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What are the symptoms of Tranebjaerg Svejgaard syndrome ?
|
What are the signs and symptoms of Tranebjaerg Svejgaard syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Tranebjaerg Svejgaard 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) Cognitive impairment 90% Dry skin 90% High forehead 90% Macrotia 90% Muscular hypotonia 90% Neurological speech impairment 90% Open mouth 90% Seizures 90% Strabismus 90% Abnormality of the palate 50% Abnormality of the tongue 50% Anteverted nares 50% Incoordination 50% Mandibular prognathia 50% Respiratory insufficiency 50% Scoliosis 50% Thick lower lip vermilion 50% Wide mouth 50% Wide nasal bridge 50% Arachnodactyly 7.5% Camptodactyly of finger 7.5% Clinodactyly of the 5th finger 7.5% Cryptorchidism 7.5% Delayed skeletal maturation 7.5% Hemiplegia/hemiparesis 7.5% Hypermetropia 7.5% Hypertelorism 7.5% Joint hypermobility 7.5% Long penis 7.5% Palmoplantar keratoderma 7.5% Proximal placement of thumb 7.5% Single transverse palmar crease 7.5% Intellectual disability - Psoriasis - X-linked inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
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What is (are) Fragile X Syndrome ?
|
Fragile X syndrome is the most common form of inherited developmental disability. A problem with a specific gene causes the disease. Normally, the gene makes a protein you need for brain development. But the problem causes a person to make little or none of the protein. This causes the symptoms of Fragile X. People with only a small change in the gene might not show any signs of Fragile X. People with bigger changes can have severe symptoms. These might include - Intelligence problems, ranging from learning disabilities to severe intellectual disabilities - Social and emotional problems, such as aggression in boys or shyness in girls - Speech and language problems, especially in boys A genetic blood test can diagnose Fragile X. There is no cure. You can treat some symptoms with educational, behavioral, or physical therapy, and with medicines. Getting treatment early can help. NIH: National Institute of Child Health and Human Development
|
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What is (are) Metaplastic carcinoma of the breast ?
|
Metaplastic carcinoma of the breast is a rare form of breast cancer. The tumor cells differ in type from that of the typical ductal or lobular breast cancers. The cells look like skin cells or cells that make bone. Some women experience no early signs or symptoms, while others experience general symptoms of breast cancers, such as new breast lumps. Treatment of metaplastic carcinoma of the breast is similar to that of invasive ductal cancer.
|
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What is (are) What I need to know about Interstitial Cystitis/Painful Bladder Syndrome ?
|
Interstitial cystitis*painful bladder syndrome (IC/PBS) is one of several conditions that causes bladder pain and a need to urinate frequently and urgently. Some doctors have started using the term bladder pain syndrome (BPS) to describe this condition.
Your bladder is a balloon-shaped organ where your body holds urine. When you have a bladder problem, you may notice certain signs or symptoms.
*See Pronounciation Guide for tips on how to say the words in bold type.
|
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What are the symptoms of Autosomal recessive hyper IgE syndrome ?
|
What are the signs and symptoms of Autosomal recessive hyper IgE syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Autosomal recessive hyper IgE 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) Asthma 90% Cellular immunodeficiency 90% Decreased antibody level in blood 90% Eczema 90% Otitis media 90% Sinusitis 90% Skin ulcer 90% Verrucae 90% Atopic dermatitis - Autosomal recessive inheritance - Cerebral vasculitis - Eosinophilia - Hemiplegia - Infantile onset - Neoplasm - Recurrent bacterial infections - Recurrent fungal infections - Recurrent sinopulmonary infections - Recurrent viral infections - Subarachnoid hemorrhage - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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How many people are affected by Baller-Gerold syndrome ?
|
The prevalence of Baller-Gerold syndrome is unknown, but this rare condition probably affects fewer than 1 per million people. Fewer than 40 cases have been reported in the medical literature.
|
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What are the treatments for hereditary sensory and autonomic neuropathy type V ?
|
These resources address the diagnosis or management of HSAN5: - Genetic Testing Registry: Congenital sensory neuropathy with selective loss of small myelinated fibers These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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How many people are affected by hereditary paraganglioma-pheochromocytoma ?
|
Hereditary paraganglioma-pheochromocytoma occurs in approximately 1 in 1 million people.
|
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What are the symptoms of Mitochondrial neurogastrointestinal encephalopathy syndrome ?
|
What are the signs and symptoms of Mitochondrial neurogastrointestinal encephalopathy syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Mitochondrial neurogastrointestinal encephalopathy 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) Abdominal pain - Areflexia - Autosomal recessive inheritance - Cachexia - Constipation - Death in early adulthood - Decreased activity of cytochrome C oxidase in muscle tissue - Distal amyotrophy - Distal muscle weakness - Distal sensory impairment - Gastrointestinal dysmotility - Gastroparesis - Hypointensity of cerebral white matter on MRI - Intermittent diarrhea - Lactic acidosis - Leukoencephalopathy - Malabsorption - Malnutrition - Mitochondrial myopathy - Multiple mitochondrial DNA deletions - Progressive - Progressive external ophthalmoplegia - Ptosis - Ragged-red muscle fibers - Sensorineural hearing impairment - Subsarcolemmal accumulations of abnormally shaped mitochondria - Vomiting - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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How many people are affected by metatropic dysplasia ?
|
Metatropic dysplasia is a rare disease; its exact prevalence is unknown. More than 80 affected individuals have been reported in the scientific literature.
|
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What are the genetic changes related to fragile X-associated tremor/ataxia syndrome ?
