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

[User] What is (are) Bereavement ?

[Assistant] Bereavement is the period of grief and mourning after a death. When you grieve, it's part of the normal process of reacting to a loss. You may experience grief as a mental, physical, social or emotional reaction. Mental reactions can include anger, guilt, anxiety, sadness and despair. Physical reactions can include sleeping problems, changes in appetite, physical problems or illness.     How long bereavement lasts can depend on how close you were to the person who died, if the person's death was expected and other factors. Friends, family and faith may be sources of support. Grief counseling or grief therapy is also helpful to some people.     NIH: National Cancer Institute


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[User] What is (are) Hereditary neuralgic amyotrophy ?

[Assistant] Hereditary neuralgic amyotrophy is a type of nervous system disease that affects the brachial plexus. Common signs and symptoms include episodes of severe pain and muscle wasting in one or both shoulders and arms.  Attacks may be spontaneous or triggered (e.g., by exercise, childbirth, surgery, infection etc.).  Secondary complications, such as decreased sensation, abnormal sensations (e.g., numbness and tingling), chronic pain, and impaired movement may develop overtime. Affected members in some families may share additional distinct physical and facial characteristics. Hereditary neuralgic amyotrophy can be caused by mutations in the SEPT9 gene.  It is inherited in an autosomal dominant fashion.


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[User] What is (are) What I need to know about Kidney Failure and How Its Treated ?

[Assistant]
You and your doctor will work together to choose a treatment that's best for you. The publications of the NIDDK Kidney Failure Series can help you learn about the specific issues you will face.

Booklets

- What I need to know about Kidney Failure and How its Treated  - Treatment Methods for Kidney Failure: Hemodialysis  - Treatment Methods for Kidney Failure: Peritoneal Dialysis  - Treatment Methods for Kidney Failure: Kidney Transplantation  - Kidney Failure: Eat Right to Feel Right on Hemodialysis

Fact Sheets

- Kidney Failure: What to Expect  - Vascular Access for Hemodialysis  - Hemodialysis Dose and Adequacy  - Peritoneal Dialysis Dose and Adequacy  - Amyloidosis and Kidney Disease  - Anemia in Chronic Kidney Disease  - Chronic Kidney Disease-Mineral and Bone Disorder  - Financial Help for Treatment of Kidney Failure

Learning as much as you can about your treatment will help make you an important member of your health care team.

This content is provided as a service of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health. The NIDDK translates and disseminates research findings through its clearinghouses and education programs to increase knowledge and understanding about health and disease among patients, health professionals, and the public. Content produced by the NIDDK is carefully reviewed by NIDDK scientists and other experts.

The NIDDK would like to thank: Neil R. Powe, M.D., M.P.H., M.B.A., University of California, San Francisco; Delphine Tuot, M.D.C.M., M.A.S., University of California, San Francisco; Vicki McClelland and Brian Testerman, both of the Free Medical Clinic of Northern Shenandoah Valley in Winchester, VA

This information is not copyrighted. The NIDDK encourages people to share this content freely.

September 2014


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[User] What are the genetic changes related to long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency ?

[Assistant] Mutations in the HADHA gene cause LCHAD deficiency. The HADHA gene provides instructions for making part of an enzyme complex called mitochondrial trifunctional protein. This enzyme complex functions in mitochondria, the energy-producing centers within cells. As the name suggests, mitochondrial trifunctional protein contains three enzymes that each perform a different function. This enzyme complex is required to break down (metabolize) a group of fats called long-chain fatty acids. Long-chain fatty acids are found in foods such as milk and certain oils. These fatty acids are stored in the body's fat tissues. Fatty acids are a major source of energy for the heart and muscles. During periods of fasting, fatty acids are also an important energy source for the liver and other tissues.  Mutations in the HADHA gene that cause LCHAD deficiency disrupt one of the functions of this enzyme complex. These mutations prevent the normal processing of long-chain fatty acids from food and body fat. As a result, these fatty acids are not converted to energy, which can lead to some features of this disorder, such as lethargy and hypoglycemia. Long-chain fatty acids or partially metabolized fatty acids may also build up and damage the liver, heart, muscles, and retina. This abnormal buildup causes the other signs and symptoms of LCHAD deficiency.


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[User] What is (are) dopamine transporter deficiency syndrome ?

[Assistant] Dopamine transporter deficiency syndrome is a rare movement disorder. The condition is also known as infantile parkinsonism-dystonia because the problems with movement (dystonia and parkinsonism, described below) usually start in infancy and worsen over time. However, the features of the condition sometimes do not appear until childhood or later.  People with dopamine transporter deficiency syndrome develop a pattern of involuntary, sustained muscle contractions known as dystonia. The dystonia is widespread (generalized), affecting many different muscles. The continuous muscle cramping and spasms cause difficulty with basic activities, including speaking, eating, drinking, picking up objects, and walking.  As the condition worsens, affected individuals develop parkinsonism, which is a group of movement abnormalities including tremors, unusually slow movement (bradykinesia), rigidity, and an inability to hold the body upright and balanced (postural instability). Other signs and symptoms that can develop include abnormal eye movements; reduced facial expression (hypomimia); disturbed sleep; frequent episodes of pneumonia; and problems with the digestive system, including a backflow of acidic stomach contents into the esophagus (gastroesophageal reflux) and constipation.  People with dopamine transporter deficiency syndrome may have a shortened lifespan, although the long-term effects of this condition are not fully understood. Children with this condition have died from pneumonia and breathing problems. When the first signs and symptoms appear later in life, affected individuals may survive into adulthood.


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[User] How many people are affected by Ohdo syndrome, Say-Barber-Biesecker-Young-Simpson variant ?

[Assistant] The SBBYS variant of Ohdo syndrome is estimated to occur in fewer than 1 per million people. At least 19 cases have been reported in the medical literature.


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[User] What is (are) Carbon Monoxide Poisoning ?

[Assistant] Carbon monoxide (CO) is a gas that has no odor or color. But it is very dangerous. It can cause sudden illness and death. CO is found in combustion fumes, such as those made by cars and trucks, lanterns, stoves, gas ranges and heating systems. CO from these fumes can build up in places that don't have a good flow of fresh air. You can be poisoned by breathing them in. The most common symptoms of CO poisoning are       -  Headache    -  Dizziness    -  Weakness    -  Nausea    -  Vomiting    -  Chest pain    -  Confusion       It is often hard to tell if someone has CO poisoning, because the symptoms may be like those of other illnesses. People who are sleeping or intoxicated can die from CO poisoning before they have symptoms. A CO detector can warn you if you have high levels of CO in your home.     Centers for Disease Control and Prevention


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[User] What is (are) 17 alpha-hydroxylase/17,20-lyase deficiency ?

