every one male carrier, although offered no data to explain this assertion of a gender difference in the rate of typhoid carriers. [ 107 ]  As far as treatment, the authors suggest: \"When recognized, carriers must be instructed as to the disposal of excreta as well as to the importance of personal cleanliness. They should be forbidden to handle food or drink intended for others, and their movements and whereabouts must be reported to the public health officers\". [ 107 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8873", "text": "Today, typhoid  carriers  exist all over the world, but the highest incidence of  asymptomatic  infection is likely to occur in South/Southeast Asian and Sub-Saharan countries. [ 1 ] [ 108 ]  The  Los Angeles County department of public health  tracks typhoid carriers and reports the number of carriers identified within the county yearly; between 2006 and 2016 0\u20134 new cases of typhoid carriers were identified per year. [ 1 ]  Cases of typhoid fever  must be reported  within one working day from identification. As of 2018, chronic typhoid carriers must sign a \"Carrier Agreement\" and are required to test for typhoid shedding twice yearly, ideally every 6 months. [ 109 ]  Carriers may be released from their agreements upon fulfilling \"release\" requirements, based on completion of a personalized treatment plan designed with medical professionals. [ 109 ]  Fecal or gallbladder carrier release requirements: 6 consecutive negative feces and urine specimens submitted at 1-month or greater intervals beginning at least 7 days after completion of therapy. [ 109 ]  Urinary or kidney carrier release requirements: 6 consecutive negative urine specimens submitted at 1-month or greater intervals beginning at least 7 days after completion of therapy. [ 109 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8874", "text": "Due to the nature of asymptomatic cases, many questions remain about how individuals can tolerate infection for long periods, how to identify such cases, and efficient options for treatment. Researchers are working to understand asymptomatic infection with  Salmonella  species by studying infections in laboratory animals, which will ultimately lead to improved prevention and treatment options for typhoid carriers. In 2002, John Gunn described the ability of  Salmonella  sp. to form  biofilms  on  gallstones  in mice, providing a model for studying carriage in the gallbladder. [ 110 ]   Denise Monack  and  Stanley Falkow  described a mouse model of asymptomatic intestinal and systemic infection in 2004, and  Monack  went on to demonstrate that a subpopulation of  superspreaders  are responsible for the majority of transmission to new hosts, following the  80/20 rule  of disease transmission, and that the intestinal microbiota likely plays a role in transmission. [ 111 ] [ 112 ]   Monack 's mouse model allows long-term carriage of  Salmonella  in  mesenteric lymph nodes ,  spleen  and  liver . [ 111 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8875", "text": "British bacteriologist  Almroth Edward Wright  first developed an effective typhoid vaccine at the Army Medical School in  Netley ,  Hampshire . It was introduced in 1896 and used successfully by the British during the  Second Boer War  in South Africa. [ 113 ]  At that time, typhoid often killed more soldiers at war than were lost due to enemy combat. Wright further developed his vaccine at a newly opened research department at  St Mary's Hospital  Medical School in London in 1902, where he established a method for measuring protective substances ( opsonin ) in human blood. [ 114 ]  Wright's version of the typhoid vaccine was produced by growing the bacterium at  body temperature  in broth, then heating the bacteria to 60\u00a0\u00b0C to \"heat inactivate\" the pathogen, killing it, while keeping the surface  antigens  intact. The heat-killed bacteria was then injected into a patient. [ 82 ]  To show evidence of the vaccine's efficacy, Wright then collected serum samples from patients several weeks post-vaccination, and tested their serum's ability to  agglutinate  live typhoid bacteria. A \"positive\" result was represented by clumping of bacteria, indicating that the body was producing anti-serum (now called  antibodies ) against the pathogen. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8876", "text": "Citing the example of the Second Boer War, during which many soldiers died from easily preventable diseases, Wright convinced the  British Army  that 10 million vaccine doses should be produced for the troops being sent to the  Western Front , thereby saving up to half a million lives during  World War I . [ 115 ]  The British Army was the only combatant at the outbreak of the war to have its troops fully immunized against the bacterium. For the first time, their casualties due to combat exceeded those from disease. [ 116 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8877", "text": "In 1909,  Frederick F. Russell , a  U.S. Army  physician, adopted Wright's typhoid vaccine for use with the Army, and two years later, his vaccination program became the first in which an entire army was immunized. It eliminated typhoid as a significant cause of morbidity and mortality in the U.S. military. [ 117 ]  Typhoid vaccination for members of the American military became mandatory in 1911. [ 82 ]  Before the vaccine, the rate of typhoid fever in the military was 14,000 or greater per 100,000 soldiers. By World War I, the rate of typhoid in American soldiers was 37 per 100,000. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8878", "text": "During the Second World War, the United States Army authorized the use of a trivalent vaccine \u2013 containing heat-inactivated Typhoid,  Paratyphi  A and  Paratyphi  B pathogens. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8879", "text": "In 1934, the discovery of the  Vi capsular  antigen by  Arthur Felix  and  Miss S. R. Margaret Pitt  enabled the development of the safer Vi Antigen vaccine \u2013 which is widely in use today. [ 118 ]  Arthur Felix and Margaret Pitt also isolated the strain Ty2, which became the parent strain of  Ty21a , the strain used as a live-attenuated vaccine for typhoid fever today. [ 119 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8880", "text": "Chloramphenicol  was isolated from  Streptomyces  by  David Gotlieb  during the 1940s. [ 82 ]  In 1948 American army doctors tested its efficacy in treating typhoid patients in  Kuala Lumpur , Malaysia. [ 82 ]  Individuals who received a full course of treatment cleared the infection, whereas patients given a lower dose had a relapse. [ 82 ]  Asymptomatic carriers continued to shed bacilli despite chloramphenicol treatment \u2013 only ill patients were improved with chloramphenicol. [ 82 ]  Resistance to chloramphenicol became frequent in Southeast Asia by the 1950s, and today chloramphenicol is only used as a last resort due to the high prevalence of resistance. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8881", "text": "The disease has been referred to by various names, often associated with symptoms, such as gastric fever, enteric fever, abdominal typhus, infantile remittant fever, slow fever, nervous fever, pythogenic fever, [ 120 ]  drain fever, and low fever. [ 121 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8882", "text": "Ulcerative colitis  ( UC ) is one of the two types of  inflammatory bowel disease  (IBD), with the other type being  Crohn's disease . [ 1 ]  It is a  long-term condition  that results in  inflammation  and  ulcers  of the  colon  and  rectum . [ 1 ] [ 7 ]  The primary symptoms of active disease are  abdominal pain  and  diarrhea  mixed with  blood  ( hematochezia ). [ 1 ]   Weight loss ,  fever , and  anemia  may also occur. [ 1 ]  Often, symptoms come on slowly and can range from mild to severe. [ 1 ]  Symptoms typically occur intermittently with periods of no symptoms between flares. [ 1 ]  Complications may include abnormal dilation of the colon ( megacolon ), inflammation of the eye, joints, or liver, and  colon cancer . [ 1 ] [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8883", "text": "The cause of UC is unknown. [ 1 ]  Theories involve  immune system dysfunction ,  genetics , changes in the  normal gut bacteria , and environmental factors. [ 1 ] [ 8 ]  Rates tend to be higher in the developed world with some proposing this to be the result of  less exposure to intestinal infections , or to a  Western diet  and lifestyle. [ 7 ] [ 9 ]  The removal of the appendix at an early age may be protective. [ 9 ]  Diagnosis is typically by  colonoscopy  with  tissue biopsies . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8884", "text": "Several medications are used to treat symptoms and bring about and maintain remission, including  aminosalicylates  such as  mesalazine  or  sulfasalazine ,  steroids ,  immunosuppressants  such as  azathioprine , and   biologic therapy . [ 1 ]   Removal of the colon by surgery  may be necessary if the disease is severe, does not respond to treatment, or if complications such as colon cancer develop. [ 1 ]   Removal of the colon and rectum  generally cures the condition. [ 1 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8885", "text": "People with ulcerative colitis usually present with  diarrhea  mixed with  blood , [ 12 ]  of gradual onset that persists for an extended period of time (weeks). It is estimated that 90% of people experience rectal bleeding (of varying severity), 90% experience watery or loose stools with increased stool frequency (diarrhea), and 75-90% of people experience bowel urgency. [ 13 ]  Additional symptoms may include fecal incontinence, mucous rectal discharge, and nocturnal defecations. [ 12 ]  With  proctitis  (inflammation of the rectum), people with UC may experience urgency or  rectal tenesmus , which is the urgent desire to evacuate the bowels but with the passage of little stool. [ 12 ]  Tenesmus may be misinterpreted as  constipation , due to the urge to defecate despite small volume of stool passage. Bloody diarrhea and abdominal pain may be more prominent features in severe disease. [ 12 ]  The severity of abdominal pain with UC varies from mild discomfort to very painful bowel movements and abdominal cramping. [ 14 ]  High frequency of bowel movements, weight loss, nausea, fatigue, and fever are also common during disease flares. Chronic bleeding from the GI tract, chronic inflammation, and iron deficiency often leads to  anemia , which can affect quality of life. [ 15 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8886", "text": "The clinical presentation of ulcerative colitis depends on the extent of the disease process. [ 16 ]  Up to 15% of individuals may have severe disease upon initial onset of symptoms. [ 12 ]  A substantial proportion (up to 45%) of people with a history of UC without any ongoing symptoms (clinical remission) have objective evidence of ongoing inflammation. [ 17 ]  Ulcerative colitis is associated with a generalized inflammatory process that can affect many parts of the body. Sometimes, these associated extra-intestinal symptoms are the initial signs of the disease. [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8887", "text": "In contrast to Crohn's disease, which can affect areas of the gastrointestinal tract outside of the colon, ulcerative colitis is usually confined to the colon. Inflammation in ulcerative colitis is usually continuous, typically involving the rectum, with involvement extending proximally (to  sigmoid colon , ascending colon, etc.). [ 19 ]  In contrast, inflammation with Crohn's disease is often patchy, with so-called \"skip lesions\" (intermittent regions of inflamed bowel). [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8888", "text": "The disease is classified by the extent of involvement, depending on how far the disease extends: [ 14 ]   proctitis  (rectal inflammation), left sided colitis (inflammation extending to descending colon), and extensive colitis (inflammation proximal to the descending colon). [ 19 ]  Proctosigmoiditis describes inflammation of the rectum and sigmoid colon. Pancolitis describes involvement of the entire colon, extending from the rectum to the cecum. While usually associated with Crohn's disease,  ileitis  (inflammation of the ileum) also occurs in UC. About 17% of individuals with UC have ileitis. [ 21 ]  Ileitis more commonly occurs in the setting of pancolitis (occurring in 20% of cases of pancolitis), [ 12 ]  and tends to correlate with the activity of colitis. This so-called \"backwash ileitis\" can occur in 10\u201320% of people with  pancolitis  and is believed to be of little clinical significance. [ 22 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8889", "text": "In addition to the extent of involvement, UC is also characterized by severity of disease. [ 19 ]  Severity of disease is defined by symptoms, objective markers of inflammation (endoscopic findings, blood tests), disease course, and the impact of the disease on day-to-day life. [ 19 ]  Most patients are categorized through endoscopy and fecal calprotectin levels. Indicators of low risk for future complications in mild and moderate UC include the following parameters: exhibiting less than 6 stools daily and lack of fever/weight loss. Other indicators include lack of extraintestinal symptoms, low levels of the inflammatory markers  C-reactive protein  (CRP), and  erythrocyte sedimentation rate  (ESR), and fecal  calprotectin , and later age of diagnosis (over 40 years). [ 23 ]  Mild disease correlates with fewer than four stools daily; in addition, mild urgency and rectal bleeding may occur intermittently. [ 19 ]   Mild disease lacks  systemic  signs of toxicity (e.g. fever, chills, weight changes) and exhibits normal levels of the serum inflammatory markers ESR and CRP. [ 23 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8890", "text": "Moderate to severe disease correlates with more than six stools daily, frequent bloody stools and urgency. [ 19 ]  Moderate abdominal pain, low-grade  fever , 38 to 39\u00a0\u00b0C (100 to 102\u00a0\u00b0F), and anemia may develop. [ 19 ]  ESR and CRP are usually elevated. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8891", "text": "The Mayo Score, which incorporates a combination of clinical symptoms (stool frequency and amount of rectal bleeding) with endoscopic findings and a physicians assessment of severity, is often used clinically to classify UC as mild, moderate or severe. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8892", "text": "Acute-Severe Ulcerative Colitis (ASUC) is a severe form which presents acutely and with severe symptoms. This fulminant type is associated with severe symptoms (usually diarrhea, rectal bleeding and abdominal pain) and is usually associated with systemic symptoms including fever. [ 13 ]  It is associated with a high mortality rate as compared to milder forms of UC, with a 3-month and 12 month mortality rate of 0.84% and 1% respectively. [ 13 ]  People with fulminant UC may have inflammation extending beyond just the mucosal layer, causing impaired colonic motility and leading to  toxic megacolon . Toxic megacolon represents a medical emergency, one often treated surgically. If the  serous membrane  is involved, a colonic  perforation  may ensue, which has a 50% mortality rate in people with UC. [ 24 ]  Other complications include  hemorrhage ,  venous thromboembolism , and secondary infections of the colon including  C. difficile  or  cytomegalovirus  colitis. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8893", "text": "Ulcerative colitis may improve and enter remission. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8894", "text": "UC is characterized by immune dysregulation and systemic inflammation, which may result in  symptoms  and  complications  outside the colon. Commonly affected organs include: eyes, joints, skin, and liver. [ 28 ]  The frequency of such extraintestinal manifestations has been reported as between 6 and 47%. [ 29 ] [ 30 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8895", "text": "UC may affect the mouth. About 8% of individuals with UC develop oral manifestations. [ 31 ]  The two most common oral manifestations are  aphthous stomatitis  and  angular cheilitis . [ 31 ]  Aphthous stomatitis is characterized by ulcers in the mouth, which are benign, noncontagious and often recurrent. Angular chelitis is characterized by redness at the corners of the mouth, which may include painful sores or breaks in the skin. [ 31 ]  Very rarely, benign pustules may occur in the mouth (pyostomatitis vegetans). [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8896", "text": "UC may affect the eyes manifesting in scleritis, iritis, and conjunctivitis. Patients may be asymptomatic or experience redness, burning, or itching in eyes. Inflammation may occur in the interior portion of the eye, leading to  uveitis  and  iritis . [ 32 ]  Uveitis can cause blurred vision and eye pain, especially when exposed to light ( photophobia ). Untreated, uveitis can lead to permanent vision loss. [ 32 ]  Inflammation may also involve the white part of the eye ( sclera ) or the overlying connective tissue ( episclera ), causing conditions called  scleritis  and  episcleritis . [ 33 ]  Ulcerative colitis is most commonly associated with uveitis and episcleritis. [ 34 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8897", "text": "UC may cause several joint manifestations, including a type of rheumatologic disease known as  seronegative arthritis , which may affect few large joints (oligoarthritis), the  vertebra  ( ankylosing spondylitis ) or several small joints of the hands and feet (peripheral arthritis). [ 28 ]  Often the insertion site where muscle attaches to bone ( entheses ) becomes inflamed ( enthesitis ). Inflammation may affect the  sacroiliac joint  ( sacroiliitis ). [ 18 ]  It is estimated that around 50% of IBD patients suffer from migratory arthritis. Synovitis, or inflammation of the synovial fluid surrounding a joint, can occur for months and recur in later times but usually does not erode the joint. The symptoms of arthritis include  joint pain , swelling, and  effusion , and often leads to significant morbidity. [ 18 ]  Ankylosing spondylitis and sacroilitis usually occur independent of bowel disease activity in UC. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8898", "text": "Ulcerative colitis may affect the skin. The most common type of skin manifestation,  erythema nodosum , presents in up to 3% of UC patients. It develops as raised, tender red nodules usually appearing on the outer areas of the arms or legs, especially in the anterior tibial area (shins). [ 34 ]  The nodules have diameters that measure approximately 1\u20135\u00a0cm. Erythema nodosum is due to inflammation of the underlying subcutaneous tissue ( panniculitis ), and biopsy will display focal panniculitis (although is often unnecessary in diagnosis). In contrast to joint-related manifestations, erythema nodosum often occurs alongside intestinal disease. Thus, treatment of UC can often lead to resolution of skin nodules. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8899", "text": "Another skin condition associated with UC is pyoderma gangrenosum, which presents as deep skin ulcerations. Pyoderma gangrenosum is seen in about 1% of patients with UC and its formation is usually independent of bowel inflammation. [ 13 ]  Pyoderma gangrenosum is characterized by painful lesions or  nodules  that become  ulcers  which progressively grow. The ulcers are often filled with sterile pus-like material. In some cases, pyoderma gangrenosum may require injection with corticosteroids. [ 28 ]  Treatment may also involve inhibitors of tumor necrosis factor (TNF), a cytokine that promotes cell survival. [ 35 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8900", "text": "Other associations determined between the skin and ulcerative colitis include a skin condition known as  hidradenitis suppurativa  (HS). This condition represents a chronic process in which follicles become occluded leading to recurring inflammation of nodules and abscesses and even  fistulas  tunnels in the skin that drain fluid. [ 36 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8901", "text": "Ulcerative colitis may affect the circulatory and endocrine system. UC increases the risk of blood clots in both arteries and veins; [ 37 ] [ 38 ] [ 39 ]  painful swelling of the lower legs can be a sign of  deep venous thrombosis , while difficulty breathing may be a result of  pulmonary embolism  (blood clots in the lungs). The risk of blood clots is about threefold higher in individuals with IBD. [ 38 ]  The risk of venous thromboembolism is high in ulcerative colitis due to hypercoagulability from inflammation, especially with active or extensive disease. [ 37 ]  Additional risk factors may include surgery, hospitalization, pregnancy, the use of corticosteroids and tofacitinib, a JAK inhibitor. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8902", "text": "Osteoporosis  may occur related to systemic inflammation or prolonged steroid use in the treatment of UC, which increases the risk of bone fractures. [ 18 ]   Clubbing , a deformity of the ends of the fingers, may occur. [ 18 ]   Amyloidosis  may occur, especially with severe and poorly controlled disease, which usually presents with protein in the urine ( proteinuria ) and  nephritic syndrome . [ 18 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8903", "text": "Ulcerative colitis (UC) has a significant association with  primary sclerosing cholangitis  (PSC), a progressive inflammatory disorder of small and large  bile ducts . Up to 70-90% of people with primary sclerosing cholangitis have ulcerative colitis. [ 34 ]  As many as 5% of people with UC may progress to develop primary sclerosing cholangitis. [ 28 ] [ 40 ]  PSC is more common in men, and often begins between 30 and 40 years of age. [ 28 ]  It can present asymptomatically or exhibit symptoms of itchiness (pruritis) and fatigue. Other symptoms include systemic signs such as fever and night sweats. Such symptoms are often associated with a bacterial episodic version of PSC. Upon physical exam, one may discern enlarged liver contours (hepatomegaly) or enlarged spleen (splenomegaly) as well as areas of excoriation. Yellow coloring of the skin, or jaundice, may also be present due to excess of bile byproduct buildup (bilirubin) from the biliary tract."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8904", "text": "In diagnosis, lab results often reveal a pattern indicative of biliary disease (cholestatic pattern). This is often displayed by markedly elevated alkaline phosphatase levels and milder or no elevation in liver enzyme levels. Results of  endoscopic retrograde cholangiography  (ERC) may show bile ducts with thicker walls, areas of dilation or narrowing.  However, some patients with UC and PSC have inflammation that has significantly affected only ramified  intrahepatic bile ducts  of smaller diameter, also known as \"small ducts\", which are not visualized by ERC. [ 41 ] :\u200a604,\u200a609"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8905", "text": "In some cases, primary sclerosing cholangitis occurs several years before the bowel symptoms of ulcerative colitis develop. [ 34 ]  PSC does not parallel the onset, extent, duration, or activity of the colonic inflammation in ulcerative colitis. [ 34 ]  In addition, colectomy does not have an impact on the course of primary sclerosing cholangitis in individuals with UC. [ 34 ]  PSC is associated with an increased risk of colorectal cancer and  cholangiocarcinoma  (bile duct cancer). [ 34 ] [ 28 ]  PSC is a progressive condition, and may result in cirrhosis of the liver. [ 28 ]  No specific therapy has been proven to affect the long-term course of PSC. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8906", "text": "Ulcerative colitis is an  autoimmune disease  characterized by  T-cells  infiltrating the colon. [ 43 ]  No direct causes for UC are known, but factors such as genetics, environment, and an overactive immune system play a role. [ 1 ]  UC is associated with comorbidities that produce symptoms in many areas of the body outside the digestive system."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8907", "text": "A genetic component to the cause of UC can be hypothesized based on aggregation of UC in families, variation of prevalence between different ethnicities,  genetic markers  and  linkages . [ 44 ]  In addition, the identical  twin   concordance  rate is 10%, whereas the  dizygotic twin  concordance rate is only 3%. [ 44 ] [ 45 ]  Between 8 and 14% of people with ulcerative colitis have a family history of inflammatory bowel disease. [ 12 ]  In addition, people with a first degree relative with UC have a four-fold increase in their risk of developing the disease. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8908", "text": "Twelve regions of the  genome  may be linked to UC, including, in the order of their discovery, chromosomes 16, 12, 6, 14, 5, 19, 1, and 3, [ 46 ]  but none of these  loci  has been consistently shown to be at fault, suggesting that the disorder is influenced by multiple genes. For example, chromosome band 1p36 is one such region thought to be linked to inflammatory bowel disease. [ 47 ]  Some of the putative regions encode transporter proteins such as  OCTN1  and  OCTN2 . Other potential regions involve cell scaffolding proteins such as the  MAGUK family .  