|
Mutations in the FMR1 gene increase the risk of developing FXTAS. The FMR1 gene provides instructions for making a protein called FMRP, which helps regulate the production of other proteins. FMRP plays a role in the development of synapses, which are specialized connections between nerve cells. Synapses are critical for relaying nerve impulses. Individuals with FXTAS have a mutation in which a DNA segment, known as a CGG triplet repeat, is expanded within the FMR1 gene. Normally, this DNA segment is repeated from 5 to about 40 times. In people with FXTAS, however, the CGG segment is repeated 55 to 200 times. This mutation is known as an FMR1 gene premutation. An expansion of more than 200 repeats, a full mutation, causes a more serious condition called fragile X syndrome, which is characterized by intellectual disability, learning problems, and certain physical features. For unknown reasons, the premutation leads to the overproduction of abnormal FMR1 mRNA that contains the expanded repeat region. The FMR1mRNA is the genetic blueprint for the production of FMRP. Researchers believe that the high levels of mRNA cause the signs and symptoms of FXTAS. The mRNA has been found in clumps of proteins and mRNA (intranuclear inclusions) in brain and nerve cells in people with FXTAS. It is thought that attaching to FMR1 mRNA and forming clumps keeps the other proteins from performing their functions, although the effect of the intranuclear inclusions is unclear. In addition, the repeat expansion makes producing FMRP from the mRNA blueprint more difficult, and as a result, people with the FMR1 gene premutation can have less FMRP than normal. A reduction in the protein is not thought to be involved in FXTAS. However, it may cause mild versions of the features seen in fragile X syndrome, such as prominent ears, anxiety, and mood swings.
|
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Do you have information about Medicines
|
Summary : You may need to take medicines every day, or only once in a while. Either way, you want to make sure that the medicines are safe and will help you get better. In the United States, the Food and Drug Administration is in charge of assuring the safety and effectiveness of both prescription and over-the-counter medicines. Even safe drugs can cause unwanted side effects or interactions with food or other medicines you may be taking. They may not be safe during pregnancy. To reduce the risk of reactions and make sure that you get better, it is important for you to take your medicines correctly and be careful when giving medicines to children.
|
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What is (are) What I need to know about Kidney Failure and How Its Treated ?
|
You have two kidneys. The kidneys are shaped like beans. Each kidney is about the size of a fist. They are located just below your ribcage, one on each side of your spine. Your kidneys filter your blood. Each kidney is made of 1 million little filters. During every minute of every day, these filters take out waste materials that can hurt you. They also take out extra fluid from your blood. The wastes and extra fluid make urine. The urine flows from your kidneys to your bladder through tubes called ureters.The bladder stores urine until you urinate. Then, urine leaves the body through a tube called the urethra.
*See the Pronunciation Guide for tips on how to say the the words in bold type.
|
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] |
How many people are affected by Nicolaides-Baraitser syndrome ?
|
Nicolaides-Baraitser syndrome is likely a rare condition; approximately 75 cases have been reported in the scientific literature.
|
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What are the treatments for Kallmann syndrome ?
|
These resources address the diagnosis or management of Kallmann syndrome: - Gene Review: Gene Review: Isolated Gonadotropin-Releasing Hormone (GnRH) Deficiency - Genetic Testing Registry: Hypogonadism with anosmia - Genetic Testing Registry: Kallmann syndrome 1 - Genetic Testing Registry: Kallmann syndrome 2 - Genetic Testing Registry: Kallmann syndrome 3 - Genetic Testing Registry: Kallmann syndrome 4 - MedlinePlus Encyclopedia: Hypogonadotropic Hypogonadism - MedlinePlus Encyclopedia: Smell - Impaired 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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Is juvenile idiopathic arthritis inherited ?
|
Most cases of juvenile idiopathic arthritis are sporadic, which means they occur in people with no history of the disorder in their family. A small percentage of cases of juvenile idiopathic arthritis have been reported to run in families, although the inheritance pattern of the condition is unclear. A sibling of a person with juvenile idiopathic arthritis has an estimated risk of developing the condition that is about 12 times that of the general population.
|
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What is (are) Diarrhea ?
|
Diarrhea is loose, watery stools. Having diarrhea means passing loose stools three or more times a day. Acute diarrhea is a common problem that usually lasts 1 or 2 days and goes away on its own.
Diarrhea lasting more than 2 days may be a sign of a more serious problem. Chronic diarrheadiarrhea that lasts at least 4 weeksmay be a symptom of a chronic disease. Chronic diarrhea symptoms may be continual or they may come and go.
Diarrhea of any duration may cause dehydration, which means the body lacks enough fluid and electrolyteschemicals in salts, including sodium, potassium, and chlorideto function properly. Loose stools contain more fluid and electrolytes and weigh more than solid stools.
People of all ages can get diarrhea. In the United States, adults average one bout of acute diarrhea each year,1 and young children have an average of two episodes of acute diarrhea each year.2
|
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What are the symptoms of Axenfeld-Rieger syndrome type 1 ?
|
What are the signs and symptoms of Axenfeld-Rieger syndrome type 1? The Human Phenotype Ontology provides the following list of signs and symptoms for Axenfeld-Rieger syndrome type 1. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the anterior chamber 90% Aplasia/Hypoplasia of the iris 90% Posterior embryotoxon 90% Glaucoma 50% Hearing impairment 50% Malar flattening 50% Abnormality of the hypothalamus-pituitary axis 7.5% Cutis laxa 7.5% Depressed nasal bridge 7.5% Displacement of the external urethral meatus 7.5% Frontal bossing 7.5% Hypertelorism 7.5% Microdontia 7.5% Reduced number of teeth 7.5% Telecanthus 7.5% Urogenital fistula 7.5% Abnormality of the abdominal wall - Abnormally prominent line of Schwalbe - Anal atresia - Anal stenosis - Aniridia - Autosomal dominant inheritance - Growth hormone deficiency - Hypodontia - Hypoplasia of the iris - Hypoplasia of the maxilla - Hypospadias - Megalocornea - Microcornea - Polycoria - Prominent supraorbital ridges - Rieger anomaly - Short philtrum - Strabismus - Variable expressivity - Wide nasal bridge - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) Familial juvenile hyperuricaemic nephropathy ?
|
Familial juvenile hyperuricaemic nephropathy (FJHN) is an inherited condition that affects the kidneys. The signs and symptoms vary, even among members of the same family. Many individuals with this condition develop high blood levels of a waste product called uric acid. Normally, the kidneys remove uric acid from the blood and transfer it to urine. In FJHN, the kidneys are unable to remove uric acid from the blood effectively. Beginning in the early teens, FJHN causes gout and slowly progressive kidney disease, resulting in kidney failure. People with FJHN typically require either dialysis to remove wastes from the blood or a kidney transplant. FJHN is caused by mutations in the UMOD gene and is inherited in an autosomal dominant fashion.
|
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What is (are) lamellar ichthyosis ?
