[System] The assistant is a factual and informative medical chatbot.

[User] Who is at risk for Cough? ?

[Assistant]
People at risk for cough include those who:

Are exposed to things that irritate their airways (called irritants) or things that they're allergic to (called allergens). Examples of irritants are cigarette smoke, air pollution, paint fumes, and scented products. Examples of allergens are dust, animal dander, mold, and pollens from trees, grasses, and flowers.

Have certain conditions that irritate the lungs, such as asthma, sinus infections, colds, or gastroesophageal reflux disease.

Smoke. Smoking can irritate your lungs and cause coughing. Smoking and/or exposure to secondhand smoke also can lead to medical conditions that can cause a cough.

Take certain medicines, such as ACE inhibitors and beta blockers. ACE inhibitors are used to treat high blood pressure (HBP). Beta blockers are used to treat HBP, migraine headaches, and glaucoma.

Women are more likely than men to develop a chronic cough. For more information about the substances and conditions that put you at risk for cough, go to "What Causes Cough?"


[System] The assistant is a factual and informative medical chatbot.

[User] what research (or clinical trials) is being done for Multiple System Atrophy with Orthostatic Hypotension ?

[Assistant] The NINDS supports research on disorders of the autonomic nervous system, including multiple system atrophy with orthostatic hypotension. This research is aimed at developing techniques to diagnose, treat, and prevent these disorders. Currently there are ongoing treatment trials of drugs to treat MSA.


[System] The assistant is a factual and informative medical chatbot.

[User] What is (are) Parasites - Scabies ?

[Assistant]
Scabies is an infestation of the skin by the human itch mite (Sarcoptes scabiei var. hominis). The microscopic scabies mite burrows into the upper layer of the skin where it lives and lays its eggs. The most common symptoms of scabies are intense itching and a pimple-like skin rash. The scabies mite usually is spread by direct, prolonged, skin-to-skin contact with a person who has scabies.
Scabies is found worldwide and affects people of all races and social classes. Scabies can spread rapidly under crowded conditions where close body and skin contact is frequent. Institutions such as nursing homes, extended-care facilities, and prisons are often sites of scabies outbreaks. Child care facilities also are a common site of scabies infestations.


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[User] What are the treatments for Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids ?

[Assistant] How might CLIPPERS be treated? The signs and symptoms of CLIPPERS typically improve after treatment with steroids. Initial treatment may involve a short course of high dose steroids given intravenously, and then oral steroids. Many patients experience a relapse when steroids are tapered off, so it is usually necessary to continue treatment that suppresses the immune system. Long term treatment may include a low dose of oral steroids and another type of immune suppressant, such as methotrexate or rituximab. Because there have been very few patients with CLIPPERS reported in medical journals, the best course of treatment has not yet been determined.


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[User] What are the symptoms of Valinemia ?

[Assistant] What are the signs and symptoms of Valinemia? Valinemia is thought to be extremely rare and has been described in only a few people. The condition is reportedly present from birth. Symptoms in the newborn period include lack of appetite, protein intolerance, metabolic acidosis, frequent vomiting, failure to thrive, and/or coma. The condition can become life-threatening. Abnormally low muscle tone (hypotonia); hyperkinesia; hyperactivity; excessive drowsiness; and delayed mental and physical development have also been reported. The Human Phenotype Ontology provides the following list of signs and symptoms for Valinemia. 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 - Drowsiness - Failure to thrive - Hyperkinesis - Hypervalinemia - Muscle weakness - Vomiting - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What causes Hereditary leiomyomatosis and renal cell cancer ?

[Assistant] What causes hereditary leiomyomatosis and renal cell cancer? Hereditary leiomyomatosis and renal cell cancer (HLRCC) is caused by changes (mutations) in the FH gene. This gene gives the body instructions for making an enzyme called fumarase which is needed for a series of reactions that lets cells use oxygen and energy (the citric acid cycle, or Krebs cycle). People with HLRCC are born with one mutated copy of the FH gene in each cell. The second copy of the gene in some cells can mutate later on from factors in the environment, such as radiation from the sun or an error during cell division. A mutation can interfere with fumarase's role in the citric acid cycle, which may affect the regulation of oxygen levels in cells. Long-term oxygen deficiency in cells with two mutated copies of the FH gene may contribute to tumors growth and the tendency to develop leiomyomas and/or renal cell cancer.


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[User] Is familial cylindromatosis inherited ?

[Assistant] Susceptibility to familial cylindromatosis has an autosomal dominant pattern of inheritance, which means one copy of the altered gene in each cell increases the risk of developing this condition. However, a second, non-inherited mutation is required for development of skin appendage tumors in this disorder.


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[User] What is (are) Meige disease ?

[Assistant] Meige disease is a condition that affects the normal function of the lymphatic system. The lymphatic system consists of a network of vessels that transport lymphatic fluid and immune cells throughout the body. Meige disease is characterized by the abnormal transport of lymphatic fluid. When this fluid builds up abnormally, it causes swelling (lymphedema) in the lower limbs.  Meige disease is classified as a primary lymphedema, which means it is a form of lymphedema that is not caused by other health conditions. In Meige disease, the lymphatic system abnormalities are present from birth (congenital), although the swelling is not usually apparent until puberty. The swelling often begins in the feet and ankles and progresses up the legs to the knees. Some affected individuals develop non-contagious skin infections called cellulitis or erysipelas in the legs, which can further damage the vessels that carry lymphatic fluid.


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[User] What are the treatments for Schizencephaly ?

[Assistant] Treatment generally consists of physical therapy and drugs 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.


[System] The assistant is a factual and informative medical chatbot.

[User] How many people are affected by core binding factor acute myeloid leukemia ?

[Assistant] Acute myeloid leukemia occurs in approximately 3.5 per 100,000 individuals each year. CBF-AML accounts for 12 to 15 percent of acute myeloid leukemia cases in adults.


[System] The assistant is a factual and informative medical chatbot.

[User] What is (are) isolated growth hormone deficiency ?

[Assistant] Isolated growth hormone deficiency is a condition caused by a severe shortage or absence of growth hormone. Growth hormone is a protein that is necessary for the normal growth of the body's bones and tissues. Because they do not have enough of this hormone, people with isolated growth hormone deficiency commonly experience a failure to grow at the expected rate and have unusually short stature. This condition is usually apparent by early childhood.  There are four types of isolated growth hormone deficiency differentiated by the severity of the condition, the gene involved, and the inheritance pattern.  Isolated growth hormone deficiency type IA is caused by an absence of growth hormone and is the most severe of all the types. In people with type IA, growth failure is evident in infancy as affected babies are shorter than normal at birth.  People with isolated growth hormone deficiency type IB produce very low levels of growth hormone. As a result, type IB is characterized by short stature, but this growth failure is typically not as severe as in type IA. Growth failure in people with type IB is usually apparent in early to mid-childhood.  Individuals with isolated growth hormone deficiency type II have very low levels of growth hormone and short stature that varies in severity. Growth failure in these individuals is usually evident in early to mid-childhood. It is estimated that nearly half of the individuals with type II have underdevelopment of the pituitary gland (pituitary hypoplasia). The pituitary gland is located at the base of the brain and produces many hormones, including growth hormone.  Isolated growth hormone deficiency type III is similar to type II in that affected individuals have very low levels of growth hormone and short stature that varies in severity. Growth failure in type III is usually evident in early to mid-childhood. People with type III may also have a weakened immune system and are prone to frequent infections. They produce very few B cells, which are specialized white blood cells that help protect the body against infection (agammaglobulinemia).


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[User] What is (are) Familial hypercholesterolemia ?

[Assistant] Familial hypercholesterolemia is a condition characterized by very high levels of cholesterol in the blood due to mutations in the LDLR gene. People with hypercholesterolemia have a high risk of developing a form of heart disease called coronary artery disease, as well as health problems related to the buildup of excess cholesterol in other tissues (e.g., in the tendons and skin). Familial hypercholesterolemia tends to be passed through families in an autosomal dominant fashion. There are other hereditary forms of hypercholesterolemia caused by mutations in the APOB, LDLRAP1, or PCSK9 gene. However, most cases of high cholesterol are not caused by a single inherited condition, but result from a combination of lifestyle choices and the effects of variations in many genes.


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[User] What is (are) Polymyositis ?

[Assistant] Polymyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Polymyositis affects skeletal muscles (those involved with making movement) on both sides of the body. It is rarely seen in persons under age 18; most cases are in adults between the ages of 31 and 60. Progressive muscle weakness starts in the proximal muscles (muscles closest to the trunk of the body) which eventually leads to difficulties climbing stairs, rising from a seated position, lifting objects, or reaching overhead. People with polymyositis may also experience arthritis, shortness of breath, difficulty swallowing and speaking, and heart arrhythmias. In some cases of polymyositis, distal muscles (muscles further away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Polymyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus. Polymyositis may also be associated with infectious disorders, such as HIV-AIDS.


