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What are the treatments for Hypomyelination with atrophy of basal ganglia and cerebellum ?
|
How might hypomelination with atrophy of basal ganglia and cerebellum (H-ABC) be treated? Unfortunately, there is no known cure for hypomyelination with atrophy of basal ganglia and cerebellum (H-ABC). However, there is a case report of one patient's movement difficulties improving somewhat after he took the medication levodopa-carbidopa. Another patient showed improvement in movement symptoms after taking folinic acid supplements.
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What are the genetic changes related to ankyloblepharon-ectodermal defects-cleft lip/palate syndrome ?
|
AEC syndrome is caused by mutations in the TP63 gene. This gene provides instructions for making a protein known as p63, which plays an essential role in early development. The p63 protein is a transcription factor, which means that it attaches (binds) to DNA and controls the activity of particular genes. The p63 protein turns many different genes on and off during development. It appears to be especially critical for the development of ectodermal structures, such as the skin, hair, teeth, and nails. Studies suggest that it also plays important roles in the development of the limbs, facial features, urinary system, and other organs and tissues. The TP63 gene mutations responsible for AEC syndrome interfere with the ability of p63 to turn target genes on and off at the right times. It is unclear how these changes lead to abnormal ectodermal development and the specific features of AEC syndrome.
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What to do for Treatment Methods for Kidney Failure: Peritoneal Dialysis ?
|
Eating the right foods can help you feel better while on peritoneal dialysis. Talk with your dialysis centers dietitian to find a meal plan that works for you. Your dietary needs will depend on your treatment and other factors such as your weight and activity level. Staying healthy with CKD requires watching what is in your diet:
- Protein is in foods from animals and plants. Protein provides the building blocks that maintain and repair muscles, organs, and other parts of your body. Peritoneal dialysis can remove proteins from your body, so eat high-quality, protein-rich foods such as meat, fish, and eggs. However, many high-protein foods also contain phosphorous, which can weaken your bones. Talk with your dietitian about ways to get the protein you need without getting too much phosphorous. - Phosphorus is a mineral that helps your bones stay healthy and your blood vessels and muscles work. Phosphorus is a natural part of foods rich in protein, and food producers often add it to many processed foods. Phosphorus can weaken your bones and make your skin itch if you consume too much. Peritoneal dialysis may not remove enough phosphorus from your body, so you will probably need to limit or avoid high-phosphorus foods such as milk and cheese, dried beans, peas, colas, nuts, and peanut butter. You may also need to take a pill called a phosphate binder that keeps phosphorus in your food from entering your bloodstream. - Fluid includes water and drinks such as fruit juice and milk and water in foods such as fruits, vegetables, ice cream, gelatin, soup, and ice pops. You need water for your body to function properly; however, too much can cause swelling and make your heart work harder. Over time, having too much fluid in your body can cause high blood pressure and congestive heart failure. Peritoneal dialysis might cause you to have either too much or too little fluid, depending on the strength of the solution you use. Your diet can also influence whether you have too much or too little fluid. Your dietitian will help you determine how much liquid you need to consume each day. - Sodium is a part of salt. Many canned, packaged, frozen, and fast foods contain sodium. Sodium is also a part of many condiments, seasonings, and meats. Too much sodium makes you thirsty, which makes you drink more liquid. Try to eat fresh foods that are naturally low in sodium, and look for products that say low sodium on the label, especially in canned and frozen foods. - Potassium is a mineral that helps your nerves and muscles work the right way. Peritoneal dialysis can pull too much potassium from your blood, so you may need to eat more high-potassium foods such as bananas, oranges, potatoes, and tomatoes. However, be careful not to eat too much potassium. Your dietitian will help you choose the right amount. - Calories are units for measuring the energy provided by foods and drinks. Eating foods with too many calories, such as oily and sugary foods, can make you gain weight. Your body can absorb the dextrose from your dialysis solution, which can increase your calorie intake. You may find you need to take in fewer calories to prevent weight gain. Your dietitian can help you create and follow a diet to stay at a healthy weight. - Supplements help provide some of the vitamins and minerals that may be missing from your diet. Peritoneal dialysis also removes some vitamins from your body. Your doctor may prescribe a vitamin and mineral supplement that scientists have designed specifically for people with CKD and kidney failure. Never take vitamin and mineral supplements that you can buy over the counter. They may be harmful to you. Talk with your doctor before taking any medicine, including vitamin and mineral supplements, that he or she has not prescribed for you.
You may have a difficult time changing your diet at first. Eating the right foods will help you feel better. You will have more strength and energy. More information is provided in the NIDDK health topic, Make the Kidney Connection: Food Tips and Healthy Eating Ideas.
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Who is at risk for Childhood Acute Myeloid Leukemia and Other Myeloid Malignancies? ?
|
The risk factors for childhood AML, childhood CML, JMML, and MDS are similar. Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesnt mean that you will not get cancer. Talk with your childs doctor if you think your child may be at risk. These and other factors may increase the risk of childhood AML, childhood CML, JMML, and MDS: - Having a brother or sister, especially a twin, with leukemia. - Being Hispanic. - Being exposed to cigarette smoke or alcohol before birth. - Having a personal history of aplastic anemia. - Having a personal or family history of MDS. - Having a family history of AML. - Past treatment with chemotherapy or radiation therapy. - Being exposed to ionizing radiation or chemicals such as benzene. - Having certain genetic disorders, such as: - Down syndrome. - Fanconi anemia. - Neurofibromatosis type 1. - Noonan syndrome. - Shwachman-Diamond syndrome.
|
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] |
What is (are) Fabry disease ?
|
Fabry disease is an inherited disorder that results from the buildup of a particular type of fat in the body's cells, called globotriaosylceramide or GL-3. Fabry disease affects many parts of the body. Signs and symptoms may include episodes of pain, particularly in the hands and feet (acroparesthesias); clusters of small, dark red spots on the skin called angiokeratomas; a decreased ability to sweat (hypohidrosis); cloudiness of the front part of the eye (corneal opacity); and hearing loss. Potentially severe complications can include progressive kidney damage, heart attack, and stroke. Milder forms of the disorder may appear later in life and affect only the heart or kidneys. Fabry disease is caused by mutations in the GLA gene and is inherited in an X-linked manner. Treatment may include enzyme replacement therapy (ERT); pain medications, ACE inhibitors; and chronic hemodialysis or renal transplantation for end stage renal disease.
|
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What causes Swyer-James syndrome ?
|
What causes Swyer-James syndrome? The cause of Swyer-James syndrome is not completely understood. Most experts agree that the initial abnormality occurs in the distal bronchi (air tubes that bring air to and from the lungs) after an infection during early childhood. The smaller size of the affected lung may be due to the infection inhibiting the normal growth of the lung. A number of reports have described Swyer-James syndrome following childhood histories including radiation therapy; measles; pertussis (whooping cough); tuberculosis; breathing in a foreign body; mycoplasma; and viral infections, especially adenovirus. Research has suggested that a hyper-immune reaction in the lung (producing an unusual abundance of antibodies) may play a role in sustaining airway damage after the initial infection. Some have argued a pre-existing lung abnormality may predispose individuals to the condition. Although bronchial damage of some kind during childhood is generally considered to play an important role, many affected individuals have had no known history of an airway infection. It is possible that some unknown factors present at birth may contribute to the development of Swyer-James syndrome.
|
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What are the treatments for Polycythemia Vera ?
|
Polycythemia vera (PV) doesn't have a cure. However, treatments can help control the disease and its complications. PV is treated with procedures, medicines, and other methods. You may need one or more treatments to manage the disease.
Goals of Treatment
The goals of treating PV are to control symptoms and reduce the risk of complications, especially heart attack and stroke. To do this, PV treatments reduce the number of red blood cells and the level of hemoglobin (an iron-rich protein) in the blood. This brings the thickness of your blood closer to normal.
Blood with normal thickness flows better through the blood vessels. This reduces the chance that blood clots will form and cause a heart attack or stroke.
Blood with normal thickness also ensures that your body gets enough oxygen. This can help reduce some of the signs and symptoms of PV, such as headaches, vision problems, and itching.
Studies show that treating PV greatly improves your chances of living longer.
The goal of treating secondary polycythemia is to control its underlying cause, if possible. For example, if the cause is carbon monoxide exposure, the goal is to find the source of the carbon monoxide and fix or remove it.
Treatments To Lower Red Blood Cell Levels
Phlebotomy
Phlebotomy (fle-BOT-o-me) is a procedure that removes some blood from your body. For this procedure, a needle is inserted into one of your veins. Blood from the vein flows through an airtight tube into a sterile container or bag. The process is similar to the process of donating blood.
Phlebotomy reduces your red blood cell count and starts to bring your blood thickness closer to normal.
Typically, a pint (1 unit) of blood is removed each week until your hematocrit level approaches normal. (Hematocrit is the measure of how much space red blood cells take up in your blood.)
You may need to have phlebotomy done every few months.
Medicines
Your doctor may prescribe medicines to keep your bone marrow from making too many red blood cells. Examples of these medicines include hydroxyurea and interferon-alpha.
Hydroxyurea is a medicine generally used to treat cancer. This medicine can reduce the number of red blood cells and platelets in your blood. As a result, this medicine helps improve your blood flow and bring the thickness of your blood closer to normal.
Interferon-alpha is a substance that your body normally makes. It also can be used to treat PV. Interferon-alpha can prompt your immune system to fight overactive bone marrow cells. This helps lower your red blood cell count and keep your blood flow and blood thickness closer to normal.
Radiation Treatment
Radiation treatment can help suppress overactive bone marrow cells. This helps lower your red blood cell count and keep your blood flow and blood thickness closer to normal.
However, radiation treatment can raise your risk of leukemia (blood cancer) and other blood diseases.
Treatments for Symptoms
Aspirin can relieve bone pain and burning feelings in your hands or feet that you may have as a result of PV. Aspirin also thins your blood, so it reduces the risk of blood clots.
Aspirin can have side effects, including bleeding in the stomach and intestines. For this reason, take aspirin only as your doctor recommends.
If your PV causes itching, your doctor may prescribe medicines to ease the discomfort. Your doctor also may prescribe ultraviolet light treatment to help relieve your itching.