|
Lamellar ichthyosis is a condition that mainly affects the skin. Infants with this condition are typically born with a tight, clear sheath covering their skin called a collodion membrane. This membrane usually dries and peels off during the first few weeks of life, and then it becomes obvious that affected babies have scaly skin, and eyelids and lips that are turned outward. People with lamellar ichthyosis typically have large, dark, plate-like scales covering their skin on most of their body. Infants with lamellar ichthyosis may develop infections, an excessive loss of fluids (dehydration), and respiratory problems. Affected individuals may also have hair loss (alopecia), abnormally formed fingernails and toenails (nail dystrophy), a decreased ability to sweat (hypohidrosis), an increased sensitivity to heat, and a thickening of the skin on the palms of the hands and soles of the feet (keratoderma). Less frequently, affected individuals have reddened skin (erythema) and joint deformities (contractures).
|
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] |
How many people are affected by Lowe syndrome ?
|
Lowe syndrome is an uncommon condition. It has an estimated prevalence of 1 in 500,000 people.
|
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What are the symptoms of Acromegaloid changes, cutis verticis gyrata and corneal leukoma ?
|
What are the signs and symptoms of Acromegaloid changes, cutis verticis gyrata and corneal leukoma? The Human Phenotype Ontology provides the following list of signs and symptoms for Acromegaloid changes, cutis verticis gyrata and corneal leukoma. 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 eye - Autosomal dominant inheritance - Cutis gyrata of scalp - Large hands - Mandibular prognathia - Periostosis - Soft skin - Tall stature - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
What are the symptoms of Ectodermal dysplasia with natal teeth Turnpenny type ?
|
What are the signs and symptoms of Ectodermal dysplasia with natal teeth Turnpenny type? The Human Phenotype Ontology provides the following list of signs and symptoms for Ectodermal dysplasia with natal teeth Turnpenny 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) Abnormality of the nail - Acanthosis nigricans - Autosomal dominant inheritance - Cranial hyperostosis - Ectodermal dysplasia - Hypodontia - Hypoplastic pilosebaceous units - Hypoplastic sweat glands - Natal tooth - Oligodontia - Relative macrocephaly - Short stature - Slow-growing scalp hair - Sparse eyebrow - Sparse eyelashes - Sparse scalp hair - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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Is CHMP2B-related frontotemporal dementia inherited ?
|
This condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder.
|
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What is (are) Waardenburg syndrome type 2 ?
|
Waardenburg syndrome type 2 is an inherited condition that can cause hearing loss and changes in coloring (pigmentation) of the hair, skin, and eyes. About 50 percent of those with Waardenburg syndrome type 2 have a hearing impairment or are deaf. Type 2 is one the most common forms of Waardenburg syndrome, along with type 1. Waardenburg syndrome type 2 may be caused by mutations in the MITF and SNAI2 genes. This condition is usually inherited in an autosomal dominant fashion, but can sometimes be inherited as an autosomal recessive trait.
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What are the treatments for Respiratory Distress Syndrome ?
|
Treatment for respiratory distress syndrome (RDS) usually begins as soon as an infant is born, sometimes in the delivery room.
Most infants who show signs of RDS are quickly moved to a neonatal intensive care unit (NICU). There they receive around-the-clock treatment from health care professionals who specialize in treating premature infants.
The most important treatments for RDS are:
Surfactant replacement therapy.
Breathing support from a ventilator or nasal continuous positive airway pressure (NCPAP) machine. These machines help premature infants breathe better.
Oxygen therapy.
Surfactant Replacement Therapy
Surfactant is a liquid that coats the inside of the lungs. It helps keep them open so that an infant can breathe in air once he or she is born.
Babies who have RDS are given surfactant until their lungs are able to start making the substance on their own. Surfactant usually is given through a breathing tube. The tube allows the surfactant to go directly into the baby's lungs.
Once the surfactant is given, the breathing tube is connected to a ventilator, or the baby may get breathing support from NCPAP.
Surfactant often is given right after birth in the delivery room to try to prevent or treat RDS. It also may be given several times in the days that follow, until the baby is able to breathe better.
Some women are given medicines called corticosteroids during pregnancy. These medicines can speed up surfactant production and lung development in a fetus. Even if you had these medicines, your infant may still need surfactant replacement therapy after birth.
Breathing Support
Infants who have RDS often need breathing support until their lungs start making enough surfactant. Until recently, a mechanical ventilator usually was used. The ventilator was connected to a breathing tube that ran through the infant's mouth or nose into the windpipe.
Today, more and more infants are receiving breathing support from NCPAP. NCPAP gently pushes air into the baby's lungs through prongs placed in the infant's nostrils.
Oxygen Therapy
Infants who have breathing problems may get oxygen therapy. Oxygen is given through a ventilator or NCPAP machine, or through a tube in the nose. This treatment ensures that the infants' organs get enough oxygen to work well.
For more information, go to the Health Topics Oxygen Therapy article.
Other Treatments
Other treatments for RDS include medicines, supportive therapy, and treatment for patent ductus arteriosus (PDA). PDA is a condition that affects some premature infants.
Medicines
Doctors often give antibiotics to infants who have RDS to control infections (if the doctors suspect that an infant has an infection).
Supportive Therapy
Treatment in the NICU helps limit stress on babies and meet their basic needs of warmth, nutrition, and protection. Such treatment may include:
Using a radiant warmer or incubator to keep infants warm and reduce the risk of infection.
Ongoing monitoring of blood pressure, heart rate, breathing, and temperature through sensors taped to the babies' bodies.
Using sensors on fingers or toes to check the amount of oxygen in the infants' blood.
Giving fluids and nutrients through needles or tubes inserted into the infants' veins. This helps prevent malnutrition and promotes growth. Nutrition is critical to the growth and development of the lungs. Later, babies may be given breast milk or infant formula through feeding tubes that are passed through their noses or mouths and into their throats.
Checking fluid intake to make sure that fluid doesn't build up in the babies' lungs.
Treatment for Patent Ductus Arteriosus
PDA is a possible complication of RDS. In this condition, a fetal blood vessel called the ductus arteriosus doesn't close after birth as it should.
The ductus arteriosus connects a lung artery to a heart artery. If it remains open, it can strain the heart and increase blood pressure in the lung arteries.
