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[User] What causes Cirrhosis ?

[Assistant]
Cirrhosis has various causes. Many people with cirrhosis have more than one cause of liver damage.

The list below shows common causes of cirrhosis in the United States.2 While chronic hepatitis C and alcohol-related liver disease are the most common causes of cirrhosis, the incidence of cirrhosis caused by nonalcoholic fatty liver disease is rising due to increasing rates of obesity.

Most Common Causes of Cirrhosis

Chronic hepatitis C. Hepatitis C is due to a viral infection that causes inflammation, or swelling, and damage to the liver. The hepatitis C virus spreads through contact with infected blood, such as from a needlestick accident, injection drug use, or receiving a blood transfusion before 1992. Less commonly, hepatitis C can be spread by sexual contact with an infected person or at the time of childbirth from an infected mother to her newborn.

Hepatitis C often becomes chronic, with long-term persistence of the viral infection. Chronic hepatitis C causes damage to the liver that, over years or decades, can lead to cirrhosis. Advanced therapies for chronic hepatitis C now exist, and health care providers should treat people with chronic hepatitis C before they develop severe fibrosis or cirrhosis. Unfortunately, many people first realize they have chronic hepatitis C when they develop symptoms of cirrhosis. More information is provided in the NIDDK health topic, What I need to know about Hepatitis C.

Alcohol-related liver disease. Alcoholism is the second most common cause of cirrhosis in the United States. Most people who consume alcohol do not suffer damage to the liver. However, heavy alcohol use over several years makes a person more likely to develop alcohol-related liver disease. The amount of alcohol it takes to damage the liver varies from person to person. Research suggests that drinking two or fewer drinks a day for women and three or fewer drinks a day for men may not injure the liver.3 Drinking more than these amounts leads to fat and inflammation in the liver, which over 10 to 12 years can lead to alcoholic cirrhosis.4

Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). In NAFLD, fat builds up in the liver; however, the fat buildup is not due to alcohol use. When the fat accompanies inflammation and liver cell damage, the condition is called nonalcoholic steatohepatitis, or NASH, with steato meaning fat, and hepatitis meaning inflammation of the liver. The inflammation and damage can cause fibrosis, which eventually can lead to cirrhosis.

Extra fat in the liver has many causes and is more common in people who

- are overweight or obese.  - have diabetesa condition characterized by high blood glucose, also called high blood sugar.  - have high blood cholesterol and triglycerides, called hyperlipidemia.  - have high blood pressure.  - have metabolic syndromea group of traits and medical conditions linked to being overweight and obese that makes people more likely to develop both cardiovascular disease and type 2 diabetes. Metabolic syndrome is defined as the presence of any three of the following: large waist size, high triglycerides in the blood, abnormal levels of cholesterol in the blood, high blood pressure, and higher than normal blood glucose levels. NASH may represent the liver component of the metabolic syndrome.

NASH now ranks as the third most common cause of cirrhosis in the United States. More information is provided in the NIDDK health topic, Nonalcoholic Steatohepatitis.

Chronic hepatitis B. Hepatitis B, like hepatitis C, is due to a viral infection that causes inflammation and damage to the liver. Chronic infection can lead to damage and inflammation, fibrosis, and cirrhosis. The hepatitis B virus spreads through contact with infected blood, such as by needlestick accident, injection drug use, or receiving a blood transfusion before the mid-1980s. Hepatitis B also spreads through sexual contact with an infected person and from an infected mother to child during childbirth.

In the United States, hepatitis B is somewhat uncommon, affecting less than 1 percent of the population, or fewer than one in 100 people.5 In many areas of the world, however, hepatitis B is common. In some parts of Africa and in most of Asia and the Pacific Islands, about 5 to 7 percent of the population has chronic hepatitis B. In some parts of Africa, more than 8 percent of the population has chronic hepatitis B.6 For these reasons, hepatitis B is likely the major cause of cirrhosis worldwide. However, in the United States, hepatitis B ranks well behind hepatitis C, alcohol-related liver disease, and NASH.

Therapies for chronic hepatitis B now exist and health care providers should treat people with chronic hepatitis B before they develop severe fibrosis or cirrhosis. Unfortunately, many people first realize they have chronic hepatitis B when they develop symptoms of cirrhosis.

Hepatitis B is also a preventable disease. Since the 1980s, a hepatitis B vaccine has been available and should be given to newborns and children in the United States. Adults at higher risk of getting hepatitis B should also get the vaccine. More information is provided in the NIDDK health topics, What I need to know about Hepatitis B and Hepatitis B: What Asian and Pacific Islander Americans Need to Know.

Less Common Causes of Cirrhosis

Less common causes of cirrhosis include the following:

Autoimmune hepatitis. In this form of hepatitis, the bodys immune system attacks liver cells and causes inflammation, damage, and eventually cirrhosis. Normally, the immune system protects people from infection by identifying and destroying bacteria, viruses, and other potentially harmful foreign substances. In autoimmune diseases, the bodys immune system attacks the bodys own cells and organs. Researchers believe genetics, or inherited genes, may make some people more likely to develop autoimmune diseases. At least 70 percent of those with autoimmune hepatitis are female.7 More information is provided in the NIDDK health topic, Autoimmune Hepatitis.

Diseases that damage, destroy, or block the bile ducts. Several diseases can damage, destroy, or block the ducts that carry bile from the liver to the small intestine, causing bile to back up in the liver and leading to cirrhosis. In adults, the most common of these diseases is primary biliary cirrhosis, a chronic disease that causes the small bile ducts in the liver to become inflamed and damaged and ultimately disappear. Primary sclerosing cholangitis is a disease that causes irritation, scarring, and narrowing of the larger bile ducts of the liver.

In infants and children, causes of damage to or disappearance of bile ducts that can lead to cirrhosis include

- Alagille syndrome, a collection of symptoms that indicates a genetic digestive disorder and leads to a loss of bile ducts in infancy.  - biliary atresia, a life-threatening condition that affects newborns in which bile ducts are missing. The cause is unknown. Biliary atresia is the most common reason for liver transplantation in children.8  - cystic fibrosis, an inherited disease of the lungs, intestines, pancreas, and bile ducts in which the body does not produce enough fluid and mucus becomes thick and blocks off small bile ducts. This blockage of the bile ducts can lead to cirrhosis.

Long-term blockage of the bile ducts by gallstones can cause cirrhosis. Cirrhosis may also develop if the bile ducts are mistakenly tied off or injured during surgery on the gallbladder or liver.

More information is provided in the NIDDK health topics:

- Primary Biliary Cirrhosis  - Primary Sclerosing Cholangitis  - Alagille Syndrome  - Biliary Atresia  - Gallstones

Inherited diseases that affect the liver. Inherited diseases that interfere with how the liver produces, processes, and stores enzymes, proteins, metals, and other substances can cause cirrhosis. These diseases include alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, galactosemia, and glycogen storage diseases. More information is provided in the NIDDK health topics:

- Hemochromatosis  - Wilson Disease

Rare viral infections of the liver. Hepatitis D, or hepatitis delta, and hepatitis E are two rare viral infections of the liver. Hepatitis D infection occurs only in people who have hepatitis B. People infected with chronic hepatitis B and chronic hepatitis D are more likely to develop cirrhosis than people infected with chronic hepatitis B alone.9

Hepatitis E is a virus found in domestic and wild animals, particularly pigs, and can cause hepatitis in humans. People with weakened immune systems, including people who are liver or kidney transplant recipients or who have acquired immune deficiency syndrome (AIDS), can develop chronic hepatitis E. Chronic hepatitis E can cause scarring of the liver and cirrhosis. Current treatments for chronic hepatitis D and E are experimental and only partially effective.

Other causes. Other causes of cirrhosis may include

- reactions to medications taken over a period of time.  - prolonged exposure to toxic chemicals.  - parasitic infections.  - chronic heart failure with liver congestion, a condition in which blood flow out of the liver is slowed. Liver congestion can also occur after surgery to correct a congenital heart problema heart problem that is present at birth.

Trauma to the liver or other acute, or short term, causes of damage do not cause cirrhosis. Usually, years of chronic injury are required to cause cirrhosis.


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[User] What are the symptoms of Glanzmann thrombasthenia ?

[Assistant] What are the signs and symptoms of Glanzmann thrombasthenia? The Human Phenotype Ontology provides the following list of signs and symptoms for Glanzmann thrombasthenia. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Bruising susceptibility - Decreased platelet glycoprotein IIb-IIIa - Epistaxis - Gastrointestinal hemorrhage - Gingival bleeding - Impaired platelet aggregation - Intracranial hemorrhage - Menorrhagia - Prolonged bleeding time - Purpura - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What are the symptoms of Glucose-6-phosphate dehydrogenase deficiency ?