Human leukocyte antigen  associations may even be at work. In fact, this linkage on chromosome 6 may be the most convincing and consistent of the genetic candidates. [ 46 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8909", "text": "Multiple autoimmune disorders are associated with ulcerative colitis, including  celiac disease , [ 48 ]   psoriasis , [ 49 ]   lupus erythematosus , [ 50 ]   rheumatoid arthritis , [ 51 ]   episcleritis , and  scleritis . [ 32 ]  Ulcerative colitis is also associated with  acute intermittent porphyria . [ 52 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8910", "text": "Many hypotheses have been raised for environmental factors contributing to the pathogenesis of ulcerative colitis, including  diet ,  breastfeeding  and medications. Breastfeeding may have a protective effect in the development of ulcerative colitis. [ 53 ] [ 54 ]  One study of  isotretinoin  found a small increase in the rate of UC. [ 55 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8911", "text": "As the colon is exposed to many dietary substances which may encourage  inflammation , dietary factors have been hypothesized to play a role in the  pathogenesis  of both ulcerative colitis and Crohn's disease. However, research does not show a link between diet and the development of ulcerative colitis. Few studies have investigated such an association; one study showed no  association  of refined  sugar  on the number of people affected of ulcerative colitis. [ 56 ]  High intake of  unsaturated fat  and  vitamin B6  may enhance the risk of developing ulcerative colitis. [ 57 ]  Other identified dietary factors that may influence the development and/or relapse of the disease include meat protein and alcoholic beverages. [ 58 ] [ 59 ]  Specifically, sulfur has been investigated as being involved in the cause of ulcerative colitis, but this is controversial. [ 60 ]   Sulfur restricted diets  have been investigated in people with UC and animal models of the disease. The theory of sulfur as an etiological factor is related to the  gut microbiota  and mucosal sulfide detoxification in addition to the diet. [ 61 ] [ 62 ] [ 63 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8912", "text": "As a result of  a class-action lawsuit and community settlement  with  DuPont , three  epidemiologists  conducted studies on the population surrounding a chemical plant that was exposed to PFOA at levels greater than in the general population. The studies concluded that there was an association between  PFOA  exposure and six health outcomes, one of which being ulcerative colitis. [ 64 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8913", "text": "Levels of  sulfate-reducing bacteria  tend to be higher in persons with ulcerative colitis, which could indicate higher levels of  hydrogen sulfide  in the intestine. An alternative theory suggests that the symptoms of the disease may be caused by toxic effects of the hydrogen sulfide on the cells lining the intestine. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8914", "text": "Infection by  Mycobacterium avium , subspecies  paratuberculosis , has been proposed as the ultimate cause of both ulcerative colitis and Crohn's disease. [ 66 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8915", "text": "An increased amount of colonic sulfate-reducing bacteria has been observed in some people with ulcerative colitis, resulting in higher concentrations of the toxic gas hydrogen sulfide. Human colonic mucosa is maintained by the colonic epithelial barrier and immune cells in the lamina propria (see  intestinal mucosal barrier ). The  short-chain fatty acid   n -butyrate gets oxidized through the  beta oxidation  pathway into carbon dioxide and ketone bodies. It has been shown that  n -butyrate helps supply nutrients to this epithelial barrier. Studies have proposed that hydrogen sulfide plays a role in impairing this beta-oxidation pathway by interrupting the short chain acetyl-CoA dehydrogenase, an enzyme within the pathway. Furthermore, it has been suggested that the protective effect of smoking in ulcerative colitis is due to the  hydrogen cyanide  from cigarette smoke reacting with hydrogen sulfide to produce the non-toxic isothiocyanate, thereby inhibiting sulfides from interrupting the pathway. [ 68 ]  An unrelated study suggested that the sulfur contained in red meats and alcohol may lead to an increased risk of relapse for people in remission. [ 65 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8916", "text": "Other proposed mechanisms driving the pathophysiology of ulcerative colitis involve an abnormal immune response to the normal  gut microbiota . This involves abnormal activity of  antigen presenting cells  (APCs) including  dendritic cells  and  macrophages . Normally, dendritic cells and macrophages patrol the intestinal epithelium and  phagocytose  (engulf and destroy) pathogenic microorganisms and present parts of the microorganism as  antigens  to  T-cells  to stimulate differentiation and activation of the T-cells. [ 13 ]  However, in ulcerative colitis, aberrant activity of dendritic cells and macrophages results in them phagocytosing bacteria of the normal gut microbiome. After ingesting the microbiome bacterium, the APCs release the cytokine  TNF\u03b1  which stimulates inflammatory signaling and recruits inflammatory cells to the intestines, leading to the inflammation that is characteristic of ulcerative colitis. [ 13 ]  The TNF inhibitors, including  infliximab ,  adalimumab  and  golimumab , are used to inhibit this step during the treatment of ulcerative colitis. [ 13 ]  After phagocytosing the microbe, the APCs then enter the  mesenteric lymph nodes  where they present antigens to naive T-cells while also releasing the pro-inflammatory cytokines  IL-12  and  IL-23  which lead to T cell differentiation into  Th1  and  Th17  T-cells. [ 13 ]  IL-12 and IL-23 signaling is blocked by the biologic  ustekinumab  and IL-23 is blocked by  guselkumab ,  mirikizumab  and  risankizumab , medications that are used in the treatment of ulcerative colitis. [ 13 ]  From the mesenteric lymph node, the T-cells then enter the intestinal lymphatic venule which provides transport to the intestinal epithelium where they mediate further inflammation characteristic of ulcerative colitis. [ 13 ]  The T-cells exit the lymphatic venule via the adhesion protein mucosal vascular addressin cell adhesion molecule 1  MAdCAM-1 , the ulcerative colitis biologic treatment  vedolizumab  inhibits T-cell migration out of the lymphatic venules by blocking binding to MAdCAM-1. [ 13 ]  While the medications  ozanimod  and  etrasimod  inhibit the  sphingosine-1-phosphate receptor  to prevent T-cell migration into the efferent lymphatic venules. [ 13 ]  Once the mature Th1 and Th17 T-cells exit the efferent lymphatic venule, they travel to the intestinal mucosa and cause further inflammation. T-cell mediated inflammation is thought to be driven by the  JAK-STAT  intracellular T-cell signaling pathway, leading to the  transcription ,  translation  and release of inflammatory cytokines. This T-cell JAK-STAT signaling is inhibited by the medications  tofacitinib ,  filgotinib  and  upadacitinib  which are used in the treatment of ulcerative colitis. [ 13 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8917", "text": "The initial  diagnostic  workup for ulcerative colitis consists of a complete history and physical examination, assessment of signs and symptoms, laboratory tests and endoscopy. [ 69 ]  Severe UC can exhibit high erythrocyte sedimentation rate (ESR), decreased albumin (a protein produced by the liver), and various changes in electrolytes. As discussed previously, UC patients often also display elevated alkaline phosphatase. Inflammation in the intestine may also cause higher levels of fecal calprotectin or lactoferrin. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8918", "text": "Specific testing may include the following: [ 19 ] [ 71 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8919", "text": "Although ulcerative colitis is a disease of unknown causation, inquiry should be made as to unusual factors believed to trigger the disease. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8920", "text": "The  simple clinical colitis activity index  was created in 1998 and is used to assess the severity of symptoms. [ 72 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8921", "text": "The best test for diagnosis of ulcerative colitis remains  endoscopy , which is examination of the internal surface of the bowel using a flexible camera. Initially, a flexible sigmoidoscopy may be completed to establish the diagnosis. [ 73 ]  The physician may elect to limit the extent of the initial exam if severe colitis is encountered to minimize the risk of  perforation  of the colon. However, a complete colonoscopy with entry into the terminal ileum should be performed to rule out Crohn's disease, and assess extent and severity of disease. [ 73 ]  Endoscopic findings in ulcerative colitis include:  erythema  (redness of the  mucosa ),  friability  of the mucosa, superficial ulceration, and loss of the vascular appearance of the colon. When present, ulcerations may be confluent. Pseudopolyps may be observed. [ 74 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8922", "text": "Ulcerative colitis is usually continuous from the rectum, with the rectum almost universally being involved. Perianal disease is rare. The degree of involvement endoscopically ranges from proctitis (rectal inflammation) to left sided colitis (extending to descending colon), to extensive colitis (extending proximal to descending colon). [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8923", "text": "Biopsies  of the mucosa are taken during endoscopy to confirm the diagnosis of UC and differentiate it from Crohn's disease, which is managed differently clinically. Histologic findings in ulcerative colitis includes: distortion of  crypt  architecture, crypt abscesses, and inflammatory cells in the mucosa (lymphocytes, plasma cells, and granulocytes). [ 28 ]  Unlike the transmural inflammation seen in Crohn's disease, the inflammation of ulcerative colitis is limited to the mucosa. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8924", "text": "Blood and stool tests serve primarily to assess disease severity, level of inflammation and rule out causes of infectious colitis.  All individuals with suspected ulcerative colitis should have stool testing to rule out infection. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8925", "text": "A  complete blood count  may demonstrate anemia, leukocytosis, or thrombocytosis. [ 12 ]  Anemia may be caused by inflammation or bleeding. Chronic blood loss may lead to iron deficiency as a cause for anemia, particularly microcytic anemia (small red blood cells), which can be evaluated with a serum  ferritin ,  iron ,  total iron-binding capacity  and  transferrin saturation . Anemia may be due to a complication of treatment from azathioprine, which can cause low blood counts, [ 75 ]  or sulfasalazine, which can result in folate deficiency. Thiopurine metabolites (from azathioprine) and a folate level can help. [ 76 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8926", "text": "UC may cause high levels of inflammation throughout the body, which may be quantified with serum inflammatory markers, such as CRP and ESR.  However, elevated inflammatory markers are not specific for UC and elevations are commonly seen in other conditions, including infection. In addition, inflammatory markers are not uniformly elevated in people with ulcerative colitis.  Twenty five percent of individuals with confirmed inflammation on endoscopic evaluation have a normal CRP level. [ 19 ]   Serum albumin  may also be low related to inflammation, in addition to loss of protein in the GI tract associated with bleeding and colitis.  Low serum levels of vitamin D  are associated with UC, although the significance of this finding is unclear. [ 77 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8927", "text": "Specific antibody markers may be elevated in ulcerative colitis. Specifically,  perinuclear antineutrophil cytoplasmic antibodies  (pANCA) are found in 70 percent of cases of UC. [ 19 ]  Antibodies against  Saccharomyces cerevisiae  may be present, but are more often positive in Crohn's disease compared with ulcerative colitis.  However, due to poor accuracy of these serolologic tests, they are not helpful in the diagnostic evaluation of possible inflammatory bowel disease. [ 19 ] [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8928", "text": "Several stool tests may help quantify the extent of inflammation present in the colon and rectum.   Fecal calprotectin  is elevated in inflammatory conditions affecting the colon, and is useful in distinguishing irritable bowel syndrome (noninflammatory) from a flare in inflammatory bowel disease. [ 19 ]  Fecal calprotectin is 88% sensitive and 79% specific for the diagnosis of ulcerative colitis. [ 19 ]  If the fecal calprotectin is low, the likelihood of inflammatory bowel disease are less than 1 percent. [ 12 ]   Lactoferrin  is an additional nonspecific marker of intestinal inflammation. [ 78 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8929", "text": "Overall, imaging tests, such as  x-ray  or CT scan, may be helpful in assessing for complications of ulcerative colitis, such as perforation or toxic megacolon. Bowel ultrasound (US) is a cost-effective, well-tolerated, non-invasive and readily available tool for the management of patients with inflammatory bowel disease (IBD), including UC, in clinical practice. [ 79 ]  Some studies demonstrated that bowel ultrasound is an accurate tool for assessing disease activity in people with ulcerative colitis. [ 80 ] [ 81 ]  Imaging is otherwise of limited use in diagnosing ulcerative colitis. [ 12 ] [ 28 ]  Magnetic resonance imaging (MRI) is necessary to diagnose underlying PSC. [ 28 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8930", "text": "Abdominal xray is often the test of choice and may display nonspecific findings in cases of mild or moderate ulcerative colitis. In circumstances of severe UC, radiographic findings may include thickening of the mucosa, often termed \"thumbprinting\", which indicates swelling due to fluid displacement (edema). Other findings may include colonic dilation and stool buildup evidencing constipation. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8931", "text": "Similar to xray, in mild ulcerative colitis, double contrast barium enema often shows nonspecific findings. Conversely, barium enema may display small buildups of barium in microulcerations. Severe UC can be characterized by various polyps, colonic shortening, loss of haustrae (the small bulging pouches in the colon), and narrowing of the colon. It is important to note that barium enema should not be conducted in patients exhibiting very severe symptoms as this may slow or stop stool passage through the colon causing ileus and toxic megacolon. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8932", "text": "Other methods of imaging include computed tomography (CT) and magnetic resonance imaging (MRI). Both may depict colonic wall thickening but have decreased ability to find early signs of wall changes when compared to barium enema. In cases of severe ulcerative colitis, however, they often exhibit equivalent ability to detect colonic changes. [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8933", "text": "Doppler ultrasound is the last means of imaging that may be used. Similar to the imaging methods mentioned earlier, this may show some thickened bowel wall layers. In severe cases, this may show thickening in all bowel wall layers (transmural thickness). [ 70 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8934", "text": "Several conditions may present in a similar manner as ulcerative colitis and should be excluded. Such conditions include: Crohn's disease, infectious colitis,  nonsteroidal anti-inflammatory drug  enteropathy, and  irritable bowel syndrome . Alternative causes of colitis should be considered, such as  ischemic colitis  (inadequate blood flow to the colon),  radiation colitis  (if prior exposure to  radiation therapy ), or  chemical colitis .  Pseudomembranous colitis  may occur due to  Clostridioides difficile  infection  following administration of antibiotics.  Entamoeba histolytica  is a protozoan parasite that causes intestinal inflammation. A few cases have been misdiagnosed as UC with poor outcomes occurring due to the use of corticosteroids. [ 82 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8935", "text": "The most common disease that mimics the symptoms of ulcerative colitis is Crohn's disease, as both are inflammatory bowel diseases that can affect the colon with similar symptoms. It is important to differentiate these diseases since their courses and treatments may differ. In some cases, however, it may not be possible to tell the difference, in which case the disease is classified as indeterminate colitis. [ 83 ]  Crohn's disease can be distinguished from ulcerative colitis in several ways. Characteristics that indicate Crohn's include evidence of disease around the anus (perianal disease). This includes anal fissures and abscesses as well as fistulas, which are abnormal connections between various bodily structures. [ 84 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8936", "text": "Infectious colitis is another condition that may present in similar manner to ulcerative colitis. Endoscopic findings are also oftentimes similar. One can discern whether a patient has infectious colitis by employing tissue cultures and stool studies. Biopsy of the colon is another beneficial test but is more invasive."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8937", "text": "Other forms of colitis that may present similarly include radiation and diversion colitis. Radiation colitis occurs after irradiation and often affects the rectum or sigmoid colon, similar to ulcerative colitis. Upon histology radiation colitis may indicate eosinophilic infiltrates, abnormal epithelial cells, or fibrosis. Diversion colitis, on the other hand, occurs after portions of bowel loops have been removed. Histology in this condition often shows increased growth of lymphoid tissue."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8938", "text": "In patients who have undergone transplantation, graft versus host disease may also be a differential diagnosis. This response to transplantation often causes prolonged diarrhea if the colon is affected. Typical symptoms also include rash. Involvement of the upper gastrointestinal tract may lead to difficulty swallowing or ulceration. Upon histology, graft versus host disease may present with crypt cell necrosis and breakdown products within the crypts themselves. [ 85 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8939", "text": "Standard treatment for ulcerative colitis depends on the extent of involvement and disease severity. The goal is to induce remission initially with medications, followed by the administration of maintenance medications to prevent a relapse. The concept of induction of remission and maintenance of remission is very important. The medications used to induce and maintain a remission somewhat overlap, but the treatments are different. Physicians first direct treatment to inducing remission, which involves relief of symptoms and mucosal healing of the colon's lining, and then longer-term treatment to maintain remission and prevent complications. [ 91 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8940", "text": "For acute stages of the disease, a  low fiber diet  may be recommended. [ 92 ] [ 93 ] [ 94 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8941", "text": "The first-line maintenance medication for ulcerative colitis in remission is  mesalazine  (also known as mesalamine or 5-ASA). [ 95 ] [ 96 ]  For patients with active disease limited to the  left colon  (descending colon) or proctitis, mesalazine is also the first-line agent, and a combination of  suppositories  and oral mesalazine may be tried. Adding  corticosteroids  such as  prednisone  is also common in active disease, especially if remission is not achieved through mesalazine monotherapy, [ 95 ] [ 96 ]  but they are not used in long-term treatment as their risks then outweigh their benefits. Immunosuppressive medications such as  azathioprine  and  biological agents  such as  infliximab ,  adalimumab ,  ustekinumab ,  vedolizumab , or  risankizumab  are given in severe disease or if a patient cannot achieve remission with mesalazine and corticosteroids. [ 97 ] [ 98 ]  As an alternative to mesalazine, one of its  prodrugs  such as  sulfasalazine  may be chosen for treatment of active disease or maintenance therapy, [ 99 ]  but the prodrugs have greater potential for serious side effects and have not been demonstrated to be superior to mesalazine in large trials. [ 100 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8942", "text": "A formulation of  budesonide  was approved by the U.S.  Food and Drug Administration  (FDA) for treatment of active ulcerative colitis in January 2013. [ 101 ] [ 102 ]  In 2018,  tofacitinib  was approved for treatment of moderately to severely active ulcerative colitis in the United States, the first oral medication indicated for long term use in this condition. [ 103 ]  The evidence on  methotrexate  does not show a benefit in producing remission in people with ulcerative colitis. [ 104 ]   Cyclosporine  is effective for severe UC [ 97 ]  and  tacrolimus  has also shown benefits. [ 105 ] [ 106 ] [ 107 ] [ 108 ]   Etrasimod  was approved for medical use in the United States in October 2023. [ 109 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8943", "text": "Sulfasalazine has been a major agent in the therapy of mild to moderate ulcerative colitis for over 50 years. In 1977, it was shown that 5-aminosalicylic acid (5-ASA,  mesalazine /mesalamine) was the therapeutically active component in sulfasalazine. [ 110 ]   Many 5-ASA drugs have been developed with the aim of delivering the active compound to the large intestine to maintain therapeutic efficacy but with reduction of the side effects associated with the sulfapyridine moiety in sulfasalazine.  Oral 5-ASA drugs are particularly effective in inducing and in maintaining remission in mild to moderate ulcerative colitis. [ 111 ] [ 112 ]   Rectal suppository, foam or liquid enema formulations of 5-ASA are used for colitis affecting the rectum, sigmoid or descending colon, and have been shown to be effective especially when combined with oral treatment. [ 113 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8944", "text": "Biologic treatments such as the  TNF inhibitors   infliximab ,  adalimumab , and  golimumab  are commonly used to treat people with UC who are no longer responding to corticosteroids.  Tofacitinib  and  vedolizumab  can also produce good clinical remission and response rates in UC. [ 8 ]  Biologics may be used early in treatment (step down approach), or after other treatments have failed to induce remission (step up approach); the strategy should be individualized. [ 114 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8945", "text": "Unlike aminosalicylates, biologics can cause serious side effects such as an increased risk of developing extra-intestinal cancers, [ 115 ]   heart failure ; and weakening of the immune system, resulting in a  decreased ability of the immune system to clear infections  and reactivation of latent infections such as  tuberculosis . For this reason, people on these treatments are closely monitored and are often tested for hepatitis and tuberculosis annually. [ 116 ] [ 117 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8946", "text": "Etrasimod, a once-daily oral sphingosine 1-phosphate (S1P) receptor modulator that selectively activates S1P receptor subtypes 1, 4, and 5 with no detectable activity on S1P 2 or 3, is in development for treatment of immune-mediated diseases, including ulcerative colitis, and was shown in 2 randomized trials to be effective and well tolerated as induction and maintenance therapy in patients with moderately to severely active ulcerative colitis. [ 118 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8947", "text": "Unlike  Crohn's disease , ulcerative colitis has a lesser chance of affecting smokers than non-smokers. [ 119 ] [ 120 ]  In select individuals with a history of previous tobacco use, resuming low dose smoking may improve signs and symptoms of active ulcerative colitis, [ 121 ]  but it is not recommended due to the overwhelmingly negative  health effects of tobacco . [ 122 ]  Studies using a  transdermal nicotine  patch have shown clinical and histological improvement. [ 123 ]  In one double-blind, placebo-controlled study conducted in the  United Kingdom , 48.6% of people with UC who used the nicotine patch, in conjunction with their standard treatment, showed complete resolution of symptoms. Another randomized, double-blind, placebo-controlled, single-center clinical trial conducted in the  United States  showed that 39% of people who used the patch showed significant improvement, versus 9% of those given a placebo. [ 124 ]  However, nicotine therapy is generally not recommended due to side effects and inconsistent results. [ 125 ] [ 126 ] [ 127 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8948", "text": "The gradual loss of blood from the gastrointestinal tract, as well as chronic inflammation, often leads to anemia, and professional guidelines suggest routinely monitoring for anemia with blood tests repeated every three months in active disease and annually in quiescent disease. [ 128 ]  Adequate disease control usually improves anemia of chronic disease, but iron deficiency anemia should be treated with iron supplements. The form in which treatment is administered depends both on the severity of the anemia and on the guidelines that are followed. Some advise that  parenteral iron  be used first because people respond to it more quickly, it is associated with fewer gastrointestinal side effects, and it is not associated with compliance issues. [ 129 ]  Others require oral iron to be used first, as people eventually respond and many will tolerate the side effects. [ 128 ] [ 130 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8949", "text": "Anticholinergic  drugs, more specifically  muscarinic antagonists , are sometimes used to treat abdominal cramps in connection with ulcerative colitis through their calming effect on colonic  peristalsis  (reducing both amplitude and frequency) and  intestinal tone . [ 131 ] [ 132 ]  Some medical authorities suggest over-the-counter anticholinergic drugs as potential helpful treatments for abdominal cramping in mild ulcerative colitis. [ 133 ]  However, their use is contraindicated especially in moderate to severe disease states because of the potential for anticholinergic treatment to induce  toxic megacolon  in patients with colonic inflammation. [ 134 ]  Toxic megacolon is a state in which the colon is abnormally distended, and may in severe or untreated cases lead to colonic  perforation , sepsis, and death. [ 135 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8950", "text": "Many patients affected by ulcerative colitis need immunosuppressant therapies, which may be associated with a higher risk of contracting opportunistic infectious diseases. [ 136 ] \nMany of these potentially harmful diseases, such as  Hepatitis B ,  Influenza ,  chickenpox ,  herpes zoster virus ,  pneumococcal pneumonia , or  human papilloma virus , can be prevented by vaccines. Each drug used in the treatment of IBD should be classified according to the degree of immunosuppression induced in the patient. Several guidelines suggest investigating patients' vaccination status before starting any treatment and performing vaccinations against vaccine preventable diseases when required. [ 137 ] [ 138 ]  \nCompared to the rest of the population, patients affected by IBD are known to be at higher risk of contracting some vaccine-preventable diseases. [ 139 ]  Patients treated with  Janus kinase inhibitor  showed higher risk of   Shingles . [ 140 ]   Nevertheless, despite the increased risk of infections, vaccination rates in IBD patients are known to be suboptimal and may also be lower than vaccination rates in the general population. [ 141 ] [ 142 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8951", "text": "Unlike in Crohn's disease, the gastrointestinal aspects of ulcerative colitis can generally be cured by  surgical removal of the large intestine , though extraintestinal symptoms may persist. This procedure is necessary in the event of:  exsanguinating   hemorrhage , frank perforation, or documented or strongly suspected  carcinoma . Surgery is also indicated for people with severe colitis or toxic megacolon. People with symptoms that are disabling and do not respond to drugs may wish to consider whether surgery would improve the quality of life. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8952", "text": "The removal of the entire large intestine, known as a  proctocolectomy , results in a permanent ileostomy \u2013 where a  stoma  is created by pulling the terminal ileum through the abdomen. Intestinal contents are emptied into a removable  ostomy bag  which is secured around the stoma using adhesive. [ 146 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8953", "text": "Another surgical option for ulcerative colitis that is affecting most of the large bowel is called the  ileal pouch-anal anastomosis (IPAA) . This is a two- or three-step procedure. In a three-step procedure, the first surgery is a  sub-total colectomy , in which the large bowel is removed, but the rectum remains in situ, and a temporary ileostomy is made. The second step is a  proctectomy  and formation of the ileal pouch (commonly known as a \"j-pouch\"). This involves removing the large majority of the remaining rectal stump and creating a new \"rectum\" by fashioning the end of the small intestine into a pouch and attaching it to the anus. After this procedure, a new type of ileostomy is created (known as a loop ileostomy) to allow the anastomoses to heal. The final surgery is a take-down procedure where the ileostomy is reversed and there is no longer the need for an ostomy bag. When done in two steps, a proctocolectomy \u2013 removing both the colon and rectum \u2013 is performed alongside the pouch formation and loop ileostomy. The final step is the same take-down surgery as in the three-step procedure. Time taken between each step can vary, but typically a six- to twelve-month interval is recommended between the first two steps, and a minimum of two to three months is required between the formation of the pouch and the ileostomy take-down. [ 14 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8954", "text": "While the ileal pouch procedure removes the need for an ostomy bag, it does not restore normal bowel function. In the months following the final operation, patients typically experience 8\u201315 bowel movements a day. Over time this number decreases, with many patients reporting 4\u20136 bowel movements after one year post-op. While many patients have success with this procedure, there are a number of known complications.  Pouchitis , inflammation of the ileal pouch resulting in symptoms similar to ulcerative colitis, is relatively common. Pouchitis can be acute, remitting, or chronic however treatment using antibiotics, steroids, or biologics can be highly effective. Other complications include fistulas, abscesses, and pouch failure. Depending on the severity of the condition, pouch revision surgery may need to be performed. In some cased the pouch may need to be de-functioned or removed and an ileostomy recreated. [ 147 ] [ 148 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8955", "text": "The risk of cancer arising from an ileal pouch anal anastomosis is low. [ 149 ]  However, annual surveillance with  pouchoscopy  may be considered in individuals with risk factors for dysplasia, such as a history of dysplasia or colorectal cancer, a history of PSC, refractory pouchitis, and severely inflamed atrophic pouch mucosa. [ 149 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8956", "text": "In a number of randomized clinical trials,  probiotics  have demonstrated the potential to be helpful in the treatment of ulcerative colitis. Specific types of probiotics such as  Escherichia coli  Nissle  have been shown to induce remission in some people for up to a year. [ 150 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8957", "text": "A  Cochrane  review of  controlled trials  using various probiotics found low-certainty evidence that probiotic supplements may increase the probability of clinical remission. [ 151 ]  People receiving probiotics were 73% more likely to experience disease remission and over 2x as likely to report improvement in symptoms compared to those receiving a placebo, with no clear difference in minor or serious adverse effects. [ 151 ]  Although there was no clear evidence of greater remission when probiotic supplements were compared with  5\u2010aminosalicylic acid  treatment as a  monotherapy , the likelihood of remission was 22% higher if probiotics were used in combination with 5-aminosalicylic acid therapy. [ 151 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8958", "text": "It is unclear whether probiotics help to prevent future relapse in people with stable disease activity, either as a monotherapy or  combination therapy . [ 152 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8959", "text": "Fecal microbiota transplant  involves the infusion of human probiotics through fecal enemas. Ulcerative colitis typically requires a more prolonged bacteriotherapy treatment than  Clostridioides difficile  infection does to be successful, possibly due to the time needed to heal the ulcerated epithelium. The response of ulcerative colitis is potentially very favorable with one study reporting 67.7% of people experiencing complete remission. [ 153 ]  Other studies found a benefit from using fecal microbiota transplantation. [ 154 ] [ 155 ] [ 156 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8960", "text": "A variety of alternative medicine therapies have been used for ulcerative colitis, with inconsistent results.  Curcumin (turmeric)  therapy, in conjunction with taking the medications  mesalamine  or  sulfasalazine , may be effective and safe for maintaining remission in people with quiescent ulcerative colitis. [ 157 ] [ 158 ]  The effect of  curcumin  therapy alone on quiescent ulcerative colitis is unknown. [ 158 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8961", "text": "Treatments using  cannabis  or cannabis oil are uncertain. So far, studies have not determined its effectiveness and safety. [ 159 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8962", "text": "Many interventions have been considered to manage abdominal pain in people with ulcerative colitis, including  FODMAPs  diet,  relaxation  training,  yoga ,  kefir  diet and stellate  ganglion block  treatment. It is unclear whether any of these are safe or effective at improving pain or reducing  anxiety  and  depression . [ 160 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8963", "text": "Diet can play a role in symptoms of patients with ulcerative colitis. [ 161 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8964", "text": "The most avoided foods by patients are spicy foods, dairy products, alcohol, fruits and vegetables and carbonated beverages; these foods are mainly avoided during remission and to prevent relapse. In some cases, especially in the flares period, the dietary restrictions of these patients can be very severe and can lead to a compromised nutritional state. Some patients tend to eliminate gluten spontaneously, despite not having a definite diagnosis of  Coeliac disease , because they believe that gluten can exacerbate gastrointestinal symptoms. [ 162 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8965", "text": "Many studies found that patients with IBD reported a higher frequency of depressive and anxiety disorders than the general population, and most studies confirm that women with IBD are more likely than men to develop affective disorders and show that up to 65% of them may have  depression disorder  and  anxiety disorder . [ 163 ] [ 164 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8966", "text": "A meta analysis of interventions to improve mood (including talking therapy,  antidepressants , and exercise) in people with inflammatory bowel disease found that they reduced inflammatory markers such as  C-reactive protein  and  faecal calprotectin . Psychological therapies reduced inflammation more than antidepressants or exercise. [ 165 ] [ 166 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8967", "text": "Poor prognostic factors include: age < 40 years upon diagnosis, extensive colitis, severe colitis on endoscopy, prior hospitalization, elevated CRP and low serum albumin. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8968", "text": "People with ulcerative colitis usually have an intermittent course, with periods of disease inactivity alternating with \"flares\" of disease. People with proctitis or left-sided colitis usually have a more benign course: only 15% progress proximally with their disease, and up to 20% can have sustained remission in the absence of any therapy. A subset of people experience a course of disease progress rapidly. In these cases, there is usually a failure to respond to medication and surgery often is performed within the first few years of disease onset. [ 167 ] [ 168 ]  People with more extensive disease are less likely to sustain remission, but the rate of remission is independent of the severity of the disease. [ 169 ]  Several risk factors are associated with eventual need for colectomy, including: prior hospitalization for UC, extensive colitis, need for systemic steroids, young age at diagnosis, low serum albumin, elevated inflammatory markers (CRP & ESR), and severe inflammation seen during colonoscopy. [ 97 ] [ 19 ]  Surgical removal of the large intestine is necessary in some cases. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8969", "text": "The risk of  colorectal cancer  is significantly increased in people with ulcerative colitis after ten years if involvement is beyond the  splenic flexure . People with backwash ileitis might have an increased risk for colorectal carcinoma. [ 170 ]  Those people with only proctitis usually have no increased risk. [ 19 ]  It is recommended that people have screening  colonoscopies  with random biopsies to look for  dysplasia  after eight years of disease activity, at one to two year intervals. [ 171 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8970", "text": "People with ulcerative colitis are at similar [ 172 ]  or perhaps slightly increased overall risk of  death  compared with the background population. [ 173 ]  However, the distribution of causes-of-death differs from the general population. [ 172 ]  Specific risk factors may predict worse outcomes and a higher risk of mortality in people with ulcerative colitis, including  C. difficile  infection [ 19 ]  and  cytomegalovirus infection  (due to reactivation). [ 174 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8971", "text": "Together with  Crohn's disease , about 11.2 million people were affected as of 2015 [update] . [ 175 ]  Each year it newly occurs in 1 to 20 per 100,000 people, and 5 to 500 per 100,000 individuals are affected. [ 7 ] [ 9 ]  The disease is more common in North America and Europe than other regions. [ 9 ]  Often it begins in people aged 15 to 30 years, or among those over 60. [ 1 ]  Males and females appear to be affected in equal proportions. [ 7 ]  It has also become more common since the 1950s. [ 7 ] [ 9 ]  Together, ulcerative colitis and Crohn's disease affect about a million people in the United States. [ 176 ]  With appropriate treatment the risk of death appears the same as that of the general population. [ 3 ]  The first description of ulcerative colitis occurred around the 1850s. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8972", "text": "Each year, ulcerative colitis newly occurs in 1 to 20 per 100,000 people (incidence), and there are a total of 5\u2013500 per 100,000 individuals with the disease (prevalence). [ 7 ] [ 9 ]  In 2015, a worldwide total of 47,400 people died due to inflammatory bowel disease (UC and Crohn's disease). [ 6 ]  The peak onset is between 30 and 40 years of age, [ 12 ]  with a second peak of onset occurring in the 6th decade of life. [ 177 ]  Ulcerative colitis is equally common among men and women. [ 12 ] [ 7 ]  With appropriate treatment the risk of death appears similar to that of the general population. [ 3 ]  UC has become more common since the 1950s. [ 7 ] [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8973", "text": "The geographic distribution of UC and Crohn's disease is similar worldwide, [ 178 ]  with the highest number of new cases a year of UC found in  Canada ,  New Zealand  and the  United Kingdom . [ 179 ]  The disease is more common in North America and Europe than other regions. [ 9 ]  In general, higher rates are seen in northern locations compared to southern locations in  Europe [ 180 ]  and the United States. [ 181 ]  UC is more common in western Europe compared with eastern Europe. [ 182 ]   Worldwide, the prevalence of UC varies from 2 to 299 per 100,000 people. [ 5 ]  Together, ulcerative colitis and Crohn's disease affect about a million people in the United States. [ 176 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8974", "text": "As with Crohn's disease, the rates of UC are greater among  Ashkenazi Jews  and decreases progressively in other persons of Jewish descent, non-Jewish Caucasians, Africans, Hispanics, and Asians. [ 22 ]  Appendectomy prior to age 20 for appendicitis [ 183 ]  and current tobacco use [ 184 ]  are protective against development of UC. [ 12 ]  However, former tobacco use is associated with a higher risk of developing the disease. [ 184 ] [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8975", "text": "As of 2004 [update] , the number of new cases of UC in the United States was between 2.2 and 14.3 per 100,000 per year. [ 185 ]  The number of people affected in the United States in 2004 was between 37 and 246 per 100,000. [ 185 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8976", "text": "In Canada, between 1998 and 2000, the number of new cases per year was 12.9 per 100,000 population or 4,500 new cases. The number of people affected was estimated to be 211 per 100,000 or 104,000. [ 186 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8977", "text": "In the United Kingdom 10 per 100,000 people newly develop the condition a year while the number of people affected is 243 per 100,000. Approximately 146,000 people in the United Kingdom have been diagnosed with UC. [ 187 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8978", "text": "The term ulcerative colitis was first used by  Samuel Wilks  in 1859. The term entered general medical vocabulary afterwards in 1888 with  William Hale-White  publishing a report of various cases of \"ulcerative colitis\". [ 188 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8979", "text": "UC was the first subtype of IBD to be identified. [ 188 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8980", "text": "Helminthic therapy  using the  whipworm   Trichuris suis  has been shown in a  randomized control trial  from Iowa to show benefit in people with ulcerative colitis. [ 189 ]  The therapy tests the  hygiene hypothesis  which argues that the absence of  helminths  in the colons of people in the developed world may lead to inflammation. Both helminthic therapy and fecal microbiota transplant induce a characteristic  Th2  white cell response in the diseased areas, which was unexpected given that ulcerative colitis was thought to involve Th2 overproduction. [ 189 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8981", "text": "Alicaforsen  is a first generation antisense oligodeoxynucleotide designed to bind specifically to the human  ICAM-1  messenger  RNA  through Watson-Crick base pair interactions in order to subdue expression of ICAM-1. [ 190 ]  ICAM-1 propagates an inflammatory response promoting the extravasation and activation of  leukocytes  (white blood cells) into inflamed tissue. [ 190 ]  Increased expression of ICAM-1 has been observed within the  inflamed  intestinal mucosa of ulcerative colitis patients, where ICAM-1 over production correlated with disease activity. [ 191 ]  This suggests that ICAM-1 is a potential therapeutic target in the treatment of ulcerative colitis. [ 192 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8982", "text": "Gram positive bacteria present in the lumen could be associated with extending the time of relapse for ulcerative colitis. [ 193 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8983", "text": "A series of drugs in development looks to disrupt the inflammation process by selectively targeting an  ion channel  in the inflammation signaling cascade known as KCa3.1. [ 194 ]  In a preclinical study in rats and mice, inhibition of KCa3.1 disrupted the production of Th1 cytokines IL-2 and TNF-\u03b1 and decreased colon inflammation as effectively as  sulfasalazine . [ 194 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8984", "text": "Neutrophil extracellular traps [ 195 ]  and the resulting degradation of the extracellular matrix [ 196 ]  have been reported in the colon mucosa in ulcerative colitis patients in clinical remission, indicating the involvement of the innate immune system in the etiology. [ 195 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8985", "text": "Fexofenadine , an antihistamine drug used in treatment of allergies, has shown promise in a combination therapy in some studies. [ 197 ] [ 198 ]  Opportunely, low gastrointestinal absorption (or high absorbed drug gastrointestinal secretion) of fexofenadine results in higher concentration at the site of inflammation. Thus, the drug may locally decrease histamine secretion by involved gastrointestinal mast cells and alleviate the inflammation. [ 198 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8986", "text": "There is evidence that  etrolizumab  is effective for ulcerative colitis, with phase 3 trials underway as of 2016. [ 8 ] [ 199 ] [ 200 ] [ 201 ]  Etrolizumab is a humanized monoclonal antibody that targets the \u03b27 subunit of integrins \u03b14\u03b27 and \u03b1E\u03b27, ultimately blocking migration and retention of leukocytes in the intestinal mucosa. [ 200 ]  As of early 2022,  Roche  halted clinical trials for the use of etrolizumab in the treatment of ulcerative colitis. [ 202 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8987", "text": "A type of  leukocyte apheresis , known as granulocyte and monocyte adsorptive apheresis, still requires large-scale trials to determine whether or not it is effective. [ 203 ]  Results from small trials have been tentatively positive. [ 204 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8988", "text": "Wilderness-acquired diarrhea  is a variety of  traveler's diarrhea  in which backpackers and other outdoor enthusiasts are affected. Potential sources are contaminated food or water, or \"hand-to-mouth\", directly from another person who is infected. [ 1 ] [ 2 ]  Cases generally resolve spontaneously, with or without treatment, and the cause is typically unknown. The  National Outdoor Leadership School  has recorded about one incident per 5,000 person-field days by following strict protocols on hygiene and water treatment. [ 3 ]   More limited, separate studies have presented highly varied estimated rates of affliction that range from 3 percent to 74 percent of wilderness visitors. [ 1 ] [ 4 ]   One survey found that long-distance  Appalachian Trail  hikers reported  diarrhea  as their most common illness. [ 5 ]  Based on reviews of epidemiologic data and literature, some researchers believe that the risks have been over-stated and are poorly understood by the public. [ 4 ] [ 6 ] [ 7 ] [ 8 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8989", "text": "The average  incubation periods  for  giardiasis  and  cryptosporidiosis  are each 7 days. [ 9 ] [ 10 ]  Certain other bacterial and viral agents have shorter incubation periods, although hepatitis may take weeks to manifest itself. The onset usually occurs within the first week of return from the field, but may also occur at any time while hiking. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8990", "text": "Most cases begin abruptly and usually result in increased frequency, volume, and weight of stool. Typically, a hiker experiences at least four to five loose or watery bowel movements each day. Other commonly associated symptoms are nausea, vomiting, abdominal cramping, bloating, low fever, urgency, and malaise, and usually the appetite is affected. The condition is much more serious if there is blood or  mucus  in stools, abdominal pain, or high fever.  Dehydration  is a possibility. Life-threatening illness resulting from WAD is extremely rare but can occur in people with weakened immune systems. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8991", "text": "Some people may be carriers and not exhibit symptoms. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8992", "text": "Infectious diarrhea acquired in the wilderness is caused by various  bacteria ,  viruses , and parasites ( protozoa ). The most commonly reported are the protozoa  Giardia  and  Cryptosporidium . [ 11 ]  Other infectious agents may play a larger role than generally believed [ 4 ]  and include  Campylobacter ,  hepatitis A virus ,  hepatitis E virus , enterotoxogenic  E. coli ,  E. coli  O157:H7,  Shigella , and various other viruses. More rarely,  Yersinia enterocolitica ,  Aeromonas hydrophila , and  Cyanobacterium  may also cause disease. [ 12 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8993", "text": "Giardia lamblia  cysts usually do not tolerate freezing although some cysts can survive a single freeze\u2013thaw cycle. [ 13 ]   Cysts can remain viable for nearly three months in river water when the temperature is 10\u00a0\u00b0C and about one month at 15\u201320\u00a0\u00b0C in lake water.  Cryptosporidium  may survive in cold waters (4\u00a0\u00b0C) for up to 18 months, and can even withstand freezing, although its viability is thereby greatly reduced. [ 14 ]  Many other varieties of diarrhea-causing organisms, including  Shigella  and  Salmonella typhi , and hepatitis A virus, can survive freezing for weeks to months. [ 15 ]  Virologists believe all surface water in the United States and Canada has the potential to contain human viruses, which cause a wide range of illnesses including diarrhea, polio and meningitis. [ 16 ] [ 17 ] [ 18 ]  Modes of acquiring infection from these causes are limited to fecal-oral transmission, and contaminated water and food. The major factor governing pathogen content of surface water is human and animal activity in the watershed. [ 19 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8994", "text": "It may be difficult to associate a particular case of diarrhea with a recent wilderness trip of a few days because incubation of the disease may outlast the trip. Studies of trips [ 2 ] [ 20 ]  that are much longer than the average incubation period, e.g. a week for  Cryptosporidium  and  Giardia , [ 9 ] [ 10 ]  are less susceptible to these errors since there is enough time for the diarrhea to occur during the trip. Other bacterial and viral agents have shorter incubation periods, although hepatitis may require weeks. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8995", "text": "A suspected case of wilderness-acquired diarrhea may be assessed within the general context of intestinal complaints. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. [ 21 ]  There are an estimated 99 million annual cases of intestinal infectious disease in the United States, [ 22 ]  most commonly from viruses, followed by bacteria and parasites, including Giardia and Cryptosporidium. There are an estimated 1.2 million U.S. cases of symptomatic giardiasis annually. [ 23 ]  However, only about 40% of cases are symptomatic. [ 24 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8996", "text": "Since wilderness acquired diarrhea can be caused by insufficient hygiene, contaminated water, and (possibly) increased susceptibility from vitamin deficiency, prevention methods should address these causes. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8997", "text": "The risk of fecal-oral transmission of pathogens that cause diarrhea can be significantly reduced by good hygiene, including washing hands with soap and water after urination and defecation, and washing eating utensils with warm soapy water. [ 2 ]  Additionally a  three-bowl system  can be used for washing eating utensils. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8998", "text": "Water can be treated in the wilderness through filtering, chemical disinfectants, a portable ultraviolet light device,  pasteurizing  or boiling. [ 25 ] [ 26 ]  Factors in choice may include the number of people involved, space and weight considerations, the quality of available water, personal taste and preferences, and fuel availability. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_8999", "text": "In a study of long-distance backpacking, it was found that water filters were used more consistently than chemical disinfectants. Inconsistent use of iodine or chlorine may be due to disagreeable taste, extended treatment time or treatment complexity due to water temperature and turbidity. [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9000", "text": "Because methods based on  halogens , such as iodine and chlorine, do not kill  Cryptosporidium , and because filtration misses some viruses, the best protection may require a two-step process of either filtration or coagulation- flocculation , followed by  halogenation . Boiling is effective in all situations. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9001", "text": "Iodine resins, if combined with microfiltration to remove resistant cysts, are also a viable single-step process, but may not be effective under all conditions. New one-step techniques using  chlorine dioxide , ozone, and UV radiation may prove effective, but still require validation. [ 27 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9002", "text": "Ultraviolet (UV) light for water disinfection is well established and widely used for large applications, like municipal water systems. Some hikers use small portable UV devices which meet the U.S. EPA Guide Standard and Protocol for Testing Microbiological Water Purifiers, for example, the SteriPEN. [ 28 ] [ 29 ] [ 30 ]  Another approach to portable UV water purification is  solar disinfection  (also called  sodis ). Clear water is sterilized by putting it in a clear polyethylene ( PET ) bottle and leaving it in direct sunlight for 6 hours. [ 31 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9003", "text": "Different types of water sources may have different levels of contamination: [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9004", "text": "Rain storms can either improve or worsen water quality. They can wash contaminants into water and stir up contaminated sediments with increasing flow, but can also dilute contaminants by adding large amounts of water. [ 32 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9005", "text": "Unfortunately, there have not been any epidemiological studies to validate the above, except possibly for the case of spring water. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9006", "text": "One study suggests that on very long trips in the wilderness, taking  multivitamins  may reduce the incidence of diarrhea. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9007", "text": "WAD is typically self-limited, generally resolving without specific treatment.  Oral rehydration therapy  with rehydration salts is often beneficial to replace lost fluids and  electrolytes . Clear, disinfected water or other liquids are routinely recommended. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9008", "text": "Hikers who develop three or more loose stools in a 24-hour period\u00a0\u2013 especially if associated with  nausea ,  vomiting ,  abdominal   cramps ,  fever , or  blood in stools \u00a0\u2013 should be treated by a doctor and may benefit from antibiotics, usually given for 3\u20135 days. Alternatively, a single dose  azithromycin  or  levofloxacin  may be prescribed. [ 33 ]  If diarrhea persists despite therapy, travelers should be evaluated and treated for possible parasitic infection. [ citation needed ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9009", "text": "Cryptosporidium  can be quite dangerous to patients with compromised immune systems. Alinia (nitazoxanide) is approved by the FDA for treatment of  Cryptosporidium ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9010", "text": "The risk of acquiring infectious diarrhea in the wilderness arises from inadvertent ingestion of pathogens. Various studies have sought to estimate diarrhea  attack rates  among wilderness travelers, and results have ranged widely. The variation of diarrhea rate between studies may depend on the time of year, the location of the study, the length of time the hikers were in the wilderness, [ 2 ] [ 34 ] \nthe prevention methods used, and the study methodology."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9011", "text": "The  National Outdoor Leadership School  (NOLS), which emphasizes strict hand-washing techniques, water disinfection and washing of common cooking utensils in their programs, reports that gastrointestinal illnesses occurred at a rate of only 0.26 per 1000 program days. [ 35 ]  In contrast, a  survey of long-distance  Appalachian Trail   hikers found more than half  the respondents reported at least one episode of diarrhea that lasted an average of two days. (Infectious diarrhea may last longer than an average of two days; certain forms of non-infectious diarrhea, caused by diet change etc., can be of very brief duration).  Analysis of this survey found occurrence of diarrhea was positively associated with the duration of exposure in the wilderness. During any given four-week period, as many as 7.2% of Americans may experience some form of infectious or non-infectious diarrhea. [ 21 ]  A number of behaviors each individually reduced the incidence of diarrhea: treating water; routinely washing hands with soap and water after defecation and urination; cleaning cooking utensils with soap and warm water; and taking multi-vitamins. [ 2 ] [ 20 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9012", "text": "A variety of pathogens can cause infectious diarrhea, and most cases among backpackers appear to be caused by bacteria from  feces . A study at Grand Teton National Park found 69% of diarrhea affected visitors had no identifiable cause, that 23% had diarrhea due to  Campylobacter  and 8% of patients with diarrhea had  giardiasis . Campylobacter enteritis occurred most frequently in young adults who had hiked in wilderness areas and drunk untreated surface water in the week prior. [ 36 ]  Another study tested 35 individuals before and after a trip to the Desolation Wilderness of California. Giardia cysts were found in fecal samples from two people after the trip, but they were asymptomatic. A third person was empirically treated for symptoms of giardiasis. [ 37 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9013", "text": "Fecal-oral transmission may be the most common vector for wilderness acquired diarrhea. There are differing opinions regarding the importance of routine disinfection of water during relatively brief backcountry visits. [ 6 ] [ 4 ] [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9014", "text": "Infection by fecal coliform bacteria, which indicate fecal pollution, are more common than giardiasis. [ 38 ]  Risks are highest in surface water near trails used by  pack animals  and cattle pastures. [ 39 ] [ 40 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9015", "text": "Most samples of backcountry water in the Desolation Wilderness in California have found very low or no  Giardia  cysts. [ 37 ]  The infectious dose of giardia, however, is very low, with about 2% chance of infection from a single cyst. [ 41 ]  Also, very few studies have addressed the issue of transient contamination. According to one researcher, the likely model for the risk of  Giardia  from wilderness water is pulse contamination, that is, a brief period of high cyst concentration from fecal contamination. [ 7 ] [ 42 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9016", "text": "Diarrhea acquired in the wilderness or other remote areas is typically a form of  infectious diarrhea , itself classified as a type of  secretory diarrhea . These are all considered forms of  gastroenteritis . The term may be applied in various remote areas of non-tropical developed countries (U.S., Canada, western Europe, etc.), but is less applicable in developing countries, and in the tropics, because of the different  pathogens  that are most likely to cause infection. [ 7 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9017", "text": "Alimentary Pharmacology & Therapeutics  is a bimonthly  peer-reviewed   medical journal  concerned with the effects of drugs on the human gastrointestinal and hepato-biliary systems, particularly with relevance to clinical practice. The journal publishes original papers concerned with all aspects of basic and clinical  pharmacology ,  pharmacokinetics , and the therapeutic use of  drugs  in the alimentary tract including the liver, gall bladder, and pancreas. [ 1 ]  Its  editors  are J. M. Rhodes and C. W. Howden. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9018", "text": "This article about a  pharmacology   journal  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9019", "text": "This article about a  medical journal  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9020", "text": "The American Journal of Gastroenterology  is a  peer-reviewed   medical journal  owned by the  American College of Gastroenterology . It has been published by  Lippincott Williams & Wilkins  since 2019 and was previously published by  Nature Research , [ 1 ]  Blackwell and (before 2004)  Elsevier . [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9021", "text": "The  Canadian Journal of Gastroenterology and Hepatology  is a  peer-reviewed   medical journal  covering all aspects of  gastroenterology  and  liver disease . It is published by the  Hindawi Publishing Corporation , after having been sold by  Pulsus Group  in 2015.  It was the official journal of the  Canadian Association of Gastroenterology  and the  Canadian Association for the Study of the Liver , who divested from the journal in December 2016 after the sale to Hindawi. It was established in 1987 as the  Canadian Journal of Gastroenterology  and obtained its current name in 2014."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9022", "text": "The journal is abstracted and indexed in:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9023", "text": "According to the  Journal Citation Reports , the journal has a 2016  impact factor  of 2.147. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9024", "text": "Clinical and Experimental Gastroenterology   is a  peer-reviewed   medical journal  covering research in  gastroenterology . The journal was established in 2008 and is published by  Dove Medical Press . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9025", "text": "Clinical and Translational Gastroenterology  is a monthly  peer-reviewed   open access   medical journal  covering  gastroenterology . It was established in 2010 and is published by  Springer Nature  on behalf of the  American College of Gastroenterology , of which it is the official online journal. It is also the  sister journal  of the  American Journal of Gastroenterology . [ 1 ]  According to the  Journal Citation Reports , the journal has a 2020  impact factor  of 4.488. [ 2 ]  According to 2018, it ranked 20th out of 84th in the category of  Gastroenterology & Hepatology . and making it the highest-impact open access journal in this category. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9026", "text": "Clinical Gastroenterology and Hepatology  is a monthly  peer-reviewed   medical journal  published by  Elsevier  on behalf of the  American Gastroenterological Association . It was established in January 2003. [ 1 ]  According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 13.576. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9027", "text": "Digestive Diseases and Sciences , formerly known as the  American Journal of Digestive Diseases , is a monthly peer-reviewed journal focusing on gastroenterology and hepatology. It is published by  Springer Science+Business Media  and the editor-in-chief is Jonathan Kaunitz ( David Geffen School of Medicine ). According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 3.487 (2021) and a 5-year  impact factor  of 3.522."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9028", "text": "Endoscopy  is a monthly  peer-reviewed   medical journal  published by  Thieme Medical Publishers  on behalf of the  European Society of Gastrointestinal Endoscopy . The journal covers all aspects of  gastrointestinal   endoscopy  and also publishes ESGE guidelines and an annual review of the most recent literature,  Endoscopy Essentials . Since 2013, the  editor-in-chief  has been Peter D. Siersema ( University Medical Center Utrecht )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9029", "text": "The journal is abstracted and indexed in  Index Medicus / MEDLINE / PubMed , [ 1 ]   Current Contents /Clinical Medicine, [ 2 ]  Current Contents/Life Sciences, [ 2 ]   Science Citation Index , [ 2 ]   Embase , [ 3 ]  and  Scopus . [ 4 ]  According to the  Journal Citation Reports , the journal has a 2020  impact factor  of 7.341. [ 5 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9030", "text": "The  European Journal of Gastroenterology & Hepatology  is a  peer-reviewed   medical journal  covering the fields of  gastroenterology  and  hepatology . It was established in 1989 and is published by  Lippincott Williams & Wilkins . The  editors-in-chief  are Joost PH Drenth ( Radboud University Medical Center ) and Didier Lebrec. [ 1 ]  According to the  Journal Citation Reports , the journal has a 2020  impact factor  of 2.251. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9031", "text": "Expert Review of Gastroenterology & Hepatology  is a  peer-reviewed   medical journal  covering all aspects of  gastroenterology  and  hepatology . It was established in 2007 and is published by  Informa ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9032", "text": "According to the  Journal Citation Reports , the journal has a 2018  impact factor  of 2.991. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9033", "text": "Gastroenterology  is the official  medical journal  of the  American Gastroenterological Association . Its first issue was published in 1943. It is currently published by  Elsevier . According to the  Journal Citation Reports , the journal has a 2020  impact factor  of 22.682, ranking it 4th among 92 journals in the category \"Gasteroenterology & Hepatology\". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9034", "text": "Gastrointestinal Endoscopy  is a monthly  peer-reviewed   medical journal  covering  gastroenterology , especially as relating to  endoscopy . It is published by  Elsevier  and the official publication of the  American Society for Gastrointestinal Endoscopy . The  editor-in-chief  is Douglas G. Adler, MD, FASGE."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9035", "text": "The journal was established as the  Bulletin of the American Gastroscopic Society , was continued as the  Bulletin of Gastroscopy and Esophagoscopy  from 1959 to 1961, then as the  Bulletin of Gastrointestinal Endoscopy  until 1965 when it obtained its current name. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9036", "text": "The journal is abstracted and indexed in  Index Medicus / MEDLINE / PubMed , [ 2 ]   Current Contents /Clinical Medicine, [ 3 ]  Current Contents/Life Sciences, [ 3 ]   Science Citation Index , [ 3 ]   Embase , [ 4 ]  and  Scopus . [ 5 ]  According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 10.396. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9037", "text": "Gastrointestinal Nursing  is a monthly  peer-reviewed   nursing journal  covering research and clinical work on the practice of  gastrointestinal   nursing . It is published by MA Healthcare. It is indexed in  Scopus . [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9038", "text": "This article about a  nursing journal  is a  stub . You can help Wikipedia by  expanding it ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9039", "text": "Gut  is a monthly  peer-reviewed   medical journal  on  gastroenterology  and  hepatology . It is the journal of the  British Society of Gastroenterology  and is published by  BMJ . As of 2010, [update]  the  editor-in-chief  is  Emad El-Omar ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9040", "text": "Gut  was established in 1960 and covers  original research  on the  gastrointestinal tract ,  liver ,  pancreas , and  biliary tract . The journal has annual supplements covering the presentations from the British Society of Gastroenterology Annual General Meeting. British Society of Gastroenterology  clinical practice guidelines  are also published as supplements to the journal. As of March\u00a02010, [update]  subscribers to  Gut  also receive a copy of  Frontline Gastroenterology ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9041", "text": "Gut  is abstracted and indexed by  Medline ,  Science Citation Index ,  Current Contents /Clinical Medicine, Current Contents/Life Sciences,  Excerpta Medica ,  BIOSIS Previews  and  Scopus . According to the  Journal Citation Reports , its 2023  impact factor  is 23.1, ranking it fifth out of 143 journals in the category \"Gastroenterology and Hepatology\". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9042", "text": "According to the  Web of Science , some highly cited articles in  Gut  are:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9043", "text": "Hepatitis Monthly  is a monthly  peer-reviewed   open access   medical journal  published by Brieflands Publishing, formerly known as  Kowsar Publishing . [ 1 ]  Kowsar was included on  Beall's List  prior to the list's shutdown in 2017. [ 2 ]  The journal was established in 2002 by Seyed-Moayed Alavian, who is the journal's  editor-in-chief ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9044", "text": "The journal is abstracted and indexed in  CAB Abstracts , [ 3 ]   CINAHL , [ 4 ]   EBSCO databases , [ 5 ]   Embase , [ 6 ]   Science Citation Index Expanded , [ 7 ]  and  Scopus . [ 8 ]  According to the  Journal Citation Reports , the journal has a 2018  impact factor  of 1.578. [ 9 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9045", "text": "In August 2017, the  United States National Library of Medicine , which manages the  PubMed Central  database, determined that the journal did not satisfy their Scientific Quality Standard, and delisted the journal. [ 10 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9046", "text": "Hepatology  is a  peer-reviewed   medical journal  of  hepatology . It is published monthly by  John Wiley & Sons  on behalf of the  American Association for the Study of Liver Diseases . The journal was established in 1981 and the  editor-in-chief  is  David E Cohen  ( Weill Cornell Medical )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9047", "text": "The journal is abstracted and indexed in the following databases:"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9048", "text": "According to  Journal Citation Reports , the journal's 2020  impact factor  is 17.425, ranking it 6th out of 92 journals in the category \"Gastroenterology & Hepatology\". [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9049", "text": "The  Indian Journal of Gastroenterology  is a  peer-reviewed  bimonthly  medical journal  covering  gastroenterology . It is published by the  Indian Society of Gastroenterology  and is indexed and abstracted in  Index Medicus ,  MEDLINE , and  Excerpta Medica ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9050", "text": "The journal was established in 1982. Past  editors-in-chief  include F.P. Antia, S.R. Naik, and Philip Abraham. The journal publishes Editorials, Original Articles, Review Articles, Short Reports, Clinical Case Reports, Case Snippets, Debates and Letters."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9051", "text": "Inflammatory Bowel Diseases  is a monthly  peer-reviewed   medical journal  covering all aspects of  inflammatory bowel disease . It was established in 1995 and is published by  Oxford University Press . [ 1 ]  It is the official journal of the  Crohn's & Colitis Foundation . The  editor-in-chief  is Fabio Cominelli ( Case Western Reserve University ). [ 2 ]  According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 7.29, ranking it 22nd out of 93 journals in the category \"Gastroenterology & Hepatology\". [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9052", "text": "Intestinal Research  is a quarterly  peer-reviewed   open access   medical journal  covering the fields of  intestinal diseases  (especially  inflammatory bowel disease ). It is published by the  Korean Association for the Study of Intestinal Diseases  in collaboration with the  Asian Organization for Crohn's and Colitis ,  Chinese Society of IBD ,  Japanese Society for IBD ,  Taiwan Society of IBD , and  Colitis Crohn's Foundation (India) . The  editor-in-chief  is Toshifumi Hibi ( Kitasato University ). The journal was established in 2003 and published semiannually; as of 2012 it appears quarterly. Originally published in Korean with abstracts in English, the journal is now published exclusively in English."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9053", "text": "The  Journal of Clinical and Translational Hepatology  is a monthly  peer-reviewed   medical journal  covering  hepatology  established in 2013. It is owned by the Second Affiliated Hospital of  Chongqing Medical University  and published on their behalf by  Xia & He Publishing . The  editors-in-chief  are Hong Ren (The Second Affiliated Hospital of Chongqing Medical University), George Y. Wu ( University of Connecticut Health Center ), and Harry Hua-Xiang Xia (The First Affiliated Hospital of  Guangdong Pharmaceutical University )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9054", "text": "According to the  Journal Citation Reports , the journal has a 2022 impact factor of 3.6. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9055", "text": "Journal of Clinical Gastroenterology  is a  peer-reviewed   medical journal  covering  gastroenterology  and  hepatology , published by  Lippincott Williams & Wilkins . It was established in 1979 and the current  editor-in-chief  is Ronnie Fass, MD ( Case Western Reserve University School of Medicine )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9056", "text": "The journal is abstracted and indexed in: [ 1 ] [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9057", "text": "According to the  Journal Citation Reports , the journal has a 2013  impact factor  of 3.186. [ 3 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9058", "text": "The  Journal of Crohn's and Colitis  is a monthly  peer-reviewed   medical journal  covering  inflammatory bowel diseases . [ 1 ]  It was established in 2007 and was originally published by  Elsevier , [ 2 ]  but has been published by  Oxford University Press  since January 2015. [ 1 ]  It is the official journal of the  European Crohn's and Colitis Organisation . The  editor-in-chief  is Laurence J. Egan ( NUI Galway ). The journal has a 2022  impact factor  of 8.0. [ 3 ] [ 4 ] [ 5 ]  In 2022, it was ranked 7th by Scimago journal rankings in the field of Gastroenterology and Hepatology. [ 6 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9059", "text": "Journal of Hepatology  is a  peer-reviewed   scientific journal  that was established in 1985 by  Munksgaard International Publishers .  A supplement,  Journal of Hepatology Supplement  was also published in 1985, but ceased in the same year."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9060", "text": "Elsevier  took over publication in 2001. The journal is currently edited by Paolo Angeli and is published on a monthly basis. It is associated with the  European Association for the Study of the Liver ."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9061", "text": "Journal of Hepatology  is abstracted and indexed the following bibliographic databases: [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9062", "text": "According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 30.083. [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9063", "text": "Liver International  is a bimonthly  peer-reviewed   medical journal  covering  hepatology . It was established in 1981 under the title  Liver , obtaining its current name in 2003. [ 1 ]  It is published by  John Wiley & Sons  on behalf of the  International Association for the Study of the Liver , of which it is the official journal. The  editor-in-chief  is Luca Valenti. According to the  Journal Citation Reports , the journal has a 2021  impact factor  of 8.754, ranking it 18th out of 93 journals in the category \"Gastroenterology & Hepatology\". [ 2 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9064", "text": "Neurogastroenterology & Motility  is a bimonthly  peer-reviewed   medical journal  covering  neurogastroenterology  and  gastrointestinal motility . It was established in 1989 as the  Journal of Gastrointestinal Motility , obtaining its current name in 1994, and is published by  Wiley-Blackwell . It is the official journal of the  European Society of Neurogastroenterology and Motility , as well as the  American Neurogastroenterology and Motility Society . The  editors-in-chief  are Gianrico Farrugia ( Mayo Clinic ), Magnus Simren ( Sahlgrenska University Hospital ), and Gary Mawe ( University of Vermont )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9065", "text": "According to the  Journal Citation Reports , the journal has a 2013  impact factor  of 3.424. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9066", "text": "The  Scandinavian Journal of Gastroenterology  is a monthly  peer-reviewed   medical journal  covering the field of  gastroenterology . It is published by  Informa  and was established in 1966. The  editor in chief  is Helge Waldum. According to the  Journal Citation Reports , the journal has a 2013  impact factor  of 2.329. [ 1 ]"}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9067", "text": "World Journal of Gastroenterology  is a weekly  peer-reviewed   open access   medical journal  that covers research in  gastroenterology . It was established in 1995 and is published by  Baishideng Publishing Group . [ 1 ]  The  editor-in-chief  is Andrzej S. Tarnawski ( California State University, Long Beach )."}
{"_id": "WikiPedia_Gastroenterology$$$corpus_9068", "text": "In 2004, the journal was delisted from the  Journal Citation Reports  for excessive self-citation, [ 6 ]  but it was restored to this index in 2008, at which time its  impact factor  was determined to be 2.081. [ 7 ]  According to the  Journal Citation Reports , the journal has a 2020 impact factor of 5.742, ranking it 28th out of 92 journals in the category \"Gastroenterology and Hepatology\". [ 8 ]"}