PDA is treated with medicines, catheter procedures, and surgery. For more information, go to the Health Topics Patent Ductus Arteriosus article.
|
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316,
1780,
350,
3783,
316,
3929,
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] |
What is (are) Amyloidosis and Kidney Disease ?
|
Amyloidosis is a rare disease that occurs when amyloid proteins are deposited in tissues and organs. Amyloid proteins are abnormal proteins that the body cannot break down and recycle, as it does with normal proteins. When amyloid proteins clump together, they form amyloid deposits. The buildup of these deposits damages a persons organs and tissues. Amyloidosis can affect different organs and tissues in different people and can affect more than one organ at the same time. Amyloidosis most frequently affects the kidneys, heart, nervous system, liver, and digestive tract. The symptoms and severity of amyloidosis depend on the organs and tissues affected.
|
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33193,
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13,
11219,
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6728,
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36013,
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5917,
285,
12147,
273,
30593,
2433,
3469,
327,
253,
15384,
285,
7944,
5876,
15
] |
What is (are) Polycystic Kidney Disease ?
|
Autosomal recessive PKD is a rare genetic disorder that affects the liver as well as the kidneys. The signs of autosomal recessive PKD frequently appear in the earliest months of life, even in the womb, so health care providers often call it infantile PKD. In an autosomal recessive disorder, the child has to inherit the gene mutation from both parents to have an increased likelihood for the disorder. The chance of a child inheriting autosomal recessive mutations from both parents with a gene mutation is 25 percent, or one in four. If only one parent carries the mutated gene, the child will not get the disorder, although the child may inherit the gene mutation. The child is a carrier of the disorder and can pass the gene mutation to the next generation. Genetic testing can show whether a parent or child is a carrier of the mutated gene. Autosomal recessive disorders do not typically appear in every generation of an affected family.
The following chart shows the chance of inheriting an autosomal recessive mutation from parents who both carry the mutated gene:
Read more about how people inherit genetic conditions at the NLMs Genetics Home Reference.
|
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6380,
2515,
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253,
27218,
12822,
2588,
11665,
9067,
19039,
15
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What is (are) Pregnancy and Thyroid Disease ?
|
Thyroid disease is a disorder that affects the thyroid gland. Sometimes the body produces too much or too little thyroid hormone. Thyroid hormones regulate metabolismthe way the body uses energyand affect nearly every organ in the body. Too much thyroid hormone is called hyperthyroidism and can cause many of the bodys functions to speed up. Too little thyroid hormone is called hypothyroidism and can cause many of the bodys functions to slow down.
Thyroid hormone plays a critical role during pregnancy both in the development of a healthy baby and in maintaining the health of the mother.
Women with thyroid problems can have a healthy pregnancy and protect their fetuses health by learning about pregnancys effect on the thyroid, keeping current on their thyroid function testing, and taking the required medications.
|
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What are the symptoms of Ectrodactyly cleft palate syndrome ?
|
What are the signs and symptoms of Ectrodactyly cleft palate syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Ectrodactyly cleft palate syndrome. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the skin - Autosomal dominant inheritance - Cleft palate - Split hand - 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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Who is at risk for Testicular Cancer? ?
|
Health history can affect the risk of testicular cancer.
Anything that increases the chance of getting a disease is called a risk factor. Having a risk factor does not mean that you will get cancer; not having risk factors doesnt mean that you will not get cancer. Talk with your doctor if you think you may be at risk. Risk factors for testicular cancer include: - Having had an undescended testicle. - Having had abnormal development of the testicles. - Having a personal history of testicular cancer. - Having a family history of testicular cancer (especially in a father or brother). - Being white.
Treatment for testicular cancer can cause infertility.
Certain treatments for testicular cancer can cause infertility that may be permanent. Patients who may wish to have children should consider sperm banking before having treatment. Sperm banking is the process of freezing sperm and storing it for later use.
|
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What is (are) Hypopharyngeal Cancer ?
|
Key Points
- Hypopharyngeal cancer is a disease in which malignant (cancer) cells form in the tissues of the hypopharynx. - Use of tobacco products and heavy drinking can affect the risk of developing hypopharyngeal cancer. - Signs and symptoms of hypopharyngeal cancer include a sore throat and ear pain. - Tests that examine the throat and neck are used to help detect (find) and diagnose hypopharyngeal cancer. - Certain factors affect prognosis (chance of recovery) and treatment options.
Hypopharyngeal cancer is a disease in which malignant (cancer) cells form in the tissues of the hypopharynx.
The hypopharynx is the bottom part of the pharynx (throat). The pharynx is a hollow tube about 5 inches long that starts behind the nose, goes down the neck, and ends at the top of the trachea (windpipe) and esophagus (the tube that goes from the throat to the stomach). Air and food pass through the pharynx on the way to the trachea or the esophagus. Most hypopharyngeal cancers form in squamous cells, the thin, flat cells lining the inside of the hypopharynx. The hypopharynx has 3 different areas. Cancer may be found in 1 or more of these areas. Hypopharyngeal cancer is a type of head and neck cancer.
|
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What is (are) Movement Disorders ?
|
Imagine if parts of your body moved when you didn't want them to. If you have a movement disorder, you experience these kinds of impaired movement. Dyskinesia is abnormal uncontrolled movement and is a common symptom of many movement disorders. Tremors are a type of dyskinesia. Nerve diseases cause many movement disorders, such as Parkinson's disease. Other causes include injuries, autoimmune diseases, infections and certain medicines. Many movement disorders are inherited, which means they run in families. Treatment varies by disorder. Medicine can cure some disorders. Others get better when an underlying disease is treated. Often, however, there is no cure. In that case, the goal of treatment is to improve symptoms and relieve pain.
|
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What is (are) familial hemophagocytic lymphohistiocytosis ?
