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What is (are) Skin Cancer ?
|
Key Points
- Skin cancer is a disease in which malignant (cancer) cells form in the tissues of the skin. - There are several types of skin cancer. - Skin cancer is the most common cancer in the United States.
Skin cancer is a disease in which malignant (cancer) cells form in the tissues of the skin.
The skin is the bodys largest organ. It protects against heat, sunlight, injury, and infection. Skin also helps control body temperature and stores water, fat, and vitamin D. The skin has several layers, but the two main layers are the epidermis (upper or outer layer) and the dermis (lower or inner layer). The epidermis is made up of 3 kinds of cells: - Squamous cells are the thin, flat cells that make up most of the epidermis. - Basal cells are the round cells under the squamous cells. - Melanocytes are found throughout the lower part of the epidermis. They make melanin, the pigment that gives skin its natural color. When skin is exposed to the sun, melanocytes make more pigment, causing the skin to tan, or darken. The dermis contains blood and lymph vessels, hair follicles, and glands. See the following PDQ summaries for more information about skin cancer: - Skin Cancer Screening - Skin Cancer Treatment - Melanoma Treatment - Genetics of Skin Cancer
There are several types of skin cancer.
The most common types of skin cancer are squamous cell carcinoma, which forms in the squamous cells and basal cell carcinoma, which forms in the basal cells. Squamous cell carcinoma and basal cell carcinoma are also called nonmelanoma skin cancers. Melanoma, which forms in the melanocytes, is a less common type of skin cancer that grows and spreads quickly. Skin cancer can occur anywhere on the body, but it is most common in areas exposed to sunlight, such as the face, neck, hands, and arms.
Skin cancer is the most common cancer in the United States.
Basal cell carcinoma and squamous cell carcinoma are the most common types of skin cancer in the United States. The number of new cases of nonmelanoma skin cancer appears to be increasing every year. These nonmelanoma skin cancers can usually be cured. The number of new cases of melanoma has been increasing for at least 30 years. Melanoma is more likely to spread to nearby tissues and other parts of the body and can be harder to cure. Finding and treating melanoma skin cancer early may help prevent death from melanoma.
|
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What are the symptoms of Congenital ectodermal dysplasia with hearing loss ?
|
What are the signs and symptoms of Congenital ectodermal dysplasia with hearing loss? The Human Phenotype Ontology provides the following list of signs and symptoms for Congenital ectodermal dysplasia with hearing loss. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal hair quantity 90% Camptodactyly of finger 90% Sensorineural hearing impairment 90% Short stature 90% Arachnodactyly 50% Carious teeth 50% Coarse hair 50% Cognitive impairment 50% Hyperkeratosis 50% Kyphosis 50% Scoliosis 50% Autosomal recessive inheritance - Hidrotic ectodermal dysplasia - Joint contracture of the hand - Thoracic scoliosis - 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 the outlook for Chiari Malformation ?
|
Many people with Type I CM are asymptomatic and do not know they have the condition. Many individuals with the more severe types of CM and have surgery see a reduction in their symptoms and/or prolonged periods of relative stability, although paralysis is generally permanent.
|
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Who is at risk for Endometrial Cancer? ?
|
Health history and certain medicines can affect the risk of developing endometrial cancer. Anything that increases your chance of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesnt mean that you will not get cancer. People who think they may be at risk should discuss this with their doctor. Risk factors for endometrial cancer include the following: - Taking tamoxifen for treatment or prevention of breast cancer. - Taking estrogen alone. (Taking estrogen in combination with progestin does not appear to increase the risk of endometrial cancer.) - Being overweight. - Eating a high-fat diet. - Never giving birth. - Beginning menstruation at an early age. - Reaching menopause at an older age. - Having the gene for hereditary non-polyposis colon cancer (HNPCC). - Being white.
|
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Is ocular albinism inherited ?
|
Ocular albinism type 1 is inherited in an X-linked pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the GPR143 gene in each cell is sufficient to cause the characteristic features of ocular albinism. Because females have two copies of the X chromosome, women with only one copy of a GPR143 mutation in each cell usually do not experience vision loss or other significant eye abnormalities. They may have mild changes in retinal pigmentation that can be detected during an eye examination.
|
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What are the symptoms of Aplasia cutis congenita intestinal lymphangiectasia ?
|
What are the signs and symptoms of Aplasia cutis congenita intestinal lymphangiectasia? The Human Phenotype Ontology provides the following list of signs and symptoms for Aplasia cutis congenita intestinal lymphangiectasia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal hair quantity 90% Lymphedema 90% Single transverse palmar crease 90% Skull defect 90% Clinodactyly of the 5th finger 50% Decreased antibody level in blood 50% Hypoproteinemia 50% Lymphopenia 50% Malabsorption 50% Abnormality of coagulation 7.5% Chorioretinal coloboma 7.5% Myopia 7.5% Abnormal bleeding - Abnormality of the paranasal sinuses - Aplasia cutis congenita over the scalp vertex - Autosomal recessive inheritance - Generalized edema - Intestinal lymphangiectasia - 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 MYH9-related disorder ?
|
These resources address the diagnosis or management of MYH9-related disorder: - Gene Review: Gene Review: MYH9-Related Disorders - Genetic Testing Registry: Epstein syndrome - Genetic Testing Registry: Fechtner syndrome - Genetic Testing Registry: Macrothrombocytopenia and progressive sensorineural deafness - Genetic Testing Registry: May-Hegglin anomaly - Genetic Testing Registry: Sebastian syndrome - MedlinePlus Encyclopedia: Glomerulonephritis - MedlinePlus Encyclopedia: Thrombocytopenia These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What causes Craniometaphyseal dysplasia, autosomal dominant ?
|
What causes autosomal dominant craniometaphyseal dysplasia? Autosomal dominant craniometaphyseal dysplasia is caused by mutations in the ANKH gene. The ANKH gene provides instructions for making a protein that is present in bone and transports a molecule called pyrophosphate out of cells. Pyrophosphate helps regulate bone formation by preventing mineralization, the process by which minerals such as calcium and phosphorus are deposited in developing bones. The ANKH protein may have other, unknown functions. Mutations in the ANKH gene that cause autosomal dominant craniometaphyseal dysplasia may decrease the ANKH protein's ability to transport pyrophosphate out of cells. Reduced levels of pyrophosphate can increase bone mineralization, contributing to the bone overgrowth seen in craniometaphyseal dysplasia. Why long bones are shaped differently and only the skull bones become thicker in people with this condition remains unclear.
|
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] |
What are the treatments for DICER1 syndrome ?
|
These resources address the diagnosis or management of DICER1 syndrome: - Cancer.Net from the American Society of Clinical Oncology: Pleuropulmonary Blastoma--Childhood Treatment - Gene Review: Gene Review: DICER1-Related Disorders - Genetic Testing Registry: Pleuropulmonary blastoma These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the treatments for Glycogen storage disease type 4 ?
|
How might glycogen storage disease type 4 be treated? Management of glycogen storage disease type 4 typically focuses on the signs and symptoms that are present in each individual. Studies have show that in some cases, strict dietary therapy can help to maintain normal levels of glucose in the blood, reduce liver size, reduce symptoms, and allow for improved growth and development. Growing evidence indicates that a high-protein diet may improve muscle function in individuals with weakness or exercise intolerance and slow disease progression. Supportive care is typically needed for complications such as liver failure, heart failure, and neurologic dysfunction. Liver transplantation may be necessary for individuals with progressive liver disease. Individuals with cardiomyopathy may require the use of certain medications.
|
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What are the symptoms of Scalp defects postaxial polydactyly ?
|
What are the signs and symptoms of Scalp defects postaxial polydactyly? The Human Phenotype Ontology provides the following list of signs and symptoms for Scalp defects postaxial polydactyly. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal hair quantity 50% Encephalocele 50% Skull defect 50% Aplasia cutis congenita of scalp - Autosomal dominant inheritance - Postaxial polydactyly type A - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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Is celiac disease inherited ?
|
Celiac disease tends to cluster in families. Parents, siblings, or children (first-degree relatives) of people with celiac disease have between a 4 and 15 percent chance of developing the disorder. However, the inheritance pattern is unknown.
|
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What are the symptoms of Mucolipidosis III alpha/beta ?
|
What are the signs and symptoms of Mucolipidosis III alpha/beta? The Human Phenotype Ontology provides the following list of signs and symptoms for Mucolipidosis III alpha/beta. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal form of the vertebral bodies 90% Abnormality of the hip bone 90% Cognitive impairment 90% Craniofacial hyperostosis 90% Hearing abnormality 90% Limitation of joint mobility 90% Opacification of the corneal stroma 90% Prominent occiput 90% Short stature 90% Visual impairment 90% Acne 50% Coarse facial features 50% Hernia of the abdominal wall 50% Hyperlordosis 50% Abnormality of the aortic valve 7.5% Cleft palate 7.5% Reduced bone mineral density 7.5% Aortic regurgitation - Autosomal recessive inheritance - Broad ribs - Carpal bone hypoplasia - Craniosynostosis - Deficiency of N-acetylglucosamine-1-phosphotransferase - Dysostosis multiplex - Hyperopic astigmatism - Increased serum beta-hexosaminidase - Increased serum iduronate sulfatase activity - Intellectual disability - Irregular carpal bones - J-shaped sella turcica - Mandibular prognathia - Retinal degeneration - Scoliosis - Shallow acetabular fossae - Short long bone - Short ribs - Soft tissue swelling of interphalangeal joints - Specific learning disability - Split hand - Thickened skin - 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 narcolepsy ?
|
Narcolepsy probably results from a combination of genetic and environmental factors, some of which have been identified, but many of which remain unknown. In most cases of narcolepsy with cataplexy, and in some cases without cataplexy, sleep abnormalities result from a loss of particular brain cells (neurons) in a part of the brain called the hypothalamus. These cells normally produce chemicals called hypocretins (also known as orexins), which have many important functions in the body. In particular, hypocretins regulate the daily sleep-wake cycle. It is unclear what triggers the death of hypocretin-producing neurons in people with narcolepsy, although evidence increasingly points to an abnormality of the immune system. Researchers have identified changes in several genes that influence the risk of developing narcolepsy. The most well-studied of these genes is HLA-DQB1, which provides instructions for making part of a protein that plays an important role in the immune system. The HLA-DQB1 gene is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders (such as viruses and bacteria). The HLA-DQB1 gene has many different normal variations, allowing each person's immune system to react to a wide range of foreign proteins. A variation of the HLA-DQB1 gene called HLA-DQB1*06:02 has been strongly associated with narcolepsy, particularly in people who also have cataplexy and a loss of hypocretins. Most people with narcolepsy have the HLA-DQB1*06:02 variation, and many also have specific versions of other, closely related HLA genes. It is unclear how these genetic changes influence the risk of developing the condition. Variations in several additional genes have also been associated with narcolepsy. Many of these genes are thought to play roles in immune system function. However, variations in these genes probably make only a small contribution to the overall risk of developing narcolepsy. Other genetic and environmental factors are also likely to influence a person's chances of developing this disorder. For example, studies suggest that bacterial or viral infections such as strep throat (streptococcus), colds, and influenza may be involved in triggering narcolepsy in people who are at risk.
|
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How many people are affected by Birt-Hogg-Dub syndrome ?
|
Birt-Hogg-Dub syndrome is rare; its exact incidence is unknown. This condition has been reported in more than 400 families.
|
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What are the complications of Perineal Injury in Males ?
|
Injury to the blood vessels, nerves, and muscles in the perineum can lead to complications such as
- bladder control problems - sexual problems
Bladder control problems. The nerves in the perineum carry signals from the bladder to the spinal cord and brain, telling the brain when the bladder is full. Those same nerves carry signals from the brain to the bladder and pelvic floor muscles, directing those muscles to hold or release urine. Injury to those nerves can block or interfere with the signals, causing the bladder to squeeze at the wrong time or not to squeeze at all. Damage to the pelvic floor muscles can cause bladder and bowel control problems.