[Assistant] What are the signs and symptoms of glucose-6-phosphate dehydrogenase (G6PD) deficiency? People with G6PD deficiency do not have signs of the disease unless their red blood cells are exposed to certain chemicals in food or medicine, certain bacterial or viral infections, or to stress. Many people with this condition never experience symptoms. The most common medical problem associated with G6PD deficiency is hemolytic anemia, which occurs when red blood cells are destroyed faster than the body can replace them. This type of anemia leads to paleness, yellowing of the skin and whites of the eyes (jaundice), dark urine, fatigue, shortness of breath, enlarged spleen, and a rapid heart rate. Researchers believe that carriers of a mutation in the G6PD gene may be partially protected against malaria, an infectious disease carried by a certain type of mosquito. A reduction in the amount of functional glucose-6-dehydrogenase appears to make it more difficult for this parasite to invade red blood cells. G6PD deficiency occurs more frequently in areas of the world where malaria is common.


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[User] How many people are affected by GRN-related frontotemporal dementia ?

[Assistant] GRN-related frontotemporal dementia affects an estimated 3 to 15 per 100,000 people aged 45 to 64. This condition accounts for 5 to 10 percent of all cases of frontotemporal dementia.


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[User] How to diagnose Pierson syndrome ?

[Assistant] Is genetic testing available for Pierson syndrome? Yes. The Genetic Testing Registry (GTR) provides information about the genetic tests available for Pierson syndrome. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetics professional. According to the GTR, genetic testing for Pierson syndrome may be available for diagnosis in a person suspected of having the condition, carrier testing, and prenatal testing.


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[User] What is the outlook for Myotonia ?

[Assistant] Myotonia is a chronic disorder. Symptoms may improve later in life.


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[User] What to do for Viral Gastroenteritis ?

[Assistant]
The following steps may help relieve the symptoms of viral gastroenteritis in adults:

- drinking plenty of liquids such as fruit juices, sports drinks, caffeine-free soft drinks, and broths to replace fluids and electrolytes  - sipping small amounts of clear liquids or sucking on ice chips if vomiting is still a problem  - gradually reintroducing food, starting with bland, easy-to-digest foods such as rice, potatoes, toast or bread, cereal, lean meat, applesauce, and bananas  - avoiding fatty foods, sugary foods, dairy products, caffeine, and alcohol until recovery is complete  - getting plenty of rest

Children present special concerns. Because of their smaller body size, infants and children are likely to become dehydrated more quickly from diarrhea and vomiting. The following steps may help relieve symptoms of viral gastroenteritis and prevent dehydration in children:

- giving oral rehydration solutions such as Pedialyte, Naturalyte, Infalyte, and CeraLyte  - giving food as soon as the child is hungry  - giving infants breast milk or full strength formula, as usual, along with oral rehydration solutions

Older adults and adults with weak immune systems should also drink oral rehydration solutions to prevent dehydration.


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[User] What is (are) Kyrle disease ?

[Assistant] Kyrle disease is a skin disease characterized by the formation of large papules and is often associated with underlying hepatic, renal or diabetic disorders. It can affect both men and women throughout life, although the average age of onset is 30 years. Lesions typically begin as small papules with silvery scales that eventually grow and form red-brown nodules with a central keratin (horny) plug. The lesions occur mostly on the legs but also develop on the arms and the head and neck region. They are not typically painful may cause intense itching (pruritus). The cause of the disease is unknown; some cases appear to be idiopathic (no known cause) or inherited. The aim of treatment is to treat the underlying disease if one is associated. Lesions may self-heal without any treatment, but new lesions usually develop. Treatments that have been used to treat and reduce lesions include isotretinoin, high dose vitamin A, and tretinoin cream; emollients (skin softening agents) and oral antihistamines may be useful in relieving pruritus.


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[User] Is maternally inherited diabetes and deafness inherited ?

[Assistant] MIDD is inherited in a mitochondrial pattern, which is also known as maternal inheritance. This pattern of inheritance applies to genes contained in mtDNA. Because egg cells, but not sperm cells, contribute mitochondria to the developing embryo, children can only inherit disorders resulting from mtDNA mutations from their mother. These disorders can appear in every generation of a family and can affect both males and females, but fathers do not pass traits associated with changes in mtDNA to their children.  Most of the body's cells contain thousands of mitochondria, each with one or more copies of mtDNA. These cells can have a mix of mitochondria containing mutated and unmutated DNA (heteroplasmy). The severity of MIDD is thought to be associated with the percentage of mitochondria with the mtDNA mutation.


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[User] What is (are) Nutrition for Advanced Chronic Kidney Disease in Adults ?

[Assistant] CKD usually takes a long time to develop and does not go away. In CKD, the kidneys continue to workjust not as well as they should. Wastes may build up so gradually that the body becomes used to having those wastes in the blood. Salts containing phosphorus and potassium may rise to unsafe levels, causing heart and bone problems. Anemialow red blood cell countcan result from CKD because the kidneys stop making enough erythropoietin, a hormone that causes bone marrow to make red blood cells. After months or years, CKD may progress to permanent kidney failure, which requires a person to have a kidney transplant or regular blood filtering treatments called dialysis.


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[User] What is (are) achondrogenesis ?

[Assistant] Achondrogenesis is a group of severe disorders that affect cartilage and bone development. These conditions are characterized by a small body, short limbs, and other skeletal abnormalities. As a result of serious health problems, infants with achondrogenesis usually die before birth, are stillborn, or die soon after birth from respiratory failure. However, some infants have lived for a short time with intensive medical support.  Researchers have described at least three forms of achondrogenesis, designated as type 1A, type 1B, and type 2. The types are distinguished by their signs and symptoms, inheritance pattern, and genetic cause. However, types 1A and 1B are often hard to tell apart without genetic testing.  Achondrogenesis type 1A, which is also called the Houston-Harris type, is the least well understood of the three forms. Affected infants have extremely short limbs, a narrow chest, short ribs that fracture easily, and a lack of normal bone formation (ossification) in the skull, spine, and pelvis.  Achondrogenesis type 1B, also known as the Parenti-Fraccaro type, is characterized by extremely short limbs, a narrow chest, and a prominent, rounded abdomen. The fingers and toes are short and the feet may turn inward and upward (clubfeet). Affected infants frequently have a soft out-pouching around the belly-button (an umbilical hernia) or near the groin (an inguinal hernia).  Infants with achondrogenesis type 2, which is sometimes called the Langer-Saldino type, have short arms and legs, a narrow chest with short ribs, and underdeveloped lungs. This condition is also associated with a lack of ossification in the spine and pelvis. Distinctive facial features include a prominent forehead, a small chin, and, in some cases, an opening in the roof of the mouth (a cleft palate). The abdomen is enlarged, and affected infants often have a condition called hydrops fetalis, in which excess fluid builds up in the body before birth.


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[User] How many people are affected by eosinophil peroxidase deficiency ?

[Assistant] Approximately 100 individuals with eosinophil peroxidase deficiency have been described in the scientific literature. Based on blood test data, varying estimates of the prevalence of the condition have been reported in specific populations. Eosinophil peroxidase deficiency is estimated to occur in 8.6 in 1,000 Yemenite Jews, in 3 in 1,000 North-African Jews, and in 1 in 1,000 Iraqi Jews. In northeastern Italy, the condition occurs in approximately 1 in 14,000 individuals; in Japan it occurs in 1 in 36,000 people; and in Luxembourg, eosinophil peroxidase deficiency is thought to occur in 1 in 100,000 people.


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[User] What is (are) benign familial neonatal seizures ?

[Assistant] Benign familial neonatal seizures (BFNS) is a condition characterized by recurrent seizures in newborn babies. The seizures begin around day 3 of life and usually go away within 1 to 4 months. The seizures can involve only one side of the brain (focal seizures) or both sides (generalized seizures). Many infants with this condition have generalized tonic-clonic seizures (also known as grand mal seizures). This type of seizure involves both sides of the brain and affects the entire body, causing muscle rigidity, convulsions, and loss of consciousness.  A test called an electroencephalogram (EEG) is used to measure the electrical activity of the brain. Abnormalities on an EEG test, measured during no seizure activity, can indicate a risk for seizures. However, infants with BFNS usually have normal EEG readings. In some affected individuals, the EEG shows a specific abnormality called the theta pointu alternant pattern. By age 2, most affected individuals who had EEG abnormalities have a normal EEG reading.  Typically, seizures are the only symptom of BFNS, and most people with this condition develop normally. However, some affected individuals develop intellectual disability that becomes noticeable in early childhood. A small percentage of people with BFNS also have a condition called myokymia, which is an involuntary rippling movement of the muscles. In addition, in about 15 percent of people with BFNS, recurrent seizures (epilepsy) will come back later in life after the seizures associated with BFNS have gone away. The age that epilepsy begins is variable.


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[User] What is (are) Shaken Baby Syndrome ?

