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What is (are) Griscelli syndrome ?
Griscelli syndrome is an inherited condition characterized by unusually light (hypopigmented) skin and light silvery-gray hair starting in infancy. Researchers have identified three types of this disorder, which are distinguished by their genetic cause and pattern of signs and symptoms. Griscelli syndrome type 1 involves severe problems with brain function in addition to the distinctive skin and hair coloring. Affected individuals typically have delayed development, intellectual disability, seizures, weak muscle tone (hypotonia), and eye and vision abnormalities. Another condition called Elejalde disease has many of the same signs and symptoms, and some researchers have proposed that Griscelli syndrome type 1 and Elejalde disease are actually the same disorder. People with Griscelli syndrome type 2 have immune system abnormalities in addition to having hypopigmented skin and hair. Affected individuals are prone to recurrent infections. They also develop an immune condition called hemophagocytic lymphohistiocytosis (HLH), in which the immune system produces too many activated immune cells called T-lymphocytes and macrophages (histiocytes). Overactivity of these cells can damage organs and tissues throughout the body, causing life-threatening complications if the condition is untreated. People with Griscelli syndrome type 2 do not have the neurological abnormalities of type 1. Unusually light skin and hair coloring are the only features of Griscelli syndrome type 3. People with this form of the disorder do not have neurological abnormalities or immune system problems.
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How many people are affected by spondylocarpotarsal synostosis syndrome ?
Spondylocarpotarsal synostosis syndrome is a rare disorder; its prevalence is unknown. At least 25 affected individuals have been identified.
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What is (are) Hereditary diffuse leukoencephalopathy with spheroids ?
Hereditary diffuse leukoencephalopathy with spheroids (HDLS) is a neurological condition characterized by changes to certain areas of the brain. A hallmark of HDLS is leukoencephalopathy, which is damage to a type of brain tissue called white matter. Another common finding is axon damage due to swellings called spheroids. Damage to myelin and axons is thought to contribute to many of the neurological signs and symptoms seen in people with this condition, including the personality changes, loss of memory, changes in motor skills and dementia. HDLS is caused by mutations in the CSF1R gene. It is inherited in an autosomal dominant pattern.
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What are the treatments for Diverticular Disease ?
A health care provider may treat the symptoms of diverticulosis with a high-fiber diet or fiber supplements, medications, and possibly probiotics. Treatment for diverticular disease varies, depending on whether a person has diverticulitis or diverticular bleeding. Diverticulosis High-fiber diet. Studies have shown that a high-fiber diet can help prevent diverticular disease in people who already have diverticulosis.2 A health care provider may recommend a slow increase in dietary fiber to minimize gas and abdominal discomfort. For more information about fiber-rich foods, see Eating, Diet, and Nutrition. Fiber supplements. A health care provider may recommend taking a fiber product such as methylcellulose (Citrucel) or psyllium (Metamucil) one to three times a day. These products are available as powders, pills, or wafers and provide 0.5 to 3.5 grams of fiber per dose. Fiber products should be taken with at least 8 ounces of water. Medications. A number of studies suggest the medication mesalazine (Asacol), given either continuously or in cycles, may be effective at reducing abdominal pain and GI symptoms of diverticulosis. Research has also shown that combining mesalazine with the antibiotic rifaximin (Xifaxan) can be significantly more effective than using rifaximin alone to improve a persons symptoms and maintain periods of remission, which means being free of symptoms.4 Probiotics. Although more research is needed, probiotics may help treat the symptoms of diverticulosis, prevent the onset of diverticulitis, and reduce the chance of recurrent symptoms. Probiotics are live bacteria, like those normally found in the GI tract. Probiotics can be found in dietary supplementsin capsules, tablets, and powdersand in some foods, such as yogurt. To help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements and probiotics, with their health care provider. Read more at www.nccam.nih.gov/health/probiotics. Tips for talking with health care providers are available at www.nccam.nih.gov/timetotalk. Diverticular Bleeding Diverticular bleeding is rare. Bleeding can be severe; however, it may stop by itself and not require treatment. A person who has bleeding from the rectumeven a small amountshould see a health care provider right away. To treat the bleeding, a colonoscopy may be performed to identify the location of and stop the bleeding. A CT scan or angiogram also may be used to identify the site of the bleeding. A traditional angiogram is a special kind of x ray in which a thin, flexible tube called a catheter is threaded through a large artery, often from the groin, to the area of bleeding. Contrast medium is injected through the catheter so the artery shows up more clearly on the x ray. The procedure is performed in a hospital or an outpatient center by an x-ray technician, and the images are interpreted by a radiologist. Anesthesia is not needed, though a sedative may be given to lessen anxiety during the procedure. If the bleeding does not stop, abdominal surgery with a colon resection may be necessary. In a colon resection, the surgeon removes the affected part of the colon and joins the remaining ends of the colon together; general anesthesia is used. A blood transfusion may be needed if the person has lost a significant amount of blood. Diverticulitis Diverticulitis with mild symptoms and no complications usually requires a person to rest, take oral antibiotics, and be on a liquid diet for a period of time. If symptoms ease after a few days, the health care provider will recommend gradually adding solid foods back into the diet. Severe cases of diverticulitis with acute pain and complications will likely require a hospital stay. Most cases of severe diverticulitis are treated with intravenous (IV) antibiotics and a few days without food or drink to help the colon rest. If the period without food or drink is longer, the person may be given parenteral nutritiona method of providing an IV liquid food mixture through a special tube in the chest. The mixture contains proteins, carbohydrates, fats, vitamins, and minerals.
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What are the treatments for thiamine-responsive megaloblastic anemia syndrome ?
These resources address the diagnosis or management of thiamine-responsive megaloblastic anemia syndrome: - Gene Review: Gene Review: Thiamine-Responsive Megaloblastic Anemia Syndrome - Genetic Testing Registry: Megaloblastic anemia, thiamine-responsive, with diabetes mellitus and sensorineural deafness - MedlinePlus Encyclopedia: Optic nerve atrophy - MedlinePlus Encyclopedia: Thiamine These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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How to prevent Coronary Microvascular Disease ?
No specific studies have been done on how to prevent coronary microvascular disease. Researchers dont yet know how or in what way preventing coronary microvascular disease differs from preventing coronary heart disease. Coronary microvascular disease affects the tiny coronary arteries; coronary heart disease affects the large coronary arteries. Taking action to control risk factors for heart disease can help prevent or delay coronary heart disease. You cant control some risk factors, such as older age and family history of heart disease. However, you can take steps to prevent or control other risk factors, such as high blood pressure, overweight and obesity, high blood cholesterol, diabetes, and smoking. Heart-healthy lifestyle changes and ongoing medical care can help you lower your risk for heartdisease. Heart-Healthy Lifestyle Changes Your doctor may recommend heart-healthy lifestyle changes if you have coronary microvascular disease. Heart-healthy lifestyle changes include: Heart-healthy eating Maintaining a healthy weight Managing stress Physical activity Quitting smoking Heart-Healthy Eating Your doctor may recommend a heart-healthy eating plan, which should include: Fat-free or low-fat dairy products, such as skim milk Fish high in omega-3 fatty acids, such as salmon, tuna, and trout, about twice a week Fruits, such as apples, bananas, oranges, pears, and prunes Legumes, such as kidney beans, lentils, chickpeas, black-eyed peas, and lima beans Vegetables, such as broccoli, cabbage, and carrots Whole grains, such as oatmeal, brown rice, and corn tortillas. When following a heart-healthy diet, you should avoid eating: A lot of red meat Palm and coconut oils Sugary foods and beverages Two nutrients in your diet make blood cholesterol levels rise: Saturated fatfound mostly in foods that come from animals Trans fat (trans fatty acids)found in foods made with hydrogenated oils and fats, such as stick margarine; baked goods, such as cookies, cakes, and pies; crackers; frostings; and coffee creamers. Some trans fats also occur naturally in animal fats andmeats. Saturated fat raises your blood cholesterol more than anything else in your diet. When you follow a heart-healthy eating plan, only 5 percent to 6 percent of your daily calories should come from saturated fat. Food labels list the amounts of saturated fat. To help you stay on track, here are some examples: 1,200 calories a day 8 grams of saturated fat a day 1,500 calories a day 10 grams of saturated fat a day 1,800 calories a day 12 grams of saturated fat a day 2,000 calories a day 13 grams of saturated fat a day 2,500 calories a day 17 grams of saturated fat a day Not all fats are bad. Monounsaturated and polyunsaturated fats actually help lower blood cholesterollevels. Some sources of monounsaturated and polyunsaturated fats are: Avocados Corn, sunflower, and soybean oils Nuts and seeds, such as walnuts Olive, canola, peanut, safflower, and sesame oils Peanut butter Salmon and trout Tofu Sodium You should try to limit the amount of sodium that you eat. This means choosing and preparing foods that are lower in salt and sodium. Try to use low-sodium and no added salt foods and seasonings at the table or while cooking. Food labels tell you what you need to know about choosing foods that are lower in sodium. Try to eat no more than 2,300 milligrams of sodium a day. If you have high blood pressure, you may need to restrict your sodium intake even more. Dietary Approaches to Stop Hypertension Your doctor may recommend the Dietary Approaches to Stop Hypertension (DASH) eating