|
Familial hemophagocytic lymphohistiocytosis is a disorder in which the immune system produces too many activated immune cells (lymphocytes) called T cells, natural killer cells, B cells, and macrophages (histiocytes). Excessive amounts of immune system proteins called cytokines are also produced. This overactivation of the immune system causes fever and damages the liver and spleen, resulting in enlargement of these organs. Familial hemophagocytic lymphohistiocytosis also destroys blood-producing cells in the bone marrow, a process called hemophagocytosis. As a result, affected individuals have low numbers of red blood cells (anemia) and a reduction in the number of blood cells involved in clotting (platelets). A reduction in platelets may cause easy bruising and abnormal bleeding. The brain may also be affected in familial hemophagocytic lymphohistiocytosis. As a result, affected individuals may experience irritability, delayed closure of the bones of the skull in infants, neck stiffness, abnormal muscle tone, impaired muscle coordination, paralysis, blindness, seizures, and coma. In addition to neurological problems, familial hemophagocytic lymphohistiocytosis can cause abnormalities of the heart, kidneys, and other organs and tissues. Affected individuals also have an increased risk of developing cancers of blood-forming cells (leukemia and lymphoma). Signs and symptoms of familial hemophagocytic lymphohistiocytosis usually become apparent during infancy, although occasionally they appear later in life. They usually occur when the immune system launches an exaggerated response to an infection, but may also occur in the absence of infection. Without treatment, most people with familial hemophagocytic lymphohistiocytosis survive only a few months.
|
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] |
What are the treatments for autoimmune Addison disease ?
|
These resources address the diagnosis or management of autoimmune Addison disease: - Genetic Testing Registry: Addison's disease - MedlinePlus Encyclopedia: Addison's Disease These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the treatments for hypohidrotic ectodermal dysplasia ?
|
These resources address the diagnosis or management of hypohidrotic ectodermal dysplasia: - Gene Review: Gene Review: Hypohidrotic Ectodermal Dysplasia - Genetic Testing Registry: Autosomal dominant hypohidrotic ectodermal dysplasia - Genetic Testing Registry: Autosomal recessive hypohidrotic ectodermal dysplasia syndrome - Genetic Testing Registry: Hypohidrotic X-linked ectodermal dysplasia - MedlinePlus Encyclopedia: Ectodermal dysplasia - MedlinePlus Encyclopedia: Ozena - MedlinePlus Encyclopedia: Sweating - absent These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What are the symptoms of Lynch syndrome ?
|
What are the signs and symptoms of Lynch syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Lynch 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) Anemia 90% Constipation 90% Gastrointestinal hemorrhage 90% Intestinal obstruction 90% Malabsorption 90% Neoplasm of the colon 90% Neoplasm of the rectum 90% Weight loss 90% Biliary tract neoplasm 50% Neoplasm of the nervous system 50% Neoplasm of the pancreas 50% Neoplasm of the small intestine 50% Neoplasm of the stomach 50% Ovarian neoplasm 50% Renal neoplasm 50% Uterine neoplasm 50% Ascites 7.5% Hepatomegaly 7.5% Nausea and vomiting 7.5% Recurrent urinary tract infections 7.5% Autosomal dominant inheritance - Colon cancer - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
What is (are) 7q11.23 duplication syndrome ?
|
7q11.23 duplication syndrome is a condition that can cause a variety of neurological and behavioral problems as well as other abnormalities. People with 7q11.23 duplication syndrome typically have delayed development of speech and delayed motor skills such as crawling and walking. Speech problems and abnormalities in the way affected individuals walk and stand may persist throughout life. Affected individuals may also have weak muscle tone (hypotonia) and abnormal movements, such as involuntary movements of one side of the body that mirror intentional movements of the other side. Behavioral problems associated with this condition include anxiety disorders (such as social phobias and selective mutism, which is an inability to speak in certain circumstances), attention deficit hyperactivity disorder (ADHD), physical aggression, excessively defiant behavior (oppositional disorder), and autistic behaviors that affect communication and social interaction. While the majority of people with 7q11.23 duplication syndrome have low-average to average intelligence, intellectual development varies widely in this condition, from intellectual disability to, rarely, above-average intelligence. About one-fifth of people with 7q11.23 duplication syndrome experience seizures. About half of individuals with 7q11.23 duplication syndrome have enlargement (dilatation) of the blood vessel that carries blood from the heart to the rest of the body (the aorta); this enlargement can get worse over time. Aortic dilatation can lead to life-threatening complications if the wall of the aorta separates into layers (aortic dissection) or breaks open (ruptures). The characteristic appearance of people with 7q11.23 duplication syndrome can include a large head (macrocephaly) that is flattened in the back (brachycephaly), a broad forehead, straight eyebrows, and deep-set eyes with long eyelashes. The nose may be broad at the tip with the area separating the nostrils attaching lower than usual on the face (low insertion of the columella), resulting in a shortened area between the nose and the upper lip (philtrum). A high arch in the roof of the mouth (high-arched palate) and ear abnormalities may also occur in affected individuals.
|
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What are the treatments for What I need to know about Hepatitis C ?
|
Hepatitis C is usually not treated unless it becomes chronic. Chronic hepatitis C is treated with medicines that slow or stop the virus from damaging the liver. Your doctor will closely watch your symptoms and schedule regular blood tests to make sure the treatment is working.
Medicines for Chronic Hepatitis C
Chronic hepatitis C is most often treated with a medicine combination that attacks the hepatitis C virus. Treatment may last from 24 to 48 weeks.
Today, newer treatments with medicine for chronic hepatitis C are appearing quickly. Talk with your doctor if you have questions about treatment.
Talk with your doctor before taking other prescription medicines and over-the-counter medicines.
Liver Transplant
A liver transplant may be necessary if chronic hepatitis C causes severe liver damage that leads to liver failure. Symptoms of severe liver damage include the symptoms of hepatitis C and
- generalized itching - a longer than usual amount of time for bleeding to stop - easy bruising - swollen stomach or ankles - spiderlike blood vessels, called spider angiomas, that develop on the skin
Liver transplant is surgery to remove a diseased or injured liver and replace it with a healthy one from another person, called a donor. If your doctors tell you that you need a transplant, you should talk with them about the long-term demands of living with a liver transplant.
A team of surgeonsdoctors who specialize in surgeryperforms a liver transplant in a hospital. You will learn how to take care of yourself after you go home and about the medicines youll need to take to protect your new liver. You will continue to take medicines because hepatitis C may come back after surgery.