[Assistant] 17 alpha()-hydroxylase/17,20-lyase deficiency is a condition that affects the function of certain hormone-producing glands called the gonads (ovaries in females and testes in males) and the adrenal glands. The gonads direct sexual development before birth and during puberty and are important for reproduction. The adrenal glands, which are located on top of the kidneys, regulate the production of certain hormones, including those that control salt levels in the body. People with 17-hydroxylase/17,20-lyase deficiency have an imbalance of many of the hormones that are made in these glands. 17-hydroxylase/17,20-lyase deficiency is one of a group of disorders, known as congenital adrenal hyperplasias, that impair hormone production and disrupt sexual development and maturation.  Hormone imbalances lead to the characteristic signs and symptoms of 17-hydroxylase/17,20-lyase deficiency, which include high blood pressure (hypertension), low levels of potassium in the blood (hypokalemia), and abnormal sexual development. The severity of the features varies. Two forms of the condition are recognized: complete 17-hydroxylase/17,20-lyase deficiency, which is more severe, and partial 17-hydroxylase/17,20-lyase deficiency, which is typically less so.  Males and females are affected by disruptions to sexual development differently. Females (who have two X chromosomes) with 17-hydroxylase/17,20-lyase deficiency are born with normal external female genitalia; however, the internal reproductive organs, including the uterus and ovaries, may be underdeveloped. Women with complete 17-hydroxylase/17,20-lyase deficiency do not develop secondary sex characteristics, such as breasts and pubic hair, and do not menstruate (amenorrhea). Women with partial 17-hydroxylase/17,20-lyase deficiency may develop some secondary sex characteristics; menstruation is typically irregular or absent. Either form of the disorder results in an inability to conceive a baby (infertility).  In affected individuals who are chromosomally male (having an X and a Y chromosome), problems with sexual development lead to abnormalities of the external genitalia. The most severely affected are born with characteristically female external genitalia and are generally raised as females. However, because they do not have female internal reproductive organs, these individuals have amenorrhea and do not develop female secondary sex characteristics. These individuals have testes, but they are abnormally located in the abdomen (undescended). Sometimes, complete 17-hydroxylase/17,20-lyase deficiency leads to external genitalia that do not look clearly male or clearly female (ambiguous genitalia). Males with partial 17-hydroxylase/17,20-lyase deficiency usually have abnormal male genitalia, such as a small penis (micropenis), the opening of the urethra on the underside of the penis (hypospadias), or a scrotum divided into two lobes (bifid scrotum). Males with either complete or partial 17-hydroxylase/17,20-lyase deficiency are also infertile.


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

[User] What is (are) 22q11.2 deletion syndrome ?

[Assistant] 22q11.2 deletion syndrome is a spectrum disorder that includes conditions formerly called DiGeorge syndrome; velocardiofacial syndrome; conotruncal anomaly face syndrome; cases of Opitz G/BBB syndrome; and Cayler cardiofacial syndrome. The features and severity can vary greatly among affected people. Signs and symptoms may include cleft palate, heart defects, recurrent infections, unique facial characteristics, feeding problems, immune system disorders, kidney abnormalities, hypoparathyroidism, thrombocytopenia, scoliosis, hearing loss, developmental delay, and learning disabilities. People with this condition are also more likely to develop certain autoimmune disorders and personality disorders. In most cases, the syndrome occurs for the first time in the affected person; about 10% of cases are inherited from a parent. It is inherited in an autosomal dominant manner.


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[User] What are the symptoms of Glycogen storage disease type 6 ?

[Assistant] What are the signs and symptoms of Glycogen storage disease type 6? The Human Phenotype Ontology provides the following list of signs and symptoms for Glycogen storage disease type 6. 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) Hypoglycemia 90% Short stature 90% Autosomal recessive inheritance - Hepatomegaly - Increased hepatic glycogen content - Postnatal growth retardation - 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.


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

[User] What are the symptoms of Gestational trophoblastic tumor ?

[Assistant] What are the signs and symptoms of Gestational trophoblastic tumor? The Human Phenotype Ontology provides the following list of signs and symptoms for Gestational trophoblastic tumor. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the menstrual cycle 90% Spontaneous abortion 90% Neoplasm of the liver 50% Neoplasm of the lung 50% Neoplasm of the nervous system 50% Renal neoplasm 50% Vaginal neoplasm 50% Abnormality of the genitourinary system - Autosomal 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 causes Primrose syndrome ?

[Assistant] What causes primrose syndrome? The cause of primrose syndrome is currently unknown. Cases of affected males and a affected female have been reported in the literature. All cases seem to be sporadic. Sporadic refers to either a genetic disorder that occurs for the first time in a family due to a new mutation or the chance occurrence of a non-genetic disorder or abnormality that is not likely to recur in a family.


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

[User] What are the genetic changes related to MECP2-related severe neonatal encephalopathy ?

[Assistant] Mutations in the MECP2 gene cause MECP2-related severe neonatal encephalopathy. The MECP2 gene provides instructions for making a protein called MeCP2 that is critical for normal brain function. Researchers believe that this protein has several functions, including regulating other genes in the brain by switching them on or off as they are needed. The MeCP2 protein likely plays a role in maintaining the normal function of nerve cells, which ensures that connections (synapses) between these cells form properly. The MeCP2 protein may also control the production of different versions of certain proteins in nerve cells. Although mutations in the MECP2 gene disrupt the normal function of nerve cells, it is unclear how these mutations lead to the signs and symptoms of MECP2-related severe neonatal encephalopathy.


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[User] What is (are) hereditary fructose intolerance ?

[Assistant] Hereditary fructose intolerance is a condition that affects a person's ability to digest the sugar fructose. Fructose is a simple sugar found primarily in fruits. Affected individuals develop signs and symptoms of the disorder in infancy when fruits, juices, or other foods containing fructose are introduced into the diet. After ingesting fructose, individuals with hereditary fructose intolerance may experience nausea, bloating, abdominal pain, diarrhea, vomiting, and low blood sugar (hypoglycemia). Affected infants may fail to grow and gain weight at the expected rate (failure to thrive).  Repeated ingestion of fructose-containing foods can lead to liver and kidney damage. The liver damage can result in a yellowing of the skin and whites of the eyes (jaundice), an enlarged liver (hepatomegaly), and chronic liver disease (cirrhosis). Continued exposure to fructose may result in seizures, coma, and ultimately death from liver and kidney failure. Due to the severity of symptoms experienced when fructose is ingested, most people with hereditary fructose intolerance develop a dislike for fruits, juices, and other foods containing fructose.  Hereditary fructose intolerance should not be confused with a condition called fructose malabsorption. In people with fructose malabsorption, the cells of the intestine cannot absorb fructose normally, leading to bloating, diarrhea or constipation, flatulence, and stomach pain. Fructose malabsorption is thought to affect approximately 40 percent of individuals in the Western hemisphere; its cause is unknown.


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[User] What are the treatments for Gastrointestinal Carcinoid Tumors ?

[Assistant]
Key Points
                    - There are different types of treatment for patients with gastrointestinal carcinoid tumors.     - Four types of standard treatment are used:         - Surgery      - Radiation therapy      - Chemotherapy      - Hormone therapy         - Treatment for carcinoid syndrome may also be needed.    - New types of treatment are being tested in clinical trials.          - Targeted therapy         - Patients may want to think about taking part in a clinical trial.    - Patients can enter clinical trials before, during, or after starting their cancer treatment.    - Follow-up tests may be needed.

                    There are different types of treatment for patients with gastrointestinal carcinoid tumors.
                    Different types of treatment are available for patients with gastrointestinal carcinoid tumor. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.

                    Four types of standard treatment are used:
                    Surgery     Treatment of GI carcinoid tumors usually includes surgery. One of the following surgical procedures may be used:             -  Endoscopic resection: Surgery to remove a small tumor that is on the inside lining of the GI tract. An endoscope is inserted through the mouth and passed through the esophagus to the stomach and sometimes, the duodenum. An endoscope is a thin, tube-like instrument with a light, a lens for viewing, and a tool for removing tumor tissue.     -  Local excision: Surgery to remove the tumor and a small amount of normal tissue around it.      -  Resection: Surgery to remove part or all of the organ that contains cancer. Nearby lymph nodes may also be removed.     -  Cryosurgery: A treatment that uses an instrument to freeze and destroy carcinoid tumor tissue. This type of treatment is also called cryotherapy. The doctor may use ultrasound to guide the instrument.      -  Radiofrequency ablation: The use of a special probe with tiny electrodes that release high-energy radio waves (similar to microwaves) that kill cancer cells. The probe may be inserted through the skin or through an incision (cut) in the abdomen.     -  Liver transplant: Surgery to remove the whole liver and replace it with a healthy donated liver.     -  Hepatic artery embolization: A procedure to embolize (block) the hepatic artery, which is the main blood vessel that brings blood into the liver. Blocking the flow of blood to the liver helps kill cancer cells growing there.               Radiation therapy      Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy:            -  External radiation therapy uses a machine outside the body to send radiation toward the cancer.     -  Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer.            Radiopharmaceutical therapy is a type of internal radiation therapy. Radiation is given to the tumor using a drug that has a radioactive substance, such as iodine I 131, attached to it. The radioactive substance kills the tumor cells.     External and internal radiation therapy are used to treat gastrointestinal carcinoid tumors that have spread to other parts of the body.        Chemotherapy      Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping the cells from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy).      Chemoembolization of the hepatic artery is a type of regional chemotherapy that may be used to treat a gastrointestinal carcinoid tumor that has spread to the liver. The anticancer drug is injected into the hepatic artery through a catheter (thin tube). The drug is mixed with a substance that embolizes (blocks) the artery, and cuts off blood flow to the tumor. Most of the anticancer drug is trapped near the tumor and only a small amount of the drug reaches other parts of the body. The blockage may be temporary or permanent, depending on the substance used to block the artery. The tumor is prevented from getting the oxygen and nutrients it needs to grow. The liver continues to receive blood from the hepatic portal vein, which carries blood from the stomach and intestine.     The way the chemotherapy is given depends on the type and stage of the cancer being treated.       Hormone therapy      Hormone therapy with a somatostatin analogue is a treatment that stops extra hormones from being made. GI carcinoid tumors are treated with octreotide or lanreotide which are injected under the skin or into the muscle. Octreotide and lanreotide may also have a small effect on stopping tumor growth.