plan if you have high blood pressure. The DASH eating plan focuses on fruits, vegetables, whole grains, and other foods that are heart healthy and low in fat, cholesterol, and sodium and salt. The DASH eating plan is a good heart-healthy eating plan, even for those who dont have high blood pressure. Read more about DASH. Alcohol Try to limit alcohol intake. Too much alcohol canraise your blood pressure and triglyceride levels, a type of fat found in the blood. Alcohol also adds extra calories, which may cause weight gain. Men should have no more than two drinks containing alcohol a day. Women should have no more than one drink containing alcohol a day. One drink is: 12 ounces of beer 5 ounces of wine 1 ounces of liquor Maintaining a Healthy Weight Maintaining a healthy weight is important for overall health and can lower your risk for coronary heart disease. Aim for a Healthy Weight by following a heart-healthy eating plan and keeping physically active. Knowing your body mass index (BMI) helps you find out if youre a healthy weight in relation to your height and gives an estimate of your total body fat. To figure out your BMI, check out the National Heart, Lung, and Blood Institutes (NHLBI) online BMI calculator or talk to your doctor. A BMI: Below 18.5 is a sign that you are underweight. Between 18.5 and 24.9 is in the normal range. Between 25 and 29.9 is considered overweight. Of 30 or more is considered obese. A general goal to aim for is a BMI below 25. Your doctor or health care provider can help you set an appropriate BMI goal. Measuring waist circumference helps screen for possible health risks. If most of your fat is around your waist rather than at your hips, youre at a higher risk for heart disease and type 2 diabetes. This risk may be high with a waist size that is greater than 35 inches for women or greater than 40 inches for men. To learn how to measure your waist, visit Assessing Your Weight and Health Risk. If youre overweight or obese, try to lose weight. A loss of just 3 percent to 5 percent of your current weight can lower your triglycerides, blood glucose, and the risk of developing type 2 diabetes. Greater amounts of weight loss can improve blood pressure readings, lower LDL cholesterol, and increase HDL cholesterol. Managing Stress Research shows that the most commonly reported trigger for a heart attack is an emotionally upsetting eventparticularly one involving anger. Also, some of the ways people cope with stresssuch as drinking, smoking, or overeatingarent healthy. Learning how to manage stress, relax, and cope with problems can improve your emotional and physical health. Consider healthy stress-reducing activities, such as: A stress management program Meditation Physical activity Relaxation therapy Talking things out with friends or family Physical Activity Routine physical activity can lower many coronary heart disease risk factors, including LDL (bad) cholesterol, high blood pressure, and excess weight. Physical activity also can lower your risk for diabetes and raise your HDL cholesterol level. HDL is the good cholesterol that helps prevent coronary heart disease. Everyone should try to participate in moderate-intensity aerobic exercise at least 2hours and 30minutes per week, or vigorous aerobic exercise for 1hour and 15minutes per week. Aerobic exercise, such as brisk walking, is any exercise in which your heart beats faster and you use more oxygen than usual. The more active you are, the more you will benefit. Participate in aerobic exercise for at least 10minutes at a time spread throughout the week. Read more about physical activity at: Physical Activity and Your Heart U.S. Department of Health and Human Services 2008 Physical Activity Guidelines forAmericans Talk with your doctor before you start a new exercise plan. Ask your doctor how much and what kinds of physical activity are safe for you. Quitting Smoking If you smoke, quit. Smoking can raise your risk for coronary heart disease and heart attack and worsen other coronary heart disease risk factors. Talk with your doctor about programs and products that can help you quit smoking. Also, try to avoid secondhand smoke. If you have trouble quitting smoking on your own, consider joining a support group. Many hospitals, workplaces, and community groups offer classes to help people quit smoking. Read more about quitting smoking at Smoking and Your Heart. Ongoing Medical Care Learn more about heart disease and the traits, conditions, and habits that can raise your risk for developing it. Talk with your doctor about your risk factors for heart disease and how to controlthem. If lifestyle changes arent enough, your doctor may prescribe medicines to control your risk factors. Take all of your medicines as your doctor advises. Visit your doctor regularly and have recommended testing. Know your numbers. Ask your doctor for these three tests and have the results explained toyou: Blood pressure measurement. Fasting blood glucose. This test is for diabetes. Lipoprotein panel. This test measures total cholesterol, LDL (bad) cholesterol, HDL (good) cholesterol, and triglycerides (a type of fat in the blood). Finally, know your family history of heart disease. If you or someone in your family has heart disease, tell your doctor.
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What are the symptoms of Macular dystrophy, atypical vitelliform ?
What are the signs and symptoms of Macular dystrophy, atypical vitelliform? The Human Phenotype Ontology provides the following list of signs and symptoms for Macular dystrophy, atypical vitelliform. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Reduced visual acuity 5% Visual field defect 5% Visual impairment 5% Autosomal dominant inheritance - Late onset - Macular dystrophy - Vitelliform-like macular lesions - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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How many people are affected by Paget disease of bone ?
Classic Paget disease of bone occurs in approximately 1 percent of people older than 40 in the United States. Scientists estimate that about 1 million people in this country have the disease. It is most common in people of western European heritage. Early-onset Paget disease of bone is much rarer. This form of the disorder has been reported in only a few families.
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Who is at risk for Pulmonary Embolism? ?
Pulmonary embolism (PE) occurs equally in men and women. The risk increases with age. For every 10 years after age 60, the risk of having PE doubles. Certain inherited conditions, such as factor V Leiden, increase the risk of blood clotting and PE. Major Risk Factors Your risk for PE is high if you have deep vein thrombosis (DVT) or a history of DVT. In DVT, blood clots form in the deep veins of the bodymost often in the legs. These clots can break free, travel through the bloodstream to the lungs, and block an artery. Your risk for PE also is high if you've had the condition before. Other Risk Factors Other factors also can increase the risk for PE, such as: Being bedridden or unable to move around much Having surgery or breaking a bone (the risk goes up in the weeks following the surgery or injury) Having certain diseases or conditions, such as a stroke, paralysis (an inability to move), chronic heart disease, or high blood pressure Smoking People who have recently been treated for cancer or who have a central venous catheter are more likely to develop DVT, which increases their risk for PE. A central venous catheter is a tube placed in a vein to allow easy access to the bloodstream for medical treatment. Other risk factors for DVT include sitting for long periods (such as during long car or airplane rides), pregnancy and the 6-week period after pregnancy, and being overweight or obese. Women who take hormone therapy pills or birth control pills also are at increased risk for DVT. The risk of developing blood clots increases as your number of risk factors increases.
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What is (are) Parasites - Angiostrongyliasis (also known as Angiostrongylus Infection) ?
Angiostrongylus cantonensis is a parasitic worm of rats. It is also called the rat lungworm. The adult form of the parasite is found only in rodents. Infected rats pass larvae of the parasite in their feces. Snails and slugs get infected by ingesting the larvae. These larvae mature in snails and slugs but do not become adult worms. The life cycle is completed when rats eat infected snails or slugs and the larvae further mature to become adult worms.
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How many people are affected by hepatic veno-occlusive disease with immunodeficiency ?
VODI appears to be a rare disorder; approximately 20 affected families have been reported worldwide. Most people diagnosed with the condition have been of Lebanese ancestry. However, the disorder has also been identified in several individuals with other backgrounds in the United States and Italy.
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What are the treatments for ethylmalonic encephalopathy ?
These resources address the diagnosis or management of ethylmalonic encephalopathy: - Baby's First Test - Genetic Testing Registry: Ethylmalonic encephalopathy - MedlinePlus Encyclopedia: Skin discoloration - bluish These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What is the outlook for Tardive Dyskinesia ?
Symptoms of tardive dyskinesia may remain long after discontinuation of neuroleptic drugs. In many cases, the symptoms stop spontaneously, but in some cases they may persist indefinitely.
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How many people are affected by glycogen storage disease type VII ?
GSDVII is thought to be a rare condition; more than 100 cases have been described in the scientific literature.
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What causes What I need to know about Hirschsprung Disease ?
People with HD have constipation because they lack nerve cells in a part or all of the large intestine. The nerve cells signal muscles in the large intestine to push stool toward the anus. Without a signal to push stool along, stool will remain in the large intestine. How severe HD is depends on how much of the large intestine is affected. Short-segment HD means only the last part of the large intestine lacks nerve cells. Long-segment HD means most or all of the large intestine, and sometimes the last part of the small intestine, lacks nerve cells. In a person with HD, stool moves through the large intestine until it reaches the part lacking nerve cells. At that point, the stool moves slowly or stops, causing an intestinal obstruction.
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How many people are affected by Lenz microphthalmia syndrome ?
Lenz microphthalmia syndrome is a very rare condition; its incidence is unknown. It has been identified in only a few families worldwide.
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What are the symptoms of X-linked lissencephaly with abnormal genitalia ?