Sexual problems. The perineal nerves also carry signals between the genitals and the brain. Injury to those nerves can interfere with the sensations of sexual contact.
Signals from the brain direct the smooth muscles in the genitals to relax, causing greater blood flow into the penis. In men, damaged blood vessels can cause erectile dysfunction (ED), the inability to achieve or maintain an erection firm enough for sexual intercourse. An internal portion of the penis runs through the perineum and contains a section of the urethra. As a result, damage to the perineum may also injure the penis and urethra.
|
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What are the treatments for Osteoarthritis ?
|
Doctors consider a number of factors when choosing medicines for their patients. In particular, they look at the type of pain the patient may be having and any possible side effects from the drugs. For pain relief, doctors usually start with acetaminophen because the side effects are minimal. If acetaminophen does not relieve pain, then non-steroidal anti-inflammatory drugs such as ibuprofen and naproxen may be used. Some NSAIDs are available over the counter, while more than a dozen others, including a subclass called COX-2 inhibitors, are available only with a prescription. Corticosteroids, hyaluronic acid, and topical creams are also used. Most medicines used to treat osteoarthritis have side effects, so it is important for people to learn about the medicines they take. For example, people over age 65 and those with any history of ulcers or stomach bleeding should use non-steroidal anti-inflammatory drugs, or NSAIDs, with caution. There are measures you can take to help reduce the risk of side effects associated with NSAIDs. These include taking medications with food and avoiding stomach irritants such as alcohol, tobacco, and caffeine. In some cases, it may help to take another medication along with an NSAID to coat the stomach or block stomach acids. Although these measures may help, they are not always completely effective. For more tips on how older adults can avoid medication side effects, see Side Effects in the Taking Medicines topic.
|
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Is juvenile myoclonic epilepsy inherited ?
|
The inheritance pattern of juvenile myoclonic epilepsy is not completely understood. When the condition is caused by mutations in the GABRA1 gene, it is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. The inheritance pattern of juvenile myoclonic epilepsy caused by mutations in the EFHC1 gene is not known. Although juvenile myoclonic epilepsy can run in families, many cases occur in people with no family history of the disorder.
|
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What is (are) Gout ?
|
Gout is a common, painful form of arthritis. It causes swollen, red, hot and stiff joints. Gout happens when uric acid builds up in your body. Uric acid comes from the breakdown of substances called purines. Purines are in your body's tissues and in foods, such as liver, dried beans and peas, and anchovies. Normally, uric acid dissolves in the blood. It passes through the kidneys and out of the body in urine. But sometimes uric acid can build up and form needle-like crystals. When they form in your joints, it is very painful. The crystals can also cause kidney stones. Often, gout first attacks your big toe. It can also attack ankles, heels, knees, wrists, fingers, and elbows. At first, gout attacks usually get better in days. Eventually, attacks last longer and happen more often. You are more likely to get gout if you - Are a man - Have family member with gout - Are overweight - Drink alcohol - Eat too many foods rich in purines Gout can be hard to diagnose. Your doctor may take a sample of fluid from an inflamed joint to look for crystals. You can treat gout with medicines. Pseudogout has similar symptoms and is sometimes confused with gout. However, it is caused by calcium phosphate, not uric acid. NIH: National Institute of Arthritis and Musculoskeletal and Skin Diseases
|
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What are the genetic changes related to multiple pterygium syndrome ?
|
Mutations in the CHRNG gene cause most cases of multiple pterygium syndrome, Escobar type and a smaller percentage of cases of lethal multiple pterygium syndrome. The CHRNG gene provides instructions for making the gamma () protein component (subunit) of the acetylcholine receptor (AChR) protein. The AChR protein is found in the membrane of skeletal muscle cells and is critical for signaling between nerve and muscle cells. Signaling between these cells is necessary for movement. The AChR protein consists of five subunits. The subunit is found only in the fetal AChR protein. At about the thirty-third week of pregnancy, the subunit is replaced by another subunit to form adult AChR protein. The replacement of fetal AChR by adult AChR is the reason most people with multiple pterygium syndrome, Escobar type do not have problems with muscle movement after birth. CHRNG gene mutations result in an impaired or missing subunit. The severity of the CHRNG gene mutation influences the severity of the condition. Typically, mutations that prevent the production of any subunit will result in the lethal type, while mutations that allow the production of some subunit will lead to the Escobar type. Without a functional subunit, the fetal AChR protein cannot be assembled or properly placed in the muscle cell membrane. As a result, the fetal AChR protein cannot function and the communication between nerve cells and muscle cells in the developing fetus is impaired. A lack of signaling between nerve and muscle cells leads to akinesia and pterygium before birth, and may result in many of the other signs and symptoms of multiple pterygium syndrome. Mutations in other genes, most providing instructions for other AChR protein subunits, have been found to cause multiple pterygium syndrome. Changes in these genes can cause both the lethal and Escobar types of this condition, although they account for only a small number of cases. Some people with multiple pterygium syndrome do not have an identified mutation in any of the known genes associated with this condition. The cause of the disease in these individuals is unknown.
|
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What is (are) Duane syndrome type 2 ?
|
Duane syndrome is a disorder of eye movement. This condition prevents outward movement of the eye (toward the ear), and in some cases may also limit inward eye movement (toward the nose). As the eye moves inward, the eyelids partially close and the eyeball pulls back (retracts) into its socket. Usually only one eye is affected. Some people with Duane syndrome develop amblyopia ("lazy eye"), a condition that causes vision loss in the affected eye. Most cases occur without other signs and symptoms. There are three forms of Duane syndrome, designated types 1, 2, and 3. The types vary in which eye movements are most severely restricted (inward, outward, or both). All three types are characterized by retraction of the eyeball as the eye moves inward and are inherited in an autosomal dominant fashion.
|
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What are the symptoms of Microcephaly-albinism-digital anomalies syndrome ?
|
What are the signs and symptoms of Microcephaly-albinism-digital anomalies syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Microcephaly-albinism-digital anomalies 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) Aplasia/Hypoplasia of the distal phalanges of the toes 90% Cognitive impairment 90% Generalized hypopigmentation 90% Microcephaly 90% Ocular albinism 90% Short distal phalanx of finger 90% Albinism - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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Is autosomal recessive spastic ataxia of Charlevoix-Saguenay inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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Is ataxia with vitamin E deficiency inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What are the treatments for Brachial Plexus Injuries ?
|
Some brachial plexus injuries may heal without treatment. Many children who are injured during birth improve or recover by 3 to 4 months of age. Treatment for brachial plexus injuries includes physical therapy and, in some cases, surgery.
|
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What is (are) Choking ?
|
Food or small objects can cause choking if they get caught in your throat and block your airway. This keeps oxygen from getting to your lungs and brain. If your brain goes without oxygen for more than four minutes, you could have brain damage or die. Young children are at an especially high risk of choking. They can choke on foods like hot dogs, nuts and grapes, and on small objects like toy pieces and coins. Keep hazards out of their reach and supervise them when they eat. When someone is choking, quick action can be lifesaving. Learn how to do back blows, the Heimlich maneuver (abdominal thrusts), and CPR.
|
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What are the symptoms of Mantle cell lymphoma ?
|
What are the signs and symptoms of Mantle cell lymphoma? Common symptoms of Mantle cell lymphoma include fatigue, loss of appetite, and enlarged lymph nodes, spleen, and/or liver. Other symptoms may include night sweats, unexplained high fevers, and weight loss. The Human Phenotype Ontology provides the following list of signs and symptoms for Mantle cell lymphoma. 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) Hematological neoplasm 90% Lymphadenopathy 90% Anorexia 50% Splenomegaly 50% Weight loss 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 Pol III-related leukodystrophy ?
|
These resources address the diagnosis or management of Pol III-related leukodystrophy: - Eastman Dental Hospital: Hypodontia Clinic - Gene Review: Gene Review: Pol III-Related Leukodystrophies - Genetic Testing Registry: Pol III-related leukodystrophy - Johns Hopkins Medicine: Treating Ataxia - National Ataxia Foundation: Diagnosis of Ataxia - UCSF Benioff Children's Hospital: Hypodontia - University of Chicago Ataxia Center 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) Gastrointestinal Carcinoid Tumors ?
|
Key Points
- A gastrointestinal carcinoid tumor is cancer that forms in the lining of the gastrointestinal tract. - Health history can affect the risk of gastrointestinal carcinoid tumors. - Some gastrointestinal carcinoid tumors have no signs or symptoms in the early stages. - Carcinoid syndrome may occur if the tumor spreads to the liver or other parts of the body. - Imaging studies and tests that examine the blood and urine are used to detect (find) and diagnose gastrointestinal carcinoid tumors. - Certain factors affect prognosis (chance of recovery) and treatment options.
A gastrointestinal carcinoid tumor is cancer that forms in the lining of the gastrointestinal tract.
The gastrointestinal (GI) tract is part of the body's digestive system. It helps to digest food, takes nutrients (vitamins, minerals, carbohydrates, fats, proteins, and water) from food to be used by the body and helps pass waste material out of the body. The GI tract is made up of these and other organs: - Stomach. - Small intestine (duodenum, jejunum, and ileum). - Colon. - Rectum. Gastrointestinal carcinoid tumors form from a certain type of neuroendocrine cell (a type of cell that is like a nerve cell and a hormone -making cell). These cells are scattered throughout the chest and abdomen but most are found in the GI tract. Neuroendocrine cells make hormones that help control digestive juices and the muscles used in moving food through the stomach and intestines. A GI carcinoid tumor may also make hormones and release them into the body. GI carcinoid tumors are rare and most grow very slowly. Most of them occur in the small intestine, rectum, and appendix. Sometimes more than one tumor will form. See the following PDQ summaries for more information related to GI and other types of carcinoid tumors: - Non-Small Cell Lung Cancer Treatment. - Pancreatic Neuroendocrine Tumors (Islet Cell Tumors) Treatment. - Rectal Cancer Treatment. - Small Intestine Cancer Treatment. - Unusual Cancers of Childhood Treatment
Carcinoid syndrome may occur if the tumor spreads to the liver or other parts of the body.