[Assistant] Shaken baby syndrome is a type of inflicted traumatic brain injury that happens when a baby is violently shaken. A baby has weak neck muscles and a large, heavy head. Shaking makes the fragile brain bounce back and forth inside the skull and causes bruising, swelling, and bleeding, which can lead to permanent, severe brain damage or death. The characteristic injuries of shaken baby syndrome are subdural hemorrhages (bleeding in the brain), retinal hemorrhages (bleeding in the retina), damage to the spinal cord and neck, and fractures of the ribs and bones. These injuries may not be immediately noticeable. Symptoms of shaken baby syndrome include extreme irritability, lethargy, poor feeding, breathing problems, convulsions, vomiting, and pale or bluish skin. Shaken baby injuries usually occur in children younger than 2 years old, but may be seen in children up to the age of 5.


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[User] What are the symptoms of Dry Mouth ?

[Assistant] Dry mouth can be uncomfortable. Some people notice a sticky, dry feeling in the mouth. Others notice a burning feeling or difficulty while eating. The throat may feel dry, too, and swallowing without extra fluids can often be difficult. Also, people with dry mouth may develop mouth sores, cracked lips, and a dry, rough tongue.


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[User] What is the outlook for Childhood Hodgkin Lymphoma ?

[Assistant] Certain factors affect prognosis (chance of recovery) and treatment options. The prognosis (chance of recovery) and treatment options depend on the following:         - The stage of the cancer.    - The size of the tumor.    -  Whether there are B symptoms at diagnosis.    - The type of Hodgkin lymphoma.    - Certain features of the cancer cells.    - Whether there are too many white blood cells or too few red blood cells at the time of diagnosis.    - How well the tumor responds to initial treatment with chemotherapy.    - Whether the cancer is newly diagnosed or has recurred (come back).         The treatment options also depend on:         - The child's age and gender.    - The risk of long-term side effects.        Most children and adolescents with newly diagnosed Hodgkin lymphoma can be cured.


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[User] What is (are) Enthesitis-related juvenile idiopathic arthritis ?

[Assistant] Enthesitis-related juvenile idiopathic arthritis is a subtype of juvenile idiopathic arthritis that is characterized by both arthritis and inflammation of an enthesitis site (the point at which a ligament, tendon, or joint capsule attaches to the bone). Signs and symptoms generally develop in late childhood or early adolescence and include pain, tenderness, and swelling in joints and at the enthesis. The knee and the back of the ankle (at the Achilles tendon) are the most commonly affected parts of the body. The underlying cause of enthesitis-related juvenile idiopathic arthritis is currently unknown (idiopathic). It is very rare for more than one member of a family to have juvenile arthritis; however, research suggests that having a family member with juvenile arthritis or any autoimmune disease may increase the risk of having juvenile arthritis, in general. Treatment usually involves different types of medications to help manage symptoms and/or physical therapy.


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[User] Do you have information about Food Safety

[Assistant] Summary : Safe steps in food handling, cooking, and storage can prevent foodborne illness. There are four basic steps to food safety at home:       - Clean - always wash your fruits and vegetables, hands, counters, and cooking utensils.    - Separate - keep raw foods to themselves. Germs can spread from one food to another.    - Cook - foods need to get hot and stay hot. Heat kills germs.    - Chill - put fresh food in the refrigerator right away.       In the grocery store, avoid cans that are bulging or jars that have cracks or loose lids. Check packages to be sure food hasn't reached its expiration date.    United States Department of Agriculture


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[User] What are the treatments for Alzheimer's Caregiving ?

[Assistant] Currently, no medication can cure Alzheimers disease, but four medicines are approved to treat the symptoms of the disease. - Aricept (donezepil)for all stages of Alzheimers  - Exelon (rivastigmine)for mild to moderate Alzheimers  - Razadyne (galantamine)--for mild to moderate Alzheimers  - Namenda (memantine)for moderate to severe Alzheimers  -  Namzarec (memantine and donepezil)for moderate to severe Alzheimers Aricept (donezepil)for all stages of Alzheimers Exelon (rivastigmine)for mild to moderate Alzheimers Razadyne (galantamine)--for mild to moderate Alzheimers Namenda (memantine)for moderate to severe Alzheimers Namzarec (memantine and donepezil)for moderate to severe Alzheimers These medications can help slow down memory loss and allow people with Alzheimers to be more comfortable and independent for a longer time. If appropriate, the persons doctor may prescribe a medicine to treat behavior problems such as anxiety, depression, and aggression. Medicines to treat these behavior problems should be used only after other strategies have been tried. Talk with the doctor about which medicines are safest and most effective.


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[User] What are the symptoms of Anterior segment mesenchymal dysgenesis ?

[Assistant] What are the signs and symptoms of Anterior segment mesenchymal dysgenesis? The Human Phenotype Ontology provides the following list of signs and symptoms for Anterior segment mesenchymal dysgenesis. 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) Posterior polar cataract 47/47 Anterior segment dysgenesis 7/16 Autosomal dominant inheritance - Opacification of the corneal stroma - 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 symptoms of Childhood Acute Lymphoblastic Leukemia ?

[Assistant] Signs of childhood ALL include fever and bruising. These and other signs and symptoms may be caused by childhood ALL or by other conditions. Check with your child's doctor if your child has any of the following:         -  Fever.    - Easy bruising or bleeding.    -  Petechiae (flat, pinpoint, dark-red spots under the skin caused by bleeding).    - Bone or joint pain.    - Painless lumps in the neck, underarm, stomach, or groin.    - Pain or feeling of fullness below the ribs.    - Weakness, feeling tired, or looking pale.    - Loss of appetite.


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[User] What causes Lipodermatosclerosis ?

[Assistant] What causes lipodermatosclerosis? The exact cause of lipodermatosclerosis is unknown; however, it may be related to certain vein abnormalities and/or obesity. Lipodermatosclerosis often occurs in people with venous insufficiency. Approximately two thirds of affected people are obese.


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[User] How many people are affected by pontocerebellar hypoplasia ?

[Assistant] The prevalence of pontocerebellar hypoplasia is unknown, although most forms of the disorder appear to be very rare.


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[User] What are the treatments for Hemangioendothelioma ?

[Assistant] How might hemangioendothelioma be treated? Treatment for hemangioendothelioma may depend on the type of hemangioendothelioma present in the affected individual and the risk of recurrence or metastases. In most reported cases, surgical excision (removal) of the mass has been the only treatment. For spindle cell hemangioma, simple excision is reportedly curative; however, new growths develop in adjacent skin and soft tissues in 60% of affected individuals. For individuals with papillary intralymphatic angioendothelioma (PILA), excision of the involved lymph nodes, as well as the mass, has been recommended. Surgical excision is reportedly also the usual treatment for individuals with retiform hemangioendothelioma (although local recurrence with this type is common), epithelioid hemangioendothelioma, and composite hemangioendothelioma (with the exception of 1 case treated with interferon). Most individuals with pseudomyogenic hemangioendothelioma have been treated with simple excision, but a few individuals have also received post-surgical radiotherapy (RT). With regard to kaposiform hemangioendothelioma, some large lesions cannot be completely removed and may cause fatal complications due to the associated KasabachMerritt syndrome. In these cases, several medical therapies have been used, including systemic corticosteroids; alfa interferon; RT; embolization; and several other therapies, both alone and in various combinations. A study by Scott et al published in 2012 in the American Journal of Clinical Oncology evaluated the effectiveness of RT as either an alternative or adjunct to surgery. The authors stated that the effectiveness of definitive RT in the treatment of hemangioendothelioma in their study implies that radiation may be an acceptable alternative when surgical resection will compromise function or cosmetic result. They concluded that with no local recurrences and minimal risk of toxicity, their long-term data suggest that RT offers a highly effective management option for this disease.


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[User] What are the symptoms of Meckel syndrome type 2 ?

[Assistant] What are the signs and symptoms of Meckel syndrome type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Meckel syndrome type 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Dandy-Walker malformation 5% Microphthalmia 5% Anencephaly - Autosomal recessive inheritance - Bile duct proliferation - Bowing of the long bones - Cleft palate - Encephalocele - Intrauterine growth retardation - Meningocele - Polydactyly - Postaxial hand polydactyly - Renal cyst - 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 treatments for Costello syndrome ?

[Assistant] These resources address the diagnosis or management of Costello syndrome:  - Gene Review: Gene Review: Costello Syndrome  - Genetic Testing Registry: Costello syndrome   These resources from MedlinePlus offer information about the diagnosis and management of various health conditions:  - Diagnostic Tests  - Drug Therapy  - Surgery and Rehabilitation  - Genetic Counseling   - Palliative Care


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[User] Do you have information about Environmental Health

[Assistant] Summary : Our environment affects our health. If parts of the environment, like the air, water, or soil become polluted, it can lead to health problems. For example, asthma pollutants and chemicals in the air or in the home can trigger asthma attacks.    Some environmental risks are a part of the natural world, like radon in the soil. Others are the result of human activities, like lead poisoning from paint, or exposure to asbestos or mercury from mining or industrial use.    NIH: National Institute of Environmental Health Sciences


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[User] what research (or clinical trials) is being done for Childhood Rhabdomyosarcoma ?