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[User] Is amelogenesis imperfecta inherited ?

[Assistant] Amelogenesis imperfecta can have different inheritance patterns depending on the gene that is altered. Many cases are caused by mutations in the FAM83H gene and are inherited in an autosomal dominant pattern. This type of inheritance means one copy of the altered gene in each cell is sufficient to cause the disorder. Some cases caused by mutations in the ENAM gene also have an autosomal dominant inheritance pattern.  Amelogenesis imperfecta can also be inherited in an autosomal recessive pattern; this form of the disorder can result from mutations in the ENAM or MMP20 gene. Autosomal recessive inheritance means two copies of the gene in each cell are altered. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.  About 5 percent of amelogenesis imperfecta cases are caused by mutations in the AMELX gene and are inherited in an X-linked pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In most cases, males with X-linked amelogenesis imperfecta experience more severe dental abnormalities than females with this form of this condition.  Other cases of amelogenesis imperfecta result from new gene mutations and occur in people with no history of the disorder in their family.


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[User] What are the genetic changes related to phosphoglycerate dehydrogenase deficiency ?

[Assistant] Mutations in the PHGDH gene cause phosphoglycerate dehydrogenase deficiency. The PHGDH gene provides instructions for making the parts (subunits) that make up the phosphoglycerate dehydrogenase enzyme. Four PHGDH subunits combine to form the enzyme. This enzyme is involved in the production of the protein building block (amino acid) serine. Specifically, the enzyme converts a substance called 3-phosphoglycerate to 3-phosphohydroxypyruvate in the first step in serine production. Serine is necessary for the development and function of the brain and spinal cord (central nervous system). Serine is a part of chemical messengers called neurotransmitters that transmit signals in the nervous system. Proteins that form cell membranes and myelin also contain serine. Serine can be obtained from the diet, but brain cells must produce their own serine because dietary serine cannot cross the protective barrier that allows only certain substances to pass between blood vessels and the brain (the blood-brain barrier).  PHGDH gene mutations result in the production of an enzyme with decreased function. As a result, less 3-phosphoglycerate is converted into 3-phosphohydroxypyruvate than normal and serine production is stalled at the first step. The lack of serine likely prevents the production of proteins and neurotransmitters in the brain and impairs the formation of normal cells and myelin. These disruptions in normal brain development lead to the signs and symptoms of phosphoglycerate dehydrogenase deficiency.


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[User] What to do for Ectopic Kidney ?

[Assistant] Eating, diet, and nutrition have not been shown to play a role in causing or preventing an ectopic kidney.


[System] The assistant is a factual and informative medical chatbot.

[User] What are the treatments for Traumatic Brain Injury ?

[Assistant] Anyone with signs of moderate or severe TBI should receive medical attention as soon as possible. Because little can be done to reverse the initial brain damage caused by trauma, medical personnel try to stabilize an individual with TBI and focus on preventing further injury. Primary concerns include insuring proper oxygen supply to the brain and the rest of the body, maintaining adequate blood flow, and controlling blood pressure. Imaging tests help in determining the diagnosis and prognosis of a TBI patient. Patients with mild to moderate injuries may receive skull and neck X-rays to check for bone fractures or spinal instability. For moderate to severe cases, the imaging test is a computed tomography (CT) scan. Moderately to severely injured patients receive rehabilitation that involves individually tailored treatment programs in the areas of physical therapy, occupational therapy, speech/language therapy, physiatry (physical medicine), psychology/psychiatry, and social support.


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[User] What are the symptoms of Inguinal Hernia ?

[Assistant]
The first sign of an inguinal hernia is a small bulge on one or, rarely, on both sides of the grointhe area just above the groin crease between the lower abdomen and the thigh. The bulge may increase in size over time and usually disappears when lying down.

Other signs and symptoms can include

- discomfort or pain in the groinespecially when straining, lifting, coughing, or exercisingthat improves when resting  - feelings such as weakness, heaviness, burning, or aching in the groin  - a swollen or an enlarged scrotum in men or boys

Indirect and direct inguinal hernias may slide in and out of the abdomen into the inguinal canal. A health care provider can often move them back into the abdomen with gentle massage.


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[User] What causes Creating a Family Health History ?

[Assistant] Yes. Diet, weight, physical activity, tobacco and alcohol use, occupation, and where you live can each increase or decrease disease risk. For example, smoking increases the chance of developing heart disease and cancer. Sun exposure is the major known environmental factor associated with the development of skin cancer of all types. However, other environmental and genetic factors can also increase a persons risk. The best defense against skin cancer is to encourage sun-protective behaviors, regular skin examinations, and skin self-awareness in an effort to decrease high-risk behaviors and optimize early detection of problems.  Learn more about the causes and risk factors for skin cancer.


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[User] Do you have information about Exercise for Seniors

[Assistant] Summary : Exercise and physical activity are good for just about everyone, including older adults. There are four main types and each type is different. Doing them all will give you more benefits.       - Endurance, or aerobic, activities increase your breathing and heart rate. Brisk walking or jogging, dancing, swimming, and biking are examples.    - Strength exercises make your muscles stronger. Lifting weights or using a resistance band can build strength.    - Balance exercises help prevent falls    - Flexibility exercises stretch your muscles and can help your body stay limber       NIH: National Institute on Aging


[System] The assistant is a factual and informative medical chatbot.

[User] What are the treatments for asphyxiating thoracic dystrophy ?

[Assistant] These resources address the diagnosis or management of asphyxiating thoracic dystrophy:  - Genetic Testing Registry: Asphyxiating thoracic dystrophy 2  - Genetic Testing Registry: Asphyxiating thoracic dystrophy 4  - Genetic Testing Registry: Asphyxiating thoracic dystrophy 5  - Genetic Testing Registry: Jeune thoracic dystrophy  - Genetic Testing Registry: Short-rib thoracic dysplasia 1 with or without polydactyly  - Jeune's Center at Nationwide Children's Hospital  - MedlinePlus Encyclopedia: Chronic Renal Failure  - MedlinePlus Encyclopedia: Polydactyly   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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[User] What are the symptoms of Klinefelter syndrome ?

[Assistant] What are the signs and symptoms of Klinefelter syndrome? The signs and symptoms of Klinefelter syndrome (KS) vary among affected people. Some men with KS have no symptoms of the condition or are only mildy affected. In these cases, they may not even know that they are affected by KS. When present, symptoms may include: Small, firm testicles Delayed or incomplete puberty Breast growth (gynecomastia) Reduced facial and body hair Infertility Tall height Abnormal body proportions (long legs, short trunk, shoulder equal to hip size) Learning disablity Speech delay Whether or not a male with KS has visible symptoms depends on many factors, including how much testosterone his body makes, if he is mosaic (with both XY and XXY cells), and his age when the condition is diagnosed and treated. The Human Phenotype Ontology provides the following list of signs and symptoms for Klinefelter 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 chromosome segregation 90% Decreased fertility 90% Disproportionate tall stature 90% Neurological speech impairment 90% Abnormal hair quantity 50% Abnormality of movement 50% Clinodactyly of the 5th finger 50% Cryptorchidism 50% Eunuchoid habitus 50% Hypoplasia of penis 50% Long face 50% Mandibular prognathia 50% Obesity 50% Reduced bone mineral density 50% Scoliosis 50% Single transverse palmar crease 50% Venous insufficiency 50% Abnormality of calvarial morphology 7.5% Abnormality of the mitral valve 7.5% Neoplasm 7.5% Type II diabetes mellitus 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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[User] What are the genetic changes related to complement factor I deficiency ?

[Assistant] Complement factor I deficiency is caused by mutations in the CFI gene. This gene provides instructions for making a protein called complement factor I. This protein helps regulate a part of the body's immune response known as the complement system. The complement system is a group of proteins that work together to destroy foreign invaders (such as bacteria and viruses), trigger inflammation, and remove debris from cells and tissues. This system must be carefully regulated so it targets only unwanted materials and does not attack the body's healthy cells. Complement factor I and several related proteins protect healthy cells by preventing activation of the complement system when it is not needed.  Mutations in the CFI gene that cause complement factor I deficiency result in abnormal, nonfunctional, or absent complement factor I. The lack (deficiency) of functional complement factor I protein allows uncontrolled activation of the complement system. The unregulated activity of the complement system decreases blood levels of another complement protein called C3, reducing the immune system's ability to fight infections. In addition, the immune system may malfunction and attack its own tissues, resulting in autoimmune disorders.


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[User] What are the treatments for spinocerebellar ataxia type 3 ?

[Assistant] These resources address the diagnosis or management of SCA3:  - Gene Review: Gene Review: Spinocerebellar Ataxia Type 3  - Genetic Testing Registry: Azorean disease   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care


[System] The assistant is a factual and informative medical chatbot.

