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What are the symptoms of Glanzmann thrombasthenia ?
|
What are the signs and symptoms of Glanzmann thrombasthenia? The Human Phenotype Ontology provides the following list of signs and symptoms for Glanzmann thrombasthenia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Bruising susceptibility - Decreased platelet glycoprotein IIb-IIIa - Epistaxis - Gastrointestinal hemorrhage - Gingival bleeding - Impaired platelet aggregation - Intracranial hemorrhage - Menorrhagia - Prolonged bleeding time - Purpura - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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How many people are affected by pyridoxal 5'-phosphate-dependent epilepsy ?
|
Pyridoxal 5'-phosphate-dependent epilepsy is a rare condition; approximately 14 cases have been described in the scientific literature.
|
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What is (are) familial isolated hyperparathyroidism ?
|
Familial isolated hyperparathyroidism is an inherited condition characterized by overactivity of the parathyroid glands (hyperparathyroidism). The four parathyroid glands are located in the neck, and they release a hormone called parathyroid hormone that regulates the amount of calcium in the blood. In familial isolated hyperparathyroidism, one or more overactive parathyroid glands release excess parathyroid hormone, which causes the levels of calcium in the blood to rise (hypercalcemia). Parathyroid hormone stimulates the removal of calcium from bone and the absorption of calcium from the diet, and the mineral is then released into the bloodstream. In people with familial isolated hyperparathyroidism, the production of excess parathyroid hormone is caused by tumors that involve the parathyroid glands. Typically only one of the four parathyroid glands is affected, but in some people, more than one gland develops a tumor. The tumors are usually noncancerous (benign), in which case they are called adenomas. Rarely, people with familial isolated hyperparathyroidism develop a cancerous tumor called parathyroid carcinoma. Because the production of excess parathyroid hormone is caused by abnormalities of the parathyroid glands, familial isolated hyperparathyroidism is considered a form of primary hyperparathyroidism. Disruption of the normal calcium balance resulting from overactive parathyroid glands causes many of the common signs and symptoms of familial isolated hyperparathyroidism, such as kidney stones, nausea, vomiting, high blood pressure (hypertension), weakness, and fatigue. Because calcium is removed from bones to be released into the bloodstream, hyperparathyroidism often causes thinning of the bones (osteoporosis). The age at which familial isolated hyperparathyroidism is diagnosed varies from childhood to adulthood. Often, the first indication of the condition is elevated calcium levels identified through a routine blood test, even though the affected individual may not yet have signs or symptoms of hyperparathyroidism or hypercalcemia.
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15
] |
Is Ohdo syndrome, Say-Barber-Biesecker-Young-Simpson variant inherited ?
|
This condition has an autosomal dominant inheritance pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. Almost all reported cases have resulted from new mutations in the gene and have occurred in people with no history of the disorder in their family.
|
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] |
What to do for What I need to know about Hepatitis C ?
|
If you have chronic hepatitis C, you should do things to take care of yourself, including eating a healthy diet. Avoid drinking alcohol, which can harm the liver. Talk with your doctor before taking vitamins and other supplements.
|
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] |
How to diagnose Liddle syndrome ?
|
How is Liddle syndrome diagnosed? A diagnosis of Liddle syndrome may first be suspected by the detection of early-onset hypertension (high blood pressure), especially in the presence of family history. The diagnosis may then be confirmed by special blood and urine tests which show hypokalemia (low blood potassium levels), decreased or normal plasma levels of renin and aldosterone, metabolic alkalosis with high sodium plasma levels, and low rates of urinary excretion of sodium and aldosterone with high rates of urinary potassium excretion. The diagnosis can be further confirmed by genetic testing.
|
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5175,
15
] |
What causes Omenn syndrome ?
|
What causes Omenn syndrome? Omenn syndrome is a genetically heterogeneous condition (meaning that it may be caused by a number of different genes). While most cases are attributed to mutations in the RAG genes (RAG-1 and RAG2 genes have been mapped to chromosome band 11p13), recent reports describe Omenn syndrome in the absence of RAG mutations. Omenn syndrome caused by mutations in ARTEMIS, ADA, ILRA2, ILRA7, CHD7, and DNA ligase 4 have been described in the medical literature. Some cases of Omenn syndrome have also been found in association with 22q11 microdeletion syndrome.
|
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What to do for Kidney Stones in Children ?
|
Families may benefit from meeting with a dietitian to learn how dietary management can help in preventing stones. Depending on the underlying cause of the stone formation, medications may be necessary to prevent recurrent stones. Dietary changes and medications may be required for a long term or, quite often, for life. Some common changes include the following:
- Children who tend to make calcium oxalate stones or have hypercalciuria should eat a regular amount of dietary calcium and limit salt intake. A thiazide diuretic medication may be given to some children to reduce the amount of calcium leaking into the urine. - Children who have large amounts of oxalate in the urine may need to limit foods high in oxalate, such as chocolate, peanut butter, and dark-colored soft drinks. - Children who form uric acid or cystine stones may need extra potassium citrate or potassium carbonate in the form of a pill or liquid medication. Avoiding foods high in purinessuch as meat, fish, and shellfishmay also help prevent uric acid stones.
|
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How many people are affected by infantile neuronal ceroid lipofuscinosis ?
|
The incidence of infantile NCL is unknown. Collectively, all forms of NCL affect an estimated 1 in 100,000 individuals worldwide. NCLs are more common in Finland, where approximately 1 in 12,500 individuals are affected.
|
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What is (are) Laing distal myopathy ?
|
Laing distal myopathy is a slowly progressive muscle disorder that tends to begin in childhood. Early symptoms include weakness in the feet and ankles, followed by weakness in the hands and wrists. Weakness in the feet leads to tightening of the Achilles tendon, an inability to lift the big toe, and a high-stepping walk. Weakness in the hands makes it more difficult to lift the fingers, especially the third and fourth fingers. As the muscle weakness slowly progresses over the course of many years, other muscles of the body (e.g., neck, face, legs, hips, and shoulders) weaken. Most affected people remain mobile throughout life. Life expectancy is normal. Laing distal myopathy is caused by mutations in the MYH7 gene and is inherited in an autosomal dominant fashion.
|
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What are the treatments for citrullinemia ?
|
These resources address the diagnosis or management of citrullinemia: - Baby's First Test: Citrullinemia, Type I - Baby's First Test: Citrullinemia, Type II - Gene Review: Gene Review: Citrin Deficiency - Gene Review: Gene Review: Citrullinemia Type I - Gene Review: Gene Review: Urea Cycle Disorders Overview - Genetic Testing Registry: Citrullinemia type I - Genetic Testing Registry: Citrullinemia type II - Genetic Testing Registry: Neonatal intrahepatic cholestasis caused by citrin deficiency - MedlinePlus Encyclopedia: Hereditary Urea Cycle Abnormality 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 genetic changes related to biotin-thiamine-responsive basal ganglia disease ?
|
Biotin-thiamine-responsive basal ganglia disease is caused by mutations in the SLC19A3 gene. This gene provides instructions for making a protein called a thiamine transporter, which moves thiamine into cells. Thiamine, also known as vitamin B1, is obtained from the diet and is necessary for proper functioning of the nervous system. Mutations in the SLC19A3 gene likely result in a protein with impaired ability to transport thiamine into cells, resulting in decreased absorption of the vitamin and leading to neurological dysfunction. In this disorder, abnormalities affect several parts of the brain. Using medical imaging, generalized swelling as well as specific areas of damage (lesions) in the brain can often be seen, including in the basal ganglia. The relationship between these specific brain abnormalities and the abnormal thiamine transporter is unknown. It is unclear how biotin is related to this disorder. Some researchers suggest that the excess biotin given along with thiamine as treatment for the disorder may increase the amount of thiamine transporter that is produced, partially compensating for the impaired efficiency of the abnormal protein. Others propose that biotin transporter proteins may interact with thiamine transporters in such a way that biotin levels influence the course of the disease.
|
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] |
What is (are) Color Blindness ?
|
Most of us see our world in color. We enjoy looking at a lush green lawn or a red rose in full bloom. If you have a color vision defect, you may see these colors differently than most people. There are three main kinds of color vision defects. Red-green color vision defects are the most common. This type occurs in men more than in women. The other major types are blue-yellow color vision defects and a complete absence of color vision. Most of the time, color blindness is genetic. There is no treatment, but most people adjust and the condition doesn't limit their activities.
|
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Is autoimmune Addison disease inherited ?
|
A predisposition to develop autoimmune Addison disease is passed through generations in families, but the inheritance pattern is unknown.
|
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1,
1,
1
] |
[
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] |
How to diagnose Hereditary sensory neuropathy type 1 ?
|
Is genetic testing available for hereditary sensory neuropathy type 1? At least four genes responsible for hereditary sensory neuropathy type 1 (HSN1) have been found: HSN1A (the most common form) is associated with mutations in the SPTLC1 gene HSN1B, reported in a small number of families, is linked to a specific location on chromosome 3, but the exact gene has not yet been identified HSN1C is caused by mutations in the SPTLC2 gene HSN1D is caused by mutations in the ATL1 gene (the same gene is associated with early-onset hereditary spastic paraplegia 3A) HSN1E is caused by mutations in the DNMT1 gene The Genetic Testing Registry (GTR) provides information about genetic testing for HSN1A. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetics professional. Although the genes for some other types of HSN1 have been identified, we are not aware of clinical laboratories that offer genetic testing for them. A genetics professional may be able to help you locate laboratories that offer testing for other types of HSN1. If the genetic mutation in an affected person has been identified, testing for adult relatives at risk for developing symptoms may be possible. This is called predictive genetic testing. However, this testing is not useful in predicting age of onset, severity, type of symptoms, or rate of progression in people who currently don't have symptoms.
|
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What causes Adrenal Insufficiency and Addison's Disease ?
|
A lack of CRH or ACTH causes secondary adrenal insufficiency. The lack of these hormones in the body can be traced to several possible sources.
Stoppage of Corticosteroid Medication
A temporary form of secondary adrenal insufficiency may occur when a person who has been taking a synthetic glucocorticoid hormone, called a corticosteroid, for a long time stops taking the medication. Corticosteroids are often prescribed to treat inflammatory illnesses such as rheumatoid arthritis, asthma, and ulcerative colitis. In this case, the prescription doses often cause higher levels than those normally achieved by the glucocorticoid hormones created by the body. When a person takes corticosteroids for prolonged periods, the adrenal glands produce less of their natural hormones. Once the prescription doses of corticosteroid are stopped, the adrenal glands may be slow to restart their production of the bodys glucocorticoids. To give the adrenal glands time to regain function and prevent adrenal insufficiency, prescription corticosteroid doses should be reduced gradually over a period of weeks or even months. Even with gradual reduction, the adrenal glands might not begin to function normally for some time, so a person who has recently stopped taking prescription corticosteroids should be watched carefully for symptoms of secondary adrenal insufficiency.
Surgical Removal of Pituitary Tumors
Another cause of secondary adrenal insufficiency is surgical removal of the usually noncancerous, ACTH-producing tumors of the pituitary gland that cause Cushings syndrome. Cushings syndrome is a hormonal disorder caused by prolonged exposure of the bodys tissues to high levels of the hormone cortisol. When the tumors are removed, the source of extra ACTH is suddenly gone and a replacement hormone must be taken until the bodys adrenal glands are able to resume their normal production of cortisol. The adrenal glands might not begin to function normally for some time, so a person who has had an ACTH-producing tumor removed and is going off of his or her prescription corticosteroid replacement hormone should be watched carefully for symptoms of adrenal insufficiency.
More information is provided in the NIDDK health topic, Cushings Syndrome.