Testing for Liver Cancer
Having hepatitis C increases your risk for liver cancer, so your doctor may suggest an ultrasound test of the liver every 6 to 12 months. Finding cancer early makes it more treatable. Ultrasound is a machine that uses sound waves to create a picture of your liver. Ultrasound is performed at a hospital or radiology center by a specially trained technician. The image, called a sonogram, can show the livers size and the presence of cancerous tumors.
|
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What is (are) GM1 gangliosidosis type 1 ?
|
GM1 gangliosidosis is an inherited lysosomal storage disorder that progressively destroys nerve cells (neurons) in the brain and spinal cord. The condition may be classified into three major types based on the general age that signs and symptoms first appear: classic infantile (type 1); juvenile (type 2); and adult onset or chronic (type 3). Although the types differ in severity, their features may overlap significantly. GM1 gangliosidosis is caused by mutations in the GLB1 gene and is inherited in an autosomal recessive manner. Treatment is currently symptomatic and supportive.
|
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What are the genetic changes related to familial dilated cardiomyopathy ?
|
Mutations in more than 30 genes have been found to cause familial dilated cardiomyopathy. These genes provide instructions for making proteins that are found in cardiac muscle cells called cardiomyocytes. Many of these proteins play important roles in the contraction of the cardiac muscle through their association with cell structures called sarcomeres. Sarcomeres are the basic units of muscle contraction; they are made of proteins that generate the mechanical force needed for muscles to contract. Many other proteins associated with familial dilated cardiomyopathy make up the structural framework (the cytoskeleton) of cardiomyocytes. The remaining proteins play various roles within cardiomyocytes to ensure their proper functioning. Mutations in one gene, TTN, account for approximately 20 percent of cases of familial dilated cardiomyopathy. The TTN gene provides instructions for making a protein called titin, which is found in the sarcomeres of many types of muscle cells, including cardiomyocytes. Titin has several functions within sarcomeres. One of its most important jobs is to provide structure, flexibility, and stability to these cell structures. Titin also plays a role in chemical signaling and in assembling new sarcomeres. The TTN gene mutations that cause familial dilated cardiomyopathy result in the production of an abnormally short titin protein. It is unclear how the altered protein causes familial dilated cardiomyopathy, but it is likely that it impairs sarcomere function and disrupts chemical signaling. It is unclear how mutations in the other genes cause familial dilated cardiomyopathy. It is likely that the changes impair cardiomyocyte function and reduce the ability of these cells to contract, weakening and thinning cardiac muscle. People with familial dilated cardiomyopathy often do not have an identified mutation in any of the known associated genes. The cause of the condition in these individuals is unknown. Familial dilated cardiomyopathy is described as nonsyndromic or isolated because it typically affects only the heart. However, dilated cardiomyopathy can also occur as part of syndromes that affect other organs and tissues in the body. These forms of the condition are described as syndromic and are caused by mutations in other genes. Additionally, there are many nongenetic causes of dilated cardiomyopathy, including viral infection and chronic alcohol abuse.
|
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How many people are affected by succinate-CoA ligase deficiency ?
|
Although the exact prevalence of succinate-CoA ligase deficiency is unknown, it appears to be very rare. This condition occurs more frequently among people from the Faroe Islands in the North Atlantic Ocean.
|
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What is (are) autosomal recessive cerebellar ataxia type 1 ?
|
Autosomal recessive cerebellar ataxia type 1 (ARCA1) is a condition characterized by progressive problems with movement due to a loss (atrophy) of nerve cells in the part of the brain that coordinates movement (the cerebellum). Signs and symptoms of the disorder first appear in early to mid-adulthood. People with this condition initially experience impaired speech (dysarthria), problems with coordination and balance (ataxia), or both. They may also have difficulty with movements that involve judging distance or scale (dysmetria). Other features of ARCA1 include abnormal eye movements (nystagmus) and problems following the movements of objects with the eyes. The movement problems are slowly progressive, often resulting in the need for a cane, walker, or wheelchair.
|
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] |
What are the symptoms of Weyers ulnar ray/oligodactyly syndrome ?
|
What are the signs and symptoms of Weyers ulnar ray/oligodactyly syndrome? The Human Phenotype Ontology provides the following list of signs and symptoms for Weyers ulnar ray/oligodactyly 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) Absent thumb - Aplasia/Hypoplasia of the ulna - Autosomal dominant inheritance - Cleft palate - Cleft upper lip - High palate - Hydronephrosis - Hypoplasia of the radius - Hypotelorism - Long face - Mesomelia - Narrow face - Oligodactyly (hands) - Proximal placement of thumb - Proximal radial head dislocation - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What causes Diabetic Neuropathies: The Nerve Damage of Diabetes ?
|
The causes are probably different for different types of diabetic neuropathy. Researchers are studying how prolonged exposure to high blood glucose causes nerve damage. Nerve damage is likely due to a combination of factors:
- metabolic factors, such as high blood glucose, long duration of diabetes, abnormal blood fat levels, and possibly low levels of insulin - neurovascular factors, leading to damage to the blood vessels that carry oxygen and nutrients to nerves - autoimmune factors that cause inflammation in nerves - mechanical injury to nerves, such as carpal tunnel syndrome - inherited traits that increase susceptibility to nerve disease - lifestyle factors, such as smoking or alcohol use
|
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What to do for Smoking and the Digestive System ?
|
Eating, diet, and nutrition can play a role in causing, preventing, and treating some of the diseases and disorders of the digestive system that are affected by smoking, including heartburn and GERD, liver diseases, Crohns disease, colon polyps, pancreatitis, and gallstones. More information about eating, diet, and nutrition and these conditions can be found on the Digestive Diseases A-Z list.
|
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What are the treatments for Swyer-James syndrome ?
|
How might Swyer-James syndrome be treated? Individuals with Swyer-James syndrome reportedly have been treated conservatively in the past. However, although there are few reports published, it has been recognized that surgical treatment should be considered when infections cannot be controlled. There have been reports of affected individuals being treated with pneumonectomy (removal of a lung), lobectomy (removal of one or more lobes of a lung) or segmentectomy (removal of a specific segment). It has been proposed that individuals with Swyer-James syndrome may benefit from lung volume reduction surgery (LVRS), a procedure in which damaged tissue is removed from the lung. LVRS was reportedly performed successfully in an individual with Swyer-James syndrome, and it has been suggested that the procedure could be used for managing the condition in other affected individuals because it has shown to be effective for improving pulmonary function and symptoms.