[User] What causes Glucose transporter type 1 deficiency syndrome ?

[Assistant] What causes glucose transporter type 1 deficiency syndrome? Glucose transporter type 1 deficiency syndrome (GLUT1 deficiency syndrome) is caused by changes (mutations) in the SLC2A1 gene. This gene encodes a protein that helps transport glucose (a simple sugar) into cells where it is used as fuel. The protein is particularly important in the central nervous system since glucose is the brain's main source of energy. SLC2A1 mutations impair the function of the protein. This significantly reduces the amount of glucose available to brain cells leading to the many signs and symptoms associated with GLUT1 deficiency syndrome.


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[User] Who is at risk for Anxiety Disorders? ?

[Assistant] Generalized anxiety disorder (GAD) affects about 6.8 million American adults, including twice as many women as men. The disorder develops gradually and can begin at any point in the life cycle, although the years of highest risk are between childhood and middle age. The average age of onset is 31 years old. Social phobia affects about 15 million American adults. Women and men are equally likely to develop the disorder, which usually begins in childhood or early adolescence. There is some evidence that genetic factors are involved.  Panic disorder  affects about 6 million American adults and is twice as common in women as men. Panic attacks often begin in late adolescence or early adulthood, but not everyone who experiences panic attacks will develop panic disorder. Many people have just one attack and never have another. The tendency to develop panic attacks appears to be inherited.


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[User] What causes Tay-Sachs disease ?

[Assistant] What causes Tay-Sachs disease? Tay-Sachs disease is caused by mutations in the HEXA gene. The HEXA gene provides instructions for making part of an enzyme called beta-hexosaminidase A, which plays a critical role in the brain and spinal cord. This enzyme is located in lysosomes, which are structures in cells that break down toxic substances and act as recycling centers. Within lysosomes, beta-hexosaminidase A helps break down a fatty substance called GM2 ganglioside. Mutations in the HEXA gene disrupt the activity of beta-hexosaminidase A, which prevents the enzyme from breaking down GM2 ganglioside. As a result, this substance accumulates to toxic levels, particularly in neurons in the brain and spinal cord. Progressive damage caused by the buildup of GM2 ganglioside leads to the destruction of these neurons, which causes the signs and symptoms seen in Tay-Sachs disease,


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[User] What are the symptoms of Spinocerebellar ataxia 40 ?

[Assistant] What are the signs and symptoms of Spinocerebellar ataxia 40? The Human Phenotype Ontology provides the following list of signs and symptoms for Spinocerebellar ataxia 40. 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) Broad-based gait - Dysarthria - Dysdiadochokinesis - Hyperreflexia - Intention tremor - Pontocerebellar atrophy - Spastic paraparesis - Unsteady gait - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What is (are) Skin Cancer ?

[Assistant] Skin cancer is the most common form of cancer in the United States. The two most common types are basal cell cancer and squamous cell cancer. They usually form on the head, face, neck, hands, and arms. Another type of skin cancer, melanoma, is more dangerous but less common.     Anyone can get skin cancer, but it is more common in people who        -  Spend a lot of time in the sun or have been sunburned    -  Have light-colored skin, hair and eyes    -  Have a family member with skin cancer    -  Are over age 50       You should have your doctor check any suspicious skin markings and any changes in the way your skin looks. Treatment is more likely to work well when cancer is found early. If not treated, some types of skin cancer cells can spread to other tissues and organs. Treatments include surgery, radiation therapy, chemotherapy, photodynamic therapy (PDT), and biologic therapy. PDT uses a drug and a type of laser light to kill cancer cells. Biologic therapy boosts your body's own ability to fight cancer.    NIH: National Cancer Institute


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[User] What are the genetic changes related to alternating hemiplegia of childhood ?

[Assistant] Alternating hemiplegia of childhood is primarily caused by mutations in the ATP1A3 gene. Very rarely, a mutation in the ATP1A2 gene is involved in the condition. These genes provide instructions for making very similar proteins. They function as different forms of one piece, the alpha subunit, of a larger protein complex called Na+/K+ ATPase; the two versions of the complex are found in different parts of the brain. Both versions play a critical role in the normal function of nerve cells (neurons). Na+/K+ ATPase transports charged atoms (ions) into and out of neurons, which is an essential part of the signaling process that controls muscle movement.  Mutations in the ATP1A3 or ATP1A2 gene reduce the activity of the Na+/K+ ATPase, impairing its ability to transport ions normally. It is unclear how a malfunctioning Na+/K+ ATPase causes the episodes of paralysis or uncontrollable movements characteristic of alternating hemiplegia of childhood.


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[User] How many people are affected by T-cell immunodeficiency, congenital alopecia, and nail dystrophy ?

[Assistant] T-cell immunodeficiency, congenital alopecia, and nail dystrophy is a rare disorder. It has been diagnosed in only a few individuals, almost all of whom are members of a large extended family from a community in southern Italy.


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[User] Is C3 glomerulopathy inherited ?

[Assistant] Most cases of C3 glomerulopathy are sporadic, which means they occur in people with no history of the disorder in their family. Only a few reported families have had more than one family member with C3 glomerulopathy. However, many affected people have had close relatives with autoimmune diseases, which occur when the immune system malfunctions and attacks the body's tissues and organs. The connection between C3 glomerulopathy and autoimmune diseases is not fully understood.


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[User] What are the genetic changes related to mucolipidosis III gamma ?

[Assistant] Mutations in the GNPTG gene cause mucolipidosis III gamma. This gene provides instructions for making one part (subunit) of an enzyme called GlcNAc-1-phosphotransferase. This enzyme helps prepare certain newly made enzymes for transport to lysosomes. Lysosomes are compartments within the cell that use digestive enzymes to break down large molecules into smaller ones that can be reused by cells. GlcNAc-1-phosphotransferase is involved in the process of attaching a molecule called mannose-6-phosphate (M6P) to specific digestive enzymes. Just as luggage is tagged at the airport to direct it to the correct destination, enzymes are often "tagged" after they are made so they get to where they are needed in the cell. M6P acts as a tag that indicates a digestive enzyme should be transported to the lysosome.  Mutations in the GNPTG gene that cause mucolipidosis III gamma result in reduced activity of GlcNAc-1-phosphotransferase. These mutations disrupt the tagging of digestive enzymes with M6P, which prevents many enzymes from reaching the lysosomes. Digestive enzymes that do not receive the M6P tag end up outside the cell, where they have increased activity. The shortage of digestive enzymes within lysosomes causes large molecules to accumulate there. Conditions that cause molecules to build up inside lysosomes, including mucolipidosis III gamma, are called lysosomal storage disorders. The signs and symptoms of mucolipidosis III gamma are most likely due to the shortage of digestive enzymes inside lysosomes and the effects these enzymes have outside the cell.


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[User] What is (are) Compulsive Gambling ?

[Assistant] 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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[User] What are the symptoms of Chromosome 1q41-q42 deletion syndrome ?

[Assistant] What are the signs and symptoms of Chromosome 1q41-q42 deletion syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Chromosome 1q41-q42 deletion 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) Anteverted nares - Autosomal dominant inheritance - Cleft palate - Cleft upper lip - Coarse facial features - Congenital diaphragmatic hernia - Cryptorchidism - Deeply set eye - Depressed nasal bridge - Frontal bossing - Holoprosencephaly - Hypotelorism - Intellectual disability - Microcephaly - Microphthalmia - Microtia - Phenotypic variability - Preauricular skin tag - Seizures - Short stature - Talipes equinovarus - Upslanted palpebral fissure - Vertebral segmentation 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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[User] What is (are) Latex Allergy ?

[Assistant] Latex is a milky fluid that comes from the tropical rubber tree. Hundreds of everyday products contain latex. Repeated exposure to a protein in natural latex can make you more likely to develop a latex allergy. If your immune system detects the protein, a reaction can start in minutes. You could get a rash or asthma. In rare cases you could have a severe reaction called anaphylaxis.    Your doctor may use a physical exam and skin and blood tests to diagnose it. There are medicines to treat a reaction, but it is best to try to avoid latex. Common latex products include       - Gloves    - Condoms    - Balloons    - Rubber bands    - Shoe soles    - Pacifiers       You can find latex-free versions of these products.


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[User] What is (are) Chronic Myelogenous Leukemia ?

[Assistant]
Key Points
                    - Chronic myelogenous leukemia is a disease in which the bone marrow makes too many white blood cells.    - Leukemia may affect red blood cells, white blood cells, and platelets.    - Signs and symptoms of chronic myelogenous leukemia include fever, night sweats, and tiredness.     - Most people with CML have a gene mutation (change) called the Philadelphia chromosome.    - Tests that examine the blood and bone marrow are used to detect (find) and diagnose chronic myelogenous leukemia.    - Certain factors affect prognosis (chance of recovery) and treatment options.