The hormones made by gastrointestinal carcinoid tumors are usually destroyed by liver enzymes in the blood. If the tumor has spread to the liver and the liver enzymes cannot destroy the extra hormones made by the tumor, high amounts of these hormones may remain in the body and cause carcinoid syndrome. This can also happen if tumor cells enter the blood. Signs and symptoms of carcinoid syndrome include the following: - Redness or a feeling of warmth in the face and neck. - Abdominal pain. - Feeling bloated. - Diarrhea. - Wheezing or other trouble breathing. - Fast heartbeat. These signs and symptoms may be caused by gastrointestinal carcinoid tumors or by other conditions. Talk to your doctor if you have any of these signs or symptoms.
|
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What are the symptoms of Tetraploidy ?
|
What are the signs and symptoms of Tetraploidy? The Human Phenotype Ontology provides the following list of signs and symptoms for Tetraploidy. 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 chromosome segregation 90% Convex nasal ridge 90% Intrauterine growth retardation 90% Microcephaly 90% Narrow forehead 90% Hypoplasia of the ear cartilage 50% Radial club hand 50% Short philtrum 50% Aplasia/Hypoplasia affecting the eye 7.5% Aplasia/Hypoplasia of the lungs 7.5% Aplasia/Hypoplasia of the thymus 7.5% Arnold-Chiari malformation 7.5% Cleft palate 7.5% Preauricular skin tag 7.5% Renal hypoplasia/aplasia 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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Is Ehlers-Danlos syndrome, vascular type inherited ?
|
Is Ehlers-Danlos syndrome, vascular type inherited? Ehlers-Danlos syndrome (EDS), vascular type is inherited in an autosomal dominant manner. This means that to be affected, a person only needs a change (mutation) in one copy of the responsible gene in each cell. In some cases, an affected person inherits the mutation from an affected parent. Other cases may result from new (de novo) mutations in the gene. These cases occur in people with no history of the disorder in their family. A person with EDS, vascular type has a 50% chance with each pregnancy of passing along the altered gene to his or her child.
|
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What are the genetic changes related to Weill-Marchesani syndrome ?
|
Mutations in the ADAMTS10 and FBN1 genes can cause Weill-Marchesani syndrome. The ADAMTS10 gene provides instructions for making a protein whose function is unknown. This protein is important for normal growth before and after birth, and it appears to be involved in the development of the eyes, heart, and skeleton. Mutations in this gene disrupt the normal development of these structures, which leads to the specific features of Weill-Marchesani syndrome. A mutation in the FBN1 gene has also been found to cause Weill-Marchesani syndrome. The FBN1 gene provides instructions for making a protein called fibrillin-1. This protein is needed to form threadlike filaments, called microfibrils, that help provide strength and flexibility to connective tissue. The FBN1 mutation responsible for Weill-Marchesani syndrome leads to an unstable version of fibrillin-1. Researchers believe that the unstable protein interferes with the normal assembly of microfibrils, which weakens connective tissue and causes the abnormalities associated with Weill-Marchesani syndrome. In some people with Weill-Marchesani syndrome, no mutations in ADAMTS10 or FBN1 have been found. Researchers are looking for other genetic changes that may be responsible for the disorder in these people.
|
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What are the symptoms of Limbic encephalitis ?
|
What symptoms are associated with limbic encephalitis? Although the symptoms of the condition may vary from person to person, the cardinal sign of limbic encephalitis is severe impairment of short-term memory, with most patients having difficulties in recall. A large variety of symptoms may be associated with limbic encephalitis such as anterograde amnesia (the inability to store new memories after the onset of the condition), anxiety, depression, irritability, personality change, acute confusional state, hallucinations and seizures. Other possible symptoms may include obsessiveness, hyperthermia (increase in body temperature), weight change, hypersomnia, endocrine dysfunction, aphasia, and apraxia. The symptoms associated with limbic encephalitis can develop over a few days, weeks, or months. It is important to note the neurological symptoms generally precede diagnosis of the malignancy in 60%-75% of patients that have paraneoplastic limbic encephalitis.
|
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Is familial restrictive cardiomyopathy 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 are the treatments for hereditary sensory and autonomic neuropathy type II ?
|
These resources address the diagnosis or management of HSAN2: - Gene Review: Gene Review: Hereditary Sensory and Autonomic Neuropathy Type II - Genetic Testing Registry: Hereditary sensory and autonomic neuropathy type IIA - Genetic Testing Registry: Hereditary sensory and autonomic neuropathy type IIB These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the symptoms of Age-related Macular Degeneration ?
|
An early symptom of wet AMD is that straight lines appear wavy. If you notice this condition or other changes to your vision, contact your eye care professional at once. You need a comprehensive dilated eye exam.
|
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How to prevent Parasites - Loiasis ?
|
There are no programs to control or eliminate loiasis in affected areas. Your risk of infection may be less in areas where communities receive regular treatment for onchocerciasis or lymphatic filariasis.
There are no vaccines that protect you from loiasis. If you are going to be in an area with loiasis for a long period of time, diethylcarbamazine (DEC)—300mg taken once a week—can reduce your risk of infection. Avoiding areas where the deerflies are found, such as muddy, shaded areas along rivers or around wood fires, may also reduce your risk of infection. You may reduce your risk of bites by using insect repellants that contain DEET (N,N-Diethyl-meta-toluamide) and wearing long sleeves and long pants during the day, which is when deerflies bite. Treating your clothes with permethrin may also help. For a description of CDC's information for preventing insect bites, see CDC's Yellow Book.
More on: Insect Bite Prevention
|
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Do you have information about Mammography
|
Summary : A mammogram is an x-ray picture of the breast. It can be used to check for breast cancer in women who have no signs or symptoms of the disease. It can also be used if you have a lump or other sign of breast cancer. Screening mammography is the type of mammogram that checks you when you have no symptoms. It can help reduce the number of deaths from breast cancer among women ages 40 to 70. But it can also have drawbacks. Mammograms can sometimes find something that looks abnormal but isn't cancer. This leads to further testing and can cause you anxiety. Sometimes mammograms can miss cancer when it is there. It also exposes you to radiation. You should talk to your doctor about the benefits and drawbacks of mammograms. Together, you can decide when to start and how often to have a mammogram. Mammograms are also recommended for younger women who have symptoms of breast cancer or who have a high risk of the disease. When you have a mammogram, you stand in front of an x-ray machine. The person who takes the x-rays places your breast between two plastic plates. The plates press your breast and make it flat. This may be uncomfortable, but it helps get a clear picture. You should get a written report of your mammogram results within 30 days. NIH: National Cancer Institute
|
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How many people are affected by infantile systemic hyalinosis ?
|
The prevalence of infantile systemic hyalinosis is unknown. Fewer than 20 people with this disorder have been reported.
|
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What are the symptoms of Alzheimer's Disease ?
|
Alzheimer's disease varies from person to person so not everyone will have the same symptoms. Also, the disease progresses faster in some people than in others. In general, though, Alzheimers takes many years to develop and becomes increasingly severe over time. Memory Problems -- A Common Early Sign Memory problems are typically one of the first signs of Alzheimers disease. However, not all memory problems are caused by Alzheimers. If you or someone in your family thinks your forgetfulness is getting in the way of your normal routine, its time to see your doctor. He or she can find out whats causing these problems. A person in the early (mild) stage of Alzheimers disease may - find it hard to remember things - ask the same questions over and over - get lost in familiar places - lose things or put them in odd places - have trouble handling money and paying bills - take longer than normal to finish daily tasks - have some mood and personality changes. find it hard to remember things ask the same questions over and over get lost in familiar places lose things or put them in odd places have trouble handling money and paying bills take longer than normal to finish daily tasks have some mood and personality changes. Other thinking problems besides memory loss may be the first sign of Alzheimers disease. A person may have - trouble finding the right words - vision and spatial issues - impaired reasoning or judgment. trouble finding the right words vision and spatial issues impaired reasoning or judgment. See a chart that compares signs of Alzheimers disease with signs of normal aging. Later Signs of Alzheimers As Alzheimers disease progresses to the moderate stage, memory loss and confusion grow worse, and people may have problems recognizing family and friends. Other symptoms at this stage may include - difficulty learning new things and coping with new situations - trouble carrying out tasks that involve multiple steps, like getting dressed - impulsive behavior - forgetting the names of common things - hallucinations, delusions, or paranoia - wandering away from home. difficulty learning new things and coping with new situations trouble carrying out tasks that involve multiple steps, like getting dressed impulsive behavior forgetting the names of common things hallucinations, delusions, or paranoia wandering away from home. Symptoms of Severe Alzheimers As Alzheimers disease becomes more severe, people lose the ability to communicate. They may sleep more, lose weight, and have trouble swallowing. Often they are incontinentthey cannot control their bladder and/or bowels. Eventually, they need total care. Benefits of Early Diagnosis An early, accurate diagnosis of Alzheimer's disease helps people and their families plan for the future. It gives them time to discuss care options, find support, and make legal and financial arrangements while the person with Alzheimers can still take part in making decisions. Also, even though no medicine or other treatment can stop or slow the disease, early diagnosis offers the best chance to treat the symptoms. How Alzheimers Is Diagnosed The only definitive way to diagnose Alzheimer's disease is to find out whether plaques and tangles exist in brain tissue. To look at brain tissue, doctors perform a brain autopsy, an examination of the brain done after a person dies. Doctors can only make a diagnosis of "possible" or probable Alzheimers disease while a person is alive. Doctors with special training can diagnose Alzheimer's disease correctly up to 90 percent of the time. Doctors who can diagnose Alzheimers include geriatricians, geriatric psychiatrists, and neurologists. A geriatrician specializes in the treatment of older adults. A geriatric psychiatrist specializes in mental problems in older adults. A neurologist specializes in brain and nervous system disorders. To diagnose Alzheimers disease, doctors may - ask questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality - conduct tests to measure memory, problem solving, attention, counting, and language skills - carry out standard medical tests, such as blood and urine tests - perform brain scans to look for anything in the brain that does not look normal. ask questions about overall health, past medical problems, ability to carry out daily activities, and changes in behavior and personality conduct tests to measure memory, problem solving, attention, counting, and language skills carry out standard medical tests, such as blood and urine tests perform brain scans to look for anything in the brain that does not look normal. Test results can help doctors know if there are other possible causes of the person's symptoms. For example, thyroid problems, drug reactions, depression, brain tumors, head injury, and blood-vessel disease in the brain can cause symptoms similar to those of Alzheimer's. Many of these other conditions can be treated successfully. New Diagnostic Methods Being Studied Researchers are exploring new ways to help doctors diagnose Alzheimers disease earlier and more accurately. Some studies focus on changes in a persons memory, language, and other mental functions. Others look at changes in blood, spinal fluid, and brain-scan results that may detect Alzheimers years before symptoms appear. Watch a video that explains changes in diagnostic guidelines for Alzheimers.