Changes in the Pituitary Gland
Less commonly, secondary adrenal insufficiency occurs when the pituitary gland either decreases in size or stops producing ACTH. These events can result from
- tumors or an infection in the pituitary - loss of blood flow to the pituitary - radiation for the treatment of pituitary or nearby tumors - surgical removal of parts of the hypothalamus - surgical removal of the pituitary
|
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What are the symptoms of Charlie M syndrome ?
|
What are the signs and symptoms of Charlie M syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Charlie M syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the fingernails 90% Abnormality of the toenails 90% Brachydactyly syndrome 90% Finger syndactyly 90% Hypertelorism 90% Narrow mouth 90% Non-midline cleft lip 90% Reduced number of teeth 90% Split hand 90% Thin vermilion border 90% Abnormality of the metacarpal bones 50% Abnormality of the nose 50% Short philtrum 50% Macrotia 7.5% Triphalangeal thumb 7.5% The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) SYNGAP1-related intellectual disability ?
|
SYNGAP1-related intellectual disability is a neurological disorder characterized by moderate to severe intellectual disability that is evident in early childhood. The earliest features are typically delayed development of speech and motor skills, such as sitting, standing, and walking. Many people with this condition have weak muscle tone (hypotonia), which contributes to the difficulty with motor skills. Some affected individuals lose skills they had already acquired (developmental regression). Other features of SYNGAP1-related intellectual disability include recurrent seizures (epilepsy), hyperactivity, and autism spectrum disorders, which are conditions characterized by impaired communication and social interaction; almost everyone with SYNGAP1-related intellectual disability develops epilepsy, and about half have an autism spectrum disorder.
|
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What is (are) Quitting Smoking for Older Adults ?
|
One of the keys to successfully quitting is preparation. A great way to prepare to quit smoking is to create a quit plan. Quit plans - keep you focused on quit smoking strategies that can help you be confident and motivated to quit - help you identify challenges you will face as you quit and ways to overcome them - can improve your chances of quitting smoking for good. keep you focused on quit smoking strategies that can help you be confident and motivated to quit help you identify challenges you will face as you quit and ways to overcome them can improve your chances of quitting smoking for good. Use these steps to create your own customized quit plan. Pick a Quit Date. Make a list of reasons to quit. Decide where you will get support. Decide on your Quit methods. Plan how to avoid your triggers. Plan how to overcome cravings and urges. Decide how to reward yourself after certain milestones. Plan what to do the day before your Quit Date. Here are some quit plan resources. - Check out Worksheets for Your Quit Plan on this website. - See "Start Your Quit Plan Online Today" at SmokeFree 60Plus, a quit-smoking website from the National Cancer Institute. - Learn about the Quit Guide from the Centers from Disease Control and Prevention (CDC). Check out Worksheets for Your Quit Plan on this website. See "Start Your Quit Plan Online Today" at SmokeFree 60Plus, a quit-smoking website from the National Cancer Institute. Learn about the Quit Guide from the Centers from Disease Control and Prevention (CDC).
|
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What are the symptoms of Familial esophageal achalasia ?
|
What are the signs and symptoms of Familial esophageal achalasia? The Human Phenotype Ontology provides the following list of signs and symptoms for Familial esophageal achalasia. 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) Achalasia - Autosomal recessive inheritance - Keratoconjunctivitis sicca - Rheumatoid arthritis - Xerostomia - 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 cold-induced sweating syndrome ?
|
These resources address the diagnosis or management of cold-induced sweating syndrome: - Gene Review: Gene Review: Cold-Induced Sweating Syndrome including Crisponi Syndrome - Genetic Testing Registry: Cold-induced sweating syndrome 1 - Genetic Testing Registry: Cold-induced sweating syndrome 2 - Merck Manual Consumer Version: Excessive Sweating 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 Duodenal ulcer due to antral G-cell hyperfunction ?
|
What are the signs and symptoms of Duodenal ulcer due to antral G-cell hyperfunction? The Human Phenotype Ontology provides the following list of signs and symptoms for Duodenal ulcer due to antral G-cell hyperfunction. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal dominant inheritance - Duodenal ulcer - Hyperpepsinogenemia I - 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) Microcephalic osteodysplastic primordial dwarfism type 1 ?
|
Microcephalic osteodysplastic primordial dwarfism type 1 (MOPD1) is a genetic condition that is mainly characterized by intrauterine and post-natal growth retardation; an abnormally small head size (microcephaly); abnormal bone growth (skeletal dysplasia); distinctive facial features; and brain anomalies. Other signs and symptoms include sparse hair and eyebrows; dry skin; short limbs; dislocation of the hips and elbows; seizures; and intellectual disability. It is caused by mutations in the RNU4ATAC gene and is inherited in an autosomal recessive manner. Treatment is supportive only. The prognosis is poor with most affected individuals dying within the first year of life. MOPD types 1 and 3 were originally thought to be separate entities, but more recent reports have confirmed that the two forms are part of the same syndrome.
|
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What are the treatments for Neurofibromatosis ?
|
Treatment may include surgery, focused radiation, or chemotherapy. Surgery to remove NF2 tumors completely is one option. Surgery for vestibular schwannomas does not restore hearing and usually reduces hearing. Sometimes surgery is not performed until functional hearing is lost completely. Surgery may result in damage to the facial nerve and some degree of facial paralysis. Focused radiation of vestibular schwannoma carries of a lower risk of facial paralysis than open surgery, but is more effective o shrinking small to moderate tumors than larger tumors. Chemotherapy with a drug that targets the blood vessels of vestibular schwannoma can reduce the size of the tumor and improves hearing, but some tumors do not respond at all and sometimes respond only temporarily. Bone malformations can often be corrected surgically, and surgery can also correct cataracts and retinal abnormalities. Pain usually subsides when tumors are removed completely.
|
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] |
Is inclusion body myopathy with early-onset Paget disease and frontotemporal dementia inherited ?
|
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In some cases, an affected person inherits the mutation from one affected parent. Other cases result from new mutations in the gene and occur in people with no history of the disorder in their family.
|
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Is Branchiootorenal syndrome inherited ?
|
Is branchiootorenal syndrome inherited? Branchiootorenal syndrome may be inherited or occur sporadically. The inheritance pattern of branchiootorenal syndrome is autosomal dominant. Autosomal dominant inheritance is when one mutated copy of the gene that causes a disorder in each cell is needed for a person to be affected. Autosomal dominant conditions may occur for the first time in a person in a family due to a spontaneous gene mutation, or these conditions may be inherited from an affected parent. When a person with an autosomal dominant disorder has a child, there is a 50% chance that their child will inherit the condition.
|
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What are the treatments for ring chromosome 14 syndrome ?
|
These resources address the diagnosis or management of ring chromosome 14 syndrome: - Genetic Testing Registry: Ring chromosome 14 - MedlinePlus Encyclopedia: Chromosome 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 Hereditary diffuse leukoencephalopathy with spheroids ?
|
What causes hereditary diffuse leukoencephalopathy with spheroids (HDLS)? HDLS is caused by mutations in the CSF1R gene. This gene provides instructions for making a protein called colony stimulating factor 1 receptor (CSF-1 receptor), which is found in the outer membrane of certain types of cells. The CSF-1 receptor triggers signaling pathways that control many important cellular processes, such as cell growth and division (proliferation) and maturation of the cell to take on defined functions (differentiation). Mutations in the CSF1R gene lead to a altered CSF-1 receptor protein which is unable to stimulate cell signaling pathways. Exactly how these gene mutations cause the signs and symptoms of HDLS is unknown.
|
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what research (or clinical trials) is being done for Acid Lipase Disease ?
|
The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge abut the brain and nervous system, and to use that knowledge to reduce the burden of neurological diseaset. The NINDS conducts and supports research to understand lipid storage diseases such as acid lipase deficiency. Additional research studies hope to identify biomarkers (signs that may indicate risk of a disease and improve diagnosis) for thee lipid storage diseases that will speed the development of novel therapeutics for these disorders. Other investigators hope to establish an international disease registry designed to collect longitudinal data that would be used to improve the care and treatment of individuals with lysosomal acid lipase deficiency.
The National Library of Medicine (NLM), a part of the National Institutes of Health (NIH) within the U.S. Department of Health and Human Services, offers free searches of biomedical literature through an Internet service called PubMed. To search, go to: http://www.ncbi.nlm.nih.gov/PubMed . The NLM also offers extensive health information from NIH and other trusted sources. To research your condition, go to: http://www.medlineplus.gov .
|
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What are the symptoms of Spinocerebellar ataxia 21 ?
|
What are the signs and symptoms of Spinocerebellar ataxia 21? The Human Phenotype Ontology provides the following list of signs and symptoms for Spinocerebellar ataxia 21. 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) Nystagmus 5% Aggressive behavior - Akinesia - Apathy - Autosomal dominant inheritance - Cerebellar atrophy - Cognitive impairment - Cogwheel rigidity - Dysarthria - Dysgraphia - Gait ataxia - Hyporeflexia - Impulsivity - Intellectual disability - Limb ataxia - Microsaccadic pursuit - Parkinsonism - Postural tremor - Progressive cerebellar ataxia - Scanning speech - Slow progression - Slow saccadic eye movements - 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 Barrett esophagus inherited ?
|
Is Barrett esophagus inherited? Barrett esophagus usually occurs sporadically in people with no family history of the condition. In rare cases, it can affect more than one family member; however, it is unclear whether these cases are due to common environmental exposures or an inherited predisposition (or a combination of the two). One study found that some people with Barrett esophagus who go on to develop esophageal adenocarcinoma have changes (mutations) in the MSR1, ASCC1, and/or CTHRC1 genes. However, additional studies are needed to confirm these findings.
|
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What is (are) Kuskokwim disease ?
|
Kuskokwim disease is a congenital (present at birth) contracture disorder that occurs solely among Yup'ik Eskimos in and around the Kuskokwim River delta region of southwest Alaska. Affected individuals usually, but not always, have congenital contractures of large joints (especially knees and/or elbows) and spinal, pelvic, and foot deformities. Other skeletal features have also been reported. Kuskokwim disease has been shown to be caused by mutations in the FKBP10 gene and is inherited in an autosomal recessive manner.
|
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How many people are affected by Jervell and Lange-Nielsen syndrome ?
|
Jervell and Lange-Nielsen syndrome is uncommon; it affects an estimated 1.6 to 6 per 1 million people worldwide. This condition has a higher prevalence in Denmark, where it affects at least 1 in 200,000 people.
|
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What is (are) Congenital mirror movement disorder ?
|
Congenital mirror movement disorder (CMM) is a rare condition that is characterized by mirror movements (involuntary movements of one side of the body that mirror intentional movements on the opposite side). Affected people generally develop these movements in infancy or early childhood, which usually persist throughout their life without any related signs or symptoms. In most cases, the involuntary movements are noticeable but less pronounced than the corresponding voluntary movements; however, the severity of symptoms can vary significantly, even among family members. CMM can be caused by changes (mutations) in the DCC or RAD51 genes and inherited in an autosomal dominant manner. In some families, the exact underlying cause of CMM is unknown.
|
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What are the treatments for Stve-Wiedemann syndrome ?
|
These resources address the diagnosis or management of Stve-Wiedemann syndrome: - Genetic Testing Registry: Stuve-Wiedemann 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) Bladder Diseases ?
|
The bladder is a hollow organ in your lower abdomen that stores urine. Many conditions can affect your bladder. Some common ones are - Cystitis - inflammation of the bladder, often from an infection - Urinary incontinence - loss of bladder control - Overactive bladder - a condition in which the bladder squeezes urine out at the wrong time - Interstitial cystitis - a chronic problem that causes bladder pain and frequent, urgent urination - Bladder cancer Doctors diagnose bladder diseases using different tests. These include urine tests, x-rays, and an examination of the bladder wall with a scope called a cystoscope. Treatment depends on the cause of the problem. It may include medicines and, in severe cases, surgery. NIH: National Institute of Diabetes and Digestive and Kidney Diseases
|
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] |
What are the genetic changes related to oculocutaneous albinism ?