What are the signs and symptoms of X-linked lissencephaly with abnormal genitalia? The Human Phenotype Ontology provides the following list of signs and symptoms for X-linked lissencephaly with abnormal genitalia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of neuronal migration 90% Aplasia/Hypoplasia of the corpus callosum 90% Cognitive impairment 90% Cryptorchidism 90% Hypoplasia of penis 90% Microcephaly 90% Seizures 90% Hypohidrosis 50% Malabsorption 50% Muscular hypotonia 50% Ventriculomegaly 50% Aganglionic megacolon 7.5% Exocrine pancreatic insufficiency 7.5% Frontal bossing 7.5% Hypertonia 7.5% Patent ductus arteriosus 7.5% Ventricular septal defect 7.5% Agenesis of corpus callosum - Decreased testicular size - Diarrhea - Duane anomaly - Feeding difficulties in infancy - Gliosis - High forehead - High palate - Hyperreflexia - Lissencephaly - Long philtrum - Long upper lip - Low-set ears - Micropenis - Pachygyria - Prominent nasal bridge - Severe global developmental delay - Spasticity - Specific learning disability - Wide anterior fontanel - Wide nasal bridge - X-linked inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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Is acute promyelocytic leukemia inherited ?
Acute promyelocytic leukemia is not inherited but arises from a translocation in the body's cells that occurs after conception.
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what are public health agencies doing to prevent or control yersiniosis for Yersinia ?
The Centers for Disease Control and Prevention (CDC) monitors the frequency of Y. enterocolitica infections through the foodborne disease active surveillance network (FoodNet). In addition, CDC conducts investigations of outbreaks of yersiniosis to control them and to learn more about how to prevent these infections. CDC has collaborated in an educational campaign to increase public awareness about prevention of Y. enterocolitica infections. The U.S. Food and Drug Administration inspects imported foods and milk pasteurization plants and promotes better food preparation techniques in restaurants and food processing plants. The U.S. Department of Agriculture monitors the health of food animals and is responsible for the quality of slaughtered and processed meat. The U.S. Environmental Protection Agency regulates and monitors the safety of our drinking water supplies.
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Is Chromosome 4q deletion inherited ?
How is chromosome 4q deletion inherited? Chromosome 4q deletion is usually not inherited. The deletion often occurs sporadically as a random event during the formation of the egg or sperm. In this case, a person would have no family history of the condition but could pass the deletion on to children. Rarely, this deletion is passed down from parent to child. However, the symptoms and severity can vary between family members.
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How many people are affected by Heart Failure ?
Approximately 5 million people in the United States have heart failure. It contributes to 300,000 deaths each year. It is the number one cause of hospitalizations for people over the age of 65.
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What is (are) renal coloboma syndrome ?
Renal coloboma syndrome (also known as papillorenal syndrome) is a condition that primarily affects kidney (renal) and eye development. People with this condition typically have kidneys that are small and underdeveloped (hypoplastic), which can lead to end-stage renal disease (ESRD). This serious disease occurs when the kidneys are no longer able to filter fluids and waste products from the body effectively. It has been estimated that approximately ten percent of children with hypoplastic kidneys may have renal coloboma syndrome. The kidney problems can affect one or both kidneys. Additionally, people with renal coloboma syndrome may have a malformation in the optic nerve, a structure that carries information from the eye to the brain. Optic nerve malformations are sometimes associated with a gap or hole (coloboma) in the light-sensitive tissue at the back of the eye (the retina). The vision problems caused by these abnormalities can vary depending on the size and location of the malformation. Some people have no visual problems, while others may have severely impaired vision. Less common features of renal coloboma syndrome include backflow of urine from the bladder (vesicoureteral reflux), multiple kidney cysts, loose joints, and mild hearing loss.
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How to diagnose Viral Gastroenteritis ?
Viral gastroenteritis is usually diagnosed based on symptoms alone. People who have symptoms that are severe or last for more than a few days may want to see a health care provider for additional tests. A health care provider may ask for a stool sample to test for rotavirus or norovirus or to rule out bacteria or parasites as the cause of the gastroenteritis. During an epidemic of viral gastroenteritis, health care providers or public health officials may test stool samples to find out which virus is responsible for the outbreak.
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Is X-linked juvenile retinoschisis inherited ?
This condition is inherited in an X-linked recessive pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation would have to occur in both copies of the gene to cause the disorder. Because it is unlikely that females will have two altered copies of this gene, males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
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What are the treatments for Mowat-Wilson syndrome ?
These resources address the diagnosis or management of Mowat-Wilson syndrome: - Gene Review: Gene Review: Mowat-Wilson Syndrome - Genetic Testing Registry: Mowat-Wilson syndrome - MedlinePlus Encyclopedia: Hirschsprung's Disease These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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How many people are affected by mitochondrial complex III deficiency ?
The prevalence of mitochondrial complex III deficiency is unknown, although the condition is thought to be rare.
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What are the symptoms of Lethal congenital contracture syndrome 1 ?
What are the signs and symptoms of Lethal congenital contracture syndrome 1? The Human Phenotype Ontology provides the following list of signs and symptoms for Lethal congenital contracture syndrome 1. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the hip bone 90% Aplasia/Hypoplasia of the lungs 90% Hypertelorism 90% Short stature 90% Skeletal muscle atrophy 90% Abnormal cortical bone morphology 50% Abnormality of the elbow 50% Abnormality of the ribs 50% Amniotic constriction ring 50% Limitation of joint mobility 50% Low-set, posteriorly rotated ears 50% Polyhydramnios 50% Recurrent fractures 50% Short neck 50% Slender long bone 50% Webbed neck 50% Abnormal form of the vertebral bodies 7.5% Abnormality of the amniotic fluid - Abnormality of the thorax - Autosomal recessive inheritance - Edema - Hypoplasia of the musculature - Neonatal death - Paucity of anterior horn motor neurons - Pulmonary hypoplasia - Widening of cervical spinal canal - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the treatments for catecholaminergic polymorphic ventricular tachycardia ?
These resources address the diagnosis or management of catecholaminergic polymorphic ventricular tachycardia: - Cleveland Clinic: Management of Arrhythmias - Gene Review: Gene Review: Catecholaminergic Polymorphic Ventricular Tachycardia - Genetic Testing Registry: Catecholaminergic polymorphic ventricular tachycardia - Genetic Testing Registry: Ventricular tachycardia, catecholaminergic polymorphic, 2 - MedlinePlus Encyclopedia: Fainting - MedlinePlus Encyclopedia: Ventricular Tachycardia These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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Is Fabry disease inherited ?
How is Fabry disease inherited? Fabry disease is inherited in an X-linked pattern, which means that the gene that causes the condition is located on the X chromosome. In males (who have only one X chromosome), one mutated copy of the gene is enough to cause symptoms of the condition. Because females have two copies of the X chromosome, one mutated copy of the gene in each cell usually leads to less severe symptoms in females than in males, or may cause no symptoms at all.
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What are the symptoms of Spinocerebellar ataxia X-linked type 3 ?
What are the signs and symptoms of Spinocerebellar ataxia X-linked type 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Spinocerebellar ataxia X-linked type 3. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Cognitive impairment 90% Incoordination 90% Muscular hypotonia 90% Optic atrophy 90% Sensorineural hearing impairment 90% Areflexia - Cerebellar atrophy - Death in infancy - Dementia - Dysmetria - Dysphagia - Episodic hypoventilation - Episodic respiratory distress - Esotropia - Gastroesophageal reflux - Gliosis - Head titubation - Hyporeflexia - Infantile onset - Intention tremor - Lethargy - Muscle weakness - Neuronal loss in central nervous system - Optic disc pallor - Recurrent respiratory infections - Seizures - Spasticity - Unilateral vocal cord paralysis - Vomiting - X-linked recessive inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Jervell Lange-Nielsen syndrome ?
Jervell Lange-Nielsen syndrome is a form of long QT syndrome. Symptoms include deafness from birth, arrhythmia, fainting, and sudden death. There are two different types, Jervell Lange-Nielsen syndrome type 1 and 2. It is inherited in an autosomal recessive fashion.
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Is alkaptonuria inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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What are the treatments for multiple endocrine neoplasia ?
These resources address the diagnosis or management of multiple endocrine neoplasia: - Gene Review: Gene Review: Multiple Endocrine Neoplasia Type 1 - Gene Review: Gene Review: Multiple Endocrine Neoplasia Type 2 - Genetic Testing Registry: Familial medullary thyroid carcinoma - Genetic Testing Registry: Multiple endocrine neoplasia, type 1 - Genetic Testing Registry: Multiple endocrine neoplasia, type 2a - Genetic Testing Registry: Multiple endocrine neoplasia, type 2b - Genetic Testing Registry: Multiple endocrine neoplasia, type 4 - Genomics Education Programme (UK): Multiple Endocrine Neoplasia type 1 - Genomics Education Programme (UK): Multiple Endocrine Neoplasia type 2A - MedlinePlus Encyclopedia: Hyperparathyroidism - MedlinePlus Encyclopedia: Medullary Carcinoma of Thyroid - MedlinePlus Encyclopedia: Multiple Endocrine Neoplasia (MEN) I - MedlinePlus Encyclopedia: Multiple Endocrine Neoplasia (MEN) II - MedlinePlus Encyclopedia: Pancreatic Islet Cell Tumor - MedlinePlus Encyclopedia: Pheochromocytoma - MedlinePlus Encyclopedia: Pituitary Tumor - National Cancer Institute: Genetic Testing for Hereditary Cancer Syndromes - New York Thyroid Center: Medullary Thyroid Cancer These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What are the treatments for Charcot-Marie-Tooth disease type 2F ?
