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What causes Hemochromatosis ?
|
Primary Hemochromatosis
Inherited genetic defects cause primary hemochromatosis, and mutations in the HFE gene are associated with up to 90 percent of cases.1 The HFE gene helps regulate the amount of iron absorbed from food. The two known mutations of HFE are C282Y and H63D. C282Y defects are the most common cause of primary hemochromatosis.
People inherit two copies of the HFE geneone copy from each parent. Most people who inherit two copies of the HFE gene with the C282Y defect will have higher-than-average iron absorption. However, not all of these people will develop health problems associated with hemochromatosis. One recent study found that 31 percent of people with two copies of the C282Y defect developed health problems by their early fifties.2 Men who develop health problems from HFE defects typically develop them after age 40.1 Women who develop health problems from HFE defects typically develop them after menopause.1
People who inherit two H63D defects or one C282Y and one H63D defect may have higher-than-average iron absorption.3 However, they are unlikely to develop iron overload and organ damage.
Rare defects in other genes may also cause primary hemochromatosis. Mutations in the hemojuvelin or hepcidin genes cause juvenile hemochromatosis, a type of primary hemochromatosis. People with juvenile hemochromatosis typically develop severe iron overload and liver and heart damage between ages 15 and 30.
Secondary Hemochromatosis
Hemochromatosis that is not inherited is called secondary hemochromatosis. The most common cause of secondary hemochromatosis is frequent blood transfusions in people with severe anemia. Anemia is a condition in which red blood cells are fewer or smaller than normal, which means they carry less oxygen to the bodys cells. Types of anemia that may require frequent blood transfusions include
- congenital, or inherited, anemias such as sickle cell disease, thalassemia, and Fanconis syndrome - severe acquired anemias, which are not inherited, such as aplastic anemia and autoimmune hemolytic anemia
Liver diseasessuch as alcoholic liver disease, nonalcoholic steatohepatitis, and chronic hepatitis C infectionmay cause mild iron overload. However, this iron overload causes much less liver damage than the underlying liver disease causes.
Neonatal Hemochromatosis
Neonatal hemochromatosis is a rare disease characterized by liver failure and death in fetuses and newborns. Researchers are studying the causes of neonatal hemochromatosis and believe more than one factor may lead to the disease.
Experts previously considered neonatal hemochromatosis a type of primary hemochromatosis. However, recent studies suggest genetic defects that increase iron absorption do not cause this disease. Instead, the mothers immune system may produce antibodiesproteins made by the immune system to protect the body from foreign substances such as bacteria or virusesthat damage the liver of the fetus. Women who have had one child with neonatal hemochromatosis are at risk for having more children with the disease.4 Treating these women during pregnancy with intravenous (IV) immunoglobulina solution of antibodies from healthy peoplecan prevent fetal liver damage.4
Researchers supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) recently found that a combination of exchange transfusionremoving blood and replacing it with donor bloodand IV immunoglobulin is an effective treatment for babies born with neonatal hemochromatosis.5
|
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] |
Is Fuchs endothelial corneal dystrophy inherited ?
|
How is Fuchs endothelial corneal dystrophy inherited? The inheritance of Fuchs dystrophy is not straight forward. In some cases, Fuchs dystrophy appears to be inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. When this condition is caused by a mutation in the COL8A2 gene (which is the early-onset form of the disease), it is inherited in an autosomal dominant pattern. In addition, an autosomal dominant inheritance pattern is seen in some situations in which the condition is caused by changes in an unknown gene. However, in many cases, the inheritance pattern is unknown. Some cases result from new mutations in a gene and occur in people with no history of the disorder in their family. Due to the complex nature of the inheritance of this condition, we strongly recommend you discuss your concerns with a genetics professional.
|
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What are the genetic changes related to Tangier disease ?
|
Mutations in the ABCA1 gene cause Tangier disease. This gene provides instructions for making a protein that releases cholesterol and phospholipids from cells. These substances are used to make HDL, which transports them to the liver. Mutations in the ABCA1 gene prevent the release of cholesterol and phospholipids from cells. As a result, these substances accumulate within cells, causing certain body tissues to enlarge and the tonsils to acquire a yellowish-orange color. A buildup of cholesterol can be toxic to cells, leading to impaired cell function or cell death. In addition, the inability to transport cholesterol and phospholipids out of cells results in very low HDL levels, which increases the risk of cardiovascular disease. These combined factors cause the signs and symptoms of Tangier disease.
|
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] |
How to diagnose Parasites - Schistosomiasis ?
|
Stool or urine samples can be examined microscopically for parasite eggs (stool for S. mansoni or S. japonicum eggs and urine for S. haematobium eggs). The eggs tend to be passed intermittently and in small amounts and may not be detected, so it may be necessary to perform a blood (serologic) test.
More on: Resources for Health Professionals: Diagnosis
|
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How many people are affected by Niemann-Pick disease ?
|
Niemann-Pick disease types A and B is estimated to affect 1 in 250,000 individuals. Niemann-Pick disease type A occurs more frequently among individuals of Ashkenazi (eastern and central European) Jewish descent than in the general population. The incidence within the Ashkenazi population is approximately 1 in 40,000 individuals. Combined, Niemann-Pick disease types C1 and C2 are estimated to affect 1 in 150,000 individuals; however, type C1 is by far the more common type, accounting for 95 percent of cases. The disease occurs more frequently in people of French-Acadian descent in Nova Scotia. In Nova Scotia, a population of affected French-Acadians were previously designated as having Niemann-Pick disease type D, however, it was shown that these individuals have mutations in the gene associated with Niemann-Pick disease type C1.
|
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What is (are) Autoimmune pancreatitis ?
|
Autoimmune pancreatitis affects the pancreas, a gland behind the stomach and in front of the spine, and can also affect the bile ducts, salivary glands, kidneys, and lymph nodes. It is thought to occur when the immune system mistakenly begins to attack these healthy body tissues, glands, and organs. Common signs and symptoms include painless jaundice, weight loss, and noncancerous masses in the pancreas and other organs. Treatment often involves corticosteroids. The condition may recur following treatment, and require additional therapy.
|
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What is (are) Am I at Risk for Type 2 Diabetes? Taking Steps to Lower Your Risk of Getting Diabetes ?
|
Type 2 diabetes, formerly called adult-onset diabetes, is the most common type of diabetes. About 95 percent of people with diabetes have type 2. People can develop type 2 diabetes at any age, even during childhood. However, this type of diabetes develops most often in middle-aged and older people. People who are overweight and inactive are also more likely to develop type 2 diabetes.
In type 2 and other types of diabetes, you have too much glucose, also called sugar, in your blood. People with diabetes have problems converting food to energy. After a meal, food is broken down into glucose, which is carried by your blood to cells throughout your body. With the help of the hormone insulin, cells absorb glucose from your blood and use it for energy. Insulin is made in the pancreas, an organ located behind the stomach.
Type 2 diabetes usually begins with insulin resistance, a condition linked to excess weight in which your bodys cells do not use insulin properly. As a result, your body needs more insulin to help glucose enter cells. At first, your pancreas keeps up with the added demand by producing more insulin. But in time, your pancreas loses its ability to produce enough insulin, and blood glucose levels rise.
Over time, high blood glucose damages nerves and blood vessels, leading to problems such as heart disease, stroke, kidney disease, blindness, dental disease, and amputations. Other problems of diabetes may include increased risk of getting other diseases, loss of mobility with aging, depression, and pregnancy problems.
Treatment includes taking diabetes medicines, making wise food choices, being physically active on a regular basis, controlling blood pressure and cholesterol, and for some, taking aspirin daily.
|
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What are the treatments for Niemann-Pick disease ?
|
These resources address the diagnosis or management of Niemann-Pick disease: - Baby's First Test - Gene Review: Gene Review: Acid Sphingomyelinase Deficiency - Gene Review: Gene Review: Niemann-Pick Disease Type C - Genetic Testing Registry: Niemann-Pick disease type C1 - Genetic Testing Registry: Niemann-Pick disease type C2 - Genetic Testing Registry: Niemann-Pick disease, type A - Genetic Testing Registry: Niemann-Pick disease, type B - Genetic Testing Registry: Niemann-Pick disease, type C - Genetic Testing Registry: Niemann-Pick disease, type D - Genetic Testing Registry: Niemann-pick disease, intermediate, protracted neurovisceral - Genetic Testing Registry: Sphingomyelin/cholesterol lipidosis - MedlinePlus Encyclopedia: Niemann-Pick Disease These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What is (are) Dowling-Degos disease ?
|
Dowling-Degos disease is a skin condition characterized by a lacy or net-like (reticulate) pattern of abnormally dark skin coloring (hyperpigmentation), particularly in the body's folds and creases. These skin changes typically first appear in the armpits and groin area and can later spread to other skin folds such as the crook of the elbow and back of the knee. Less commonly, pigmentation changes can also occur on the wrist, back of the hand, face, scalp, scrotum (in males), and vulva (in females). These areas of hyperpigmentation do not darken with exposure to sunlight and cause no health problems. Individuals with Dowling-Degos disease may also have dark lesions on the face and back that resemble blackheads, red bumps around the mouth that resemble acne, or depressed or pitted scars on the face similar to acne scars but with no history of acne. Cysts within the hair follicle (pilar cysts) may develop, most commonly on the scalp. Rarely, affected individuals have patches of skin that are unusually light in color (hypopigmented). The pigmentation changes characteristic of Dowling-Degos disease typically begin in late childhood or in adolescence, although in some individuals, features of the condition do not appear until adulthood. New areas of hyperpigmentation tend to develop over time, and the other skin lesions tend to increase in number as well. While the skin changes caused by Dowling-Degos disease can be bothersome, they typically cause no health problems. A condition called Galli-Galli disease has signs and symptoms similar to those of Dowling-Degos disease. In addition to pigmentation changes, individuals with Galli-Galli disease also have a breakdown of cells in the outer layer of skin (acantholysis). Acantholysis can cause skin irritation and itchiness. These conditions used to be considered two separate disorders, but Galli-Galli disease and Dowling-Degos disease are now regarded as the same condition.
|
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What causes Cri du chat syndrome ?
|
What causes cri du chat syndrome? Cri du chat syndrome is caused by a deletion of the end of the short (p) arm of chromosome 5. This chromosomal change is written as 5p-. The size of the deletion varies among affected individuals but studies suggest that larger deletions tend to result in more severe intellectual disability and developmental delay than smaller deletions. The signs and symptoms of cri du chat syndrome are probably related to the loss of multiple genes on the short arm of chromosome 5. Researchers believe that the loss of a specific gene, CTNND2, is associated with severe intellectual disability in some people with this condition. They are working to determine how the loss of other genes in this region contributes to the characteristic features of cri du chat syndrome.
|
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How many people are affected by cystinosis ?
|
Cystinosis affects approximately 1 in 100,000 to 200,000 newborns worldwide. The incidence is higher in the province of Brittany, France, where the disorder affects 1 in 26,000 individuals.
|
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What are the treatments for SOX2 anophthalmia syndrome ?
|
These resources address the diagnosis or management of SOX2 anophthalmia syndrome: - Gene Review: Gene Review: SOX2-Related Eye Disorders - Genetic Testing Registry: Microphthalmia syndromic 3 - MedlinePlus Encyclopedia: Vision Problems 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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9776
] |
What causes Hypothyroidism ?
|
Hypothyroidism has several causes, including
- Hashimotos disease - thyroiditis, or inflammation of the thyroid - congenital hypothyroidism, or hypothyroidism that is present at birth - surgical removal of part or all of the thyroid - radiation treatment of the thyroid - some medications
Less commonly, hypothyroidism is caused by too much or too little iodine in the diet or by abnormalities of the pituitary gland.