|
Oculocutaneous albinism can result from mutations in several genes, including TYR, OCA2, TYRP1, and SLC45A2. Changes in the TYR gene cause type 1; mutations in the OCA2 gene are responsible for type 2; TYRP1 mutations cause type 3; and changes in the SLC45A2 gene result in type 4. Mutations in additional genes likely underlie the other forms of this disorder. The genes associated with oculocutaneous albinism are involved in producing a pigment called melanin, which is the substance that gives skin, hair, and eyes their color. In the retina, melanin also plays a role in normal vision. Mutations in any of these genes disrupt the ability of cells to make melanin, which reduces pigmentation in the skin, hair, and eyes. A lack of melanin in the retina leads to the vision problems characteristic of oculocutaneous albinism. Alterations in the MC1R gene can change the appearance of people with oculocutaneous albinism type 2. This gene helps regulate melanin production and is responsible for some normal variation in pigmentation. People with genetic changes in both the OCA2 and MC1R genes have many of the usual features of oculocutaneous albinism type 2, including light-colored eyes and vision problems; however, they typically have red hair instead of the usual yellow, blond, or light brown hair seen with this condition. Some individuals with oculocutaneous albinism do not have mutations in any of the known genes. In these people, the genetic cause of the condition is unknown.
|
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] |
How many people are affected by Camurati-Engelmann disease ?
|
The prevalence of Camurati-Engelmann disease is unknown. Approximately 200 cases have been reported worldwide.
|
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] |
Is Neonatal progeroid syndrome inherited ?
|
Is neonatal progeroid syndrome inherited? Although the underlying genetic cause of neonatal progeroid syndrome is unknown, studies suggest that it is likely inherited in an autosomal recessive manner. This means that to be affected, a person must have a mutation in both copies of the responsible gene in each cell. The parents of an affected person usually each carry one mutated copy of the gene and are referred to as carriers. Carriers typically do not show signs or symptoms of the condition. When two carriers of an autosomal recessive condition have children, each child has a 25% (1 in 4) risk to have the condition, a 50% (1 in 2) risk to be a carrier like each of the parents, and a 25% chance to not have the condition and not be a carrier.
|
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What are the symptoms of Osteosclerosis with ichthyosis and premature ovarian failure ?
|
What are the signs and symptoms of Osteosclerosis with ichthyosis and premature ovarian failure? The Human Phenotype Ontology provides the following list of signs and symptoms for Osteosclerosis with ichthyosis and premature ovarian failure. 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) Chorioretinal abnormality 90% Edema of the lower limbs 90% Ichthyosis 90% Increased bone mineral density 90% Secondary amenorrhea 90% 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) familial restrictive cardiomyopathy ?
|
Familial restrictive cardiomyopathy is a genetic form of heart disease. For the heart to beat normally, the heart (cardiac) muscle must contract and relax in a coordinated way. Oxygen-rich blood from the lungs travels first through the upper chambers of the heart (the atria), and then to the lower chambers of the heart (the ventricles). In people with familial restrictive cardiomyopathy, the heart muscle is stiff and cannot fully relax after each contraction. Impaired muscle relaxation causes blood to back up in the atria and lungs, which reduces the amount of blood in the ventricles. Familial restrictive cardiomyopathy can appear anytime from childhood to adulthood. The first signs and symptoms of this condition in children are failure to gain weight and grow at the expected rate (failure to thrive), extreme tiredness (fatigue), and fainting. Children who are severely affected may also have abnormal swelling or puffiness (edema), increased blood pressure, an enlarged liver, an abnormal buildup of fluid in the abdominal cavity (ascites), and lung congestion. Some children with familial restrictive cardiomyopathy do not have any obvious signs or symptoms, but they may die suddenly due to heart failure. Without treatment, the majority of affected children survive only a few years after they are diagnosed. Adults with familial restrictive cardiomyopathy typically first develop shortness of breath, fatigue, and a reduced ability to exercise. Some individuals have an irregular heart beat (arrhythmia) and may also experience a sensation of fluttering or pounding in the chest (palpitations) and dizziness. Abnormal blood clots are commonly seen in adults with this condition. Without treatment, approximately one-third of adults with familial restrictive cardiomyopathy do not survive more than five years after diagnosis.
|
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] |
What are the treatments for Coffin-Siris syndrome ?
|
How might Coffin-Siris syndrome be treated? People with Coffin-Siris syndrome may benefit from occupational, physical, and speech therapy. Developmental pediatricians may be helpful in recommending and coordinating therapeutic and educational interventions. Additional specialty care may be needed depending on the symptoms in the individual, such as by gastrointestinal, eye, kidney, heart, and hearing specialists.
|
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] |
What are the treatments for Depression ?
|
A bushy, wild-growing plant with yellow flowers, St John's wort has been used for centuries in many folk and herbal remedies. It is commonly used in Europe to treat mild depression, and it is a top-seller in the United States as well. In a study funded by the National Institutes of Health, the herb was found to be no more effective than a placebo (sugar pill) in treating adults suffering from major depression. Other research has shown that St. John's wort can interact unfavorably with other drugs. The herb interferes with certain drugs used to treat heart disease, depression, seizures, certain cancers, and organ transplant rejection. Because of these potential interactions, older adults should always consult with their doctors before taking any herbal supplement. Another product sold as a dietary supplement, S-adenosyl methionine (SAMe), has shown promise in controlled trials as helpful when added to an SSRI antidepressant that is only partially effective.
|
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] |
What is (are) Dislocations ?
|
Dislocations are joint injuries that force the ends of your bones out of position. The cause is often a fall or a blow, sometimes from playing a contact sport. You can dislocate your ankles, knees, shoulders, hips, elbows and jaw. You can also dislocate your finger and toe joints. Dislocated joints often are swollen, very painful and visibly out of place. You may not be able to move it. A dislocated joint is an emergency. If you have one, seek medical attention. Treatment depends on which joint you dislocate and the severity of the injury. It might include manipulations to reposition your bones, medicine, a splint or sling, and rehabilitation. When properly repositioned, a joint will usually function and move normally again in a few weeks. Once you dislocate a shoulder or kneecap, you are more likely to dislocate it again. Wearing protective gear during sports may help prevent dislocations.
|
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What are the genetic changes related to beta-ureidopropionase deficiency ?
|
Beta-ureidopropionase deficiency is caused by mutations in the UPB1 gene, which provides instructions for making an enzyme called beta-ureidopropionase. This enzyme is involved in the breakdown of molecules called pyrimidines, which are building blocks of DNA and its chemical cousin RNA. The beta-ureidopropionase enzyme is involved in the last step of the process that breaks down pyrimidines. This step converts N-carbamyl-beta-aminoisobutyric acid to beta-aminoisobutyric acid and also breaks down N-carbamyl-beta-alanine to beta-alanine, ammonia, and carbon dioxide. Both beta-aminoisobutyric acid and beta-alanine are thought to play roles in the nervous system. Beta-aminoisobutyric acid increases the production of a protein called leptin, which has been found to help protect brain cells from damage caused by toxins, inflammation, and other factors. Research suggests that beta-alanine is involved in sending signals between nerve cells (synaptic transmission) and in controlling the level of a chemical messenger (neurotransmitter) called dopamine. UPB1 gene mutations can reduce or eliminate beta-ureidopropionase enzyme activity. Loss of this enzyme function reduces the production of beta-aminoisobutyric acid and beta-alanine, and leads to an excess of their precursor molecules, N-carbamyl-beta-aminoisobutyric acid and N-carbamyl-beta-alanine, which are released in the urine. Reduced production of beta-aminoisobutyric acid and beta-alanine may impair the function of these molecules in the nervous system, leading to neurological problems in some people with beta-ureidopropionase deficiency. The extent of the reduction in enzyme activity caused by a particular UPB1 gene mutation, along with other genetic and environmental factors, may determine whether people with beta-ureidopropionase deficiency develop neurological problems and the severity of these problems.
|
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How many people are affected by X-linked agammaglobulinemia ?
|
XLA occurs in approximately 1 in 200,000 newborns.
|
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] |
How many people are affected by Laing distal myopathy ?
|
Although Laing distal myopathy is thought to be rare, its prevalence is unknown. Several families with the condition have been identified worldwide.
|
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Is X-linked spondyloepiphyseal dysplasia tarda inherited ?
|
X-linked spondyloepiphyseal dysplasia tarda is inherited in an X-linked recessive pattern. The TRAPPC2 gene is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. In X-linked recessive inheritance, a female with one mutated copy of the gene in each cell is called a carrier. She can pass on the altered gene, but usually does not experience signs and symptoms of the disorder. In rare cases, however, females who carry a TRAPPC2 mutation may develop arthritis in early adulthood.
|
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Who is at risk for Wilms Tumor and Other Childhood Kidney Tumors? ?
|
Having certain genetic syndromes or other conditions can increase the risk of Wilms tumor.
Anything that increases the risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn't mean that you will not get cancer. Talk to your child's doctor if you think your child may be at risk. Wilms tumor may be part of a genetic syndrome that affects growth or development. A genetic syndrome is a set of signs and symptoms or conditions that occur together and is caused by certain changes in the genes. Certain conditions can also increase a child's risk of developing Wilms tumor. These and other genetic syndromes and conditions have been linked to Wilms tumor: - WAGR syndrome (Wilms tumor, aniridia, abnormal genitourinary system, and mental retardation). - Denys-Drash syndrome (abnormal genitourinary system). - Frasier syndrome (abnormal genitourinary system). - Beckwith-Wiedemann syndrome (abnormally large growth of one side of the body or a body part, large tongue, umbilical hernia at birth, and abnormal genitourinary system). - A family history of Wilms tumor. - Aniridia (the iris, the colored part of the eye, is missing). - Isolated hemihyperplasia (abnormally large growth of one side of the body or a body part). - Urinary tract problems such as cryptorchidism or hypospadias.
Having certain conditions may increase the risk of renal cell cancer.