|
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] |
How to diagnose Parsonage Turner syndrome ?
|
How is Parsonage Turner syndrome diagnosed? A diagnosis of Parsonage Turner syndrome (PTS) is often suspected based on the presence of characteristic signs and symptoms. Specialized tests may be recommended to further investigate the shoulder pain and/or muscle weakness and to rule out other conditions that can cause similar features. These tests may include nerve conduction studies (tests that determine the ability of a specific nerve to relay a message to the brain), electromyography, magnetic resonance imaging (MRI scan) and/or an X-ray.
|
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] |
Is pulmonary alveolar microlithiasis inherited ?
|
This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.
|
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What are the symptoms of Crohn's Disease ?
|
The most common signs and symptoms of Crohn's disease are
- diarrhea - abdominal cramping and pain - weight loss
Other general signs and symptoms include
- feeling tired - nausea or loss of appetite - fever - anemiaa condition in which the body has fewer red blood cells than normal
Signs and symptoms of inflammation outside of the intestines include
- joint pain or soreness - eye irritation - skin changes that involve red, tender bumps under the skin
The symptoms a person experiences can vary depending on the severity of the inflammation and where it occurs.
|
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How many people are affected by alpha-mannosidosis ?
|
Alpha-mannosidosis is estimated to occur in approximately 1 in 500,000 people worldwide.
|
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What is (are) Beta ketothiolase deficiency ?
|
Beta-ketothiolase deficiency is an inherited disorder in which the body cannot effectively process a protein building block (amino acid) called isoleucine. This condition also impairs the body's ability to process ketones, which are molecules produced during the breakdown of fats. Signs and symptoms typically appear between the ages of 6 months and 24 months. Affected children experience episodes of vomiting, dehydration, difficulty breathing, extreme tiredness (lethargy), and occasionally seizures. These episodes, which are called ketoacidotic attacks, sometimes lead to coma. Ketoacidotic attacks are frequently triggered by infections, periods without food (fasting), or increased intake of protein-rich foods. This condition is inherited in an autosomal recessive fashion and is caused by mutations in the ACAT1 gene.
|
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] |
What is (are) aromatase deficiency ?
|
Aromatase deficiency is a condition characterized by reduced levels of the female sex hormone estrogen and increased levels of the male sex hormone testosterone. Females with aromatase deficiency have a typical female chromosome pattern (46,XX) but are born with external genitalia that do not appear clearly female or male (ambiguous genitalia). These individuals typically have normal internal reproductive organs, but develop ovarian cysts early in childhood, which impair the release of egg cells from the ovaries (ovulation). In adolescence, most affected females do not develop secondary sexual characteristics, such as breast growth and menstrual periods. They tend to develop acne and excessive body hair growth (hirsutism). Men with this condition have a typical male chromosome pattern (46,XY) and are born with male external genitalia. Some men with this condition have decreased sex drive, abnormal sperm production, or testes that are small or undescended (cryptorchidism). There are other features associated with aromatase deficiency that can affect both males and females. Affected individuals are abnormally tall because of excessive growth of long bones in the arms and legs. The abnormal bone growth results in slowed mineralization of bones (delayed bone age) and thinning of the bones (osteoporosis), which can lead to bone fractures with little trauma. Males and females with aromatase deficiency can have abnormally high blood sugar (hyperglycemia) because the body does not respond correctly to the hormone insulin. In addition, they can have excessive weight gain and a fatty liver. Women who are pregnant with fetuses that have aromatase deficiency often experience mild symptoms of the disorder even though they themselves do not have the disorder. These women may develop hirsutism, acne, an enlarged clitoris (clitoromegaly), and a deep voice. These features can appear as early as 12 weeks of pregnancy and go away soon after delivery.
|
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What is (are) Autosomal dominant partial epilepsy with auditory features ?
|
Autosomal dominant partial epilepsy with auditory features (ADPEAF) is a rare form of epilepsy, a condition that is characterized by recurrent seizures. In ADPEAF, specifically, most affected people experience secondary generalized seizures and partial seizures, some of which are associated with sound-related symptoms (such as buzzing, humming, or ringing) and/or receptive aphasia (inability to understand written or spoken words). Less commonly, seizures may cause visual hallucinations, a disturbance in the sense of smell, vertigo, or other symptoms affecting the senses. Signs and symptoms of the condition generally begin in adolescence or early adulthood. ADPEAF is caused by changes (mutations) in the LGI1 or RELN gene and is inherited in an autosomal dominant manner. The seizures associated with ADPEAF are typically well controlled with medications that are used to treat epilepsy (called antiepileptic drugs).
|
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What are the symptoms of Aromatase excess syndrome ?
|
What are the signs and symptoms of Aromatase excess syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Aromatase excess 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) Accelerated skeletal maturation - Autosomal dominant inheritance - Gynecomastia - Short stature - 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 Immune dysfunction with T-cell inactivation due to calcium entry defect 2 ?
|
What are the signs and symptoms of Immune dysfunction with T-cell inactivation due to calcium entry defect 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Immune dysfunction with T-cell inactivation due to calcium entry defect 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autoimmune hemolytic anemia - Autosomal recessive inheritance - Episodic fever - Hypoplasia of the iris - Immunodeficiency - Lymphadenopathy - Muscular hypotonia - Myopathy - Recurrent bacterial infections - Thrombocytopenia - 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 COPD ?
|
COPD is a disease that slowly worsens over time, especially if you continue to smoke. If you have COPD, you are more likely to have lung infections, which can be fatal. If the lungs are severely damaged, the heart may be affected. A person with COPD dies when the lungs and heart are unable to function and get oxygen to the body's organs and tissues, or when a complication, such as a severe infection, occurs. Treatment for COPD may help prevent complications, prolong life, and improve a person's quality of life.
|
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What are the symptoms of Pituitary hormone deficiency, combined 2 ?
|
What are the signs and symptoms of Pituitary hormone deficiency, combined 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Pituitary hormone deficiency, combined 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Adrenal insufficiency - Autosomal recessive inheritance - Hypoglycemic seizures - Hypogonadism - Hypothyroidism - Neonatal hypoglycemia - Panhypopituitarism - Prolactin deficiency - Short stature - 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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Do you have information about Secondhand Smoke
|
Summary : Secondhand smoke is a mixture of the smoke that comes from the burning end of a cigarette, cigar, or pipe, and the smoke breathed out by the smoker. It contains more than 7,000 chemicals. Hundreds of those chemicals are toxic and about 70 can cause cancer. Health effects of secondhand smoke include - Ear infections in children - More frequent and severe asthma attacks in children - Heart disease and lung cancer in adults who have never smoked There is no safe amount of secondhand smoke. Even low levels of it can be harmful. The only way to fully protect nonsmokers from secondhand smoke is not to allow smoking indoors. Centers for Disease Control and Prevention
|
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What are the treatments for focal dermal hypoplasia ?
|
These resources address the diagnosis or management of focal dermal hypoplasia: - Gene Review: Gene Review: Focal Dermal Hypoplasia - Genetic Testing Registry: Focal dermal hypoplasia - MedlinePlus Encyclopedia: Ectodermal dysplasia - MedlinePlus Encyclopedia: Omphalocele These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the symptoms of Metaphyseal dysplasia maxillary hypoplasia brachydactyly ?
|
What are the signs and symptoms of Metaphyseal dysplasia maxillary hypoplasia brachydactyly? The Human Phenotype Ontology provides the following list of signs and symptoms for Metaphyseal dysplasia maxillary hypoplasia brachydactyly. 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 dental color 90% Brachydactyly syndrome 90% Convex nasal ridge 90% Short philtrum 90% Short stature 90% Thin vermilion border 90% Abnormal form of the vertebral bodies 50% Abnormality of the femur 50% Abnormality of the humerus 50% Camptodactyly of finger 50% Craniofacial hyperostosis 50% Reduced bone mineral density 50% Cerebral cortical atrophy 7.5% Recurrent fractures 7.5% Autosomal dominant inheritance - Flared metaphysis - Hypoplasia of the maxilla - Metaphyseal dysplasia - Multiple small vertebral fractures - Osteoporosis of vertebrae - Platyspondyly - Premature loss of teeth - Short 5th metacarpal - Short middle phalanx of the 2nd finger - Short middle phalanx of the 5th finger - 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 Charcot-Marie-Tooth disease type 2B ?
|
What are the signs and symptoms of Charcot-Marie-Tooth disease type 2B? The Human Phenotype Ontology provides the following list of signs and symptoms for Charcot-Marie-Tooth disease type 2B. 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) Areflexia - Autoamputation (feet) - Autosomal dominant inheritance - Axonal degeneration/regeneration - Decreased motor nerve conduction velocity - Decreased number of peripheral myelinated nerve fibers - Distal amyotrophy - Dystrophic toenail - Foot dorsiflexor weakness - Hammertoe - Hyporeflexia - Osteomyelitis or necrosis, distal, due to sensory neuropathy (feet) - Peripheral axonal atrophy - Pes cavus - Pes planus - Steppage gait - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Urinary Tract Infections ?
|
Symptoms of a UTI in the bladder may include - cloudy, bloody, or foul-smelling urine - pain or burning during urination - strong and frequent need to urinate, even right after emptying the bladder - a mild fever below 101 degrees Fahrenheit in some people. cloudy, bloody, or foul-smelling urine pain or burning during urination strong and frequent need to urinate, even right after emptying the bladder a mild fever below 101 degrees Fahrenheit in some people. If the UTI spreads to the kidneys, symptoms may include - chills and shaking - night sweats - feeling tired or generally ill - fever above 101 degrees Fahrenheit - pain in the side, back, or groin - flushed, warm, or reddened skin - mental changes or confusion - nausea and vomiting - very bad abdominal pain in some people. chills and shaking night sweats feeling tired or generally ill fever above 101 degrees Fahrenheit pain in the side, back, or groin flushed, warm, or reddened skin mental changes or confusion nausea and vomiting very bad abdominal pain in some people. Symptoms may differ depending on age, gender, and catheter use. In some elderly people, mental changes and confusion may be the only signs of a UTI. Older women and men with a UTI are more likely to be tired, shaky, and weak. They are also more likely to have muscle aches and abdominal pain. In a person with a catheter, the only symptom may be fever that does not have another likely cause. Learn more about the signs and symptoms of urinary tract infections in adults.
|
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What is (are) Learning Disorders ?
|
Learning disorders affect how a person understands, remembers and responds to new information. People with learning disorders may have problems - Listening or paying attention - Speaking - Reading or writing - Doing math Although learning disorders occur in very young children, they are usually not recognized until the child reaches school age. About one-third of children who have learning disabilities also have ADHD, which makes it hard to focus. Evaluation and testing by a trained professional can help identify a learning disorder. The next step is special education, which involves helping your child in the areas where he or she needs the most help. Sometimes tutors or speech or language therapists also work with the children. Learning disorders do not go away, but strategies to work around them can make them less of a problem. NIH: National Institute of Neurological Disorders and Stroke
|
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What is the outlook for Dyslexia ?
|
For those with dyslexia, the prognosis is mixed. The disability affects such a wide range of people and produces such different symptoms and varying degrees of severity that predictions are hard to make. The prognosis is generally good, however, for individuals whose dyslexia is identified early, who have supportive family and friends and a strong self-image, and who are involved in a proper remediation program.
