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How many people are affected by aromatase excess syndrome ?
|
The prevalence of aromatase excess syndrome is unknown; more than 20 cases have been described in the medical literature.
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What is (are) Mycetoma ?
|
Mycetoma is a chronic infection that is caused by fungi or actinomycetes (bacteria that produce filaments, like fungi). The first symptom of the condition is generally painless swelling beneath the skin, which progresses to a nodule (lump) over several years. Eventually, affected people experience massive swelling and hardening of the affected area; skin rupture; and formation of sinus tracts (holes) that discharge pus and grains filled with organisms. Some affected people have no discomfort while others report itching and/or pain. Mycetoma is rare in the United States, but is commonly diagnosed in Africa, Mexico and India. In these countries, it occurs most frequently in farmers, shepherds, and people living in rural areas. Frequent exposure to penetrating wounds by thorns or splinters is a risk factor. Treatment varies based on the cause of the condition and may include antibiotics or antifungal medications.
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How to diagnose Parasites - Cysticercosis ?
|
If you think that you may have cysticercosis, please see your health care provider. Your health care provider will ask you about your symptoms, where you have travelled, and what kinds of foods you eat. The diagnosis of neurocysticercosis usually requires MRI or CT brain scans. Blood tests may be useful to help diagnose an infection, but they may not always be positive in light infections.
If you have been diagnosed with cysticercosis, you and your family members should be tested for intestinal tapeworm infection. See the taeniasis section for more information on intestinal tapeworm infections.
More on: Taeniasis
More on: Resources for Health Professionals: Diagnosis
|
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What are the genetic changes related to hereditary myopathy with early respiratory failure ?
|
HMERF can be caused by a mutation in the TTN gene. This gene provides instructions for making a protein called titin. Titin plays an important role in muscles the body uses for movement (skeletal muscles) and in heart (cardiac) muscle. Within muscle cells, titin is an essential component of structures called sarcomeres. Sarcomeres are the basic units of muscle contraction; they are made of proteins that generate the mechanical force needed for muscles to contract. Titin has several functions within sarcomeres. One of its most important jobs is to provide structure, flexibility, and stability to these cell structures. Titin also plays a role in chemical signaling and in assembling new sarcomeres. The TTN gene mutation responsible for HMERF leads to the production of an altered version of the titin protein. Studies suggest that this change may disrupt titin's interactions with other proteins within sarcomeres and interfere with the protein's role in chemical signaling. Consequently, muscle fibers become damaged and weaken over time. It is unclear why these effects are usually limited to proximal muscles and muscles involved in breathing. Some people with the characteristic features of HMERF do not have identified mutations in the TTN gene. In these cases, the genetic cause of the condition is unknown.
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What are the treatments for Kidney Disease ?
|
Kidney disease can get worse over time, and may lead to kidney failure. Kidney failure means advanced kidney damage with less than 15% normal function. Most people with kidney failure have symptoms from the build up of waste products and extra water in their body. End-stage renal disease (ESRD) is kidney failure treated by dialysis or kidney transplant. If kidney disease progresses to kidney failure, the goal of treatment changes. Since the kidneys no longer work well enough to maintain health, it is necessary to choose a treatment in order to maintain health. There are two main options for this: dialysis and transplantation. Some patients choose not to treat kidney failure with dialysis or a transplant. Instead, they receive supportive care to treat their symptoms. Before you and your health care team decide on a treatment plan, it is important that you understand how each treatment option is likely to affect how long you will live or how good you will feel. If your kidney disease is progressing, talk with your health care provider about choosing a treatment that is right for you. (Watch the video to learn more about dialysis decisions. To enlarge the videos on this page, click the brackets in the lower right-hand corner of the video screen. To reduce the videos, press the Escape (Esc) button on your keyboard.) Two Kinds of Dialysis Dialysis is a treatment that takes waste products and extra fluid out of your body. In hemodialysis, your blood passes through a filter outside of your body and the clean blood is returned to your body. In hemodialysis, blood is run through a filter outside of your body and the clean blood is returned to the body. Hemodialysis is usually done at a dialysis center three times a week, but it can also be done at home. Each session usually lasts between three and four hours. Peritoneal dialysis is another way to remove wastes from your blood. This kind of dialysis uses the lining of your abdominal cavity (the space in your body that holds organs like the stomach, intestines, and liver) to filter your blood. It works by putting a special fluid into your abdomen that absorbs waste products in your blood as it passes through small blood vessels in this lining. This fluid with the waste products is then drained away. A key benefit of peritoneal dialysis is that it can be done at home, while you sleep. Hemodialysis and peritoneal dialysis do not cure kidney failure. They are treatments that help replace the function of the kidneys and may help you feel better and live longer. But, for some people who have many health problems and are age 75 or older, studies show that treatment with dialysis may not help. If You Are on Dialysis Although patients with kidney failure are now living longer than ever, over the years, kidney disease can cause problems such as - depression - heart disease - bone disease - arthritis - nerve damage - malnutrition. depression heart disease bone disease arthritis nerve damage malnutrition. To stay as healthy as possible for as long as possible while on dialysis, - follow your dietitian's advice, - take your medicines, and - follow healthy lifestyle and diet habits to keep a healthy weight and control blood pressure, blood sugar, and cholesterol. follow your dietitian's advice, take your medicines, and follow healthy lifestyle and diet habits to keep a healthy weight and control blood pressure, blood sugar, and cholesterol. Dialysis can be a special challenge for older adults, especially those who have other diseases or conditions. For example, for hemodialysis, a person must be able to leave home, travel to the dialysis facility, and sit for 4 hours during treatment. Peritoneal dialysis can be done at home, but someone needs to help. Often, older adults need help with some or all of these activities. They and their families need to think about these issues as they choose treatment options and living facilities. Learn more about dialysis. Eating, Diet, and Nutrition on Dialysis For people who are on dialysis or approaching total kidney failure, adequate nutrition is important for maintaining energy, strength, healthy sleep patterns, bone health, heart health, and good mental health. The diet should be based on the type of treatment the person is getting. - People on hemodialysis must watch how much fluid they drink and avoid eating foods with too much sodium, potassium, and phosphorus. - In contrast, people on peritoneal dialysisa type of dialysis that uses the lining of the abdomen, or belly, to filter the blood inside the bodymay be able to eat more potassium-rich foods because peritoneal dialysis removes potassium from the body more efficiently than hemodialysis. - Both hemodialysis and peritoneal dialysis can remove proteins from the body, so anyone on either form of dialysis should eat protein-rich foods such as meat, fish, and eggs. People on hemodialysis must watch how much fluid they drink and avoid eating foods with too much sodium, potassium, and phosphorus. In contrast, people on peritoneal dialysisa type of dialysis that uses the lining of the abdomen, or belly, to filter the blood inside the bodymay be able to eat more potassium-rich foods because peritoneal dialysis removes potassium from the body more efficiently than hemodialysis. Both hemodialysis and peritoneal dialysis can remove proteins from the body, so anyone on either form of dialysis should eat protein-rich foods such as meat, fish, and eggs. All dialysis centers have a renal dietitian, who helps people with kidney failure make healthy food choices. People who are on dialysis should talk with their clinics renal dietitian. The renal dietitian can help make a meal plan that will help their treatment work well. Kidney Transplantation Some people with kidney failure -- including older adults -- may be able to receive a kidney transplant. This involves having a healthy kidney from another person surgically placed into your body. The new, donated kidney does the work the failed kidneys used to do. The donated kidney can come from someone you dont know who has recently died, or from a living person -- usually a family member. But you might also be able to receive a kidney from an unrelated donor, including your spouse or a friend. Due to the shortage of kidneys, patients on the waiting list for a deceased donor kidney may wait many years. (Watch the video to learn more about kidney transplantation.) Kidney transplantation is a treatment for kidney failure -- not a cure. You will need to see your healthcare provider regularly. And you will need to take medicines for as long as you have your transplant. These medicines suppress your immune system so it doesn't reject the transplanted kidney. Eating, Diet, and Nutrition After a Transplant After a transplant, it is still important to make healthy food choices. It is still important to eat foods with less salt. This may help you keep a healthy blood pressure. You should also choose foods that are healthy for your heart, like fresh fruits, fresh or frozen vegetables, whole grains, and low-fat dairy foods. If you were on dialysis before the transplant, you may find that your diet after transplant is much easier to follow. You can drink more fluids and eat many of the fruits and vegetables you had to eat less of while on dialysis. You may even need to gain a little weight, but be careful not to gain weight too quickly. All transplant clinics have a renal dietitian, who helps people with kidney failure make healthy food choices. People who have had a transplant should talk with their clinics renal dietitian. The renal dietitian can help make a meal plan that will help keep the new kidney healthy. Learn more about kidney transplantation. Choosing Not to Treat With Dialysis or Transplant You may choose not to treat kidney failure with dialysis or a transplant. Instead, you may choose to focus on treating its complications. If you choose this path, you will still get care from your health care team. Your care may include - medicines to protect remaining kidney function for as long as possible - medicines to treat symptoms of kidney failure (such as nausea, anemia, and poor appetite) - advice on diet and lifestyle choices, and - care to ease symptoms, provide relief from physical and emotional pain, and enhance quality of life. medicines to protect remaining kidney function for as long as possible medicines to treat symptoms of kidney failure (such as nausea, anemia, and poor appetite) advice on diet and lifestyle choices, and care to ease symptoms, provide relief from physical and emotional pain, and enhance quality of life. You have the right to choose not to start dialysis or undergo transplant surgery. You may choose not to treat with dialysis or transplant if you feel that the burdens would outweigh the benefits. Or, you may make this choice if you feel these treatments would lower your quality of life. Only you know what it is like for you to live with kidney failure. Treatment with no dialysis or transplant may be a choice for you if - you and your doctor feel dialysis or transplant will not improve your health. For some people who have many health problems and are age 75 or older, studies show that treatment with dialysis may not help. - you feel youve accomplished what you wanted in life. - family and friends support your decision. you and your doctor feel dialysis or transplant will not improve your health. For some people who have many health problems and are age 75 or older, studies show that treatment with dialysis may not help. you feel youve accomplished what you wanted in life. family and friends support your decision. Choosing the Right Treatment Not all treatments are right for all people. Talk to your doctor and other health professionals -- including nurses, dietitians, and diabetes educators -- to figure out the best treatment plan for you. The right choice for you depends upon your medical condition, lifestyle, and personal likes and dislikes. Each treatment option may have a different effect on - how long you live - your overall health - what and how much you can do - how well you can get around - how you feel emotionally - how well you can think, learn, and remember - your sex life. how long you live your overall health what and how much you can do how well you can get around how you feel emotionally how well you can think, learn, and remember your sex life.
|
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] |
Is purine nucleoside phosphorylase 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) paroxysmal extreme pain disorder ?
|
Paroxysmal extreme pain disorder is a condition characterized by skin redness and warmth (flushing) and attacks of severe pain in various parts of the body. The area of flushing typically corresponds to the site of the pain. The pain attacks experienced by people with paroxysmal extreme pain disorder usually last seconds to minutes, but in some cases can last hours. These attacks can start as early as infancy. Early in life, the pain is typically concentrated in the lower part of the body, especially around the rectum, and is usually triggered by a bowel movement. Some children may develop constipation, which is thought to be due to fear of triggering a pain attack. Pain attacks in these young children may also be accompanied by seizures, slow heartbeat, or short pauses in breathing (apnea). As a person with paroxysmal extreme pain disorder ages, the location of pain changes. Pain attacks switch from affecting the lower body to affecting the head and face, especially the eyes and jaw. Triggers of these pain attacks include changes in temperature (such as a cold wind) and emotional distress as well as eating spicy foods and drinking cold drinks. Paroxysmal extreme pain disorder is considered a form of peripheral neuropathy because it affects the peripheral nervous system, which connects the brain and spinal cord to muscles and to cells that detect sensations such as touch, smell, and pain.
|
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what research (or clinical trials) is being done for Microcephaly ?