How might Charcot-Marie-Tooth disease type 2F be treated? Treatment for Charcot-Marie-Tooth disease type 2 mainly focuses on the specific symptoms present. Affected individuals are often managed by a team of various specialists that includes neurologists, physiatrists, orthopedic surgeons, and physical and occupational therapists. Depending on the individual's signs and symptoms, the following may be indicated: Special shoes, including those with good ankle support Ankle/foot orthoses (AFO) to correct foot drop and aid with walking Orthopedic surgery to correct severe pes cavus Forearm crutches or canes for stability (fewer than 5% of affected individuals need wheelchairs) Treatment of sleep apnea or restless legs Treatment of pain and depression as needed
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What is (are) L1 syndrome ?
L1 syndrome is an inherited disorder that primarily affects the nervous system. L1 syndrome involves a variety of features that were once thought to be distinct disorders, but are now considered to be part of the same syndrome. The most common characteristics of L1 syndrome are muscle stiffness (spasticity) of the lower limbs, intellectual disability, increased fluid in the center of the brain (hydrocephalus), and thumbs bent toward the palm (adducted thumbs). People with L1 syndrome can also have difficulty speaking (aphasia), seizures, and underdeveloped or absent tissue connecting the left and right halves of the brain (agenesis of the corpus callosum). The symptoms of L1 syndrome vary widely among affected individuals, even among members of the same family. Because this disorder involves spasticity of the lower limbs, L1 syndrome is sometimes referred to as spastic paraplegia type 1 (SPG1).
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Do you have information about Radiation Therapy
Summary : Radiation therapy is a cancer treatment. It uses high doses of radiation to kill cancer cells and stop them from spreading. About half of all cancer patients receive it. The radiation may be external, from special machines, or internal, from radioactive substances that a doctor places inside your body. The type of radiation therapy you receive depends on many factors, including - The type of cancer - The size of the cancer - The cancer's location in the body - How close the cancer is to normal tissues that are sensitive to radiation - How far into the body the radiation needs to travel - Your general health and medical history - Whether you will have other types of cancer treatment - Other factors, such as your age and other medical conditions Radiation therapy can damage normal cells as well as cancer cells. Treatment must be carefully planned to minimize side effects. Common side effects include skin changes and fatigue. Other side effects depend on the part of your body being treated. Sometimes radiation is used with other treatments, like surgery or chemotherapy. NIH: National Cancer Institute
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What are the symptoms of Spastic paraplegia 14 ?
What are the signs and symptoms of Spastic paraplegia 14? The Human Phenotype Ontology provides the following list of signs and symptoms for Spastic paraplegia 14. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Adult onset - Autosomal recessive inheritance - Babinski sign - Hyperreflexia - Intellectual disability, mild - Lower limb muscle weakness - Lower limb spasticity - Motor axonal neuropathy - Pes cavus - Progressive - Spastic gait - Spastic paraplegia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Skin Cancer ?
Once cancer has been found, the doctor will need to determine the extent, or stage, of the cancer. Through staging, the doctor can tell if the cancer has spread and, if so, to what parts of the body. More tests may be performed to help determine the stage. Knowing the stage of the disease helps you and the doctor plan treatment. Staging will let the doctor know - the size of the tumor and exactly where it is - if the cancer has spread from the original tumor site - if cancer is present in nearby lymph nodes - if cancer is present in other parts of the body. the size of the tumor and exactly where it is if the cancer has spread from the original tumor site if cancer is present in nearby lymph nodes if cancer is present in other parts of the body. The choice of treatment is based on many factors, including the size of the tumor, its location in the layers of the skin, and whether it has spread to other parts of the body. For stage 0, I, II or III cancers, the main goals are to treat the cancer and reduce the risk of it returning. For stage IV cancer, the goal is to improve symptoms and prolong survival.
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What is (are) Czech dysplasia ?
Czech dysplasia is an inherited condition that affects joint function and bone development. People with this condition have joint pain (osteoarthritis) that begins in adolescence or early adulthood. The joint pain mainly affects the hips, knees, shoulders, and spine and may impair mobility. People with Czech dysplasia often have shortened bones in their third and fourth toes, which make their first two toes appear unusually long. Affected individuals may have flattened bones of the spine (platyspondyly) or an abnormal spinal curvature, such as a rounded upper back that also curves to the side (kyphoscoliosis). Some people with Czech dysplasia have progressive hearing loss.
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Is congenital sucrase-isomaltase deficiency inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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What are the symptoms of Glomerulopathy with fibronectin deposits 2 ?
What are the signs and symptoms of Glomerulopathy with fibronectin deposits 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Glomerulopathy with fibronectin deposits 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Edema of the lower limbs 90% Glomerulopathy 90% Hematuria 90% Hypertension 90% Nephrotic syndrome 90% Proteinuria 90% Renal insufficiency 90% Intracranial hemorrhage 7.5% Autosomal dominant inheritance - Generalized distal tubular acidosis - Microscopic hematuria - Renal cell carcinoma - Slow progression - Stage 5 chronic kidney disease - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the genetic changes related to frontometaphyseal dysplasia ?
Mutations in the FLNA gene cause frontometaphyseal dysplasia. The FLNA gene provides instructions for producing the protein filamin A, which helps build the network of protein filaments (cytoskeleton) that gives structure to cells and allows them to change shape and move. Filamin A binds to another protein called actin, and helps the actin to form the branching network of filaments that make up the cytoskeleton. Filamin A also links actin to many other proteins to perform various functions within the cell. A small number of mutations in the FLNA gene have been identified in people with frontometaphyseal dysplasia. These mutations are described as "gain-of-function" because they appear to enhance the activity of the filamin A protein or give the protein a new, atypical function. Researchers believe that the mutations may change the way the filamin A protein helps regulate processes involved in skeletal development, but it is not known how changes in the protein relate to the specific signs and symptoms of frontometaphyseal dysplasia.
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what research (or clinical trials) is being done for Hydromyelia ?
The National Institute of Neurological Disorders and Stroke (NINDS) conducts research related to hydromyelia in its clinics and laboratories at The National Institutes of Health (NIH) and supports additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure abnormalities of the spinal cord such as hydromyelia.
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What is the outlook for Merkel Cell Carcinoma ?
Certain factors affect prognosis (chance of recovery) and treatment options. The prognosis (chance of recovery) and treatment options depend on the following: - The stage of the cancer (the size of the tumor and whether it has spread to the lymph nodes or other parts of the body). - Where the cancer is in the body. - Whether the cancer has just been diagnosed or has recurred (come back). - The patient's age and general health. Prognosis also depends on how deeply the tumor has grown into the skin.
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What causes Hypophosphatemic rickets ?
What causes hypophosphatemic rickets? Hypophosphatemic rickets is almost always hereditary and may be caused by mutations in any of several genes. The specific gene involved determines the way it is inherited. Most commonly, it is caused by a mutation in the PHEX gene. Other genes that can be responsible for the condition include the CLCN5, DMP1, ENPP1, FGF23, and SLC34A3 genes. The genes associated with hereditary hypophosphatemic rickets are involved in keeping a proper balance of phosphate in the body. Many of these genes directly or indirectly regulate a protein that normally inhibits the kidneys' ability to reabsorb phosphate into the blood. Mutations affecting the function of these genes increase the production (or reduce the breakdown) of the protein, causing the protein to be overactive. The overactivity of the protein reduces phosphate reabsorption by the kidneys, leading to the features of the condition. Rarer, sporadic, acquired cases are sometimes associated with benign (non-cancerous) mesenchymal tumors that decrease resorption of phosphate.
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Is Fanconi anemia inherited ?
Fanconi anemia is most often inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition. Very rarely, this condition is inherited in an X-linked recessive pattern. The gene associated with X-linked recessive Fanconi anemia is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation would have to occur in both copies of the gene to cause the disorder. Because it is unlikely that females will have two altered copies of this gene, males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
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What are the symptoms of Cataract-microcephaly-failure to thrive-kyphoscoliosis ?
What are the signs and symptoms of Cataract-microcephaly-failure to thrive-kyphoscoliosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Cataract-microcephaly-failure to thrive-kyphoscoliosis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the face - Autosomal recessive inheritance - Cataract - Failure to thrive - Hip dislocation - Intellectual disability, progressive - Intellectual disability, severe - Kyphoscoliosis - Microcephaly - Small for gestational age - Spasticity - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What causes Primary Biliary Cirrhosis ?
The causes of primary biliary cirrhosis are unknown. Most research suggests it is an autoimmune disease. The immune system protects people from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. An autoimmune disease is a disorder in which the bodys immune system attacks the bodys own cells and organs. In primary biliary cirrhosis, the immune system attacks the small bile ducts in the liver. Genetics, or inherited genes, can make a person more likely to develop primary biliary cirrhosis. Primary biliary cirrhosis is more common in people who have a parent or siblingparticularly an identical twinwith the disease. In people who are genetically more likely to develop primary biliary cirrhosis, environmental factors may trigger or worsen the disease, including - exposure to toxic chemicals - smoking - infections Genetics can also make some people more likely to develop other autoimmune diseases, such as - autoimmune hepatitis, a disease in which the bodys immune system attacks liver cells - Sjgrens syndrome, a condition in which the immune system attacks the glands that produce tears and saliva - autoimmune thyroid dysfunctions, conditions in which the immune system attacks the thyroid gland
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What are the genetic changes related to mevalonate kinase deficiency ?