Other ways to reduce itching include:
Avoiding hot baths. Cooler water can limit irritation to your skin.
Gently patting yourself dry after bathing. Vigorous rubbing with a towel can irritate your skin.
Taking starch baths. Add half a box of starch to a tub of lukewarm water. This can help soothe your skin.
Experimental Treatments
Researchers are studying other treatments for PV. An experimental treatment for itching involves taking low doses of selective serotonin reuptake inhibitors (SSRIs). This type of medicine is used to treat depression. In clinical trials, SSRIs reduced itching in people who had PV.
Imatinib mesylate is a medicine that's approved for treating leukemia. In clinical trials, this medicine helped reduce the need for phlebotomy in people who had PV. This medicine also helped reduce the size of enlarged spleens.
Researchers also are trying to find a treatment that can block or limit the effects of an abnormal JAK2 gene. (A mutation, or change, in the JAK2 gene is the major cause of PV.)
|
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What is (are) Axenfeld-Rieger syndrome type 2 ?
|
Axenfeld-Rieger syndrome is a group of eye disorders that affects the development of the eye. Common eye symptoms include cornea defects, which is the clear covering on the front of the eye, and iris defects, which is the colored part of the eye. People with this syndrome may have an off-center pupil (corectopia) or extra holes in the eyes that can look like multiple pupils (polycoria). About 50% of people with this syndrome develop glaucoma, which is a serious condition that increases pressure inside of the eye. This may cause vision loss or blindness. Click here to view a diagram of the eye. Even though Axenfeld-Rieger syndrome is primarily an eye disorder, this syndrome is also associated with symptoms that affect other parts of the body. Most people with this syndrome have distinctive facial features and many have issues with their teeth, including unusually small teeth (microdontia) or fewer than normal teeth (oligodontia). Some people have extra folds of skin around their belly button, heart defects, or other more rare birth defects. There are three types of Axenfeld-Rieger syndrome and each has a different genetic cause. Axenfeld-Rieger syndrome type 1 is caused by spelling mistakes (mutations) in the PITX2 gene. Axenfeld-Rieger syndrome type 3 is caused by mutations in the FOXC1 gene. The gene that causes Axenfeld-Rieger syndrome type 2 is not known, but it is located on chromosome 13. Axenfeld-Rieger syndrome has an autosomal dominant pattern of inheritance.
|
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what research (or clinical trials) is being done for Krabbe Disease ?
|
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system and to use that knowledge to reduce the burden of neurological disease. The NINDS is a component of the National Institutes of Health, the largest supporter of biomedical research in the world. Hamatopoietic stem cell transplantation -- using stem cells from umbilical cord blood or bone marrow -- has been shown to benefit some individuals when given early in the course of the disease. Scientists plan to test hematopoietic stem cell transplantation plus gene therapy to see if it dramatically increases life expectancy in a mouse model of the disease. Also in a mouse mode, NINDS-funded scientists are testing a combined treatment approach that uses a harmless virus to increase protein production, along with blood stem cell transplantation and small-molecule-based drugs, to reduce neuroinflammation, cell death, and nerve cell degeneration seen in Krabbe disease.
|
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What are the symptoms of Familial isolated hyperparathyroidism ?
|
What are the signs and symptoms of Familial isolated hyperparathyroidism? The Human Phenotype Ontology provides the following list of signs and symptoms for Familial isolated hyperparathyroidism. 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) Autosomal dominant inheritance - Hypercalcemia - Primary hyperparathyroidism - 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 Muscular dystrophy white matter spongiosis ?
|
What are the signs and symptoms of Muscular dystrophy white matter spongiosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Muscular dystrophy white matter spongiosis. 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 palate 90% Cognitive impairment 90% EMG abnormality 90% Facial palsy 90% Macrocephaly 90% Muscular hypotonia 90% Myotonia 90% Narrow face 90% Seizures 90% Skeletal muscle atrophy 90% Respiratory insufficiency 50% 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) Muscular Dystrophy ?
|
Muscular dystrophy (MD) is a group of more than 30 inherited diseases. They all cause muscle weakness and muscle loss. Some forms of MD appear in infancy or childhood. Others may not appear until middle age or later. The different types can vary in whom they affect, which muscles they affect, and what the symptoms are. All forms of MD grow worse as the person's muscles get weaker. Most people with MD eventually lose the ability to walk. There is no cure for muscular dystrophy. Treatments can help with the symptoms and prevent complications. They include physical and speech therapy, orthopedic devices, surgery, and medications. Some people with MD have mild cases that worsen slowly. Others cases are disabling and severe. NIH: National Institute of Neurological Disorders and Stroke
|
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What are the symptoms of Filippi syndrome ?
|
What are the signs and symptoms of Filippi syndrome? Filippi syndrome is characterized by growth delays before and after birth, a low birth weight, and short stature. Affected individuals are also born with abnormalities of the head and facial area (craniofacial abnormalities), resulting in a distinctive facial appearance. Affected infants typically have a small head (microcephaly), a high forehead, a broad bridge of the nose, thin nostrils, an abnormally thin upper lip, and widely spaced eyes (hypertelorism). Filippi syndrome is also characterized by mild to severe intellectual disability; some affected individuals may have abnormal language and speech development, potentially resulting in an inability to speak. Abnormalities of the fingers and toes have also been reported. These may include webbing or fusion of the fingers and toes (syndactyly). The severity of the syndactyly may be variable, ranging from webbing of skin and other soft tissues to fusion of bone within the affected fingers or toes. Affected individuals can also have extra fingers and/or toes (polydactyly). In addition, the fingers and toes may appear unusually short (brachydactyly), particularly due to abnormalities of the bones within the hands and feet. Some individuals may have additional physical abnormalities including delayed bone age, incomplete closure of the roof of the mouth (cleft palate), and a dislocated elbow. In some affected males, the testes may fail to descend into the scrotum (cryptorchidism). In one report, skin and teeth abnormalities were also noted. The Human Phenotype Ontology provides the following list of signs and symptoms for Filippi 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) Clinodactyly of the 5th finger 90% Cognitive impairment 90% Cryptorchidism 90% Finger syndactyly 90% Microcephaly 90% Neurological speech impairment 90% Prominent nasal bridge 90% Short stature 90% Underdeveloped nasal alae 90% Delayed skeletal maturation 50% Frontal bossing 50% Single transverse palmar crease 50% Hypertrichosis 5% Hypodontia 5% Sparse hair 5% 2-4 toe syndactyly - Autosomal recessive inheritance - Broad forehead - Cerebellar atrophy - Decreased body weight - Dystonia - Intellectual disability - Intrauterine growth retardation - Microdontia - Optic atrophy - Postnatal growth retardation - Proptosis - Seizures - Short philtrum - Thin vermilion border - Ventricular septal defect - Visual impairment - Wide nasal bridge - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
What are the genetic changes related to hypomagnesemia with secondary hypocalcemia ?
|
Hypomagnesemia with secondary hypocalcemia is caused by mutations in the TRPM6 gene. This gene provides instructions for making a protein that acts as a channel, which allows charged atoms (ions) of magnesium (Mg2+) to flow into cells; the channel may also allow small amounts of calcium ions (Ca2+) to pass into cells. Magnesium is involved in many cell processes, including production of cellular energy, maintenance of DNA building blocks (nucleotides), protein production, and cell growth and death. Magnesium and calcium are also required for the normal functioning of nerve cells that control muscle movement (motor neurons). The TRPM6 channel is embedded in the membrane of epithelial cells that line the large intestine, structures in the kidneys known as distal convoluted tubules, the lungs, and the testes in males. When the body needs additional Mg2+, the TRPM6 channel allows it to be absorbed in the intestine and filtered from the fluids that pass through the kidneys by the distal convoluted tubules. When the body has sufficient or too much Mg2+, the TRPM6 channel does not filter out the Mg2+ from fluids but allows the ion to be released from the kidney cells into the urine. The channel also helps to regulate Ca2+, but to a lesser degree. Most TRPM6 gene mutations that cause hypomagnesemia with secondary hypocalcemia result in a lack of functional protein. A loss of functional TRPM6 channels prevent Mg2+ absorption in the intestine and cause excessive amounts of Mg2+ to be excreted by the kidneys and released in the urine. A lack of Mg2+ in the body impairs the production of parathyroid hormone, which likely reduces blood Ca2+ levels. Additionally, hypomagnesemia and hypocalcemia can disrupt many cell processes and impair the function of motor neurons, leading to neurological problems and movement disorders. If the condition is not effectively treated and low Mg2+ levels persist, signs and symptoms can worsen over time and may lead to early death.
|
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What are the treatments for Heart Attack ?
|
There are many medicines that are used to treat a heart attack. - Clot-busters or thrombolytic drugs dissolve blood clots that are blocking blood flow to the heart. - Beta blockers decrease the workload on your heart by slowing your heart rate. - Angiotensin-converting enzyme (ACE) inhibitors lower your blood pressure and reduce the strain on your heart. - Nitrates, such as nitroglycerin relax blood vessels and relieve chest pain. - Anticoagulants thin the blood and prevent clots from forming in your arteries. - Antiplatelet medications, such as aspirin and clopidogrel, stop platelets from clumping together to form clots. These medications are given to people who have had a heart attack, have angina, or have had angioplasty. Clot-busters or thrombolytic drugs dissolve blood clots that are blocking blood flow to the heart. Beta blockers decrease the workload on your heart by slowing your heart rate. Angiotensin-converting enzyme (ACE) inhibitors lower your blood pressure and reduce the strain on your heart. Nitrates, such as nitroglycerin relax blood vessels and relieve chest pain. Anticoagulants thin the blood and prevent clots from forming in your arteries. Antiplatelet medications, such as aspirin and clopidogrel, stop platelets from clumping together to form clots. These medications are given to people who have had a heart attack, have angina, or have had angioplasty. Doctors may also prescribe medicines to relieve pain and anxiety, or to treat irregular heart rhythms which often occur during a heart attack.
|
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How many people are affected by spinocerebellar ataxia type 36 ?
|
Approximately 100 individuals with SCA36 have been reported in the scientific literature. Almost all of these individuals have been from two regions: western Japan and the Costa de Morte in Galicia, Spain.
|
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Is Craniometaphyseal dysplasia, autosomal dominant inherited ?