[Assistant]
New types of treatment are being tested in clinical trials.
                    This summary section describes treatments that are being studied in clinical trials. It may not mention every new treatment being studied. Information about clinical trials is available from the NCI website.     High-dose chemotherapy with stem cell transplant     High-dose chemotherapy with stem cell transplant is a way of giving high doses of chemotherapy and replacing blood -forming cells destroyed by the cancer treatment. Stem cells (immature blood cells) are removed from the blood or bone marrow of the patient or a donor and are frozen and stored. After the chemotherapy is completed, the stored stem cells are thawed and given back to the patient through an infusion. These reinfused stem cells grow into (and restore) the body's blood cells.       Immunotherapy     Immunotherapy is a treatment that uses the patients immune system to fight cancer. Substances made by the body or made in a laboratory are used to boost, direct, or restore the bodys natural defenses against cancer. This type of cancer treatment is also called biologic therapy or biotherapy.    There are different types of immunotherapy:            -  Immune checkpoint inhibitor therapy uses the body's immune system to kill cancer cells. Two types of immune checkpoint inhibitors are being studied in the treatment of childhood rhabdomyosarcoma that has come back after treatment:                  -  CTLA-4 is a protein on the surface of T cells that helps keep the bodys immune responses in check. When CTLA-4 attaches to another protein called B7 on a cancer cell, it stops the T cell from killing the cancer cell. CTLA-4 inhibitors attach to CTLA-4 and allow the T cells to kill cancer cells. Ipilimumab is a type of CTLA-4 inhibitor.       -  PD-1 is a protein on the surface of T cells that helps keep the bodys immune responses in check. When PD-1 attaches to another protein called PDL-1 on a cancer cell, it stops the T cell from killing the cancer cell. PD-1 inhibitors attach to PDL-1 and allow the T cells to kill cancer cells. Nivolumab and pembrolizumab are PD-1 inhibitors.                -  Vaccine therapy is a type of immunotherapy being studied to treat metastatic rhabdomyosarcoma.              Targeted therapy     Targeted therapy is a type of treatment that uses drugs or other substances to attack cancer cells. Targeted therapies usually cause less harm to normal cells than chemotherapy or radiation do. There are different types of targeted therapy:            -  mTOR inhibitors stop the protein that helps cells divide and survive. Sirolimus is a type of mTOR inhibitor therapy being studied in the treatment of recurrent rhabdomyosarcoma.     -  Tyrosine kinase inhibitors are small-molecule drugs that go through the cell membrane and work inside cancer cells to block signals that cancer cells need to grow and divide. MK-1775 is a tyrosine kinase inhibitor being studied in the treatment of recurrent rhabdomyosarcoma.     -  Antibody-drug conjugates are made up of a monoclonal antibody attached to a drug. The monoclonal antibody binds to specific proteins or receptors found on certain cells, including cancer cells. The drug enters these cells and kills them without harming other cells. Lorvotuzumab mertansine is an antibody-drug conjugate being studied in the treatment of recurrent rhabdomyosarcoma.

                    Patients may want to think about taking part in a clinical trial.
                    For some patients, taking part in a clinical trial may be the best treatment choice. Clinical trials are part of the cancer research process. Clinical trials are done to find out if new cancer treatments are safe and effective or better than the standard treatment.   Many of today's standard treatments for cancer are based on earlier clinical trials. Patients who take part in a clinical trial may receive the standard treatment or be among the first to receive a new treatment.   Patients who take part in clinical trials also help improve the way cancer will be treated in the future. Even when clinical trials do not lead to effective new treatments, they often answer important questions and help move research forward.

                    Patients can enter clinical trials before, during, or after starting their cancer treatment.
                    Some clinical trials only include patients who have not yet received treatment. Other trials test treatments for patients whose cancer has not gotten better. There are also clinical trials that test new ways to stop cancer from recurring (coming back) or reduce the side effects of cancer treatment.   Clinical trials are taking place in many parts of the country. See the Treatment Options section that follows for links to current treatment clinical trials. These have been retrieved from NCI's listing of clinical trials.


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[User] Is Epidermolysis bullosa acquisita inherited ?

[Assistant] Is epidermolysis bullosa acquisita inherited? Unlike the genetic forms of epidermolysis bullosa, epidermolysis bullosa acquisita (EBA) is considered an acquired, sporadic disease. This means that it generally occurs in people with no history of the condition in their families. There have been a couple of reports of families with more than one affected person, suggesting a genetic component may be involved. This could mean that EBA may develop in a person who is "genetically susceptible." However, the condition is not thought to be due to any specific gene(s).


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[User] What is (are) GM1 gangliosidosis type 3 ?

[Assistant] GM1 gangliosidosis is an inherited lysosomal storage disorder that progressively destroys nerve cells (neurons) in the brain and spinal cord. The condition may be classified into three major types based on the general age that signs and symptoms first appear: classic infantile (type 1); juvenile (type 2); and adult onset or chronic (type 3). Although the types differ in severity, their features may overlap significantly. GM1 gangliosidosis is caused by mutations in the GLB1 gene and is inherited in an autosomal recessive manner. Treatment is currently symptomatic and supportive.


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[User] What is (are) Knee Replacement ?

[Assistant] Knee replacement is surgery for people with severe knee damage. Knee replacement can relieve pain and allow you to be more active. Your doctor may recommend it if you have knee pain and medicine and other treatments are not helping you anymore.    When you have a total knee replacement, the surgeon removes damaged cartilage and bone from the surface of your knee joint and replaces them with a man-made surface of metal and plastic. In a partial knee replacement, the surgeon only replaces one part of your knee joint. The surgery can cause scarring, blood clots, and, rarely, infections. After a knee replacement, you will no longer be able to do certain activities, such as jogging and high-impact sports.


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[User] What is (are) Townes-Brocks Syndrome ?

[Assistant] Townes-Brocks syndrome is a genetic condition that affects several parts of the body. The most common features of this condition are an obstruction of the anal opening (imperforate anus), abnormally shaped ears, and hand malformations that most often affect the thumb. Most people with this condition have at least two of these three major features.  Other possible signs and symptoms of Townes-Brocks syndrome include kidney abnormalities, mild to profound hearing loss, heart defects, and genital malformations. These features vary among affected individuals, even within the same family. Intellectual disability or learning problems have also been reported in about 10 percent of people with Townes-Brocks syndrome.


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[User] What is (are) Rh deficiency syndrome ?

[Assistant] The Rh deficiency syndrome, also known as Rh-null syndrome, is a blood disorder where people have red blood cells (RBCs) lacking all Rh antigens. The Rh antigens maintain the integrity of the RBC membrane and therefore, RBCs which lack Rh antigens have an abnormal shape. There are two types of Rh deficiency syndrome: The regulator type is associated with many different changes (mutations) in the RHAG gene .  The amorph type is caused by inactive copies of a gene (silent alleles) at the RH locus. As a result, the RBCs do not express any of the Rh antigens. The absence of the Rh complex alters the RBC shape, increases its tendency to break down (osmotic fragility), and shortens its lifespan, resulting in a hemolytic anemia that is usually mild. These patients are at risk of having adverse transfusion reactions because they may produce antibodies against several of the Rh antigens and can only receive blood from people who have the same condition. Rh deficiency syndrome is inherited in an autosomal recessive manner. Management is individualized according to the severity of hemolytic anemia.


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[User] What is the outlook for AIDS-Related Lymphoma ?

[Assistant] Certain factors affect prognosis (chance of recovery) and treatment options. The prognosis (chance of recovery) and treatment options depend on the following:          - The stage of the cancer.    - The age of the patient.    - The number of CD4 lymphocytes (a type of white blood cell) in the blood.    - The number of places in the body lymphoma is found outside the lymph system.    - Whether the patient has a history of intravenous (IV) drug use.    - The patient's ability to carry out regular daily activities.


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[User] What is (are) Leiomyosarcoma ?

[Assistant] Leiomyosarcoma is a rare cancerous tumor that consists of smooth (involuntary) muscle cells. Leiomyosarcoma is a type of sarcoma. It spreads through the blood stream and can affect the lungs, liver, blood vessels, or any other soft tissue in the body. The exact cause of leiomyosarcoma is not known, although genetic and environmental factors appear to be involved. It is most often found in the uterus or abdomen.


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[User] How many people are affected by adermatoglyphia ?

[Assistant] Adermatoglyphia appears to be a rare condition. Only a few affected families have been identified worldwide.


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[User] What is (are) myotonia congenita ?