                    Treatment for carcinoid syndrome may also be needed.
                    Treatment of carcinoid syndrome may include the following:          - Hormone therapy with a somatostatin analogue stops extra hormones from being made. Carcinoid syndrome is treated with octreotide or lanreotide to lessen flushing and diarrhea. Octreotide and lanreotide may also help slow tumor growth.     -  Interferon therapy stimulates the bodys immune system to work better and lessens flushing and diarrhea. Interferon may also help slow tumor growth.    - Taking medicine for diarrhea.    - Taking medicine for skin rashes.    - Taking medicine to breathe easier.    - Taking medicine before having anesthesia for a medical procedure.        Other ways to help treat carcinoid syndrome include avoiding things that cause flushing or difficulty breathing such as alcohol, nuts, certain cheeses and foods with capsaicin, such as chili peppers. Avoiding stressful situations and certain types of physical activity can also help treat carcinoid syndrome.   For some patients with carcinoid heart syndrome, a heart valve replacement may be done.

                    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.     Targeted therapy      Targeted therapy is a type of treatment that uses drugs or other substances to identify and attack specific cancer cells without harming normal cells. Several types of targeted therapy are being studied in the treatment of GI carcinoid tumors.

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

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

                    Follow-up tests may be needed.
                    Some of the tests that were done to diagnose the cancer or to find out the stage of the cancer may be repeated. Some tests will be repeated in order to see how well the treatment is working. Decisions about whether to continue, change, or stop treatment may be based on the results of these tests.   Some of the tests will continue to be done from time to time after treatment has ended. The results of these tests can show if your condition has changed or if the cancer has recurred (come back). These tests are sometimes called follow-up tests or check-ups.

		            Treatment Options for Gastrointestinal Carcinoid Tumors

		                    Carcinoid Tumors in the Stomach
		                    Treatment of gastrointestinal (GI) carcinoid tumors in the stomach may include the following:         -  Endoscopic surgery (resection) for small tumors.    - Surgery (resection) to remove part or all of the stomach. Nearby lymph nodes for larger tumors, tumors that grow deep into the stomach wall, or tumors that are growing and spreading quickly may also be removed.        For patients with GI carcinoid tumors in the stomach and MEN1 syndrome, treatment may also include:         - Surgery (resection) to remove tumors in the duodenum (first part of the small intestine, that connects to the stomach).    -  Hormone therapy.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with localized gastrointestinal carcinoid tumor and regional gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Carcinoid Tumors in the Small Intestine
		                    It is not clear what the best treatment is for GI carcinoid tumors in the duodenum (first part of the small intestine, that connects to the stomach). Treatment may include the following:         -  Endoscopic surgery (resection) for small tumors.    - Surgery (local excision) to remove slightly larger tumors.    - Surgery (resection) to remove the tumor and nearby lymph nodes.        Treatment of GI carcinoid tumors in the jejunum (middle part of the small intestine) and ileum (last part of the small intestine, that connects to the colon) may include the following:         -  Surgery (resection) to remove the tumor and the membrane that connects the intestines to the back of the abdominal wall. Nearby lymph nodes are also removed.    - A second surgery to remove the membrane that connects the intestines to the back of the abdominal wall, if any tumor remains or the tumor continues to grow.    -  Hormone therapy.         Check the list of NCI-supported cancer clinical trials that are now accepting patients with localized gastrointestinal carcinoid tumor and regional gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Carcinoid Tumors in the Appendix
		                    Treatment of GI carcinoid tumors in the appendix may include the following:         -  Surgery (resection) to remove the appendix.    - Surgery (resection) to remove the right side of the colon including the appendix. Nearby lymph nodes are also removed.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with localized gastrointestinal carcinoid tumor and regional gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Carcinoid Tumors in the Colon
		                    Treatment of GI carcinoid tumors in the colon may include the following:         -  Surgery (resection) to remove part of the colon and nearby  lymph nodes, in order to remove as much of the cancer as possible.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with localized gastrointestinal carcinoid tumor and regional gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Carcinoid Tumors in the Rectum
		                    Treatment of GI carcinoid tumors in the rectum may include the following:         -  Endoscopic surgery (resection) for tumors that are smaller than 1 centimeter.    - Surgery (resection) for tumors that are larger than 2 centimeters or that have spread to the muscle layer of the rectal wall. This may be either:               - surgery to remove part of the rectum; or      -  surgery to remove the anus, the rectum, and part of the colon through an incision made in the abdomen.                 It is not clear what the best treatment is for tumors that are 1 to 2 centimeters. Treatment may include the following:         - Endoscopic surgery (resection).    - Surgery (resection) to remove part of the rectum.    - Surgery (resection) to remove the anus, the rectum, and part of the colon through an incision made in the abdomen.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with localized gastrointestinal carcinoid tumor and regional gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Metastatic Gastrointestinal Carcinoid Tumors
		                    Distant metastases    Treatment of distant metastases of GI carcinoid tumors is usually palliative therapy to relieve symptoms and improve quality of life. Treatment may include the following:          -  Surgery (resection) to remove as much of the tumor as possible.    -  Hormone therapy.    -  Radiopharmaceutical therapy.    -  External radiation therapy for cancer that has spread to the bone, brain, or spinal cord.    - A clinical trial of a new treatment.         Liver metastases    Treatment of cancer that has spread to the liver may include the following:          - Surgery (local excision) to remove the tumor from the liver.    -  Hepatic artery embolization.    -  Cryosurgery.    -  Radiofrequency ablation.    - Liver transplant.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with metastatic gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.

		                    Recurrent Gastrointestinal Carcinoid Tumors
		                    Treatment of recurrent GI carcinoid tumors may include the following:          -  Surgery (local excision) to remove part or all of the tumor.    - A clinical trial of a new treatment.        Check the list of NCI-supported cancer clinical trials that are now accepting patients with recurrent gastrointestinal carcinoid tumor. For more specific results, refine the search by using other search features, such as the location of the trial, the type of treatment, or the name of the drug. Talk with your doctor about clinical trials that may be right for you. General information about clinical trials is available from the NCI website.


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[User] What are the genetic changes related to alveolar capillary dysplasia with misalignment of pulmonary veins ?