Hashimotos Disease
Hashimotos disease, also called chronic lymphocytic thyroiditis, is the most common cause of hypothyroidism in the United States.1 Hashimotos disease is a form of chronic inflammation of the thyroid gland. Hashimotos disease is also an autoimmune disorder.
Normally, the immune system protects the body against foreign invaderssuch as viruses and bacteriathat can cause illness. But in autoimmune diseases, the immune system attacks the bodys own cells and organs. With Hashimotos disease, the immune system attacks the thyroid, causing inflammation and interfering with its ability to produce thyroid hormones.
More information is provided in the NIDDK health topic, Hashimotos Disease.
Thyroiditis
Thyroiditis causes stored thyroid hormone to leak out of the thyroid gland. At first, the leakage raises hormone levels in the blood, leading to hyperthyroidismwhen thyroid hormone levels are too highthat lasts for 1 or 2 months. Most people then develop hypothyroidism before the thyroid is completely healed.
Several types of thyroiditis can cause hyperthyroidism followed by hypothyroidism:
- Subacute thyroiditis. This condition involves painful inflammation and enlargement of the thyroid. Experts are not sure what causes subacute thyroiditis, but it may be related to a viral or bacterial infection. The condition usually goes away on its own in a few months. - Postpartum thyroiditis. This type of thyroiditis develops after a woman gives birth. For more information, see the section titled What happens with pregnancy and thyroid conditions? - Silent thyroiditis. This type of thyroiditis is called silent because it is painless, as is postpartum thyroiditis, even though the thyroid may be enlarged. Like postpartum thyroiditis, silent thyroiditis is probably an autoimmune condition and sometimes develops into permanent hypothyroidism.
Congenital Hypothyroidism
Some babies are born with a thyroid that is not fully developed or does not function properly. If untreated, congenital hypothyroidism can lead to mental retardation and growth failure. Early treatment can prevent these complications, so most newborns in the United States are screened for hypothyroidism.
Surgical Removal of the Thyroid
When part of the thyroid is removed, the remaining part may produce normal amounts of thyroid hormone, but some people who have this surgery develop hypothyroidism. Removal of the entire thyroid always results in hypothyroidism.
Part or all of the thyroid may be surgically removed as a treatment for
- hyperthyroidism - a large goiter, which is an enlarged thyroid that may cause the neck to appear swollen and can interfere with normal breathing and swallowing - thyroid nodules, which are noncancerous tumors, called adenomas, or lumps in the thyroid that can produce excess thyroid hormone - thyroid cancer
Radiation Treatment of the Thyroid
Radioactive iodine, a common treatment for hyperthyroidism, gradually destroys the cells of the thyroid. Most people who receive radioactive iodine treatment eventually develop hypothyroidism. People with Hodgkins disease, other lymphomas, and head or neck cancers are treated with radiation, which can also damage the thyroid.
Medications
Some drugs can interfere with thyroid hormone production and lead to hypothyroidism, including
- amiodarone, a heart medication - interferon alpha, a cancer medication - lithium, a bipolar disorder medication - interleukin-2, a kidney cancer medication
|
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] |
How many people are affected by autosomal recessive congenital stationary night blindness ?
|
Autosomal recessive congenital stationary night blindness is likely a rare disease; however, its prevalence is unknown.
|
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] |
What is (are) Turner syndrome ?
|
Turner syndrome is a chromosomal disorder that affects development in females. It is characterized by a person having one X chromosome in each cell (females without Turner syndrome have two X chromosomes in each cell). Signs and symptoms may include short stature; premature ovarian failure; a "webbed" neck; a low hairline at the back of the neck; and swelling (lymphedema) of the hands and feet. Some people with Turner syndrome have skeletal abnormalities, kidney problems, and/or a congenital heart defect. Most affected girls and women have normal intelligence, but some have developmental delays, learning disabilities, and/or behavior problems. Turner syndrome is typically not inherited, but it can be inherited in rare cases. Treatment may include growth hormone therapy for short stature and estrogen therapy to help stimulate sexual development. While most women with Turner syndrome are infertile, assisted reproductive techniques can help some women become pregnant.
|
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Is L1 syndrome inherited ?
|
This condition is inherited in an X-linked recessive pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation would have to occur in both copies of the gene to cause the disorder. Because it is unlikely that females will have two altered copies of this gene, males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
|
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What causes Trisomy 17 mosaicism ?
|
What causes trisomy 17 mosaicism? Trisomy 17 mosaicism can arise due to errors in cell division that occur after conception. For example, at the time of conception, the fetus may actually have trisomy 17 in all of its cells; however, during cell division, some of the cells lose the extra chromosome 17. Alternatively, the fetus may initially have had only two copies of chromosome 17, but due to errors in cell division some of the cells end up with an extra copy of chromosome 17. Either of these two scenarios result in trisomy 17 mosaicism. To read more about trisomy mosaicism, visit the following links from the Medical Genetics Department at the University of British Columbia in Canada. What is mosaicism? How does trisomy mosaicism occur?
|
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What is (are) spastic paraplegia type 3A ?
|
Spastic paraplegia type 3A is one of a group of genetic disorders known as hereditary spastic paraplegias. These disorders are characterized by muscle stiffness (spasticity) and weakness in the lower limbs (paraplegia). Hereditary spastic paraplegias are often divided into two types: pure and complex. The pure types involve only the lower limbs, while the complex types also involve other areas of the body; additional features can include changes in vision, changes in intellectual functioning, difficulty walking, and disturbances in nerve function (neuropathy). Spastic paraplegia type 3A is usually a pure hereditary spastic paraplegia, although a few complex cases have been reported. In addition to spasticity and weakness, which typically affect both legs equally, people with spastic paraplegia type 3A can also experience progressive muscle wasting (amyotrophy) in the lower limbs, reduced bladder control, an abnormal curvature of the spine (scoliosis), loss of sensation in the feet (peripheral neuropathy), or high arches of the feet (pes cavus). The signs and symptoms of spastic paraplegia type 3A usually appear before the age of 10; the average age of onset is 4 years. In some affected individuals the condition slowly worsens over time, sometimes leading to a need for walking support.
|
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What are the symptoms of Intellectual deficit - short stature - hypertelorism ?
|
What are the signs and symptoms of Intellectual deficit - short stature - hypertelorism? The Human Phenotype Ontology provides the following list of signs and symptoms for Intellectual deficit - short stature - hypertelorism. 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) Anteverted nares 90% Broad forehead 90% Frontal bossing 90% Hypertelorism 90% Hypoplasia of the zygomatic bone 90% Clinodactyly of the 5th finger 50% Cognitive impairment 50% Long philtrum 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 are the treatments for Uterine Sarcoma ?
|
Key Points
- There are different types of treatment for patients with uterine sarcoma. - Four types of standard treatment are used: - Surgery - Radiation therapy - Chemotherapy - Hormone therapy - New types of treatment are being tested in clinical trials. - Patients may want to think about taking part in a clinical trial. - Patients can enter clinical trials before, during, or after starting their cancer treatment. - Follow-up tests may be needed.
There are different types of treatment for patients with uterine sarcoma.
Different types of treatments are available for patients with uterine sarcoma. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.
Four types of standard treatment are used:
Surgery Surgery is the most common treatment for uterine sarcoma, as described in the Stages of Uterine Sarcoma section of this summary. Even if the doctor removes all the cancer that can be seen at the time of the surgery, some patients may be given chemotherapy or radiation therapy after surgery to kill any cancer cells that are left. Treatment given after the surgery, to lower the risk that the cancer will come back, is called adjuvant therapy. Radiation therapy Radiation therapy is a cancer treatment that uses high energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy: - External radiation therapy uses a machine outside the body to send radiation toward the cancer. - Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. The way the radiation therapy is given depends on the type and stage of the cancer being treated. External and internal radiation therapy are used to treat uterine sarcoma, and may also be used as palliative therapy to relieve symptoms and improve quality of life. Chemotherapy Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). The way the chemotherapy is given depends on the type and stage of the cancer being treated. Hormone therapy Hormone therapy is a cancer treatment that removes hormones or blocks their action and stops cancer cells from growing. Hormones are substances produced by glands in the body and circulated in the bloodstream. Some hormones can cause certain cancers to grow. If tests show the cancer cells have places where hormones can attach (receptors), drugs, surgery, or radiation therapy is used to reduce the production of hormones or block them from working.
New types of treatment are being tested in clinical trials.
Information about clinical trials is available from the NCI website.
Patients may want to think about taking part in a clinical trial.
For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment. Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment. Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.
Patients can enter clinical trials before, during, or after starting their cancer treatment.
Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment. Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
Follow-up tests may be needed.
Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests. Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.
Treatment Options by Stage
Stage I Uterine Sarcoma
Treatment of stage I uterine sarcoma may include the following: - Surgery (total abdominal hysterectomy, bilateral salpingo-oophorectomy, and lymphadenectomy). - Surgery followed by radiation therapy to the pelvis. - Surgery followed by chemotherapy. Check the list of NCI-supported cancer clinical trials that are now accepting patients with stage I uterine sarcoma. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.
Stage II Uterine Sarcoma
Treatment of stage II uterine sarcoma may include the following: - Surgery (total abdominal hysterectomy, bilateral salpingo-oophorectomy, and lymphadenectomy). - Surgery followed by radiation therapy to the pelvis. - Surgery followed by chemotherapy. Check the list of NCI-supported cancer clinical trials that are now accepting patients with stage II uterine sarcoma. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.
Stage III Uterine Sarcoma
Treatment of stage III uterine sarcoma may include the following: - Surgery (total abdominal hysterectomy, bilateral salpingo-oophorectomy, and lymphadenectomy). - A clinical trial of surgery followed by radiation therapy to the pelvis. - A clinical trial of surgery followed by chemotherapy. Check the list of NCI-supported cancer clinical trials that are now accepting patients with stage III uterine sarcoma. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.
Stage IV Uterine Sarcoma
There is no standard treatment for patients with stage IV uterine sarcoma. Treatment may include a clinical trial using chemotherapy. Check the list of NCI-supported cancer clinical trials that are now accepting patients with stage IV uterine sarcoma. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.
|
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How many people are affected by fish-eye disease ?
|
Fish-eye disease is a rare disorder. Approximately 30 cases have been reported in the medical literature.
|
[
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What are the symptoms of Chondrosarcoma ?
|
What are the signs and symptoms of Chondrosarcoma? The Human Phenotype Ontology provides the following list of signs and symptoms for Chondrosarcoma. 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 - Chondrosarcoma - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
How to diagnose Danon disease ?
|
Is genetic testing available for Danon disease? Yes. GeneTests lists laboratories offering clinical genetic testing for Danon disease. Clinical genetic tests are ordered to help diagnose a person or family and to aid in decisions regarding medical care or reproductive issues. Talk to your health care provider or a genetic professional to learn more about your testing options. Click on the link above to view a list of testing laboratories.
|
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How to prevent Crimean-Congo Hemorrhagic Fever (CCHF) ?
|
Agricultural workers and others working with animals should use insect repellent on exposed skin and clothing. Insect repellants containing DEET (N, N-diethyl-m-toluamide) are the most effective in warding off ticks. Wearing gloves and other protective clothing is recommended. Individuals should also avoid contact with the blood and body fluids of livestock or humans who show symptoms of infection. It is important for healthcare workers to use proper infection control precautions to prevent occupational exposure.