Renal cell cancer may be related to the following conditions: - Von Hippel-Lindau disease (an inherited condition that causes abnormal growth of blood vessels). Children with Von Hippel-Lindau disease should be checked yearly for renal cell cancer with an ultrasound of the abdomen or an MRI (magnetic resonance imaging) beginning at age 8 to 11 years. - Tuberous sclerosis (an inherited disease marked by noncancerous fatty cysts in the kidney). - Familial renal cell cancer (an inherited condition that occurs when certain changes in the genes that cause kidney cancer are passed down from the parent to the child). - Renal medullary cancer (a rare kidney cancer that grows and spreads quickly). - Hereditary leiomyomatosis (an inherited disorder that increases the risk of having cancer of the kidney, skin, and uterus). Prior chemotherapy or radiation therapy for a childhood cancer, such as neuroblastoma, soft tissue sarcoma, leukemia, or Wilms tumor may also increase the risk of renal cell cancer. See the Second Cancers section in the PDQ summary about Late Effects of Treatment for Childhood Cancer for more information.
|
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What causes Inflammatory myofibroblastic tumor ?
|
What causes inflammatory myofibroblastic tumors? The underlying cause of inflammatory myofibroblastic tumors (IMTs) remains unknown. While some researchers believe it is a true neoplasm, others believe that it represents an immunologic response to an infectious or noninfectious agent. Several associations have been reported between IMT and infections, including: organizing pneumonia Mycobacterium avium intracellulare Corynebacterium equi (a bacteria that affects the lungs) Campylobacter jejuni (a common cause of gastroenteritis) Bacillus sphaericus Coxiella burnetii Epstein-Barr virus E. coli occlusive phlebitis of intrahepatic veins Associations have also been reported between IMT and: previous abdominal surgery trauma ventriculoperitoneal shunt radiation therapy steroid usage An inflammatory reaction to an underlying, low-grade malignancy has also been proposed as a cause. Because there is limited information available to support or refute any of these, the mechanism behind the development of IMTs is still unclear.
|
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] |
Is Split hand split foot nystagmus inherited ?
|
How is split hand split foot nystagmus inherited? Split hand split foot nystagmus is thought to be inherited in an autosomal dominant fashion. A person with an autosomal dominant condition has a 50% chance of passing the condition on to their children. Click here to learn more about autosomal dominant inheritance. Sometimes a person is the only one in their family with the autosomal dominant disorder. One explanation for this is that the person has a de novo or new mutation. De novo mutations refer to a change in a gene that is present for the first time in one family member as a result of a mutation in the mothers egg or fathers sperm, or in the fertilized egg itself. In addition, there have been a couple of case reports where unaffected parents had more than one child with split hand split foot nystagmus. It is thought that this may have been due to germline mosaicism. In germline mosaicism, one of the unaffected parents has the disease-causing genetic mutation in some of his/her eggs or sperm only. Click here to learn more about mosaicism.
|
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How to diagnose Pityriasis lichenoides chronica ?
|
How is pityriasis lichenoides chronica diagnosed? The clinical appearance of pityriasis lichenoides chronica suggests the diagnosis. However, since it can look like psoriasis, lichen planus, or the common bug bite, a skin biopsy is recommended to confirm the diagnosis. A dermatologist is the type of specialist who is most often involved in the diagnosis and care of patients with this condition.
|
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] |
what research (or clinical trials) is being done for Primary CNS Lymphoma ?
|
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. Targeted therapy Targeted therapy is a type of treatment that uses drugs or other substances to attack cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation therapy do. Monoclonal antibody therapy is one type of targeted therapy being studied in the treatment of primary CNS lymphoma. Monoclonal antibody therapy is a cancer treatment that uses antibodies made in the laboratory from a single type of immune system cell. These antibodies can identify substances on cancer cells or normal substances that may help cancer cells grow. The antibodies attach to the substances and kill the cancer cells, block their growth, or keep them from spreading. Monoclonal antibodies are given by infusion. They may be used alone or to carry drugs, toxins, or radioactive material directly to cancer cells. Rituximab is a type of monoclonal antibody used to treat newly diagnosed primary CNS lymphoma in patients who do not have AIDS.
Patients may want to think about taking part in a clinical trial.
For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment. Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment. Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.
Patients can enter clinical trials before, during, or after starting their cancer treatment.
Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment. Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.
|
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] |
What are the symptoms of Progressive hemifacial atrophy ?
|
What are the signs and symptoms of Progressive hemifacial atrophy? The Human Phenotype Ontology provides the following list of signs and symptoms for Progressive hemifacial atrophy. 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) Irregular hyperpigmentation 90% Abnormality of the musculature 50% Aplasia/Hypoplasia of the skin 50% Asymmetric growth 50% Seizures 50% Deeply set eye 7.5% Heterochromia iridis 7.5% Ptosis 7.5% Alopecia areata - Ataxia - Blepharophimosis - Delayed eruption of teeth - Dental malocclusion - Hemifacial atrophy - Horner syndrome - Kyphosis - Microtia - Migraine - Onset - Poliosis - Short mandibular rami - Sporadic - Trigeminal neuralgia - 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 FG syndrome ?
|
How might FG syndrome be treated? Treatment is aimed at addressing the individual symptoms present in each case. This often involves care by a team of providers which may include pediatricians, neurologists, cardiologists, surgeons, gastroenterologists, and psychologists. Early intervention and special education services should be initiated as soon as possible so that each child can reach his fullest potential. GeneReviews provides a detailed list of management strategies.
|
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What is (are) Chronic Myeloproliferative Neoplasms ?
|
Key Points
- Myeloproliferative neoplasms are a group of diseases in which the bone marrow makes too many red blood cells, white blood cells, or platelets. - There are 6 types of chronic myeloproliferative neoplasms. - Tests that examine the blood and bone marrow are used to detect (find) and diagnose chronic myeloproliferative neoplasms.
Myeloproliferative neoplasms are a group of diseases in which the bone marrow makes too many red blood cells, white blood cells, or platelets.
Normally, the bone marrow makes blood stem cells (immature cells) that become mature blood cells over time. A blood stem cell may become a myeloid stem cell or a lymphoid stem cell. A lymphoid stem cell becomes a white blood cell. A myeloid stem cell becomes one of three types of mature blood cells: - Red blood cells that carry oxygen and other substances to all tissues of the body. - White blood cells that fight infection and disease. - Platelets that form blood clots to stop bleeding. In myeloproliferative neoplasms, too many blood stem cells become one or more types of blood cells. The neoplasms usually get worse slowly as the number of extra blood cells increases.
There are 6 types of chronic myeloproliferative neoplasms.
The type of myeloproliferative neoplasm is based on whether too many red blood cells, white blood cells, or platelets are being made. Sometimes the body will make too many of more than one type of blood cell, but usually one type of blood cell is affected more than the others are. Chronic myeloproliferative neoplasms include the following 6 types: - Chronic myelogenous leukemia. - Polycythemia vera. - Primary myelofibrosis (also called chronic idiopathic myelofibrosis). - Essential thrombocythemia. - Chronic neutrophilic leukemia. - Chronic eosinophilic leukemia. These types are described below. Chronic myeloproliferative neoplasms sometimes become acute leukemia, in which too many abnormal white blood cells are made.
|
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] |
What are the genetic changes related to Proteus syndrome ?
|
Proteus syndrome results from a mutation in the AKT1 gene. This genetic change is not inherited from a parent; it arises randomly in one cell during the early stages of development before birth. As cells continue to grow and divide, some cells will have the mutation and other cells will not. This mixture of cells with and without a genetic mutation is known as mosaicism. The AKT1 gene helps regulate cell growth and division (proliferation) and cell death. A mutation in this gene disrupts a cell's ability to regulate its own growth, allowing it to grow and divide abnormally. Increased cell proliferation in various tissues and organs leads to the abnormal growth characteristic of Proteus syndrome. Studies suggest that an AKT1 gene mutation is more common in groups of cells that experience overgrowth than in the parts of the body that grow normally. In some published case reports, mutations in a gene called PTEN have been associated with Proteus syndrome. However, many researchers now believe that individuals with PTEN gene mutations and asymmetric overgrowth do not meet the strict guidelines for a diagnosis of Proteus syndrome. Instead, these individuals actually have condition that is considered part of a larger group of disorders called PTEN hamartoma tumor syndrome. One name that has been proposed for the condition is segmental overgrowth, lipomatosis, arteriovenous malformations, and epidermal nevus (SOLAMEN) syndrome; another is type 2 segmental Cowden syndrome. However, some scientific articles still refer to PTEN-related Proteus syndrome.
|
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What is (are) Ohdo syndrome, Say-Barber-Biesecker-Young-Simpson variant ?
|
The Say-Barber-Biesecker-Young-Simpson (SBBYS) variant of Ohdo syndrome is a rare condition characterized by genital abnormalities in males, missing or underdeveloped kneecaps (patellae), intellectual disability, distinctive facial features, and abnormalities affecting other parts of the body. Males with the SBBYS variant of Ohdo syndrome typically have undescended testes (cryptorchidism). Females with this condition have normal genitalia. Missing or underdeveloped patellae is the most common skeletal abnormality associated with the SBBYS variant of Ohdo syndrome. Affected individuals also have joint stiffness involving the hips, knees, and ankles that can impair movement. Although joints in the lower body are stiff, joints in the arms and upper body may be unusually loose (lax). Many people with this condition have long thumbs and first (big) toes. The SBBYS variant of Ohdo syndrome is also associated with delayed development and intellectual disability, which are often severe. Many affected infants have weak muscle tone (hypotonia) that leads to breathing and feeding difficulties. The SBBYS variant of Ohdo syndrome is characterized by a mask-like, non-expressive face. Additionally, affected individuals may have distinctive facial features such as prominent cheeks, a broad nasal bridge or a nose with a rounded tip, a narrowing of the eye opening (blepharophimosis), droopy eyelids (ptosis), and abnormalities of the tear (lacrimal) glands. About one-third of affected individuals are born with an opening in the roof of the mouth called a cleft palate. The SBBYS variant of Ohdo syndrome can also be associated with heart defects and dental problems.
|
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What are the treatments for aspartylglucosaminuria ?
|
These resources address the diagnosis or management of aspartylglucosaminuria: - Genetic Testing Registry: Aspartylglycosaminuria 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 Hydrolethalus syndrome ?
|
What are the signs and symptoms of Hydrolethalus syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Hydrolethalus 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) Polyhydramnios 92% Severe hydrocephalus 92% Microphthalmia 86% Postaxial hand polydactyly 77% Cleft in skull base 76% Stillbirth 73% Abnormality of the pinna 70% Low-set ears 70% Abnormal lung lobation 66% Laryngeal hypoplasia 57% Tracheal stenosis 57% Cleft palate 55% Talipes equinovarus 52% Complete atrioventricular canal defect 48% Duplication of phalanx of hallux 47% Bifid uterus 33% Hypospadias 33% Upper limb undergrowth 24% Hydronephrosis 16% Abnormal cortical gyration - Abnormality of the vagina - Absent septum pellucidum - Accessory spleen - Adrenal gland dysgenesis - Agenesis of corpus callosum - Agenesis of the diaphragm - Arrhinencephaly - Autosomal recessive inheritance - Bifid nose - Broad neck - Dandy-Walker malformation - Heterotopia - Intrauterine growth retardation - Median cleft lip - Omphalocele - Preaxial hand polydactyly - Proximal tibial hypoplasia - Ventricular septal defect - 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 Pyruvate dehydrogenase deficiency inherited ?
|
How is pyruvate dehydrogenase deficiency inherited? Pyruvate dehydrogenase deficiency is most commonly caused by mutations in the E1 alpha gene, which is located on the X chromosome (one of the sex chromosomes) and is typically inherited in an X-linked dominant manner. Dominant inheritance occurs when an abnormal gene from one parent is capable of causing disease, even though a matching gene from the other parent is normal. The abnormal gene "dominates" the gene pair. Females have two X chromosomes (one from each parent) and males have one X chromosome from the mother and one Y chromosome from the father. For an X-linked dominant disorder, because one mutated gene is enough to cause the condition, both males and females can have the condition. Because males have no other copy of the X chromosome with a working gene, affected males usually have more severe disease than affected females (who have another X chromosome with a working gene). If the father carries the abnormal X gene, all of his daughters will inherit the disease and none of his sons will have the disease. If the mother carries the abnormal X gene, there is a 50% (1 in 2) chance for each child (whether male or female) to inherit the disease. The condition may also be caused by a new mutation that first appears in an affected individual, without either parent carrying an abnormal gene for the condition. The other genes that are thought to cause pyruvate dehydrogenase deficiency appear to be inherited in an autosomal recessive manner and are not on the sex chromosomes. This means that two non-working copies of the gene that is causing the condition must be present for an individual to have the condition. When an individual has an autosomal recessive condition, each of that person's parents have a non-working copy of the gene and are referred to as "carriers." When 2 carriers for the same condition are having children, there is a 25% (1 in 4) chance for each child to have the condition, a 50% (1 in 2) chance for each child to be a carrier like each of the parents, and a 25% chance for each child to not have the condition and not be a carrier.
|
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] |
What is (are) Diabetic Neuropathies: The Nerve Damage of Diabetes ?
|
Autonomic neuropathy affects the nerves that control the heart, regulate blood pressure, and control blood glucose levels. Autonomic neuropathy also affects other internal organs, causing problems with digestion, respiratory function, urination, sexual response, and vision. In addition, the system that restores blood glucose levels to normal after a hypoglycemic episode may be affected, resulting in loss of the warning symptoms of hypoglycemia.