[Assistant] Myotonia congenita is a disorder that affects muscles used for movement (skeletal muscles). Beginning in childhood, people with this condition experience bouts of sustained muscle tensing (myotonia) that prevent muscles from relaxing normally. Although myotonia can affect any skeletal muscles, including muscles of the face and tongue, it occurs most often in the legs. Myotonia causes muscle stiffness that can interfere with movement. In some people the stiffness is very mild, while in other cases it may be severe enough to interfere with walking, running, and other activities of daily life. These muscle problems are particularly noticeable during movement following a period of rest. Many affected individuals find that repeated movements can temporarily alleviate their muscle stiffness, a phenomenon known as the warm-up effect.  The two major types of myotonia congenita are known as Thomsen disease and Becker disease. These conditions are distinguished by the severity of their symptoms and their patterns of inheritance. Becker disease usually appears later in childhood than Thomsen disease and causes more severe muscle stiffness, particularly in males. People with Becker disease often experience temporary attacks of muscle weakness, particularly in the arms and hands, brought on by movement after periods of rest. They may also develop mild, permanent muscle weakness over time. This muscle weakness is not seen in people with Thomsen disease.


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[User] Who is at risk for Aplastic Anemia? ?

[Assistant]
Aplastic anemia is a rare but serious blood disorder. People of all ages can develop aplastic anemia. However, it's most common in adolescents, young adults, and the elderly. Men and women are equally likely to have it.

The disorder is two to three times more common in Asian countries.

Your risk of aplastic anemia is higher if you:

Have been exposed to toxins

Have taken certain medicines or had radiation or chemotherapy (treatments for cancer)

Have certain infectious diseases, autoimmune disorders, or inherited conditions

For more information, go to "What Causes Aplastic Anemia?"


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[User] What causes Congenital anosmia ?

[Assistant] What causes congenital anosmia? Congenital anosmia may occur as an isolated abnormality or be associated with specific genetic disorders (such as Kallmann syndrome and congenital insensitivity to pain). Most cases of isolated congenital anosmia (not associated with additional symptoms) occur sporadically in people with no family history of the condition. In these people, the exact underlying cause of the condition is unknown. Most likely, there is more than one cause. Scientists suspect that the condition occurs due to abnormal development of the olfactory system (the sensory system used for sense of smell) prior to birth. This may include abnormalities of the nasal cavity, disruptions in the pathway that carries information from the nose to the brain, and/or malformations of the portion of the brain that processes sense of smell. Rarely, isolated congenital anosmia can affect more than one family member. This suggests that there may be a genetic component in some cases. One study found that some people affected by isolated congenital anosmia have changes (mutations) in PROKR2 or PROK2, two genes that have previously been reported in people with Kallmann syndrome (an inherited condition associated with congenital anosmia and other symptoms). To date, no other disease-causing genes have been identified.


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[User] What is (are) Aicardi-Goutieres Syndrome Disorder ?

[Assistant]
Aicardi-Goutieres syndrome (AGS) is an inherited encephalopathy that affects newborn infants and usually results in severe mental and physical handicap. There are two forms of the syndrome: an early-onset form that is severe, and a late-onset form that has less impact upon neurological function. The early-onset form affects about 20 percent of all babies who have AGS. These infants are born with neurological and liver abnormalities, such as enlargement of the liver and spleen and elevated liver enzymes. Their jittery behavior and poor feeding ability mimic congenital viral infection.

Babies with later-onset AGS begin having symptoms after the first weeks or months of normal development, which appear as a progressive decline in head growth, weak or stiffened muscles (spasticity), and cognitive and developmental delays that range from moderate to severe. Symptoms last for several months, and include irritability, inconsolable crying, intermittent fever, seizures, and loss of developmental skills. Children may also have puffy swelling on the fingers, toes, and ears that resemble chilblains. A number of children have a noticeable startle reaction to sudden noise. For babies with the later-onset form, as symptoms lessen, there is no further worsening of the disease.

AGS is difficult to diagnose since many of the symptoms are similar to those of other disorders. Diagnosis is made based on the clinical symptoms of the disease, as well as characteristic brain abnormalities that can be seen in an MRI brain scan. Cerebrospinal fluid (CSF), taken using a "spinal tap," can also be tested for increased levels of a specific immune system cell (a lymphocyte), which indicates a condition known as chronic lymphocytosis. These cells are normally only elevated during infection, so that lymphocytosis without evidence of infection can be used as an indicator of AGS. CSF may also be tested for elevated levels of a substance known as interferon-gamma, which can also support a diagnosis of AGS.

The mutations of four different genes are associated with AGS:

- Aicardi-Goutieres syndrome-1 (AGS1) and AGS5 (an autosomal dominant form) are caused by a mutation in the TREX1 gene, - AGS2 is caused by a mutation in the RNASEH2B gene, - AGS3 is caused by a mutation in the RNASEH2C gene, - AGS4 is caused by a mutation in the RNASEH2A gene.

Most cases of AGS are inherited in an autosomal recessive manner, which means that both parents of a child with AGS must carry a single copy of the defective gene responsible for the disease. Parents do not have any symptoms of disease, but with every child they have together, there is a one in four chance that the baby will receive two copies of the defective gene and inherit AGS.

NOTE: AGS is distinct from the similarly named Aicardi syndrome (characterized by absence of a brain structure (corpus callosum), and spinal, skeletal, and eye abnormalities).


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[User] What are the complications of Knee Replacement ?

[Assistant] While new technology and advances in surgical techniques have greatly reduced the risks involved with knee replacements, there are still some risks you should be aware of. Two of the most common possible problems are blood clots and infection. Preventing Blood Clots Blood clots can occur in the veins of your legs after knee replacement surgery. To reduce the risk of clots, your doctor may have you elevate your leg periodically and prescribe special exercises, support hose, or blood thinners. Preventing Infections Infection can occur when bacteria enter the bloodstream from skin or urinary tract infections. To reduce the risk of infection, your doctors may prescribe antibiotics for you to take prior to your surgery and for a short time afterward. Other Complications Other complications, such as new or ongoing pain, stiffness, fracture, bleeding, or injury to the blood vessels can occur. Serious medical complications, such as heart attack or stroke, are very rare. Warning Signs To Watch For To minimize the risk of complications, it is important to recognize signs of potential problems early and contact your doctor. For example, tenderness, redness, and swelling of your calf or swelling of your thigh, ankle, calf, or foot could be warning signs of a possible blood clot. Warning signs of infection include fever or chills, tenderness and swelling of the wound, and drainage from the wound. You should call your doctor if you experience any of these symptoms. It is important to get instructions from your doctor before leaving the hospital and follow them carefully once you get home. Doing so will give you the greatest chance of a successful surgery.


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[User] How to diagnose Rheumatoid Arthritis ?

[Assistant] Rheumatoid arthritis can be difficult to diagnose in its early stages because the full range of symptoms develops over time, and only a few symptoms may be present in the early stages. As part of the diagnosis, your doctor will look for symptoms such as swelling, warmth, pain, and limitations in joint motion throughout your body. Your doctor may ask you questions about the intensity of your pain symptoms, how often they occur, and what makes the pain better or worse.


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[User] What is (are) Diverticular Disease ?

[Assistant]
Fiber is a substance in foods that comes from plants. Fiber helps soften stool so it moves smoothly through the colon and is easier to pass. Soluble fiber dissolves in water and is found in beans, fruit, and oat products. Insoluble fiber does not dissolve in water and is found in whole-grain products and vegetables. Both kinds of fiber help prevent constipation.

Constipation is a condition in which an adult has fewer than three bowel movements a week or has bowel movements with stools that are hard, dry, and small, making them painful or difficult to pass.

High-fiber foods also have many benefits in preventing and controlling chronic diseases, such as cardiovascular disease, obesity, diabetes, and cancer.2


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[User] What are the treatments for Acute Disseminated Encephalomyelitis ?

[Assistant] Treatment for ADEM is targeted at suppressing inflammation in the brain using anti-inflammatory drugs. Most individuals respond to several days of intravenous corticosteroids such as methylprednisolone, followed by oral corticosteroid treatment. When corticosteroids fail to work, plasmapheresis or intravenous immunoglobulin therapy are possible secondary treatment options that are reported to help in some severe cases. Additional treatment is symptomatic and supportive.


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[User] What is (are) Vesicoureteral Reflux ?

[Assistant]
Vesicoureteral reflux is the abnormal flow of urine from the bladder to the upper urinary tract. The urinary tract is the bodys drainage system for removing wastes and extra water. The urinary tract includes two kidneys, two ureters, a bladder, and a urethra. Blood flows through the kidneys, and the kidneys filter out wastes and extra water, making urine. The urine travels down two narrow tubes called the ureters. The urine is then stored in a balloonlike organ called the bladder. When the bladder empties, urine flows out of the body through a tube called the urethra at the bottom of the bladder.

In VUR, urine may flow backrefluxinto one or both ureters and, in some cases, to one or both kidneys. VUR that affects only one ureter and kidney is called unilateral reflux, and VUR that affects both ureters and kidneys is called bilateral reflux.


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[User] What are the symptoms of Osteopetrosis autosomal recessive 7 ?