                    Chronic myelogenous leukemia is a disease in which the bone marrow makes too many white blood cells.
                    Chronic myelogenous leukemia (also called CML or chronic granulocytic leukemia) is a slowly progressing blood and bone marrow disease that usually occurs during or after middle age, and rarely occurs in children.

                    Leukemia may affect red blood cells, white blood cells, and 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.    -  Platelets that form blood clots to stop bleeding.    -  Granulocytes (white blood cells) that fight infection and disease.         In CML, too many blood stem cells become a type of white blood cell called granulocytes. These granulocytes are abnormal and do not become healthy white blood cells. They are also called leukemia cells. The leukemia cells can build up in the blood and bone marrow so there is less room for healthy white blood cells, red blood cells, and platelets. When this happens, infection, anemia, or easy bleeding may occur.   This summary is about chronic myelogenous leukemia. See the following PDQ summaries for more information about leukemia:          -  Adult Acute Lymphoblastic Leukemia Treatment     -  Childhood Acute Lymphoblastic Leukemia Treatment     -  Adult Acute Myeloid Leukemia Treatment     -  Childhood Acute Myeloid Leukemia/Other Myeloid Malignancies Treatment     -  Chronic Lymphocytic Leukemia Treatment     -  Hairy Cell Leukemia Treatment


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[User] How to diagnose Polycythemia Vera ?

[Assistant]
Polycythemia vera (PV) may not cause signs or symptoms for years. The disease often is found during routine blood tests done for other reasons. If the results of your blood tests aren't normal, your doctor may want to do more tests.

Your doctor will diagnose PV based on your signs and symptoms, your age and overall health, your medical history, a physical exam, and test results.

During the physical exam, your doctor will look for signs of PV. He or she will check for an enlarged spleen, red skin on your face, and bleeding from your gums.

If your doctor confirms that you have polycythemia, the next step is to find out whether you have primary polycythemia (polycythemia vera) or secondary polycythemia.

Your medical history and physical exam may confirm which type of polycythemia you have. If not, you may have tests that check the level of the hormone erythropoietin (EPO) in your blood.

People who have PV have very low levels of EPO. People who have secondary polycythemia usually have normal or high levels of EPO.

Specialists Involved

If your primary care doctor thinks you have PV, he or she may refer you to a hematologist. A hematologist is a doctor who specializes in diagnosing and treating blood diseases and conditions.

Diagnostic Tests

You may have blood tests to diagnose PV. These tests include a complete blood count (CBC) and other tests, if necessary.

Complete Blood Count

Often, the first test used to diagnose PV is a CBC. The CBC measures many parts of your blood.

This test checks your hemoglobin (HEE-muh-glow-bin) and hematocrit (hee-MAT-oh-crit) levels. Hemoglobin is an iron-rich protein that helps red blood cells carry oxygen from the lungs to the rest of the body. Hematocrit is a measure of how much space red blood cells take up in your blood. A high level of hemoglobin or hematocrit may be a sign of PV.

The CBC also checks the number of red blood cells, white blood cells, and platelets in your blood. Abnormal results may be a sign of PV, a blood disorder, an infection, or another condition.

In addition to high red blood cell counts, people who have PV also may have high white blood cell and/or platelet counts.

Other Blood Tests

Blood smear. For this test, a small sample of blood is drawn from a vein, usually in your arm. The blood sample is examined under a microscope.

A blood smear can show whether you have a higher than normal number of red blood cells. The test also can show abnormal blood cells that are linked to myelofibrosis and other conditions related to PV.

Erythropoietin level. This blood test measures the level of EPO in your blood. EPO is a hormone that prompts your bone marrow to make new blood cells. People who have PV have very low levels of EPO. People who have secondary polycythemia usually have normal or high levels of EPO.

Bone Marrow Tests

Bone marrow tests can show whether your bone marrow is healthy. These tests also show whether your bone marrow is making normal amounts of blood cells.

The two bone marrow tests are aspiration (as-pi-RA-shun) and biopsy. For aspiration, your doctor removes a small amount of fluid bone marrow through a needle. For a biopsy, your doctor removes a small amount of bone marrow tissue through a larger needle. The samples are then examined under a microscope.

If the tests show that your bone marrow is making too many blood cells, it may be a sign that you have PV.


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[User] What are the treatments for Hemifacial microsomia ?

[Assistant] How might hemifacial microsomia be treated? Treatment of hemifacial microsomia varies depending on the features present and the severity in each affected person. Various types of surgeries may be needed in many cases. Some children need breathing support or a tracheostomy soon after birth if the jaw is severely affected. However in most cases, airway problems can be managed without surgery. Those with a jaw deformity and/or clefts may have feeding problems and may need supplemental feedings through a nasogastric tube to support growth and weight gain. Babies born with cleft lip or palate can have surgical repairs done during the first year. Cleft lip repair is typically performed when the child is 3-6 months old, while cleft palate surgery is generally performed when the child is about a year old. A lateral facial cleft, one of the most severe abnormalities associated with the condition, also requires reconstruction in stages. If eye closure is incomplete due to eyelid abnormalities or facial paralysis is present, a child may need eye protection or surgery. Surgery may also be used for eyelid differences to reposition the lower lids and corners of the eyes. Some children with abnormally shaped or missing ears may choose to have a series of reconstructive surgeries to make the ear appear more normal. Children with skin, cheek and other soft tissue deficiencies may need augmentation procedures such as fat grafting or tissue transfer. Severe bone abnormalities may require surgery as well. Because multiple body systems may be involved in hemifacial microsomia, affected people should continually be monitored for complications.


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[User] What are the complications of Primary Biliary Cirrhosis ?

[Assistant]
Most complications of primary biliary cirrhosis are related to cirrhosis and start after primary biliary cirrhosis progresses to cirrhosis. In some cases, portal hypertension and esophageal varices may develop before cirrhosis.

Portal hypertension. The portal vein carries blood from the stomach, intestines, spleen, gallbladder, and pancreas to the liver. In cirrhosis, scar tissue partially blocks the normal flow of blood, which increases the pressure in the portal vein. This condition is called portal hypertension. Portal hypertension is a common complication of cirrhosis. This condition may lead to other complications, such as

- edemaswelling due to a buildup of fluidin the feet, ankles, or legs, and ascitesa buildup of fluid in the abdomen  - enlarged blood vessels, called varices, in the esophagus, stomach, or both  - an enlarged spleen, called splenomegaly  - mental confusion due to a buildup of toxins that are ordinarily removed by the liver, a condition called hepatic encephalopathy

Edema and ascites. Liver failure causes fluid buildup that results in edema and ascites. Ascites can lead to spontaneous bacterial peritonitis, a serious infection that requires immediate medical attention.

Varices. Portal hypertension may cause enlarged blood vessels in the esophagus, stomach, or both. These enlarged blood vessels, called esophageal or gastric varices, cause the vessel walls to become thin and blood pressure to increase, making the blood vessels more likely to burst. If they burst, serious bleeding can occur in the esophagus or upper stomach, requiring immediate medical attention.

Splenomegaly. Portal hypertension may cause the spleen to enlarge and retain white blood cells and platelets, reducing the numbers of these cells and platelets in the blood. A low platelet count may be the first evidence that a person has developed cirrhosis.

Hepatic encephalopathy. A failing liver cannot remove toxins from the blood, so they eventually accumulate in the brain. The buildup of toxins in the brain is called hepatic encephalopathy. This condition can decrease mental function and cause stupor and even coma. Stupor is an unconscious, sleeplike state from which a person can only be aroused briefly by a strong stimulus, such as a sharp pain. Coma is an unconscious, sleeplike state from which a person cannot be aroused. Signs of decreased mental function include

- confusion  - personality changes  - memory loss  - trouble concentrating  - a change in sleep habits

Metabolic bone diseases. Some people with cirrhosis develop a metabolic bone disease, which is a disorder of bone strength usually caused by abnormalities of vitamin D, bone mass, bone structure, or minerals, such as calcium and phosphorous. Osteopenia is a condition in which the bones become less dense, making them weaker. When bone loss becomes more severe, the condition is referred to as osteoporosis. People with these conditions are more likely to develop bone fractures.

Gallstones and bile duct stones. If cirrhosis prevents bile from flowing freely to and from the gallbladder, the bile hardens into gallstones. Symptoms of gallstones include abdominal pain and recurrent bacterial cholangitisirritated or infected bile ducts. Stones may also form in and block the bile ducts, causing pain, jaundice, and bacterial cholangitis.

Steatorrhea. Steatorrhea is a condition in which the body cannot absorb fat, causing a buildup of fat in the stool and loose, greasy, and foul-smelling bowel movements. Steatorrhea may be caused by impairment of bile delivery to the small intestine or by the pancreas not producing enough digestive enzymes.