An inactivated, mouse-brain derived vaccine against CCHF has been developed and is used on a small scale in Eastern Europe. However, there is no safe and effective vaccine currently available for human use. Further research is needed to develop these potential vaccines as well as determine the efficacy of different treatment options including ribavirin and other antiviral drugs.
|
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What is (are) Stroke ?
|
Atherosclerosis, also known as hardening of the arteries, is the most common blood vessel disease. It is caused by the buildup of fatty deposits in the arteries, and is a risk factor for stroke.
|
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How many people are affected by Axenfeld-Rieger syndrome ?
|
Axenfeld-Rieger syndrome has an estimated prevalence of 1 in 200,000 people.
|
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What is (are) familial idiopathic basal ganglia calcification ?
|
Familial idiopathic basal ganglia calcification (FIBGC, formerly known as Fahr disease) is a condition characterized by abnormal deposits of calcium (calcification) in the brain. These calcium deposits typically occur in the basal ganglia, which are structures deep within the brain that help start and control movement; however, other brain regions can also be affected. The signs and symptoms of FIBGC include movement disorders and psychiatric or behavioral difficulties. These problems begin in adulthood, usually in a person's thirties. The movement difficulties experienced by people with FIBGC include involuntary tensing of various muscles (dystonia), problems coordinating movements (ataxia), and uncontrollable movements of the limbs (choreoathetosis). Affected individuals often have seizures as well. The psychiatric and behavioral problems include difficulty concentrating, memory loss, changes in personality, a distorted view of reality (psychosis), and decline in intellectual function (dementia). An estimated 20 to 30 percent of people with FIBGC have one of these psychiatric disorders. The severity of this condition varies among affected individuals; some people have no symptoms related to the brain calcification, whereas other people have significant movement and psychiatric problems.
|
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What are the genetic changes related to Poland syndrome ?
|
The cause of Poland syndrome is unknown. Researchers have suggested that it may result from a disruption of blood flow during development before birth. This disruption is thought to occur at about the sixth week of embryonic development and affect blood vessels that will become the subclavian and vertebral arteries on each side of the body. The arteries normally supply blood to embryonic tissues that give rise to the chest wall and hand on their respective sides. Variations in the site and extent of the disruption may explain the range of signs and symptoms that occur in Poland syndrome. Abnormality of an embryonic structure called the apical ectodermal ridge, which helps direct early limb development, may also be involved in this disorder. Rare cases of Poland syndrome are thought to be caused by a genetic change that can be passed down in families, but no related genes have been identified.
|
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Is 3MC syndrome inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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How to diagnose Graves' Disease ?
|
Health care providers can sometimes diagnose Graves disease based only on a physical examination and a medical history. Blood tests and other diagnostic tests, such as the following, then confirm the diagnosis.
TSH test. The ultrasensitive TSH test is usually the first test performed. This test detects even tiny amounts of TSH in the blood and is the most accurate measure of thyroid activity available.
T3 and T4 test. Another blood test used to diagnose Graves disease measures T3 and T4 levels. In making a diagnosis, health care providers look for below-normal levels of TSH, normal to elevated levels of T4, and elevated levels of T3.
Because the combination of low TSH and high T3 and T4 can occur with other thyroid problems, health care providers may order other tests to finalize the diagnosis. The following two tests use small, safe doses of radioactive iodine because the thyroid uses iodine to make thyroid hormone.
Radioactive iodine uptake test. This test measures the amount of iodine the thyroid collects from the bloodstream. High levels of iodine uptake can indicate Graves disease.
Thyroid scan. This scan shows how and where iodine is distributed in the thyroid. With Graves disease the entire thyroid is involved, so the iodine shows up throughout the gland. Other causes of hyperthyroidism such as nodulessmall lumps in the glandshow a different pattern of iodine distribution.
TSI test. Health care providers may also recommend the TSI test, although this test usually isnt necessary to diagnose Graves disease. This test, also called a TSH antibody test, measures the level of TSI in the blood. Most people with Graves disease have this antibody, but people whose hyperthyroidism is caused by other conditions do not.
More information about testing for thyroid problems is provided in the NIDDK health topic, Thyroid Tests.
|
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Is Prader-Willi syndrome inherited ?
|
Most cases of Prader-Willi syndrome are not inherited, particularly those caused by a deletion in the paternal chromosome 15 or by maternal uniparental disomy. These genetic changes occur as random events during the formation of reproductive cells (eggs and sperm) or in early embryonic development. Affected people typically have no history of the disorder in their family. Rarely, a genetic change responsible for Prader-Willi syndrome can be inherited. For example, it is possible for a genetic change that abnormally inactivates genes on the paternal chromosome 15 to be passed from one generation to the next.
|
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How to prevent Anemia ?
|
You might be able to prevent repeat episodes of some types of anemia, especially those caused by lack of iron or vitamins. Dietary changes or supplements can prevent these types of anemia from occurring again.
Treating anemia's underlying cause may prevent the condition (or prevent repeat episodes). For example, if medicine is causing your anemia, your doctor may prescribe another type of medicine.
To prevent anemia from getting worse, tell your doctor about all of your signs and symptoms. Talk with your doctor about the tests you may need and follow your treatment plan.
You can't prevent some types of inherited anemia, such as sickle cell anemia. If you have an inherited anemia, talk with your doctor about treatment and ongoing care.
|
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] |
How many people are affected by hereditary antithrombin deficiency ?
|
Hereditary antithrombin deficiency is estimated to occur in about 1 in 2,000 to 3,000 individuals. Of people who have experienced an abnormal blood clot, about 1 in 20 to 200 have hereditary antithrombin deficiency.
|
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Who is at risk for Kawasaki Disease? ?
|
Kawasaki disease affects children of all races and ages and both genders. It occurs most often in children of Asian and Pacific Island descent.
The disease is more likely to affect boys than girls. Most cases occur in children younger than 5 years old. Kawasaki disease is rare in children older than 8.
|
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Do you have information about X-Rays
|
Summary : X-rays are a type of radiation called electromagnetic waves. X-ray imaging creates pictures of the inside of your body. The images show the parts of your body in different shades of black and white. This is because different tissues absorb different amounts of radiation. Calcium in bones absorbs x-rays the most, so bones look white. Fat and other soft tissues absorb less, and look gray. Air absorbs the least, so lungs look black. The most familiar use of x-rays is checking for broken bones, but x-rays are also used in other ways. For example, chest x-rays can spot pneumonia. Mammograms use x-rays to look for breast cancer. When you have an x-ray, you may wear a lead apron to protect certain parts of your body. The amount of radiation you get from an x-ray is small. For example, a chest x-ray gives out a radiation dose similar to the amount of radiation you're naturally exposed to from the environment over 10 days.
|
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] |
What are the treatments for Frontal fibrosing alopecia ?
|
How might frontal fibrosing alopecia be treated? Unfortunately, there is currently no cure for frontal fibrosing alopecia (FFA). Because the hair loss associated with this condition is thought to be caused by inflammation of hair follicles, treatment often involves using anti-inflammatory medications or ointments, such as corticosteroids or hydroxychloroquine (brand name Plaquenil), to reduce inflammation and suppress the body's immune system. Medications that block the production of the male hormone 5-alpha reductase have been reported to stop further hair loss in some women. Researchers continue to question whether treatment is effective or if hair loss in FFA just stops naturally.
|
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Is Fryns syndrome inherited ?
|
How is Fryns syndrome inherited? Although the exact cause of Fryns syndrome is not currently known (and no disease-causing gene has yet been identified), it is thought to be genetic because it tends to "run in families" and has features common to other genetic disorders. It appears to be inherited in an autosomal recessive manner. This means that both copies of the disease-causing gene in each cell of the body (one copy inherited from each parent) have mutations. The parents of an affected individual are referred to as carriers, who typically do not show signs or symptoms of the condition. When two carriers of an autosomal recessive condition have children, each child has a 25% (1 in 4) risk to have the condition, a 50% (1 in 2) risk to be a carrier like each of the parents, and a 25% chance to not have the condition and not be a carrier.
|
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What are the symptoms of Hydrops, Ectopic calcification, Moth-eaten skeletal dysplasia ?
|
What are the signs and symptoms of Hydrops, Ectopic calcification, Moth-eaten skeletal dysplasia? The diagnostic findings of HEM (hydrops fetalis, severe micromelia, and ectopic calcification) have been present in all cases reported in the medical literature thus far. The following are several of the other signs and symptoms that have been reported in some patients with HEM : Polydactyly (presence of more than 5 fingers on the hands or 5 toes on the feet) Reduced number of ribs Omphalocele Intestinal malformation Abnormal fingernails Less than normal number of lobes in the lung (hypolobated lungs) Cystic hygroma The Human Phenotype Ontology provides the following list of signs and symptoms for Hydrops, Ectopic calcification, Moth-eaten skeletal dysplasia. 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 bone mineral density 90% Abnormality of erythrocytes 90% Abnormality of pelvic girdle bone morphology 90% Abnormality of the ribs 90% Brachydactyly syndrome 90% Limb undergrowth 90% Lymphedema 90% Short stature 90% Decreased skull ossification 50% Malar flattening 50% Narrow chest 50% Skull defect 50% Toxemia of pregnancy 50% 11 pairs of ribs - Abnormal foot bone ossification - Abnormal joint morphology - Abnormal lung lobation - Abnormal ossification involving the femoral head and neck - Abnormal pelvis bone ossification - Abnormality of cholesterol metabolism - Abnormality of the calcaneus - Abnormality of the scapula - Abnormality of the vertebral spinous processes - Absent or minimally ossified vertebral bodies - Absent toenail - Anterior rib punctate calcifications - Autosomal recessive inheritance - Barrel-shaped chest - Bone marrow hypocellularity - Bowing of the long bones - Broad palm - Cardiomegaly - Cystic hygroma - Depressed nasal bridge - Diaphyseal thickening - Disproportionate short-limb short stature - Epiphyseal stippling - Extramedullary hematopoiesis - Flared metaphysis - Hepatic calcification - Hepatomegaly - Hepatosplenomegaly - High forehead - Horizontal sacrum - Hypertelorism - Hypoplasia of the maxilla - Hypoplastic fingernail - Hypoplastic vertebral bodies - Intestinal malrotation - Laryngeal calcification - Lethal skeletal dysplasia - Long clavicles - Low-set ears - Macrocephaly - Mesomelia - Metaphyseal cupping - Micromelia - Misalignment of teeth - Multiple prenatal fractures - Neonatal death - Nonimmune hydrops fetalis - Omphalocele - Pancreatic islet-cell hyperplasia - Patchy variation in bone mineral density - Pleural effusion - Polyhydramnios - Postaxial foot polydactyly - Postaxial hand polydactyly - Pulmonary hypoplasia - Punctate vertebral calcifications - Rhizomelia - Sandal gap - Sclerosis of skull base - Severe hydrops fetalis - Short diaphyses - Short phalanx of finger - Short ribs - Sternal punctate calcifications - Stillbirth - Supernumerary vertebral ossification centers - Tracheal calcification - Ulnar deviation of the hand - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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] |
What causes Stroke ?
|
Ischemic Stroke and Transient Ischemic Attack
An ischemic stroke or transient ischemic attack (TIA) occurs if an artery that supplies oxygen-rich blood to the brain becomes blocked. Many medical conditions can increase the risk of ischemic stroke or TIA.
For example, atherosclerosis (ath-er-o-skler-O-sis) is a disease in which a fatty substance called plaque builds up on the inner walls of the arteries. Plaque hardens and narrows the arteries, which limits the flow of blood to tissues and organs (such as the heart and brain).
Plaque in an artery can crack or rupture (break open). Blood platelets (PLATE-lets), which are disc-shaped cell fragments, stick to the site of the plaque injury and clump together to form blood clots. These clots can partly or fully block an artery.
Plaque can build up in any artery in the body, including arteries in the heart, brain, and neck. The two main arteries on each side of the neck are called the carotid (ka-ROT-id) arteries. These arteries supply oxygen-rich blood to the brain, face, scalp, and neck.