Mutations in the MVK gene cause mevalonate kinase deficiency. The MVK gene provides instructions for making the mevalonate kinase enzyme. This enzyme is involved in the production of cholesterol, which is later converted into steroid hormones and bile acids. Steroid hormones are needed for normal development and reproduction, and bile acids are used to digest fats. Mevalonate kinase also helps to produce other substances that are necessary for certain cellular functions, such as cell growth, cell maturation (differentiation), formation of the cell's structural framework (the cytoskeleton), gene activity (expression), and protein production and modification. Most MVK gene mutations that cause mevalonate kinase deficiency result in an enzyme that is unstable and folded into an incorrect 3-dimensional shape, leading to a reduction of mevalonate kinase enzyme activity. Despite this shortage (deficiency) of mevalonate kinase activity, people with mevalonate kinase deficiency typically have normal production of cholesterol, steroid hormones, and bile acids. It is unclear how a lack of mevalonate kinase activity causes the signs and symptoms of this condition. Some researchers believe the features may be due to a buildup of mevalonic acid, the substance that mevalonate kinase normally acts on. Other researchers think that a shortage of the substances produced from mevalonic acid, such as those substances necessary for certain cellular functions, causes the fever episodes and other features of this condition. The severity of the enzyme deficiency determines the severity of the condition. People who have approximately 1 to 20 percent of normal mevalonate kinase activity typically develop HIDS. Individuals who have less than 1 percent of normal enzyme activity usually develop MVA.
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What causes Asbestos-Related Lung Diseases ?
Significant exposure to asbestos fibers causes asbestos-related lung diseases. "Significant" usually means you were exposed for at least several months to visible dust from the fibers. Asbestos fibers are very small. When you breathe in, they can get stuck deep in your lungs. The fibers remain in your lung tissue for a long time and may cause scarring and inflammation. This can lead to pleural plaque and widespread pleural thickening, pleural effusion, asbestosis, lung cancer, or mesothelioma. Generally, asbestos-related lung diseases develop 10 to 40 or more years after a person has been exposed to asbestos. Being around products that contain asbestos isn't a danger, as long as the asbestos is enclosed. This prevents the fibers from getting into the air.
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What is (are) McCune-Albright syndrome ?
McCune-Albright syndrome is a disorder that affects the bones, skin, and several hormone-producing (endocrine) tissues. People with McCune-Albright syndrome develop areas of abnormal scar-like (fibrous) tissue in their bones, a condition called polyostotic fibrous dysplasia. Polyostotic means the abnormal areas (lesions) may occur in many bones; often they are confined to one side of the body. Replacement of bone with fibrous tissue may lead to fractures, uneven growth, and deformity. When lesions occur in the bones of the skull and jaw it can result in uneven (asymmetric) growth of the face. Asymmetry may also occur in the long bones; uneven growth of leg bones may cause limping. Abnormal curvature of the spine (scoliosis) may also occur. Bone lesions may become cancerous, but this happens in fewer than 1 percent of people with McCune-Albright syndrome. In addition to bone abnormalities, affected individuals usually have light brown patches of skin called caf-au-lait spots, which may be present from birth. The irregular borders of the caf-au-lait spots in McCune-Albright syndrome are often compared to a map of the coast of Maine. By contrast, caf-au-lait spots in other disorders have smooth borders, which are compared to the coast of California. Like the bone lesions, the caf-au-lait spots in McCune-Albright syndrome often appear on only one side of the body. Girls with McCune-Albright syndrome usually reach puberty early. These girls usually have menstrual bleeding by age two, many years before secondary sex characteristics such as breast enlargement and pubic hair are evident. This early onset of menstruation is believed to be caused by excess estrogen, a female sex hormone, produced by cysts that develop in one of the ovaries. Less commonly, boys with McCune-Albright syndrome may also experience early puberty. Other endocrine problems may also occur in people with McCune-Albright syndrome. The thyroid gland, a butterfly-shaped organ at the base of the neck, may become enlarged (a condition called a goiter) or develop masses called nodules. About 50 percent of affected individuals produce excessive amounts of thyroid hormone (hyperthyroidism), resulting in a fast heart rate, high blood pressure, weight loss, tremors, sweating, and other symptoms. The pituitary gland (a structure at the base of the brain that makes several hormones) may produce too much growth hormone. Excess growth hormone can result in acromegaly, a condition characterized by large hands and feet, arthritis, and distinctive facial features that are often described as "coarse." Rarely, affected individuals develop Cushing's syndrome, an excess of the hormone cortisol produced by the adrenal glands, which are small glands located on top of each kidney. Cushing's syndrome causes weight gain in the face and upper body, slowed growth in children, fragile skin, fatigue, and other health problems.
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What are the symptoms of Alpha-ketoglutarate dehydrogenase deficiency ?
What are the signs and symptoms of Alpha-ketoglutarate dehydrogenase deficiency? The Human Phenotype Ontology provides the following list of signs and symptoms for Alpha-ketoglutarate dehydrogenase deficiency. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Cognitive impairment 90% Hypertonia 90% Incoordination 90% Short stature 90% Skeletal muscle atrophy 90% Abnormality of movement 50% Abnormality of the salivary glands 50% Hydrocephalus 50% Autosomal recessive inheritance - Congenital lactic acidosis - Death in childhood - Increased serum lactate - Metabolic acidosis - Muscular hypotonia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Cough ?
A cough is a natural reflex that protects your lungs. Coughing helps clear your airways of lung irritants, such as smoke and mucus (a slimy substance). This helps prevent infections. A cough also can be a symptom of a medical problem. Prolonged coughing can cause unpleasant side effects, such as chest pain, exhaustion, light-headedness, and loss of bladder control. Coughing also can interfere with sleep, socializing, and work. Overview Coughing occurs when the nerve endings in your airways become irritated. The airways are tubes that carry air into and out of your lungs. Certain substances (such as smoke and pollen), medical conditions, and medicines can irritate these nerve endings. A cough can be acute, subacute, or chronic, depending on how long it lasts. An acute cough lasts less than 3 weeks. Common causes of an acute cough are a common cold or other upper respiratory (RES-pi-rah-tor-e) infections. Examples of other upper respiratory infections include the flu, pneumonia (nu-MO-ne-ah), and whooping cough. A subacute cough lasts 3 to 8 weeks. This type of cough remains even after a cold or other respiratory infection is over. A chronic cough lasts more than 8 weeks. Common causes of a chronic cough are upper airway cough syndrome (UACS); asthma; and gastroesophageal (GAS-tro-eh-so-fa-JE-al) reflux disease, or GERD. "UACS" is a term used to describe conditions that inflame the upper airways and cause a cough. Examples include sinus infections and allergies. These conditions can cause mucus to run down your throat from the back of your nose. This is called postnasal drip. Asthma is a long-term lung disease that inflames and narrows the airways. GERD occurs if acid from your stomach backs up into your throat. Outlook The best way to treat a cough is to treat its cause. For example, asthma is treated with medicines that open the airways. Your doctor may recommend cough medicine if the cause of your cough is unknown and the cough causes a lot of discomfort. Cough medicines may harm children. If your child has a cough, talk with his or her doctor about how to treat it.
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How many people are affected by hypochondrogenesis ?
Hypochondrogenesis and achondrogenesis, type 2 (a similar skeletal disorder) together affect 1 in 40,000 to 60,000 newborns.
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What are the genetic changes related to craniofacial microsomia ?
It is unclear what genes are involved in craniofacial microsomia. This condition results from problems in the development of structures in the embryo called the first and second pharyngeal arches (also called branchial or visceral arches). Tissue layers in the six pairs of pharyngeal arches give rise to the muscles, arteries, nerves, and cartilage of the face and neck. Specifically, the first and second pharyngeal arches develop into the lower jaw, the nerves and muscles used for chewing and facial expression, the external ear, and the bones of the middle ear. Interference with the normal development of these structures can result in the abnormalities characteristic of craniofacial microsomia. There are several factors that can disrupt the normal development of the first and second pharyngeal arches and lead to craniofacial microsomia. Some individuals with this condition have chromosomal abnormalities such as deletions or duplications of genetic material; these individuals often have additional developmental problems or malformations. Occasionally, craniofacial microsomia occurs in multiple members of a family in a pattern that suggests inheritance of a causative gene mutation, but the gene or genes involved are unknown. In other families, individuals seem to inherit a predisposition to the disorder. The risk of craniofacial microsomia can also be increased by environmental factors, such as certain drugs taken by the mother during pregnancy. In most affected individuals, the cause of the disorder is unknown. It is not well understood why certain disruptions to development affect the first and second pharyngeal arches in particular. Researchers suggest that these structures may develop together in such a way that they respond as a unit to these disruptions.
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What are the treatments for Menkes Disease ?
Treatment with daily copper injections may improve the outcome in Menkes disease if it begins within days after birth. Other treatment is symptomatic and supportive.
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What is the outlook for Wilson Disease ?
Early onset of the disease may foretell a worse prognosis than later onset. If the disorder is detected early and treated appropriately, an individual with WD can usually enjoy normal health and a normal lifespan. If not treated, however, WD can cause brain damage, liver failure, and death. The disease requires lifelong treatment.
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What are the symptoms of Osteopetrosis autosomal dominant type 1 ?