Hypoglycemia Unawareness
Normally, symptoms such as shakiness, sweating, and palpitations occur when blood glucose levels drop below 70 mg/dL. In people with autonomic neuropathy, symptoms may not occur, making hypoglycemia difficult to recognize. Problems other than neuropathy can also cause hypoglycemia unawareness.
Heart and Blood Vessels
The heart and blood vessels are part of the cardiovascular system, which controls blood circulation. Damage to nerves in the cardiovascular system interferes with the body's ability to adjust blood pressure and heart rate. As a result, blood pressure may drop sharply after sitting or standing, causing a person to feel light-headed or even to faint. Damage to the nerves that control heart rate can mean that the heart rate stays high, instead of rising and falling in response to normal body functions and physical activity.
Digestive System
Nerve damage to the digestive system most commonly causes constipation. Damage can also cause the stomach to empty too slowly, a condition called gastroparesis. Severe gastroparesis can lead to persistent nausea and vomiting, bloating, and loss of appetite. Gastroparesis can also make blood glucose levels fluctuate widely, due to abnormal food digestion.
Nerve damage to the esophagus may make swallowing difficult, while nerve damage to the bowels can cause constipation alternating with frequent, uncontrolled diarrhea, especially at night. Problems with the digestive system can lead to weight loss.
Urinary Tract and Sex Organs
Autonomic neuropathy often affects the organs that control urination and sexual function. Nerve damage can prevent the bladder from emptying completely, allowing bacteria to grow in the bladder and kidneys and causing urinary tract infections. When the nerves of the bladder are damaged, urinary incontinence may result because a person may not be able to sense when the bladder is full or control the muscles that release urine.
Autonomic neuropathy can also gradually decrease sexual response in men and women, although the sex drive may be unchanged. A man may be unable to have erections or may reach sexual climax without ejaculating normally. A woman may have difficulty with arousal, lubrication, or orgasm.
Sweat Glands
Autonomic neuropathy can affect the nerves that control sweating. When nerve damage prevents the sweat glands from working properly, the body cannot regulate its temperature as it should. Nerve damage can also cause profuse sweating at night or while eating.
Eyes
Finally, autonomic neuropathy can affect the pupils of the eyes, making them less responsive to changes in light. As a result, a person may not be able to see well when a light is turned on in a dark room or may have trouble driving at night.
|
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] |
How many people are affected by spinal muscular atrophy with progressive myoclonic epilepsy ?
|
SMA-PME is a rare disorder; approximately a dozen affected families have been described in the scientific literature.
|
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] |
What are the treatments for Osteochondritis dissecans ?
|
How might osteochondritis dissecans be treated? The primary aim of treatment for osteochondritis dissecans is to restore normal function of the affected joint, relieve pain and prevent osteoarthritis. Treatment for the condition varies depending on many factors including the age of the affected person and the severity of the symptoms. In children and young teens, osteochondritis dissecans often heals overtime without surgical treatment. These cases are often managed with rest and in some cases, crutches and/or splinting to relieve pain and swelling. If non-surgical treatments are not successful or the case is particularly severe (i.e. the cartilage and bone are moving around within the joint space), surgery may be recommended. Following surgery, physical therapy is often necessary to improve the strength and range of motion of the affected joint.
|
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] |
How many people are affected by lactose intolerance ?
|
Lactose intolerance in infancy resulting from congenital lactase deficiency is a rare disorder. Its incidence is unknown. This condition is most common in Finland, where it affects an estimated 1 in 60,000 newborns. Approximately 65 percent of the human population has a reduced ability to digest lactose after infancy. Lactose intolerance in adulthood is most prevalent in people of East Asian descent, affecting more than 90 percent of adults in some of these communities. Lactose intolerance is also very common in people of West African, Arab, Jewish, Greek, and Italian descent. The prevalence of lactose intolerance is lowest in populations with a long history of dependence on unfermented milk products as an important food source. For example, only about 5 percent of people of Northern European descent are lactose intolerant.
|
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] |
What are the treatments for familial cold autoinflammatory syndrome ?
|
These resources address the diagnosis or management of familial cold autoinflammatory syndrome: - Genetic Testing Registry: Familial cold autoinflammatory syndrome 2 - Genetic Testing Registry: Familial cold urticaria 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 genetic changes related to lysinuric protein intolerance ?
|
Mutations in the SLC7A7 gene cause lysinuric protein intolerance. The SLC7A7 gene provides instructions for producing a protein called y+L amino acid transporter 1 (y+LAT-1), which is involved in transporting lysine, arginine, and ornithine between cells in the body. The transportation of amino acids from the small intestines and kidneys to the rest of the body is necessary for the body to be able to use proteins. Mutations in the y+LAT-1 protein disrupt the transportation of amino acids, leading to a shortage of lysine, arginine, and ornithine in the body and an abnormally large amount of these amino acids in urine. A shortage of lysine, arginine, and ornithine disrupts many vital functions. Arginine and ornithine are involved in a cellular process called the urea cycle, which processes excess nitrogen (in the form of ammonia) that is generated when protein is used by the body. The lack of arginine and ornithine in the urea cycle causes elevated levels of ammonia in the blood. Lysine is particularly abundant in collagen molecules that give structure and strength to connective tissues such as skin, tendons, and ligaments. A deficiency of lysine contributes to the short stature and osteoporosis seen in people with lysinuric protein intolerance. Other features of lysinuric protein intolerance are thought to result from abnormal protein transport (such as protein deposits in the lungs) or a lack of protein that can be used by the body (protein malnutrition).
|
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How many people are affected by STING-associated vasculopathy with onset in infancy ?
|
The prevalence of this condition is unknown. Only a few affected individuals have been described in the medical literature.
|
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What is (are) Limb-girdle muscular dystrophy ?
|
Limb-girdle muscular dystrophy is a group of disorders which affect the voluntary muscles around the hips and shoulders. The conditions are progressive, leading to a loss of muscle strength and bulk over a number of years. Onset may occur in childhood, adolescence, young adulthood, or even later. Males and females are affected in equal numbers. Most forms of limb girdle muscular dystrophy are inherited in an autosomal recessive manner. Several rare forms are inherited in an autosomal dominant pattern. While there are no treatments which directly reverse the muscle weakness associated with this condition, supportive treatment can decrease the complications. There are at least 20 different types of limb-girdle muscular dystrophy.
|
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What are the symptoms of Tuberous sclerosis, type 1 ?
|
What are the signs and symptoms of Tuberous sclerosis, type 1? The Human Phenotype Ontology provides the following list of signs and symptoms for Tuberous sclerosis, type 1. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Intellectual disability 30% Abnormality of the respiratory system - Achromatic retinal patches - Astrocytoma - Attention deficit hyperactivity disorder - Autism - Autosomal dominant inheritance - Cafe-au-lait spot - Cerebral calcification - Chordoma - Dental enamel pits - Ependymoma - Gingival fibromatosis - Hypomelanotic macule - Hypothyroidism - Infantile spasms - Optic glioma - Phenotypic variability - Precocious puberty - Premature chromatid separation - Projection of scalp hair onto lateral cheek - Renal angiomyolipoma - Renal cell carcinoma - Renal cyst - Shagreen patch - Specific learning disability - Subcutaneous nodule - Subependymal nodules - Subungual fibromas - Wolff-Parkinson-White syndrome - 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 Prosopagnosia, hereditary ?
|
What are the signs and symptoms of Prosopagnosia, hereditary? The Human Phenotype Ontology provides the following list of signs and symptoms for Prosopagnosia, hereditary. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal dominant inheritance - Prosopagnosia - 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) Diabetic Kidney Disease ?
|
The kidneys are two bean-shaped organs, each about the size of a fist. They are located just below the rib cage, one on each side of the spine. Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2 quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to the bladder through tubes called ureters. The bladder stores urine.
When the bladder empties, urine flows out of the body through a tube called the urethra, located at the bottom of the bladder. In men the urethra is long, while in women it is short.
Kidneys work at the microscopic level. The kidney is not one large filter. Each kidney is made up of about a million filtering units called nephrons. Each nephron filters a small amount of blood. The nephron includes a filter, called the glomerulus, and a tubule. The nephrons work through a two-step process. The glomerulus lets fluid and waste products pass through it; however, it prevents blood cells and large molecules, mostly proteins, from passing. The filtered fluid then passes through the tubule, which sends needed minerals back to the bloodstream and removes wastes. The final product becomes urine.
|
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What are the symptoms of Precocious puberty ?
|
What are the signs and symptoms of Precocious puberty? The Human Phenotype Ontology provides the following list of signs and symptoms for Precocious puberty. 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) Hypothyroidism 7.5% Autosomal dominant inheritance - Elevated follicle stimulating hormone - Elevated luteinizing hormone - Isosexual precocious puberty - 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 is (are) severe congenital neutropenia ?
|
Severe congenital neutropenia is a condition that causes affected individuals to be prone to recurrent infections. People with this condition have a shortage (deficiency) of neutrophils, a type of white blood cell that plays a role in inflammation and in fighting infection. The deficiency of neutrophils, called neutropenia, is apparent at birth or soon afterward. It leads to recurrent infections beginning in infancy, including infections of the sinuses, lungs, and liver. Affected individuals can also develop fevers and inflammation of the gums (gingivitis) and skin. Approximately 40 percent of affected people have decreased bone density (osteopenia) and may develop osteoporosis, a condition that makes bones progressively more brittle and prone to fracture. In people with severe congenital neutropenia, these bone disorders can begin at any time from infancy through adulthood. Approximately 20 percent of people with severe congenital neutropenia develop cancer of the blood-forming tissue (leukemia) or a disease of the blood and bone marrow (myelodysplastic syndrome) during adolescence. Some people with severe congenital neutropenia have additional health problems such as seizures, developmental delay, or heart and genital abnormalities.