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What are the genetic changes related to aceruloplasminemia ?
|
Mutations in the CP gene cause aceruloplasminemia. The CP gene provides instructions for making a protein called ceruloplasmin, which is involved in iron transport and processing. Ceruloplasmin helps move iron from the organs and tissues of the body and prepares it for incorporation into a molecule called transferrin, which transports it to red blood cells to help carry oxygen. CP gene mutations result in the production of ceruloplasmin protein that is unstable or nonfunctional, or they prevent the protein from being released (secreted) by the cells in which it is made. When ceruloplasmin is unavailable, transport of iron out of the body's tissues is impaired. The resulting iron accumulation damages cells in those tissues, leading to neurological dysfunction, and the other health problems seen in aceruloplasminemia.
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What is (are) Traumatic Brain Injury ?
|
Traumatic brain injury (TBI), a form ofacquired brain injury, occurs when a sudden trauma causes damage to the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue.Symptoms of a TBI can be mild, moderate, or severe, depending on the extent of the damage to the brain. A person with a mild TBI may remain conscious or may experience a loss of consciousness for a few seconds or minutes. Other symptoms of mild TBI include headache, confusion, lightheadedness, dizziness, blurred vision or tired eyes, ringing in the ears, bad taste in the mouth, fatigue or lethargy, a change in sleep patterns, behavioral or mood changes, and trouble with memory, concentration, attention, or thinking. A person with a moderate or severe TBI may show these same symptoms, but may also have a headache that gets worse or does not go away, repeated vomiting or nausea, convulsions or seizures, an inability to awaken from sleep, dilation of one or both pupils of the eyes, slurred speech, weakness or numbness in the extremities, loss of coordination, and increased confusion, restlessness, or agitation.
|
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What are the treatments for Meige disease ?
|
These resources address the diagnosis or management of Meige disease: - Genetic Testing Registry: Lymphedema praecox - Johns Hopkins Medicine: Lymphedema Management These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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How many people are affected by mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes ?
|
The exact incidence of MELAS is unknown. It is one of the more common conditions in a group known as mitochondrial diseases. Together, mitochondrial diseases occur in about 1 in 4,000 people.
|
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What are the genetic changes related to Romano-Ward syndrome ?
|
Mutations in the KCNE1, KCNE2, KCNH2, KCNQ1, and SCN5A genes cause Romano-Ward syndrome. These genes provide instructions for making proteins that act as channels across the cell membrane. These channels transport positively charged atoms (ions), such as potassium and sodium, into and out of cells. In cardiac muscle, ion channels play critical roles in maintaining the heart's normal rhythm. Mutations in any of these genes alter the structure or function of these channels, which changes the flow of ions between cells. A disruption in ion transport alters the way the heart beats, leading to the abnormal heart rhythm characteristic of Romano-Ward syndrome. Unlike most genes related to Romano-Ward syndrome, the ANK2 gene does not provide instructions for making an ion channel. The ANK2 protein, ankyrin-2, ensures that certain other proteins (particularly ion channels) are inserted into the cell membrane appropriately. A mutation in the ANK2 gene likely alters the flow of ions between cells in the heart, which disrupts the heart's normal rhythm. ANK2 mutations can cause a variety of heart problems, including the irregular heartbeat often found in Romano-Ward syndrome. It is unclear whether mutations in the ANK2 gene cause Romano-Ward syndrome or lead to another heart condition with some of the same signs and symptoms.
|
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Do you have information about Teen Development
|
Summary : As a teenager, you go through many physical, mental, emotional, and social changes. The biggest change is puberty, the process of becoming sexually mature. It usually happens between ages 10 and 14 for girls and ages 12 and 16 for boys. As your body changes, you may have questions about sexual health. During this time, you start to develop your own unique personality and opinions. Some changes that you might notice include - Increased independence from your parents - More concerns about body image and clothes - More influence from peers - Greater ability to sense right and wrong All of these changes can sometimes seem overwhelming. Some sadness or moodiness can be normal. But feeling very sad, hopeless, or worthless could be warning signs of a mental health problem. If you need help, talk to your parents, school counselor, or health care provider. Centers for Disease Control and Prevention
|
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What are the treatments for Horner syndrome ?
|
These resources address the diagnosis or management of Horner syndrome: - Genetic Testing Registry: Horner syndrome, congenital 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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Who is at risk for Metabolic Syndrome? ?
|
People at greatest risk for metabolic syndrome have these underlying causes:
Abdominal obesity (a large waistline)
An inactive lifestyle
Insulin resistance
Some people are at risk for metabolic syndrome because they take medicines that cause weight gain or changes in blood pressure, blood cholesterol, and blood sugar levels. These medicines most often are used to treat inflammation, allergies, HIV, and depression and other types of mental illness.
Populations Affected
Some racial and ethnic groups in the United States are at higher risk for metabolic syndrome than others. Mexican Americans have the highest rate of metabolic syndrome, followed by whites and blacks.
Other groups at increased risk for metabolic syndrome include:
People who have a personal history of diabetes
People who have a sibling or parent who hasdiabetes
Women when compared with men
Women who have a personal history of polycystic ovarian syndrome (a tendency to develop cysts on the ovaries)
Heart Disease Risk
Metabolic syndrome increases your risk for coronary heart disease. Other risk factors, besides metabolic syndrome, also increase your risk for heart disease. For example, a high LDL (bad) cholesterol level and smoking are major risk factors for heart disease. For details about all of the risk factors for heart disease, go to the Coronary Heart Disease Risk Factors HealthTopic.
Even if you dont have metabolic syndrome, you should find out your short-term risk for heart disease. The National Cholesterol Education Program (NCEP) divides short-term heart disease risk into four categories. Your risk category depends on which risk factors you have and how many you have.
Your risk factors are used to calculate your 10-year risk of developing heart disease. The NCEP has an online calculator that you can use to estimate your 10-year risk of having a heart attack.
High risk: Youre in this category if you already have heart disease or diabetes, or if your 10-year risk score is more than 20 percent.
Moderately high risk: Youre in this category if you have two or more risk factors and your 10-year risk score is 10 percent to 20 percent.
Moderate risk: Youre in this category if you have two or more risk factors and your 10-year risk score is less than 10 percent.
Lower risk: Youre in this category if you have zero or one risk factor.
Even if your 10-year risk score isnt high, metabolic syndrome will increase your risk for coronary heart disease over time.
|
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What is (are) essential thrombocythemia ?
|
Essential thrombocythemia is a condition characterized by an increased number of platelets (thrombocythemia). Platelets (thrombocytes) are blood cell fragments involved in blood clotting. While some people with this condition have no symptoms, others develop problems associated with the excess platelets. Abnormal blood clotting (thrombosis) is common in people with essential thrombocythemia and causes many signs and symptoms of this condition. Clots that block blood flow to the brain can cause strokes or temporary stroke-like episodes known as transient ischemic attacks. Thrombosis in the legs can cause leg pain, swelling, or both. In addition, clots can travel to the lungs (pulmonary embolism), blocking blood flow in the lungs and causing chest pain and difficulty breathing (dyspnea). Another problem in essential thrombocythemia is abnormal bleeding, which occurs more often in people with a very high number of platelets. Affected people may have nosebleeds, bleeding gums, or bleeding in the gastrointestinal tract. It is thought that bleeding occurs because a specific protein in the blood that helps with clotting is reduced, although why the protein is reduced is unclear. Other signs and symptoms of essential thrombocythemia include an enlarged spleen (splenomegaly); weakness; headaches; or a sensation in the skin of burning, tingling, or prickling. Some people with essential thrombocythemia have episodes of severe pain, redness, and swelling (erythromelalgia), which commonly occur in the hands and feet.
|
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What causes Dominant dystrophic epidermolysis bullosa ?
|
What causes dominant dystrophic epidermolysis bullosa? Dominant dystrophic epidermolysis bullosa (DDEB) is caused by mutations in the COL7A1 gene. The COL7A1 gene provides instructions for making a protein that is used to assemble type VII collagen. Collagen gives structure and strength to connective tissues, such as skin, tendons, and ligaments, throughout the body. Type VII collagen plays an important role in strengthening and stabilizing the skin. It is the main component of structures called anchoring fibrils, which anchor the top layer of skin, called the epidermis, to an underlying layer called the dermis. COL7A1 mutations alter the structure or disrupt the production of type VII collagen, which impairs its ability to help connect the epidermis to the dermis. When type VII collagen is abnormal or missing, friction or other minor trauma can cause the two skin layers to separate. This separation leads to the formation of blisters, which can cause extensive scarring as they heal. A diagram of the skin structure including the area of skin implicated in DDEB is provided by the National Institute of Arthritis and Musculoskeletal and Skin Diseases. Click on the link for more.
|
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What is (are) Colorectal Cancer ?
|
Cancer of the colon or rectum is called colorectal cancer. The colon and the rectum are part of the large intestine, which is part of the digestive system. Colorectal cancer occurs when malignant tumors form in the lining of the large intestine, also called the large bowel.
|
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How many people are affected by X-linked creatine deficiency ?
|
The prevalence of X-linked creatine deficiency is unknown. More than 150 affected individuals have been identified. The disorder has been estimated to account for between 1 and 2 percent of males with intellectual disability.
|
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How many people are affected by type 1 diabetes ?
|
Type 1 diabetes occurs in 10 to 20 per 100,000 people per year in the United States. By age 18, approximately 1 in 300 people in the United States develop type 1 diabetes. The disorder occurs with similar frequencies in Europe, the United Kingdom, Canada, and New Zealand. Type 1 diabetes occurs much less frequently in Asia and South America, with reported incidences as low as 1 in 1 million per year. For unknown reasons, during the past 20 years the worldwide incidence of type 1 diabetes has been increasing by 2 to 5 percent each year. Type 1 diabetes accounts for 5 to 10 percent of cases of diabetes worldwide. Most people with diabetes have type 2 diabetes, in which the body continues to produce insulin but becomes less able to use it.
|
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What are the treatments for Hyper-IgD syndrome ?
|
How might hyper IgD syndrome be treated? There is no cure for hyper IgD syndrome and currently no established treatment. Management is focused on supportive care. Some patients have responded to high-dose prednisone. Simvastatin, Anakinria (an IL-1 receptor antagonist) and TNF inhibitors have recently shown some success in controlling inflammatory attacks. Consultations with the following specialists may be helpful: dermatologist, rheumatologist, and infectious disease specialist (to evaluate periodic fever).
|
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What is (are) Niemann-Pick disease ?