|
How is autosomal dominant craniometaphyseal dysplasia inherited? Autosomal dominant craniometaphyseal dysplasia is inherited in an autosomal dominant pattern, which means one altered copy of the ANKH gene in each cell is sufficient to cause the disorder. Individuals with autosomal dominant craniometaphyseal dysplasia typically have one parent who also has the condition. Less often, cases result from new mutations in the gene and occur in people with no history of the disorder in their family.
|
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How many people are affected by core binding factor acute myeloid leukemia ?
|
Acute myeloid leukemia occurs in approximately 3.5 per 100,000 individuals each year. CBF-AML accounts for 12 to 15 percent of acute myeloid leukemia cases in adults.
|
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What are the treatments for lysinuric protein intolerance ?
|
These resources address the diagnosis or management of lysinuric protein intolerance: - Gene Review: Gene Review: Lysinuric Protein Intolerance - Genetic Testing Registry: Lysinuric protein intolerance - MedlinePlus Encyclopedia: Aminoaciduria - MedlinePlus Encyclopedia: Malabsorption 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) Alopecia areata ?
|
Alopecia areata (AA) is an autoimmune disease in which the immune system mistakenly attacks the hair follicles. In most cases, hair falls out in small, round patches on the scalp. Although uncommon, hair loss can be more extensive in some people and affect other parts of the body. This condition can progress to complete loss of scalp hair (alopecia totalis) or total loss of all body hair (alopecia universalis). Although the exact cause of AA is unknown, roughly 20% of affected people have a family member with alopecia, suggesting that genetic factors may contribute to the development of the condition. There is no cure or approved therapy for AA; however, some people find that medications approved for other purposes can help regrow hair.
|
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What is (are) Long QT syndrome 8 ?
|
Timothy syndrome is a type of long QT syndrome. It affects many parts of the body including the heart, fingers, toes, face, and the nervous system. It is characterized by long QT syndrome, although some people with Timothy syndrome also have other heart defects that affect the hearts ability to pump blood effectively. Other symptoms of Timothy syndrome include fusion of the skin between fingers or toes and distinctive facial features. In addition, many children with this syndrome have developmental delay and characteristic features of autism. Mental retardation and seizures can also occur in children with Timothy syndrome. There are two forms of Timothy syndrome. Type 1 includes all of the characteristic features described. Type 2 causes a more severe form of long QT syndrome and does not appear to cause fusion of skin between fingers or toes. All cases of Timothy syndrome appear to be due to changes in the CACNA1C gene. This syndrome is inherited in an autosomal dominant manner. However, most cases are not inherited from an affected parent, but occur for the first time in a family due to a spontaneous or random change in the CACNA1C gene.
|
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What is (are) Pleural Disorders ?
|
Your pleura is a large, thin sheet of tissue that wraps around the outside of your lungs and lines the inside of your chest cavity. Between the layers of the pleura is a very thin space. Normally it's filled with a small amount of fluid. The fluid helps the two layers of the pleura glide smoothly past each other as your lungs breathe air in and out. Disorders of the pleura include - Pleurisy - inflammation of the pleura that causes sharp pain with breathing - Pleural effusion - excess fluid in the pleural space - Pneumothorax - buildup of air or gas in the pleural space - Hemothorax - buildup of blood in the pleural space Many different conditions can cause pleural problems. Viral infection is the most common cause of pleurisy. The most common cause of pleural effusion is congestive heart failure. Lung diseases, like COPD, tuberculosis, and acute lung injury, cause pneumothorax. Injury to the chest is the most common cause of hemothorax. Treatment focuses on removing fluid, air, or blood from the pleural space, relieving symptoms, and treating the underlying condition. NIH: National Heart, Lung, and Blood Institute
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What is (are) Globozoospermia ?
|
Globozoospermia is a rare form of male infertility. Men affected by this condition have abnormal sperm with a round (rather than oval) head and no acrosome (a cap-like covering which contains enzymes that break down the outer membrane of an egg cell). As a result of these abnormalities, the sperm are unable to fertilize an egg cell, leading to male factor infertility. Approximately 70% of men with globozoospermia have changes (mutations) in the DPY19L2 gene, which are inherited in an autosomal recessive manner. In the remaining cases, the underlying cause of the condition is unknown; however, researchers suspect that mutations in other genes likely cause globozoospermia. Although there is currently no cure for the condition, certain assisted reproductive technologies (ICSI combined with assisted egg cell activation, specifically) can help men affected by the condition conceive children.
|
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What is (are) Sexual Assault ?
|
Sexual assault is any sexual activity to which you haven't freely given your consent. This includes completed or attempted sex acts that are against your will. Sometimes it can involve a victim who is unable to consent. It also includes abusive sexual contact. It can happen to men, women or children. The attacker can be anyone - a current or former partner, a family member, a person in position of power or trust, a friend, an acquaintance, or a stranger. Sexual assault can affect your health in many ways. It can lead to long-term health and emotional problems. It is important to seek help if you have been assaulted. First, get to a safe place. Then dial 9-1-1 or go to a hospital for medical care. You may want to have counseling to deal with your feelings. The most important thing to know is that the assault was not your fault. Centers for Disease Control and Prevention
|
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What are the treatments for Kuru ?
|
There were no treatments that could control or cure kuru, other than discouraging the practice of cannibalism. Currently, there are no cures or treatments for any of the other TSE diseases.
|
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What are the treatments for Chronic Fatigue Syndrome (CFS) ?
|
Introduction
Managing chronic fatigue syndrome can be as complex as the illness itself. There is no cure, no prescription drugs have been developed specifically for CFS, and symptoms can vary a lot over time. Thus, people with CFS should closely monitor their health and let their doctor know of any changes; and doctors should regularly monitor their patients' conditions and change treatment strategies as needed.
A team approach that involves doctors and patients is one key to successfully managing CFS. Patients and their doctors can work together to create an individualized treatment program that best meets the needs of the patient with CFS. This program should be based on a combination of therapies that address symptoms, coping techniques, and managing normal daily activities.
CFS affects patients in different ways, and the treatment plan should be tailored to address symptoms that are most disruptive or disabling for each patient. Helping the patient get relief from symptoms is the main goal of treatment. However, expecting a patient to return to usual activities should not be the immediate goal because the physical and mental exertion needed to try to reach that goal may aggravate the illness.
Because CFS is a complicated illness, its management may require input from a variety of medical professionals. Primary care providers can develop effective treatment plans based on their experience in treating other illnesses. Patients benefit when they can work in collaboration with a team of doctors and other health care professionals, who might also include rehabilitation specialists, mental health professionals, and physical or exercise therapists.
Difficulties of Living with CFS
Living with chronic fatigue syndrome can be difficult. Like other debilitating chronic illnesses, CFS can have a devastating impact on patients' daily lives and require them to make major lifestyle changes to adapt to many new limitations.
Common difficulties for CFS patients include problems coping with:
- the changing and unpredictable symptoms
- a decrease in stamina that interferes with activities of daily life
- memory and concentration problems that seriously hurt work or school performance
- loss of independence, livelihood, and economic security
- alterations in relationships with partners, family members, and friends
- worries about raising children
Feelings of anger, guilt, anxiety, isolation and abandonment are common in CFS patients. While it's OK to have such feelings, unresolved emotions and stress can make symptoms worse, interfere with prescription drug therapies, and make recovery harder.
|
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What is (are) Zika Virus ?
|
Zika is a virus that is spread by mosquitoes. A pregnant mother can pass it to her baby during pregnancy or around the time of birth. A man can spread it to his partner during sexual contact. There have also been reports that the virus has spread through blood transfusions. There have been outbreaks of Zika virus in Africa, Southeast Asia, the Pacific Islands, parts of the Caribbean, and Central and South America. Most people who get the virus do not get sick. One in five people do get symptoms, which can include a fever, rash, joint pain, and conjunctivitis (pinkeye). Symptoms are usually mild, and start 2 to 7 days after being bitten by an infected mosquito. A blood test can tell whether you have the infection. There are no vaccines or medicines to treat it. Drinking lots of fluids, resting, and taking acetaminophen might help. Zika can cause microcephaly (a serious birth defect of the brain) and other problems in babies whose mothers were infected while pregnant. The Centers for Disease Control and Prevention recommends that pregnant women do not travel to areas where there is a Zika virus outbreak. If you do decide to travel, first talk to your doctor. You should also be careful to prevent mosquito bites: - Use insect repellent - Wear clothes that cover your arms, legs, and feet - Stay in places that have air conditioning or that use window and door screens Centers for Disease Control and Prevention
|
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What are the treatments for Hendra Virus Disease (HeV) ?
|
The drug ribavirin has been shown to be effective against the viruses in vitro, but the clinical usefulness of this drug is uncertain.
A post-exposure therapy with a Nipah/Hendra neutralizing antibody, efficacious in animal models is in human preclinical development stages in Australia.
|
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What are the symptoms of Familial joint instability syndrome ?
|
What are the signs and symptoms of Familial joint instability syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Familial joint instability 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 hip bone 90% Joint hypermobility 90% Patellar dislocation 90% Abnormality of the elbow 7.5% Abnormality of the femur 7.5% Abnormality of the shoulder 7.5% Hernia of the abdominal wall 7.5% Autosomal dominant inheritance - Congenital hip dislocation - Joint laxity - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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Is MYH9-related disorder 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. In most cases, an affected person inherits the mutation from one affected parent. Approximately 30 percent of cases result from new mutations in the gene and occur in people with no history of the disorder in their family.
|
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Is Russell-Silver syndrome inherited ?
|
Most cases of Russell-Silver syndrome are sporadic, which means they occur in people with no history of the disorder in their family. Less commonly, Russell-Silver syndrome can run in families. In some affected families, the condition appears to have an autosomal dominant pattern of inheritance. Autosomal dominant inheritance means one copy of a genetic change in each cell is sufficient to cause the disorder. In other families, the condition has an autosomal recessive pattern of inheritance. Autosomal recessive inheritance means both copies of a gene are altered in each cell. 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) Pituitary Disorders ?
|
Your pituitary gland is a pea-sized gland at the base of your brain. The pituitary is the "master control gland" - it makes hormones that affect growth and the functions of other glands in the body. With pituitary disorders, you often have too much or too little of one of your hormones. Injuries can cause pituitary disorders, but the most common cause is a pituitary tumor.
|
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Is 18q deletion syndrome inherited ?
|
Most cases of 18q deletion syndrome are not inherited. The deletion occurs most often 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. In some cases, 18q deletion syndrome is inherited, usually from a mildly affected parent. The deletion can also be inherited from an unaffected parent who carries a chromosomal rearrangement called a balanced translocation, in which no genetic material is gained or lost. Individuals with a balanced translocation do not usually have any related health problems; however, the translocation can become unbalanced as it is passed to the next generation. Children who inherit an unbalanced translocation can have a chromosomal rearrangement with extra or missing genetic material. Individuals with 18q deletion syndrome who inherit an unbalanced translocation are missing genetic material from the long arm of chromosome 18, which results in the signs and symptoms of this disorder.
|
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what research (or clinical trials) is being done for Thymoma and Thymic Carcinoma ?
|
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.