[Assistant] ACD/MPV can be caused by mutations in the FOXF1 gene. The protein produced from the FOXF1 gene is a transcription factor, which means that it attaches (binds) to specific regions of DNA and helps control the activity of many other genes. The FOXF1 protein is important in development of the lungs and their blood vessels. The FOXF1 protein is also involved in the development of the gastrointestinal tract. Mutations in the FOXF1 gene that cause ACD/MPV result in an inactive protein that cannot regulate development, leading to abnormal formation of the pulmonary blood vessels and gastrointestinal tract.  ACD/MPV can also be caused by a deletion of genetic material on the long arm of chromosome 16 in a region known as 16q24.1. This region includes several genes, including the FOXF1 gene. Deletion of one copy of the FOXF1 gene in each cell reduces the production of the FOXF1 protein. A shortage of FOXF1 protein affects the development of pulmonary blood vessels and causes the main features of ACD/MPV. Researchers suggest that the loss of other genes in this region probably causes the additional abnormalities, such as heart defects, seen in some infants with this disorder. Like FOXF1, these genes also provide instructions for making transcription factors that regulate development of various body systems before birth.  In about 60 percent of affected infants, the genetic cause of ACD/MPV is unknown.


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[User] How to diagnose Parasites - Cysticercosis ?

[Assistant]
If you think that you may have cysticercosis, please see your health care provider. Your health care provider will ask you about your symptoms, where you have travelled, and what kinds of foods you eat. The diagnosis of neurocysticercosis usually requires MRI or CT brain scans. Blood tests may be useful to help diagnose an infection, but they may not always be positive in light infections.

If you have been diagnosed with cysticercosis, you and your family members should be tested for intestinal tapeworm infection. See the taeniasis section for more information on intestinal tapeworm infections.

More on: Taeniasis

More on: Resources for Health Professionals: Diagnosis


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[User] What are the treatments for Post-Polio Syndrome ?

[Assistant] Presently, no prevention has been found that can stop deterioration or reverse the deficits caused by the syndrome A number of controlled studies have demonstrated that nonfatiguing exercises may improve muscle strength and reduce tiredness. Doctors recommend that polio survivors follow standard healthy lifestyle practices: consuming a well-balanced diet, exercising judiciously (preferably under the supervision of an experienced health professional), and visiting a doctor regularly. There has been much debate about whether to encourage or discourage exercise for polio survivors or individuals who already have PPS. A commonsense approach, in which people use individual tolerance as their limit, is currently recommended. Preliminary studies indicate that intravenous immunoglobulin therapy may reduce pain, increase quality of life, and improve strength modestly.


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[User] Is Juvenile retinoschisis inherited ?

[Assistant] How is juvenile retinoschisis inherited? Juvenile retinoschisis is inherited in an x-linked recessive pattern. The gene associated with this condition is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present in both copies of the gene to cause the disorder. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons. In X-linked recessive inheritance, a female with one mutated copy of the gene (mutation) in each cell is called a carrier. She can pass on the mutation, but usually does not experience signs and symptoms of the condition. Carrier women have a 50% chance of passing the mutation to their children, males who inherit the mutation will be affected; females who inherit the mutation will be carriers and will nearly always have normal vision. Carrier testing for at-risk female relatives and prenatal testing for pregnancies at increased risk are possible if the disease-causing mutation in the family is known.


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[User] What are the genetic changes related to van der Woude syndrome ?

[Assistant] Mutations in the IRF6 gene cause van der Woude syndrome. The IRF6 gene provides instructions for making a protein that plays an important role in early development. This protein is a transcription factor, which means that it attaches (binds) to specific regions of DNA and helps control the activity of particular genes.  The IRF6 protein is active in cells that give rise to tissues in the head and face. It is also involved in the development of other parts of the body, including the skin and genitals.  Mutations in the IRF6 gene that cause van der Woude syndrome prevent one copy of the gene in each cell from making any functional protein. A shortage of the IRF6 protein affects the development and maturation of tissues in the face, resulting in the signs and symptoms of van der Woude syndrome.


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[User] How many people are affected by von Hippel-Lindau syndrome ?

[Assistant] The incidence of von Hippel-Lindau syndrome is estimated to be 1 in 36,000 individuals.


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[User] What is (are) Fainting ?

[Assistant] Fainting is a temporary loss of consciousness. If you're about to faint, you'll feel dizzy, lightheaded, or nauseous. Your field of vision may "white out" or "black out." Your skin may be cold and clammy. You lose muscle control at the same time, and may fall down.    Fainting usually happens when your blood pressure drops suddenly, causing a decrease in blood flow to your brain. It is more common in older people. Some causes of fainting include       - Heat or dehydration     - Emotional distress     - Standing up too quickly     - Certain medicines     - Drop in blood sugar     - Heart problems        When someone faints, make sure that the airway is clear and check for breathing. The person should stay lying down for 10-15 minutes. Most people recover completely. Fainting is usually nothing to worry about, but it can sometimes be a sign of a serious problem. If you faint, it's important to see your health care provider and find out why it happened.


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[User] What are the symptoms of Ichthyosis, leukocyte vacuoles, alopecia, and sclerosing cholangitis ?

[Assistant] What are the signs and symptoms of Ichthyosis, leukocyte vacuoles, alopecia, and sclerosing cholangitis? The Human Phenotype Ontology provides the following list of signs and symptoms for Ichthyosis, leukocyte vacuoles, alopecia, and sclerosing cholangitis. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the eyelashes 90% Aplasia/Hypoplasia of the eyebrow 90% Hepatomegaly 90% Ichthyosis 90% Splenomegaly 90% Abnormality of dental enamel 7.5% Acanthosis nigricans 7.5% Portal hypertension 7.5% Reduced number of teeth 7.5% Abnormality of blood and blood-forming tissues - Alopecia - Autosomal recessive inheritance - Cholangitis - Dry skin - Hypodontia - Hypoplasia of dental enamel - Hypotrichosis - Jaundice - Oligodontia - Orthokeratosis - Parakeratosis - Sparse eyelashes - 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) Langerhans cell histiocytosis ?

[Assistant] Langerhans cell histiocytosis (LCH) is a disorder that primarily affects children, but is also found in adults of all ages. People with LCH produce too many Langerhans cells or histiocytes, a form of white blood cell found in healthy people that is supposed to protect the body from infection. In people with LCH, these cells multiply excessively and build up in certain areas of the body, causing tumors called granulomas to form. The symptoms vary among affected individuals, and the cause of LCH is unknown. In most cases, this condition is not life-threatening. Some people do experience life-long problems associated with LCH.


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[User] How to diagnose Peters plus syndrome ?

[Assistant] Is there genetic testing available for Peters plus syndrome? Genetic testing is available for Peters plus syndrome. Click here to obtain a list of clinical laboratories offering genetic testing. Carrier testing for at-risk family members and prenatal diagnosis for pregnancies at increased risk are possible if the disease-causing mutations in the family are known. To learn more about the various options available to you, we recommend you work with your health care provider or a genetics professional to contact the laboratories offering prenatal testing.


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[User] What are the symptoms of Limb-girdle muscular dystrophy type 2I ?

[Assistant] What are the signs and symptoms of Limb-girdle muscular dystrophy type 2I? The Human Phenotype Ontology provides the following list of signs and symptoms for Limb-girdle muscular dystrophy type 2I. 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) Exercise-induced myoglobinuria 25% Achilles tendon contracture - Autosomal recessive inheritance - Calf muscle hypertrophy - Congenital muscular dystrophy - Difficulty climbing stairs - Difficulty walking - Dilated cardiomyopathy - Elevated serum creatine phosphokinase - Frequent falls - Hyperlordosis - Impaired left ventricular function - Kyphosis - Macroglossia - Muscle cramps - Myalgia - Nocturnal hypoventilation - Pelvic girdle muscle weakness - Proximal muscle weakness - Restrictive respiratory insufficiency - Scoliosis - Shoulder girdle muscle weakness - Thigh hypertrophy - Toe walking - Variable expressivity - Vertebral fusion - Waddling gait - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What are the treatments for erythrokeratodermia variabilis et progressiva ?

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


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[User] What is (are) Osteopathia striata cranial sclerosis ?