|
Niemann-Pick disease is a condition that affects many body systems. It has a wide range of symptoms that vary in severity. Niemann-Pick disease is divided into four main types: type A, type B, type C1, and type C2. These types are classified on the basis of genetic cause and the signs and symptoms of the condition. Infants with Niemann-Pick disease type A usually develop an enlarged liver and spleen (hepatosplenomegaly) by age 3 months and fail to gain weight and grow at the expected rate (failure to thrive). The affected children develop normally until around age 1 year when they experience a progressive loss of mental abilities and movement (psychomotor regression). Children with Niemann-Pick disease type A also develop widespread lung damage (interstitial lung disease) that can cause recurrent lung infections and eventually lead to respiratory failure. All affected children have an eye abnormality called a cherry-red spot, which can be identified with an eye examination. Children with Niemann-Pick disease type A generally do not survive past early childhood. Niemann-Pick disease type B usually presents in mid-childhood. The signs and symptoms of this type are similar to type A, but not as severe. People with Niemann-Pick disease type B often have hepatosplenomegaly, recurrent lung infections, and a low number of platelets in the blood (thrombocytopenia). They also have short stature and slowed mineralization of bone (delayed bone age). About one-third of affected individuals have the cherry-red spot eye abnormality or neurological impairment. People with Niemann-Pick disease type B usually survive into adulthood. The signs and symptoms of Niemann-Pick disease types C1 and C2 are very similar; these types differ only in their genetic cause. Niemann-Pick disease types C1 and C2 usually become apparent in childhood, although signs and symptoms can develop at any time. People with these types usually develop difficulty coordinating movements (ataxia), an inability to move the eyes vertically (vertical supranuclear gaze palsy), poor muscle tone (dystonia), severe liver disease, and interstitial lung disease. Individuals with Niemann-Pick disease types C1 and C2 have problems with speech and swallowing that worsen over time, eventually interfering with feeding. Affected individuals often experience progressive decline in intellectual function and about one-third have seizures. People with these types may survive into adulthood.
|
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What is (are) Primary Biliary Cirrhosis ?
|
Primary biliary cirrhosis is a chronic, or long lasting, disease that causes the small bile ducts in the liver to become inflamed and damaged and ultimately disappear.
The bile ducts carry a fluid called bile from the liver to the gallbladder, where it is stored. When food enters the stomach after a meal, the gallbladder contracts, and the bile ducts carry bile to the duodenum, the first part of the small intestine, for use in digestion. The liver makes bile, which is made up of bile acids, cholesterol, fats, and fluids. Bile helps the body absorb fats, cholesterol, and fat-soluble vitamins. Bile also carries cholesterol, toxins, and waste products to the intestines, where the body removes them. When chronic inflammation, or swelling, damages the bile ducts, bile and toxic wastes build up in the liver, damaging liver tissue.
This damage to the liver tissue can lead to cirrhosis, a condition in which the liver slowly deteriorates and is unable to function normally. In cirrhosis, scar tissue replaces healthy liver tissue, partially blocking the flow of blood through the liver.
The liver is the bodys largest internal organ. The liver is called the bodys metabolic factory because of the important role it plays in metabolismthe way cells change food into energy after food is digested and absorbed into the blood. The liver has many functions, including
- taking up, storing, and processing nutrients from foodincluding fat, sugar, and proteinand delivering them to the rest of the body when needed - making new proteins, such as clotting factors and immune factors - producing bile - removing waste products the kidneys cannot remove, such as fats, cholesterol, toxins, and medications
A healthy liver is necessary for survival. The liver can regenerate most of its own cells when they become damaged. However, if injury to the liver is too severe or long lasting, regeneration is incomplete, and the liver creates scar tissue. Scarring of the liver may lead to cirrhosis.
The buildup of scar tissue that causes cirrhosis is usually a slow and gradual process. In the early stages of cirrhosis, the liver continues to function. However, as cirrhosis gets worse and scar tissue replaces more healthy tissue, the liver will begin to fail. Chronic liver failure, which is also called end-stage liver disease, progresses over months, years, or even decades. With end-stage liver disease, the liver can no longer perform important functions or effectively replace damaged cells.
Primary biliary cirrhosis usually occurs between the ages of 30 and 65 and affects women more often than men.1
|
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625,
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685,
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15,
18
] |
How many people are affected by Graves disease ?
|
Graves disease affects about 1 in 200 people. The disease occurs more often in women than in men, which may be related to hormonal factors. Graves disease is the most common cause of thyroid overactivity (hyperthyroidism) in the United States.
|
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2347,
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[
2347,
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24085,
37739,
10,
275,
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1986,
2077,
15
] |
what research (or clinical trials) is being done for Postural Tachycardia Syndrome ?
|
The National Institute of Neurological Disorders and Stroke (NINDS) and other Institutes of the National Institutes of Health (NIH) conduct research related to POTS and support additional research through grants to major research institutions across the country. Much of this research focuses on finding better ways to prevent, treat, and ultimately cure disorders such as POTS. NINDS-funded researchers are investigating if low levels of the hormone aldosterone contribute to low blood volume in individuals with POTS, and if high levels of angiotensin II, a peptide that helps regulate blood volume, leads to decreased adrenal sensitivity. Other NINDS-funded research is investigating the hypothesis that POTS is a syndrome of different subtypes, with different underlying mechanisms. Additionally, the NINDS funds the Autonomic Rare Diseases Consortium to further understand disorders such as orthostatic hypotension and hopefully alter the course of disease.
|
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8064,
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347,
9373,
48051,
37251,
2452,
285,
18670,
6990,
253,
2282,
273,
2728,
15
] |
How to diagnose Intestinal Pseudo-obstruction ?
|
To diagnose intestinal pseudo-obstruction, a health care provider may suggest the person consult a gastroenterologista doctor who specializes in digestive diseases. A health care provider will perform a physical exam; take a complete medical history, imaging studies, and a biopsy; and perform blood tests. A health care provider may order other tests to confirm the diagnosis. The health care provider also will look for the cause of the condition, such as an underlying illness.
Intestinal pseudo-obstruction can be difficult to diagnose, especially primary intestinal pseudo-obstruction. As a result, a correct diagnosis may take a long time.
Physical Exam
A physical exam is one of the first things a health care provider may do to help diagnose intestinal pseudo-obstruction. During a physical exam, a health care provider usually
- examines a persons body - uses a stethoscope to listen to bodily sounds - taps on specific areas of the persons body
Medical History
The health care provider will ask a person to provide a medical and family history to help diagnose intestinal pseudo-obstruction.
Imaging Studies
A health care provider may order the following imaging studies:
- Abdominal x ray. An x ray is a picture recorded on film or a computer that a technician takes using low-level radiation. The amount of radiation used is small. An x-ray technician takes the x ray at a hospital or an outpatient center, and a radiologista doctor who specializes in medical imaginginterprets the images. A person does not need anesthesia. The person will lie on a table or stand during the x ray. The technician positions the x-ray machine over the abdominal area. The person will hold his or her breath as the technician takes the picture so that the picture will not be blurry. The technician may ask the person to change position for additional pictures. An x ray of the abdominal area will show whether symptoms are due to an intestinal blockage. - Upper GI series. A health care provider may order an upper GI series to look at the small intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images; the health care provider may give infants and children anesthesia. A person should not eat or drink for 8 hours before the procedure, if possible. During the procedure, the person will stand or sit in front of an x-ray machine and drink barium, a chalky liquid. Infants lie on a table and the technician will give them barium through a tiny tube placed in the nose that runs into the stomach. Barium coats the lining of the small intestine, making signs of obstruction show up more clearly on x rays. A person may experience bloating and nausea for a short time after the test. Barium liquid in the GI tract causes stools to be white or light colored for several days or longer in people with intestinal pseudo-obstruction. A health care provider will give the person specific instructions about eating and drinking after the test. - Lower GI series. A health care provider may order a lower GI series, an x-ray exam to look at the large intestine. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. A person does not need anesthesia. The health care provider may provide written bowel prep instructions to follow at home before the test. The health care provider may ask the person to follow a clear liquid diet for 1 to 3 days before the procedure. A person may need to use a laxative or an enema before the test. A laxative is medication that loosens stool and increases bowel movements. An enema involves flushing water or laxative into the anus using a special squirt bottle. For the test, the person will lie on a table while the health care provider inserts a flexible tube into the persons anus. The health care provider will fill the large intestine with barium, making signs of underlying problems show up more clearly on x rays. The test can show problems with the large intestine that are causing the persons symptoms. Barium liquid in the GI tract causes stools to be white or light colored for several days or longer in people with intestinal pseudo-obstruction. Enemas and repeated bowel movements may cause anal soreness. A health care provider will provide specific instructions about eating and drinking after the test. - Computerized tomography (CT) scan. CT scans use a combination of x rays and computer technology to create images. An x-ray technician performs the test at a hospital or an outpatient center, and a radiologist interprets the images. For a CT scan, a health care provider may give the person a solution to drink and an injection of a special dye, called contrast medium. CT scans require the person to lie on a table that slides into a tunnel-shaped device where the technician takes the x rays. CT scans can show both the internal and external intestinal wall. The health care provider may give children a sedative to help them fall asleep for the test. - Upper GI endoscopy. This procedure involves using an endoscopea small, flexible tube with a lightto see the upper GI tract, which includes the esophagus, stomach, and duodenum. A gastroenterologist performs the test at a hospital or an outpatient center. The gastroenterologist carefully feeds the endoscope down the esophagus and into the stomach and duodenum. A small camera mounted on the endoscope transmits a video image to a monitor, allowing close examination of the intestinal lining. A health care provider may give a person a liquid anesthetic to gargle or may spray anesthetic on the back of the persons throat. A health care provider will place an intravenous (IV) needle in a vein in the arm to administer sedation. Sedatives help patients stay relaxed and comfortable. This test can show blockages or other conditions in the upper small intestine. A gastroenterologist may obtain a biopsy of the lining of the small intestine during an upper GI endoscopy.
Biopsy
A gastroenterologist can obtain a biopsy of the intestinal wall during endoscopy or during surgery, if the person has surgery for intestinal pseudo-obstruction and the cause is unknown. If the health care provider needs to examine the nerves in the intestinal wall, a deeper biopsy, which a gastroenterologist can typically obtain only during surgery, is necessary.
A biopsy is a procedure that involves taking a piece of the intestinal wall tissue for examination with a microscope. A health care provider performs the biopsy in a hospital and uses light sedation and local anesthetic; the health care provider uses general anesthesia if performing the biopsy during surgery. A pathologista doctor who specializes in diagnosing diseasesexamines the intestinal tissue in a lab. Diagnosing problems in the nerve pathways of the intestinal tissue requires special techniques that are not widely available.
A health care provider can also use a biopsy obtained during endoscopy to rule out celiac disease. Celiac disease is an autoimmune disorder in which people cannot tolerate gluten because it damages the lining of their small intestine and prevents absorption of nutrients. Gluten is a protein found in wheat, rye, and barley and in products such as vitamin and nutrient supplements, lip balms, and certain medications.