When plaque builds up in the carotid arteries, the condition is called carotid artery disease. Carotid artery disease causes many of the ischemic strokes and TIAs that occur in the United States.
An embolic stroke (a type of ischemic stroke) or TIA also can occur if a blood clot or piece of plaque breaks away from the wall of an artery. The clot or plaque can travel through the bloodstream and get stuck in one of the brains arteries. This stops blood flow through the artery and damages brain cells.
Heart conditions and blood disorders also can cause blood clots that can lead to a stroke or TIA. For example, atrial fibrillation (A-tre-al fi-bri-LA-shun), or AF, is a common cause of embolic stroke.
In AF, the upper chambers of the heart contract in a very fast and irregular way. As a result, some blood pools in the heart. The pooling increases the risk of blood clots forming in the heart chambers.
An ischemic stroke or TIA also can occur because of lesions caused by atherosclerosis. These lesions may form in the small arteries of the brain, and they can block blood flow to the brain.
Hemorrhagic Stroke
Sudden bleeding in the brain can cause a hemorrhagic stroke. The bleeding causes swelling of the brain and increased pressure in the skull. The swelling and pressure damage brain cells and tissues.
Examples of conditions that can cause a hemorrhagic stroke include high blood pressure, aneurysms, and arteriovenous (ar-TEER-e-o-VE-nus) malformations (AVMs).
"Blood pressure" is the force of blood pushing against the walls of the arteries as the heart pumps blood. If blood pressure rises and stays high over time, it can damage the body in many ways.
Aneurysms are balloon-like bulges in an artery that can stretch and burst. AVMs are tangles of faulty arteries and veins that can rupture within the brain. High blood pressure can increase the risk of hemorrhagic stroke in people who have aneurysms or AVMs.
|
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] |
Is Crouzon syndrome inherited ?
|
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.
|
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] |
What is (are) Acanthamoeba - Granulomatous Amebic Encephalitis (GAE); Keratitis ?
|
Acanthamoeba is a microscopic, free-living ameba (single-celled living organism) commonly found in the environment that can cause rare, but severe, illness. Acanthamoeba causes three main types of illness involving the eye (Acanthamoeba keratitis), the brain and spinal cord (Granulomatous Encephalitis), and infections that can spread throughout the entire body (disseminated infection).
|
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What is (are) warfarin sensitivity ?
|
Warfarin sensitivity is a condition in which individuals have a low tolerance for the drug warfarin. Warfarin is an anticoagulant, which means that it thins the blood, preventing blood clots from forming. Warfarin is often prescribed to prevent blood clots in people with heart valve disease who have replacement heart valves, people with an irregular heart beat (atrial fibrillation), or those with a history of heart attack, stroke, or a prior blood clot in the deep veins of the arms or legs (deep vein thrombosis). Many people with warfarin sensitivity take longer than normal to break down (metabolize) warfarin, so the medication is in their body longer than usual and they require lower doses. These individuals are classified as "slow metabolizers" of warfarin. Other people with warfarin sensitivity do not need as much drug to prevent clots because their clot forming process is already slower than average and can be inhibited by low warfarin doses. If people with warfarin sensitivity take the average dose (or more) of warfarin, they are at risk of an overdose, which can cause abnormal bleeding in the brain, gastrointestinal tract, or other tissues, and may lead to serious health problems or death. Warfarin sensitivity does not appear to cause any health problems other than those associated with warfarin drug treatment.
|
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What causes Congenital laryngeal palsy ?
|
What is the cause of congenital laryngeal paralysis? The cause is often unknown (idiopathic). Congenital bilateral vocal cord paralysis may occur as a result of the immaturity of the nerve or muscle (neuromuscular) or as a result of central nervous system problems, such as Arnold-Chiari syndrome, cerebral palsy, hydrocephalus, myelomeningocele, spine bifida, hypoxia (lack of oxygen in the blood), or bleeding. In other cases the vocal cords' paralysis is acquired. For example, a birth trauma may cause tension in the neck and lead to bilateral vocal cord paralyses that can last 6-9 months. Other causes may include: Surgical Trauma Malignancies Delayed endotracheal intubation Neurological diseases Strokes Choking Diseases that result in inflammation of the vocal cords or the laryngeal cartilage (Wegener's granulomatosis, sarcoidosis or polychondritis, gout, syphilis and tuberculosis (resulting in mechanical attachment of the vocal cords) Diabetes mellitus, which may lead to a neuropathy resulting in vocal cord paralysis Gastroesophageal reflux (GER). The unilateral paralysis is usually idiopathic but may also be secondary to mediastinal lesions, such as tumors or vascular malformations or iatrogenic (caused by damage to the left recurrent laryngeal nerve during surgery in this area, such as heart surgery). It may also result from problems of the mechanical structures of the larynx as the cricoarytenoid joint. The following online resources provide more information on the cause of congenital laryngeal paralysis: American Academy of Otolaringology Medscape Reference - Congenital Malformations of the Larynx
|
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What are the treatments for Ovarian small cell carcinoma ?
|
What treatments are available for ovarian small cell carcinoma? Ovarian small cell carcinoma is often treated with surgery and chemotherapy. Radiation therapy may also be used in some cases. Because this tumor is derived from the primitive germ cells (eggs) of the ovary, it is often treated with a chemotherapy regimen similar to what is used to treat ovarian germ cell tumors. Specifically, platinum and etoposide based chemotherapy is typically used to treat ovarian small cell carcinoma.
|
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What is (are) Alcohol Use and Older Adults ?
|
Blood alcohol concentration (BAC) measures the percentage of ethanolthe chemical name for alcohol in alcoholic beveragesin a persons blood. As you drink, you increase your blood alcohol concentration (BAC) level. The higher the BAC, the more impaired a person is. In all states, it is against the law for people to drive if their blood alcohol concentration is above .08. The effects of increased blood alcohol levels can include - reduced inhibitions - slurred speech - motor impairment - confusion - memory problems - concentration problems - coma - breathing problems - death. reduced inhibitions slurred speech motor impairment confusion memory problems concentration problems coma breathing problems death. Learn more about the risks of alcohol overdose.
|
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Is Schwartz-Jampel syndrome inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What are the genetic changes related to Smith-Lemli-Opitz syndrome ?
|
Mutations in the DHCR7 gene cause Smith-Lemli-Opitz syndrome. The DHCR7 gene provides instructions for making an enzyme called 7-dehydrocholesterol reductase. This enzyme is responsible for the final step in the production of cholesterol. Cholesterol is a waxy, fat-like substance that is produced in the body and obtained from foods that come from animals (particularly egg yolks, meat, poultry, fish, and dairy products). Cholesterol is necessary for normal embryonic development and has important functions both before and after birth. It is a structural component of cell membranes and the protective substance covering nerve cells (myelin). Additionally, cholesterol plays a role in the production of certain hormones and digestive acids. Mutations in the DHCR7 gene reduce or eliminate the activity of 7-dehydrocholesterol reductase, preventing cells from producing enough cholesterol. A lack of this enzyme also allows potentially toxic byproducts of cholesterol production to build up in the blood, nervous system, and other tissues. The combination of low cholesterol levels and an accumulation of other substances likely disrupts the growth and development of many body systems. It is not known, however, how this disturbance in cholesterol production leads to the specific features of Smith-Lemli-Opitz syndrome.
|
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What are the genetic changes related to common variable immune deficiency ?
|
CVID is believed to result from mutations in genes that are involved in the development and function of immune system cells called B cells. B cells are specialized white blood cells that help protect the body against infection. When B cells mature, they produce special proteins called antibodies (also known as immunoglobulins). These proteins attach to foreign particles, marking them for destruction. Mutations in the genes associated with CVID result in dysfunctional B cells that cannot make sufficient amounts of antibodies. People with CVID have a shortage (deficiency) of specific antibodies called immunoglobulin G (IgG), immunoglobulin A (IgA), and immunoglobulin M (IgM). Some have a deficiency of all three antibodies, while others are lacking only IgG and IgA. A shortage of these antibodies makes it difficult for people with this disorder to fight off infections. Abnormal and deficient immune responses over time likely contribute to the increased cancer risk. In addition, vaccines for diseases such as measles and influenza do not provide protection for people with CVID because they cannot produce an antibody response. Mutations in at least 10 genes have been associated with CVID. Approximately 10 percent of affected individuals have mutations in the TNFRSF13B gene. The protein produced from this gene plays a role in the survival and maturation of B cells and in the production of antibodies. TNFRSF13B gene mutations disrupt B cell function and antibody production, leading to immune dysfunction. Other genes associated with CVID are also involved in the function and maturation of immune system cells, particularly of B cells; mutations in these genes account for only a small percentage of cases. In most cases of CVID, the cause is unknown, but it is likely a combination of genetic and environmental factors.
|
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What are the treatments for branchio-oculo-facial syndrome ?
|
These resources address the diagnosis or management of branchio-oculo-facial syndrome: - Gene Review: Gene Review: Branchiooculofacial Syndrome - Genetic Testing Registry: Branchiooculofacial syndrome - MedlinePlus Encyclopedia: Cleft Lip and Palate These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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How to prevent What I need to know about Gestational Diabetes ?
|
You can do a lot to prevent or delay type 2 diabetes by making these lifestyle changes:
- Reach and stay at a healthy weight. Try to reach your prepregnancy weight 6 to 12 months after your baby is born. Then, if you still weigh too much, work to lose at least 5 to 7 percent of your body weight and keep it off. For example, if you weigh 200 pounds, losing 10 to 14 pounds can greatly reduce your chance of getting diabetes. - Be physically active for at least 30 minutes most days of the week. - Follow a healthy eating plan. Eat more grains, fruits, and vegetables. Cut down on fat and calories. Your health care team can help you design a meal plan. - Ask your doctor if you should take the diabetes medicine metformin. Metformin can lower your chances of having type 2 diabetes, especially if you are younger and heavier and have prediabetes or if you have had gestational diabetes.
These changes can help you enjoy a longer, healthier life. Your health care team can give you information and support to help you make these changes.
By delaying or preventing type 2 diabetes, you will also lower your chances of having heart and blood vessel disease and other problems as you get older.
Talk with your doctor if you are thinking about having another baby. For the safety of your baby, your blood glucose needs to be at healthy levels before you get pregnant again. Your doctor can help ensure you are ready for your next child.
|
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Is Albright's hereditary osteodystrophy inherited ?
|
How is progressive osseous heteroplasia 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. People normally inherit one copy of each gene from their mother and one copy from their father. For most genes, both copies are active, or "turned on," in all cells. For a small subset of genes, however, only one of the two copies is active. For some of these genes, only the copy inherited from a person's father (the paternal copy) is active, while for other genes, only the copy inherited from a person's mother (the maternal copy) is active. These differences in gene activation based on the gene's parent of origin are caused by a phenomenon called genomic imprinting. The GNAS gene has a complex genomic imprinting pattern. In some cells of the body the maternal copy of the gene is active, while in others the paternal copy is active. Progressive osseous heteroplasia occurs when mutations affect the paternal copy of the gene. Thus, progressive heteroplasia is usually inherited from the father.
|
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What is (are) Metabolic Syndrome ?
|
Metabolicsyndrome is the name for a group of risk factors that raises your risk for heart disease and other health problems, such as diabetes and stroke.
The term "metabolic" refers to the biochemical processes involved in the body's normal functioning. Risk factors are traits, conditions, or habits that increase your chance of developing a disease.
In this article, "heart disease" refers to coronary heart disease (CHD). CHD is a condition in which a waxy substance called plaque builds up inside the coronary (heart) arteries.