[Assistant] Osteopathia striata cranial sclerosis is a type of skeletal dysplasia, which refers to a group of genetic conditions that affect the bones and hinder growth and development. The severity of the condition and the associated symptoms vary significantly from person to person, even within a single family. Features of the condition are generally present at birth and may include skeletal abnormalities (particularly at the ends of long bones), sclerosis (hardening) of the craniofacial bones, macrocephaly (unusually large head size), and characteristic facial features. Some affected people may also have developmental delay, hearing loss, heart defects and/or ophthalmoplegia (paralysis of the muscles surrounding the eyes). Osteopathia striata cranial sclerosis is caused by changes (mutations) in the WTX gene and is inherited in an X-linked dominant manner. Treatment is based on the signs and symptoms present in each person.


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[User] What is (are) histiocytosis-lymphadenopathy plus syndrome ?

[Assistant] Histiocytosis-lymphadenopathy plus syndrome (also known as SLC29A3 spectrum disorder) is a group of conditions with overlapping signs and symptoms that affect many parts of the body. This group of disorders includes H syndrome, pigmented hypertrichosis with insulin-dependent diabetes mellitus (PHID), Faisalabad histiocytosis, and familial Rosai-Dorfman disease (also known as sinus histiocytosis with massive lymphadenopathy or SHML). These conditions were once thought to be distinct disorders; however, because of the overlapping features and shared genetic cause, they are now considered to be part of the same disease spectrum. While some affected individuals have signs and symptoms characteristic of one of the conditions, others have a range of features from two or more of the conditions. The pattern of signs and symptoms can vary even within the same family.  A feature common to the disorders in this spectrum is histiocytosis, which is the overgrowth of immune system cells called histiocytes. The cells abnormally accumulate in one or more tissues in the body, which can lead to organ or tissue damage. The buildup often occurs in the lymph nodes, leading to swelling of the lymph nodes (lymphadenopathy). Other areas of cell accumulation can include the skin, kidneys, brain and spinal cord (central nervous system), or digestive tract.  This spectrum is known as histiocytosis-lymphadenopathy plus syndrome because the disorders that make up the spectrum can have additional signs and symptoms. A characteristic feature of H syndrome is abnormal patches of skin (lesions), typically on the lower body. These lesions are unusually dark (hyperpigmented) and have excessive hair growth (hypertrichosis). In addition, histiocytes accumulate at the site of the skin lesions. Other features of H syndrome include enlargement of the liver (hepatomegaly), heart abnormalities, hearing loss, reduced amounts of hormones that direct sexual development (hypogonadism), and short stature.  Like H syndrome, PHID causes patches of hyperpigmented skin with hypertrichosis. PHID is also characterized by the development of type 1 diabetes (also known as insulin-dependent diabetes mellitus), which usually begins in childhood. Type 1 diabetes occurs when the body does not produce enough of the hormone insulin, leading to dysregulation of blood sugar levels.  Faisalabad histiocytosis typically causes lymphadenopathy and swelling of the eyelids due to accumulation of histiocytes. Affected individuals can also have joint deformities called contractures in their fingers or toes and hearing loss.  The most common feature of familial Rosai-Dorfman disease is lymphadenopathy, usually affecting lymph nodes in the neck. Histiocytes can also accumulate in other parts of the body.


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[User] What causes Tracheobronchopathia osteoplastica ?

[Assistant] What causes tracheobronchopathia osteoplastica? The underlying cause of tracheobronchopathia osteoplastica (TO) remains unknown. Several theories have been proposed, including chronic airway inflammation, exostosis (formation of new bone), and metaplasia (abnormal cell changes) in the affected tissue. Numerous cases have been reported in association with different conditions including allergic rhinitis. However, no theories have been validated. There is no known genetic susceptibility to the development of TO.


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[User] Is X-linked myotubular myopathy inherited ?

[Assistant] X-linked myotubular myopathy is inherited in an X-linked recessive pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In males (who have only one X chromosome), one altered copy of the gene in each cell is sufficient to cause the condition. In females (who have two X chromosomes), a mutation must be present 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.  In X-linked myotubular myopathy, the affected male inherits one altered copy from his mother in 80 to 90 percent of cases. In the remaining 10 to 20 percent of cases, the disorder results from a new mutation in the gene that occurs during the formation of a parent's reproductive cells (eggs or sperm) or in early embryonic development. Females with one altered copy of the MTM1 gene generally do not experience signs and symptoms of the disorder. In rare cases, however, females who have one altered copy of the MTM1 gene experience some mild muscle weakness.


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[User] What are the symptoms of Ectodermal dysplasia, hidrotic, Christianson-Fourie type ?

[Assistant] What are the signs and symptoms of Ectodermal dysplasia, hidrotic, Christianson-Fourie type? The Human Phenotype Ontology provides the following list of signs and symptoms for Ectodermal dysplasia, hidrotic, Christianson-Fourie type. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal hair quantity 90% Abnormality of the eye 90% Abnormality of the fingernails 90% Aplasia/Hypoplasia of the eyebrow 90% Arrhythmia 7.5% Absent eyebrow - Autosomal dominant inheritance - Bradycardia - Fair hair - Hidrotic ectodermal dysplasia - Nail dystrophy - Paroxysmal supraventricular tachycardia - Short eyelashes - Sparse axillary hair - Sparse pubic hair - Sparse scalp hair - Thick nail - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What are the genetic changes related to Laron syndrome ?

[Assistant] Laron syndrome is caused by mutations in the GHR gene. This gene provides instructions for making a protein called the growth hormone receptor. The receptor is present on the outer membrane of cells throughout the body, particularly liver cells. As its name suggests, the growth hormone receptor attaches (binds) to growth hormone; the two proteins fit together like a key in a lock. When growth hormone is bound to its receptor, it triggers signaling that stimulates the growth and division of cells. This signaling also leads to the production, primarily by liver cells, of another important growth-promoting hormone called insulin-like growth factor I (IGF-I).  Growth hormone and IGF-I have a wide variety of effects on the growth and function of many parts of the body. For example, these hormones stimulate the growth and division of cells called chondrocytes, which play a critical role in producing new bone tissue. Growth hormone and IGF-I also influence metabolism, including how the body uses and stores carbohydrates, proteins, and fats from food.  Mutations in the GHR gene impair the receptor's ability to bind to growth hormone or to trigger signaling within cells. As a result, even when growth hormone is available, cells are unable to respond by producing IGF-I and stimulating growth and division. The cells' inability to react to growth hormone, which is described as growth hormone insensitivity, disrupts the normal growth and function of many different tissues. Short stature results when growth hormone cannot adequately stimulate the growth of bones. Changes in metabolism caused by insensitivity to growth hormone and the resulting shortage of IGF-I cause many of the other features of the condition, including obesity.  Researchers are working to determine how mutations in the GHR gene may protect people with Laron syndrome from developing cancer and type 2 diabetes. Studies suggest that insensitivity to growth hormone may help prevent the uncontrolled growth and division of cells that can lead to the development of cancerous tumors. Growth hormone insensitivity also appears to alter how the body responds to insulin, which is a hormone that regulates blood sugar levels. Resistance to the effects of insulin is a major risk factor for type 2 diabetes. People with Laron syndrome have the opposite situation, an increased sensitivity to insulin, which likely helps explain their reduced risk of this common disease.


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[User] Is ankyloblepharon-ectodermal defects-cleft lip/palate syndrome inherited ?

[Assistant] This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.


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[User] What is (are) Hepatoblastoma ?

[Assistant] Hepatoblastoma is a rare malignant (cancerous) tumor of the liver that usually occurs in the first 3 years of life. In early stages of the condition, there may be no concerning signs or symptoms. As the tumor gets larger, affected children may experience a painful, abdominal lump; swelling of the abdomen; unexplained weight loss; loss of appetite; and/or nausea and vomiting. The exact underlying cause of hepatoblastoma is poorly understood. Risk factors for the tumor include prematurity with a very low birth weight, early exposure to hepatitis B infection, biliary atresia, and several different genetic conditions (i.e. Beckwith-Wiedemann syndrome, familial adenomatous polyposis, Aicardi syndrome, Glycogen storage disease, and Simpson-Golabi-Behmel syndrome). Treatment varies based on the severity of the condition but may include a combination of surgery, watchful waiting, chemotherapy, and/or radiation therapy.