[Assistant] What are the signs and symptoms of Osteopetrosis autosomal recessive 7? The Human Phenotype Ontology provides the following list of signs and symptoms for Osteopetrosis autosomal recessive 7. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Decreased antibody level in blood 3/4 Abnormal trabecular bone morphology - Anemia - Autosomal recessive inheritance - Nystagmus - Optic nerve compression - Osteopetrosis - Progressive visual loss - Recurrent pneumonia - 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 treatments for Reye's Syndrome ?

[Assistant] There is no cure for RS. Successful management, which depends on early diagnosis, is primarily aimed at protecting the brain against irreversible damage by reducing brain swelling, reversing the metabolic injury, preventing complications in the lungs, and anticipating cardiac arrest. It has been learned that several inborn errors of metabolism mimic RS in that the first manifestation of these errors may be an encephalopathy with liver dysfunction. These disorders must be considered in all suspected cases of RS. Some evidence suggests that treatment in the end stages of RS with hypertonic IV glucose solutions may prevent progression of the syndrome.


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[User] What is the outlook for Coma ?

[Assistant] The outcome for coma and persistent vegetative state depends on the cause, severity, and site of neurological damage. Individuals may emerge from coma with a combination of physical, intellectual, and psychological difficulties that need special attention. Recovery usually occurs gradually, with some acquiring more and more ability to respond. Some individuals never progress beyond very basic responses, but many recover full awareness. Individuals recovering from coma require close medical supervision. A coma rarely lasts more than 2 to 4 weeks. Some patients may regain a degree of awareness after persistent vegetative state. Others may remain in that state for years or even decades. The most common cause of death for someone in a persistent vegetative state is infection, such as pneumonia.


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[User] Is Tracheobronchopathia osteoplastica inherited ?

[Assistant] Is tracheobronchopathia osteoplastica inherited? There is no known genetic susceptibility to the development of TO, and it typically occurs in people with no known history of the condition in their family. Familial occurrence has been reported only once, in a woman and her daughter.


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[User] What is (are) Aicardi-Goutieres syndrome ?

[Assistant] Aicardi-Goutieres syndrome is a disorder that mainly affects the brain, the immune system, and the skin.  Most newborns with Aicardi-Goutieres syndrome do not show any signs or symptoms of the disorder at birth. However, about 20 percent are born with a combination of features that include an enlarged liver and spleen (hepatosplenomegaly), elevated blood levels of liver enzymes, a decrease in blood platelets (thrombocytopenia), and abnormal neurological responses. While this combination of signs and symptoms is typically associated with the immune system's response to congenital viral infection, no actual infection is found in these infants. For this reason, Aicardi-Goutieres syndrome is sometimes referred to as a "mimic of congenital infection."  Within the first year of life most individuals with Aicardi-Goutieres syndrome experience an episode of severe brain dysfunction (encephalopathy), typically lasting for several months. During this phase of the disorder, affected babies are usually extremely irritable and do not feed well. They may develop intermittent fevers in the absence of infection (sterile pyrexias) and may have seizures. They stop developing new skills and begin losing skills they had already acquired (developmental regression). Growth of the brain and skull slows down, resulting in an abnormally small head size (microcephaly). In this phase of the disorder, white blood cells and molecules associated with inflammation can be detected in the cerebrospinal fluid, which is the fluid that surrounds the brain and spinal cord (central nervous system). These abnormal findings are consistent with inflammation and tissue damage in the central nervous system.  The encephalopathic phase of Aicardi-Goutieres syndrome leaves behind permanent neurological damage that is usually severe. Medical imaging reveals deterioration of white matter in the brain (leukodystrophy). White matter consists of nerve fibers covered by myelin, which is a substance that insulates and protects nerves. Affected individuals also have abnormal deposits of calcium (calcification) in the brain.  Most people with Aicardi-Goutieres syndrome have profound intellectual disability. They also have significant neuromuscular problems including muscle stiffness (spasticity); involuntary tensing of various muscles (dystonia), especially those in the arms; and weak muscle tone (hypotonia) in the trunk.  About 40 percent of people with Aicardi-Goutieres syndrome have painful, itchy skin lesions, usually on the fingers, toes, and ears. These puffy, red lesions, which are called chilblains, are caused by inflammation of small blood vessels. They may be brought on or made worse by exposure to cold. Vision problems, joint stiffness, and mouth ulcers may also occur in this disorder.  As a result of the severe neurological problems usually associated with Aicardi-Goutieres syndrome, most people with this disorder do not survive past childhood. However, some affected individuals who have later onset and milder neurological problems may live into adulthood.


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[User] what research (or clinical trials) is being done for Neurodegeneration with Brain Iron Accumulation ?

[Assistant] The mission of the National Institute of Neurological Disorders and Stroke (NINDS) is to seek fundamental knowledge about the brain and nervous system, and to use that knowledge to reduce the burden of neurological disease. NINDS-funded researchers are developing a mouse model of an NBIA disorder to gain insight into the causes of the disease and accelerate ongoing efforts to identify therapeutics to treat it..


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[User] Is X-linked chondrodysplasia punctata 1 inherited ?

[Assistant] This condition is inherited in an X-linked recessive pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the ARSE gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation would have to occur in both copies of the gene to cause the disorder. Because it is unlikely that females will have two altered copies of this gene, males are affected by X-linked recessive disorders much more frequently than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.


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[User] What are the genetic changes related to infantile systemic hyalinosis ?

[Assistant] Mutations in the ANTXR2 gene (also known as the CMG2 gene) cause infantile systemic hyalinosis. The ANTXR2 gene provides instructions for making a protein involved in the formation of tiny blood vessels (capillaries). Researchers believe that the ANTXR2 protein is also important for maintaining the structure of basement membranes, which are thin, sheet-like structures that separate and support cells in many tissues.  The signs and symptoms of infantile systemic hyalinosis are caused by the accumulation of a hyaline substance in different parts of the body. The nature of this substance is not well known, but it is likely made up of protein and sugar molecules. Researchers suspect that mutations in the ANTXR2 gene disrupt the formation of basement membranes, allowing the hyaline substance to leak through and build up in various body tissues.


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[User] What is (are) Cole disease ?

[Assistant] Cole disease is a disorder that affects the skin. People with this disorder have areas of unusually light-colored skin (hypopigmentation), typically on the arms and legs, and spots of thickened skin on the palms of the hands and the soles of the feet (punctate palmoplantar keratoderma). These skin features are present at birth or develop in the first year of life.  In some cases, individuals with Cole disease develop abnormal accumulations of the mineral calcium (calcifications) in the tendons, which can cause pain during movement. Calcifications may also occur in the skin or breast tissue.


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[User] What is (are) COL4A1-related brain small-vessel disease ?

[Assistant] COL4A1-related brain small-vessel disease is part of a group of conditions called the COL4A1-related disorders. The conditions in this group have a range of signs and symptoms that involve fragile blood vessels. COL4A1-related brain small-vessel disease is characterized by weakening of the blood vessels in the brain. Stroke is often the first symptom of this condition, typically occurring in mid-adulthood. In affected individuals, stroke is usually caused by bleeding in the brain (hemorrhagic stroke) rather than a lack of blood flow in the brain (ischemic stroke), although either type can occur. Individuals with this condition are at increased risk of having more than one stroke in their lifetime. People with COL4A1-related brain small vessel disease also have leukoencephalopathy, which is a change in a type of brain tissue called white matter that can be seen with magnetic resonance imaging (MRI). Affected individuals may also experience seizures and migraine headaches accompanied by visual sensations known as auras.  Some people with COL4A1-related brain small-vessel disease have an eye abnormality called Axenfeld-Rieger anomaly. Axenfeld-Rieger anomaly involves underdevelopment and eventual tearing of the colored part of the eye (iris) and a pupil that is not in the center of the eye. Other eye problems experienced by people with COL4A1-related brain small-vessel disease include clouding of the lens of the eye (cataract) and the presence of arteries that twist and turn abnormally within the light-sensitive tissue at the back of the eye (arterial retinal tortuosity). Axenfeld-Rieger anomaly and cataract can cause impaired vision. Arterial retinal tortuosity can cause episodes of bleeding within the eye following any minor trauma to the eye, leading to temporary vision loss.  The severity of the condition varies greatly among affected individuals. Some individuals with COL4A1-related brain small-vessel disease do not have any signs or symptoms of the condition.


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[User] What are the treatments for Prostate Cancer ?

[Assistant] Hormonal therapy deprives cancer cells of the male hormones they need to grow and survive. This treatment is often used for prostate cancer that has spread to other parts of the body. Sometimes doctors use hormonal therapy to try to keep the cancer from coming back after surgery or radiation treatment. Side effects can include impotence, hot flashes, loss of sexual desire, and thinning of bones.


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[User] What are the symptoms of Mosaic trisomy 8 ?