Liver cancer. Liver cancer is common in people with cirrhosis. Liver cancer has a high mortality rate. Current treatments are limited and only fully successful if a health care provider detects the cancer early, before the tumor is too large. For this reason, health care providers should check people with cirrhosis for signs of liver cancer every 6 to 12 months. Health care providers use blood tests, ultrasound, or both to check for signs of liver cancer.


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[User] What is the outlook for Narcolepsy ?

[Assistant] None of the currently available medications enables people with narcolepsy to consistently maintain a fully normal state of alertness. But EDS and cataplexy, the most disabling symptoms of the disorder, can be controlled in most patients with drug treatment. Often the treatment regimen is modified as symptoms change. Whatever the age of onset, patients find that the symptoms tend to get worse over the two to three decades after the first symptoms appear. Many older patients find that some daytime symptoms decrease in severity after age 60.


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[User] What are the genetic changes related to cranioectodermal dysplasia ?

[Assistant] Cranioectodermal dysplasia is caused by mutations in one of at least four genes: the WDR35, IFT122, WDR19, or IFT43 gene. The protein produced from each of these genes is one piece (subunit) of a protein complex called IFT complex A (IFT-A). This complex is found in finger-like structures called cilia that stick out from the surface of cells. These structures are important for the development and function of many types of cells and tissues. The IFT-A complex is involved in a process called intraflagellar transport, which moves substances within cilia. This movement is essential for the assembly and maintenance of these structures. The IFT-A complex carries materials from the tip to the base of cilia.  Mutations in any of the four mentioned genes reduce the amount or function of one of the IFT-A subunits. Shortage or abnormal function of a single component of the IFT-A complex impairs the function of the entire complex, disrupting the assembly and maintenance of cilia. These mutations lead to a smaller number of cilia and to abnormalities in their shape and structure. Although the mechanism is unclear, a loss of normal cilia impedes proper development of bone, ectodermal tissues, and other tissues and organs, leading to the features of cranioectodermal dysplasia.  About 40 percent of people with cranioectodermal dysplasia have mutations in one of the four known genes. The cause of the condition in people without mutations in one of these genes is unknown.


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[User] What are the stages of Lip and Oral Cavity Cancer ?

[Assistant]
Key Points
                    - After lip and oral cavity cancer has been diagnosed, tests are done to find out if cancer cells have spread within the lip and oral cavity or to other parts of the body.     - There are three ways that cancer spreads in the body.    - Cancer may spread from where it began to other parts of the body.    - The following stages are used for lip and oral cavity cancer:         - Stage 0 (Carcinoma in Situ)     - Stage I     - Stage II     - Stage III     - Stage IV

                    After lip and oral cavity cancer has been diagnosed, tests are done to find out if cancer cells have spread within the lip and oral cavity or to other parts of the body.
                    The process used to find out if cancer has spread within the lip and oral cavity or to other parts of the body is called staging. The information gathered from the staging process determines the stage of the disease. It is important to know the stage in order to plan treatment. The results of the tests used to diagnose lip and oral cavity cancer are also used to stage the disease. (See the General Information section.)

                    There are three ways that cancer spreads in the body.
                    Cancer can spread through tissue, the lymph system, and the blood:         - Tissue. The cancer spreads from where it began by growing into nearby areas.     - Lymph system. The cancer spreads from where it began by getting into the lymph system. The cancer travels through the lymph vessels to other parts of the body.     - Blood. The cancer spreads from where it began by getting into the blood. The cancer travels through the blood vessels to other parts of the body.

                    Cancer may spread from where it began to other parts of the body.
                    When cancer spreads to another part of the body, it is called metastasis. Cancer cells break away from where they began (the primary tumor) and travel through the lymph system or blood.         - Lymph system. The cancer gets into the lymph system, travels through the lymph vessels, and forms a tumor (metastatic tumor) in another part of the body.    - Blood. The cancer gets into the blood, travels through the blood vessels, and forms a tumor (metastatic tumor) in another part of the body.        The metastatic tumor is the same type of cancer as the primary tumor. For example, if lip cancer spreads to the lung, the cancer cells in the lung are actually lip cancer cells. The disease is metastatic lip cancer, not lung cancer.

                    The following stages are used for lip and oral cavity cancer:
                    Stage 0 (Carcinoma in Situ)    In stage 0, abnormal cells are found in the lining of the lips and oral cavity. These abnormal cells may become cancer and spread into nearby normal tissue. Stage 0 is also called carcinoma in situ.        Stage I    In stage I, cancer has formed and the tumor is 2 centimeters or smaller. Cancer has not spread to the lymph nodes.        Stage II    In stage II, the tumor is larger than 2 centimeters but not larger than 4 centimeters, and cancer has not spread to the lymph nodes.       Stage III    In stage III, the tumor:            - may be any size and has spread to one lymph node that is 3 centimeters or smaller, on the same side of the neck as the tumor; or     - is larger than 4 centimeters.              Stage IV     Stage IV is divided into stages IVA, IVB, and IVC.            - In stage IVA, the tumor:                  - has spread through tissue in the lip or oral cavity into nearby tissue and/or bone (jaw, tongue, floor of mouth, maxillary sinus, or skin on the chin or nose); cancer may have spread to one lymph node that is 3 centimeters or smaller, on the same side of the neck as the tumor; or       -  is any size or has spread through tissue in the lip or oral cavity into nearby tissue and/or bone (jaw, tongue, floor of mouth, maxillary sinus, or skin on the chin or nose), and cancer has spread:                           -  to one lymph node on the same side of the neck as the tumor and the lymph node is larger than 3 centimeters but not larger than 6 centimeters; or          - to more than one lymph node on the same side of the neck as the tumor and the lymph nodes are not larger than 6 centimeters; or          - to lymph nodes on the opposite side of the neck as the tumor or on both sides of the neck, and the lymph nodes are not larger than 6 centimeters.                                  - In stage IVB, the tumor:                  - may be any size and has spread to one or more lymph nodes that are larger than 6 centimeters; or       - has spread further into the muscles or bones in the oral cavity, or to the base of the skull and/or the carotid artery. Cancer may have spread to one or more lymph nodes anywhere in the neck.                 - In stage IVC, the tumor has spread beyond the lip or oral cavity to distant parts of the body, such as the lungs. The tumor may be any size and may have spread to the lymph nodes.


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[User] What are the symptoms of Tarsal tunnel syndrome ?

[Assistant] What symptoms are commonly seen in tarsal tunnel syndrome? The symptoms of tarsal tunnel syndrome can vary from person to person. The most common symptom of tarsal tunnel syndrome is foot and ankle pain. Individuals may also experience a burning or tingling sensation and numbness. These symptoms may occur when a person stands, walks, or wears a particular type of shoe. Pain usually worsens during walking and is relieved by rest.


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[User] What causes Rickets ?

[Assistant] What causes rickets? Rickets is caused by a lack of vitamin D. A child might not get enough vitamin D if he or she: Has dark skin Spends too little time outside Has on sunscreen all the time when out of doors Doesn't eat foods containing vitamin D because of lactose intolerance or a strict vegetarian diet Is breastfed without receiving vitamin D supplements Can't make or use vitamin D because of a medical disorder such as celiac disease Has an inherited disorder that affects vitamin D levels


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[User] What are the genetic changes related to Ghosal hematodiaphyseal dysplasia ?

[Assistant] Ghosal hematodiaphyseal dysplasia results from mutations in the TBXAS1 gene. This gene provides instructions for making an enzyme called thromboxane A synthase 1, which acts as part of a chemical signaling pathway involved in normal blood clotting (hemostasis). Based on its role in Ghosal hematodiaphyseal dysplasia, researchers suspect that thromboxane A synthase 1 may also be important for bone remodeling, which is a normal process in which old bone is removed and new bone is created to replace it, and for the production of red blood cells in bone marrow.  Mutations in the TBXAS1 gene severely reduce the activity of thromboxane A synthase 1. Studies suggest that a lack of this enzyme's activity may lead to abnormal bone remodeling and fibrosis of the bone marrow. However, the mechanism by which a shortage of thromboxane A synthase 1 activity leads to the particular abnormalities characteristic of Ghosal hematodiaphyseal dysplasia is unclear.


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[User] What are the symptoms of GOSR2-related progressive myoclonus ataxia ?

[Assistant] What are the signs and symptoms of GOSR2-related progressive myoclonus ataxia? The Human Phenotype Ontology provides the following list of signs and symptoms for GOSR2-related progressive myoclonus ataxia. 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) Absence seizures - Areflexia - Ataxia - Atonic seizures - Autosomal recessive inheritance - Difficulty walking - Dysarthria - Elevated serum creatine phosphokinase - Myoclonus - Progressive - Scoliosis - Tremor - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What is (are) Melnick-Needles syndrome ?