|
The National Institute of Neurological Disorders and Stroke (NINDS), one of several institutes of the National Institutes of Health (NIH), conducts and funds research aimed at understanding normal brain development, as well as disease-related disorders of the brain and nervous system. Other NIH institutes and centers also support research on disorders that may affect development. Among several projects, scientists are studying genetic mechanisms and identifying novel genes involved with brain development. Animal models are helping scientists to better understand the pathology of human disease, and to discover how the sizes of tissues and organs are impacted by developmental variability. Other researchers hope to gain a better understanding of normal brain development and the molecular and cellular mechanisms of microcephaly.
|
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What is (are) Nablus mask-like facial syndrome ?
|
Nablus mask-like facial syndrome is a rare microdeletion syndrome that is characterized by a mask-like facial appearance. Facial features include narrowing of the eye opening (blepharophimosis); tight appearing glistening facial skin; and flat and broad nose. Other features include malformed ears; unusual scalp hair pattern; permanently bent fingers and toes (camptodactyly); joint deformities (contractures) that restrict movement in the hands and feet; unusual dentition; mild developmental delay; undescended testicles in males (cryptorchidism); and a happy disposition. This condition is caused by a deletion at chromosome 8q22.1.
|
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What are the symptoms of Alopecia, epilepsy, pyorrhea, mental subnormality ?
|
What are the signs and symptoms of Alopecia, epilepsy, pyorrhea, mental subnormality? The Human Phenotype Ontology provides the following list of signs and symptoms for Alopecia, epilepsy, pyorrhea, mental subnormality. 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 eyelashes 90% Abnormality of the teeth 90% Alopecia 90% Aplasia/Hypoplasia of the eyebrow 90% EEG abnormality 90% Gingivitis 90% Memory impairment 90% Seizures 50% Hearing impairment 7.5% Hydrocephalus 7.5% Melanocytic nevus 7.5% Alopecia universalis - Autosomal dominant inheritance - Congenital alopecia totalis - Intellectual disability, mild - Periodontitis - 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) Florid cemento-osseous dysplasia ?
|
Florid cemento-osseous dysplasia is characterized by lesions in the upper and/or lower jaw that occur when normal bone is replaced with a mix of connective tissue and abnormal bone. It tends to affect middle aged women, particularly women of African American and Asian descent. The lesions often affect both sides of the jaw and are symmetrical. The number, size, and shape of the lesions vary. Occasionally the lesions expand and may cause discomfort, pain, or mild disfigurement. The radiographic appearance of the lesions are important for diagnosis.
|
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What is (are) Cholesteatoma ?
|
Cholesteatoma is a type of skin cyst located in the middle ear. It can be congenital (present from birth), but it more commonly occurs as a complication of chronic ear infection. The hallmark symptom is a painless discharge from the ear. Hearing loss, dizziness, and facial muscle paralysis are rare but can result from continued cholesteatoma growth. Surgery can stop infections and prevent complications.
|
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What is (are) Mainzer-Saldino syndrome ?
|
Mainzer-Saldino syndrome is a disorder characterized by kidney disease, eye problems, and skeletal abnormalities. People with Mainzer-Saldino syndrome have chronic kidney disease that begins in childhood and gets worse over time. The rate at which the kidney disease worsens is variable, but the condition eventually leads to kidney failure in most affected individuals. Degeneration of the light-sensitive tissue at the back of the eye (the retina) almost always occurs in this disorder, but the age at which this feature develops varies. Some affected individuals are blind or have severe vision impairment beginning in infancy, with the pattern of vision loss resembling a condition called Leber congenital amaurosis. In other people with Mainzer-Saldino syndrome, the retinal degeneration begins in childhood, but some vision is retained into early adulthood. The vision loss in these affected individuals resembles a category of retinal disorders called rod-cone dystrophies. The most common rod-cone dystrophy is called retinitis pigmentosa, and the vision problems in Mainzer-Saldino syndrome are sometimes referred to as such. However, the abnormal deposits of pigment in the retina from which retinitis pigmentosa gets its name are often not found in Mainzer-Saldino syndrome. As a result, some researchers use terms such as "atypical retinitis pigmentosa without pigment" to describe the retinal degeneration that occurs in Mainzer-Saldino syndrome. The skeletal abnormality most characteristic of Mainzer-Saldino syndrome consists of cone-shaped ends of the bones (epiphyses) in the fingers (phalanges) that can be seen on x-ray images after the first year of life. Affected individuals may also have abnormalities of the thigh bones that occur in the epiphyses and adjacent areas where bone growth occurs (the metaphyses). Occasionally, other skeletal abnormalities occur, including short stature and premature fusion of certain skull bones (craniosynostosis) that affects the shape of the head and face. Affected individuals may also have a small rib cage, which sometimes causes breathing problems in infancy, but the breathing problems are usually mild. A small number of individuals with this disorder have additional problems affecting other organs. These can include liver disease resulting in a buildup of scar tissue in the liver (hepatic fibrosis); cerebellar ataxia, which is difficulty with coordination and balance arising from problems with a part of the brain called the cerebellum; and mild intellectual disability.
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What are the treatments for Achalasia ?
|
How might achalasia be treated? The aim of treatment is to reduce the pressure at the lower esophageal sphincter. Therapy may involve: Injection with botulinum toxin (Botox) to help relax the sphincter muscles (used as a temporary fix) Medications, such as long-acting nitrates (i.e. isosorbide dinitrate) or calcium channel blockers (i.e. nifedipine), to relax the lower esophagus sphincter Surgery (Heller myotomy) to decrease the pressure in the lower sphincter Pneumatic balloon dilation of the esophagus at the location of the narrowing (done during esophagogastroduodenoscopy) You can learn more about these treatment options by clicking on the following links: eMedicine Esophageal Motility Disorders Merck Manuals Motility Disorders A doctor should help to determine the best treatment for each individual situation.
|
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What is (are) Nausea and Vomiting ?
|
Nausea is an uneasy or unsettled feeling in the stomach together with an urge to vomit. Nausea and vomiting, or throwing up, are not diseases. They can be symptoms of many different conditions. These include morning sickness during pregnancy, infections, migraine headaches, motion sickness, food poisoning, cancer chemotherapy or other medicines. For vomiting in children and adults, avoid solid foods until vomiting has stopped for at least six hours. Then work back to a normal diet. Drink small amounts of clear liquids to avoid dehydration. Nausea and vomiting are common. Usually, they are not serious. You should see a doctor immediately if you suspect poisoning or if you have - Vomited for longer than 24 hours - Blood in the vomit - Severe abdominal pain - Headache and stiff neck - Signs of dehydration, such as dry mouth, infrequent urination or dark urine
|
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Is Mayer-Rokitansky-Kster-Hauser syndrome inherited ?
|
Most cases of MRKH syndrome occur in people with no history of the disorder in their family. Less often, MRKH syndrome is passed through generations in families. Its inheritance pattern is usually unclear because the signs and symptoms of the condition frequently vary among affected individuals in the same family. However, in some families, the condition appears to have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance means that one copy of the altered gene in each cell is typically sufficient to cause the disorder, although no genes have been associated with MRKH syndrome.
|
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What is (are) multiminicore disease ?
|
Multiminicore disease is a disorder that primarily affects muscles used for movement (skeletal muscles). This condition causes muscle weakness and related health problems that range from mild to life-threatening. Researchers have identified at least four forms of multiminicore disease, which can be distinguished by their characteristic signs and symptoms. The most common form, called the classic form, causes muscle weakness beginning in infancy or early childhood. This weakness is most noticeable in muscles of the trunk and neck (axial muscles) and is less severe in the arm and leg muscles. Muscle weakness causes affected infants to appear "floppy" (hypotonic) and can delay the development of motor skills such as sitting, standing, and walking. The disease causes muscles of the ribcage and spine to stiffen. When combined with weakness of the muscles needed for breathing, this stiffness leads to severe or life-threatening respiratory problems. Almost all children with multiminicore disease develop an abnormal curvature of the spine (scoliosis), which appears during childhood and steadily worsens over time. Other forms of multiminicore disease have different patterns of signs and symptoms. They are less common than the classic form, together accounting for about 25 percent of all cases. The atypical forms of the condition tend to be milder and cause few or no problems with breathing. The moderate form with hand involvement causes muscle weakness and looseness of the joints, particularly in the arms and hands. Another form of multiminicore disease, known as the antenatal form with arthrogryposis, is characterized by stiff, rigid joints throughout the body (arthrogryposis), distinctive facial features, and other birth defects. Paralysis of the eye muscles (external ophthalmoplegia) is a primary feature of another atypical form of multiminicore disease. This form of the condition also causes general muscle weakness and feeding difficulties that appear in the first year of life. Many people with multiminicore disease also have an increased risk of a developing a severe reaction to certain drugs used during surgery and other invasive procedures. This reaction is called malignant hyperthermia. Malignant hyperthermia occurs in response to some anesthetic gases, which are used to block the sensation of pain, and with a particular type of muscle relaxant. If given these drugs, people at risk for malignant hyperthermia may experience muscle rigidity, breakdown of muscle fibers (rhabdomyolysis), a high fever, increased acid levels in the blood and other tissues (acidosis), and a rapid heart rate. The complications of malignant hyperthermia can be life-threatening unless they are treated promptly. Multiminicore disease gets its name from small, disorganized areas called minicores, which are found in muscle fibers of many affected individuals. These abnormal regions can only be seen under a microscope. Although the presence of minicores can help doctors diagnose multiminicore disease, it is unclear how they are related to muscle weakness and the other features of this condition.
|
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] |
What is (are) neutral lipid storage disease with myopathy ?
|
Neutral lipid storage disease with myopathy is a condition in which fats (lipids) are stored abnormally in organs and tissues throughout the body. People with this condition have muscle weakness (myopathy) due to the accumulation of fats in muscle tissue. Other features of this condition may include a fatty liver, a weakened and enlarged heart (cardiomyopathy), inflammation of the pancreas (pancreatitis), reduced thyroid activity (hypothyroidism), and type 2 diabetes mellitus (the most common form of diabetes). Signs and symptoms of neutral lipid storage disease with myopathy vary greatly among affected individuals.
|
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What are the treatments for 5-alpha reductase deficiency ?
|
These resources address the diagnosis or management of 5-alpha reductase deficiency: - Genetic Testing Registry: 3-Oxo-5 alpha-steroid delta 4-dehydrogenase deficiency - MedlinePlus Encyclopedia: Ambiguous Genitalia - MedlinePlus Encyclopedia: Intersex 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) Lymphedema-distichiasis syndrome ?
|
Lymphedema distichiasis syndrome is a condition that affects the normal function of the lymphatic system (part of the immune system that produces and transports fluids and immune cells throughout the body). People with this condition are born with extra eyelashes (distichiasis) and develop puffiness or swelling (lymphedema) of the limbs by the time they are in their forties. The abnormal eyelashes, which grow along the inner lining of the eyelid, often touch the eyeball and can cause damage to the clear covering of the eye (cornea). Other eye problems such as an irregular curvature of the cornea causing blurred vision (astigmatism) or scarring of the cornea may also occur. Other health problems, varicose veins, droopy eyelids (ptosis), heart abnormalities, and an opening in the roof of the mouth (a cleft palate), may also be present. Lymphedema-distichiasis syndrome is caused by mutations in the FOXC2 gene. This condition is inherited in an autosomal dominant pattern.
|
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] |
What are the treatments for globozoospermia ?
|
These resources address the diagnosis or management of globozoospermia: - Association for Reproductive Medicine: Semen Analysis - Centers for Disease Control: Assisted Reproductive Technology (ART) - Genetic Testing Registry: Globozoospermia - MedlinePlus Encyclopedia: Semen Analysis - MedlinePlus Health Topic: Assisted Reproductive Technology 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 symptoms of 3 methylglutaconic aciduria type V ?
|
What are the signs and symptoms of 3 methylglutaconic aciduria type V? The Human Phenotype Ontology provides the following list of signs and symptoms for 3 methylglutaconic aciduria type V. 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) 3-Methylglutaric aciduria - Autosomal recessive inheritance - Congestive heart failure - Cryptorchidism - Decreased testicular size - Dilated cardiomyopathy - Glutaric aciduria - Hypospadias - Intellectual disability - Intrauterine growth retardation - Microvesicular hepatic steatosis - Muscle weakness - Noncompaction cardiomyopathy - Nonprogressive cerebellar ataxia - Normochromic microcytic anemia - Optic atrophy - Prolonged QT interval - Sudden cardiac death - 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 Varicose Veins ?
|
Weak or damaged valves in the veins can cause varicose veins. After your arteries and capillaries deliver oxygen-rich blood to your body, your veins return the blood to your heart. The veins in your legs must work against gravity to do this.