Plaque hardens and narrows the arteries, reducing blood flow to your heart muscle. This can lead to chest pain, a heart attack, heart damage, or even death.
Metabolic Risk Factors
The five conditions described below are metabolic risk factors. You can have any one of these risk factors by itself, but they tend to occur together. You must have at least three metabolic risk factors to be diagnosed with metabolic syndrome.
A large waistline. This also is called abdominal obesity or "having an apple shape." Excess fat in the stomach area is a greater risk factor for heart disease than excess fat in other parts of the body, such as on the hips.
A high triglyceride level (or you're on medicine to treat high triglycerides). Triglycerides are a type of fat found in the blood.
A low HDL cholesterol level (or you're on medicine to treat low HDL cholesterol). HDL sometimes is called "good" cholesterol. This is because it helps remove cholesterol from your arteries. A low HDL cholesterol level raises your risk for heart disease.
High blood pressure (or you're on medicine to treat high blood pressure). Blood pressure is the force of blood pushing against the walls of your arteries as your heart pumps blood. If this pressure rises and stays high over time, it can damage your heart and lead to plaque buildup.
High fasting blood sugar (or you're on medicine to treat high blood sugar). Mildly high blood sugar may be an early sign of diabetes.
Overview
Your risk for heart disease, diabetes, and stroke increases with the number of metabolic risk factors you have. The risk of having metabolic syndrome is closely linked to overweight and obesity and a lack of physical activity.
Insulin resistance also may increase your risk for metabolic syndrome. Insulin resistance is a condition in which the body cant use its insulin properly. Insulin is a hormone that helps move blood sugar into cells where its used for energy. Insulin resistance can lead to high blood sugar levels, and its closely linked to overweight and obesity.Genetics (ethnicity and family history) and older age are other factors that may play a role in causing metabolic syndrome.
Outlook
Metabolic syndrome is becoming more common due to a rise in obesity rates among adults. In the future, metabolic syndrome may overtake smoking as the leading risk factor for heart disease.
It is possible to prevent or delay metabolic syndrome, mainly with lifestyle changes. A healthy lifestyle is a lifelong commitment. Successfully controlling metabolic syndrome requires long-term effort and teamwork with your health care providers.
|
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] |
What is (are) Parkinson disease ?
|
Parkinson disease is a progressive disorder of the nervous system. The disorder affects several regions of the brain, especially an area called the substantia nigra that controls balance and movement. Often the first symptom of Parkinson disease is trembling or shaking (tremor) of a limb, especially when the body is at rest. Typically, the tremor begins on one side of the body, usually in one hand. Tremors can also affect the arms, legs, feet, and face. Other characteristic symptoms of Parkinson disease include rigidity or stiffness of the limbs and torso, slow movement (bradykinesia) or an inability to move (akinesia), and impaired balance and coordination (postural instability). These symptoms worsen slowly over time. Parkinson disease can also affect emotions and thinking ability (cognition). Some affected individuals develop psychiatric conditions such as depression and visual hallucinations. People with Parkinson disease also have an increased risk of developing dementia, which is a decline in intellectual functions including judgment and memory. Generally, Parkinson disease that begins after age 50 is called late-onset disease. The condition is described as early-onset disease if signs and symptoms begin before age 50. Early-onset cases that begin before age 20 are sometimes referred to as juvenile-onset Parkinson disease.
|
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What to do for Prevent diabetes problems: Keep your kidneys healthy ?
|
Your dietitian or doctor may suggest a special eating plan for you. You may have to avoid a diet high in protein, fat, sodium, and potassium.
- Cut back on protein, especially animal products such as meat. Damaged kidneys may fail to remove protein waste products from your blood. Diets high in protein make your kidneys work harder and fail sooner. - Avoid a high-fat diet. High-fat diets are high in cholesterol. Cholesterol is a type of fat found in your bodys cells, blood, and many foods. Your body needs some cholesterol to work the right way. For example, your body uses cholesterol to make certain essential hormones and maintain nerve function. However, your body makes all the cholesterol it needs. If you often eat foods that are high in cholesterol, or if high cholesterol runs in your family, extra cholesterol in your blood can build up over time in the walls of your blood vessels and arteries. High blood cholesterol can lead to heart disease and stroke, some of the biggest health problems for people with diabetes. - Avoid high-sodium foods. Sodium is a mineral found in salt and other foods. High levels of sodium may raise your blood pressure. Some high-sodium foods include canned food, frozen dinners, and hot dogs. The amount of sodium is listed on the food label, so you can see which foods have the highest levels. Try to limit your sodium to less than a teaspoon a day, or about 2,300 milligrams (mg) a day. If you have high blood pressure or are African American, middle-aged, or older, aim for no more than 1,500 mg of sodium per day. Ask your doctor or your dietitian about how much sodium you can have. - Ask your doctor about the amount of potassium you need. Potassium is a mineral that helps your heartbeat stay regular and muscles work right. Healthy kidneys keep the right amount of potassium in your body. However, if you have severe kidney damage, high levels of potassium may cause an abnormal heart rhythm or even make your heart stop, called cardiac arrest. Some high-potassium foods include apricots, bananas, oranges, and potatoes.
More information about healthy eating and kidney disease is provided in the NIDDK health topics: - Eat Right to Feel Right on Hemodialysis - Nutrition for Advanced Chronic Kidney Disease in Adults - Nutrition for Early Chronic Kidney Disease in Adults - What I need to know about Eating and Diabetes
|
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What is (are) Absence of Tibia ?
|
Absence of tibia is a rare birth defect that is characterized by deficiency of the tibia (the shinbone) with other bones of the lower leg relatively intact. The condition may affect one or both legs. Some cases are isolated birth defects, while others are associated with a variety of skeletal and other malformations. It can also be a part of a recognized syndrome such as Werner's syndrome, tibial hemimelia-polysyndactyly-triphalangeal thumb syndrome, and CHARGE syndrome. The underlying cause is generally unknown. Although most isolated cases occur sporadically in people with no family history of the condition, absence of the tibia can rarely affect more than one family member. Treatment varies based on the severity of the condition, but generally involves surgery (i.e. amputation or reconstructive surgery with a prosthesis adapted to growth).
|
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] |
What is (are) Ovarian, Fallopian Tube, and Primary Peritoneal Cancer ?
|
Key Points
- Ovarian, fallopian tube, and primary peritoneal cancers are diseases in which malignant (cancer) cells form in the ovaries, fallopian tubes, or peritoneum. - In the United States, ovarian cancer is the fifth leading cause of cancer death in women. - Different factors increase or decrease the risk of getting ovarian, fallopian tube, and primary peritoneal cancer.
Ovarian, fallopian tube, and primary peritoneal cancers are diseases in which malignant (cancer) cells form in the ovaries, fallopian tubes, or peritoneum.
The ovaries are a pair of organs in the female reproductive system. They are located in the pelvis, one on each side of the uterus (the hollow, pear-shaped organ where a fetus grows). Each ovary is about the size and shape of an almond. The ovaries produce eggs and female hormones (chemicals that control the way certain cells or organs function). The fallopian tubes are a pair of long, slender tubes, one on each side of the uterus. Eggs pass from the ovaries, through the fallopian tubes, to the uterus. Cancer sometimes begins at the end of the fallopian tube near the ovary and spreads to the ovary. The peritoneum is the tissue that lines the abdominal wall and covers organs in the abdomen. Primary peritoneal cancer is cancer that forms in the peritoneum and has not spread there from another part of the body. Cancer sometimes begins in the peritoneum and spreads to the ovary. Ovarian epithelial cancer, fallopian tube cancer, and primary peritoneal cancer form in the same type of tissue. Studies of screening tests look at these cancers together. See the following PDQ summaries for more information about ovarian, fallopian tube, and primary peritoneal cancers: - Ovarian, Fallopian Tube, and Primary Peritoneal Cancer Prevention - Genetics of Breast and Gynecologic Cancers - Ovarian Epithelial, Fallopian Tube, and Primary Peritoneal Cancer Treatment - Ovarian Germ Cell Tumors Treatment - Ovarian Low Malignant Potential Tumors Treatment
In the United States, ovarian cancer is the fifth leading cause of cancer death in women.
Ovarian cancer is also the leading cause of death from cancer of the female reproductive system. Over the last 20 years, the number of new cases of ovarian cancer has gone down slightly in white women and in black women. Since 2005, the number of deaths from ovarian cancer also decreased slightly in white and black women.
|
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] |
What causes Human T-cell leukemia virus type 1 ?
|
What causes human T-cell leukemia virus, type 1? Human T-cell leukemia virus, type 1 (HTLV-1) occurs when a person is infected by the human T-cell leukemia retrovirus. HTLV-1 is spread by blood transfusions, sexual contact and sharing needles. It can also be spread from mother to child during birth or breast-feeding. It is unclear why some people with HTLV-1 develop adult T-cell leukemia (ATL), HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) or other medical conditions, while others remain asymptomatic (show no signs or symptoms) their entire lives.
|
[
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How to prevent Kidney Stones in Children ?
|
To prevent kidney stones, health care providers and their patients must understand what is causing the stones to form. Especially in children with suspected metabolic abnormalities or with recurrent stones, a 24-hour urine collection is obtained to measure daily urine volume and to determine if any underlying mineral abnormality is making a child more likely to form stones. Based on the analysis of the collected urine, the treatment can be individualized to address a metabolic problem.
In all circumstances, children should drink plenty of fluids to keep the urine diluted and flush away substances that could form kidney stones. Urine should be almost clear.
|
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What are the treatments for Dystonias ?
|
No one treatment has been found to be universally effective. Instead, doctors use a variety of therapies (medications, surgery, and other treatments such as physical therapy, splinting, stress management, and biofeedback) aimed at reducing or eliminating muscle spasms and pain. Since response to drugs varies among individuals and even in the same person over time, the most effective therapy is often individualized.
|
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What is (are) Diverticulosis and Diverticulitis ?
|
Diverticula are small pouches that bulge outward through the colon, or large intestine. If you have these pouches, you have a condition called diverticulosis. It becomes more common as people age. About half of all people over age 60 have it. Doctors believe the main cause is a low-fiber diet. Most people with diverticulosis don't have symptoms. Sometimes it causes mild cramps, bloating or constipation. Diverticulosis is often found through tests ordered for something else. For example, it is often found during a colonoscopy to screen for cancer. A high-fiber diet and mild pain reliever will often relieve symptoms. If the pouches become inflamed or infected, you have a condition called diverticulitis. The most common symptom is abdominal pain, usually on the left side. You may also have fever, nausea, vomiting, chills, cramping, and constipation. In serious cases, diverticulitis can lead to bleeding, tears, or blockages. Your doctor will do a physical exam and imaging tests to diagnose it. Treatment may include antibiotics, pain relievers, and a liquid diet. A serious case may require a hospital stay or surgery. NIH: National Institute of Diabetes and Digestive and Kidney Diseases
|
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What is (are) Pheochromocytoma ?
|
Pheochromocytoma is a rare tumor that usually starts in the cells of one of your adrenal glands. Although they are usually benign, pheochromocytomas often cause the adrenal gland to make too many hormones. This can lead to high blood pressure and cause symptoms such as - Headaches - Sweating - Pounding of the heart - Being shaky - Being extremely pale Sometimes pheochromocytoma is part of another condition called multiple endocrine neoplasia syndrome (MEN). People with MEN often have other cancers and other problems involving hormones. Doctors use lab tests and imaging tests to diagnose it. Surgery is the most common treatment. Other options include radiation therapy, chemotherapy, and targeted therapy. Targeted therapy uses substances that attack cancer cells without harming normal cells. NIH: National Cancer Institute
|
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What are the symptoms of Split hand/foot malformation X-linked ?
|
What are the signs and symptoms of Split hand/foot malformation X-linked? The Human Phenotype Ontology provides the following list of signs and symptoms for Split hand/foot malformation X-linked. 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) Finger syndactyly - Short metacarpal - Short phalanx of finger - Split foot - Split hand - X-linked inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) Solitary Kidney ?
|
When a person has only one kidney or one working kidney, this kidney is called a solitary kidney. The three main causes of a solitary kidney are
- birth defects. People with kidney agenesis are born with only one kidney. People born with kidney dysplasia have both kidneys; however, one kidney does not function. Many people with kidney agenesis or kidney dysplasia do not discover that they have a solitary kidney until they have an x ray, an ultrasound, or surgery for an unrelated condition. - surgical removal of a kidney. Some people must have a kidney removed to treat cancer or another disease or injury. When a kidney is removed surgically due to disease or for donation, both the kidney and ureter are removed. - kidney donation. A growing number of people are donating a kidney to be transplanted into a family member or friend whose kidneys have failed.