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[User] What is (are) Machado-Joseph Disease ?

[Assistant] Machado-Joseph disease (MJD), which is also called spinocerebellar ataxia type 3, is a rare hereditary ataxia (ataxia is a medical term meaning lack of muscle control). The disease is characterized by slowly progressive clumsiness and weakness in the arms and legs, spasticity, a staggering lurching gait easily mistaken for drunkenness, difficulty with speech and swallowing, involuntary eye movements, double vision, and frequent urination. Some individuals also have dystonia (sustained muscle contractions that cause twisting of the body and limbs, repetitive movements, abnormal postures, and rigidity) or symptoms similar to those of Parkinson's disease. Others have twitching of the face or tongue, or peculiar bulging eyes. Almost all individuals with MJD experience vision problems, including double vision or blurred vision, loss of the ability to distinguish color and/or contrast, and inability to control eye movements.


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[User] What are the symptoms of Pallister-Killian mosaic syndrome ?

[Assistant] What are the signs and symptoms of Pallister-Killian mosaic syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Pallister-Killian mosaic syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormal hair quantity 90% Aplasia/Hypoplasia of the eyebrow 90% Cognitive impairment 90% Decreased body weight 90% Delayed eruption of teeth 90% Delayed skeletal maturation 90% Downturned corners of mouth 90% Hypohidrosis 90% Joint hypermobility 90% Long philtrum 90% Muscular hypotonia 90% Ptosis 90% Short neck 90% Thin vermilion border 90% Anteverted nares 50% Coarse facial features 50% Frontal bossing 50% Hypertelorism 50% Short nose 50% Telecanthus 50% Upslanted palpebral fissure 50% Abnormality of the soft palate 7.5% Strabismus 7.5% Urogenital fistula 7.5% Anal atresia - Anal stenosis - Anteriorly placed anus - Aortic valve stenosis - Aplasia of the uterus - Atria septal defect - Bifid uvula - Broad foot - Broad palm - Cataract - Cleft palate - Clinodactyly of the 5th finger - Coarctation of aorta - Congenital diaphragmatic hernia - Congenital hip dislocation - Cryptorchidism - Depressed nasal bridge - Epicanthus - Flexion contracture - Full cheeks - Hearing impairment - Hyperpigmented streaks - Hypertonia - Hypertrophic cardiomyopathy - Hypopigmented streaks - Hypoplastic labia majora - Hypospadias - Inguinal hernia - Intellectual disability, profound - Intestinal malrotation - Kyphoscoliosis - Macrocephaly - Macroglossia - Macrotia - Mesomelia - Mesomelic/rhizomelic limb shortening - Obesity - Omphalocele - Patent ductus arteriosus - Postaxial foot polydactyly - Postaxial hand polydactyly - Postnatal microcephaly - Prominent forehead - Proptosis - Pulmonary hypoplasia - Renal cyst - Renal dysplasia - Rhizomelia - Seizures - Short phalanx of finger - Short toe - Single transverse palmar crease - Small scrotum - Somatic mosaicism - Sparse anterior scalp hair - Sparse eyebrow - Sparse eyelashes - Stenosis of the external auditory canal - Stillbirth - Supernumerary nipple - Umbilical hernia - Ventricular septal defect - Webbed neck - Wide nasal bridge - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What is (are) Progressive bulbar palsy ?

[Assistant] Progressive bulbar palsy involves the brain stem. The brain stem is the part of the brain needed for swallowing, speaking, chewing, and other functions. Signs and symptoms of progressive bulbar palsy include difficulty swallowing, weak jaw and facial muscles, progressive loss of speech, and weakening of the tongue. Additional symptoms include less prominent weakness in the arms and legs, and outbursts of laughing or crying (called emotional lability). Progressive bulbar palsy is considered a variant form of amyotrophic lateral sclerosis (ALS). Many people with progressive bulbar palsy later develop ALS. While there is no cure for progressive bulbar palsy or for ALS, doctors can treat symptoms.


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[User] What is (are) Dermatomyositis ?

[Assistant] Dermatomyositis is one of a group of muscle diseases known as the inflammatory myopathies, which are characterized by chronic muscle inflammation accompanied by muscle weakness. Dermatomyositis cardinal symptom is a skin rash that precedes, accompanies, or follows progressive muscle weakness. The rash looks patchy, with purple or red discolorations, and characteristically develops on the eyelids and on muscles used to extend or straighten joints, including knuckles, elbows, knees, and toes. Red rashes may also occur on the face, neck, shoulders, upper chest, back, and other locations, and there may be swelling in the affected areas. The rash sometimes occurs without obvious muscle involvement. Adults with dermatomyositis may experience weight loss, a low-grade fever, inflamed lungs, and be sensitive to light such that the rash or muscle disease gets worse. Children and adults with dermatomyositis may develop calcium deposits, which appear as hard bumps under the skin or in the muscle (called calcinosis). Calcinosis most often occurs 1-3 years after the disease begins. These deposits are seen more often in children with dermatomyositis than in adults. In some cases of dermatomyositis, distal muscles (muscles located away from the trunk of the body, such as those in the forearms and around the ankles and wrists) may be affected as the disease progresses. Dermatomyositis may be associated with collagen-vascular or autoimmune diseases, such as lupus.


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[User] Is glycogen storage disease type III 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.


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[User] Do you have information about Statins

[Assistant] Summary : Statins are drugs used to lower cholesterol. Your body needs some cholesterol to work properly. But if you have too much in your blood, it can stick to the walls of your arteries and narrow or even block them.    If diet and exercise don't reduce your cholesterol levels, you may need to take medicine. Often, this medicine is a statin. Statins interfere with the production of cholesterol in your liver. They lower bad cholesterol levels and raise good cholesterol levels. This can slow the formation of plaques in your arteries.    Statins are relatively safe for most people. But they are not recommended for pregnant patients or those with active or chronic liver disease. They can also cause serious muscle problems. Some statins also interact adversely with other drugs. You may have fewer side effects with one statin drug than another.     Researchers are also studying the use of statins for other conditions.    Food and Drug Administration


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[User] What is (are) Gorlin syndrome ?

[Assistant] Gorlin syndrome, also known as nevoid basal cell carcinoma syndrome, is a condition that affects many areas of the body and increases the risk of developing various cancerous and noncancerous tumors.  In people with Gorlin syndrome, the type of cancer diagnosed most often is basal cell carcinoma, which is the most common form of skin cancer. Individuals with Gorlin syndrome typically begin to develop basal cell carcinomas during adolescence or early adulthood. These cancers occur most often on the face, chest, and back. The number of basal cell carcinomas that develop during a person's lifetime varies among affected individuals. Some people with Gorlin syndrome never develop any basal cell carcinomas, while others may develop thousands of these cancers. Individuals with lighter skin are more likely to develop basal cell carcinomas than are people with darker skin.  Most people with Gorlin syndrome also develop noncancerous (benign) tumors of the jaw, called keratocystic odontogenic tumors. These tumors usually first appear during adolescence, and new tumors form until about age 30. Keratocystic odontogenic tumors rarely develop later in adulthood. If untreated, these tumors may cause painful facial swelling and tooth displacement.  Individuals with Gorlin syndrome have a higher risk than the general population of developing other tumors. A small proportion of affected individuals develop a brain tumor called medulloblastoma during childhood. A type of benign tumor called a fibroma can occur in the heart or in a woman's ovaries. Heart (cardiac) fibromas often do not cause any symptoms, but they may obstruct blood flow or cause irregular heartbeats (arrhythmia). Ovarian fibromas are not thought to affect a woman's ability to have children (fertility).  Other features of Gorlin syndrome include small depressions (pits) in the skin of the palms of the hands and soles of the feet; an unusually large head size (macrocephaly) with a prominent forehead; and skeletal abnormalities involving the spine, ribs, or skull. These signs and symptoms are typically apparent from birth or become evident in early childhood.