|
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What is (are) Myhre syndrome ?
|
Myhre syndrome is a rare inherited disorder characterized by intellectual disability, short stature, unusual facial features, and various bone (skeletal) abnormalities. Other findings may include hearing impairment, abnormal enlargement of the muscles (muscle hypertrophy), and/or joint stiffness. Myhre syndrome is caused by mutations in the SMAD4 gene. This condition is inherited in an autosomal dominant pattern. Most cases are due to a new mutation.
|
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How many people are affected by Mowat-Wilson syndrome ?
|
The prevalence of Mowat-Wilson syndrome is unknown. More than 200 people with this condition have been reported in the medical literature.
|
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What is the outlook for Encephaloceles ?
|
The prognosis for individuals with encephaloceles varies depending on the type of brain tissue involved, the location of the sacs, and the accompanying brain malformations.
|
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What are the symptoms of Hemophilia B ?
|
What are the signs and symptoms of Hemophilia B? The Human Phenotype Ontology provides the following list of signs and symptoms for Hemophilia B. 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 bleeding - Degenerative joint disease - Gastrointestinal hemorrhage - Joint hemorrhage - Persistent bleeding after trauma - Prolonged partial thromboplastin time - Prolonged whole-blood clotting time - Reduced factor IX activity - X-linked recessive inheritance - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Osteogenesis imperfecta type VII ?
|
What are the signs and symptoms of Osteogenesis imperfecta type VII? The Human Phenotype Ontology provides the following list of signs and symptoms for Osteogenesis imperfecta type VII. 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) Absent pulmonary artery - Autosomal recessive inheritance - Blue sclerae - Bowing of the legs - Breech presentation - Coxa vara - Crumpled long bones - Death in infancy - Decreased calvarial ossification - Delayed cranial suture closure - Externally rotated/abducted legs - Hydronephrosis - Hypoplastic pulmonary veins - Long philtrum - Micromelia - Multiple prenatal fractures - Multiple rib fractures - Narrow chest - Osteopenia - Pectus excavatum - Proptosis - Protrusio acetabuli - Recurrent fractures - Rhizomelia - Round face - Scoliosis - Vertebral compression fractures - Wide anterior fontanel - Wide cranial sutures - Wormian bones - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
How to diagnose Orofaciodigital syndrome 1 ?
|
Is genetic testing available for orofaciodigital syndrome 1 (OFD1)? Genetic testing for orofaciodigital syndrome 1 is clinically available. OFD1 is the only gene currently known to be associated with this condition. Testing is often used to confirm or establish the diagnosis in an individual when OFD1 is suspected. A change (mutation) in the OFD1 gene is detected in up to 85% of individuals who have OFD1. You can find laboratories offering clinical genetic testing for OFD1 on a website called GeneTests. To see a listing of clinical testing laboratories click here. GeneTests does not currently list laboratories doing research testing for OFD1.
|
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What are the genetic changes related to spastic paraplegia type 7 ?
|
Mutations in the SPG7 gene cause spastic paraplegia type 7. The SPG7 gene provides instructions for producing a protein called paraplegin. Located within the inner membrane of the energy-producing centers of cells (mitochondria), paraplegin is one of the proteins that form a complex called the m-AAA protease. The m-AAA protease is responsible for assembling ribosomes (cellular structures that process the cell's genetic instructions to create proteins) and removing nonfunctional proteins in the mitochondria. When there is a mutation in paraplegin, the m-AAA protease cannot function correctly. Nonfunctional m-AAA proteases cause a build up of unusable proteins in the mitochondria of nerve cells, which can result in swelling of the cell, reduced cell signaling, and impaired cell movement, leading to the major signs and symptoms of spastic paraplegia type 7.
|
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What are the treatments for Chapare Hemorrhagic Fever (CHHF) ?
|
Supportive therapy is important in CHHF. This includes:
- maintenance of hydration
- management of shock
- sedation
- pain relief
- usual precautions for patients with bleeding disorders
- transfusions (when necessary)
Use of convalescent plasma therapy for treatment of AHF reduces mortality significantly and anecdotal evidence shows that the antiviral drug ribavirin may also hold promise for treating AHF. Ribavirin has also been considered for preventing development of disease in people exposed to other arenaviruses.
Recovery
The precise mortality of CHHF is unknown and the only described case was fatal.
Patients who have suffered from other arenaviruses may continue to excrete virus in urine or semen for weeks after recovery. For this reason, these fluids should be monitored for infectivity, since convalescent patients have the potential to infect others (particularly sexual partners) via these fluids.
|
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] |
What are the symptoms of Crigler Najjar syndrome, type 2 ?
|
What are the signs and symptoms of Crigler Najjar syndrome, type 2? The Human Phenotype Ontology provides the following list of signs and symptoms for Crigler Najjar syndrome, type 2. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Abnormality of the liver 90% Autosomal recessive inheritance - Jaundice - Unconjugated hyperbilirubinemia - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What is (are) Klippel-Feil syndrome ?