What are the signs and symptoms of Osteopetrosis autosomal dominant type 1? The Human Phenotype Ontology provides the following list of signs and symptoms for Osteopetrosis autosomal dominant type 1. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of pelvic girdle bone morphology - Abnormality of the vertebral column - Autosomal dominant inheritance - Conductive hearing impairment - Generalized osteosclerosis - Headache - Osteopetrosis - Thickened calvaria - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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Is Hashimoto thyroiditis inherited ?
The inheritance pattern of Hashimoto thyroiditis is unclear because many genetic and environmental factors appear to be involved. However, the condition can cluster in families, and having a close relative with Hashimoto thyroiditis or another autoimmune disorder likely increases a person's risk of developing the condition.
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How many people are affected by pyruvate carboxylase deficiency ?
Pyruvate carboxylase deficiency is a rare condition, with an estimated incidence of 1 in 250,000 births worldwide. This disorder appears to be much more common in some Algonkian Indian tribes in eastern Canada.
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What are the symptoms of Spondylometaphyseal dysplasia with dentinogenesis imperfecta ?
What are the signs and symptoms of Spondylometaphyseal dysplasia with dentinogenesis imperfecta? The Human Phenotype Ontology provides the following list of signs and symptoms for Spondylometaphyseal dysplasia with dentinogenesis imperfecta. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Brachydactyly syndrome 90% Joint hypermobility 90% Micromelia 90% Narrow chest 90% Platyspondyly 90% Short stature 90% Delayed eruption of teeth 50% Scoliosis 50% Depressed nasal bridge 7.5% Frontal bossing 7.5% Patent ductus arteriosus 7.5% Short nose 7.5% Strabismus 7.5% Autosomal dominant inheritance - Biconvex vertebral bodies - Cone-shaped epiphyses of the phalanges of the hand - Coronal cleft vertebrae - Delayed ossification of carpal bones - Dentinogenesis imperfecta - Flared iliac wings - Flat acetabular roof - Genu recurvatum - Genu varum - Irregular epiphyses - Long philtrum - Mesomelia - Metaphyseal cupping - Metaphyseal widening - Motor delay - Narrow face - Osteoporosis - Pectus carinatum - Prominent forehead - Respiratory distress - Short long bone - Short metacarpal - Short phalanx of finger - Small epiphyses - Spondylometaphyseal dysplasia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the treatments for Yellow nail syndrome ?
How are the respiratory conditions associated with yellow nail syndrome treated? You can find further information on treatment of pleural effusions, bronchitis, sinusitis, and pneumonia at the following links to MedlinePlus.gov, the National Library of Medicine Web site designed to help you research your health questions. Pleural effusions: http://www.nlm.nih.gov/medlineplus/ency/article/000086.htm Bronchitis: http://www.nlm.nih.gov/medlineplus/chronicbronchitis.html Sinusitis: http://www.nlm.nih.gov/medlineplus/sinusitis.html Pneumonia: http://www.nlm.nih.gov/medlineplus/pneumonia.html
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What causes Hereditary lymphedema type II ?
What causes hereditary lymphedema type II? The cause of hereditary lymphedema type II is unknown. The condition is thought to be genetic because it tends to run in families. Researchers have studied many genes associated with the lymphatic system; however, to date, no specific genetic change has been associated with this type of lymphedema.
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What is (are) Miller-Dieker syndrome ?
Miller-Dieker syndrome is a genetic condition characterized by lissencephaly, typical facial features, and severe neurologic abnormalities. Symptoms may include severe intellectual disability, developmental delay, seizures, muscle stiffness, weak muscle tone and feeding difficulties. Miller-Dieker syndrome is caused by a deletion of genetic material near the end of the short (p) arm of chromosome 17. Treatment is symptomatic and supportive.
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How to prevent Cardiogenic Shock ?
The best way to prevent cardiogenic shock is to lower your risk for coronary heart disease (CHD) and heart attack. (For more information, go to the National Heart, Lung, and Blood Institute's "Your Guide to a Healthy Heart.") If you already have CHD, its important to get ongoing treatment from a doctor who has experience treating heart problems. If you have a heart attack, you should get treatment right away to try to prevent cardiogenic shock and other possible complications. Act in time. Know the warning signs of a heart attack so you can act fast to get treatment. Many heart attack victims wait 2 hours or more after their symptoms begin before they seek medical help. Delays in treatment increase the risk of complications and death. If you think you're having a heart attack, call 911 for help. Don't drive yourself or have friends or family drive you to the hospital. Call an ambulance so that medical personnel can begin life-saving treatment on the way to the emergency room.
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How to diagnose Nephrotic Syndrome in Adults ?
Urine samples are taken to diagnose people suspected of having nephrotic syndrome. Nephrotic syndrome is diagnosed when large amounts of protein are found in the urine. The blood protein albumin makes up much of the protein that is lost, though many other important proteins are also lost in nephrotic syndrome. The presence of albumin in the urine can be detected with a dipstick test performed on a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine. Patches on the dipstick change color when protein is present in urine. A more precise measurement is usually needed to confirm the diagnosis. Either a single urine sample or a 24-hour collection of urine can be sent to a lab for analysis. With the single urine sample, the lab measures both albumin and creatinine, a waste product of normal muscle breakdown. The comparison of the measurements is called a urine albumin-to-creatinine ratio. A urine sample containing more than 30 milligrams of albumin for each gram of creatinine may signal a problem. With a 24-hour collection of urine, the lab measures only the amount of albumin present. The single urine sample is easier to collect than the 24-hour sample and is usually sufficient to confirm diagnosis, though the 24-hour collection may be used in some cases. Once nephrotic syndrome is diagnosed, blood tests are usually needed to check for systemic diseases that may be causing the nephrotic syndrome and to find out how well the kidneys are working overall. A blood test involves drawing blood at a health care providers office or commercial facility and sending the sample to a lab for analysis. Though blood tests can point toward systemic diseases, a kidney biopsy is usually needed to diagnose the specific underlying disease causing the nephrotic syndrome and to determine the best treatment. A kidney biopsy is a procedure that involves taking a piece of kidney tissue for examination with a microscope. Kidney biopsies are performed by a health care provider in a hospital with light sedation and local anesthetic. A biopsy is often not needed for a person with diabetes because the persons medical history and lab tests may be enough to diagnose the problem as being a result of diabetes.
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Is primary hyperoxaluria inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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What is (are) Nuclear Gene-Encoded Leigh Syndrome ?
Nuclear gene-encoded Leigh syndrome is a progressive neurological disease. It usually first becomes apparent in infancy with developmental delay or regression. Rarely, the disease begins in adolescence or adulthood. Symptoms progress to include generalized weakness, lack of muscle tone, spasticity, movement disorders, cerebellar ataxia, and peripheral neuropathy. Other signs and symptoms may include an increase in the heart muscle size (hypertrophic cardiomyopathy); excessive body hair (hypertrichosis); anemia; kidney or liver problems; and lung or heart failure. Nuclear gene-encoded Leigh syndrome (and Leigh-like syndrome, a term used for cases with similar features but that do not fulfill the diagnostic criteria for Leigh syndrome) may be caused by mutations in any of several genes and can be inherited in an autosomal recessive or X-linked manner. While treatment for some cases of Leigh-like syndrome may be available, management is generally supportive and focuses on the symptoms present.
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Who is at risk for Acanthamoeba - Granulomatous Amebic Encephalitis (GAE); Keratitis? ?
Acanthamoeba keratitis Acanthamoeba keratitis is a rare disease that can affect anyone, but is most common in individuals who wear contact lenses. In the United States, an estimated 85% of cases occur in contact lens users. The incidence of the disease in developed countries is approximately one to 33 cases per million contact lens wearers. For people who wear contact lenses, certain practices can increase the risk of getting Acanthamoeba keratitis: - Storing and handling lenses improperly - Disinfecting lenses improperly (such as using tap water or topping off solutions when cleaning the lenses or lens case) - Swimming, using a hot tub, or showering while wearing lenses - Coming into contact with contaminated water - Having a history of trauma to the cornea Contact lens wearers who practice proper lens care and non-contact lens wearers can still develop the infection. For additional information on contact lens care and prevention of Acanthamoeba keratitis visit CDC’s web page on Prevention and Control. There have been no reports of Acanthamoeba keratitis being spread from one person to another. Granulomatous Amebic Encephalitis (GAE) Granulomatous Amebic Encephalitis (GAE) and disseminated infection are very rare forms of Acanthamoeba infection and primarily affect people with compromised immune systems. While unusual, disseminated infection can also affect healthy children and adults. Conditions that may increase a patient’s risk for GAE and disseminated infection include: - AIDS - Organ/Tissue transplant - Steroids or excessive use of antibiotics - Diabetes Mellitus - Cancer - Disorders in which white blood cells in the lymphatic tissue are over-produced or abnormal - Disorders in which blood cells or blood clotting mechanisms do not function properly or are abnormal - Liver cirrhosis - Lupus
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How to diagnose Mastocytic enterocolitis ?
How is mastocytic enterocolits diagnosed? Mastocytic enterocolitis is diagnosed after an endoscopic procedure in which the doctor takes samples of tissues (biopsies) from the lining of the intestines. The tissue is then sent to a pathologist who looks at it under the microscope. Mast cells may be hard to see on biopsies without a special stain for tryptase, an enzyme present in mast cells. Mastocytic enterocolitis is diagnosed when excess mast cells are present in the small bowel or the colon.
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What to do for Lactose Intolerance ?