Blood Tests
A blood test involves drawing blood at a health care providers office or a commercial facility and sending the sample to a lab for analysis. The blood test can show the presence of other diseases or conditions that may be causing a persons symptoms. The blood test also can show levels of essential vitamins and minerals to help detect malnutrition.
Manometry
Manometry is a test that measures muscle pressure and movements in the GI tract, such as how well the smooth muscles of the stomach and small intestine contract and relax. A gastroenterologist performs the test at a hospital or an outpatient center. While the person is under sedation, a health care provider places a thin tube, or manometry tube, into the stomach and moves it down into the small intestine. A gastroenterologist may use an endoscope to place this tube. A health care provider will move the person to a manometry room and connect the manometry tube to a computer. When the person wakes up from sedation, the computer records the pressure inside the intestine while the person is fasting and after the person has eaten a meal. Manometry can confirm the diagnosis of intestinal pseudo-obstruction and show the extent of the condition.
Gastric Emptying Tests
Gastric emptying tests can show if a disorder called gastroparesis is causing a persons symptoms. People with gastroparesis, which literally refers to a paralyzed stomach, have severely delayed gastric emptying, or the delayed movement of food from the stomach to the small intestine. Some patients with intestinal pseudo-obstruction also have gastroparesis.
Types of gastric emptying tests include the following:
- Gastric emptying scintigraphy. This test involves eating a bland mealsuch as eggs or an egg substitutethat contains a small amount of radioactive material. A specially trained technician performs the test in a radiology center or hospital, and a radiologist interprets the results; the person does not need anesthesia. An external camera scans the abdomen to show where the radioactive material is located. The radiologist is then able to measure the rate of gastric emptying at 1, 2, 3, and 4 hours after the meal. Normal values depend on the composition of the meal. With some meals, if more than 10 percent of the meal is still in the stomach at 4 hours, a health care provider confirms the diagnosis of gastroparesis. Obtaining scans for 4 hours after the meal is essential. When the technician only obtains scans 1 to 2 hours after the meal, the results are often unreliable. - Breath test. With this test, the person eats a meal containing a small amount of nonradioactive material. Then, the health care provider takes breath samples over a period of several hours to measure the amount of nonradioactive material in the exhaled breath. The results allow the health care provider to calculate how fast the stomach is emptying. - SmartPill. The SmartPill is a small electronic device in capsule form. The SmartPill test is available at specialized outpatient centers. The person swallows the device so that it can move through the entire digestive tract and send information to a cell-phone-sized receiver worn around the persons waist or neck. The recorded information provides details about how quickly food travels through each part of the digestive tract.
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Is Wolff-Parkinson-White syndrome inherited ?
|
Most cases of Wolff-Parkinson-White syndrome occur in people with no apparent family history of the condition. These cases are described as sporadic and are not inherited. Familial Wolff-Parkinson-White syndrome accounts for only a small percentage of all cases of this condition. The familial form of the disorder typically has an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell is sufficient to cause the condition. In most cases, a person with familial Wolff-Parkinson-White syndrome has inherited the condition from an affected parent.
|
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What are the symptoms of Congenital dyserythropoietic anemia type 2 ?
|
What are the signs and symptoms of Congenital dyserythropoietic anemia type 2? The signs and symptoms of CDA II include jaundice, gallstones and an enlarged liver and spleen. This condition also causes the body to absorb too much iron, which builds up and can damage tissues and organs. In particular, iron overload can lead to an abnormal heart rhythm (arrhythmia), congestive heart failure, diabetes, and chronic liver disease (cirrhosis). Rarely, people with CDA type II have mediastinal tumors. During pregnancy and other special circumstances (such as anemic crisis, major surgery and infections), blood transfusions may be necessary. The Human Phenotype Ontology provides the following list of signs and symptoms for Congenital dyserythropoietic anemia type 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Anemia of inadequate production - Autosomal recessive inheritance - Cholelithiasis - Endopolyploidy on chromosome studies of bone marrow - Jaundice - Reduced activity of N-acetylglucosaminyltransferase II - Reticulocytosis - Splenomegaly - 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) L-arginine:glycine amidinotransferase deficiency ?
|
L-arginine:glycine amidinotransferase (AGAT) deficiency is a rare condition that primarily affects the brain. People with AGAT deficiency generally have mild to moderate intellectual disability. Other signs and symptoms may include seizures, delayed language development, muscle weakness, failure to thrive, autistic behaviors, and delayed motor milestones (i.e. walking, sitting). AGAT deficiency is caused by changes (mutations) in the GATM gene and is inherited in an autosomal recessive manner. Treatment of AGAT deficiency is focused on increasing cerebral creatine levels and generally consists of supplementation with creatine monohydrate.
|
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What is (are) Apraxia ?
|
Apraxia (called "dyspraxia" if mild) is a neurological disorder characterized by loss of the ability to execute or carry out skilled movements and gestures, despite having the desire and the physical ability to perform them. Apraxia results from dysfunction of the cerebral hemispheres of the brain, especially the parietal lobe, and can arise from many diseases or damage to the brain. There are several kinds of apraxia, which may occur alone or together. The most common is buccofacial or orofacial apraxia, which causes the inability to carry out facial movements on command such as licking lips, whistling, coughing, or winking. Other types of apraxia include limb-kinetic apraxia (the inability to make fine, precise movements with an arm or leg), ideomotor apraxia (the inability to make the proper movement in response to a verbal command), ideational apraxia (the inability to coordinate activities with multiple, sequential movements, such as dressing, eating, and bathing), verbal apraxia (difficulty coordinating mouth and speech movements), constructional apraxia (the inability to copy, draw, or construct simple figures), and oculomotor apraxia (difficulty moving the eyes on command). Apraxia may be accompanied by a language disorder called aphasia. Corticobasal ganglionic degeneration is a disease that causes a variety of types of apraxia, especially in elderly adults.
|
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What are the treatments for cri-du-chat syndrome ?
|
These resources address the diagnosis or management of cri-du-chat syndrome: - Cri du Chat Syndrome Support Group (UK): Diagnosis - Cri du Chat Syndrome Support Group (UK): Therapies - Genetic Testing Registry: 5p partial monosomy syndrome - MedlinePlus Encyclopedia: Cri du Chat 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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What is (are) X-linked lissencephaly with abnormal genitalia ?
|
X-linked lissencephaly with abnormal genitalia (XLAG) is a condition that affects the development of the brain and genitalia. It occurs most often in males. XLAG is characterized by abnormal brain development that results in the brain having a smooth appearance (lissencephaly) instead of its normal folds and grooves. Individuals without any folds in the brain (agyria) typically have more severe symptoms than people with reduced folds and grooves (pachygyria). Individuals with XLAG may also have a lack of development (agenesis) of the tissue connecting the left and right halves of the brain (corpus callosum). The brain abnormalities can cause severe intellectual disability and developmental delay, abnormal muscle stiffness (spasticity), weak muscle tone (hypotonia), and feeding difficulties. Starting soon after birth, babies with XLAG have frequent and recurrent seizures (epilepsy). Most children with XLAG do not survive past early childhood. Another key feature of XLAG in males is abnormal genitalia that can include an unusually small penis (micropenis), undescended testes (cryptorchidism), or external genitalia that do not look clearly male or clearly female (ambiguous genitalia). Additional signs and symptoms of XLAG include chronic diarrhea, periods of increased blood sugar (transient hyperglycemia), and problems with body temperature regulation.
|
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] |
What is (are) Skin Pigmentation Disorders ?
|
Pigmentation means coloring. Skin pigmentation disorders affect the color of your skin. Your skin gets its color from a pigment called melanin. Special cells in the skin make melanin. When these cells become damaged or unhealthy, it affects melanin production. Some pigmentation disorders affect just patches of skin. Others affect your entire body. If your body makes too much melanin, your skin gets darker. Pregnancy, Addison's disease, and sun exposure all can make your skin darker. If your body makes too little melanin, your skin gets lighter. Vitiligo is a condition that causes patches of light skin. Albinism is a genetic condition affecting a person's skin. A person with albinism may have no color, lighter than normal skin color, or patchy missing skin color. Infections, blisters and burns can also cause lighter skin.
|
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What is (are) Multiple sclerosis ?
|
Multiple sclerosis (MS) is a degenerative disorder that affects the central nervous system, specifically the brain and the spinal cord. The disorder is characterized by destruction of the myelin, the fatty tissue that surrounds and protects the nerve fibers and promotes the transmission of nerve impulses, and damage to nerve cells. The symptoms vary widely from person to person, and may include sensory disturbances in the limbs, problems with muscle control, tremors, muscle stiffness (spasticity), exaggerated reflexes (hyperreflexia), weakness, difficulty walking, poor bladder control, and vision problems. Most patients have periods during which they have symptoms (clinical attacks). The clinical attacks are typically followed by periods without any symptoms (remission). After several years, the symptoms worsen continuously. Multiple sclerosis is considered an autoimmune disorder but the exact cause is unknown. Risk factors for developing multiple sclerosis include genetic factors like changes in the HLA-DRB1 gene and in the IL7R gene and environmental factors, such as exposure to the Epstein-Barr virus, low levels of vitamin D, and smoking. The goal of treatment of MS is to decrease attacks and the inflammation within the central nervous system.
|
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What is (are) Cytomegalovirus Infections ?
|
Cytomegalovirus (CMV) is a virus found around the world. It is related to the viruses that cause chickenpox and infectious mononucleosis (mono). Between 50 percent and 80 percent of adults in the United States have had a CMV infection by age 40. Once CMV is in a person's body, it stays there for life. CMV is spread through close contact with body fluids. Most people with CMV don't get sick and don't know that they've been infected. But infection with the virus can be serious in babies and people with weak immune systems. If a woman gets CMV when she is pregnant, she can pass it on to her baby. Usually the babies do not have health problems. But some babies can develop lifelong disabilities. A blood test can tell whether a person has ever been infected with CMV. Most people with CMV don't need treatment. If you have a weakened immune system, your doctor may prescribe antiviral medicine. Good hygiene, including proper hand washing, may help prevent infections. Centers for Disease Control and Prevention
|
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What are the symptoms of Multicentric osteolysis nephropathy ?
|
What are the signs and symptoms of Multicentric osteolysis nephropathy? The Human Phenotype Ontology provides the following list of signs and symptoms for Multicentric osteolysis nephropathy. 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 metacarpal bones 90% Decreased body weight 90% EMG abnormality 90% Gait disturbance 90% Limitation of joint mobility 90% Proptosis 90% Proteinuria 90% Skeletal muscle atrophy 90% Slender long bone 90% Triangular face 90% Camptodactyly of finger 50% Nephropathy 50% Abnormality of epiphysis morphology 7.5% Downturned corners of mouth 7.5% Polyhydramnios 7.5% Telecanthus 7.5% Wide nasal bridge 7.5% Ankle swelling - Arthralgia - Autosomal dominant inheritance - Carpal osteolysis - Hypertension - Hypoplasia of the maxilla - Metacarpal osteolysis - Metatarsal osteolysis - Osteolysis involving tarsal bones - Osteopenia - Pes cavus - Renal insufficiency - Ulnar deviation of the hand or of fingers of the hand - Wrist swelling - 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) Parasites - Taeniasis ?
|
Taeniasis in humans is a parasitic infection caused by the tapeworm species Taenia saginata (beef tapeworm), Taenia solium (pork tapeworm), and Taenia asiatica (Asian tapeworm). Humans can become infected with these tapeworms by eating raw or undercooked beef (T. saginata) or pork (T. solium and T. asiatica). People with taeniasis may not know they have a tapeworm infection because symptoms are usually mild or nonexistent.