[Assistant] Melnick-Needles syndrome is a disorder involving abnormalities in skeletal development and other health problems. It is a member of a group of related conditions called otopalatodigital spectrum disorders, which also includes otopalatodigital syndrome type 1, otopalatodigital syndrome type 2, and frontometaphyseal dysplasia. In general, these disorders involve hearing loss caused by malformations in the tiny bones in the ears (ossicles), problems in the development of the roof of the mouth (palate), and skeletal abnormalities involving the fingers and/or toes (digits).  Melnick-Needles syndrome is usually the most severe of the otopalatodigital spectrum disorders. People with this condition are usually of short stature, have an abnormal curvature of the spine (scoliosis), partial dislocation (subluxation) of certain joints, and unusually long fingers and toes. They may have bowed limbs; underdeveloped, irregular ribs that can cause problems with breathing; and other abnormal or absent bones.  Characteristic facial features may include bulging eyes with prominent brow ridges, excess hair growth on the forehead, round cheeks, a very small lower jaw and chin (micrognathia), and misaligned teeth. One side of the face may appear noticeably different from the other (facial asymmetry). Some individuals with this disorder have hearing loss.  In addition to skeletal abnormalities, individuals with Melnick-Needles syndrome may have obstruction of the ducts between the kidneys and bladder (ureters) or heart defects.  Males with Melnick-Needles syndrome generally have much more severe signs and symptoms than do females, and in almost all cases die before or soon after birth.


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[User] What is (are) Glucose transporter type 1 deficiency syndrome ?

[Assistant] Glucose transporter type 1 deficiency syndrome (GLUT1 deficiency syndrome) is an inherited condition that affects the nervous system. Signs and symptoms generally develop within the first few months of life and may include recurrent seizures (epilepsy) and involuntary eye movements. Affected people may also have microcephaly (unusually small head size) that develops after birth, developmental delay, intellectual disability and other neurological problems such as spasticity, ataxia (difficulty coordinating movements), and dysarthria. Approximately 10% of affected people have the "non-epileptic" form of GLUT1 deficiency syndrome which is associated with all the typical symptoms of the condition without seizures. GLUT1 deficiency syndrome is caused by changes (mutations) in the SLC2A1 gene and is inherited in an autosomal dominant manner. Although there is currently no cure for GLUT1 deficiency syndrome, a special diet (called a ketogenic diet) may help alleviate symptoms.


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[User] Is Nephrocalcinosis inherited ?

[Assistant] Is nephrocalcinosis inherited? Nephrocalcinosis may be caused by a large variety of things, including underlying disorders, certain medications and supplements, and infections. Nephrocalcinosis itself is not inherited. However, the underlying condition that is causing nephrocalcinosis in an individual may be inherited. Some inherited conditions that may be associated with nephrocalcinosis in affected individuals are: Multiple endocrine neoplasia type 1 (MEN1) Familial distal renal tubular acidosis Chronic granulomatous disease Primary hyperoxaluria Bartter syndrome primary hyperaldosteronism Liddle syndrome 11-beta hydroxylase deficiency, a form of congenital adrenal hyperplasia (CAH) Autosomal dominant hypophosphatemic rickets and X-linked hypophosphatemic conditions


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[User] What is (are) Female Infertility ?

[Assistant] Infertility means not being able to get pregnant after at least one year of trying (or 6 months if the woman is over age 35). If a woman keeps having miscarriages, it is also called infertility. Female infertility can result from age, physical problems, hormone problems, and lifestyle or environmental factors.    Most cases of infertility in women result from problems with producing eggs. In premature ovarian failure, the ovaries stop functioning before natural menopause. In polycystic ovary syndrome (PCOS), the ovaries may not release an egg regularly or they may not release a healthy egg.    About a third of the time, infertility is because of a problem with the woman. One third of the time, it is a problem with the man. Sometimes no cause can be found.    If you think you might be infertile, see your doctor. There are tests that may tell if you have fertility problems. When it is possible to find the cause, treatments may include medicines, surgery, or assisted reproductive technologies. Happily, many couples treated for infertility are able to have babies.    Dept. of Health and Human Services Office on Women's Health


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[User] What is (are) Tietz syndrome ?

[Assistant] Tietz syndrome is a disorder characterized by profound hearing loss from birth, fair skin, and light-colored hair. The hearing loss in affected individuals is caused by abnormalities of the inner ear (sensorineural hearing loss) and is present from birth. Although people with Tietz syndrome are born with white hair and very pale skin, their hair color often darkens over time to blond or red. The skin of affected individuals, which sunburns very easily, may tan slightly or develop reddish freckles with limited sun exposure; however, their skin and hair color remain lighter than those of other members of their family.  Tietz syndrome also affects the eyes. The colored part of the eye (the iris) in affected individuals is blue, and specialized cells in the eye called retinal pigment epithelial cells lack their normal pigment. The retinal pigment epithelium nourishes the retina, the part of the eye that detects light and color. The changes to the retinal pigment epithelium are generally detectable only by an eye examination; it is unclear whether the changes affect vision.


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[User] What is (are) Primary hyperparathyroidism ?

[Assistant] Hyperparathyroidism is an endocrine disorder in which the parathyroid glands in the neck produce too much parathyroid hormone (PTH). Signs and symptoms are often mild and nonspecific, such as a feeling of weakness and fatigue, depression, or aches and pains. With more severe disease, a person may have a loss of appetite, nausea, vomiting, constipation, confusion or impaired thinking and memory, and increased thirst and urination. Patients may have thinning of the bones without symptoms, but with risk of fractures. There are two main types of hyperparathyroidism: primary hyperparathyroidism and secondary hyperparathyroidism. Surgery to remove the parathyroid gland(s) is the main treatment for the disorder. Some patients with mild disease do not require treatment.


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[User] What is (are) Urinary Tract Infections ?

[Assistant] The urinary system is the body's drainage system for removing wastes and extra water. It includes two kidneys, two ureters, a bladder, and a urethra. Urinary tract infections (UTIs) are the second most common type of infection in the body.    You may have a UTI if you notice       - Pain or burning when you urinate    - Fever, tiredness, or shakiness    - An urge to urinate often    - Pressure in your lower belly     - Urine that smells bad or looks cloudy or reddish    - Pain in your back or side below the ribs       People of any age or sex can get UTIs. But about four times as many women get UTIs as men. You're also at higher risk if you have diabetes, need a tube to drain your bladder, or have a spinal cord injury.    If you think you have a UTI it is important to see your doctor. Your doctor can tell if you have a UTI with a urine test. Treatment is with antibiotics.     NIH: National Institute of Diabetes and Digestive and Kidney Diseases


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[User] How many people are affected by familial paroxysmal kinesigenic dyskinesia ?

[Assistant] Familial paroxysmal kinesigenic dyskinesia is estimated to occur in 1 in 150,000 individuals. For unknown reasons, this condition affects more males than females.


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[User] What is the outlook for Gastrointestinal Carcinoid Tumors ?

[Assistant] Certain factors affect prognosis (chance of recovery) and treatment options. The prognosis (chance of recovery) and treatment options depend on the following:         - Where the tumor is in the gastrointestinal tract.    - The size of the tumor.     - Whether the cancer has spread from the stomach and intestines to other parts of the body, such as the liver or lymph nodes.    - Whether the patient has carcinoid syndrome or has carcinoid heart syndrome.    - Whether the cancer can be completely removed by surgery.     - Whether the cancer is newly diagnosed or has recurred.


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[User] What is (are) Bobble-head doll syndrome ?

[Assistant] Bobble-head doll syndrome (BHDS) is a rare neurological condition that is typically first seen in childhood. The signs and symptoms of BHDS include characteristic up and down head movements that increase during walking and excitement and decrease during concentration. Although the specific cause of this condition is unknown, BHDS is often seen with cysts in the third ventricle of the brain that also cause hydrocephalus (water on the brain). Treatment for BHDS may involve surgical removal of the cyst causing the condition or using a shunt to drain excess water on the brain.


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[User] what research (or clinical trials) is being done for Hemifacial Spasm ?

[Assistant] The National Institute of Neurological Disorders and Stroke (NINDS) conducts and supports research related to hemifacial spams through grants to major research institutions across the country. Much of this research focuses on better ways to prevent, treat, and ultimately cure neurological disorders, such as hemifacial spasm.


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[User] What is (are) TAR syndrome ?