- Lactose is a sugar found in milk and milk products. - Lactose intolerance is a condition in which people have digestive symptomssuch as bloating, diarrhea, and gasafter eating or drinking milk or milk products. - A health care provider makes a diagnosis of lactose intolerance based on medical, family, and diet history, including a review of symptoms; a physical exam; and medical tests. - Basing a diagnosis on symptoms alone may be misleading because digestive symptoms can occur for many reasons other than lactose intolerance. - Most people with lactose intolerance can tolerate some amount of lactose in their diet and do not need to avoid milk or milk products completely. However, individuals vary in the amount of lactose they can tolerate. - Research suggests that adults and adolescents with lactose malabsorption could eat or drink at least 12 grams of lactose in one sitting without symptoms or with only minor symptoms. This amount is the amount of lactose in 1 cup of milk. - Many people can manage the symptoms of lactose intolerance by changing their diet. Some people may only need to limit the amount of lactose they eat or drink. Others may need to avoid lactose altogether. - People may find it helpful to talk with a health care provider or a registered dietitian to determine if their diet provides adequate nutrients including calcium and vitamin D. To help ensure coordinated and safe care, people should discuss their use of complementary and alternative medical practices, including their use of dietary supplements, with their health care provider. - Lactose is in all milk and milk products. Manufacturers also often add milk and milk products to boxed, canned, frozen, packaged, and prepared foods. People can check the ingredients on food labels to find possible sources of lactose in food products.
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What are the symptoms of Osteopetrosis autosomal recessive 3 ?
What are the signs and symptoms of Osteopetrosis autosomal recessive 3? The Human Phenotype Ontology provides the following list of signs and symptoms for Osteopetrosis autosomal recessive 3. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of epiphysis morphology 90% Abnormality of the renal tubule 90% Anemia 90% Aseptic necrosis 90% Bone pain 90% Cognitive impairment 90% Genu valgum 90% Hepatomegaly 90% Increased bone mineral density 90% Recurrent fractures 90% Reduced bone mineral density 90% Splenomegaly 90% Abnormality of dental morphology 50% Carious teeth 50% Cerebral calcification 50% Mandibular prognathia 50% Peripheral neuropathy 50% Thrombocytopenia 50% Optic atrophy 7.5% Visual impairment 7.5% Autosomal recessive inheritance - Basal ganglia calcification - Cranial hyperostosis - Dental malocclusion - Diaphyseal sclerosis - Distal renal tubular acidosis - Elevated serum acid phosphatase - Extramedullary hematopoiesis - Hepatosplenomegaly - Intellectual disability - Optic nerve compression - Osteopetrosis - Periodic hypokalemic paresis - Short stature - Visual loss - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the genetic changes related to branchiootorenal/branchiootic syndrome ?
Mutations in three genes, EYA1, SIX1, and SIX5, have been reported in people with BOR/BO syndrome. About 40 percent of people with this condition have a mutation in the EYA1 gene. SIX1 gene mutations are a much less common cause of the disorder. SIX5 gene mutations have been found in a small number of people with BOR syndrome, although researchers question whether mutations in this gene cause the condition. Some affected individuals originally reported to have SIX5 gene mutations were later found to have EYA1 gene mutations as well, and researchers suspect that the EYA1 gene mutations may be the actual cause of the condition in these people. The proteins produced from the EYA1, SIX1, and SIX5 genes play important roles in development before birth. The EYA1 protein interacts with several other proteins, including SIX1 and SIX5, to regulate the activity of genes involved in many aspects of embryonic development. Research suggests that these protein interactions are essential for the normal formation of many organs and tissues, including the second branchial arch, ears, and kidneys. Mutations in the EYA1, SIX1, or SIX5 gene may disrupt the proteins' ability to interact with one another and regulate gene activity. The resulting genetic changes affect the development of organs and tissues before birth, which leads to the characteristic features of BOR/BO syndrome. Some people with BOR/BO syndrome do not have an identified mutation in any of the genes listed above. In these cases, the cause of the condition is unknown.
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How many people are affected by aromatic l-amino acid decarboxylase deficiency ?
AADC deficiency is a rare disorder. Only about 100 people with this condition have been described in the medical literature worldwide; about 20 percent of these individuals are from Taiwan.
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what research (or clinical trials) is being done for Lambert-Eaton Myasthenic Syndrome ?
The NINDS supports research on neuromuscular disorders such as LEMS with the ultimate goal of finding ways to treat, prevent, and cure them.
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What are the treatments for piebaldism ?
These resources address the diagnosis or management of piebaldism: - Genetic Testing Registry: Partial albinism These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What is (are) Parasites - Zoonotic Hookworm ?
There are many different species of hookworms, some are human parasites and some are animal parasites. People can be infected by larvae of animal hookworms, usually dog and cat hookworms. The most common result of animal hookworm infection is a skin condition called cutaneous larva migrans.
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what research (or clinical trials) is being done for Childhood Astrocytomas ?
New types of treatment are being tested in clinical trials. This summary section describes treatments that are being studied in clinical trials. It may not mention every new treatment being studied. Information about clinical trials is available from the NCI website. Other drug therapy Lenalidomide is a type of angiogenesis inhibitor. It prevents the growth of new blood vessels that are needed by a tumor to grow. Patients may want to think about taking part in a clinical trial. For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment. Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment. Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward. Patients can enter clinical trials before, during, or after starting their cancer treatment. Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment. Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
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What are the genetic changes related to Pol III-related leukodystrophy ?
Pol III-related leukodystrophy is caused by mutations in the POLR3A or POLR3B gene. These genes provide instructions for making the two largest parts (subunits) of an enzyme called RNA polymerase III. This enzyme is involved in the production (synthesis) of ribonucleic acid (RNA), a chemical cousin of DNA. The RNA polymerase III enzyme attaches (binds) to DNA and synthesizes RNA in accordance with the instructions carried by the DNA, a process called transcription. RNA polymerase III helps synthesize several forms of RNA, including ribosomal RNA (rRNA) and transfer RNA (tRNA). Molecules of rRNA and tRNA assemble protein building blocks (amino acids) into working proteins; this process is essential for the normal functioning and survival of cells. Researchers suggest that mutations in the POLR3A or POLR3B gene may impair the ability of subunits of the RNA polymerase III enzyme to assemble properly or result in an RNA polymerase III with impaired ability to bind to DNA. Reduced function of the RNA polymerase III molecule likely affects development and function of many parts of the body, including the nervous system and the teeth, but the relationship between POLR3A and POLR3B gene mutations and the specific signs and symptoms of Pol III-related leukodystrophy is unknown.
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What are the symptoms of Richieri Costa Da Silva syndrome ?
What are the signs and symptoms of Richieri Costa Da Silva syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Richieri Costa Da Silva syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Absent tibia - Autosomal recessive inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the treatments for cholesteryl ester storage disease ?
These resources address the diagnosis or management of cholesteryl ester storage disease: - Genetic Testing Registry: Lysosomal acid lipase deficiency - MedlinePlus Encyclopedia: Atherosclerosis - MedlinePlus Encyclopedia: Cirrhosis These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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what research (or clinical trials) is being done for Pompe Disease ?
The National Institute of Neurological Disorders and Stroke (NINDS) supports Pompe research through grants to major research institutions across the country. Research related to Pompe disease is conducted in one of the laboratories of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) at the National Institutes of Health. Much of Pompe-related research focuses on finding better ways to prevent, treat, and ultimately cure this disorder.
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What are the symptoms of Lymphocytic vasculitis ?
What are the signs and symptoms of Lymphocytic vasculitis? Lymphocytic vasculitis can cause a number of different symptoms. Hives, red or purplish discolored patches, a bump (nodule), or an open sore (ulcer) have all been described as symptoms of this condition. The size, location, and severity of symptoms varies widely among affected individuals. Additional symptoms may occur if the vasculitis also affects internal organs; this is known as systemic vasculitis. The symptoms of systemic vasculitis depend on which organs are affected and to what degree. The Human Phenotype Ontology provides the following list of signs and symptoms for Lymphocytic vasculitis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of metabolism/homeostasis - Autosomal dominant inheritance - Nodular inflammatory vasculitis - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) SAPHO syndrome ?
SAPHO syndrome involves any combination of: Synovitis (inflammation of the joints), Acne, Pustulosis (thick yellow blisters containing pus) often on the palms and soles, Hyperostosis (increase in bone substance) and Osteitis (inflammation of the bones). The cause of SAPHO syndrome is unknown and treatment is focused on managing symptoms.
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What are the treatments for Gitelman syndrome ?
These resources address the diagnosis or management of Gitelman syndrome: - Genetic Testing Registry: Familial hypokalemia-hypomagnesemia These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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What is (are) Leukodystrophy ?
A leukodystrophy is a type of rare genetic disorder that affects the brain, spinal cord, and other nerves in the body. It is caused by destruction of the white matter of the brain. The white matter degrades due to defects of the myelin, which is a fatty covering that insulates nerves in the brain. Myelin is needed to protect the nerves and the nerves can't function normally without it. These disorders are progressive, meaning they tend to get worse with time. The leukodystrophies are a group of disorders caused by spelling mistakes (mutations) in the genes involved in making myelin. Specific leukodystrophies include metachromatic leukodystrophy, Krabbe leukodystrophy, X-linked adrenoleukodystrophy, Pelizaeus-Merzbacher disease, Canavan disease, and Alexander disease. The most common symptom of a leukodystrophy is a decline in functioning of an infant or child who previously appeared healthy. This gradual loss may be seen with issues in body tone, movements, gait, speech, ability to eat, vision, hearing, and behavior.