Patients may want to think about taking part in a clinical trial.
For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment. Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment. Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.
Patients can enter clinical trials before, during, or after starting their cancer treatment.
Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment. Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
|
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What is (are) Acute Lymphocytic Leukemia ?
|
Leukemia is cancer of the white blood cells. White blood cells help your body fight infection. Your blood cells form in your bone marrow. In leukemia, however, the bone marrow produces abnormal white blood cells. These cells crowd out the healthy blood cells, making it hard for blood to do its work. In acute lymphocytic leukemia (ALL), also called acute lymphoblastic leukemia, there are too many of specific types of white blood cells called lymphocytes or lymphoblasts. ALL is the most common type of cancer in children. Possible risk factors for ALL include being male, being white, previous chemotherapy treatment, exposure to radiation, and for adults, being older than 70. Symptoms of ALL include: - Weakness or feeling tired - Fever - Easy bruising or bleeding - Bleeding under the skin - Shortness of breath - Weight loss or loss of appetite - Pain in the bones or stomach - Pain or a feeling of fullness below the ribs - Painless lumps in the neck, underarm, stomach, or groin Tests that examine the blood and bone marrow diagnose ALL. Treatments include chemotherapy, radiation therapy, stem cell transplants, and targeted therapy. Targeted therapy uses substances that attack cancer cells without harming normal cells. Once the leukemia is in remission, you need additional treatment to make sure that it does not come back. NIH: National Cancer Institute
|
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What is (are) Secondary adrenal insufficiency ?
|
Adrenal insufficiency is an endocrine disorder that occurs when the adrenal glands do not produce enough of certain hormones. Secondary adrenal insufficiency occurs when the pituitary gland (a pea-sized gland at the base of the brain) fails to produce enough adrenocorticotropin (ACTH), a hormone that stimulates the adrenal glands to produce the hormone cortisol. The lack of these hormones in the body can be caused by reduction or cessation of corticosteroid medication, the surgical removal of pituitary tumors, or changes in the pituitary gland. Symptoms of secondary adrenal insufficiency may include severe fatigue, loss of appetite, weight loss, nausea, vomiting, diarrhea, muscle weakness, irritability, and depression. Treatment includes replacing the hormones that the adrenal glands are not making. The dose of each medication is adjusted to meet the needs of each affected individual.
|
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What is (are) lysinuric protein intolerance ?
|
Lysinuric protein intolerance is a disorder caused by the body's inability to digest and use certain protein building blocks (amino acids), namely lysine, arginine, and ornithine. Because the body cannot effectively break down these amino acids, which are found in many protein-rich foods, nausea and vomiting are typically experienced after ingesting protein. People with lysinuric protein intolerance have features associated with protein intolerance, including an enlarged liver and spleen (hepatosplenomegaly), short stature, muscle weakness, impaired immune function, and progressively brittle bones that are prone to fracture (osteoporosis). A lung disorder called pulmonary alveolar proteinosis may also develop. This disorder is characterized by protein deposits in the lungs, which interfere with lung function and can be life-threatening. An accumulation of amino acids in the kidneys can cause end-stage renal disease (ESRD) in which the kidneys become unable to filter fluids and waste products from the body effectively. A lack of certain amino acids can cause elevated levels of ammonia in the blood. If ammonia levels are too high for too long, they can cause coma and intellectual disability. The signs and symptoms of lysinuric protein intolerance typically appear after infants are weaned and receive greater amounts of protein from solid foods.
|
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What is the outlook for SUNCT Headache ?
|
There is no cure for these headaches. The disorder is not fatal but can cause considerable discomfort.
|
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What are the treatments for myoclonic epilepsy with ragged-red fibers ?
|
These resources address the diagnosis or management of MERRF: - Gene Review: Gene Review: MERRF - Genetic Testing Registry: Myoclonus with epilepsy with ragged red fibers - Kennedy Krieger Institute: Mitochondrial Disorders - MedlinePlus Encyclopedia: Lipoma - MedlinePlus Encyclopedia: Optic nerve atrophy - MedlinePlus Encyclopedia: Peripheral Neuropathy - MitoAction: Tips and Tools for Living with Mito - United Mitochondrial Disease Foundation: Treatments and Therapies 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 3MC syndrome ?
|
3MC syndrome is a rare disorder; its exact prevalence is unknown.
|
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What is (are) hypermanganesemia with dystonia, polycythemia, and cirrhosis ?
|
Hypermanganesemia with dystonia, polycythemia, and cirrhosis (HMDPC) is an inherited disorder in which excessive amounts of the element manganese accumulate in the body, particularly in the brain, liver, and blood (hypermanganesemia). Signs and symptoms of this condition can appear in childhood (early-onset), typically between ages 2 and 15, or in adulthood (adult-onset). Manganese accumulates in a region of the brain responsible for the coordination of movement, causing neurological problems that make controlling movement difficult. Most children with the early-onset form of HMDPC experience involuntary tensing of the muscles in the arms and legs (four-limb dystonia), which often leads to a characteristic high-stepping walk described as a "cock-walk gait." Other neurological symptoms in affected children include involuntary trembling (tremor), unusually slow movement (bradykinesia), and slurred speech (dysarthria). The adult-onset form of HMDPC is characterized by a pattern of movement abnormalities known as parkinsonism, which includes bradykinesia, tremor, muscle rigidity, and an inability to hold the body upright and balanced (postural instability). Affected individuals have an increased number of red blood cells (polycythemia) and low levels of iron stored in the body. Additional features of HMDPC can include an enlarged liver (hepatomegaly), scarring (fibrosis) in the liver, and irreversible liver disease (cirrhosis).
|
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How many people are affected by Sheldon-Hall syndrome ?
|
The prevalence of Sheldon-Hall syndrome is unknown; however, it is thought to be the most common type of distal arthrogryposis. About 100 affected individuals have been described in the medical literature.
|
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What are the symptoms of Patent Ductus Arteriosus ?
|
A heart murmur may be the only sign that a baby has patent ductus arteriosus (PDA). A heart murmur is an extra or unusual sound heard during the heartbeat. Heart murmurs also have other causes besides PDA, and most murmurs are harmless.
Some infants may develop signs or symptoms of volume overload on the heart and excess blood flow in the lungs. Signs and symptoms may include:
Fast breathing, working hard to breathe, or shortness of breath. Premature infants may need increased oxygen or help breathing from a ventilator.
Poor feeding and poor weight gain.
Tiring easily.
Sweating with exertion, such as while feeding.
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What is (are) familial pityriasis rubra pilaris ?
|
Familial pityriasis rubra pilaris is a rare genetic condition that affects the skin. The name of the condition reflects its major features: The term "pityriasis" refers to scaling; "rubra" means redness; and "pilaris" suggests the involvement of hair follicles in this disorder. Affected individuals have a salmon-colored skin rash covered in fine scales. This rash occurs in patches all over the body, with distinct areas of unaffected skin between the patches. Affected individuals also develop bumps called follicular keratoses that occur around hair follicles. The skin on the palms of the hands and soles of the feet often becomes thick, hard, and callused, a condition known as palmoplantar keratoderma. Researchers have distinguished six types of pityriasis rubra pilaris based on the features of the disorder and the age at which signs and symptoms appear. The familial form is usually considered part of type V, which is also known as the atypical juvenile type. People with familial pityriasis rubra pilaris typically have skin abnormalities from birth or early childhood, and these skin problems persist throughout life.
|
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Do you have information about Foot Health
|
Summary : Each step you take involves a complex network of bones, muscles, tendons, and ligaments. This, combined with all of the weight they carry, explains why feet can have problems. To keep your feet healthy - Examine your feet regularly - Wear comfortable shoes that fit - Wash your feet daily with soap and lukewarm water - Trim your toenails straight across and not too short Your foot health can be a clue to your overall health. For example, joint stiffness could mean arthritis. Tingling or numbness could be a sign of diabetes. Swelling might indicate kidney disease, heart disease, or high blood pressure. Good foot care and regular foot checks are an important part of your health care. If you have foot problems, be sure to talk to your doctor. NIH: National Institute on Aging
|
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What is (are) Krabbe Disease ?
|
Krabbe disease is a rare, inherited metabolic disorder in which harmful amounts of lipids (fatty materials such as oils and waxes) build up in various cells and tissues in the body and destroys brain cells. Krabbe disease, also known as globoid cell leukodystrophy, ischaracterized by the presence of globoid cells (cells that have more than one nucleus) that break down the nerves protective myelin coating. Krabbe disease is caused by a deficiency of galactocerebrosidase, an essential enzyme for myelin metabolism. The disease most often affects infants, with onset before age 6 months, but can occur in adolescence or adulthood. Symptoms include severe deterioration of mental and motor skills, muscle weakness, hypertonia (inability of a muscle to stretch), myoclonic seizures (sudden, shock-like contractions of the limbs), and spasticity (involuntary and awkward movement). Other symptoms may include irritability, unexplained fever, blindness, difficulty with swallowing, and deafness.