In general, people with a solitary kidney lead full, healthy lives. However, some people are more likely to develop kidney disease.
|
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Is Book syndrome inherited ?
|
How is Book syndrome inherited? To our knowledge, Book syndrome has only been reported in one, large Swedish family (25 cases in 4 generations) and in one other isolated case. In the Swedish family, the syndrome was inherited in an autosomal dominant manner. In autosomal dominant inheritance, having a mutation in only one copy of the responsible gene is enough to cause signs and symptoms of the condition. When a person with an autosomal dominant condition has children, each child has a 50% (1 in 2) risk to inherit the mutated copy of the gene.
|
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What are the genetic changes related to porphyria ?
|
Each form of porphyria results from mutations in one of these genes: ALAD, ALAS2, CPOX, FECH, HMBS, PPOX, UROD, or UROS. The genes related to porphyria provide instructions for making the enzymes needed to produce heme. Mutations in most of these genes reduce enzyme activity, which limits the amount of heme the body can produce. As a result, compounds called porphyrins and porphyrin precursors, which are formed during the process of heme production, can build up abnormally in the liver and other organs. When these substances accumulate in the skin and interact with sunlight, they cause the cutaneous forms of porphyria. The acute forms of the disease occur when porphyrins and porphyrin precursors build up in and damage the nervous system. One type of porphyria, porphyria cutanea tarda, results from both genetic and nongenetic factors. About 20 percent of cases are related to mutations in the UROD gene. The remaining cases are not associated with UROD gene mutations and are classified as sporadic. Many factors contribute to the development of porphyria cutanea tarda. These include an increased amount of iron in the liver, alcohol consumption, smoking, hepatitis C or HIV infection, or certain hormones. Mutations in the HFE gene (which cause an iron overload disorder called hemochromatosis) are also associated with porphyria cutanea tarda. Other, as-yet-unidentified genetic factors may also play a role in this form of porphyria.
|
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What causes Leukonychia totalis ?
|
What causes leukonychia totalis? Leukonychia totalis (also called total leukonychia) is thought to be due to abnormal keratinization (conversion into keratin) of the nail plate. Keratin is a protein that is a major component of the epidermis (outer layer of skin), hair, nails, and horny tissues. The condition is usually inherited, following either an autosomal dominant or autosomal recessive inheritance pattern. These inherited forms can be caused by mutations in the PLCD1 gene. In some cases, leukonychia occurs in association with other underlying abnormalities or syndromes. Conditions that have been reported include palmoplantar keratoderma; certain types of cysts; severe keratosis pilaris; pili torti; hypotrichosis (lack of hair growth); onychorrhexis (brittle nails); koilonychia (spoon-shaped nails); Bart-Pumphrey syndrome; and Buschkell-Gorlin syndrome, when it occurs with sebaceous cysts and kidney stones. It has also reportedly been associated with typhoid fever, leprosy, cirrhosis, nail biting, trichinosis, and cytotoxic drugs (drugs that are toxic to cells). In a few cases, the cause of leukonychia is unknown (idiopathic).
|
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What causes Mowat-Wilson syndrome ?
|
What causes Mowat-Wilson syndrome? Mowat-Wilson syndrome is caused by mutations in the ZEB2 (also known as ZFHX1B or SIP-1) gene. This gene provides instructions for making a protein that plays a critical role in the formation of many organs and tissues before birth. It is a transcription factor, which means that it attaches (binds) to specific regions of DNA and helps control the activity of particular genes. Researchers believe that ZEB2 protein is involved in the development of tissues that give rise to the nervous system, digestive tract, facial features, heart, and other organs. Mowat-Wilson syndrome almost always results from the loss of one working copy of the ZEB2 gene in each cell. In some cases, the entire gene is deleted. In other cases, mutations within the gene lead to the production of an abnormally short, nonfunctional version of the ZEB2 protein. A shortage of this protein disrupts the normal development of many organs and tissues, which causes the varied signs and symptoms of Mowat-Wilson syndrome.
|
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What are the symptoms of 1q44 microdeletion syndrome ?
|
What are the signs and symptoms of 1q44 microdeletion syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for 1q44 microdeletion 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) Cognitive impairment 90% Muscular hypotonia 90% Neurological speech impairment 90% Seizures 90% Thin vermilion border 90% Abnormality of the cardiac septa 50% Abnormality of the philtrum 50% Aplasia/Hypoplasia of the corpus callosum 50% Hypertelorism 50% Microcephaly 50% Short stature 50% Strabismus 50% Telecanthus 50% Upslanted palpebral fissure 50% Ventriculomegaly 50% Abnormality of the palate 7.5% Displacement of the external urethral meatus 7.5% Frontal bossing 7.5% High forehead 7.5% Hydrocephalus 7.5% Intestinal malrotation 7.5% Narrow forehead 7.5% Optic atrophy 7.5% Preauricular skin tag 7.5% Prominent metopic ridge 7.5% Renal hypoplasia/aplasia 7.5% Scoliosis 7.5% Synophrys 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 Hypophosphatasia ?
|
What are the signs and symptoms of Hypophosphatasia? The signs and symptoms of hypophosphatasia vary widely and can appear anywhere from before birth to adulthood. The most severe forms of the disorder tend to occur before birth and in early infancy. Hypophosphatasia weakens and softens the bones, causing skeletal abnormalities similar to another childhood bone disorder called rickets. Affected infants are born with short limbs, an abnormally shaped chest, and soft skull bones. Additional complications in infancy include poor feeding and a failure to gain weight, respiratory problems, and high levels of calcium in the blood (hypercalcemia), which can lead to recurrent vomiting and kidney problems. These complications are life-threatening in some cases. The forms of hypophosphatasia that appear in childhood or adulthood are typically less severe than those that appear in infancy. Early loss of primary (baby) teeth is one of the first signs of the condition in children. Affected children may have short stature with bowed legs or knock knees, enlarged wrist and ankle joints, and an abnormal skull shape. Adult forms of hypophosphatasia are characterized by a softening of the bones known as osteomalacia. In adults, recurrent fractures in the foot and thigh bones can lead to chronic pain. Affected adults may lose their secondary (adult) teeth prematurely and are at increased risk for joint pain and inflammation. The mildest form of this condition, called odontohypophosphatasia, only affects the teeth. People with this disorder typically experience abnormal tooth development and premature tooth loss, but do not have the skeletal abnormalities seen in other forms of hypophosphatasia. The Human Phenotype Ontology provides the following list of signs and symptoms for Hypophosphatasia. 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 metaphyses 90% Abnormality of the ribs 90% Abnormality of the teeth 90% Bowing of the long bones 90% Craniosynostosis 90% Emphysema 90% Narrow chest 90% Sacrococcygeal pilonidal abnormality 90% Short stature 90% Anemia 50% Behavioral abnormality 50% Hypercalcemia 50% Muscular hypotonia 50% Recurrent fractures 50% Respiratory insufficiency 50% Seizures 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 are the symptoms of Lip and Oral Cavity Cancer ?
|
Signs of lip and oral cavity cancer include a sore or lump on the lips or in the mouth. These and other signs and symptoms may be caused by lip and oral cavity cancer or by other conditions. Check with your doctor if you have any of the following: - A sore on the lip or in the mouth that does not heal. - A lump or thickening on the lips or gums or in the mouth. - A white or red patch on the gums, tongue, or lining of the mouth. - Bleeding, pain, or numbness in the lip or mouth. - Change in voice. - Loose teeth or dentures that no longer fit well. - Trouble chewing or swallowing or moving the tongue or jaw. - Swelling of jaw. - Sore throat or feeling that something is caught in the throat. Lip and oral cavity cancer may not have any symptoms and is sometimes found during a regular dental exam.
|
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What are the symptoms of Thyroid cancer, follicular ?
|
What are the signs and symptoms of Thyroid cancer, follicular? The Human Phenotype Ontology provides the following list of signs and symptoms for Thyroid cancer, follicular. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of metabolism/homeostasis - Autosomal dominant inheritance - Follicular thyroid carcinoma - 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) SOX2 anophthalmia syndrome ?
|
SOX2 anophthalmia syndrome is a rare disorder characterized by abnormal development of the eyes and other parts of the body. People with SOX2 anophthalmia syndrome are usually born without eyeballs (anophthalmia), although some individuals have small eyes (microphthalmia). The term anophthalmia is often used interchangeably with severe microphthalmia because individuals with no visible eyeballs typically have some remaining eye tissue. These eye problems can cause significant vision loss. While both eyes are usually affected in SOX2 anophthalmia syndrome, one eye may be more affected than the other. Individuals with SOX2 anophthalmia syndrome may also have seizures, brain abnormalities, slow growth, delayed development of motor skills (such as walking), and mild to severe learning disabilities. Some people with this condition are born with a blocked esophagus (esophageal atresia), which is often accompanied by an abnormal connection between the esophagus and the trachea (tracheoesophageal fistula). Genital abnormalities have been described in affected individuals, especially males. Male genital abnormalities include undescended testes (cryptorchidism) and an unusually small penis (micropenis).
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What are the genetic changes related to genitopatellar syndrome ?
|
Genitopatellar syndrome is caused by mutations in the KAT6B gene. This gene provides instructions for making a type of enzyme called a histone acetyltransferase. These enzymes modify histones, which are structural proteins that attach (bind) to DNA and give chromosomes their shape. By adding a small molecule called an acetyl group to histones, histone acetyltransferases control the activity of certain genes. Little is known about the function of the histone acetyltransferase produced from the KAT6B gene. It appears to regulate genes that are important for early development, including development of the skeleton and nervous system. The mutations that cause genitopatellar syndrome occur near the end of the KAT6B gene and lead to the production of a shortened histone acetyltransferase enzyme. Researchers suspect that the shortened enzyme may function differently than the full-length version, altering the regulation of various genes during early development. However, it is unclear how these changes lead to the specific features of genitopatellar syndrome.
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What are the symptoms of Pseudopelade of Brocq ?
|
What are the signs and symptoms of Pseudopelade of Brocq? The Human Phenotype Ontology provides the following list of signs and symptoms for Pseudopelade of Brocq. 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) Alopecia 90% Hypertrichosis 90% Lichenification 90% Skin ulcer 50% Abnormality of the nail 7.5% Aplasia/Hypoplasia of the eyebrow 7.5% Cheilitis 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 is (are) Kidney Failure: Eat Right to Feel Right on Hemodialysis ?
|
Phosphorus is a mineral found in many foods. If you have too much phosphorus in your blood, it pulls calcium from your bones. Losing calcium will make your bones weak and likely to break. Also, too much phosphorus may make your skin itch. Foods like milk and cheese, dried beans, peas, colas, nuts, and peanut butter are high in phosphorus. Usually, people on dialysis are limited to 1/2 cup of milk per day. The renal dietitian will give you more specific information regarding phosphorus.