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[User] What is (are) Prostate Cancer ?

[Assistant] The prostate is a male sex gland, about the size of a large walnut. It is located below the bladder and in front of the rectum. The prostate's main function is to make fluid for semen, a white substance that carries sperm. Prostate cancer occurs when a tumor forms in the tissue of the prostate. In its early stage, prostate cancer needs the male hormone testosterone to grow and survive.


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[User] What is (are) Castleman disease ?

[Assistant] Castleman disease (CD) is a rare condition that affects the lymph nodes and related tissues. There are two main forms: unicentric CD and multicentric CD. Unicentric CD is a "localized" condition that is generally confined to a single set of lymph nodes, while multicentric CD is a "systemic" disease that affects multiple sets of lymph nodes and other tissues throughout the body. The exact underlying cause of CD is currently unknown; however, it is thought to occur sporadically in people with no family history of the condition. Treatment varies based on the form of the condition, the severity of symptoms and whether or not the affected person also has an HIV and/or human herpes virus type 8 (HHV-8) infection. For more specific information about each form of CD, please visit GARD's unicentric Castleman disease and multicentric Castleman disease pages.


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[User] What are the treatments for La Crosse encephalitis ?

[Assistant] How might La Crosse (LAC) encephalitis be treated? There is no specific treatment for LAC encephalitis. Severe cases are treated with supportive therapy which may include hospitalization, respiratory support, IV fluids and prevention of other infections.[9633]


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

[Assistant] Mutations in the FGFR3 gene cause thanatophoric dysplasia. Both types of this condition result from mutations in the FGFR3 gene. This gene provides instructions for making a protein that is involved in the development and maintenance of bone and brain tissue. Mutations in this gene cause the FGFR3 protein to be overly active, which leads to the severe disturbances in bone growth that are characteristic of thanatophoric dysplasia. It is not known how FGFR3 mutations cause the brain and skin abnormalities associated with this disorder.


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[User] What are the symptoms of Coronary Heart Disease ?

[Assistant]
A common symptom of coronary heart disease (CHD) is angina. Angina is chest pain or discomfort that occurs if an area of your heart muscle doesn't get enough oxygen-rich blood.

Angina may feel like pressure or squeezing in your chest. You also may feel it in your shoulders, arms, neck, jaw, or back. Angina pain may even feel like indigestion. The pain tends to get worse with activity and go away with rest. Emotional stress also can trigger the pain.

Another common symptom of CHD is shortness of breath. This symptom occurs if CHD causes heart failure. When you have heart failure, your heart can't pump enough blood to meet your bodys needs. Fluid builds up in your lungs, making it hard to breathe.

The severity of these symptoms varies. They may get more severe as the buildup of plaque continues to narrow the coronary arteries.

Signs and Symptoms of Heart Problems Related to Coronary Heart Disease

Some people who have CHD have no signs or symptomsa condition called silent CHD. The disease might not be diagnosed until a person has signs or symptoms of a heart attack, heart failure, or an arrhythmia (an irregular heartbeat).

Heart Attack

A heart attack occurs if the flow of oxygen-rich blood to a section of heart muscle is cut off. This can happen if an area of plaque in a coronary artery ruptures (breaks open).

Blood cell fragments called platelets stick to the site of the injury and may clump together to form blood clots. If a clot becomes large enough, it can mostly or completely block blood flow through a coronary artery.

If the blockage isnt treated quickly, the portion of heart muscle fed by the artery begins to die. Healthy heart tissue is replaced with scar tissue. This heart damage may not be obvious, or it may cause severe or long-lasting problems.

Heart With Muscle Damage and a Blocked Artery

The most common heart attack symptom is chest pain or discomfort. Most heart attacks involve discomfort in the center or left side of the chest that often lasts for more than a few minutes or goes away and comes back.

The discomfort can feel like uncomfortable pressure, squeezing, fullness, or pain. The feeling can be mild or severe. Heart attack pain sometimes feels like indigestion or heartburn.

The symptoms of angina can be similar to the symptoms of a heart attack. Angina pain usually lasts for only a few minutes and goes away with rest.

Chest pain or discomfort that doesnt go away or changes from its usual pattern (for example, occurs more often or while youre resting) might be a sign of a heart attack. If you dont know whether your chest pain is angina or a heart attack, call 911.

All chest pain should be checked by a doctor.

Other common signs and symptoms of a heart attack include:

Upper body discomfort in one or both arms, the back, neck, jaw, or upper part of the stomach

Shortness of breath, which may occur with or before chest discomfort

Nausea (feeling sick to your stomach), vomiting, light-headedness or fainting, or breaking out in a cold sweat

Sleep problems, fatigue (tiredness), or lack of energy

For more information, go to the Health Topics Heart Attack article.

Heart Failure

Heart failure is a condition in which your heart can't pump enough blood to meet your bodys needs. Heart failure doesn't mean that your heart has stopped or is about to stop working.

The most common signs and symptoms of heart failure are shortness of breath or trouble breathing; fatigue; and swelling in the ankles, feet, legs, stomach, and veins in the neck.

All of these symptoms are the result of fluid buildup in your body. When symptoms start, you may feel tired and short of breath after routine physical effort, like climbing stairs.

For more information, go to the Health Topics Heart Failure article.

Arrhythmia

An arrhythmia is a problem with the rate or rhythm of the heartbeat. When you have an arrhythmia, you may notice that your heart is skipping beats or beating too fast.

Some people describe arrhythmias as a fluttering feeling in the chest. These feelings are called palpitations (pal-pih-TA-shuns).

Some arrhythmias can cause your heart to suddenly stop beating. This condition is called sudden cardiac arrest (SCA). SCA usually causes death if it's not treated within minutes.

For more information, go to the Health Topics Arrhythmia article.


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[User] What are the treatments for Andermann syndrome ?

[Assistant] These resources address the diagnosis or management of Andermann syndrome:  - Gene Review: Gene Review: Hereditary Motor and Sensory Neuropathy with Agenesis of the Corpus Callosum  - Genetic Testing Registry: Andermann 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 Nutrition

[Assistant] Summary : Food provides the energy and nutrients you need to be healthy. Nutrients include proteins, carbohydrates, fats, vitamins, minerals, and water.     Healthy eating is not hard. The key is to       -  Eat a variety of foods, including vegetables, fruits, and whole-grain products    -  Eat lean meats, poultry, fish, beans, and low-fat dairy products     -  Drink lots of water    -  Limit salt, sugar, alcohol, saturated fat, and trans fat in your diet       Saturated fats are usually fats that come from animals. Look for trans fat on the labels of processed foods, margarines, and shortenings.    Centers for Disease Control and Prevention


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[User] What are the treatments for Diabetic Kidney Disease ?

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A health care provider may treat kidney failure due to diabetic kidney disease with dialysis or a kidney transplant. In some cases, people with diabetic kidney disease receive kidney and pancreas transplants.

In most cases, people with diabetic kidney disease start dialysis earlier than people with kidney failure who do not have diabetes. People with diabetic end-stage kidney disease who receive a kidney transplant have a much better survival rate than those people on dialysis, although survival rates for those on dialysis have increasingly improved over time. However, people who receive a kidney transplant and do not have diabetes have a higher survival rate than people with diabetic kidney disease who receive a transplant.5

More information about treatment options for kidney failure is provided in the NIDDK health topics:

- Treatment Methods for Kidney Failure: Hemodialysis  - Treatment Methods for Kidney Failure: Peritoneal Dialysis  - Treatment Methods for Kidney Failure: Transplantation


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[User] What is the outlook for Migraine ?

[Assistant] Responsive prevention and treatment of migraine is incredibly important. Evidence shows an increased sensitivity after each successive attack, eventually leading to chronic daily migraine in some individuals With proper combination of drugs for prevention and treatment of migraine attacks most individuals can overcome much of the discomfort from this debilitating disorder. Women whose migraine attacks occur in association with their menstrual cycle are likely to have fewer attacks and milder symptoms after menopause.