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What are the treatments for Best vitelliform macular dystrophy ?
|
How might Best vitelliform macular dystrophy be treated? There is no specific treatment for Best vitelliform macular dystrophy (BVMD) at this time. Low vision aids help affected people with significant loss of visual acuity. Laser photocoagulation, photodynamic therapy, and anti-VEGF (vascular endothelial growth factor) agents such as bevacizumab have shown limited success in treating some of the secondary features of BVMD such as choroidal neovascularization (when abnormal blood vessels grow under the macula and retina).
|
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What are the treatments for Jackson-Weiss syndrome ?
|
These resources address the diagnosis or management of Jackson-Weiss syndrome: - Gene Review: Gene Review: FGFR-Related Craniosynostosis Syndromes - Genetic Testing Registry: Jackson-Weiss syndrome - MedlinePlus Encyclopedia: Craniosynostosis 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 Prostate Cancer ?
|
Choosing Treatment There are a number of ways to treat prostate cancer, and the doctor will develop a treatment to fit each man's needs. The choice of treatment mostly depends on the stage of the disease and the grade of the tumor. But doctors also consider a man's age, general health, and his feelings about the treatments and their possible side effects. Treatment for prostate cancer may involve watchful waiting, surgery, radiation therapy, or hormonal therapy. Some men receive a combination of therapies. A cure is the goal for men whose prostate cancer is diagnosed early. Weighing Treatment Options You and your doctor will want to consider both the benefits and possible side effects of each option, especially the effects on sexual activity and urination, and other concerns about quality of life. Surgery, radiation therapy, and hormonal therapy all have the potential to disrupt sexual desire or performance for a short while or permanently. Discuss your concerns with your health care provider. Several options are available to help you manage sexual problems related to prostate cancer treatment. Watchful Waiting The doctor may suggest watchful waiting for some men who have prostate cancer that is found at an early stage and appears to be growing slowly. Also, watchful waiting may be advised for older men or men with other serious medical problems. For these men, the risks and possible side effects of surgery, radiation therapy, or hormonal therapy may outweigh the possible benefits. Doctors monitor these patients with regular check-ups. If symptoms appear or get worse, the doctor may recommend active treatment. Surgery Surgery is used to remove the cancer. It is a common treatment for early stage prostate cancer. The surgeon may remove the entire prostate with a type of surgery called radical prostatectomy or, in some cases, remove only part of it. Sometimes the surgeon will also remove nearby lymph nodes. Side effects of the operation may include lack of sexual function or impotence, or problems holding urine or incontinence. Improvements in surgery now make it possible for some men to keep their sexual function. In some cases, doctors can use a technique known as nerve-sparing surgery. This may save the nerves that control erection. However, men with large tumors or tumors that are very close to the nerves may not be able to have this surgery. Some men with trouble holding urine may regain control within several weeks of surgery. Others continue to have problems that require them to wear a pad. Radiation Therapy Radiation therapy uses high-energy x-rays to kill cancer cells and shrink tumors. Doctors may recommend it instead of surgery, or after surgery, to destroy any cancer cells that may remain in the area. In advanced stages, the doctor may recommend radiation to relieve pain or other symptoms. It may also be used in combination with hormonal therapy. Radiation can cause problems with impotence and bowel function. The radiation may come from a machine, which is external radiation, or from tiny radioactive seeds placed inside or near the tumor, which is internal radiation. Men who receive only the radioactive seeds usually have small tumors. Some men receive both kinds of radiation therapy. For external radiation therapy, patients go to the hospital or clinic -- usually for several weeks. Internal radiation may require patients to stay in the hospital for a short time. Hormonal Therapy Hormonal therapy deprives cancer cells of the male hormones they need to grow and survive. This treatment is often used for prostate cancer that has spread to other parts of the body. Sometimes doctors use hormonal therapy to try to keep the cancer from coming back after surgery or radiation treatment. Side effects can include impotence, hot flashes, loss of sexual desire, and thinning of bones. Some hormone therapies increase the risk of blood clots. Monitoring Treatment Regardless of the type of treatment you receive, you will be closely monitored to see how well the treatment is working. Monitoring may include - a PSA blood test -- usually every 3 months to 1 year. - bone scan and/or CT scan to see if the cancer has spread. - a complete blood count to monitor for signs and symptoms of anemia. - looking for signs or symptoms that the disease might be progressing, such as fatigue, increased pain, or decreased bowel and bladder function. a PSA blood test -- usually every 3 months to 1 year. bone scan and/or CT scan to see if the cancer has spread. a complete blood count to monitor for signs and symptoms of anemia. looking for signs or symptoms that the disease might be progressing, such as fatigue, increased pain, or decreased bowel and bladder function.
|
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what research (or clinical trials) is being done for Locked-In Syndrome ?
|
The NINDS supports research on neurological disorders that can cause locked-in syndrome. The goals of this research are to find ways to prevent, treat, and cure these disorders.
|
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What are the treatments for Hemolytic Anemia ?
|
Treatments for hemolytic anemia include blood transfusions, medicines, plasmapheresis (PLAZ-meh-feh-RE-sis), surgery, blood and marrow stem cell transplants, and lifestyle changes.
People who have mild hemolytic anemia may not need treatment, as long as the condition doesn't worsen. People who have severe hemolytic anemia usually need ongoing treatment. Severe hemolytic anemia can be fatal if it's not properly treated.
Goals of Treatment
The goals of treating hemolytic anemia include:
Reducing or stopping the destruction of red blood cells
Increasing the red blood cell count to an acceptable level
Treating the underlying cause of the condition
Treatment will depend on the type, cause, and severity of the hemolytic anemia you have. Your doctor also will consider your age, overall health, and medical history.
If you have an inherited form of hemolytic anemia, it's a lifelong condition that may require ongoing treatment. If you have an acquired form of hemolytic anemia, it may go away if its cause can be found and corrected.
Blood Transfusions
Blood transfusions are used to treat severe or life-threatening hemolytic anemia.
A blood transfusion is a common procedure in which blood is given to you through an intravenous (IV) line in one of your blood vessels. Transfusions require careful matching of donated blood with the recipient's blood.
For more information, go to the Health Topics Blood Transfusion article.
Medicines
Medicines can improve some types of hemolytic anemia, especially autoimmune hemolytic anemia (AIHA). Corticosteroid medicines, such as prednisone, can stop your immune system from, or limit its ability to, make antibodies (proteins) against red blood cells.
If you don't respond to corticosteroids, your doctor may prescribe other medicines to suppress your immune system. Examples include the medicines rituximab and cyclosporine.
If you have severe sickle cell anemia, your doctor may recommend a medicine called hydroxyurea. This medicine prompts your body to make fetal hemoglobin. Fetal hemoglobin is the type of hemoglobin that newborns have.
In people who have sickle cell anemia, fetal hemoglobin helps prevent red blood cells from sickling and improves anemia.
Plasmapheresis
Plasmapheresis is a procedure that removes antibodies from the blood. For this procedure, blood is taken from your body using a needle inserted into a vein.
The plasma, which contains the antibodies, is separated from the rest of the blood. Then, plasma from a donor and the rest of the blood is put back in your body.
This treatment may help if other treatments for immune hemolytic anemia don't work.
Surgery
Some people who have hemolytic anemia may need surgery to remove their spleens. The spleen is an organ in the abdomen. A healthy spleen helps fight infection and filters out old or damaged blood cells.
An enlarged or diseased spleen may remove more red blood cells than normal, causing anemia. Removing the spleen can stop or reduce high rates of red blood cell destruction.
Blood and Marrow Stem Cell Transplant
In some types of hemolytic anemia, such as thalassemias, the bone marrow doesn't make enough healthy red blood cells. The red blood cells it does make may be destroyed before their normal lifespan is over. Blood and marrow stem cell transplants may be used to treat these types of hemolytic anemia.
A blood and marrow stem cell transplant replaces damaged stem cells with healthy ones from another person (a donor).
During the transplant, which is like a blood transfusion, you get donated stem cells through a tube placed in a vein. Once the stem cells are in your body, they travel to your bone marrow and begin making new blood cells.
For more information, go to the Health Topics Blood and Marrow Stem Cell Transplant article.
Lifestyle Changes
If you have AIHA with cold-reactive antibodies, try to avoid cold temperatures. This can help prevent the breakdown of red blood cells. It's very important to protect your fingers, toes, and ears from the cold.
To protect yourself, you can:
Wear gloves or mittens when taking food out of the refrigerator or freezer.
Wear a hat, scarf, and a coat with snug cuffs during cold weather.
Turn down air conditioning or dress warmly while in air-conditioned spaces.
Warm up the car before driving in cold weather.
People born with glucose-6-phosphate dehydrogenase (G6PD) deficiency can avoid substances that may trigger anemia. For example, avoid fava beans, naphthalene (a substance found in some moth balls), and certain medicines (as your doctor advises).
|
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] |
What is (are) What I need to know about Lactose Intolerance ?
|
Lactose
*
intestine
lactase
,
enzyme
*See the Pronunciation Guide for tips on how to say the words in bold type.
|
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What is (are) Glutaric acidemia type III ?
|
Glutaric acidemia type III is a rare metabolic condition characterized by persistent, isolated accumulation or excretion of glutaric acid. No specific phenotype has been described, as symptoms vary and some individuals remain symptom-free. Unlike other types of glutaric acidemia, this type is caused by a peroxisomal rather than a mitochondrial dysfunction. Mutations in the C7ORF10 gene on chromosome 7p14 have been identified in some people with glutaric acidemia type III and the condition follows an autosomal recessive pattern of inheritance. Treatment with riboflavin has been helpful in some patients.
|
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Who is at risk for Adult Soft Tissue Sarcoma? ?
|
Having certain inherited disorders can increase the risk of adult soft tissue sarcoma. Anything that increases your risk of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesn't mean that you will not get cancer. Talk with your doctor if you think you may be at risk. Risk factors for soft tissue sarcoma include the following inherited disorders: - Retinoblastoma. - Neurofibromatosis type 1 (NF1; von Recklinghausen disease). - Tuberous sclerosis (Bourneville disease). - Familial adenomatous polyposis (FAP; Gardner syndrome). - Li-Fraumeni syndrome. - Werner syndrome (adult progeria). - Nevoid basal cell carcinoma syndrome (Gorlin syndrome). Other risk factors for soft tissue sarcoma include the following: - Past treatment with radiation therapy for certain cancers. - Being exposed to certain chemicals, such as Thorotrast (thorium dioxide), vinyl chloride, or arsenic. - Having swelling (lymphedema) in the arms or legs for a long time.
|
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What are the treatments for Coffin Lowry Syndrome ?
|
There is no cure and no standard course of treatment for Coffin-Lowry syndrome. Treatment is symptomatic and supportive, and may include physical and speech therapy and educational services.
|
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What are the symptoms of Mental retardation X-linked, South African type ?
|
What are the signs and symptoms of Mental retardation X-linked, South African type? The Human Phenotype Ontology provides the following list of signs and symptoms for Mental retardation X-linked, South African type. 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 cerebellum 90% Cognitive impairment 90% Decreased body weight 90% Incoordination 90% Long face 90% Macrotia 90% Narrow face 90% Neurological speech impairment 90% Seizures 90% Strabismus 90% Thick eyebrow 90% Adducted thumb 50% Aplasia/Hypoplasia of the corpus callosum 50% Autism 50% Cerebral cortical atrophy 50% Feeding difficulties in infancy 50% Gait disturbance 50% Microcephaly 50% Nystagmus 50% Ophthalmoparesis 50% Pectus excavatum 50% Ventriculomegaly 50% Deeply set eye 7.5% Joint hypermobility 7.5% Mandibular prognathia 7.5% Skeletal muscle atrophy 7.5% Abnormality of the foot - Absent speech - Bowel incontinence - Cerebellar atrophy - Drooling - Dysphagia - Flexion contracture - Happy demeanor - Hyperkinesis - Intellectual disability, progressive - Intellectual disability, severe - Long nose - Loss of ability to walk in first decade - Muscular hypotonia - Mutism - Narrow chest - Neuronal loss in central nervous system - Open mouth - Ophthalmoplegia - Photosensitive tonic-clonic seizures - Sleep disturbance - Slender finger - Truncal ataxia - Urinary incontinence - X-linked dominant inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
What are the symptoms of Prinzmetal's variant angina ?
|
What are the symptoms of Prinzmetal's variant angina? The main symptom of Prinzmetal's variant angina is chest pain (angina) with the following characteristics: Occurs under the chest bone Described as squeezing, constricting, tightness, pressure, crushing Is usually severe and may radiate to the neck, jaw, shoulder, or arm Often occurs at rest Typically occurs at the same time each day, usually between midnight and 8am. Duration of pain is 5 to 30 minutes Pain is relieved by nitroglycerin Loss of consciousness
|
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] |
What is (are) prolidase deficiency ?
|
Prolidase deficiency is a disorder that causes a wide variety of symptoms. The disorder typically becomes apparent during infancy. Affected individuals may have enlargement of the spleen (splenomegaly); in some cases, both the spleen and liver are enlarged (hepatosplenomegaly). Diarrhea, vomiting, and dehydration may also occur. People with prolidase deficiency are susceptible to severe infections of the skin or ears, or potentially life-threatening respiratory tract infections. Some individuals with prolidase deficiency have chronic lung disease. Characteristic facial features in people with prolidase deficiency include prominent eyes that are widely spaced (hypertelorism), a high forehead, a flat bridge of the nose, and a very small lower jaw and chin (micrognathia). Affected children may experience delayed development, and about 75 percent of people with prolidase deficiency have intellectual disability that may range from mild to severe. People with prolidase deficiency often develop skin lesions, especially on their hands, feet, lower legs, and face. The severity of the skin involvement, which usually begins during childhood, may range from a mild rash to severe skin ulcers. Skin ulcers, especially on the legs, may not heal completely, resulting in complications including infection and amputation. The severity of symptoms in prolidase deficiency varies greatly among affected individuals. Some people with this disorder do not have any symptoms. In these individuals the condition can be detected by laboratory tests such as newborn screening tests or tests offered to relatives of affected individuals.
|
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How to diagnose Hemochromatosis ?
|
Health care providers use medical and family history, a physical exam, and routine blood tests to diagnose hemochromatosis or other conditions that could cause the same symptoms or complications.