You probably will need to take a phosphate binder like Renagel, PhosLo, Tums, or calcium carbonate to control the phosphorus in your blood between dialysis sessions. These medications act like sponges to soak up, or bind, phosphorus while it is in the stomach. Because it is bound, the phosphorus does not get into the blood. Instead, it is passed out of the body in the stool.
|
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How many people are affected by McLeod neuroacanthocytosis syndrome ?
|
McLeod neuroacanthocytosis syndrome is rare; approximately 150 cases have been reported worldwide.
|
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What is (are) Kuskokwim syndrome ?
|
Kuskokwim syndrome is characterized by joint deformities called contractures that restrict the movement of affected joints. This condition has been found only in a population of native Alaskans known as Yup'ik Eskimos, who live in and around a region of southwest Alaska known as the Kuskokwim River Delta. In Kuskokwim syndrome, contractures most commonly affect the knees, ankles, and elbows, although other joints, particularly of the lower body, can be affected. The contractures are usually present at birth and worsen during childhood. They tend to stabilize after childhood, and they remain throughout life. Some individuals with this condition have other bone abnormalities, most commonly affecting the spine, pelvis, and feet. Affected individuals can develop an inward curve of the lower back (lordosis), a spine that curves to the side (scoliosis), wedge-shaped spinal bones, or an abnormality of the collarbones (clavicles) described as clubbing. Affected individuals are typically shorter than their peers and they may have an abnormally large head (macrocephaly).
|
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What are the genetic changes related to primary myelofibrosis ?
|
Mutations in the JAK2, MPL, CALR, and TET2 genes are associated with most cases of primary myelofibrosis. The JAK2 and MPL genes provide instructions for making proteins that promote the growth and division (proliferation) of blood cells. The CALR gene provides instructions for making a protein with multiple functions, including ensuring the proper folding of newly formed proteins and maintaining the correct levels of stored calcium in cells. The TET2 gene provides instructions for making a protein whose function is unknown. The proteins produced from the JAK2 and MPL genes are both part of a signaling pathway called the JAK/STAT pathway, which transmits chemical signals from outside the cell to the cell's nucleus. The protein produced from the MPL gene, called thrombopoietin receptor, turns on (activates) the pathway, and the JAK2 protein transmits signals after activation. Through the JAK/STAT pathway, these two proteins promote the proliferation of blood cells, particularly a type of blood cell known as a megakaryocyte. Mutations in either the JAK2 gene or the MPL gene that are associated with primary myelofibrosis lead to overactivation of the JAK/STAT pathway. The abnormal activation of JAK/STAT signaling leads to overproduction of abnormal megakaryocytes, and these megakaryocytes stimulate another type of cell to release collagen. Collagen is a protein that normally provides structural support for the cells in the bone marrow. However, in primary myelofibrosis, the excess collagen forms scar tissue in the bone marrow. Although mutations in the CALR gene and the TET2 gene are relatively common in primary myelofibrosis, it is unclear how these mutations are involved in the development of the condition. Some people with primary myelofibrosis do not have a mutation in any of the known genes associated with this condition. Researchers are working to identify other genes that may be involved in the condition.
|
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] |
What are the treatments for Intrahepatic cholangiocarcinoma ?
|
How might intrahepatic cholangiocarcinoma be treated? Can it be cured? Surgery to completely remove the bile duct and tumor is the only option that can possibly lead to a cure for patients. The type of operation will depend on the size and location of the cancer. For cases of intrahepatic cancers that cannot be surgically removed, a liver transplantation may be an option. In some cases, a liver transplant might even cure the cancer. Finally, radiation and chemotherapy are also treatment options available for intrahepatic cholangiocarcioma either in addition to surgery or on their own.
|
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What is (are) Satoyoshi syndrome ?
|
Satoyoshi syndrome is a rare condition characterized by progressive, painful, intermittent muscle spasms, diarrhea or unusual malabsorption, amenorrhea, alopecia universalis, short stature, and skeletal abnormalities. Progressive painful intermittent muscle spasms usually start between 6 to 15 years of age. Alopecia universalis also appears around age 10. About half of affected individuals experience malabsorption, specifically of carbohydrates. The skeletal abnormalities may be secondary to muscle spasms. The main endocrine disorder is primary amenorrhea. All cases have apparently been sporadic, even when occurring in large families. The exact cause is unknown; but some researchers have speculated that Satoyoshi syndrome is an autoimmune disorder.
|
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Is spondylocostal dysostosis inherited ?
|
Spondylocostal dysostosis can have different inheritance patterns. Types 1, 2, 3, and 4 are 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. AD spondylocostal dysostosis is inherited in an autosomal dominant pattern. Autosomal dominant inheritance means that one copy of an altered gene in each cell is sufficient to cause the disorder, although in these cases no causative genes have been identified. The signs and symptoms of spondylocostal dysostosis are typically more severe with autosomal recessive inheritance.
|
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Is Hallermann-Streiff syndrome inherited ?
|
How is Hallermann-Streiff syndrome inherited? The majority of cases of Hallermann-Streiff syndrome appear to be sporadic (occurring in individuals with no history of the condition in the family). There have been reports of affected individuals having multiple, unaffected children. Although some have reported it appears to be inherited in an autosomal recessive manner in a small number of cases, others have argued that there is little evidence for this being a recessively inherited disorder. Therefore, the mode of inheritance of the condition remains unclear.
|
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What is (are) abdominal wall defect ?
|
An abdominal wall defect is an opening in the abdomen through which various abdominal organs can protrude. This opening varies in size and can usually be diagnosed early in fetal development, typically between the tenth and fourteenth weeks of pregnancy. There are two main types of abdominal wall defects: omphalocele and gastroschisis. Omphalocele is an opening in the center of the abdominal wall where the umbilical cord meets the abdomen. Organs (typically the intestines, stomach, and liver) protrude through the opening into the umbilical cord and are covered by the same protective membrane that covers the umbilical cord. Gastroschisis is a defect in the abdominal wall, usually to the right of the umbilical cord, through which the large and small intestines protrude (although other organs may sometimes bulge out). There is no membrane covering the exposed organs in gastroschisis. Fetuses with omphalocele may grow slowly before birth (intrauterine growth retardation) and they may be born prematurely. Individuals with omphalocele frequently have multiple birth defects, such as a congenital heart defect. Additionally, underdevelopment of the lungs is often associated with omphalocele because the abdominal organs normally provide a framework for chest wall growth. When those organs are misplaced, the chest wall does not form properly, providing a smaller than normal space for the lungs to develop. As a result, many infants with omphalocele have respiratory insufficiency and may need to be supported with a machine to help them breathe (mechanical ventilation). Rarely, affected individuals who have breathing problems in infancy experience recurrent lung infections or asthma later in life. Affected infants often have gastrointestinal problems including a backflow of stomach acids into the esophagus (gastroesophageal reflux) and feeding difficulty; these problems can persist even after treatment of omphalocele. Large omphaloceles or those associated with multiple additional health problems are more often associated with fetal death than cases in which omphalocele occurs alone (isolated). Omphalocele is a feature of many genetic syndromes. Nearly half of individuals with omphalocele have a condition caused by an extra copy of one of the chromosomes in each of their cells (trisomy). Up to one-third of people born with omphalocele have a genetic condition called Beckwith-Wiedemann syndrome. Affected individuals may have additional signs and symptoms associated with these genetic conditions. Individuals who have gastroschisis rarely have other birth defects and seldom have chromosome abnormalities or a genetic condition. Most affected individuals experience intrauterine growth retardation and are small at birth; many affected infants are born prematurely. With gastroschisis, the protruding organs are not covered by a protective membrane and are susceptible to damage due to direct contact with amniotic fluid in the womb. Components of the amniotic fluid may trigger immune responses and inflammatory reactions against the intestines that can damage the tissue. Constriction around exposed organs at the abdominal wall opening late in fetal development may also contribute to organ injury. Intestinal damage causes impairment of the muscle contractions that move food through the digestive tract (peristalsis) in most children with gastroschisis. In these individuals, peristalsis usually improves in a few months and intestinal muscle contractions normalize. Rarely, children with gastroschisis have a narrowing or absence of a portion of intestine (intestinal atresia) or twisting of the intestine. After birth, these intestinal malformations can lead to problems with digestive function, further loss of intestinal tissue, and a condition called short bowel syndrome that occurs when areas of the small intestine are missing, causing dehydration and poor absorption of nutrients. Depending on the severity of the condition, intravenous feedings (parenteral nutrition) may be required. The health of an individual with gastroschisis depends largely on how damaged his or her intestine was before birth. When the abdominal wall defect is repaired and normal intestinal function is recovered, the vast majority of affected individuals have no health problems related to the repaired defect later in life.
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452,
642,
1786,
3237,
2905,
281,
253,
33172,
7071,
1996,
275,
1495,
15
] |
What is the outlook for Behcet's Disease ?
|
Behcet's disease is a lifelong disorder that comes and goes. Permanent remission of symptoms has not been reported.
|
[
1276,
310,
253,
29338,
323,
2325,
31728,
292,
434,
18742,
3736,
4678,
31728,
292,
434,
2728,
310,
247,
36536,
8984,
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3249,
285,
4566,
15,
367,
47605,
31701,
273,
5917,
556,
417,
644,
2361,
15
] |
[
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1
] |
[
1276,
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323,
2325,
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285,
4566,
15,
367,
47605,
31701,
273,
5917,
556,
417,
644,
2361,
15
] |
How many people are affected by Wilson disease ?
|
Wilson disease is a rare disorder that affects approximately 1 in 30,000 individuals.
|
[
2347,
1142,
952,
403,
5876,
407,
10520,
2728,
3736,
39440,
2728,
310,
247,
7520,
8984,
326,
11852,
5512,
337,
275,
1884,
13,
933,
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15
] |
[
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1
] |
[
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326,
11852,
5512,
337,
275,
1884,
13,
933,
4292,
15
] |
What are the treatments for renal coloboma syndrome ?
|
These resources address the diagnosis or management of renal coloboma syndrome: - Gene Review: Gene Review: Renal Coloboma Syndrome - Genetic Testing Registry: Renal coloboma syndrome 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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] |
[
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1,
1,
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1,
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1,
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] |
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9776
] |
What are the genetic changes related to familial hypobetalipoproteinemia ?
|
Most cases of FHBL are caused by mutations in the APOB gene. This gene provides instructions for making two versions of the apolipoprotein B protein: a short version called apolipoprotein B-48 and a longer version known as apolipoprotein B-100. Both of these proteins are components of lipoproteins, which transport fats and cholesterol in the blood. Most APOB gene mutations that lead to FHBL cause both versions of apolipoprotein B to be abnormally short. The severity of the condition largely depends on the length of these two versions of apolipoprotein B. Severely shortened versions cannot partner with lipoproteins and transport fats and cholesterol. Proteins that are only slightly shortened retain some function but partner less effectively with lipoproteins. Generally, the signs and symptoms of FHBL are worse if both versions of apolipoprotein B are severely shortened. Mild or no signs and symptoms result when the proteins are only slightly shortened. All of these protein changes lead to a reduction of functional apolipoprotein B. As a result, the transportation of dietary fats and cholesterol is decreased or absent. A decrease in fat transport reduces the body's ability to absorb fats and fat-soluble vitamins from the diet. Although APOB gene mutations are responsible for most cases of FHBL, mutations in a few other genes account for a small number of cases. Some people with FHBL do not have identified mutations in any of these genes. Changes in other, unidentified genes are likely involved in this condition.