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[User] What are the symptoms of Dihydrolipoamide dehydrogenase deficiency ?

[Assistant] What are the signs and symptoms of Dihydrolipoamide dehydrogenase deficiency? The signs and symptoms of dihydrolipoamide dehydrogenase (DLD) deficiency can vary widely among affected people. Early-onset DLD deficiency typically appears in early infancy with decreased muscle tone (hypotonia), lethargy, and lactic acidosis. Lactic acidosis can cause nausea, vomiting, severe breathing problems, and an abnormal heartbeat. Symptoms typically occur in episodes that may be triggered by illness, injury, or other stresses on the body. Affected infants often do not survive their initial episode or may die within the first few years of life during a recurrent episode. Children who live beyond the first two to three years often have growth delays and neurological problems such as intellectual disability, spasticity, ataxia, and seizures. However, normal intellect has been reported in a few people with the early-onset form of DLD deficiency. Isolated liver involvement, which can range from hepatomegaly (enlarged liver) to life-threatening liver failure, can also occur in the newborn period, or as late as the 3rd decade of life. A few people with DLD deficiency have become affected later in childhood with ataxia and dystonia, with normal cognitive development. Rarely, affected people have muscle weakness (particularly during exercise) or a weakened heart muscle (cardiomyopathy). The Human Phenotype Ontology provides the following list of signs and symptoms for Dihydrolipoamide dehydrogenase deficiency. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Aminoaciduria 90% Cognitive impairment 50% Gait disturbance 50% Hepatomegaly 50% Microcephaly 50% Muscular hypotonia 50% Hepatic failure 7.5% Hypoglycemia 7.5% Decreased liver function 5% Elevated hepatic transaminases 5% Ataxia - Autosomal recessive inheritance - Dystonia - Encephalopathy - Feeding difficulties - Hypertrophic cardiomyopathy - Lactic acidosis - Lethargy - Metabolic acidosis - Seizures - Variable expressivity - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What are the treatments for Colorectal Cancer ?

[Assistant] For surgery, the main side effects are short-term pain and tenderness around the area of the operation. For chemotherapy, the side effects depend on which drugs you take and what the dosages are. Most often the side effects include nausea, vomiting, and hair loss. For radiation therapy, fatigue, loss of appetite, nausea, and diarrhea may occur. There are many new drugs that have greatly reduced the degree of nausea that used to be experienced because of some of these treatments.


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[User] What is (are) Familial stomach cancer ?

[Assistant] Familial stomach cancer is a cluster of stomach cancer within a family. Most cases of stomach cancer occur sporadically in people with little to no family history of the condition; however, approximately 10% of stomach cancer is considered "familial." Although the underlying cause of some familial cases is unknown, genetic changes (mutations) are identified in a subset of people affected by gastric cancer. Hereditary cancer syndromes associated with a predisposition to gastric cancer include hereditary diffuse gastric cancer, Lynch syndrome, Li-Fraumeni syndrome, familial adenomatous polyposis, and Peutz-Jeghers syndrome. In other families, the cluster of stomach cancers may be due to a combination of gene(s) and/or other shared factors such as environment and lifestyle. Depending on the estimated risk, high-risk cancer screening and/or prophylactic surgeries are typically recommended in people who have an increased risk for stomach cancer based on their personal and/or family histories.


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[User] Is Limb-girdle muscular dystrophy inherited ?

[Assistant] How is limb-girdle muscular dystrophy inherited? Limb-girdle muscular dystrophy (LGMD) is most often inherited in an autosomal recessive manner; less commonly, rare sub-types may be inherited in an autosomal dominant manner.  There may be difficulties diagnosing the condition accurately, and often the mode of inheritance cannot be determined. Therefore, it may be challenging to determine the exact recurrence risks for some families. Establishing the type of LGMD in an affected individual can be useful for discussing the clinical course of the disease as well as for determining who else in the family may be at risk for the condition.


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[User] What are the symptoms of Dicarboxylic aminoaciduria ?

[Assistant] What are the signs and symptoms of Dicarboxylic aminoaciduria? There are no common signs or symptoms of dicarboxylic aminoaciduria. Hypoglycemia, developmental and neurological abnormalities, and obsessive compulsive tendencies were described in individual cases. Others that have been diagnosed had virtually no signs or symptoms. The Human Phenotype Ontology provides the following list of signs and symptoms for Dicarboxylic aminoaciduria. 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) Aminoaciduria - Autosomal recessive inheritance - Fasting hypoglycemia - Intellectual disability - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.


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[User] What causes Prevent diabetes problems: Keep your heart and blood vessels healthy ?

[Assistant]
Narrowed blood vessels leave a smaller opening for blood to flow through. Having narrowed blood vessels is like turning on a garden hose and holding your thumb over the opening. The smaller opening makes the water shoot out with more pressure. In the same way, narrowed blood vessels lead to high blood pressure. Other factors, such as kidney problems and being overweight, also can lead to high blood pressure.

Many people with diabetes also have high blood pressure. If you have heart, eye, or kidney problems from diabetes, high blood pressure can make them worse.

You will see your blood pressure written with two numbers separated by a slash. For example, your reading might be 120/70, said as "120 over 70." For most people with diabetes, the target is to keep the first number below 140 and the second number below 80, unless their doctor sets a different target.

If you have high blood pressure, ask your doctor how to lower it. Your doctor may ask you to take blood pressure medicine every day. Some types of blood pressure medicine can also help keep your kidneys healthy.

You may also be able to control your blood pressure by

- eating more fruits and vegetables  - eating less salt and high-sodium foods  - losing weight if you need to  - being physically active  - not smoking  - limiting alcoholic drinks


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[User] What is (are) Head Lice ?

[Assistant] Head lice are parasitic wingless insects. They live on people's heads and feed on their blood. An adult louse is about the size of a sesame seed. The eggs, called nits, are even smaller - about the size of a knot in thread. Lice and nits are found on or near the scalp, most often at the neckline and behind the ears.    Lice spread by close person-to-person contact. It is possible, but not common, to get lice by sharing personal belongings such as hats or hairbrushes. Children ages 3-11 and their families get head lice most often. Personal hygiene has nothing to do with getting head lice. Head lice do not spread disease.    Symptoms are        - Tickling feeling in the hair    - Frequent itching    - Sores from scratching    - Irritability and difficulty sleeping. Head lice are most active in the dark.       Treatment is recommended for people who have an active infestation of head lice. All household members and other close contacts should be checked and treated if necessary. Some experts also recommend treating anyone who shares a bed with an infested person. It is important to treat everyone at the same time.    Centers for Disease Control and Prevention


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[User] What are the genetic changes related to 46,XX testicular disorder of sex development ?

[Assistant] People normally have 46 chromosomes in each cell. Two of the 46 chromosomes, known as X and Y, are called sex chromosomes because they help determine whether a person will develop male or female sex characteristics. Females typically have two X chromosomes (46,XX), and males usually have one X chromosome and one Y chromosome (46,XY).  The SRY gene, normally located on the Y chromosome, provides instructions for making the sex-determining region Y protein. The sex-determining region Y protein causes a fetus to develop as a male.  In about 80 percent of individuals with 46,XX testicular disorder of sex development, the condition results from an abnormal exchange of genetic material between chromosomes (translocation). This exchange occurs as a random event during the formation of sperm cells in the affected person's father. The translocation causes the SRY gene to be misplaced, almost always onto an X chromosome. If a fetus is conceived from a sperm cell with an X chromosome bearing the SRY gene, it will develop as a male despite not having a Y chromosome. This form of the condition is called SRY-positive 46,XX testicular disorder of sex development.  About 20 percent of people with 46,XX testicular disorder of sex development do not have the SRY gene. This form of the condition is called SRY-negative 46,XX testicular disorder of sex development. The cause of the disorder in these individuals is unknown. They are more likely to have ambiguous genitalia than are people with the SRY-positive form.