[Assistant] What are the signs and symptoms of Mosaic trisomy 8? The facial features are usually mild and can include elongation of the skull (scaphocephaly), prominent forehead, widely-spaced eyes, deeply set eyes, broad upturned nose, micrognathia, and ear abnormalities. Additional features can include: agenesis of the corpus callosum, highly arched or cleft palate, short and large neck, high stature, elongated thin trunk, and narrow shoulders and pelvis. Kidney and cardiac abnormalities are frequent. Camptodactyly, stiff joints, absent malformed kneecap, vertebral malformations such as scoliosis, as well as eye abnormalities also commonly observed. Most affected individuals have moderate intellectual disabilities (IQ between 50 and 75), with some people having a normal intelligence. There is no correlation between the percentage of trisomic cells and the severity of the intellectual deficit. Mosaic trisomy 8 also seems to predispose to Wilms tumors, myelodysplasias, and myeloid leukemia. The Human Phenotype Ontology provides the following list of signs and symptoms for Mosaic trisomy 8. 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% Cognitive impairment 90% Abnormality of pelvic girdle bone morphology 50% Abnormality of the antihelix 50% Abnormality of the ribs 50% Abnormality of the shoulder 50% Anteverted nares 50% Camptodactyly of finger 50% Deep palmar crease 50% Deep plantar creases 50% Deeply set eye 50% Dolichocephaly 50% Frontal bossing 50% Hypertelorism 50% Large earlobe 50% Limitation of joint mobility 50% Long face 50% Low-set, posteriorly rotated ears 50% Narrow chest 50% Opacification of the corneal stroma 50% Patellar aplasia 50% Scoliosis 50% Strabismus 50% Vertebral segmentation defect 50% Vesicoureteral reflux 50% Aplasia/Hypoplasia of the corpus callosum 7.5% Cleft palate 7.5% Cryptorchidism 7.5% Deviation of finger 7.5% Hearing impairment 7.5% Hypopigmented skin patches 7.5% Irregular hyperpigmentation 7.5% Short neck 7.5% Short stature 7.5% Tall stature 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] How many people are affected by Miyoshi myopathy ?

[Assistant] The exact prevalence of Miyoshi myopathy is unknown. In Japan, where the condition was first described, it is estimated to affect 1 in 440,000 individuals.


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[User] Who is at risk for Rh Incompatibility? ?

[Assistant]
An Rh-negative woman who conceives a child with an Rh-positive man is at risk for Rhincompatibility.

Rh factor is inherited (passed from parents to children through the genes). If you're Rh-negative and the father of your baby is Rh-positive, the baby has a 50 percent or more chance of having Rh-positive blood.

Simple blood tests can show whether you and the father of your baby are Rh-positive or Rh-negative.

If you're Rh-negative, your risk of problems from Rh incompatibility is higher if you were exposed to Rh-positive blood before the pregnancy. This may have happened during:

An earlier pregnancy (usually during delivery). You also may have been exposed to Rh-positive blood if you had bleeding or abdominal trauma (for example, from a car accident) during the pregnancy.

An ectopic pregnancy, a miscarriage, or an induced abortion. (An ectopic pregnancy is a pregnancy that starts outside of the uterus, or womb.)

A mismatched blood transfusion or blood and marrow stem cell transplant.

An injection or puncture with a needle or other object containing Rh-positive blood.

Certain tests also can expose you to Rh-positive blood. Examples include amniocentesis (AM-ne-o-sen-TE-sis) and chorionic villus (ko-re-ON-ik VIL-us) sampling (CVS).

Amniocentesis is a test that you may have during pregnancy. Your doctor uses a needle to remove a small amount of fluid from the sac around your baby. The fluid is then tested for various reasons.

CVS also may be done during pregnancy. For this test, your doctor threads a thin tube through the vagina and cervix to the placenta. He or she removes a tissue sample from the placenta using gentle suction. The tissue sample is tested for various reasons.

Unless you were treated with the medicine that prevents Rh antibodies (Rh immune globulin) after each of these events, you're at risk for Rh incompatibility during current and future pregnancies.


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[User] What is (are) osteoporosis-pseudoglioma syndrome ?

[Assistant] Osteoporosis-pseudoglioma syndrome is a rare condition characterized by severe thinning of the bones (osteoporosis) and eye abnormalities that lead to vision loss. In people with this condition, osteoporosis is usually recognized in early childhood. It is caused by a shortage of minerals, such as calcium, in bones (decreased bone mineral density), which makes the bones brittle and prone to fracture. Affected individuals often have multiple bone fractures, including in the bones that form the spine (vertebrae). Multiple fractures can cause collapse of the affected vertebrae (compressed vertebrae), abnormal side-to-side curvature of the spine (scoliosis), short stature, and limb deformities. Decreased bone mineral density can also cause softening or thinning of the skull (craniotabes).  Most affected individuals have impaired vision at birth or by early infancy and are blind by young adulthood. Vision problems are usually caused by one of several eye conditions, grouped together as pseudoglioma, that affect the light-sensitive tissue at the back of the eye (the retina), although other eye conditions have been identified in affected individuals. Pseudogliomas are so named because, on examination, the conditions resemble an eye tumor known as a retinal glioma.  Rarely, people with osteoporosis-pseudoglioma syndrome have additional signs or symptoms such as mild intellectual disability, weak muscle tone (hypotonia), abnormally flexible joints, or seizures.


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[User] What to do for Diabetic Kidney Disease ?

[Assistant] - Diabetic kidney disease, also called diabetic nephropathy, is kidney disease caused by diabetes.  - People with diabetes have high blood glucose, also called high blood sugar or hyperglycemia.  - At the onset of diabetes, blood flow into the kidneys increases, which may strain the glomeruli and lessen their ability to filter blood.  - Higher levels of blood glucose lead to the buildup of extra material in the glomeruli, which increases the force of the blood moving through the kidneys and creates stress in the glomeruli.  - Many people with diabetes can develop high blood pressure, another factor in the development of kidney disease. High blood pressure, also called hypertension, is an increase in the amount of force that blood places on blood vessels as it moves through the entire body.  - Diabetic kidney disease takes many years to develop.  - People with diabetic kidney disease do not have any symptoms in the early stages. As kidney disease progresses, a person can develop edema, or swelling. Edema happens when the kidneys cannot get rid of the extra fluid and salt in the body. Edema can occur in the legs, feet, or ankles and less often in the hands or face.  - Once kidney function decreases further, symptoms may include      - appetite loss    - nausea    - vomiting    - drowsiness, or feeling tired    - trouble concentrating    - sleep problems    - increased or decreased urination    - generalized itching or numbness    - dry skin    - headaches    - weight loss    - darkened skin    - muscle cramps    - shortness of breath    - chest pain    - People can prevent or slow the progression of diabetic kidney disease by      - taking medication to control high blood pressure    - managing blood glucose levels    - making changes in their eating, diet, and nutrition    - losing weight if they are overweight or obese    - getting regular physical activity


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[User] What is (are) Dyggve-Melchior-Clausen syndrome ?

[Assistant] Dyggve-Melchior-Clausen (DMC) syndrome is a rare, progressive genetic condition characterized by abnormal skeletal development, microcephaly, and intellectual disability. Only about 100 cases have been reported to date. Skeletal abnormalities may include a barrel-shaped chest with a short truck, partial dislocation of the hips, knock knees, bowlegs, and decreased joint mobility. A small number of affected individuals experience instability in the upper neck vertebrae that can lead to spinal cord compression, weakness and paralysis. Normally, there is growth deficiency resulting in short stature. DMC is caused by mutations in the DYM gene and is inherited in an autosomal recessive manner. Some researchers have described an X-linked pattern of inheritance, which has not been confirmed to date.


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[User] What are the treatments for X-linked adrenoleukodystrophy ?

[Assistant] These resources address the diagnosis or management of X-linked adrenoleukodystrophy:  - Gene Review: Gene Review: X-Linked Adrenoleukodystrophy  - Genetic Testing Registry: Adrenoleukodystrophy  - Genomics Education Programme (UK)  - MedlinePlus Encyclopedia: Adrenoleukodystrophy  - National Marrow Donor Program  - X-linked Adrenoleukodystrophy Database: Diagnosis of X-ALD   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] How many people are affected by Acromegaly ?

[Assistant] Small pituitary adenomas are common, affecting about 17 percent of the population.1 However, research suggests most of these tumors do not cause symptoms and rarely produce excess GH.2 Scientists estimate that three to four out of every million people develop acromegaly each year and about 60 out of every million people suffer from the disease at any time.3 Because the clinical diagnosis of acromegaly is often missed, these numbers probably underestimate the frequency of the disease.


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[User] What is (are) Harlequin ichthyosis ?

[Assistant] Harlequin ichthyosis is a severe genetic disorder that mainly affects the skin. The newborn infant is covered with plates of thick skin that crack and split apart. The thick plates can pull at and distort facial features and can restrict breathing and eating. Mutations in the ABCA12 gene cause harlequin ichthyosis. This condition is inherited in an autosomal recessive pattern.


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[User] What is the outlook for Pseudotumor Cerebri ?

[Assistant] The disorder may cause progressive, permanent visual loss in some patients. In some cases, pseudotumor cerebri recurs.