- Medical and family history. Taking a medical and family history is one of the first things a health care provider may do to help diagnose hemochromatosis. The health care provider will look for clues that may indicate hemochromatosis, such as a family history of arthritis or unexplained liver disease. - Physical exam. After taking a medical history, a health care provider will perform a physical exam, which may help diagnose hemochromatosis. During a physical exam, a health care provider usually - examines a patients body - uses a stethoscope to listen to bodily sounds - taps on specific areas of the patients body - 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. Blood tests can determine whether the amount of iron stored in the body is higher than normal:1 - The transferrin saturation test shows how much iron is bound to the protein that carries iron in the blood. Transferrin saturation values above or equal to 45 percent are considered abnormal. - The serum ferritin test detects the amount of ferritina protein that stores ironin the blood. Levels above 300 g/L in men and 200 g/L in women are considered abnormal. Levels above 1,000 g/L in men or women indicate a high chance of iron overload and organ damage. If either test shows higher-than-average levels of iron in the body, health care providers can order a special blood test that can detect two copies of the C282Y mutation to confirm the diagnosis. If the mutation is not present, health care providers will look for other causes. - Liver biopsy. Health care providers may perform a liver biopsy, a procedure that involves taking a piece of liver tissue for examination with a microscope for signs of damage or disease. The health care provider may ask the patient to temporarily stop taking certain medications before the liver biopsy. The health care provider may ask the patient to fast for 8 hours before the procedure. During the procedure, the patient lies on a table, right hand resting above the head. The health care provider applies a local anesthetic to the area where he or she will insert the biopsy needle. If needed, a health care provider will also give sedatives and pain medication. The health care provider uses a needle to take a small piece of liver tissue. He or she may use ultrasound, computerized tomography scans, or other imaging techniques to guide the needle. After the biopsy, the patient must lie on the right side for up to 2 hours and is monitored an additional 2 to 4 hours before being sent home. A health care provider performs a liver biopsy at a hospital or an outpatient center. The health care provider sends the liver sample to a pathology lab where the pathologista doctor who specializes in diagnosing diseaselooks at the tissue with a microscope and sends a report to the patients health care provider. The biopsy shows how much iron has accumulated in the liver and whether the patient has liver damage.
Hemochromatosis is rare, and health care providers may not think to test for this disease. Thus, the disease is often not diagnosed or treated. The initial symptoms can be diverse, vague, and similar to the symptoms of many other diseases. Health care providers may focus on the symptoms and complications caused by hemochromatosis rather than on the underlying iron overload. However, if a health care provider diagnoses and treats the iron overload caused by hemochromatosis before organ damage has occurred, a person can live a normal, healthy life.
Who should be tested for hemochromatosis? Experts recommend testing for hemochromatosis in people who have symptoms, complications, or a family history of the disease. Some researchers have suggested widespread screening for the C282Y mutation in the general population. However, screening is not cost-effective. Although the C282Y mutation occurs quite frequently, the disease caused by the mutation is rare, and many people with two copies of the mutation never develop iron overload or organ damage. Researchers and public health officials suggest the following: - Siblings of people who have hemochromatosis should have their blood tested to see if they have the C282Y mutation. - Parents, children, and other close relatives of people who have hemochromatosis should consider being tested. - Health care providers should consider testing people who have severe and continuing fatigue, unexplained cirrhosis, joint pain or arthritis, heart problems, erectile dysfunction, or diabetes because these health issues may result from hemochromatosis.
|
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What is (are) Agnosia ?
|
Agnosia is a rare disorder characterized by an inability to recognize and identify objects or persons. People with agnosia may have difficulty recognizing the geometric features of an object or face or may be able to perceive the geometric features but not know what the object is used for or whether a face is familiar or not. Agnosia can be limited to one sensory modality such as vision or hearing. For example, a person may have difficulty in recognizing an object as a cup or identifying a sound as a cough. Agnosia can result from strokes, dementia, developmental disorders, or other neurological conditions. It typically results from damage to specific brain areas in the occipital or parietal lobes of the brain. People with agnosia may retain their cognitive abilities in other areas.
|
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What are the treatments for Urinary Incontinence in Men ?
|
Treatment depends on the type of UI.
Urgency Incontinence
As a first line of therapy for urgency incontinence, a health care professional may recommend the following techniques to treat a mans problem:
- behavioral and lifestyle changes - bladder training - pelvic floor exercises - urgency suppression
If those treatments are not successful, the following additional measures may help urgency incontinence:
- medications - electrical nerve stimulation - bulking agents - surgery
A health care professional may recommend other treatments for men with urgency incontinence caused by BPH. More information is provided in the NIDDK health topic, Prostate Enlargement: Benign Prostatic Hyperplasia.
Behavioral and lifestyle changes. Men with urgency incontinence may be able to reduce leaks by making behavioral and lifestyle changes:
- Eating, diet, and nutrition. Men with urgency incontinence can change the amount and type of liquid they drink. A man can try limiting bladder irritantsincluding caffeinated drinks such as tea or coffee and carbonated beveragesto decrease leaks. Men also should limit alcoholic drinks, which can increase urine production. A health care professional can help a man determine how much he should drink based on his health, how active he is, and where he lives. To decrease nighttime trips to the restroom, men may want to stop drinking liquids several hours before bed. - Engaging in physical activity. Although a man may be reluctant to engage in physical activity when he has urgency incontinence, regular exercise is important for good overall health and for preventing and treating UI. - Losing weight. Men who are overweight should talk with a health care professional about strategies for losing weight, which can help improve UI. - Preventing constipation. Gastrointestinal (GI) problems, especially constipation, can make urinary tract health worse and can lead to UI. The opposite is also true: Urinary problems, such as UI, can make GI problems worse. More information about how to prevent constipation through diet and physical activity is provided in the NIDDK health topic, Constipation.
To Help Prevent Bladder Problems, Stop Smoking People who smoke should stop. Quitting smoking at any age promotes bladder health and overall health. Smoking increases a persons chance of developing stress incontinence, as it increases coughing. Some people say smoking worsens their bladder irritation. Smoking causes most cases of bladder cancer. People who smoke for many years have a higher risk of bladder cancer than nonsmokers or those who smoke for a short time.2 People who smoke should ask for help so they do not have to try quitting alone. Call 1-800-QUITNOW (1-800-784-8669) for more information.
Bladder training. Bladder training is changing urination habits to decrease incidents of UI. The health care professional may suggest a man use the restroom at regular timed intervals, called timed voiding, based on the mans bladder diary. A man can gradually lengthen the time between trips to the restroom to help stretch the bladder so it can hold more urine.
Pelvic floor muscle exercises. Pelvic floor muscle, or Kegel, exercises involve strengthening pelvic floor muscles. Strong pelvic floor muscles hold in urine more effectively than weak muscles. A man does not need special equipment for Kegel exercises. The exercises involve tightening and relaxing the muscles that control urine flow. Pelvic floor exercises should not be performed during urination. A health care professional can help a man learn proper technique. More information is provided in the NIDDK health topic, Kegel Exercise Tips.
Men also may learn how to perform Kegel exercises properly by using biofeedback. Biofeedback uses special sensors to measure bodily functions, such as muscle contractions that control urination. A video monitor displays the measurements as graphs, and sounds indicate when the man is using the correct muscles. The health care professional uses the information to help the man change abnormal function of the pelvic floor muscles. At home, the man practices to improve muscle function. The man can perform the exercises while lying down, sitting at a desk, or standing up. Success with pelvic floor exercises depends on the cause of UI, its severity, and the mans ability to perform the exercises.
Urgency suppression. By using certain techniques, a man can suppress the urge to urinate, called urgency suppression. Urgency suppression is a way for a man to train his bladder to maintain control so he does not have to panic about finding a restroom. Some men use distraction techniques to take their mind off the urge to urinate. Other men find taking long, relaxing breaths and being still can help. Doing pelvic floor exercises also can help suppress the urge to urinate.
Medications. Health care professionals may prescribe medications that relax the bladder, decrease bladder spasms, or treat prostate enlargement to treat urgency incontinence in men.
- Antimuscarinics. Antimuscarinics can help relax bladder muscles and prevent bladder spasms. These medications include oxybutynin (Oxytrol), tolterodine (Detrol), darifenacin (Enablex), trospium (Sanctura), fesoterodine (Toviaz), and solifenacin (VESIcare). They are available in pill, liquid, and patch form. - Tricyclic antidepressants. Tricyclic antidepressants such as imipramine (Tofranil) can calm nerve signals, decreasing spasms in bladder muscles. - Alpha-blockers. Terazosin (Hytrin), doxazosin (Cardura), tamsulosin (Flomax), alfuzosin (Uroxatral), and silodosin (Rapaflo) are used to treat problems caused by prostate enlargement and bladder outlet obstruction. These medications relax the smooth muscle of the prostate and bladder neck, which lets urine flow normally and prevents abnormal bladder contractions that can lead to urgency incontinence. - 5-alpha reductase inhibitors. Finasteride (Proscar) and dutasteride (Avodart) block the production of the male hormone dihydrotestosterone, which accumulates in the prostate and may cause prostate growth. These medications may help to relieve urgency incontinence problems by shrinking an enlarged prostate. - Beta-3 agonists. Mirabegron (Myrbetriq) is a beta-3 agonist a person takes by mouth to help prevent symptoms of urgency incontinence. Mirabegron suppresses involuntary bladder contractions. - Botox. A health care professional may use onabotulinumtoxinA (Botox), also called botulinum toxin type A, to treat UI in men with neurological conditions such as spinal cord injury or multiple sclerosis. Injecting Botox into the bladder relaxes the bladder, increasing storage capacity and decreasing UI. A health care professional performs the procedure during an office visit. A man receives local anesthesia. The health care professional uses a cystoscope to guide the needle for injecting the Botox. Botox is effective for up to 10 months.3
Electrical nerve stimulation. If behavioral and lifestyle changes and medications do not improve symptoms, a urologist may suggest electrical nerve stimulation as an option to prevent UI, urinary frequencyurination more often than normaland other symptoms. Electrical nerve stimulation involves altering bladder reflexes using pulses of electricity. The two most common types of electrical nerve stimulation are percutaneous tibial nerve stimulation and sacral nerve stimulation.4
- Percutaneous tibial nerve stimulation uses electrical stimulation of the tibial nerve, which is located in the ankle, on a weekly basis. The patient receives local anesthesia for the procedure. In an outpatient center, a urologist inserts a battery-operated stimulator beneath the skin near the tibial nerve. Electrical stimulation of the tibial nerve prevents bladder activity by interfering with the pathway between the bladder and the spinal cord or brain. Although researchers consider percutaneous tibial nerve stimulation safe, they continue to study the exact ways that it prevents symptoms and how long the treatment can last. - Sacral nerve stimulation involves implanting a battery-operated stimulator beneath the skin in the lower back near the sacral nerve. The procedure takes place in an outpatient center using local anesthesia. Based on the patients feedback, the health care professional can adjust the amount of stimulation so it works best for that individual. The electrical pulses enter the body for minutes to hours, two or more times a day, either through wires placed on the lower back or just above the pubic areabetween the navel and the pubic hair. Sacral nerve stimulation may increase blood flow to the bladder, strengthen pelvic muscles that help control the bladder, and trigger the release of natural substances that block pain. The patient can turn the stimulator on or off at any time.