One-way valves inside the veins open to let blood flow through, and then they shut to keep blood from flowing backward. If the valves are weak or damaged, blood can back up and pool in your veins. This causes the veins to swell.
Weak vein walls may cause weak valves. Normally, the walls of the veins are elastic (stretchy). If these walls become weak, they lose their normal elasticity. They become like an overstretched rubber band. This makes the walls of the veins longer and wider, and it causes the flaps of the valves to separate.
When the valve flaps separate, blood can flow backward through the valves. The backflow of blood fills the veins and stretches the walls even more. As a result, the veins get bigger, swell, and often twist as they try to squeeze into their normal space. These are varicose veins.
Normal Vein and Varicose Vein
Figure A shows a normal vein with a working valve and normal blood flow. Figure B shows a varicose vein with a deformed valve, abnormal blood flow, and thin, stretched walls. The middle image shows where varicose veins might appear in a leg.
Older age or a family history of varicose veins may raise your risk for weak vein walls. You also may be at higher risk if you have increased pressure in your veins due to overweight or obesity or pregnancy.
|
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What are the treatments for Dyssynergia Cerebellaris Myoclonica ?
|
Treatment of Dyssynergia Cerebellaris Myoclonica is symptomatic. Myoclonus and seizures may be treated with drugs like valproate.
|
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How many people are affected by Jacobsen syndrome ?
|
The estimated incidence of Jacobsen syndrome is 1 in 100,000 newborns. More than 200 affected individuals have been reported.
|
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What is (are) Eisenmenger syndrome ?
|
Eisenmenger syndrome is a rare progressive heart condition caused by a structural error in the heart, typically a "hole in the heart" (ventricular septal defect) present at birth (congenital heart defect). This causes abnormal blood flow in the heart, resulting in high pressure within the pulmonary artery, the main blood vessel that connects the heart to the lungs (pulmonary hypertension).
|
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What is (are) Leukoencephalopathy with vanishing white matter ?
|
Leukoencephalopathy with vanishing white matter is a progressive disorder that mainly affects the central nervous system (CNS). This disorder causes deterioration of white matter, which consists of nerve fibers covered by myelin (the substance that protects the nerves). Most affected people begin to have signs and symptoms during childhood, but symptoms may first become apparent anywhere from before birth to adulthood. Symptoms may include difficulty coordinating movements (ataxia); muscle stiffness (spasticity); and optic atrophy. Symptoms may worsen rapidly with episodes of fever, after head trauma, or with other stresses on the body. This disorder may be caused by mutations in any of 5 genes and is inherited in an autosomal recessive manner. There is no specific treatment, and prognosis seems to correlate with the age of onset, the earliest forms being more severe.
|
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] |
Is Tylosis with esophageal cancer inherited ?
|
How is Tylosis with esophageal cancer inherited? This condition has an autosomal dominant pattern of inheritance, which means that a mutation in one copy of the altered gene in each cell is sufficient to cause the disorder. Affected individuals typically have one parent with the condition.
|
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What is (are) Migraine ?
|
If you suffer from migraine headaches, you're not alone. About 12 percent of the U.S. population gets them. Migraines are recurring attacks of moderate to severe pain. The pain is throbbing or pulsing, and is often on one side of the head. During migraines, people are very sensitive to light and sound. They may also become nauseated and vomit. Migraine is three times more common in women than in men. Some people can tell when they are about to have a migraine because they see flashing lights or zigzag lines or they temporarily lose their vision. Many things can trigger a migraine. These include - Anxiety - Stress - Lack of food or sleep - Exposure to light - Hormonal changes (in women) Doctors used to believe migraines were linked to the opening and narrowing of blood vessels in the head. Now they believe the cause is related to genes that control the activity of some brain cells. Medicines can help prevent migraine attacks or help relieve symptoms of attacks when they happen. For many people, treatments to relieve stress can also help. NIH: National Institute of Neurological Disorders and Stroke
|
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How many people are affected by lysinuric protein intolerance ?
|
Lysinuric protein intolerance is estimated to occur in 1 in 60,000 newborns in Finland and 1 in 57,000 newborns in Japan. Outside these populations this condition occurs less frequently, but the exact incidence is unknown.
|
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What is (are) 2-hydroxyglutaric aciduria ?
|
2-hydroxyglutaric aciduria is a condition that causes progressive damage to the brain. The major types of this disorder are called D-2-hydroxyglutaric aciduria (D-2-HGA), L-2-hydroxyglutaric aciduria (L-2-HGA), and combined D,L-2-hydroxyglutaric aciduria (D,L-2-HGA). The main features of D-2-HGA are delayed development, seizures, weak muscle tone (hypotonia), and abnormalities in the largest part of the brain (the cerebrum), which controls many important functions such as muscle movement, speech, vision, thinking, emotion, and memory. Researchers have described two subtypes of D-2-HGA, type I and type II. The two subtypes are distinguished by their genetic cause and pattern of inheritance, although they also have some differences in signs and symptoms. Type II tends to begin earlier and often causes more severe health problems than type I. Type II may also be associated with a weakened and enlarged heart (cardiomyopathy), a feature that is typically not found with type I. L-2-HGA particularly affects a region of the brain called the cerebellum, which is involved in coordinating movements. As a result, many affected individuals have problems with balance and muscle coordination (ataxia). Additional features of L-2-HGA can include delayed development, seizures, speech difficulties, and an unusually large head (macrocephaly). Typically, signs and symptoms of this disorder begin during infancy or early childhood. The disorder worsens over time, usually leading to severe disability by early adulthood. Combined D,L-2-HGA causes severe brain abnormalities that become apparent in early infancy. Affected infants have severe seizures, weak muscle tone (hypotonia), and breathing and feeding problems. They usually survive only into infancy or early childhood.
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Is Williams syndrome inherited ?
|
Is Williams syndrome inherited?
|
[
2513,
8757,
9237,
20265,
3736,
2513,
8757,
9237,
20265,
32
] |
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1,
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[
2513,
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32
] |
What are the symptoms of Meckel syndrome type 2 ?
|
What are the signs and symptoms of Meckel syndrome type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Meckel syndrome type 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) Dandy-Walker malformation 5% Microphthalmia 5% Anencephaly - Autosomal recessive inheritance - Bile duct proliferation - Bowing of the long bones - Cleft palate - Encephalocele - Intrauterine growth retardation - Meningocele - Polydactyly - Postaxial hand polydactyly - Renal cyst - 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 symptoms of Fuhrmann syndrome ?
|
What are the signs and symptoms of Fuhrmann syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Fuhrmann 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) Abnormality of the fibula 90% Adactyly 90% Aplasia/Hypoplasia of the fibula 90% Aplasia/Hypoplasia of the ulna 90% Femoral bowing 90% Hypoplasia of the radius 90% Radial bowing 90% Short stature 90% Talipes 90% Tarsal synostosis 90% Aplasia/Hypoplasia of the 5th finger 75% Aplasia/hypoplasia of the femur 75% Congenital hip dislocation 75% Hypoplastic iliac wing 75% Hypoplastic pelvis 75% Oligodactyly (feet) 75% Patellar aplasia 75% Abnormal finger flexion creases 50% Abnormality of the femur 50% Abnormality of the fingernails 50% Abnormality of the hip bone 50% Abnormality of the metacarpal bones 50% Anonychia 50% Bowing of the long bones 50% Clinodactyly of the 5th finger 50% Hypoplastic toenails 50% Postaxial hand polydactyly 50% Sacrococcygeal pilonidal abnormality 50% Single transverse palmar crease 50% Symphalangism affecting the phalanges of the hand 50% Ulnar deviation of finger 50% Aplasia/Hypoplasia involving the metacarpal bones 33% Aplasia/Hypoplasia of metatarsal bones 33% Oligodactyly (hands) 33% Talipes equinovarus 33% Toe syndactyly 33% Finger syndactyly 7.5% Low-set, posteriorly rotated ears 7.5% Macrotia 7.5% Short distal phalanx of finger 7.5% Split hand 7.5% Absent toenail - Amenorrhea - Aplasia/Hypoplasia of the phalanges of the hand - Autosomal recessive inheritance - Fibular aplasia - 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) Cluttering ?
|
Cluttering is a disorder that affects the way a person speaks. It is characterized by a rapid speaking rate and inability to maintain normally expected sound, syllable, phrase, and pausing patterns while speaking. Other symptoms may include stuttering; language or phonological errors (problems organizing sounds); and attention deficits. The disorder seems to result from disorganized speech planning, talking too fast or in spurts, or simply being unsure of what one wants to say. Therapy generally focuses on the symptoms present in each individual and may include slowing the rate of speech and clearly producing speech sounds (articulating). Articulation and language problems are often reduced if the affected individual can achieve a slower rate of speech.
|
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What is (are) Vesicoureteral Reflux ?
|
The two types of VUR are primary and secondary. Most cases of VUR are primary and typically affect only one ureter and kidney. With primary VUR, a child is born with a ureter that did not grow long enough during the childs development in the womb. The valve formed by the ureter pressing against the bladder wall does not close properly, so urine refluxes from the bladder to the ureter and eventually to the kidney. This type of VUR can get better or disappear as a child gets older. As a child grows, the ureter gets longer and function of the valve improves.
Secondary VUR occurs when a blockage in the urinary tract causes an increase in pressure and pushes urine back up into the ureters. Children with secondary VUR often have bilateral reflux. VUR caused by a physical defect typically results from an abnormal fold of tissue in the urethra that keeps urine from flowing freely out of the bladder.
VUR is usually classified as grade I through V, with grade I being the least severe and grade V being the most severe.
|
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What is the outlook for Pituitary Tumors ?
|
If diagnosed early enough, the prognosis is usually excellent. If diagnosis is delayed, even a non-functioning tumor can cause problems if it grows large enough to press on the optic nerves, the brain, or the carotid arteries (the vessels that bring blood to the brain). Early diagnosis and treatment is the key to a good prognosis.
|
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What are the treatments for Age-related Macular Degeneration ?
|
Wet AMD can be treated with laser surgery, photodynamic therapy, and drugs that are injected into the eye. None of these treatments is a cure for wet AMD. The disease and loss of vision may progress despite treatment.
|
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What is (are) cone-rod dystrophy ?
|
Cone-rod dystrophy is a group of related eye disorders that causes vision loss, which becomes more severe over time. These disorders affect the retina, which is the layer of light-sensitive tissue at the back of the eye. In people with cone-rod dystrophy, vision loss occurs as the light-sensing cells of the retina gradually deteriorate. The first signs and symptoms of cone-rod dystrophy, which often occur in childhood, are usually decreased sharpness of vision (visual acuity) and increased sensitivity to light (photophobia). These features are typically followed by impaired color vision (dyschromatopsia), blind spots (scotomas) in the center of the visual field, and partial side (peripheral) vision loss. Over time, affected individuals develop night blindness and a worsening of their peripheral vision, which can limit independent mobility. Decreasing visual acuity makes reading increasingly difficult and most affected individuals are legally blind by mid-adulthood. As the condition progresses, individuals may develop involuntary eye movements (nystagmus). There are more than 30 types of cone-rod dystrophy, which are distinguished by their genetic cause and their pattern of inheritance: autosomal recessive, autosomal dominant, or X-linked (each of which is described below). Additionally, cone-rod dystrophy can occur alone without any other signs and symptoms or it can occur as part of a syndrome that affects multiple parts of the body.
|
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what research (or clinical trials) is being done for Neurosyphilis ?
|
The National Institute of Neurological Disorders and Stroke supports and conducts research on neurodegenerative disorders, such as neurosyphilis, in an effort to find ways to prevent, treat, and ultimately cure these disorders.
|
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] |
How many people are affected by Bannayan-Riley-Ruvalcaba syndrome ?
|
The prevalence of Bannayan-Riley-Ruvalcaba syndrome is unknown, although it appears to be rare. Several dozen cases have been reported in the medical literature. Researchers suspect that the disorder is underdiagnosed because its signs and symptoms vary and some of them are subtle.
|
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] |
What to do for Graves' Disease ?
|
Experts recommend that people eat a balanced diet to obtain most nutrients. More information about diet and nutrition is provided by the National Agricultural Library available at www.nutrition.gov.