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] |
What are the treatments for cone-rod dystrophy ?
|
These resources address the diagnosis or management of cone-rod dystrophy: - Cleveland Clinic: Eye Examinations: What to Expect - Genetic Testing Registry: CONE-ROD DYSTROPHY, AIPL1-RELATED - Genetic Testing Registry: Cone-rod dystrophy - Genetic Testing Registry: Cone-rod dystrophy 1 - Genetic Testing Registry: Cone-rod dystrophy 10 - Genetic Testing Registry: Cone-rod dystrophy 11 - Genetic Testing Registry: Cone-rod dystrophy 12 - Genetic Testing Registry: Cone-rod dystrophy 13 - Genetic Testing Registry: Cone-rod dystrophy 15 - Genetic Testing Registry: Cone-rod dystrophy 16 - Genetic Testing Registry: Cone-rod dystrophy 17 - Genetic Testing Registry: Cone-rod dystrophy 18 - Genetic Testing Registry: Cone-rod dystrophy 19 - Genetic Testing Registry: Cone-rod dystrophy 2 - Genetic Testing Registry: Cone-rod dystrophy 20 - Genetic Testing Registry: Cone-rod dystrophy 21 - Genetic Testing Registry: Cone-rod dystrophy 3 - Genetic Testing Registry: Cone-rod dystrophy 5 - Genetic Testing Registry: Cone-rod dystrophy 6 - Genetic Testing Registry: Cone-rod dystrophy 7 - Genetic Testing Registry: Cone-rod dystrophy 8 - Genetic Testing Registry: Cone-rod dystrophy 9 - Genetic Testing Registry: Cone-rod dystrophy X-linked 3 - Genetic Testing Registry: Cone-rod dystrophy, X-linked 1 - MedlinePlus Encyclopedia: Color Vision Test - MedlinePlus Encyclopedia: Visual Acuity Test - MedlinePlus Encyclopedia: Visual Field 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 are the treatments for Breast Cancer ?
|
Certain drugs that have been used successfully in other cancers are now being used to treat some breast cancers. A mix of drugs may increase the length of time you will live, or the length of time you will live without cancer. In addition, certain drugs like Herceptin and Tykerb taken in combination with chemotherapy, can help women with specific genetic breast cancer mutations better than chemotherapy alone.
|
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] |
How many people are affected by X-linked severe combined immunodeficiency ?
|
X-linked SCID is the most common form of severe combined immunodeficiency. Its exact incidence is unknown, but the condition probably affects at least 1 in 50,000 to 100,000 newborns.
|
[
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How many people are affected by breast cancer ?
|
Breast cancer is the second most commonly diagnosed cancer in women. (Only skin cancer is more common.) About one in eight women in the United States will develop invasive breast cancer in her lifetime. Researchers estimate that more than 230,000 new cases of invasive breast cancer will be diagnosed in U.S. women in 2015. Male breast cancer represents less than 1 percent of all breast cancer diagnoses. Scientists estimate that about 2,300 new cases of breast cancer will be diagnosed in men in 2015. Particular gene mutations associated with breast cancer are more common among certain geographic or ethnic groups, such as people of Ashkenazi (central or eastern European) Jewish heritage and people of Norwegian, Icelandic, or Dutch ancestry.
|
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] |
What to do for Henoch-Schnlein Purpura ?
|
Eating, diet, and nutrition have not been shown to play a role in causing or preventing HSP.
|
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Is retroperitoneal fibrosis inherited ?
|
Most cases of retroperitoneal fibrosis are sporadic, which means that they occur in people with no apparent history of the disorder in their family. In rare cases, the condition has been reported to occur in a few members of the same family, but the inheritance pattern is unknown.
|
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] |
What is (are) X-linked sideroblastic anemia ?
|
X-linked sideroblastic anemia is an inherited disorder that prevents developing red blood cells (erythroblasts) from making enough hemoglobin. People with X-linked sideroblastic anemia have mature red blood cells that are smaller than normal (microcytic) and appear pale (hypochromic) because of the shortage of hemoglobin. This disorder also leads to an abnormal accumulation of iron in red blood cells. The iron-loaded erythroblasts, which are present in bone marrow, are called ring sideroblasts. These abnormal cells give the condition its name. The signs and symptoms of X-linked sideroblastic anemia result from a combination of reduced hemoglobin and an overload of iron. They range from mild to severe and most often appear in young adulthood. Common features include fatigue, dizziness, a rapid heartbeat, pale skin, and an enlarged liver and spleen (hepatosplenomegaly). Over time, severe medical problems such as heart disease and liver damage (cirrhosis) can result from the buildup of excess iron in these organs. X-linked sideroblastic anemia is caused by mutation in the ALAS2 gene. In rare cases, mutations are found in both the HFE gene and the ALAS2 gene, resulting in a more severe form of X-linked sideroblastic anemia. X-linked sideroblastic anemia is inherited in an X-linked recessive pattern.
|
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What are the symptoms of Infantile convulsions and paroxysmal choreoathetosis, familial ?
|
What are the signs and symptoms of Infantile convulsions and paroxysmal choreoathetosis, familial? The Human Phenotype Ontology provides the following list of signs and symptoms for Infantile convulsions and paroxysmal choreoathetosis, familial. 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) Chorea 90% EEG abnormality 90% Seizures 90% Incoordination 50% Migraine 50% Stereotypic behavior 7.5% Anxiety - Autosomal dominant inheritance - Focal seizures, afebril - Generalized seizures - Normal interictal EEG - Paroxysmal choreoathetosis - Paroxysmal dystonia - 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) Pediatric Crohn's disease ?
|
Crohn's disease is a type of inflammatory bowel disease (IBD), the general name for conditions that cause inflammation in the gastrointestinal (GI) tract. Common signs and symptoms include abdominal pain and cramping, diarrhea, and weight loss. Other general symptoms include feeling tired, nausea and loss of appetite, fever, and anemia. Complications of Crohn's disease may include intestinal blockage, fistulas, anal fissures, ulcers, malnutrition, and inflammation in other areas of the body. Crohn's disease can occur in people of all age groups but is most often diagnosed in young adults. The exact cause is unknown, but is thought to involve both genetic and environmental factors. It appears to run in some families. Treatment is aimed at relieving symptoms and reducing inflammation, but some people require surgery.
|
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] |
what are marine toxins?
|
Marine toxins are naturally occurring chemicals that can contaminate certain seafood. The seafood contaminated with these chemicals frequently looks, smells, and tastes normal. When humans eat such seafood, disease can result.
|
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What is (are) Cat Scratch Disease ?
|
Cat scratch disease (CSD) is an illness caused by the bacterium Bartonella henselae. Almost half of all cats carry the infection at some point. The infection does not make cats sick. However, the scratch or bite of an infected cat can cause symptoms in people, including - Swollen lymph nodes, especially around the head, neck, and upper limbs - Fever - Headache - Fatigue - Poor appetite For people with weak immune systems, CSD may cause more serious problems. The best way to avoid CSD is to avoid rough play with cats that could lead to scratches or bites. If you do get a scratch or bite, wash it well with soap and water. If the bite or scratch gets infected or if you have symptoms of CSD, call your doctor. Centers for Disease Control and Prevention
|
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What are the symptoms of Diabetic Retinopathy ?
|
Diabetic retinopathy often has no early warning signs. Don't wait for symptoms. Be sure to have a comprehensive dilated eye exam at least once a year to detect the disease before it causes damage to your vision. Vision Changes May Indicate Bleeding In the early stages of diabetic retinopathy, you may not notice any changes in your vision. But if diabetic retinopathy reaches its final stage, proliferative retinopathy, bleeding can occur. If this happens, at first, you will see a few specks of blood, or spots, floating in your vision. If spots occur, see your eye care professional as soon as possible. Early Treatment is Important You may need treatment before more serious bleeding or hemorrhages occur causing vision loss or possibly blindness. Hemorrhages tend to happen more than once, often during sleep. See how to find an eye care professional. Here is a list of questions to ask your eye care professional. Sometimes the spots clear without treatment, and you will see better. However, bleeding can reoccur and cause severely blurred vision. You need to be examined by your eye care professional at the first sign of blurred vision, before more bleeding occurs. If left untreated, proliferative retinopathy can cause severe vision loss and even blindness. Also, the earlier you receive treatment, the more likely treatment will be successful. Detection Diabetic retinopathy and macular edema are detected during a comprehensive eye exam that includes a visual acuity test, dilated eye exam, and tonometry. A visual acuity test is an eye chart test that measures how well you see at various distances. During the dilated eye exam, your eye care professional checks your retina for early signs of the disease, including - leaking blood vessels - retinal swelling such as macular edema - pale, fatty deposits on the retina -- signs of leaking blood vessels - damaged nerve tissue leaking blood vessels retinal swelling such as macular edema pale, fatty deposits on the retina -- signs of leaking blood vessels damaged nerve tissue Watch an animation showing what a comprehensive dilated eye exam involves. With tonometry, an instrument measures the pressure inside the eye. Numbing drops may be applied to your eye for this test. If your eye care professional believes you need treatment for macular edema, he or she may suggest a fluorescein angiogram. In this test, a special dye is injected into your arm. Pictures are taken as the dye passes through the blood vessels in your retina. The test allows your eye care professional to identify any leaking blood vessels and recommend treatment.
|
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] |
Is ALG6-congenital disorder of glycosylation 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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] |
Is spastic paraplegia type 31 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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[
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] |
What is (are) 9q22.3 microdeletion ?
|
9q22.3 microdeletion is a chromosomal change in which a small piece of chromosome 9 is deleted in each cell. The deletion occurs on the long (q) arm of the chromosome in a region designated q22.3. This chromosomal change is associated with delayed development, intellectual disability, certain physical abnormalities, and the characteristic features of a genetic condition called Gorlin syndrome. Many individuals with a 9q22.3 microdeletion have delayed development, particularly affecting the development of motor skills such as sitting, standing, and walking. In some people, the delays are temporary and improve in childhood. More severely affected individuals have permanent developmental disabilities along with intellectual impairment and learning problems. Rarely, seizures have been reported in people with a 9q22.3 microdeletion. About 20 percent of people with a 9q22.3 microdeletion experience overgrowth (macrosomia), which results in increased height and weight compared to unaffected peers. The macrosomia often begins before birth and continues into childhood. Other physical changes that can be associated with a 9q22.3 microdeletion include the premature fusion of certain bones in the skull (metopic craniosynostosis) and a buildup of fluid in the brain (hydrocephalus). Affected individuals can also have distinctive facial features such as a prominent forehead with vertical skin creases, upward- or downward-slanting eyes, a short nose, and a long space between the nose and upper lip (philtrum). 9q22.3 microdeletions also cause the characteristic features of Gorlin syndrome (also known as nevoid basal cell carcinoma syndrome). This genetic condition affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumors. In people with Gorlin syndrome, the type of cancer diagnosed most often is basal cell carcinoma, which is the most common form of skin cancer. Most people with this condition also develop noncancerous (benign) tumors of the jaw, called keratocystic odontogenic tumors, which can cause facial swelling and tooth displacement. Other types of tumors that occur more often in people with Gorlin syndrome include a form of childhood brain cancer called a medulloblastoma and a type of benign tumor called a fibroma that occurs in the heart or in a woman's ovaries. Other features of Gorlin syndrome include small depressions (pits) in the skin of the palms of the hands and soles of the feet; an unusually large head size (macrocephaly) with a prominent forehead; and skeletal abnormalities involving the spine, ribs, or skull.
|
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What is (are) What I need to know about Lactose Intolerance ?
|
Lactose intolerance means you have symptoms such as bloating, diarrhea, and gas after you have milk or milk products.