A patient may consider getting an implanted device that delivers regular impulses to the bladder. A urologist places a wire next to the tailbone and attaches it to a permanent stimulator under the skin.
Bulking agents. A urologist injects bulking agents, such as collagen and carbon spheres, near the urinary sphincter to treat incontinence. The bulking agent makes the tissues thicker and helps close the bladder opening. Before the procedure, the health care professional may perform a skin test to make sure the man doesnt have an allergic reaction to the bulking agent. A urologist performs the procedure during an office visit. The man receives local anesthesia. The urologist uses a cystoscopea tubelike instrument used to look inside the urethra and bladderto guide the needle for injection of the bulking agent. Over time, the body may slowly eliminate certain bulking agents, so a man may need to have injections again.
Surgery. As a last resort, surgery to treat urgency incontinence in men includes the artificial urinary sphincter (AUS) and the male sling. A health care professional performs the surgery in a hospital with regional or general anesthesia. Most men can leave the hospital the same day, although some may need to stay overnight.
- AUS. An AUS is an implanted device that keeps the urethra closed until the man is ready to urinate. The device has three parts: a cuff that fits around the urethra, a small balloon reservoir placed in the abdomen, and a pump placed in the scrotumthe sac that holds the testicles. The cuff contains a liquid that makes it fit tightly around the urethra to prevent urine from leaking. When it is time to urinate, the man squeezes the pump with his fingers to deflate the cuff. The liquid moves to the balloon reservoir and lets urine flow through the urethra. When the bladder is empty, the cuff automatically refills in the next 2 to 5 minutes to keep the urethra tightly closed. - Male sling. A health care professional performs a sling procedure, also called urethral compression procedure, to add support to the urethra, which can sometimes better control urination. Through an incision in the tissue between the scrotum and the rectum, also called the perineum, the health care professional uses a piece of human tissue or mesh to compress the urethra against the pubic bone. The surgeon secures the ends of the tissue or mesh around the pelvic bones. The lifting and compression of the urethra sometimes provides better control over urination.
Stress Incontinence
Men who have stress incontinence can use the same techniques for treating urgency incontinence.
Functional Incontinence
Men with functional incontinence may wear protective undergarments if they worry about reaching a restroom in time. These products include adult diapers or pads and are available from drugstores, grocery stores, and medical supply stores. Men who have functional incontinence should talk to a health care professional about its cause and how to prevent or treat functional incontinence.
Overflow Incontinence
A health care professional treats overflow incontinence caused by a blockage in the urinary tract with surgery to remove the obstruction. Men with overflow incontinence that is not caused by a blockage may need to use a catheter to empty the bladder. A catheter is a thin, flexible tube that is inserted through the urethra into the bladder to drain urine. A health care professional can teach a man how to use a catheter. A man may need to use a catheter once in a while, a few times a day, or all the time. Catheters that are used continuously drain urine from the bladder into a bag that is attached to the mans thigh with a strap. Men using a continuous catheter should watch for symptoms of an infection.
Transient Incontinence
A health care professional treats transient incontinence by addressing the underlying cause. For example, if a medication is causing increased urine production leading to UI, a health care professional may try lowering the dose or prescribing a different medication. A health care professional may prescribe bacteria-fighting medications called antibiotics to treat UTIs.
|
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] |
What are the treatments for hereditary leiomyomatosis and renal cell cancer ?
|
These resources address the diagnosis or management of HLRCC: - Gene Review: Gene Review: Hereditary Leiomyomatosis and Renal Cell Cancer - Genetic Testing Registry: Hereditary leiomyomatosis and renal cell cancer - MedlinePlus Encyclopedia: Renal Cell Carcinoma 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) Non-Small Cell Lung Cancer ?
|
Key Points
- Non-small cell lung cancer is a disease in which malignant (cancer) cells form in the tissues of the lung. - There are several types of non-small cell lung cancer. - Smoking is the major risk factor for non-small cell lung cancer. - Signs of non-small cell lung cancer include a cough that doesn't go away and shortness of breath. - Tests that examine the lungs are used to detect (find), diagnose, and stage non-small cell lung cancer. - Certain factors affect prognosis (chance of recovery) and treatment options. - For most patients with non-small cell lung cancer, current treatments do not cure the cancer.
Non-small cell lung cancer is a disease in which malignant (cancer) cells form in the tissues of the lung.
The lungs are a pair of cone-shaped breathing organs in the chest. The lungs bring oxygen into the body as you breathe in. They release carbon dioxide, a waste product of the bodys cells, as you breathe out. Each lung has sections called lobes. The left lung has two lobes. The right lung is slightly larger and has three lobes. Two tubes called bronchi lead from the trachea (windpipe) to the right and left lungs. The bronchi are sometimes also involved in lung cancer. Tiny air sacs called alveoli and small tubes called bronchioles make up the inside of the lungs. A thin membrane called the pleura covers the outside of each lung and lines the inside wall of the chest cavity. This creates a sac called the pleural cavity. The pleural cavity normally contains a small amount of fluid that helps the lungs move smoothly in the chest when you breathe. There are two main types of lung cancer: non-small cell lung cancer and small cell lung cancer. See the following PDQ summaries for more information about lung cancer: - Small Cell Lung Cancer Treatment - Unusual Cancers of Childhood Treatment - Lung Cancer Prevention - Lung Cancer Screening
There are several types of non-small cell lung cancer.
Each type of non-small cell lung cancer has different kinds of cancer cells. The cancer cells of each type grow and spread in different ways. The types of non-small cell lung cancer are named for the kinds of cells found in the cancer and how the cells look under a microscope: - Squamous cell carcinoma: Cancer that begins in squamous cells, which are thin, flat cells that look like fish scales. This is also called epidermoid carcinoma. - Large cell carcinoma: Cancer that may begin in several types of large cells. - Adenocarcinoma: Cancer that begins in the cells that line the alveoli and make substances such as mucus. Other less common types of non-small cell lung cancer are: pleomorphic, carcinoid tumor, salivary gland carcinoma, and unclassified carcinoma.
For most patients with non-small cell lung cancer, current treatments do not cure the cancer.
If lung cancer is found, taking part in one of the many clinical trials being done to improve treatment should be considered. Clinical trials are taking place in most parts of the country for patients with all stages of non-small cell lung cancer. Information about ongoing clinical trials is available from the NCI website.
|
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] |
What are the treatments for dystonia 6 ?
|
These resources address the diagnosis or management of dystonia 6: - Gene Review: Gene Review: Dystonia Overview - Genetic Testing Registry: Dystonia 6, torsion 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 Noonan syndrome 2 ?
|
How might Noonan syndrome be treated? Management generally focuses on the specific signs and symptoms present in each person. Treatments for the complications of Noonan syndrome (such as cardiovascular abnormalities) are generally standard and do not differ from treatment in the general population. Developmental disabilities are addressed by early intervention programs and individualized education strategies. Treatment for serious bleeding depends upon the specific factor deficiency or platelet abnormality. Growth hormone treatment increases growth velocity. More detailed information about treatment for Noonan syndrome can be viewed on the GeneReviews Web site.
|
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] |
What is (are) Compulsive Gambling ?
|
Many people enjoy gambling, whether it's betting on a horse or playing poker on the Internet. Most people who gamble don't have a problem, but some lose control of their gambling. Signs of problem gambling include - Always thinking about gambling - Lying about gambling - Spending work or family time gambling - Feeling bad after you gamble, but not quitting - Gambling with money you need for other things If you have concerns about your gambling, ask for help. Your health care provider can work with you to find the treatment that's best for you. NIH: National Institutes of Health
|
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What are the symptoms of HurlerScheie syndrome ?
|
What are the signs and symptoms of HurlerScheie syndrome ? The Human Phenotype Ontology provides the following list of signs and symptoms for HurlerScheie syndrome . If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal form of the vertebral bodies 90% Abnormality of the heart valves 90% Abnormality of the tonsils 90% Coarse facial features 90% Hepatomegaly 90% Hernia 90% Limitation of joint mobility 90% Opacification of the corneal stroma 90% Short stature 90% Sinusitis 90% Skeletal dysplasia 90% Splenomegaly 90% Abnormal pyramidal signs 50% Decreased nerve conduction velocity 50% Sensorineural hearing impairment 50% Spinal canal stenosis 50% Hypertrichosis 7.5% Hypertrophic cardiomyopathy 7.5% Aortic regurgitation - Autosomal recessive inheritance - Corneal opacity - Depressed nasal bridge - Dysostosis multiplex - Hirsutism - Joint stiffness - Kyphosis - Mitral regurgitation - Obstructive sleep apnea - Pulmonary hypertension - Recurrent respiratory infections - Scoliosis - Thick vermilion border - Tracheal stenosis - Umbilical hernia - 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 Viral Hepatitis: A through E and Beyond ?
|
Symptoms include
- jaundice, which causes a yellowing of the skin and eyes - fatigue - abdominal pain - loss of appetite - nausea - vomiting - diarrhea - low grade fever - headache
However, some people do not have symptoms.
|
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What are the genetic changes related to galactosemia ?
|
Mutations in the GALT, GALK1, and GALE genes cause galactosemia. These genes provide instructions for making enzymes that are essential for processing galactose obtained from the diet. These enzymes break down galactose into another simple sugar, glucose, and other molecules that the body can store or use for energy. Mutations in the GALT gene cause classic galactosemia (type I). Most of these genetic changes almost completely eliminate the activity of the enzyme produced from the GALT gene, preventing the normal processing of galactose and resulting in the life-threatening signs and symptoms of this disorder. Another GALT gene mutation, known as the Duarte variant, reduces but does not eliminate the activity of the enzyme. People with the Duarte variant tend to have much milder features of galactosemia. Galactosemia type II results from mutations in the GALK1 gene, while mutations in the GALE gene underlie galactosemia type III. Like the enzyme produced from the GALT gene, the enzymes made from the GALK1 and GALE genes play important roles in processing galactose. A shortage of any of these critical enzymes allows galactose and related compounds to build up to toxic levels in the body. The accumulation of these substances damages tissues and organs, leading to the characteristic features of galactosemia.
|
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] |
What are the treatments for Schizencephaly ?
|
How might schizencephaly be treated? The best treatment options for people with schizencephaly depend on many factors, including the severity of the condition and the signs and symptoms present. For example, people with developmental delay (i.e. delayed motor milestones) or partial paralysis may be referred for physical therapy and/or occupational therapy. Medications are often prescribed to prevent seizures. In cases that are complicated by hydrocephalus, a surgically implanted tube, called a shunt, is often used to divert fluid to another area of the body where it can be absorbed.
|
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What are the symptoms of Juvenile myelomonocytic leukemia ?
|
What are the signs and symptoms of Juvenile myelomonocytic leukemia? The Human Phenotype Ontology provides the following list of signs and symptoms for Juvenile myelomonocytic leukemia. 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) Juvenile myelomonocytic leukemia - Somatic mutation - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
How many people are affected by Weyers acrofacial dysostosis ?
|
Weyers acrofacial dysostosis appears to be a rare disorder. Only a few affected families have been identified worldwide.
|
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15
] |
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