Dietary Supplements
Iodine is an essential mineral for the thyroid. However, people with autoimmune thyroid disease may be sensitive to harmful side effects from iodine. Taking iodine drops or eating foods containing large amounts of iodinesuch as seaweed, dulse, or kelpmay cause or worsen hyperthyroidism. More information about iodine is provided by the National Library of Medicine in the fact sheet, Iodine in diet, available at www.nlm.nih.gov/medlineplus.
Women need more iodine when they are pregnantabout 250 micrograms a daybecause the baby gets iodine from the mothers diet. In the United States, about 7 percent of pregnant women may not get enough iodine in their diet or through prenatal vitamins.3 Choosing iodized saltsalt supplemented with iodineover plain salt and prenatal vitamins containing iodine will ensure this need is met.
To help ensure coordinated and safe care, people should discuss their use of dietary supplements, such as iodine, with their health care provider. Tips for talking with health care providers are available through the National Center for Complementary and Integrative Health.
3 Zimmerman MB. Iodine deficiency in pregnancy and the effects of maternal iodine supplementation on the offspring: a review. American Journal of Clinical Nutrition. 2009;89(2):668S672S.
|
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What is (are) Parasites - Trichinellosis (also known as Trichinosis) ?
|
Trichinellosis, also called trichinosis, is caused by eating raw or undercooked meat of animals infected with the larvae of a species of worm called Trichinella. Infection occurs commonly in certain wild carnivorous (meat-eating) animals such as bear or cougar, or omnivorous (meat and plant-eating) animals such as domestic pigs or wild boar.
|
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What are the treatments for Tracheobronchomalacia ?
|
How might tracheobronchomalacia be treated? Treatment is only medically necessary in people who have signs and symptoms of tracheobronchomalacia (TBM). Management of symptomatic TBM first involves identifying underlying conditions contributing to symptoms, such as chronic inflammation, compression, or injury. Initial treatment will target these underlying medical concerns. If symptoms persist, people with TBM may undergo pulmonary function tests or other assessments to help guide therapy choice and allow monitoring of the response to treatment. Treatment options may include: Silicone and/or long-term stenting Surgical correction Continuous positive airway pressure (CPAP) Tracheostomy (often used as a last resort as it can sometimes worsen TBM) We strongly recommend that you discuss your treatment options with a healthcare provider.
|
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Do you have information about Food Labeling
|
Summary : Most packaged foods in the U.S. have food labels. On every food label you will see - Serving size, number of servings, and number of calories per serving - Information on the amount of dietary fat, cholesterol, dietary fiber, dietary sodium, carbohydrates, dietary proteins, vitamins, and minerals in each serving - Definitions for terms such as low-fat and high-fiber - Information to help you see how a food fits into an overall daily diet Food and Drug Administration
|
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] |
What are the symptoms of Hypopharyngeal Cancer ?
|
Signs and symptoms of hypopharyngeal cancer include a sore throat and ear pain. These and other signs and symptoms may be caused by hypopharyngeal cancer or by other conditions. Check with your doctor if you have any of the following: - A sore throat that does not go away. - Ear pain. - A lump in the neck. - Painful or difficult swallowing. - A change in voice.
|
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What are the treatments for primary hyperoxaluria ?
|
These resources address the diagnosis or management of primary hyperoxaluria: - Gene Review: Gene Review: Primary Hyperoxaluria Type 1 - Gene Review: Gene Review: Primary Hyperoxaluria Type 2 - Gene Review: Gene Review: Primary Hyperoxaluria Type 3 - Genetic Testing Registry: Hyperoxaluria - Genetic Testing Registry: Primary hyperoxaluria 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 symptoms of Diffuse mesangial sclerosis ?
|
What are the signs and symptoms of Diffuse mesangial sclerosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Diffuse mesangial sclerosis. 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) Focal segmental glomerulosclerosis 5% Autosomal recessive inheritance - Childhood onset - Diffuse mesangial sclerosis - Nephroblastoma (Wilms tumor) - Nephrotic syndrome - Progressive - Renal insufficiency - 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) Renal Artery Stenosis ?
|
Renal artery stenosis is the narrowing of one or both renal arteries. Renal means kidney and stenosis means narrowing. The renal arteries are blood vessels that carry blood to the kidneys from the aortathe main blood vessel that carries blood from the heart to arteries throughout the body.
RVH is high blood pressure caused by RAS. Blood pressure is written with two numbers separated by a slash, 120/80, and is said as 120 over 80. The top number is called the systolic pressure and represents the pressure as the heart beats and pushes blood through the blood vessels. The bottom number is called the diastolic pressure and represents the pressure as blood vessels relax between heartbeats. A persons blood pressure is considered normal if it stays at or below 120/80. High blood pressure is a systolic pressure of 140 or above or a diastolic pressure of 90 or above.1
|
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What are the treatments for Striatonigral Degeneration ?
|
There is no cure for striatonigral degeneration, and treatments for the disorder have variable success. Treatments used for Parkinson's disease are recommended. However, unlike Parkinson's disease, striatonigral degeneration is not responsive to levodopa. Dopamine and anticholinergics provide some benefit. Generally, treatment is reevaluated as the disorder progresses.
|
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What are the treatments for Rh Incompatibility ?
|
Rh incompatibility is treated with a medicine called Rh immune globulin. Treatment for a baby who has hemolytic anemia will vary based on the severity of the condition.
Goals of Treatment
The goals of treating Rh incompatibility are to ensure that your baby is healthy and to lower your risk for the condition in future pregnancies.
Treatment for Rh Incompatibility
If Rh incompatibility is diagnosed during your pregnancy, you'll receive Rh immune globulin in your seventh month of pregnancy and again within 72 hours of delivery.
You also may receive Rh immune globulin if the risk of blood transfer between you and the baby is high (for example, if you've had a miscarriage, ectopic pregnancy, or bleeding during pregnancy).
Rh immune globulin contains Rh antibodies that attach to the Rh-positive blood cells in your blood. When this happens, your body doesn't react to the baby's Rh-positive cells as a foreign substance. As a result, your body doesn't make Rh antibodies. Rh immune globulin must be given at the correct times to work properly.
Once you have formed Rh antibodies, the medicine will no longer help. That's why a woman who has Rh-negative blood must be treated with the medicine with each pregnancy or any other event that allows her blood to mix with Rh-positive blood.
Rh immune globulin is injected into the muscle of your arm or buttock. Side effects may include soreness at the injection site and a slight fever. The medicine also may be injected into a vein.
Treatment for Hemolytic Anemia
Several options are available for treating hemolytic anemia in a baby. In mild cases, no treatment may be needed. If treatment is needed, the baby may be given a medicine called erythropoietin and iron supplements. These treatments can prompt the body to make red blood cells.
If the hemolytic anemia is severe, the baby may get a blood transfusion through the umbilical cord. If the hemolytic anemia is severe and the baby is almost full-term, your doctor may induce labor early. This allows the baby's doctor to begin treatment right away.
A newborn who has severe anemia may be treated with a blood exchange transfusion. The procedure involves slowly removing the newborn's blood and replacing it with fresh blood or plasma from a donor.
Newborns also may be treated with special lights to reduce the amount of bilirubin in their blood. These babies may have jaundice (a yellowish color of the skin and whites of the eyes). High levels of bilirubin cause jaundice.
Reducing the blood's bilirubin level is important because high levels of this compound can cause brain damage. High levels of bilirubin often are seen in babies who have hemolytic anemia. This is because the compound forms when red blood cells break down.
|
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What are the symptoms of Microgastria limb reduction defect ?
|
What are the signs and symptoms of Microgastria limb reduction defect? The Human Phenotype Ontology provides the following list of signs and symptoms for Microgastria limb reduction defect. 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 spleen 90% Aplasia/Hypoplasia of the radius 90% Aplasia/Hypoplasia of the thumb 90% Microgastria 90% Abnormality of the humerus 50% Abnormality of the metacarpal bones 50% Abnormality of the ulna 50% Congenital muscular torticollis 50% Frontal bossing 50% Multicystic kidney dysplasia 50% Plagiocephaly 50% Abnormal localization of kidney 7.5% Abnormal lung lobation 7.5% Abnormality of neuronal migration 7.5% Abnormality of the clavicle 7.5% Absent hand 7.5% Amelia 7.5% Aplasia/Hypoplasia affecting the eye 7.5% Aplasia/Hypoplasia of the corpus callosum 7.5% Atria septal defect 7.5% Elbow dislocation 7.5% Hepatomegaly 7.5% Holoprosencephaly 7.5% Intestinal malrotation 7.5% Phocomelia 7.5% Renal hypoplasia/aplasia 7.5% Split hand 7.5% Tracheoesophageal fistula 7.5% Truncus arteriosus 7.5% Urogenital fistula 7.5% Absent gallbladder - Absent thumb - Aganglionic megacolon - Agenesis of corpus callosum - Anophthalmia - Arrhinencephaly - Asplenia - Bicornuate uterus - Biliary tract abnormality - Cryptorchidism - Cystic renal dysplasia - Failure to thrive - Fusion of the left and right thalami - Gastroesophageal reflux - Horseshoe kidney - Hypoplasia of the radius - Hypoplasia of the ulna - Oligodactyly (hands) - Pelvic kidney - Polymicrogyria - Secundum atrial septal defect - Sporadic - Type I truncus arteriosus - Unilateral renal agenesis - 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) X-linked chondrodysplasia punctata 2 ?
|
X-linked chondrodysplasia punctata 2 is a disorder characterized by bone, skin, and eye abnormalities. It occurs almost exclusively in females. Although the signs and symptoms of this condition vary widely, almost all affected individuals have chondrodysplasia punctata, an abnormality that appears on x-rays as spots (stippling) near the ends of bones and in cartilage. In this form of chondrodysplasia punctata, the stippling typically affects the long bones in the arms and legs, the ribs, the spinal bones (vertebrae), and the cartilage that makes up the windpipe (trachea). The stippling is apparent in infancy but disappears in early childhood. Other skeletal abnormalities seen in people with X-linked chondrodysplasia punctata 2 include shortening of the bones in the upper arms and thighs (rhizomelia) that is often different on the right and left sides, and progressive abnormal curvature of the spine (kyphoscoliosis). As a result of these abnormalities, people with this condition tend to have short stature. Infants with X-linked chondrodysplasia punctata 2 are born with dry, scaly patches of skin (ichthyosis) in a linear or spiral (whorled) pattern. The scaly patches fade over time, leaving abnormally colored blotches of skin without hair (follicular atrophoderma). Most affected individuals also have sparse, coarse hair on their scalps. Most people with X-linked chondrodysplasia punctata 2 have clouding of the lens of the eye (cataracts) from birth or early childhood. Other eye abnormalities that have been associated with this disorder include unusually small eyes (microphthalmia) and small corneas (microcornea). The cornea is the clear front surface of the eye. These eye abnormalities can impair vision. In affected females, X-linked chondrodysplasia punctata 2 is typically associated with normal intelligence and a normal lifespan. However, a much more severe form of the condition has been reported in a small number of males. Affected males have some of the same features as affected females, as well as weak muscle tone (hypotonia), changes in the structure of the brain, moderately to profoundly delayed development, seizures, distinctive facial features, and other birth defects. The health problems associated with X-linked chondrodysplasia punctata 2 are often life-threatening in males.
|
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Is Doyne honeycomb retinal dystrophy inherited ?
|
How is Doyne honeycomb retinal dystrophy inherited? Doyne honeycomb retinal dystrophy (DHRD) is inherited in an autosomal dominant manner. This means that having only one changed (mutated) copy of the responsible gene in each cell is enough to cause signs and symptoms of the condition. When a person with an autosomal dominant condition has children, each child has a 50% (1 in 2) risk to inherit the mutated gene from the affected parent. Children who do not inherit the mutated gene will not develop or pass on the disease.
|
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What is (are) Age-related Macular Degeneration ?