If your small intestine does not produce much lactase, you cannot break down much lactose. Lactose that does not break down goes to your colon. The colon is an organ that absorbs water from stool and changes it from a liquid to a solid form. In your colon, bacteria that normally live in the colon break down the lactose and create fluid and gas, causing you to have symptoms.
The causes of low lactase in your small intestine can include the following:
- In some people, the small intestine makes less lactase starting at about age 2, which may lead to symptoms of lactose intolerance. Other people start to have symptoms later, when they are teenagers or adults. - Infection, disease, or other problems that harm the small intestine can cause low lactase levels. Low lactase levels can cause you to become lactose intolerant until your small intestine heals. - Being born early may cause babies to be lactose intolerant for a short time after they are born. - In a rare form of lactose intolerance, the small intestine produces little or no lactase enzyme from birth.
Not all people with low lactase levels have symptoms. If you have symptoms, you are lactose intolerant.
Most people who are lactose intolerant can have some milk or milk products and not have symptoms. The amount of lactose that causes symptoms is different from person to person.
People sometimes confuse lactose intolerance with a milk allergy. While lactose intolerance is a digestive problem, a milk allergy is a reaction by the bodys immune system to one or more milk proteins. If you have a milk allergy, having even a small amount of milk or milk product can be life threatening. A milk allergy most commonly occurs in the first year of life. Lactose intolerance occurs more often during the teen years or adulthood.
|
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What is (are) Alexander Disease ?
|
Alexander disease is one of a group of neurological conditions known as the leukodystrophies, disorders that are the result of abnormalities in myelin, the white matter that protects nerve fibers in the brain. Alexander disease is a progressive and often fatal disease. The destruction of white matter is accompanied by the formation of Rosenthal fibers, which are abnormal clumps of protein that accumulate in non-neuronal cells of the brain called astrocytes. Rosenthal fibers are sometimes found in other disorders, but not in the same amount or area of the brain that are featured in Alexander disease. The infantile form is the most common type of Alexander disease. It has an onset during the first two years of life. Usually there are both mental and physical developmental delays, followed by the loss of developmental milestones, an abnormal increase in head size, and seizures. The juvenile form of Alexander disease is less common and has an onset between the ages of two and thirteen. These children may have excessive vomiting, difficulty swallowing and speaking, poor coordination, and loss of motor control. Adult-onset forms of Alexander disease are less common. The symptoms sometimes mimic those of Parkinsons disease or multiple sclerosis, or may present primarily as a psychiatric disorder. The disease occurs in both males and females, and there are no ethnic, racial, geographic, or cultural/economic differences in its distribution.
|
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What are the complications of Shingles ?
|
The most common complication of shingles is pain -- a condition called post-herpetic neuralgia (PHN). People with PHN have severe pain in the areas where they had the shingles rash, even after the rash clears up. In most patients, the pain usually clears up in a few weeks or months, but some people can have pain from PHN for years. Shingles may also lead to other serious complications. - Outbreaks that start on the face or eyes can cause vision or hearing problems. Even permanent blindness can result if the cornea of the eye is affected. - Bacterial infection of the open sores can lead to scarring. - In a very small number of cases, bacteria can cause more serious conditions, including toxic shock syndrome and necrotizing fasciitis, a severe infection that destroys the soft tissue under the skin. - The burning waves of pain, loss of sleep, and interference with even basic life activities can cause serious depression. - In patients with immune deficiency, the rash can be much more extensive than usual and the illness can be complicated by pneumonia. These cases are more serious, but they are rarely fatal. - Very rarely, shingles can also lead to pneumonia, brain inflammation (encephalitis), or death. Outbreaks that start on the face or eyes can cause vision or hearing problems. Even permanent blindness can result if the cornea of the eye is affected. Bacterial infection of the open sores can lead to scarring. In a very small number of cases, bacteria can cause more serious conditions, including toxic shock syndrome and necrotizing fasciitis, a severe infection that destroys the soft tissue under the skin. The burning waves of pain, loss of sleep, and interference with even basic life activities can cause serious depression. In patients with immune deficiency, the rash can be much more extensive than usual and the illness can be complicated by pneumonia. These cases are more serious, but they are rarely fatal. Very rarely, shingles can also lead to pneumonia, brain inflammation (encephalitis), or death.
|
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What are the symptoms of Autosomal dominant partial epilepsy with auditory features ?
|
What are the signs and symptoms of Autosomal dominant partial epilepsy with auditory features? The Human Phenotype Ontology provides the following list of signs and symptoms for Autosomal dominant partial epilepsy with auditory features. 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) Auditory auras - Autosomal dominant inheritance - Bilateral convulsive seizures - Focal seizures with impairment of consciousness or awareness - Focal seizures without impairment of consciousness or awareness - Incomplete penetrance - 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) Hypoglycemia ?
|
Hypoglycemia, also called low blood glucose or low blood sugar, occurs when blood glucose drops below normal levels. Glucose, an important source of energy for the body, comes from food. Carbohydrates are the main dietary source of glucose. Rice, potatoes, bread, tortillas, cereal, milk, fruit, and sweets are all carbohydrate-rich foods.
After a meal, glucose is absorbed into the bloodstream and carried to the body's cells. Insulin, a hormone made by the pancreas, helps the cells use glucose for energy. If a person takes in more glucose than the body needs at the time, the body stores the extra glucose in the liver and muscles in a form called glycogen. The body can use glycogen for energy between meals. Extra glucose can also be changed to fat and stored in fat cells. Fat can also be used for energy.
When blood glucose begins to fall, glucagonanother hormone made by the pancreassignals the liver to break down glycogen and release glucose into the bloodstream. Blood glucose will then rise toward a normal level. In some people with diabetes, this glucagon response to hypoglycemia is impaired and other hormones such as epinephrine, also called adrenaline, may raise the blood glucose level. But with diabetes treated with insulin or pills that increase insulin production, glucose levels can't easily return to the normal range.
Hypoglycemia can happen suddenly. It is usually mild and can be treated quickly and easily by eating or drinking a small amount of glucose-rich food. If left untreated, hypoglycemia can get worse and cause confusion, clumsiness, or fainting. Severe hypoglycemia can lead to seizures, coma, and even death.
In adults and children older than 10 years, hypoglycemia is uncommon except as a side effect of diabetes treatment. Hypoglycemia can also result, however, from other medications or diseases, hormone or enzyme deficiencies, or tumors.
|
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What is (are) High Blood Pressure ?
|
"DASH" stands for "Dietary Approaches to Stop Hypertension." This is the name of a clinical study that tested the effects of nutrients in food on blood pressure. Study results indicated that you can reduce high blood pressure by following an eating plan that emphasizes fruits, vegetables, and fat-free or low-fat milk and milk products, and that is low in saturated fat, cholesterol, total fat, and added sugars. The DASH eating plan also includes whole grains, poultry, fish, and nuts, and has reduced amounts of red meats, sweets, added sugars, and beverages containing sugars. A second study, called "DASH-Sodium," showed that eating less salt also lowered blood pressure in people following either the DASH eating plan or the typical American diet. But those following DASH, especially those with high blood pressure, benefited the most. For more information on using the DASH eating plan, see Your Guide to Lowering Your Blood Pressure with DASH.
|
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What are the symptoms of Cockayne syndrome ?
|
What are the signs and symptoms of Cockayne syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Cockayne 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 blistering of the skin 90% Abnormality of the nose 90% Carious teeth 90% Cognitive impairment 90% Cutaneous photosensitivity 90% Deeply set eye 90% Hyperreflexia 90% Hypertonia 90% Incoordination 90% Macrotia 90% Microcephaly 90% Peripheral neuropathy 90% Prematurely aged appearance 90% Retinopathy 90% Sensorineural hearing impairment 90% Short stature 90% Abnormal hair quantity 50% Abnormality of the foot 50% Aplasia/Hypoplasia of the skin 50% Atypical scarring of skin 50% Cerebral calcification 50% Cerebral cortical atrophy 50% Chorioretinal abnormality 50% Decreased nerve conduction velocity 50% Dental malocclusion 50% Disproportionate tall stature 50% EEG abnormality 50% Fine hair 50% Generalized hyperpigmentation 50% Hypertension 50% Kyphosis 50% Large hands 50% Limitation of joint mobility 50% Strabismus 50% Tremor 50% Abnormality of pelvic girdle bone morphology 7.5% Abnormality of retinal pigmentation 7.5% Abnormality of the palate 7.5% Aplasia/Hypoplasia affecting the eye 7.5% Breast aplasia 7.5% Cataract 7.5% Cryptorchidism 7.5% Delayed eruption of teeth 7.5% Glomerulopathy 7.5% Hypertrophic cardiomyopathy 7.5% Nephrotic syndrome 7.5% Optic atrophy 7.5% Oral cleft 7.5% Platyspondyly 7.5% Seizures 7.5% Telangiectasia of the skin 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 Trismus-pseudocamptodactyly syndrome ?