[Assistant] TAR syndrome is characterized by the absence of a bone called the radius in each forearm, short stature, and thrombocytopenia. The thrombocytopenia often appears first in infancy but becomes less severe or returns to normal over time. Infants and young children are particularly vulnerable to episodes of severe bleeding which may occur in the brain and other organs. Children who survive this period and do not have damaging bleeding in the brain usually have a normal life expectancy and normal intellectual development. Other signs and symptoms vary but may include heart defects, kidney defects, and other skeletal abnormalities. About half of people with TAR syndrome also have difficulty digesting cow's milk. TAR syndrome is thought be caused by a deletion of genes on chromosome 1q21.1 in concert with another genetic change that has yet to be identified. Click here to see a diagram of chromosome 1.


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[User] Do you have information about Drinking Water

[Assistant] Summary : We all need to drink water. How much you need depends on your size, activity level, and the weather where you live.    The water you drink is a combination of surface water and groundwater. Surface water includes rivers, lakes and reservoirs. Groundwater comes from underground. The United States has one of the safest water supplies in the world, but drinking water quality can vary from place to place. It depends on the condition of the source water and the treatment it receives. Treatment may include adding fluoride to prevent cavities and chlorine to kill germs.     Your water supplier must give you annual reports on drinking water. The reports include where your water came from and what contaminants are in it.    Centers for Disease Control and Prevention


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[User] What are the treatments for Diabetes, Heart Disease, and Stroke ?

[Assistant]
You can keep track of the ABCs of diabetes to make sure your treatment is working. Talk with your health care provider about the best targets for you.

A stands for A1C (a test that measures blood glucose control). Have an A1C test at least twice a year. It shows your average blood glucose level over the past 3 months. Talk with your doctor about whether you should check your blood glucose at home and how to do it.

A1C target        Below 7 percent, unless your doctor sets a different target

Blood glucose targets        Before meals    90 to 130 mg/dL        1 to 2 hours after the start of a meal    Less than 180 mg/dL

B is for blood pressure. Have it checked at every office visit.

Blood pressure target        Below 140/80 mm Hg, unless your doctor sets a different target

C is for cholesterol. Have it checked at least once a year.

Blood fat (cholesterol) targets        LDL (bad) cholesterol    Under 100 mg/dL        Triglycerides    Under 150 mg/dL        HDL (good) cholesterol For men: above 40 mg/dL For women: above 50 mg/dL

Control of the ABCs of diabetes can reduce your risk for heart disease and stroke. If your blood glucose, blood pressure, and cholesterol levels aren't on target, ask your doctor what changes in diet, activity, and medications can help you reach these goals.


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[User] What is (are) Mabry syndrome ?

[Assistant] Mabry syndrome is a condition characterized by intellectual disability, distinctive facial features, increased levels of an enzyme called alkaline phosphatase in the blood (hyperphosphatasia), and other signs and symptoms.  People with Mabry syndrome have intellectual disability that is often moderate to severe. They typically have little to no speech development and are delayed in the development of motor skills (such as sitting, crawling, and walking). Many affected individuals have low muscle tone (hypotonia) and develop recurrent seizures (epilepsy) in early childhood. Seizures are usually the generalized tonic-clonic type, which involve muscle rigidity, convulsions, and loss of consciousness.  Individuals with Mabry syndrome have distinctive facial features that include wide-set eyes (hypertelorism), long openings of the eyelids (long palpebral fissures), a nose with a broad bridge and a rounded tip, downturned corners of the mouth, and a thin upper lip. These facial features usually become less pronounced over time.  Hyperphosphatasia begins within the first year of life in people with Mabry syndrome. There are many different types of alkaline phosphatase found in tissues; the type that is increased in Mabry syndrome is called the tissue non-specific type and is found throughout the body. In affected individuals, alkaline phosphatase levels in the blood are usually increased by one to two times the normal amount, but can be up to 20 times higher than normal. The elevated enzyme levels remain relatively stable over a person's lifetime. Hyperphosphatasia appears to cause no negative health effects, but this finding can help health professionals diagnose Mabry syndrome.  Another common feature of Mabry syndrome is shortened bones at the ends of fingers (brachytelephalangy), which can be seen on x-ray imaging. Underdeveloped fingernails (nail hypoplasia) may also occur. Sometimes, individuals with Mabry syndrome have abnormalities of the digestive system, including narrowing or blockage of the anus (anal stenosis or anal atresia) or Hirschsprung disease, a disorder that causes severe constipation or blockage of the intestine. Rarely, affected individuals experience hearing loss.  The signs and symptoms of Mabry syndrome vary among affected individuals. Those who are least severely affected have only intellectual disability and hyperphosphatasia, without distinctive facial features or the other health problems listed above.


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[User] What are the treatments for Pineocytoma ?

[Assistant] How might a pineocytoma be treated? Because pineocytomas are quite rare, there are no consensus guidelines on the best treatment for these tumors. However, surgery to remove the entire tumor is considered the standard treatment. Because these tumors are located deep in the brain, it is important that the risks of surgery be carefully considered in each person.  Radiation therapy is sometimes used following surgery to destroy any tumor cells that may remain, but the benefit of this additional treatment is questionable.


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[User] What are the symptoms of Gracile bone dysplasia ?

[Assistant] What are the signs and symptoms of Gracile bone dysplasia? The Human Phenotype Ontology provides the following list of signs and symptoms for Gracile bone dysplasia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of bone mineral density 90% Abnormality of the spleen 90% Bowing of the long bones 90% Decreased skull ossification 90% Micromelia 90% Narrow mouth 90% Recurrent fractures 90% Short philtrum 90% Short stature 90% Skeletal dysplasia 90% Slender long bone 90% Tented upper lip vermilion 90% Abnormality of pelvic girdle bone morphology 50% Abnormality of the clavicle 50% Abnormality of the fingernails 50% Abnormality of the helix 50% Abnormality of the metacarpal bones 50% Abnormality of the metaphyses 50% Abnormality of the ribs 50% Anteverted nares 50% Aplasia/Hypoplasia affecting the eye 50% Aplasia/Hypoplasia of the lungs 50% Aplasia/Hypoplasia of the thymus 50% Brachydactyly syndrome 50% Cloverleaf skull 50% Depressed nasal bridge 50% Enlarged thorax 50% Frontal bossing 50% Hypoplasia of penis 50% Intrauterine growth retardation 50% Low-set, posteriorly rotated ears 50% Malar flattening 50% Platyspondyly 50% Renal hypoplasia/aplasia 50% Respiratory insufficiency 50% Short distal phalanx of finger 50% Short nose 50% Short toe 50% Tapered finger 50% Wide nasal bridge 50% Abnormality of neuronal migration 7.5% Abnormality of the fontanelles or cranial sutures 7.5% Aplasia/Hypoplasia involving the nose 7.5% Aplasia/Hypoplasia of the eyebrow 7.5% Blepharophimosis 7.5% Blue sclerae 7.5% Cataract 7.5% Cleft palate 7.5% Cryptorchidism 7.5% Displacement of the external urethral meatus 7.5% Hepatomegaly 7.5% Hypertelorism 7.5% Hypotelorism 7.5% Iris coloboma 7.5% Microcornea 7.5% Muscular hypotonia 7.5% Oligohydramnios 7.5% Rocker bottom foot 7.5% Upslanted palpebral fissure 7.5% Asplenia 5% Aniridia - Ascites - Autosomal dominant inheritance - Failure to thrive - Flared metaphysis - Hydrocephalus - Hypocalcemia - Hypoplastic spleen - Micropenis - Microphthalmia - Prominent forehead - Seizures - 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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[User] what research (or clinical trials) is being done for Diabetic Retinopathy ?

[Assistant] The National Eye Institute, or NEI, is conducting and supporting research that seeks better ways to detect, treat, and prevent vision loss in people with diabetes. This research is conducted through studies in the laboratory and with patients. For example, researchers are studying drugs for the treatment of proliferative retinopathy that may reduce the need for laser surgery.


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[User] How many people are affected by X-linked sideroblastic anemia and ataxia ?

[Assistant] X-linked sideroblastic anemia and ataxia is a rare disorder; only a few affected families have been reported.


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[User] Is Hereditary diffuse leukoencephalopathy with spheroids inherited ?

[Assistant] How is hereditary diffuse leukoencephalopathy with spheroids (HDLS) inherited? HDLS is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. In most cases, an affected person inherits the mutation from one affected parent. 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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[User] Is Binswanger's disease inherited ?

[Assistant] Is Binswanger's disease an inherited condition? Although Binswanger's disease is not considered an inherited condition, genetics may play a role in many of the conditions and risk factors that are associated with the disease (i.e. atherosclerosis, blood clots).


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[User] How many people are affected by Lenz microphthalmia syndrome ?

[Assistant] Lenz microphthalmia syndrome is a very rare condition; its incidence is unknown. It has been identified in only a few families worldwide.


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[User] What is (are) Peripheral Arterial Disease (P.A.D.) ?