|
Age-related macular degeneration, also known as AMD, is an eye disease that affects the macula, a part of the retina. The retina sends light from the eye to the brain, and the macula allows you to see fine detail. AMD Blurs Central Vision AMD blurs the sharp central vision you need for straight-ahead activities such as reading, sewing, and driving. AMD causes no pain. How AMD Progresses In some cases, AMD advances so slowly that people notice little change in their vision. In others, the disease progresses faster and may lead to a loss of vision in both eyes. AMD is a common eye condition among people age 50 and older. It is a leading cause of vision loss in older adults. Two Forms of AMD There are two forms of age-related macular degeneration -- dry and wet.
|
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What are the treatments for Weill-Marchesani syndrome ?
|
How might Weill-Marchesani syndrome be treated? There is no cure for Weill-Marchesani syndrome, and treatment focuses addressing the symptoms that develop. Individuals with this condition often need a team of medical specialists, including pediatricians, eye specialists (ophthalmologists and optometrists), orthopedists, and cardiologists. Regular eye exams are important for early diagnosis of eye problems. Corrective glasses, visual aids, or eye surgery may be needed to improve vision. Increased pressure within the eye (glaucoma) may be treated with eye drops, laser therapy, surgical removal of the iris or lens. Contraction or dilation of the pupils can cause glaucoma in some people with Weill-Marchesani syndrome. Medications that contract the pupil must be avoided, and medications that dilate the pupils must be given with care. Joint stiffness and bone abnormalities can cause complications if anesthesia is needed for a procedure. It is important to inform a physician of the diagnosis before receiving anesthesia, as it can impact airway management.
|
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What are the symptoms of Fetal hydantoin syndrome ?
|
What are the signs and symptoms of Fetal hydantoin syndrome? There is a wide range in the nature and severity of characteristics associated with fetal hydantoin syndrome. Of infants born to women who used phenytoin during pregnancy, 10-30% are reported to show some of the characteristics associated with this syndrome. Few infants exposed only to phenytoin have all of the characteristic that have been reported. Children with this condition may be small at birth, with increased hair on the body and face, and with poorly developed fingernails and toenails. They may also have poor muscle tone. Facial features that may be present with this syndrome include a flat bridge of the nose; an underdeveloped vertical groove in the center of the upper lip (philtrum); a large mouth; and malformed ears. Features specific to the eyes may include down-slanted eyes; widely spaced eyes (hypertelorism); crossed eyes (strabismus); drooping eyelids (ptosis); and/or epicanthal folds (skin folds of the eyelid covering the inner corner of the eye). Other features that have been reported include a short or webbed neck and low-set hair line. Growth deficiencies may include underdeveloped fingers and/or toes, malformed nails, as well as finger-like thumbs. These features are often associated with growth delay and varying degrees of developmental delay. The risk for an affected child to be neurologically impaired is estimated at 1 to 11 % (two to three times higher than for the general population). The risk of cleft lip and/or palate and heart defects is estimated to be about five times higher among exposed infants. Some case reports have suggested an increased risk for the occurrence of benign (noncancerous) or malignant (cancerous) tumors, such as neuroblastoma or other neonatal tumors (ependymoma, ectodermal tumors, Wilms tumor). The Human Phenotype Ontology provides the following list of signs and symptoms for Fetal hydantoin 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) Abnormal dermatoglyphics 90% Depressed nasal ridge 90% Hearing abnormality 90% Low-set, posteriorly rotated ears 90% Short nose 90% Abnormality of the fontanelles or cranial sutures 50% Abnormality of the nipple 50% Anonychia 50% Bifid scrotum 50% Brachydactyly syndrome 50% Coarse hair 50% Cognitive impairment 50% Epicanthus 50% Hernia 50% Hypertelorism 50% Intrauterine growth retardation 50% Low posterior hairline 50% Microcephaly 50% Ptosis 50% Short stature 50% Strabismus 50% Thickened nuchal skin fold 50% Triphalangeal thumb 50% Wide mouth 50% Abnormality of the cardiovascular system 7.5% Cleft palate 7.5% Cryptorchidism 7.5% Neoplasm 7.5% 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 symptoms of Amyotrophic lateral sclerosis type 6 ?
|
What are the signs and symptoms of Amyotrophic lateral sclerosis type 6? The Human Phenotype Ontology provides the following list of signs and symptoms for Amyotrophic lateral sclerosis type 6. 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) Amyotrophic lateral sclerosis - Autosomal dominant inheritance - Fasciculations - Gait disturbance - Hyporeflexia - Neuronal loss in central nervous system - Proximal amyotrophy - 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) white sponge nevus ?
|
White sponge nevus is a condition characterized by the formation of white patches of tissue called nevi (singular: nevus) that appear as thickened, velvety, sponge-like tissue. The nevi are most commonly found on the moist lining of the mouth (oral mucosa), especially on the inside of the cheeks (buccal mucosa). Affected individuals usually develop multiple nevi. Rarely, white sponge nevi also occur on the mucosae (singular: mucosa) of the nose, esophagus, genitals, or anus. The nevi are caused by a noncancerous (benign) overgrowth of cells. White sponge nevus can be present from birth but usually first appears during early childhood. The size and location of the nevi can change over time. In the oral mucosa, both sides of the mouth are usually affected. The nevi are generally painless, but the folds of extra tissue can promote bacterial growth, which can lead to infection that may cause discomfort. The altered texture and appearance of the affected tissue, especially the oral mucosa, can be bothersome for some affected individuals.
|
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What are the symptoms of Xeroderma pigmentosum type 7 ?
|
What are the signs and symptoms of Xeroderma pigmentosum type 7? The Human Phenotype Ontology provides the following list of signs and symptoms for Xeroderma pigmentosum type 7. 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) Ataxia 5% Cataract 5% Growth delay 5% Microcephaly 5% Microphthalmia 5% Pes cavus 5% Spasticity 5% Tremor 5% Autosomal recessive inheritance - Cutaneous photosensitivity - Defective DNA repair after ultraviolet radiation damage - 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) Kidney Failure: Eat Right to Feel Right on Hemodialysis ?
|
Before you were on dialysis, your doctor may have told you to follow a low-protein diet. Being on dialysis changes this. Most people on dialysis are encouraged to eat as much high-quality protein as they can. Protein helps you keep muscle and repair tissue. The better nourished you are, the healthier you will be. You will also have greater resistance to infection and recover from surgery more quickly.
Your body breaks protein down into a waste product called urea. If urea builds up in your blood, it's a sign you have become very sick. Eating mostly high-quality proteins is important because they produce less waste than others. High-quality proteins come from meat, fish, poultry, and eggs (especially egg whites).
Talk With a Dietitian Meat, fish, and chicken are good sources of protein. Talk with a dietitian about the meats you eat. I will eat ______ servings of meat each day. A regular serving size is 3 ounces. This is about the size of the palm of your hand or a deck of cards. Try to choose lean (low-fat) meats that are also low in phosphorus. If you are a vegetarian, ask about other ways to get your protein. Low-fat milk is a good source of protein. But milk is high in phosphorus and potassium. And milk adds to your fluid intake. Talk with a dietitian to see if milk fits into your food plan. I (will) (will not) drink milk. I will drink ______ cup(s) of milk a day.
|
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] |
Is 1p36 deletion syndrome inherited ?
|
Most cases of 1p36 deletion syndrome are not inherited. They result from a chromosomal deletion that occurs as a random event during the formation of reproductive cells (eggs or sperm) or in early fetal development. Affected people typically have no history of the disorder in their family. About 20 percent of people with 1p36 deletion syndrome inherit the chromosome with a deleted segment from an unaffected parent. In these cases, the parent carries a chromosomal rearrangement called a balanced translocation, in which no genetic material is gained or lost. Balanced translocations usually do not cause any health problems; however, they can become unbalanced as they are passed to the next generation. Children who inherit an unbalanced translocation can have a chromosomal rearrangement with extra or missing genetic material. Individuals with 1p36 deletion syndrome who inherit an unbalanced translocation are missing genetic material from the short arm of chromosome 1, which results in birth defects and other health problems characteristic of this disorder.
|
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What are the symptoms of Essential Thrombocythemia ?
|
Patients with essential thrombocythemia may have no signs or symptoms. Essential thrombocythemia often does not cause early signs or symptoms. It may be found during a routine blood test. Signs and symptoms may be caused by essential thrombocytopenia or by other conditions. Check with your doctor if you have any of the following: - Headache. - Burning or tingling in the hands or feet. - Redness and warmth of the hands or feet. - Vision or hearing problems. Platelets are sticky. When there are too many platelets, they may clump together and make it hard for the blood to flow. Clots may form in blood vessels and there may also be increased bleeding. These can cause serious health problems such as stroke or heart attack.
|
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] |
What are the treatments for Salih myopathy ?
|
These resources address the diagnosis or management of Salih myopathy: - Gene Review: Gene Review: Salih Myopathy - Genetic Testing Registry: Myopathy, early-onset, with fatal cardiomyopathy 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 Hearing Loss ?
|
Approximately 17 percent, or 36 million, of American adults say that they have some degree of hearing loss. Hearing loss is a common condition in older adults. Roughly one-third of Americans 65 to 74 years of age and 47 percent of those 75 and older have hearing loss.
|
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What are the treatments for isolated growth hormone deficiency ?
|
These resources address the diagnosis or management of isolated growth hormone deficiency: - Genetic Testing Registry: Ateleiotic dwarfism - Genetic Testing Registry: Autosomal dominant isolated somatotropin deficiency - Genetic Testing Registry: Isolated growth hormone deficiency type 1B - Genetic Testing Registry: X-linked agammaglobulinemia with growth hormone deficiency - MedlinePlus Encyclopedia: Growth Hormone Test 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) Locked-In Syndrome ?
|
Locked-in syndrome is a rare neurological disorder characterized by complete paralysis of voluntary muscles in all parts of the body except for those that control eye movement. It may result from traumatic brain injury, diseases of the circulatory system, diseases that destroy the myelin sheath surrounding nerve cells, or medication overdose. Individuals with locked-in syndrome are conscious and can think and reason, but are unable to speak or move. The disorder leaves individuals completely mute and paralyzed. Communication may be possible with blinking eye movements
|
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What is the outlook for Cushing's Syndrome ?
|
The prognosis for those with Cushing's syndrome varies depending on the cause of the disease. Most cases of Cushing's syndrome can be cured. Many individuals with Cushing's syndrome show significant improvement with treatment, although some may find recovery complicated by various aspects of the causative illness. Some kinds of tumors may recur.
|
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What causes Achondrogenesis ?
|
What causes achondrogenesis? Research has shown that changes (mutations) in the SLC26A2 and COL2A1 genes cause achondrogenesis types 1B and 2, respectively. The genetic cause of achondrogenesis type 1A remains unknown. The SLC26A2 gene provides instructions for making a protein that is important for the normal development of cartilage and for the conversion of cartilage to bone. The COL2A1 gene provides instructions for making a protein that forms a type of collagen found mostly in cartilage and in the clear gel that fills the eyeball (vitreous). Mutations in these genes result in the production of proteins that are unable to properly perform their jobs within the body.
|
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What are the genetic changes related to arrhythmogenic right ventricular cardiomyopathy ?
|
ARVC can result from mutations in at least eight genes. Many of these genes are involved in the function of desmosomes, which are structures that attach heart muscle cells to one another. Desmosomes provide strength to the myocardium and play a role in signaling between neighboring cells. Mutations in the genes responsible for ARVC often impair the normal function of desmosomes. Without normal desmosomes, cells of the myocardium detach from one another and die, particularly when the heart muscle is placed under stress (such as during vigorous exercise). These changes primarily affect the myocardium surrounding the right ventricle, one of the two lower chambers of the heart. The damaged myocardium is gradually replaced by fat and scar tissue. As this abnormal tissue builds up, the walls of the right ventricle become stretched out, preventing the heart from pumping blood effectively. These changes also disrupt the electrical signals that control the heartbeat, which can lead to arrhythmia. Gene mutations have been found in 30 to 40 percent of people with ARVC. Mutations in a gene called PKP2 are most common. In people without an identified mutation, the cause of the disorder is unknown. Researchers are looking for additional genetic factors, particularly those involved in the function of desmosomes, that may play a role in causing ARVC.
|
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Is hyperferritinemia-cataract syndrome inherited ?
|
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.
|
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Is Autoimmune atrophic gastritis inherited ?
|
Is autoimmune atrophic gastritis inherited? In some cases, more than one family member can be affected by autoimmune atrophic gastritis. Although the underlying genetic cause has not been identified, studies suggest that the condition may be inherited in an autosomal dominant manner in these families. In autosomal dominant conditions, an affected person only needs a change (mutation) in one copy of the responsible gene in each cell. In some cases, an affected person inherits the mutation from an affected parent. Other cases may result from new (de novo) mutations in the gene. These cases occur in people with no history of the disorder in their family. A person with the condition has a 50% chance with each pregnancy of passing along the altered gene to his or her child.
|
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What are the treatments for Pudendal Neuralgia ?
|
What treatments are available for pudendal neuralgia? There are no established guidelines for the treatment of pudendal neuralgia. Treatment may include medications, the use of a specialized cushion while sitting, nerve block, surgery to remove nearby tissues that may be pressing on the pudendal nerve, or nerve stimulation.
|
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What are the treatments for Cirrhosis ?
|
Treatment for cirrhosis depends on the cause of the disease and whether complications are present. In the early stages of cirrhosis, the goals of treatment are to slow the progression of tissue scarring in the liver and prevent complications. As cirrhosis progresses, a person may need additional treatments and hospitalization to manage complications. Treatment may include the following:
Avoiding Alcohol and Illegal Substances
People with cirrhosis should not drink any alcohol or take any illegal substances, as both will cause more liver damage.