|
What are the signs and symptoms of Trismus-pseudocamptodactyly syndrome? While the symptoms of trismus-pseudocamptodactyly syndrome vary from patient to patient, characteristic symptoms include the inability to open the mouth wide (e.g., less than 6 mm, just under 1/4 of an inch) and shortened muscles, including of the hamstrings and calf muscles. As a result of shortened muscles some infants with trismus-pseudocamptodactyly syndrome have closed or clinched fists, club foot, metatarsus adductus, and calcaneovalgus (where the foot bends sharply at the ankle) at birth. Children with this syndrome may crawl on their knuckles. In adulthood the syndrome may cause reduced hand dexterity, however hand limitation does not often interfere with normal function. The most serious complications of the condition occur as a result of the limited mobility of the mouth, including impairment of adequate calorie intake, speech development, dental care, and difficulty with intubation. The Human Phenotype Ontology provides the following list of signs and symptoms for Trismus-pseudocamptodactyly 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 musculature 90% Limitation of joint mobility 90% Short stature 90% Symphalangism affecting the phalanges of the hand 90% Abnormality of the hip bone 7.5% Mandibular prognathia 7.5% Ptosis 7.5% Deep philtrum 5% Macrocephaly 5% Autosomal dominant inheritance - Cutaneous syndactyly of toes - Distal arthrogryposis - Dysphagia - Facial asymmetry - Feeding difficulties - Hammertoe - Hip dislocation - Talipes equinovarus - Trismus - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the genetic changes related to ALG6-congenital disorder of glycosylation ?
|
ALG6-CDG is caused by mutations in the ALG6 gene. This gene provides instructions for making an enzyme that is involved in a process called glycosylation. Glycosylation is the process by which sugar molecules (monosaccharides) and complex chains of sugar molecules (oligosaccharides) are added to proteins and fats. Glycosylation modifies proteins and fats so they can perform a wider variety of functions. The enzyme produced from the ALG6 gene transfers a simple sugar called glucose to the growing oligosaccharide. Once the correct number of sugar molecules are linked together, the oligosaccharide is attached to a protein or fat. ALG6 gene mutations lead to the production of an abnormal enzyme with reduced or no activity. Without a properly functioning enzyme, glycosylation cannot proceed normally, and oligosaccharides are incomplete. As a result, glycosylation is reduced or absent. The wide variety of signs and symptoms in ALG6-CDG are likely due to impaired glycosylation of proteins and fats that are needed for normal function in many organs and tissues, including the brain, eyes, liver, and hormone-producing (endocrine) system.
|
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How to diagnose Amyloidosis corneal ?
|
Is genetic testing available for lattice corneal dystrophy? Yes. GeneTests lists the names of laboratories that are performing genetic testing for lattice corneal dystrophy. Most of the laboratories listed through GeneTests do not accept direct contact from patients and their families; therefore, if you are interested in learning more, you will need to work with a health care provider or a genetics professional. To view the contact information for the clinical laboratories, conducting testing for lattice dystrophy type 1 and 3a click here. To access the contact information for the research laboratories performing genetic testing for lattice dystrophy type 3 click here.
|
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How many people are affected by atopic dermatitis ?
|
Atopic dermatitis is a common disorder that affects 10 to 20 percent of children and 5 to 10 percent of adults.
|
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Is spastic paraplegia type 15 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) Trichorhinophalangeal syndrome type 3 ?
|
Trichorhinophalangeal syndrome type 3 (TRPS3), also known as Sugio-Kajii syndrome, is an extremely rare inherited multisystem disorder. TRPS3 is characterized by short stature, sparse hair, a bulbous nasal tip and cone-shaped epiphyses (the growing ends of bones), as well as severe generalized shortening of all finger and toe bones (brachydactyly). The range and severity of symptoms may vary from case to case. TRPS3 is caused by mutations in the TRPS1 gene which is localized to 8q24.12. TRPS3 is inherited in an autosomal dominant manner.
|
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What are the genetic changes related to Kawasaki disease ?
|
The causes of Kawasaki disease are not well understood. The disorder is generally regarded as being the result of an abnormal immune system activation, but the triggers of this abnormal response are unknown. Because cases of the disorder tend to cluster geographically and by season, researchers have suggested that an infection may be involved. However, no infectious agent (such as a virus or bacteria) has been identified. A variation in the ITPKC gene has been associated with an increased risk of Kawasaki disease. The ITPKC gene provides instructions for making an enzyme called inositol 1,4,5-trisphosphate 3-kinase C. This enzyme helps limit the activity of immune system cells called T cells. T cells identify foreign substances and defend the body against infection. Reducing the activity of T cells when appropriate prevents the overproduction of immune proteins called cytokines that lead to inflammation and which, in excess, cause tissue damage. Researchers suggest that the ITPKC gene variation may interfere with the body's ability to reduce T cell activity, leading to inflammation that damages blood vessels and results in the signs and symptoms of Kawasaki disease. It appears likely that other factors, including changes in other genes, also influence the development of this complex disorder.
|
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What are the treatments for mucopolysaccharidosis type II ?
|
These resources address the diagnosis or management of mucopolysaccharidosis type II: - Baby's First Test - Gene Review: Gene Review: Mucopolysaccharidosis Type II - Genetic Testing Registry: Mucopolysaccharidosis, MPS-II - MedlinePlus Encyclopedia: Hunter syndrome - MedlinePlus Encyclopedia: Mucopolysaccharides These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the treatments for Breast Cancer ?
|
Even if the surgeon removes all of the cancer that can be seen at the time of surgery, a woman may still receive follow-up treatment. This may include radiation therapy, chemotherapy, or hormone therapy to try to kill any cancer cells that may be left. Treatment that a patient receives after surgery to increase the chances of a cure is called adjuvant therapy.
|
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What are the treatments for aniridia ?
|
These resources address the diagnosis or management of aniridia: - Gene Review: Gene Review: Aniridia - Genetic Testing Registry: Congenital aniridia 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 causes Myelodysplastic/myeloproliferative disease ?
|
What causes myelodysplastic/myeloproliferative disease? In most cases, the cause of myelodysplastic/myeloproliferative disease is unknown, and there is limited information regarding potential causes. No specific genetic defects have been identified for any of the diseases. The specific cause of chronic myelomonocytic leukemia (CMML) is unknown, but exposure to occupational and environmental carcinogens (agents that can cause cancer), ionizing radiation, and cytotoxic agents (agents that are toxic to cells) have been associated in some cases. The cause of juvenile myelomonocytic leukemia (JMML) is not known; however, children with neurofibromatosis type 1 (NF1) are at increased risk for developing JMML, and up to 14% of cases of JMML occur in children with NF1. Atypical chronic myelogenous leukemia (aCML) has been associated with cytogenetic (chromosomal) abnormalities in as many as 80% of individuals with the disease; however, no cytogenetic abnormality is specific. Myelodysplastic/myeloproliferative neoplasm, unclassifiable (MDS/ MPN-UC) (also known as mixed myeloproliferative/ myelodysplastic syndrome) also has no known cause.
|
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what research (or clinical trials) is being done for Hereditary Spastic Paraplegia ?
|
The NINDS supports research on genetic disorders such as HSP. More than 30 genes that are responsible for several forms of HSP have been identified, and many more will likely be identified in the future. These genes generally encode proteins that normally help maintain the function of axons in the spinal cord. Understanding how mutations of these genes cause HSP should lead to ways to prevent, treat, and cure HSP.
|
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] |
What is (are) Renal oncocytoma ?
|
Renal oncocytoma is a benign (noncancerous) growth of the kidney. They generally do not cause any signs or symptoms and are often discovered incidentally (by chance) while a person is undergoing diagnostic imaging for other conditions. Some people with renal oncocytoma will have abdominal or flank pain; blood in the urine; and/or an abdominal mass. Although these tumors can occur in people of all ages, they most commonly develop in men who are over age 50. The exact underlying cause of most isolated (single tumor affecting one kidney) renal oncocytomas is unknown; however, multiple and bilateral (affecting both kidneys) renal oncocytomas sometimes occur in people with certain genetic syndromes such as tuberous sclerosis complex and Birt-Hogg-Dube syndrome. Although many benign tumors do not require treatment unless they are causing unpleasant symptoms, it can be difficult to confidently differentiate a renal oncocytoma from renal cell carcinoma. Most affected people are, therefore, treated with surgery which allows for confirmation of the diagnosis.
|
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How to prevent Hearing Loss ?
|
Washing your hands frequently can help prevent upper respiratory infections, which can lead to an ear infection called otitis media. The ear infection otitis media can be a cause of long-term hearing loss. Also, ask your doctor about a yearly flu shot to help prevent flu-related ear infections. If you still get an ear infection, see a doctor immediately before it becomes more serious.
|
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What are the genetic changes related to familial pityriasis rubra pilaris ?
|
In most cases of pityriasis rubra pilaris, the cause of the condition is unknown. However, mutations in the CARD14 gene have been found to cause the familial form of the disorder in a few affected families. The CARD14 gene provides instructions for making a protein that turns on (activates) a group of interacting proteins known as nuclear factor-kappa-B (NF-B). NF-B regulates the activity of multiple genes, including genes that control the body's immune responses and inflammatory reactions. It also protects cells from certain signals that would otherwise cause them to self-destruct (undergo apoptosis). The CARD14 protein is found in many of the body's tissues, but it is particularly abundant in the skin. NF-B signaling appears to play an important role in regulating inflammation in the skin. Mutations in the CARD14 gene lead to overactivation of NF-B signaling, which triggers an abnormal inflammatory response. Researchers are working to determine how these changes lead to the specific features of familial pityriasis rubra pilaris.
|
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What are the treatments for warfarin sensitivity ?
|
These resources address the diagnosis or management of warfarin sensitivity: - Food and Drug Administration Medication Guide - MedlinePlus Drugs & Supplements: Warfarin - My46 Trait Profile - PharmGKB - WarfarinDosing.org 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) Mucolipidosis type 4 ?