T. solium tapeworm infections can lead to cysticercosis, which is a disease that can cause seizures, so it is important seek treatment.
|
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What are the symptoms of Eyebrows duplication of, with stretchable skin and syndactyly ?
|
What are the signs and symptoms of Eyebrows duplication of, with stretchable skin and syndactyly? The Human Phenotype Ontology provides the following list of signs and symptoms for Eyebrows duplication of, with stretchable skin and syndactyly. 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 calvarial morphology 90% Abnormality of the eyebrow 90% Abnormality of the eyelashes 90% Cryptorchidism 90% Finger syndactyly 90% Ptosis 90% Shagreen patch 90% 2-3 toe syndactyly - 2-4 finger syndactyly - Autosomal recessive inheritance - Hyperextensible skin of chest - Hyperextensible skin of face - Hypermobility of interphalangeal joints - Long eyelashes - Partial duplication of eyebrows - Periorbital wrinkles - 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 Extragonadal Germ Cell Tumors ?
|
Key Points
- There are different types of treatment for patients with extragonadal germ cell tumors. - Three types of standard treatment are used: - Radiation therapy - Chemotherapy - Surgery - New types of treatment are being tested in clinical trials. - High-dose chemotherapy with stem cell transplant - 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 extragonadal germ cell tumors.
Different types of treatments are available for patients with extragonadal germ cell tumors. 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.
Three types of standard treatment are used:
Radiation therapy Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy: - External radiation therapy uses a machine outside the body to send radiation toward the cancer. - Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. The way the radiation therapy is given depends on the type and stage of the cancer being treated. External radiation therapy is used to treat seminoma. 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 in 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. Surgery Patients who have benign tumors or tumor remaining after chemotherapy or radiation therapy may need to have surgery.
New types of treatment are being tested in clinical trials.
This summary section describes treatments that are being studied in clinical trials. It may not mention every new treatment being studied. Information about clinical trials is available from the NCI website. High-dose chemotherapy with stem cell transplant High-dose chemotherapy with stem cell transplant is a method of giving high doses of chemotherapy and replacing blood -forming cells destroyed by the cancer treatment. Stem cells (immature blood cells) are removed from the blood or bone marrow of the patient or a donor and are frozen and stored. After the chemotherapy is completed, the stored stem cells are thawed and given back to the patient through an infusion. These reinfused stem cells grow into (and restore) the body's blood cells.
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. After initial treatment for extragonadal germ cell tumors, blood levels of AFP and other tumor markers continue to be checked to find out how well the treatment is working.
Treatment Options for Extragonadal Germ Cell Tumors
Benign Teratoma
Treatment of benign teratomas is surgery. Check the list of NCI-supported cancer clinical trials that are now accepting patients with benign teratoma. 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.
Seminoma
Treatment of seminoma extragonadal germ cell tumors may include the following: - Radiation therapy for small tumors in one area, followed by watchful waiting if there is tumor remaining after treatment. - Chemotherapy for larger tumors or tumors that have spread. If a tumor smaller than 3 centimeters remains after chemotherapy, watchful waiting follows. If a larger tumor remains after treatment, surgery or watchful waiting follow. Check the list of NCI-supported cancer clinical trials that are now accepting patients with extragonadal seminoma. 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.
Nonseminoma
Treatment of nonseminoma extragonadal germ cell tumors may include the following: - Combination chemotherapy followed by surgery to remove any remaining tumor. - A clinical trial of a new treatment. Check the list of NCI-supported cancer clinical trials that are now accepting patients with malignant extragonadal non-seminomatous germ cell tumor. 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.
Recurrent or Refractory Extragonadal Germ Cell Tumors
Treatment of extragonadal germ cell tumors that are recurrent (come back after being treated) or refractory (do not get better during treatment) may include the following: - Chemotherapy. - A clinical trial of high-dose chemotherapy with stem cell transplant. - A clinical trial of a new treatment. Check the list of NCI-supported cancer clinical trials that are now accepting patients with recurrent extragonadal germ cell tumor. 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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15
] |
What is (are) Landau-Kleffner syndrome ?
|
Landau-Kleffner syndrome (LKS) is a rare, childhood neurological disorder characterized by the sudden or gradual development of aphasia (the inability to understand or express language) and an abnormal electro-encephalogram (EEG). The disorder usually occurs in children between age 2 and 8. Typically, children with LKS develop normally but then lose their language skills for no apparent reason. While many of the affected individuals have seizures, some do not. The disorder is difficult to diagnose and may be misdiagnosed as autism, pervasive developmental disorder, hearing impairment, learning disability, auditory/verbal processing disorder, attention deficit disorder, intellectual disability, childhood schizophrenia, or emotional/behavioral problems. Treatment for LKS usually consists of medications, such as anticonvulsants and corticosteroids, and speech therapy, which should be started promptly. The prognosis varies. Some children may have a permanent language disorder, while others may regain much of their language abilities (although it may take months or years).
|
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What are the treatments for Dumping Syndrome ?
|
Treatment for dumping syndrome includes changes in eating, diet, and nutrition; medication; and, in some cases, surgery. Many people with dumping syndrome have mild symptoms that improve over time with simple dietary changes.
|
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What is (are) propionic acidemia ?
|
Propionic acidemia is an inherited disorder in which the body is unable to process certain parts of proteins and lipids (fats) properly. It is classified as an organic acid disorder, which is a condition that leads to an abnormal buildup of particular acids known as organic acids. Abnormal levels of organic acids in the blood (organic acidemia), urine (organic aciduria), and tissues can be toxic and can cause serious health problems. In most cases, the features of propionic acidemia become apparent within a few days after birth. The initial symptoms include poor feeding, vomiting, loss of appetite, weak muscle tone (hypotonia), and lack of energy (lethargy). These symptoms sometimes progress to more serious medical problems, including heart abnormalities, seizures, coma, and possibly death. Less commonly, the signs and symptoms of propionic acidemia appear during childhood and may come and go over time. Some affected children experience intellectual disability or delayed development. In children with this later-onset form of the condition, episodes of more serious health problems can be triggered by prolonged periods without food (fasting), fever, or infections.
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what research (or clinical trials) is being done for Polymyositis ?
|
The National Institute of Neurological Disorders and Stroke (NINDS) and other institutes of the National Institutes of Health (NIH) conduct research relating to polymyositis in laboratories at the NIH and support additional research through grants to major medical institutions across the country. Currently funded research is exploring patterns of gene expression among the inflammatory myopathies, the role of viral infection as a precursor to the disorders, and the safety and efficacy of various treatment regimens.
|
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What are the symptoms of Spinocerebellar ataxia autosomal recessive 7 ?
|
What are the signs and symptoms of Spinocerebellar ataxia autosomal recessive 7? The Human Phenotype Ontology provides the following list of signs and symptoms for Spinocerebellar ataxia autosomal recessive 7. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Ataxia - Autosomal recessive inheritance - Babinski sign - Cerebellar atrophy - Clumsiness - Diplopia - Dysarthria - Gait ataxia - Hypermetric saccades - Hyperreflexia - Juvenile onset - Limb ataxia - Nystagmus - Postural tremor - Saccadic smooth pursuit - Slow progression - 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 Epilepsy ?
|
Once epilepsy is diagnosed, it is important to begin treatment as soon as possible. For about 70 percent of those diagnosed with epilepsy, seizures can be controlled with modern medicines and surgical techniques. Some drugs are more effective for specific types of seizures. An individual with seizures, particularly those that are not easily controlled, may want to see a neurologist specifically trained to treat epilepsy. In some children, special diets may help to control seizures when medications are either not effective or cause serious side effects.
|
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What are the symptoms of Glutamine deficiency, congenital ?
|
What are the signs and symptoms of Glutamine deficiency, congenital? The Human Phenotype Ontology provides the following list of signs and symptoms for Glutamine deficiency, congenital. 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) Death in infancy 7.5% Flexion contracture 5% Micromelia 5% Apnea - Autosomal recessive inheritance - Bradycardia - Brain atrophy - CNS hypomyelination - Depressed nasal bridge - Encephalopathy - Hyperammonemia - Hyperreflexia - Hypoplasia of the corpus callosum - Low-set ears - Muscular hypotonia - Periventricular cysts - Respiratory insufficiency - Seizures - Severe global developmental delay - Skin rash - Subependymal cysts - Ventriculomegaly - Wide nasal bridge - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Homocarnosinosis ?
|
What are the signs and symptoms of Homocarnosinosis? The Human Phenotype Ontology provides the following list of signs and symptoms for Homocarnosinosis. 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 retinal pigmentation - Abnormality of skin pigmentation - Autosomal recessive inheritance - Carnosinuria - Intellectual disability - Spastic paraplegia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) Malaria ?
|
Malaria is a serious and sometimes fatal disease caused by a parasite that commonly infects a certain type of mosquito which feeds on humans. Infection with malaria parasites may result in a wide variety of symptoms, ranging from absent or very mild symptoms to severe disease and even death. People who get malaria are typically very sick with high fevers, shaking chills, and flu-like illness. In general, malaria is a curable disease if diagnosed and treated promptly and correctly. Treatment depends on many factors including disease severity, the species of malaria parasite causing the infection and the part of the world in which the infection was acquired.
|
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What are the genetic changes related to mucopolysaccharidosis type IV ?
|
Mutations in the GALNS and GLB1 genes cause MPS IV. These genes provide instructions for producing enzymes involved in the breakdown of large sugar molecules called glycosaminoglycans (GAGs). GAGs were originally called mucopolysaccharides, which is where this condition gets its name. When MPS IV is caused by mutations in the GALNS gene it is called MPS IV type A (MPS IVA), and when it is caused by mutations in the GLB1 gene it is called MPS IV type B (MPS IVB). In general, the two types of MPS IV cannot be distinguished by their signs and symptoms. Mutations in the GALNS and GLB1 genes reduce or completely eliminate the activity of the enzymes produced from these genes. Without these enzymes, GAGs accumulate within cells, specifically inside the lysosomes. Lysosomes are compartments in the cell that break down and recycle different types of molecules. Conditions such as MPS IV that cause molecules to build up inside the lysosomes are called lysosomal storage disorders. In MPS IV, GAGs accumulate to toxic levels in many tissues and organs, particularly in the bones. The accumulation of GAGs causes the bone deformities in this disorder. Researchers believe that the buildup of GAGs may also cause the features of MPS IV by interfering with the functions of other proteins inside lysosomes and disrupting the movement of molecules inside the cell.
|
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