Preventing Problems with Medications
People with cirrhosis should be careful about starting new medications and should consult a health care provider before taking prescription medications, over-the-counter medications, or vitamins. People with cirrhosis should avoid complementary and alternative medications, such as herbs.
Cirrhosis slows the livers ability to filter medications from the blood. When this slowdown occurs, medications act longer than expected and build up in the body. Some medications and vitamins may also affect liver function.
Viral Hepatitis Vaccination and Screening
All people with cirrhosis should consider vaccination against hepatitis A and B. An infection with one of these hepatitis viruses can cause cirrhosis to get worse. Vaccination can easily prevent both infections.
People with cirrhosis should also get a screening blood test for hepatitis C.
Treating Causes of Cirrhosis
Health care providers can treat some causes of cirrhosis, for example, by prescribing antiviral medications for hepatitis B and C. In some instances, these medications cure the viral infection. Health care providers treat autoimmune hepatitis with corticosteroids and other medications that suppress the immune system. Health care providers can treat hemochromatosis and Wilson diseaseinherited forms of liver disease caused by the buildup of iron or copper in the liverif detected early. Health care providers usually treat liver diseases due to blockage or loss of bile ducts with ursodiol (Actigall, Urso). Ursodiol is a nontoxic bile acid that people can take orally. Ursodiol replaces the bile acids that are normally produced by the liver, which are toxic and build up in the liver when the bile ducts are blocked.
Treating Symptoms and Complications of Cirrhosis
Itching and abdominal pain. A health care provider may give medications to treat various symptoms of cirrhosis, such as itching and abdominal pain.
Portal hypertension. A health care provider may prescribe a beta-blocker or nitrate to treat portal hypertension. Beta-blockers lower blood pressure by helping the heart beat slower and with less force, and nitrates relax and widen blood vessels to let more blood flow to the heart and reduce the hearts workload.
Varices. Beta-blockers can lower the pressure in varices and reduce the likelihood of bleeding. Bleeding in the stomach or esophagus requires an immediate upper endoscopy. This procedure involves using an endoscopea small, flexible tube with a lightto look for varices. The health care provider may use the endoscope to perform a band ligation, a procedure that involves placing a special rubber band around the varices that causes the tissue to die and fall off. A gastroenterologista doctor who specializes in digestive diseasesperforms the procedure at a hospital or an outpatient center. People who have had varices in the past may need to take medication to prevent future episodes.
Edema and ascites. Health care providers prescribe diureticsmedications that remove fluid from the bodyto treat edema and ascites. A health care provider may remove large amounts of ascitic fluid from the abdomen and check for spontaneous bacterial peritonitis. A health care provider may prescribe bacteria-fighting medications called antibiotics to prevent infection. He or she may prescribe oral antibiotics; however, severe infection with ascites requires intravenous (IV) antibiotics.
Hepatic encephalopathy. A health care provider treats hepatic encephalopathy by cleansing the bowel with lactulose, a laxative given orally or as an enemaa liquid put into the rectum. A health care provider may also add antibiotics to the treatment. Hepatic encephalopathy may improve as other complications of cirrhosis are controlled.
Hepatorenal syndrome. Some people with cirrhosis who develop hepatorenal syndrome must undergo regular dialysis treatment, which filters wastes and extra fluid from the body by means other than the kidneys. People may also need medications to improve blood flow through the kidneys.
Osteoporosis. A health care provider may prescribe bisphosphonate medications to improve bone density.
Gallstones and bile duct stones. A health care provider may use surgery to remove gallstones. He or she may use endoscopic retrograde cholangiopancreatography, which uses balloons and basketlike devices, to retrieve the bile duct stones.
Liver cancer. A health care provider may recommend screening tests every 6 to 12 months to check for signs of liver cancer. Screening tests can find cancer before the person has symptoms of the disease. Cancer treatment is usually more effective when the health care provider finds the disease early. Health care providers use blood tests, ultrasound, or both to screen for liver cancer in people with cirrhosis. He or she may treat cancer with a combination of surgery, radiation, and chemotherapy.
|
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] |
what research (or clinical trials) is being done for Prostate Cancer ?
|
Scientists continue to look at new ways to prevent, treat, and diagnose prostate cancer. Research has already led to a number of advances in these areas. Dietary Research Several studies are under way to explore the causes of prostate cancer. Some researchers think that diet may affect a man's chances of developing prostate cancer. For example, some studies show that prostate cancer is more common in populations that consume a high-fat diet, particularly animal fat, and in populations with diets that lack certain nutrients. Research on Testosterone Some research suggests that high levels of testosterone may increase a man's risk of prostate cancer. The difference in prostate cancer risk among racial groups could be related to high testosterone levels, but it also could result from diet or other lifestyle factors. Genetic Research Researchers are studying changes in genes that may increase the risk for developing prostate cancer. Some studies are looking at the genes of men who were diagnosed with prostate cancer at a relatively young age, such as less than 55 years old, and the genes of families who have several members with the disease. Other studies are trying to identify which genes, or arrangements of genes, are most likely to lead to prostate cancer. Much more work is needed, however, before scientists can say exactly how genetic changes relate to prostate cancer. Prevention Research Several studies have explored ways to prevent prostate cancer. In October 2008, initial results of a study on the use of the dietary supplements vitamin E and selenium found that they did not provide any benefit in reducing the number of new cases of the disease. A few studies suggest that a diet that regularly includes tomato-based foods may help protect men from prostate cancer, but there are no studies that conclusively prove this hypothesis. According to results of a study that was re-analyzed in 2013, men who took finasteride, a drug that affects male hormone levels, reduced their chances of getting prostate cancer by nearly 30 percent compared to men who took a placebo. Unlike earlier findings from this study, this new analysis showed no increased risk of late stage disease due to use of finasteride. Stopping Prostate Cancer from Returning Scientists are also looking at ways to stop prostate cancer from returning in men who have already been treated for the disease. These approaches use drugs such as finasteride, flutamide, nilutamide, and LH-RH agonists that manipulate hormone levels. In 2010, the FDA approved a therapeutic cancer vaccine, Provenge, for use in some men with metastatic prostate cancer. Provenge may provide a 4-month improvement in overall survival compared with a placebo vaccine. Other similar vaccine therapies are in development. Research on New Blood Tests Some researchers are working to develop new blood tests to detect the antibodies that the immune system produces to fight prostate cancer. When used along with PSA testing, the antibody tests may provide more accurate results about whether or not a man has prostate cancer. Researching New Approaches to Treatment Through research, doctors are trying to find new, more effective ways to treat prostate cancer. Cryosurgery -- destroying cancer by freezing it -- is under study as an alternative to surgery and radiation therapy. To avoid damaging healthy tissue, the doctor places an instrument known as a cryoprobe in direct contact with the tumor to freeze it. Doctors are studying new ways of using radiation therapy and hormonal therapy, too. Studies have shown that hormonal therapy given after radiation therapy can help certain men whose cancer has spread to nearby tissues. Scientists are also testing the effectiveness of chemotherapy and biological therapy for men whose cancer does not respond, or stops responding, to hormonal therapy. They are also exploring new ways to schedule and combine various treatments. For example, they are studying hormonal therapy to find out if using it to shrink the tumor before a man has surgery or radiation might be a useful approach. For men with early stage prostate cancer, researchers are also comparing treatment with watchful waiting. The results of this work will help doctors know whether to treat early stage prostate cancer immediately or only later on, if symptoms occur or worsen.
|
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3576,
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2923,
4745,
390,
760,
1996,
327,
13,
604,
5917,
2826,
390,
548,
8243,
15
] |
What causes Gas in the Digestive Tract ?
|
Most foods that contain carbohydrates can cause gas. In contrast, fats and proteins cause little gas. Foods that produce gas in one person may not cause gas in someone else, depending on how well individuals digest carbohydrates and the type of bacteria present in the intestines.
Some foods that may cause gas include
- beans - vegetables such as broccoli, cauliflower, cabbage, brussels sprouts, onions, mushrooms, artichokes, and asparagus - fruits such as pears, apples, and peaches - whole grains such as whole wheat and bran - sodas; fruit drinks, especially apple juice and pear juice; and other drinks that contain high-fructose corn syrup, a sweetener made from corn - milk and milk products such as cheese, ice cream, and yogurt - packaged foodssuch as bread, cereal, and salad dressingthat contain small amounts of lactose, a sugar found in milk and foods made with milk - sugar-free candies and gums that contain sugar alcohols such as sorbitol, mannitol, and xylitol
|
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2713,
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] |
How many people are affected by epidermal nevus ?
|
Epidermal nevi affect approximately 1 in 1,000 people.
|
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How many people are affected by Koolen-de Vries syndrome ?
|
The prevalence of Koolen-de Vries syndrome is estimated to be 1 in 16,000. However, the underlying genetic cause is often not identified in people with intellectual disability, so this condition is likely underdiagnosed.
|
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What is (are) Lipoid Proteinosis ?
|
Lipoid proteinosis (LP) is a rare disease that affects the skin and the brain. Three distinctive features characterize the disease: a hoarse voice, unusual growths on the skin and mucus membranes, and damage to the temporal lobes or hippocampus of the brain. The symptoms of LP may begin as early as infancy with hoarseness or a weak cry, due to growths on the vocal cords. Skin lesions appear sometime in the next 3 years, leaving acne- or pox-like scars on the face, hands, and mucous membranes. The most characteristic symptom of LP is waxy, yellow, bead-like bumps along the upper and lower edges of the eyelids. Brain damage develops over time and is associated with the development of cognitive abilities and epileptic seizures. Damage to the amygdala, a part of the brain that regulates emotions and perceptions, leads to difficulties in discriminating facial expressions and in making realistic judgments about the trustworthiness of other people. LP is a hereditary disease that equally affects males and females. Nearly a quarter of all reported cases have been in the Afrikaner population of South Africa, but the disease is increasingly being reported from other parts of the world including India. The gene responsible for LP has recently been identified. It performs an unknown function in the skin related to the production of collagen.
|
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what research (or clinical trials) is being done for Hairy Cell Leukemia ?
|
New types of treatment are being tested in clinical trials.
Information about clinical trials is available from the NCI website.