|
Mucolipidosis type 4 is a metabolic condition that affects the body's ability to process certain carbohydrates and fats. As a result, these materials accumulate in cells leading to the various signs and symptoms of the condition. Most people with mucolipidosis type 4 develop severe psychomotor (mental and motor skills) delay by the end of the first year of life and visual impairment that worsens over time. Other common features of the condition include limited or absent speech; intellectual disability; hypotonia that gradually progresses to spasticity; problems controlling hand movements; impaired production of stomach acids; and iron deficiency. Approximately 5% of affected people have a mild form of the condition (known as atypical mucolipidosis type 4) which is associated with milder psychomotor delay and less severe eye abnormalities. Mucolipidosis type 4 is caused by changes (mutations) in the MCOLN1 gene and is inherited in an autosomal recessive manner. Treatment is based on the signs and symptoms present in each person.
|
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How many people are affected by congenital cataracts, facial dysmorphism, and neuropathy ?
|
The prevalence of CCFDN is unknown. The disorder has been identified in about 150 individuals of Romani ethnicity. Thus far, no affected individuals have been observed outside this community.
|
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What are the symptoms of Pulmonary edema of mountaineers ?
|
What are the signs and symptoms of Pulmonary edema of mountaineers? The Human Phenotype Ontology provides the following list of signs and symptoms for Pulmonary edema of mountaineers. 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) Autosomal dominant inheritance - Elevated pulmonary artery pressure - Pulmonary edema - 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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320,
7520,
390,
1846,
15
] |
How to diagnose Henoch-Schnlein Purpura ?
|
A diagnosis of HSP is suspected when a person has the characteristic rash and one of the following:
- abdominal pain - joint pain - antibody deposits on the skin - hematuria or proteinuria
Antibody deposits on the skin can confirm the diagnosis of HSP. These deposits can be detected using a skin biopsy, a procedure that involves taking a piece of skin tissue for examination with a microscope. A skin biopsy is performed by a health care provider in a hospital with little or no sedation and local anesthetic. The skin tissue is examined in a lab by a pathologista doctor who specializes in diagnosing diseases.
A kidney biopsy may also be needed. A kidney biopsy is performed by a health care provider in a hospital with light sedation and local anesthetic. The health care provider uses imaging techniques such as ultrasound or a computerized tomography scan to guide the biopsy needle into the organ. The kidney tissue is examined in a lab by a pathologist. The test can confirm diagnosis and be used to determine the extent of kidney involvement, which will help guide treatment decisions.
Hematuria and proteinuria are detected using urinalysis, which is testing of a urine sample. The urine sample is collected in a special container in a health care providers office or commercial facility and can be tested in the same location or sent to a lab for analysis. For the test, a nurse or technician places a strip of chemically treated paper, called a dipstick, into the urine sample. Patches on the dipstick change color when blood or protein are present in urine.
|
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] |
What are the symptoms of Multiple epiphyseal dysplasia 1 ?
|
What are the signs and symptoms of Multiple epiphyseal dysplasia 1? The Human Phenotype Ontology provides the following list of signs and symptoms for Multiple epiphyseal dysplasia 1. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the hip bone 50% Arthralgia 50% Brachydactyly syndrome 50% Micromelia 50% Genu valgum 7.5% Genu varum 7.5% Autosomal dominant inheritance - Avascular necrosis of the capital femoral epiphysis - Broad femoral neck - Delayed epiphyseal ossification - Disproportionate short-limb short stature - Epiphyseal dysplasia - Generalized joint laxity - Hip osteoarthritis - Irregular epiphyses - Irregular vertebral endplates - Joint stiffness - Limited hip movement - Mild short stature - Ovoid vertebral bodies - Short femoral neck - Short metacarpal - Short phalanx of finger - Small epiphyses - Waddling gait - 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) Creutzfeldt-Jakob Disease ?
|
Creutzfeldt-Jakob disease (CJD) is a rare, degenerative,fatal brain disorder. Typically, onset of symptoms occurs at about age 60. There are three major categories of CJD: sporadic (the most common form, in which people do not have any risk factors for the disease); hereditary (in which the person has a family member with the disease and tests positive for a genetic mutation), and acquired (in which the disease is transmitted by exposure to brain and nervous system tissue, usually through certain medical procedures. A form called variant CJD can be acquired by eating meat from cattle affected by a disease similar to CJD, called bovine spongiform encephalopathy (commonly called mad cow disease). Symptoms of CJD include problems with muscular coordination, personality changes including progressive and severe mental impairment, impaired vision that may lead to blindness, and involuntary muscle jerks called myoclonus. People eventually lose the ability to move and speak and enter a coma. Tests that help in the diagnosis of CJD include electroencephalography (which measures brain waves), detection of certain proteins in the fluid that surrounds the brain and spinal cord, and magnetic resonance imaging.. The first concern is to rule out treatable forms of dementia such as encephalitis or chronic meningitis. The only way to confirm a diagnosis of CJD is by brain biopsy or autopsy. In a brain biopsy, a neurosurgeon removes a small piece of tissue from the person's brain so that it can be examined by a neurologist. Because a correct diagnosis of CJD does not help the individual, a brain biopsy is discouraged unless it is need to rule out a treatable disorder. .
|
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What are the symptoms of Mousa Al din Al Nassar syndrome ?
|
What are the signs and symptoms of Mousa Al din Al Nassar syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Mousa Al din Al Nassar 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) Cataract 90% Corneal dystrophy 90% Hypertonia 90% Incoordination 90% Myopia 90% Aplasia/Hypoplasia of the cerebellum 50% Decreased antibody level in blood 50% EMG abnormality 50% Gait disturbance 50% Hemiplegia/hemiparesis 50% Optic atrophy 50% Autosomal recessive inheritance - Congenital cataract - Spastic ataxia - Spinocerebellar tract degeneration - 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) Horizontal gaze palsy with progressive scoliosis ?
|
Horizontal gaze palsy with progressive scoliosis (HGPPS) is a rare disorder that affects vision and also causes an abnormal curvature of the spine (scoliosis). People with this condition are unable to move their eyes side-to-side (horizontally) and must turn their head instead of moving their eyes to track moving objects. Scoliosis develops in infancy or childhood and worsens over time. Scoliosis can be painful and may interfere with movement so it is often treated with surgery early in life. HGPPS is caused by changes (mutations) in the ROBO3 gene and is inherited in an autosomal recessive manner. Treatment is based on the signs and symptoms present in each person.
|
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What are the symptoms of Arthrogryposis, distal, with hypopituitarism, intellectual disability and facial anomalies ?
|
What are the signs and symptoms of Arthrogryposis, distal, with hypopituitarism, intellectual disability and facial anomalies? The Human Phenotype Ontology provides the following list of signs and symptoms for Arthrogryposis, distal, with hypopituitarism, intellectual disability and facial anomalies. 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) Autosomal recessive inheritance - Camptodactyly of finger - Distal arthrogryposis - Full cheeks - Growth hormone deficiency - Hammertoe - Intellectual disability, progressive - Intellectual disability, severe - Square face - 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) erythromelalgia ?
|
Erythromelalgia is a condition characterized by episodes of pain, redness, and swelling in various parts of the body, particularly the hands and feet. These episodes are usually triggered by increased body temperature, which may be caused by exercise or entering a warm room. Ingesting alcohol or spicy foods may also trigger an episode. Wearing warm socks, tight shoes, or gloves can cause a pain episode so debilitating that it can impede everyday activities such as wearing shoes and walking. Pain episodes can prevent an affected person from going to school or work regularly. The signs and symptoms of erythromelalgia typically begin in childhood, although mildly affected individuals may have their first pain episode later in life. As individuals with erythromelalgia get older and the disease progresses, the hands and feet may be constantly red, and the affected areas can extend from the hands to the arms, shoulders, and face, and from the feet to the entire legs. Erythromelalgia is often 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 is (are) Hereditary spherocytosis ?
|
Hereditary spherocytosis is a condition characterized by hemolytic anemia (when red blood cells are destroyed earlier than normal). Signs and symptoms can range from mild to severe and may include pale skin, fatigue, anemia, jaundice, gallstones, and enlargement of the spleen. Some people with a severe form may have short stature, delayed sexual development, and skeletal abnormalities. The condition is caused by mutations in any of several genes, such as the ANK1, EPB42, SLC4A1, SPTA1, and SPTB genes. It is most commonly inherited in an autosomal dominant manner, but may be inherited in an autosomal recessive manner. There are different types of hereditary spherocytosis, which are distinguished by severity and genetic cause. Depending on severity, treatment may involve splenectomy, red cell transfusions, folic acid supplementation, and/or cholecystectomy.
|
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What to do for Monogenic Forms of Diabetes: Neonatal Diabetes Mellitus and Maturity-onset Diabetes of the Young ?
|
#NAME?
|
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Is Northern epilepsy 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) Gallstones ?
|
Your gallbladder is a pear-shaped organ under your liver. It stores bile, a fluid made by your liver to digest fat. As your stomach and intestines digest food, your gallbladder releases bile through a tube called the common bile duct. The duct connects your gallbladder and liver to your small intestine. Your gallbladder is most likely to give you trouble if something blocks the flow of bile through the bile ducts. That is usually a gallstone. Gallstones form when substances in bile harden. Gallstone attacks usually happen after you eat. Signs of a gallstone attack may include nausea, vomiting, or pain in the abdomen, back, or just under the right arm. Gallstones are most common among older adults, women, overweight people, Native Americans and Mexican Americans. Gallstones are often found during imaging tests for other health conditions. If you do not have symptoms, you usually do not need treatment. The most common treatment is removal of the gallbladder. Fortunately, you can live without a gallbladder. Bile has other ways to reach your small intestine. NIH: National Institute of Diabetes and Digestive and Kidney Diseases
|
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What are the symptoms of Familial hypocalciuric hypercalcemia type 2 ?
|
What are the signs and symptoms of Familial hypocalciuric hypercalcemia type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Familial hypocalciuric hypercalcemia 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) Nephrolithiasis 5% Peptic ulcer 5% Chondrocalcinosis - Hypercalcemia - Hypermagnesemia - Hypocalciuria - Multiple lipomas - Pancreatitis - Parathormone-independent increased renal tubular calcium reabsorption - Primary hyperparathyroidism - 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 harlequin ichthyosis ?
|
These resources address the diagnosis or management of harlequin ichthyosis: - Gene Review: Gene Review: Autosomal Recessive Congenital Ichthyosis - Genetic Testing Registry: Autosomal recessive congenital ichthyosis 4B 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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