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What are the symptoms of L-arginine:glycine amidinotransferase deficiency ?
What are the signs and symptoms of L-arginine:glycine amidinotransferase deficiency? The Human Phenotype Ontology provides the following list of signs and symptoms for L-arginine:glycine amidinotransferase deficiency. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Gowers sign 5% Abnormality of creatine metabolism - Autism - Autosomal recessive inheritance - Delayed speech and language development - Failure to thrive - Infantile onset - Intellectual disability - Organic aciduria - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Edema ?
Edema means swelling caused by fluid in your body's tissues. It usually occurs in the feet, ankles and legs, but it can involve your entire body. Causes of edema include - Eating too much salt - Sunburn - Heart failure - Kidney disease - Liver problems from cirrhosis - Pregnancy - Problems with lymph nodes, especially after mastectomy - Some medicines - Standing or walking a lot when the weather is warm To keep swelling down, your health care provider may recommend keeping your legs raised when sitting, wearing support stockings, limiting how much salt you eat, or taking a medicine called a diuretic - also called a water pill.
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What are the symptoms of Cirrhosis ?
Many people with cirrhosis have no symptoms in the early stages of the disease. However, as the disease progresses, a person may experience the following symptoms: - fatigue, or feeling tired - weakness - itching - loss of appetite - weight loss - nausea - bloating of the abdomen from ascitesa buildup of fluid in the abdomen - edemaswelling due to a buildup of fluidin the feet, ankles, or legs - spiderlike blood vessels, called spider angiomas, on the skin - jaundice, a condition that causes the skin and whites of the eyes to turn yellow
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Is carbamoyl phosphate synthetase I deficiency inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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What is (are) Neurological Consequences of Cytomegalovirus Infection ?
Cytomegalovirus (CMV) is a virus found throughout the world that infects between 50 to 80 percent of all adults in the United States by the age of 40. CMV is in the same family of viruses that causes cold sores (herpes simplex virus), infectious mononucleosis (Epstein-Barr virus), and chickenpox/shingles (varicella zoster virus). Most people who acquire CVM as children or adults display no signs of illness or have mild symptoms such as fever, fatigue, or tender lymph nodes. People with a compromised immune system may have more severe forms of infection involving the nervous system. A hallmark of CMV infection is that the virus cycles through periods of dormancy and active infection during the life of the individual Infected persons of any age periodically shed the virus in their body fluids, such as saliva, urine, blood, tears, semen, or breast milk. CMV is most commonly transmitted when infected body fluids come in contact with the mucous membranes of an uninfected person, but the virus can also pass from mother to fetus during pregnancy.
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How many people are affected by mucolipidosis III gamma ?
Mucolipidosis III gamma is a rare disorder, although its exact prevalence is unknown. It is estimated to occur in about 1 in 100,000 to 400,000 individuals worldwide.
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What is (are) Wolff-Parkinson-White syndrome ?
Wolff-Parkinson-White syndrome is a condition characterized by abnormal electrical pathways in the heart that cause a disruption of the heart's normal rhythm (arrhythmia). The heartbeat is controlled by electrical signals that move through the heart in a highly coordinated way. A specialized cluster of cells called the atrioventricular node conducts electrical impulses from the heart's upper chambers (the atria) to the lower chambers (the ventricles). Impulses move through the atrioventricular node during each heartbeat, stimulating the ventricles to contract slightly later than the atria. People with Wolff-Parkinson-White syndrome are born with an extra connection in the heart, called an accessory pathway, that allows electrical signals to bypass the atrioventricular node and move from the atria to the ventricles faster than usual. The accessory pathway may also transmit electrical impulses abnormally from the ventricles back to the atria. This extra connection can disrupt the coordinated movement of electrical signals through the heart, leading to an abnormally fast heartbeat (tachycardia) and other arrhythmias. Resulting symptoms include dizziness, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, and fainting (syncope). In rare cases, arrhythmias associated with Wolff-Parkinson-White syndrome can lead to cardiac arrest and sudden death. The most common arrhythmia associated with Wolff-Parkinson-White syndrome is called paroxysmal supraventricular tachycardia. Complications of Wolff-Parkinson-White syndrome can occur at any age, although some individuals born with an accessory pathway in the heart never experience any health problems associated with the condition. Wolff-Parkinson-White syndrome often occurs with other structural abnormalities of the heart or underlying heart disease. The most common heart defect associated with the condition is Ebstein anomaly, which affects the valve that allows blood to flow from the right atrium to the right ventricle (the tricuspid valve). Additionally, Wolff-Parkinson-White syndrome can be a component of several other genetic syndromes, including hypokalemic periodic paralysis (a condition that causes episodes of extreme muscle weakness), Pompe disease (a disorder characterized by the storage of excess glycogen), and tuberous sclerosis (a condition that results in the growth of noncancerous tumors in many parts of the body).
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What are the symptoms of Craniosynostosis, anal anomalies, and porokeratosis ?
What are the signs and symptoms of Craniosynostosis, anal anomalies, and porokeratosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Craniosynostosis, anal anomalies, and porokeratosis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the clavicle 90% Abnormality of the eyelashes 90% Aplasia/Hypoplasia of the eyebrow 90% Displacement of the external urethral meatus 90% Frontal bossing 90% Hyperkeratosis 90% Urogenital fistula 90% Cognitive impairment 50% Ectopic anus 50% Hearing impairment 50% Malar flattening 50% Proptosis 50% Thick lower lip vermilion 50% Wide mouth 50% Cleft palate 7.5% Kyphosis 7.5% Anal atresia - Autosomal recessive inheritance - Brachycephaly - Coronal craniosynostosis - Delayed cranial suture closure - Ectropion - Hypoplasia of midface - Hypospadias - Lambdoidal craniosynostosis - Parietal foramina - Porokeratosis - Ptosis - Rectovaginal fistula - Sagittal craniosynostosis - Sensorineural hearing impairment - Short clavicles - Short ribs - Sparse eyebrow - Sparse eyelashes - Sparse scalp hair - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Hypopituitarism ?
Hypopituitarism occurs when the body has low levels of certain hormones made by the pituitary gland. The pituitary gland normally makes several hormones (including growth hormone, thyroid stimulating hormone, adrenocorticotropic hormone, prolactin, follicle stimulating hormone and luteinizing hormone, vasopressin, and oxytocin). These hormones are important for directing body growth and development, and for regulating blood pressure and metabolism. Symptoms of this condition vary and depend on which hormones are affected. Treatment depends on the cause of this condition; once the cause is corrected, medication (hormone replacement therapy) must be taken to provide the body with the normal amount of hormones.
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What are the symptoms of Sprengel deformity ?
What are the signs and symptoms of Sprengel deformity? Signs and symptoms of Sprengel deformity can vary depending on the severity and whether additional skeletal or muscular abnormalities are present. Some people may not have noticeable signs or symptoms. It more commonly occurs on the left side, but can occur on both sides (bilaterally). In addition to shoulder asymmetry, the elevated shoulder blade may cause a lump in the back of the base of the neck; underdeveloped or incomplete muscles in the surrounding area; and limited movement of the shoulder and arm on the affected side. Some people have bone, cartilage or fiber- like tissue between the shoulder blade and the spinal bones (vertebrae) next to it. Other features that have been found in association with Sprengel deformity include: scoliosis Klippel Feil syndrome limb length discrepancy an underdeveloped backbone (hemivertebrae) missing, fused, or extra ribs (cervical ribs) abnormalities of the collarbone abnormalities of the chest organs of the body displaced on the opposite side (ex: liver on the left and heart on the right) spina bifida occulta cleft palate The Human Phenotype Ontology provides the following list of signs and symptoms for Sprengel deformity. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the shoulder 90% Sprengel anomaly 90% Cleft palate 7.5% Autosomal dominant inheritance - Cervical segmentation defect - Hemivertebrae - Neck muscle hypoplasia - Rib segmentation abnormalities - Scoliosis - Shoulder muscle hypoplasia - Spina bifida occulta - Sporadic - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What are the treatments for Schimke immuno-osseous dysplasia ?
These resources address the diagnosis or management of Schimke immuno-osseous dysplasia: - Gene Review: Gene Review: Schimke Immunoosseous Dysplasia - Genetic Testing Registry: Schimke immunoosseous dysplasia These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
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Is mitochondrial trifunctional protein deficiency inherited ?
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
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How many people are affected by dopamine beta-hydroxylase deficiency ?
Dopamine -hydroxylase deficiency is a very rare disorder. Fewer than 20 affected individuals, all of Western European descent, have been described in the scientific literature.
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What is (are) Aromatic L-amino acid decarboxylase deficiency ?
Aromatic l-amino acid decarboxylase (AADC) deficiency is an inherited condition that affects the way signals are passed between certain cells in the nervous system. Individuals affected by this condition often have severe movement disorders, abnormal eye movements, autonomic symptoms, and neurological impairment. The condition is caused by mutations in the DDC gene. It is inherited in an autosomal recessive pattern. Treatment includes a variety of medications which may result in varying levels of success in individual patients. Physical, occupational, and speech therapy may also be of benefit.
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