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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Is autosomal dominant hyper-IgE syndrome inherited ?
|
AD-HIES has an autosomal dominant pattern of inheritance, which means one copy of an altered gene in each cell is sufficient to cause the disorder. In about half of all cases caused by STAT3 gene mutations, an affected person inherits the genetic change from an affected parent. Other cases result from new mutations in this gene. These cases occur in people with no history of the disorder in their family.
|
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What is (are) Peptic Ulcer ?
|
A peptic ulcer is a sore in the lining of your stomach or your duodenum, the first part of your small intestine. A burning stomach pain is the most common symptom. The pain - Starts between meals or during the night - Briefly stops if you eat or take antacids - Lasts for minutes to hours - Comes and goes for several days or weeks Peptic ulcers happen when the acids that help you digest food damage the walls of the stomach or duodenum. The most common cause is infection with a bacterium called Helicobacter pylori. Another cause is the long-term use of nonsteroidal anti-inflammatory medicines (NSAIDs) such as aspirin and ibuprofen. Stress and spicy foods do not cause ulcers, but can make them worse. To see if you have an H. pylori infection, your doctor will test your blood, breath, or stool. Your doctor also may look inside your stomach and duodenum by doing an endoscopy or x-ray. Peptic ulcers will get worse if not treated. Treatment may include medicines to reduce stomach acids or antibiotics to kill H. pylori. Antacids and milk can't heal peptic ulcers. Not smoking and avoiding alcohol can help. You may need surgery if your ulcers don't heal. NIH: National Institute of Diabetes and Digestive and Kidney Diseases
|
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What is (are) High Blood Pressure ?
|
Blood pressure is the force of blood pushing against the walls of the blood vessels as the heart pumps blood. If your blood pressure rises and stays high over time, its called high blood pressure. High blood pressure is dangerous because it makes the heart work too hard, and the high force of the blood flow can harm arteries and organs such as the heart, kidneys, brain, and eyes.
|
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What are the symptoms of Intellectual disability-developmental delay-contractures syndrome ?
|
What are the signs and symptoms of Intellectual disability-developmental delay-contractures syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Intellectual disability-developmental delay-contractures 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) Abnormality of movement 90% Clinodactyly of the 5th finger 90% Cognitive impairment 90% Limitation of joint mobility 90% Neurological speech impairment 90% Ophthalmoparesis 90% Skeletal muscle atrophy 90% Kyphosis 7.5% Ptosis 7.5% Scoliosis 7.5% Strabismus 7.5% Oculomotor apraxia 5% Apnea - Apraxia - Areflexia - Broad alveolar ridges - Camptodactyly - Cerebral atrophy - Congenital foot contractures - Congenital onset - Decreased fetal movement - Delayed myelination - Delayed speech and language development - Distal amyotrophy - Drooling - Dystonia - Facial palsy - Feeding difficulties - High anterior hairline - High palate - Hip dislocation - Hyperlordosis - Intellectual disability, mild - Long philtrum - Low-set ears - Muscular hypotonia - Narrow chest - Neonatal respiratory distress - Proximal placement of thumb - Retrognathia - Seizures - Short neck - Short stature - Smooth philtrum - Spasticity - Talipes equinovarus - Upslanted palpebral fissure - U-Shaped upper lip vermilion - 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 are the symptoms of Rutherfurd syndrome ?
|
What are the signs and symptoms of Rutherfurd syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Rutherfurd 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) Delayed eruption of teeth 90% Gingival overgrowth 90% Opacification of the corneal stroma 90% Reduced number of teeth 90% Behavioral abnormality 50% Cognitive impairment 50% Autosomal dominant inheritance - Corneal dystrophy - Delayed eruption of primary teeth - Failure of eruption of permanent teeth - 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) Joubert Syndrome ?
|
Joubert syndrome is a rare brain malformation characterized by the absence or underdevelopment of the cerebellar vermis- an area of the brain that controls balance and coordination -- as well as a malformed brain stem (molar tooth sign). The most common features of Joubert syndrome in infants include abnormally rapid breathing (hyperpnea), decreased muscle tone (hypotonia), abnormal eye movements, impaired intellectual development, and the inability to coordinate voluntary muscle movements (ataxia). Physical deformities may be present, such as extra fingers and toes (polydactyly), cleft lip or palate, and tongue abnormalities. Kidney and liver abnormalities can develop, and seizures may also occur. Many cases of Joubert syndrome appear to be sporadic (not inherited). In most other cases, Joubert syndrome is inherited in an autosomal recessive manner (meaning both parents must have a copy of the mutation) via mutation in at least 10 different genes, including NPHP1, AHI1, and CEP290.
|
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What causes Chronic hiccups ?
|
What causes chronic hiccups? Although the exact underlying cause of chronic hiccups is often unknown, many factors can contribute to the development of hiccups. For example, common triggers for hiccups include hot or spicy foods and liquids; harmful fumes; surgery; and/or certain medications. Chronic hiccups can also be associated with a variety of health problems including: Pneumonia, pleurisy and other conditions that irritate the diaphragm Brain abnormalities (i.e. strokes, tumors, injuries, infections) Metabolic disorders Gastrointestinal (esophagus, stomach, small/large intestines) diseases Psychological problems such as hysteria, shock, fear, and personality disorders Liver abnormalities Kidney disorders For a comprehensive listings of factors that can cause chronic hiccups, please click here.
|
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What is (are) Myotonia Congenita ?
|
Myotonia congenita is an inherited neuromuscular disorder characterized by the inability of muscles to quickly relax after a voluntary contraction. The condition is present from early childhood, but symptoms can be mild. Most children will be 2 or 3 years old when parents first notice their muscle stiffness, particularly in the legs, often provoked by sudden activity after rest. The disease doesnt cause muscle wasting; in fact, it may cause muscle enlargement. Muscle strength is increased. There are two forms of the disorder: Becker-type, which is the most common form; and Thomsens disease, which is a rare and milder form. The disorder is cause by mutations in a gene responsible for shutting off electrical excitation in the muscles.
|
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] |
How many people are affected by autosomal dominant hypocalcemia ?
|
The prevalence of autosomal dominant hypocalcemia is unknown. The condition is likely underdiagnosed because it often causes no signs or symptoms.
|
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What are the treatments for Adult Non-Hodgkin Lymphoma ?
|
Key Points
- There are different types of treatment for patients with non-Hodgkin lymphoma. - Patients with non-Hodgkin lymphoma should have their treatment planned by a team of health care providers who are experts in treating lymphomas. - Patients may develop late effects that appear months or years after their treatment for non-Hodgkin lymphoma. - Nine types of standard treatment are used: - Radiation therapy - Chemotherapy - Immunotherapy - Targeted therapy - Plasmapheresis - Watchful waiting - Antibiotic therapy - Surgery - Stem cell transplant - New types of treatment are being tested in clinical trials. - Vaccine therapy - Patients may want to think about taking part in a clinical trial. - Patients can enter clinical trials before, during, or after starting their cancer treatment. - Follow-up tests may be needed.
There are different types of treatment for patients with non-Hodgkin lymphoma.
Different types of treatment are available for patients with non-Hodgkin lymphoma. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment. For pregnant women with non-Hodgkin lymphoma, treatment is carefully chosen to protect the baby. Treatment decisions are based on the mothers wishes, the stage of the non-Hodgkin lymphoma, and the age of the baby. The treatment plan may change as the signs and symptoms, cancer, and pregnancy change. Choosing the most appropriate cancer treatment is a decision that ideally involves the patient, family, and health care team.
Patients with non-Hodgkin lymphoma should have their treatment planned by a team of health care providers who are experts in treating lymphomas.
Treatment will be overseen by a medical oncologist, a doctor who specializes in treating cancer, or a hematologist, a doctor who specializes in treating blood cancers. The medical oncologist may refer you to other health care providers who have experience and are experts in treating adult non-Hodgkin lymphoma and who specialize in certain areas of medicine. These may include the following specialists: - Neurosurgeon. - Neurologist. - Radiation oncologist. - Endocrinologist. - Rehabilitation specialist. - Other oncology specialists.
Patients may develop late effects that appear months or years after their treatment for non-Hodgkin lymphoma.
Side effects from cancer treatment that begin during or after treatment and continue for months or years are called late effects. Treatment with chemotherapy, radiation therapy, or stem cell transplant for non-Hodgkin lymphoma may increase the risk of late effects. Late effects of cancer treatment may include the following: - Heart problems. - Infertility (inability to have children). - Loss of bone density. - Neuropathy (nerve damage that causes numbness or trouble walking). - A second cancer, such as: - Lung cancer. - Brain cancer. - Kidney cancer. - Bladder cancer. - Melanoma. - Hodgkin lymphoma. - Myelodysplastic syndrome. - Acute myeloid leukemia. Some late effects may be treated or controlled. It is important to talk with your doctor about the effects cancer treatment can have on you. Regular follow-up to check for late effects is important.
Nine types of standard treatment are used:
Radiation therapy Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy: - External radiation therapy uses a machine outside the body to send radiation toward the cancer. - Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. Total-body irradiation is a type of external radiation therapy that is given to the entire body. It may be given before a stem cell transplant. The way the radiation therapy is given depends on the type and stage of the cancer being treated. External radiation therapy is used to treat adult non-Hodgkin lymphoma, and may also be used as palliative therapy to relieve symptoms and improve quality of life. For pregnant women with non-Hodgkin lymphoma, radiation therapy should be given after delivery, if possible, to avoid any risk to the baby. If treatment is needed right away, pregnant women may decide to continue the pregnancy and receive radiation therapy. However, lead used to shield the baby may not protect it from scattered radiation that could possibly cause cancer in the future. Chemotherapy Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid (intrathecal chemotherapy), an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). Combination chemotherapy is treatment using two or more anticancer drugs. Steroid drugs may be added, to lessen inflammation and lower the body's immune response. The way the chemotherapy is given depends on the type and stage of the cancer being treated. Intrathecal chemotherapy may also be used in the treatment of lymphoma that first forms in the testicles or sinuses (hollow areas) around the nose, diffuse large B-cell lymphoma, Burkitt lymphoma, lymphoblastic lymphoma, and some aggressive T-cell lymphomas. It is given to lessen the chance that lymphoma cells will spread to the brain and spinal cord. This is called CNS prophylaxis. In pregnant women, the baby is exposed to chemotherapy when the mother is treated, and some anticancer drugs cause birth defects. Because anticancer drugs are passed to the baby through the mother, both must be watched closely when chemotherapy is given. See Drugs Approved for Non-Hodgkin Lymphoma for more information. Immunotherapy Immunotherapy is a treatment that uses the patients immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the bodys natural defenses against cancer. Immunomodulators are a type of immunotherapy. Lenalidomide is an immunomodulator used to treat adult non-Hodgkin lymphoma. See Drugs Approved for Non-Hodgkin Lymphoma for more information. Targeted therapy Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells without harming normal cells. Monoclonal antibody therapy, proteasome inhibitor therapy, and kinase inhibitor therapy are types of targeted therapy used to treat adult non-Hodgkin lymphoma. Monoclonal antibody therapy is a cancer treatment that uses antibodies made in the laboratory from a single type of immune system cell. These antibodies can identify substances on cancer cells or normal substances that may help cancer cells grow. The antibodies attach to the substances and kill the cancer cells, block their growth, or keep them from spreading. They may be used alone or to carry drugs, toxins, or radioactive material directly to cancer cells. Rituximab is a monoclonal antibody used to treat many types of non-Hodgkin lymphoma. Monoclonal antibodies that have been joined to radioactive material are called radiolabeled monoclonal antibodies. Yttrium Y 90-ibritumomab tiuxetan is an example of a radiolabeled monoclonal antibody. Monoclonal antibodies are given by infusion. Proteasome inhibitor therapy blocks the action of proteasomes in cancer cells and may prevent the growth of tumors. Kinase inhibitor therapy, such as idelalisib, blocks certain proteins, which may help keep lymphoma cells from growing and may kill them. It is used to treat indolent lymphoma. Ibrutinib, a type of Bruton's tyrosine kinase inhibitor therapy, is used to treat lymphoplasmacytic lymphoma and mantle cell lymphoma. See Drugs Approved for Non-Hodgkin Lymphoma for more information. Plasmapheresis If the blood becomes thick with extra antibody proteins and affects circulation, plasmapheresis is done to remove extra plasma and antibody proteins from the blood. In this procedure, blood is removed from the patient and sent through a machine that separates the plasma (the liquid part of the blood) from the blood cells. The patient's plasma contains the unneeded antibodies and is not returned to the patient. The normal blood cells are returned to the bloodstream along with donated plasma or a plasma replacement. Plasmapheresis does not keep new antibodies from forming. Watchful waiting Watchful waiting is closely monitoring a patients condition without giving any treatment until signs or symptoms appear or change. Antibiotic therapy Antibiotic therapy is a treatment that uses drugs to treat infections and cancer caused by bacteria and other microorganisms. See Drugs Approved for Non-Hodgkin Lymphoma for more information. Surgery Surgery may be used to remove the lymphoma in certain patients with indolent or aggressive non-Hodgkin lymphoma. The type of surgery used depends on where the lymphoma formed in the body: - Local excision for certain patients with mucosa-associated lymphoid tissue (MALT) lymphoma, PTLD, and small bowel T-cell lymphoma. - Splenectomy for patients with marginal zone lymphoma of the spleen. Patients who have a heart, lung, liver, kidney, or pancreas transplant usually need to take drugs to suppress their immune system for the rest of their lives. Long-term immunosuppression after an organ transplant can cause a certain type of non-Hodgkin lymphoma called post-transplant lymphoproliferative disorder (PLTD). Small bowel surgery is often needed to diagnose celiac disease in adults who develop a type of T-cell lymphoma. Stem cell transplant Stem cell transplant is a method of giving high doses of chemotherapy and/or total-body irradiation and then replacing blood-forming cells destroyed by the cancer treatment. Stem cells (immature blood cells) are removed from the blood or bone marrow of the patient (autologous transplant) or a donor (allogeneic transplant) and are frozen and stored. After the chemotherapy and/or radiation therapy is completed, the stored stem cells are thawed and given back to the patient through an infusion. These reinfused stem cells grow into (and restore) the bodys blood cells.