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[User] What are the symptoms of Keratosis follicularis spinulosa decalvans ?

[Assistant] What are the signs and symptoms of Keratosis follicularis spinulosa decalvans? The Human Phenotype Ontology provides the following list of signs and symptoms for Keratosis follicularis spinulosa decalvans. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Alopecia 90% Aplasia/Hypoplasia of the eyebrow 90% Hyperkeratosis 90% Ichthyosis 90% Abnormality of the fingernails 50% Blepharitis 50% Myopia 50% Opacification of the corneal stroma 50% Retinal detachment 50% Abnormality of dental color 7.5% Abnormality of dental enamel 7.5% Carious teeth 7.5% Eczema 7.5% Conjunctivitis - Corneal dystrophy - Dry skin - Dystrophic fingernails - Ectropion - Facial erythema - Follicular hyperkeratosis - Heterogeneous - Keratitis - Nail dysplasia - Palmoplantar keratoderma - Perifollicular fibrosis - Photophobia - Scarring alopecia of scalp - Sparse eyebrow - Sparse eyelashes - X-linked recessive inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What is (are) Neuronal ceroid lipofuscinosis 7 ?

[Assistant] Neuronal ceroid lipofuscinosis 7 (CLN7-NCL) is a rare condition that affects the nervous system. Signs and symptoms of the condition generally develop in early childhood (average age 5 years) and may include loss of muscle coordination (ataxia), seizures that do not respond to medications, muscle twitches (myoclonus), visual impairment, and developmental regression (the loss of previously acquired skills). CLN7-NCL is caused by changes (mutations) in the MFSD8 gene and is inherited in an autosomal recessive manner. Treatment options are limited to therapies that can help relieve some of the symptoms.


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[User] What is (are) Myoepithelial carcinoma ?

[Assistant] Myoepithelial carcinoma is a rare malignant tumor that usually occurs in the salivary glands but can also occur in skin and soft tissues. The name of this cancer comes from the appearance of the tumor cells under the microscope. Approximately 66% of these tumors occur in the parotid gland. The average age of patients is reported to be 55 years.


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[User] What is (are) Neurogenic diabetes insipidus ?

[Assistant] Neurogenic diabetes insipidus is a disease that causes frequent urination. This type of diabetes insipidus results from damage to the pituitary gland, which disrupts the normal storage and release of antidiuretic hormone (ADH). When this hormone reaches the kidneys, it directs them to make less urine. Damage to the pituitary gland can be caused by different diseases as well as by head injuries, neurosurgery, or genetic disorders. To treat the ADH deficiency that results from any kind of damage to the pituitary, a synthetic hormone called desmopressin can be taken by an injection, a nasal spray, or a pill.


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[User] What are the genetic changes related to mucopolysaccharidosis type VII ?

[Assistant] Mutations in the GUSB gene cause MPS VII. This gene provides instructions for producing the beta-glucuronidase (-glucuronidase) enzyme, which is involved in the breakdown of large sugar molecules called glycosaminoglycans (GAGs). GAGs were originally called mucopolysaccharides, which is where this condition gets its name. Mutations in the GUSB gene reduce or completely eliminate the function of -glucuronidase. The shortage (deficiency) of -glucuronidase leads to the accumulation of GAGs within cells, specifically inside the lysosomes. Lysosomes are compartments in the cell that digest and recycle different types of molecules. Conditions such as MPS VII that cause molecules to build up inside the lysosomes are called lysosomal storage disorders. The accumulation of GAGs increases the size of the lysosomes, which is why many tissues and organs are enlarged in this disorder. Researchers believe that the GAGs may also interfere with the functions of other proteins inside the lysosomes and disrupt many normal functions of cells.


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[User] What is (are) Hemorrhoids ?

[Assistant]
Hemorrhoids are swollen and inflamed veins around the anus or in the lower rectum. The rectum is the last part of the large intestine leading to the anus. The anus is the opening at the end of the digestive tract where bowel contents leave the body.

External hemorrhoids are located under the skin around the anus. Internal hemorrhoids develop in the lower rectum. Internal hemorrhoids may protrude, or prolapse, through the anus. Most prolapsed hemorrhoids shrink back inside the rectum on their own. Severely prolapsed hemorrhoids may protrude permanently and require treatment.


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[User] What are the symptoms of Hyperinsulinemic hypoglycemia familial 2 ?

[Assistant] What are the signs and symptoms of Hyperinsulinemic hypoglycemia familial 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Hyperinsulinemic hypoglycemia familial 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Hyperinsulinemic hypoglycemia - Hypoglycemia - Large for gestational age - Pancreatic islet-cell hyperplasia - 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 to do for What I need to know about Living with Kidney Failure ?

[Assistant]
Eating the right foods can help you feel better when you are on dialysis or have a kidney transplant. Staying healthy with kidney failure requires watching how much of these elements are included in your diet:

- Protein is in many foods you eat. Protein is in foods from animals and plants. Most diets include both types of protein. Protein provides the building blocks that maintain and repair muscles, organs, and other parts of the body. Too much protein can cause waste to build up in your blood, making your kidneys work harder. However, if you are on hemodialysis or peritoneal dialysis, you need lots of protein to replace the protein that dialysis removes.  - Phosphorus is a mineral that keeps your bones healthy. Phosphorus also keeps blood vessels and muscles working. This mineral is found naturally in foods rich in protein, such as meat, poultry, fish, nuts, beans, and dairy products. Phosphorus is also added to many processed foods. You need phosphorus to turn food into energy; however, too much can cause your bones to weaken.  - Water is in drinks and in foods such as fruits, vegetables, ice cream, gelatin, soup, and popsicles. Your body needs water; however, too much can cause fluid to build up in your body and make your heart work harder.  - Sodium is a part of salt. You can find sodium in many canned, packaged, and fast foods and in seasonings and meats. You need sodium to help control the amount of fluid in your body; however, too much can cause high blood pressure.  - Potassium is a mineral that helps your nerves and muscles work the right way. Potassium is found in fruits and vegetables such as oranges, bananas, tomatoes, and potatoes. You need potassium for healthy nerves and brain cells; however, too much can make your heartbeat irregular.  - Calories are found in all foods and are especially high in oils and sugary foods. You need calories for energy; however, too many can cause weight gain and high blood sugar.

Talk with your clinics renal dietitian to find a meal plan that works for you. Each treatment requires a different diet. If you are on hemodialysis, you have to stay away from foods such as potatoes and oranges because they have lots of potassium. If you are on peritoneal dialysis, eating potassium is fine. Instead, you may need to watch your calories. Your food needs will also depend on your weight and activity level.

Changing your diet may be hard at first. Eating the right foods will help you feel better. You will have more strength and energy. Having more energy will help you live a fuller, healthier life. More information is provided in the NIDDK health topic, Eat Right to Feel Right on Hemodialysis.


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[User] What is (are) Leukemia ?

[Assistant] Cancer begins in cells, which make up the blood and other tissues. Normally, cells grow, divide, and produce more cells as needed to keep the body healthy and functioning properly. Sometimes, however, the process of creating a new cell goes wrong -- cells become abnormal and form more cells in an uncontrolled way.


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[User] How many people are affected by neurofibromatosis type 1 ?

[Assistant] Neurofibromatosis type 1 occurs in 1 in 3,000 to 4,000 people worldwide.


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[User] What is (are) sickle cell disease ?

[Assistant] Sickle cell disease is a group of disorders that affects hemoglobin, the molecule in red blood cells that delivers oxygen to cells throughout the body. People with this disorder have atypical hemoglobin molecules called hemoglobin S, which can distort red blood cells into a sickle, or crescent, shape.  Signs and symptoms of sickle cell disease usually begin in early childhood. Characteristic features of this disorder include a low number of red blood cells (anemia), repeated infections, and periodic episodes of pain. The severity of symptoms varies from person to person. Some people have mild symptoms, while others are frequently hospitalized for more serious complications.  The signs and symptoms of sickle cell disease are caused by the sickling of red blood cells. When red blood cells sickle, they break down prematurely, which can lead to anemia. Anemia can cause shortness of breath, fatigue, and delayed growth and development in children. The rapid breakdown of red blood cells may also cause yellowing of the eyes and skin, which are signs of jaundice. Painful episodes can occur when sickled red blood cells, which are stiff and inflexible, get stuck in small blood vessels. These episodes deprive tissues and organs of oxygen-rich blood and can lead to organ damage, especially in the lungs, kidneys, spleen, and brain. A particularly serious complication of sickle cell disease is high blood pressure in the blood vessels that supply the lungs (pulmonary hypertension). Pulmonary hypertension occurs in about one-third of adults with sickle cell disease and can lead to heart failure.


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[User] Is Schwartz-Jampel syndrome inherited ?

[Assistant] This condition is inherited in an autosomal recessive pattern, which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition each carry one copy of the mutated gene, but they typically do not show signs and symptoms of the condition.