|
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3206,
275,
436,
1617,
15
] |
[
1,
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What are the symptoms of Leri Weill dyschondrosteosis ?
|
What are the signs and symptoms of Leri Weill dyschondrosteosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Leri Weill dyschondrosteosis. 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 femur 90% Abnormality of the hip bone 90% Abnormality of the humeroulnar joint 90% Abnormality of the humerus 90% Abnormality of the metacarpal bones 90% Abnormality of the metaphyses 90% Abnormality of the tibia 90% Abnormality of the ulna 90% Anonychia 90% Aplasia/Hypoplasia of the radius 90% Aplastic/hypoplastic toenail 90% Arthralgia 90% Bone pain 90% Brachydactyly syndrome 90% Clinodactyly of the 5th finger 90% Cone-shaped epiphysis 90% Depressed nasal bridge 90% Exostoses 90% Genu varum 90% Limitation of joint mobility 90% Madelung deformity 90% Micromelia 90% Patellar aplasia 90% Short stature 90% Abnormality of calvarial morphology 50% Elbow dislocation 50% Genu valgum 50% Osteoarthritis 50% Scoliosis 50% Nephropathy 7.5% Abnormality of the carpal bones - Abnormality of the metatarsal bones - Autosomal dominant inheritance - Coxa valga - Disproportionate short-limb short stature - Dorsal subluxation of ulna - Fibular hypoplasia - High palate - Hypoplasia of the radius - Hypoplasia of the ulna - Increased carrying angle - Limited elbow movement - Limited wrist movement - Mesomelia - Multiple exostoses - Radial bowing - Short 4th metacarpal - Short tibia - Short toe - Skeletal muscle hypertrophy - Tibial bowing - 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 Congenital sucrase-isomaltase deficiency ?
|
What are the signs and symptoms of Congenital sucrase-isomaltase deficiency? Affected infants usually develop symptoms soon after they first ingest sucrose, which is found in modified milk formulas, fruits, or starches. Symptoms may include explosive, watery diarrhea resulting in abnormally low levels of body fluids (dehydration), abdominal swelling (distension), and/or abdominal discomfort. In addition, some affected infants may experience malnutrition, resulting from malabsorption of essential nutrients, and/or failure to thrive, resulting from nutritional deficiencies. In some cases, individuals may exhibit irritability; colic; abrasion and/or irritation (excoriation) of the skin on the buttocks as a result of prolonged diarrhea episodes; and/or vomiting. Symptoms of this disorder vary among affected individuals, but are usually more severe in infants and young children than in adults. Symptoms exhibited in infants and young children are usually more pronounced than those of the affected adults because the diet of younger individuals often includes a higher carbohydrate intake. In addition, the time it takes for intestinal digestion is less in infants or young children. The Human Phenotype Ontology provides the following list of signs and symptoms for Congenital sucrase-isomaltase deficiency. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of metabolism/homeostasis - Autosomal recessive inheritance - Diarrhea - Malabsorption - Nephrolithiasis - 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) Actinomycosis ?
|
Actinomycosis is a chronic bacterial infection that commonly affects the face and neck. It is usually caused by an anaerobic bacteria called Actinomyces israelii. Actinomyces are normal inhabitants of the mouth, gastrointestinal tract, and female genital tract, and do not cause an infection unless there is a break in the skin or mucosa. The infection usually occurs in the face and neck, but can sometimes occur in the chest, abdomen, pelvis, or other areas of the body. The infection is not contagious.
|
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What is (are) sickle cell disease ?
|
Sickle cell disease is a group of disorders that affects hemoglobin, the molecule in red blood cells that delivers oxygen to cells throughout the body. People with this disorder have atypical hemoglobin molecules called hemoglobin S, which can distort red blood cells into a sickle, or crescent, shape. Signs and symptoms of sickle cell disease usually begin in early childhood. Characteristic features of this disorder include a low number of red blood cells (anemia), repeated infections, and periodic episodes of pain. The severity of symptoms varies from person to person. Some people have mild symptoms, while others are frequently hospitalized for more serious complications. The signs and symptoms of sickle cell disease are caused by the sickling of red blood cells. When red blood cells sickle, they break down prematurely, which can lead to anemia. Anemia can cause shortness of breath, fatigue, and delayed growth and development in children. The rapid breakdown of red blood cells may also cause yellowing of the eyes and skin, which are signs of jaundice. Painful episodes can occur when sickled red blood cells, which are stiff and inflexible, get stuck in small blood vessels. These episodes deprive tissues and organs of oxygen-rich blood and can lead to organ damage, especially in the lungs, kidneys, spleen, and brain. A particularly serious complication of sickle cell disease is high blood pressure in the blood vessels that supply the lungs (pulmonary hypertension). Pulmonary hypertension occurs in about one-third of adults with sickle cell disease and can lead to heart failure.
|
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] |
What are the symptoms of Paralysis agitans, juvenile, of Hunt ?
|
What are the signs and symptoms of Paralysis agitans, juvenile, of Hunt? The Human Phenotype Ontology provides the following list of signs and symptoms for Paralysis agitans, juvenile, of Hunt. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of metabolism/homeostasis - Autosomal dominant inheritance - Bradykinesia - Dysarthria - Gait disturbance - Mask-like facies - Parkinsonism - Rigidity - Slow progression - Tremor - 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 acromicric dysplasia ?
|
Acromicric dysplasia is caused by mutations in the FBN1 gene, which provides instructions for making a large protein called fibrillin-1. This protein is transported out of cells into the extracellular matrix, which is an intricate lattice of proteins and other molecules that forms in the spaces between cells. In this matrix, molecules of fibrillin-1 attach (bind) to each other and to other proteins to form threadlike filaments called microfibrils. The microfibrils become part of the fibers that provide strength and flexibility to connective tissues, which support the bones, skin, and other tissues and organs. Additionally, microfibrils store molecules called growth factors, including transforming growth factor beta (TGF-), and release them at various times to control the growth and repair of tissues and organs throughout the body. Most of the FBN1 gene mutations that cause acromicric dysplasia change single protein building blocks in the fibrillin-1 protein. The mutations result in a reduction and disorganization of the microfibrils. Without enough normal microfibrils to store TGF-, the growth factor is abnormally active. These effects likely contribute to the physical abnormalities that occur in acromicric dysplasia, but the mechanisms are unclear.
|
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what research (or clinical trials) is being done for Adult Central Nervous System Tumors ?
|
New types of treatment are being tested in clinical trials.
This summary section refers to new treatments being studied in clinical trials, but it may not mention every new treatment being studied. Information about clinical trials is available from the NCI website. Proton beam radiation therapy Proton beam radiation therapy is a type of high-energy, external radiation therapy that uses streams of protons (small, positively-charged pieces of matter) to make radiation. This type of radiation kills tumor cells with little damage to nearby tissues. It is used to treat cancers of the head, neck, and spine and organs such as the brain, eye, lung, and prostate. Proton beam radiation is different from x-ray radiation. Biologic therapy Biologic therapy is a treatment that uses the patients immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the bodys natural defenses against cancer. This type of cancer treatment is also called biotherapy or immunotherapy. Biologic therapy is being studied for the treatment of some types of brain tumors. Treatments may include the following: - Dendritic cell vaccine therapy. - Gene therapy.
Patients may want to think about taking part in a clinical trial.
For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment. Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment. Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.
Patients can enter clinical trials before, during, or after starting their cancer treatment.
Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment. Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
|
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] |
What are the symptoms of Amish infantile epilepsy syndrome ?
|
What are the signs and symptoms of Amish infantile epilepsy syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Amish infantile epilepsy 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) Hearing impairment 5% Microcephaly 5% Absent speech - Autosomal recessive inheritance - Choreoathetosis - Cortical visual impairment - Developmental regression - Developmental stagnation at onset of seizures - Failure to thrive - Feeding difficulties in infancy - Generalized tonic-clonic seizures - Global brain atrophy - Hyporeflexia of upper limbs - Irritability - Lower limb hyperreflexia - Muscular hypotonia - Myoclonus - Optic atrophy - Status epilepticus - Visual loss - Vomiting - 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) Pinworms ?
|
Pinworms are small parasites that can live in the colon and rectum. You get them when you swallow their eggs. The eggs hatch inside your intestines. While you sleep, the female pinworms leave the intestines through the anus and lay eggs on nearby skin. Pinworms spread easily. When people who are infected touch their anus, the eggs attach to their fingertips. They can spread the eggs to others directly through their hands, or through contaminated clothing, bedding, food, or other articles. The eggs can live on household surfaces for up to 2 weeks. The infection is more common in children. Many people have no symptoms at all. Some people feel itching around the anus or vagina. The itching may become intense, interfere with sleep, and make you irritable. Your health care provider can diagnose pinworm infection by finding the eggs. A common way to collect the eggs is with a sticky piece of clear tape. Mild infections may not need treatment. If you do need medicine, everyone in the household should take it. To prevent becoming infected or reinfected with pinworms, - Bathe after waking up - Wash your pajamas and bed sheets often - Wash your hands regularly, especially after using the bathroom or changing diapers - Change your underwear every day - Avoid nail biting - Avoid scratching the anal area NIH: National Institute of Allergy and Infectious Diseases
|
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41185,
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41,
27,
3313,
6516,
273,
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2124,
285,
49078,
784,
35852
] |
How many people are affected by Warsaw breakage syndrome ?
|
Warsaw breakage syndrome is a rare condition; at least four cases have been described in the medical literature.
|
[
2347,
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275,
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3739,
6239,
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] |
What is (are) Infectious Arthritis ?
|
Most kinds of arthritis cause pain and swelling in your joints. Joints are places where two bones meet, such as your elbow or knee. Infectious arthritis is an infection in the joint. The infection comes from a bacterial, viral, or fungal infection that spreads from another part of the body. Symptoms of infectious arthritis include - Intense pain in the joint - Joint redness and swelling - Chills and fever - Inability to move the area with the infected joint One type of infectious arthritis is reactive arthritis. The reaction is to an infection somewhere else in your body. The joint is usually the knee, ankle, or toe. Sometimes, reactive arthritis is set off by an infection in the bladder, or in the urethra, which carries urine out of the body. In women, an infection in the vagina can cause the reaction. For both men and women, it can start with bacteria passed on during sex. Another form of reactive arthritis starts with eating food or handling something that has bacteria on it. To diagnose infectious arthritis, your health care provider may do tests of your blood, urine, and joint fluid. Treatment includes medicines and sometimes surgery.
|
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4536,
5869,
15
] |
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17012,
3797,
26114,
285,
4536,
5869,
15
] |
What is (are) Hypothalamic dysfunction ?
|
Hypothalamic dysfunction refers to a condition in which the hypothalamus is not working properly. The hypothalamus produces hormones that control body temperature, hunger, moods, release of hormones from many glands such as the pituitary gland, sex drive, sleep, and thirst. The signs and symptoms patients have vary depending on the hormones missing. A number of different causes including anorexia, bleeding, genetic disorder, tumors, and more have been linked to hypothalamic dysfunction. Treatment depends on the cause of the hypothalamic dysfunction.
|
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327,
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273,
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12614,
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15
] |
How to diagnose Renal Tubular Acidosis ?
|
To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which type of RTA a person has. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of acidosis.
|
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2433,
15
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[
1,
1,
1,
1,
1,
1,
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1,
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1,
1,
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1,
1,
1,
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1,
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1,
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1,
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1,
1,
1,
1,
1,
1,
1,
1,
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1,
1,
1,
1,
1,
1,
1,
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1,
1,
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1,
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1,
1,
1,
1,
1,
1,
1,
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1,
1,
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1,
1,
1
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2433,
15
] |
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