[Assistant] Peripheral arterial disease (P.A.D.) is a disease in which plaque (plak) builds up in the arteries that carry blood to your head, organs, and limbs. Plaque is made up of fat, cholesterol, calcium, fibrous tissue, and other substances in the blood. P.A.D. currently affects millions of Americans, and about 1 in every 20 Americans over the age of 50 has P.A.D.


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[User] What is (are) Porphyria ?

[Assistant]
Each of the eight types of porphyria corresponds to low levels of a specific enzyme in the heme biosynthetic pathway. Experts often classify porphyrias as acute or cutaneous based on the symptoms a person experiences:

- Acute porphyrias affect the nervous system. They occur rapidly and last only a short time.  - Cutaneous porphyrias affect the skin.

Two types of acute porphyrias, hereditary coproporphyria and variegate porphyria, can also have cutaneous symptoms.

Experts also classify porphyrias as erythropoietic or hepatic:

- In erythropoietic porphyrias, the body overproduces porphyrins, mainly in the bone marrow.  - In hepatic porphyrias, the body overproduces porphyrins and porphyrin precursors, mainly in the liver.

Table 1 lists each type of porphyria, the deficient enzyme responsible for the disorder, and the main location of porphyrin buildup.

Table 1. Types of porphyria

Type of Porphyria    Deficient Enzyme    Main Location of Porphyrin Buildup                  delta-aminolevulinate-dehydratase deficiency porphyria    delta-aminolevulinic acid dehydratase    liver        acute intermittent porphyria    porphobilinogen deaminase    liver        hereditary coproporphyria    coproporphyrinogen oxidase    liver        variegate porphyria    protoporphyrinogen oxidase    liver                congenital erythropoietic porphyria    uroporphyrinogen III cosynthase    bone marrow        porphyria cutanea tarda    uroporphyrinogen decarboxylase (~75% deficiency)    liver        hepatoerythropoietic porphyria    uroporphyrinogen decarboxylase (~90% deficiency)    bone marrow        erythropoietic protoporphyria*    ferrochelatase (~75% deficiency)    bone marrow

*Protoporphyria XLPP is a variant of erythropoietic protoporphyria.


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[User] What are the symptoms of Spondylometaphyseal dysplasia type A4 ?

[Assistant] What are the signs and symptoms of Spondylometaphyseal dysplasia type A4? The Human Phenotype Ontology provides the following list of signs and symptoms for Spondylometaphyseal dysplasia type A4. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the hip bone 90% Micromelia 90% Platyspondyly 90% Short stature 90% Brachydactyly syndrome 50% Enlarged thorax 7.5% Limitation of joint mobility 7.5% Autosomal recessive inheritance - Broad ischia - Costochondral joint sclerosis - Coxa valga - Disproportionate short-limb short stature - Dolichocephaly - Enlargement of the costochondral junction - Flat acetabular roof - Hypoplasia of the capital femoral epiphysis - Irregular capital femoral epiphysis - Irregular patellae - Metaphyseal irregularity - Metaphyseal sclerosis - Metaphyseal widening - Narrow greater sacrosciatic notches - Osteoporotic metatarsal - Osteoporotic tarsals - Ovoid vertebral bodies - Pectus carinatum - Sclerotic humeral metaphysis - Severe short stature - Spondylometaphyseal dysplasia - 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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[User] What is (are) Chikungunya ?

[Assistant] Chikungunya is a virus that spread by the same kinds of mosquitoes that spread dengue and Zika virus. Rarely, it can spread from mother to newborn around the time of birth. It may also possibly spread through infected blood. There have been outbreaks of chikungunya virus in Africa, Asia, Europe, the Indian and Pacific Oceans, the Caribbean, and Central and South America.    Most people who are infected will have symptoms, which can be severe. They usually start 3-7 days after being bitten by an infected mosquito. The most common symptoms are fever and joint pain. Other symptoms may include headache, muscle pain, joint swelling, and rash.    Most people feel better within a week. In some cases, however, the joint pain may last for months. People at risk for more severe disease include newborns, older adults, and people with diseases such as high blood pressure, diabetes, or heart disease.    A blood test can show whether you have chikungunya virus. There are no vaccines or medicines to treat it. Drinking lots of fluids, resting, and taking non-aspirin pain relievers might help.    The best way to prevent chikungunya infection is to avoid mosquito bites:       - Use insect repellent    - Wear clothes that cover your arms, legs, and feet    - Stay in places that have air conditioning or that use window and door screens       Centers for Disease Control and Prevention


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[User] What are the treatments for Pyelonephritis: Kidney Infection ?

[Assistant]
Pyelonephritis is treated with antibiotics, which may need to be taken for several weeks. While a urine sample is sent to a lab for culture, the health care provider may begin treatment with an antibiotic that fights the most common types of bacteria. Once culture results are known and the bacteria is clearly identified, the health care provider may switch the antibiotic to one that more effectively targets the bacteria. Antibiotics may be given through a vein, orally, or both. Urinary tract obstructions are often treated with surgery.

Severely ill patients may be hospitalized and limited to bed rest until they can take the fluids and medications they need on their own. Fluids and medications may be given intravenously during this time.

In adults, repeat urine cultures should be performed after treatment has ended to make sure the infection does not recur. If a repeat test shows infection, another 14-day course of antibiotics is prescribed; if infection recurs again, antibiotics are prescribed for 6 weeks.


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[User] What are the symptoms of Pretibial epidermolysis bullosa ?

[Assistant] What are the signs and symptoms of Pretibial epidermolysis bullosa? The Human Phenotype Ontology provides the following list of signs and symptoms for Pretibial epidermolysis bullosa. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal blistering of the skin 90% Abnormality of the fingernails 90% Abnormality of the toenails 90% Atypical scarring of skin 50% Pruritus 50% Hyperkeratosis 7.5% Lichenification 7.5% Autosomal dominant inheritance - Pretibial blistering - 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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[User] What is (are) Varicose Veins ?

[Assistant]
Espaol

Varicose (VAR-i-kos) veins are swollen, twisted veins that you can see just under the surface of the skin. These veins usually occur in the legs, but they also can form in other parts of the body.

Varicose veins are a common condition. They usually cause few signs and symptoms. Sometimes varicose veins cause mild to moderate pain, blood clots, skin ulcers (sores), or other problems.

Overview

Veins are blood vessels that carry blood from your body's tissues to your heart. Your heart pumps the blood to your lungs to pick up oxygen. The oxygen-rich blood then is pumped to your body through blood vessels called arteries.

From your arteries, the blood flows through tiny blood vessels called capillaries, where it gives up its oxygen to the body's tissues. Your blood then returns to your heart through your veins to pick up more oxygen. For more information about blood flow, go to the Health Topics How the Heart Works article.

Veins have one-way valves that help keep blood flowing toward your heart. If the valves are weak or damaged, blood can back up and pool in your veins. This causes the veins to swell, which can lead to varicose veins.

Many factors can raise your risk for varicose veins. Examples of these factors include family history, older age, gender, pregnancy, overweight or obesity, lack of movement, and leg trauma.

Varicose veins are treated with lifestyle changes and medical procedures. The goals of treatment are to relieve symptoms, prevent complications, and improve appearance.

Outlook

Varicose veins usually don't cause medical problems. If they do, your doctor may simply suggest making lifestyle changes.

Sometimes varicose veins cause pain, blood clots, skin ulcers, or other problems. If this happens, your doctor may recommend one or more medical procedures. Some people choose to have these procedures to improve the way their veins look or to relieve pain.

Many treatments for varicose veins are quick and easy and don't require a long recovery.


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[User] How to diagnose Prolactinoma ?

[Assistant]
A doctor will test for prolactin blood levels in women with unexplained milk secretion, called galactorrhea, or with irregular menses or infertility and in men with impaired sexual function and, in rare cases, milk secretion. If prolactin levels are high, a doctor will test thyroid function and ask first about other conditions and medications known to raise prolactin secretion. The doctor may also request magnetic resonance imaging (MRI), which is the most sensitive test for detecting pituitary tumors and determining their size. MRI scans may be repeated periodically to assess tumor progression and the effects of therapy. Computerized tomography (CT) scan also gives an image of the pituitary but is less precise than the MRI.

The doctor will also look for damage to surrounding tissues and perform tests to assess whether production of other pituitary hormones is normal. Depending on the size of the tumor, the doctor may request an eye exam with measurement of visual fields.


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[User] What are the symptoms of Charcot-Marie-Tooth disease type 1D ?

[Assistant] What are the signs and symptoms of Charcot-Marie-Tooth disease type 1D? The Human Phenotype Ontology provides the following list of signs and symptoms for Charcot-Marie-Tooth disease type 1D. 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 - Decreased motor nerve conduction velocity - Distal amyotrophy - Distal muscle weakness - Foot dorsiflexor weakness - Juvenile onset - Steppage gait - Upper limb muscle weakness - Variable expressivity - 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.