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. Vaccine therapy Vaccine therapy is a type of biologic therapy. Biologic therapy is a treatment that uses the patients immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the bodys natural defenses against cancer. This type of cancer treatment is also called biotherapy or immunotherapy. Vaccine therapy can also be a type of targeted therapy.
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.
Follow-up tests may be needed.
Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests. Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.
Treatment Options for Non-Hodgkin Lymphoma During Pregnancy
Indolent Non-Hodgkin Lymphoma During Pregnancy
Women who have indolent (slow-growing) non-Hodgkin lymphoma during pregnancy may be treated with watchful waiting until after they give birth. (See the Treatment Options for Indolent Non-Hodgkin Lymphoma section for more information.)
Aggressive Non-Hodgkin Lymphoma During Pregnancy
Treatment of aggressive non-Hodgkin lymphoma during pregnancy may include the following: - Treatment given right away based on the type of non-Hodgkin lymphoma to increase the mother's chance of survival. Treatment may include combination chemotherapy and rituximab. - Early delivery of the baby followed by treatment based on the type of non-Hodgkin lymphoma. - If in the first trimester of pregnancy, medical oncologists may advise ending the pregnancy so that treatment may begin. Treatment depends on the type of non-Hodgkin lymphoma.
|
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41,
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5914,
24964,
15
] |
How many people are affected by X-linked juvenile retinoschisis ?
|
The prevalence of X-linked juvenile retinoschisis is estimated to be 1 in 5,000 to 25,000 men worldwide.
|
[
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[
1,
1,
1,
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1,
1,
1,
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1,
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1,
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15
] |
What is (are) Cavernous Malformation ?
|
Cerebral cavernous malformations (CCMs) are vascular lesions comprised of clusters of tightly packed, abnormally thin-walled small blood vessels (capillaries) that displace normal neurological tissue in the brain or spinal cord. The vessels are filled with slow-moving or stagnant blood that is usually clotted or in a state of decomposition. Cavernous malformations can occur in the brain, spinal cord, and some other body regions. In the brain and spinal cord these cavernous lesions are quite fragile and are prone to bleeding, causing hemorrhagic strokes (bleeding into the brain), seizures, and neurological deficits. CCMs can range in size from a few fractions of an inch to several inches in diameter, depending on the number of blood vessels involved. Some people develop multiple lesions while others never experience related medical problems. Hereditary forms of CCM are caused by mutations in one of three CCM disease genes: CCM1, CCM2, and CCM3. A large population with hereditary CCM disease is found in New Mexico and the Southwestern United States, in which the disease is caused by mutations in the gene CCM1 (or KRIT1).
|
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What causes Hemochromatosis ?
|
The two types of hemochromatosis are primary and secondary. Each type has a different cause.
Primary Hemochromatosis
Primary hemochromatosis is caused by a defect in the genes that control how much iron you absorb from food. This form of the disease sometimes is called hereditary or classical hemochromatosis. Primary hemochromatosis is more common than the secondary form of the disease.
The genes usually involved in primary hemochromatosis are called HFE genes. Faulty HFE genes cause the body to absorb too much iron. If you inherit two copies of the faulty HFE gene (one from each parent), you're at risk for iron overload and signs and symptoms of hemochromatosis.
If you inherit one faulty HFE gene and one normal HFE gene, you're a hemochromatosis "carrier." Carriers usually don't develop the disease. However, they can pass the faulty gene on to their children. Estimates suggest that about 1 in 10 people in the United States are hemochromatosis carriers.
If two parents are carriers of the faulty HFE gene, then each of their children has a 1 in 4 chance of inheriting two faulty HFE genes.
Although less common, other faulty genes also can cause hemochromatosis. Researchers continue to study what changes to normal genes may cause the disease.
Secondary Hemochromatosis
Secondary hemochromatosis usually is the result of another disease or condition that causes iron overload. Examples of such diseases and conditions include:
Certain types of anemia, such as thalassemias and sideroblastic anemia
Atransferrinemia and aceruloplasminemiaboth are rare, inherited diseases
Chronic liver diseases, such as chronic hepatitis C infection, alcoholic liver disease, or nonalcoholic steatohepatitis
Other factors also can cause secondary hemochromatosis, including:
Blood transfusions
Oral iron pills or iron injections, with or without very high vitamin C intake (vitamin C helps your body absorb iron)
Long-term kidney dialysis
|
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Is 5q minus syndrome inherited ?
|
This condition is generally not inherited but arises from a mutation in the body's cells that occurs after conception. This alteration is called a somatic mutation. Affected people typically have no history of the disorder in their family.
|
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Is hereditary antithrombin deficiency inherited ?
|
Hereditary antithrombin deficiency is typically inherited in an autosomal dominant pattern, which means one altered copy of the SERPINC1 gene in each cell is sufficient to cause the disorder. Inheriting two altered copies of this gene in each cell is usually incompatible with life; however, a few severely affected individuals have been reported with mutations in both copies of the SERPINC1 gene in each cell.
|
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What are the genetic changes related to granulomatosis with polyangiitis ?
|
The genetic basis of GPA is not well understood. Having a particular version of the HLA-DPB1 gene is the strongest genetic risk factor for developing this condition, although several other genes, some of which have not been identified, may be involved. It is likely that a combination of genetic and environmental factors lead to GPA. GPA is an autoimmune disorder. Such disorders occur when the immune system malfunctions and attacks the body's own tissues and organs. Approximately 90 percent of people with GPA have an abnormal immune protein called an anti-neutrophil cytoplasmic antibody (ANCA) in their blood. Antibodies normally bind to specific foreign particles and germs, marking them for destruction, but ANCAs attack normal human proteins. Most people with GPA have an ANCA that attacks the human protein proteinase 3 (PR3). A few affected individuals have an ANCA that attacks a protein called myeloperoxidase (MPO). When these antibodies attach to the protein they recognize, they trigger inflammation, which contributes to the signs and symptoms of GPA. The HLA-DPB1 gene belongs to a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders (such as viruses and bacteria). Each HLA gene has many different normal variations, allowing each person's immune system to react to a wide range of foreign proteins. A particular variant of the HLA-DPB1 gene called HLA-DPB1*0401 has been found more frequently in people with GPA, especially those with ANCAs, than in people without the condition. Because the HLA-DPB1 gene is involved in the immune system, changes in it might be related to the autoimmune response and inflammation in the respiratory tract and kidneys characteristic of GPA. However, it is unclear what specific role the HLA-DPB1*0401 gene variant plays in development of this condition.
|
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What are the genetic changes related to juvenile myoclonic epilepsy ?
|
The genetics of juvenile myoclonic epilepsy are complex and not completely understood. Mutations in one of several genes can cause or increase susceptibility to this condition. The most studied of these genes are the GABRA1 gene and the EFHC1 gene, although mutations in at least three other genes have been identified in people with this condition. Many people with juvenile myoclonic epilepsy do not have mutations in any of these genes. Changes in other, unidentified genes are likely involved in this condition. A mutation in the GABRA1 gene has been identified in several members of a large family with juvenile myoclonic epilepsy. The GABRA1 gene provides instructions for making one piece, the alpha-1 (1) subunit, of the GABAA receptor protein. The GABAA receptor acts as a channel that allows negatively charged chlorine atoms (chloride ions) to cross the cell membrane. After infancy, the influx of chloride ions creates an environment in the cell that inhibits signaling between nerve cells (neurons) and prevents the brain from being overloaded with too many signals. Mutations in the GABRA1 gene lead to an altered 1 subunit and a decrease in the number of GABAA receptors available. As a result, the signaling between neurons is not controlled, which can lead to overstimulation of neurons. Researchers believe that the overstimulation of certain neurons in the brain triggers the abnormal brain activity associated with seizures. Mutations in the EFHC1 gene have been associated with juvenile myoclonic epilepsy in a small number of people. The EFHC1 gene provides instructions for making a protein that also plays a role in neuron activity, although its function is not completely understood. The EFHC1 protein is attached to another protein that acts as a calcium channel. This protein allows positively charged calcium ions to cross the cell membrane. The movement of these ions is critical for normal signaling between neurons. The EFHC1 protein is thought to help regulate the balance of calcium ions inside the cell, although the mechanism is unclear. In addition, studies show that the EFHC1 protein may be involved in the self-destruction of cells. EFHC1 gene mutations reduce the function of the EFHC1 protein. Researchers suggest that this reduction causes an increase in the number of neurons and disrupts the calcium balance. Together, these effects may lead to overstimulation of neurons and trigger seizures.
|
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What is (are) AL amyloidosis ?
|
AL amyloidosisis the most common form of amyloidosis, a group of disorders in which an abnormal protein called amyloid builds up in tissues and organs. The signs and symptoms of AL amyloidosis vary among patients because the build up may occur in the tongue, intestines, muscles, joints, nerves, skin, ligaments, heart, liver, spleen, or kidneys. To diagnose AL amyloidosis, healthcare professionals use blood or urine tests to identify signs of amyloid protein and a biopsy to confirm the diagnosis. Treatment may include chemotherapy directed at the abnormal plasma cells, stem cell transplantation, or other treatments based on which symptoms have developed.
|
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What are the symptoms of Madelung disease ?
|
What are the signs and symptoms of Madelung disease? The signs and symptoms of Madelung disease vary from person to person. The condition is characterized by the symmetric growth of fatty tumors (lipomas) around the neck, shoulders, upper arms and/or upper trunk. In some affected people, these fatty deposits may grow rapidly over the course of months, while others experience a slower progression over the course of years. The lipomas can be associated with significant physical deformity and may lead to a loss of neck mobility and pain. In the majority of cases, the disease is benign; however, lipomas can become cancerous in rare circumstances. People with Madelung disease may also develop peripheral neuropathy and neurological disturbances including difficulty swallowing, hoarseness, sleep problems, tachycardia (rapid heart rate), fluctuation in blood pressure, and breathing issues. In some cases, it may be associated with other metabolic abnormalities or diseases such as hypertension, diabetes mellitus, hypothyroidism, and liver disease. The Human Phenotype Ontology provides the following list of signs and symptoms for Madelung disease. 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) Arthralgia 90% Limitation of joint mobility 90% Multiple lipomas 90% Gait disturbance 50% Hepatomegaly 50% Insulin resistance 50% Paresthesia 50% Abnormality of the skin - Autosomal dominant inheritance - Lipoma - Peripheral neuropathy - 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 juvenile Batten disease ?
|
These resources address the diagnosis or management of juvenile Batten disease: - Batten Disease Diagnostic and Clinical Research Center at the University of Rochester Medical Center - Batten Disease Support and Research Association: Centers of Excellence - Gene Review: Gene Review: Neuronal Ceroid-Lipofuscinoses - Genetic Testing Registry: Juvenile neuronal ceroid lipofuscinosis 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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