|
Klippel-Feil syndrome is a bone disorder characterized by the abnormal joining (fusion) of two or more spinal bones in the neck (cervical vertebrae). The vertebral fusion is present from birth. Three major features result from this vertebral fusion: a short neck, the resulting appearance of a low hairline at the back of the head, and a limited range of motion in the neck. Most affected people have one or two of these characteristic features. Less than half of all individuals with Klippel-Feil syndrome have all three classic features of this condition. In people with Klippel-Feil syndrome, the fused vertebrae can limit the range of movement of the neck and back as well as lead to chronic headaches and muscle pain in the neck and back that range in severity. People with minimal bone involvement often have fewer problems compared to individuals with several vertebrae affected. The shortened neck can cause a slight difference in the size and shape of the right and left sides of the face (facial asymmetry). Trauma to the spine, such as a fall or car accident, can aggravate problems in the fused area. Fusion of the vertebrae can lead to nerve damage in the head, neck, or back. Over time, individuals with Klippel-Feil syndrome can develop a narrowing of the spinal canal (spinal stenosis) in the neck, which can compress and damage the spinal cord. Rarely, spinal nerve abnormalities may cause abnormal sensations or involuntary movements in people with Klippel-Feil syndrome. Affected individuals may develop a painful joint disorder called osteoarthritis around the areas of fused bone or experience painful involuntary tensing of the neck muscles (cervical dystonia). In addition to the fused cervical bones, people with this condition may have abnormalities in other vertebrae. Many people with Klippel-Feil syndrome have abnormal side-to-side curvature of the spine (scoliosis) due to malformation of the vertebrae; fusion of additional vertebrae below the neck may also occur. People with Klippel-Feil syndrome may have a wide variety of other features in addition to their spine abnormalities. Some people with this condition have hearing difficulties, eye abnormalities, an opening in the roof of the mouth (cleft palate), genitourinary problems such as abnormal kidneys or reproductive organs, heart abnormalities, or lung defects that can cause breathing problems. Affected individuals may have other skeletal defects including arms or legs of unequal length (limb length discrepancy), which can result in misalignment of the hips or knees. Additionally, the shoulder blades may be underdeveloped so that they sit abnormally high on the back, a condition called Sprengel deformity. Rarely, structural brain abnormalities or a type of birth defect that occurs during the development of the brain and spinal cord (neural tube defect) can occur in people with Klippel-Feil syndrome. In some cases, Klippel-Feil syndrome occurs as a feature of another disorder or syndrome, such as Wildervanck syndrome or hemifacial microsomia. In these instances, affected individuals have the signs and symptoms of both Klippel-Feil syndrome and the additional disorder.
|
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What are the symptoms of Cone-rod dystrophy 6 ?
|
What are the signs and symptoms of Cone-rod dystrophy 6? The Human Phenotype Ontology provides the following list of signs and symptoms for Cone-rod dystrophy 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) Autosomal dominant inheritance - Childhood onset - Cone/cone-rod dystrophy - Peripheral visual field loss - Reduced visual acuity - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the symptoms of Milroy disease ?
|
What are the signs and symptoms of Milroy disease? The most common symptom of Milroy disease is build-up of fluids (lymphedema) in the lower limbs, which is usually present from birth or before birth. However, the degree and distribution of swelling varies among affected people. It sometimes progresses, but may improve in some cases. Other signs and symptoms may include hydrocele and/or urethral abnormalities in males; prominent veins; upslanting toenails; papillomatosis (development of wart-like growths); and cellulitis. Cellulitis may cause additional swelling. The Human Phenotype Ontology provides the following list of signs and symptoms for Milroy disease. 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 amniotic fluid - Abnormality of the nail - Autosomal dominant inheritance - Congenital onset - Hemangioma - Hydrocele testis - Hyperkeratosis over edematous areas - Hypoplasia of lymphatic vessels - Nonimmune hydrops fetalis - Predominantly lower limb lymphedema - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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] |
What is (are) High Blood Pressure ?
|
High blood pressure is a common disease in which blood flows through blood vessels (arteries) at higher than normal pressures. What Is Blood Pressure? Blood pressure is the force of blood pushing against the walls of the blood vessels as the heart pumps blood. If your blood pressure rises and stays high over time, its called high blood pressure. High blood pressure is dangerous because it makes the heart work too hard, and the high force of the blood flow can harm arteries and organs such as the heart, kidneys, brain, and eyes. Types of High Blood Pressure There are two main types of high blood pressure: primary and secondary high blood pressure. - Primary, or essential, high blood pressure is the most common type of high blood pressure. This type of high blood pressure tends to develop over years as a person ages. - Secondary high blood pressure is caused by another medical condition or use of certain medicines. This type usually resolves after the cause is treated or removed. Primary, or essential, high blood pressure is the most common type of high blood pressure. This type of high blood pressure tends to develop over years as a person ages. Secondary high blood pressure is caused by another medical condition or use of certain medicines. This type usually resolves after the cause is treated or removed. Measuring Blood Pressure Blood pressure is always given as two numbers, the systolic and diastolic pressures. Both are important. - Systolic Pressure is the pressure of blood against the artery walls when the heart beats. - Diastolic Pressure is the pressure of blood against the artery walls when the heart is at rest between beats. Systolic Pressure is the pressure of blood against the artery walls when the heart beats. Diastolic Pressure is the pressure of blood against the artery walls when the heart is at rest between beats. Usually these numbers are written one above or before the other -- for example, 120/80 mmHg. The top, or first, number is the systolic and the bottom, or second number, is the diastolic. If your blood pressure is 120/80, you say that it is "120 over 80." Normal Blood Pressure Normal blood pressure for adults is defined as a systolic pressure below 120 mmHg and a diastolic pressure below 80 mmHg. It is normal for blood pressures to change when you sleep, wake up, or are excited or nervous. When you are active, it is normal for your blood pressure to increase. However, once the activity stops, your blood pressure returns to your normal baseline range. Blood pressure normally rises with age and body size. Newborn babies often have very low blood pressure numbers that are considered normal for babies, while older teens have numbers similar to adults. Abnormal Blood Pressure Abnormal blood pressure is higher than 120/80 mmHg. If either your systolic or diastolic blood pressure is higher than normal (120/80) but not high enough to be considered high blood pressure (140/90), you have pre-hypertension. Pre-hypertension is a top number between 120 and 139 or a bottom number between 80 and 89 mmHg. For example, blood pressure readings of 138/82, 128/70, or 115/86 are all in the "pre-hypertension" range. (Click the table on the right to see the stages of high blood pressure in adults.) A systolic blood pressure of 140 mmHg or higher, or a diastolic blood pressure of 90 mmHg or higher, is considered high blood pressure, or hypertension. Hypertension is the medical term for high blood pressure. If you have diabetes or chronic kidney disease, your recommended blood pressure levels are a systolic blood pressure of 130 mmHg or lower, and a diastolic blood pressure of 80 mmHg or lower. Usually Has No Symptoms High blood pressure is often called "the silent killer" because it usually has no symptoms. Occasionally, headaches may occur. Some people may not find out they have high blood pressure until they have trouble with their heart, kidneys, or eyes. When high blood pressure is not diagnosed and treated, it can lead to other life-threatening conditions, including heart attack, heart failure, stroke, and kidney failure. It can also lead to vision changes or blindness. Possible Complications Over Time Over time, high blood pressure can cause - your heart to work too hard and become larger or weaker, which can lead to heart failure. - small bulges (aneurysms) to worsen in your blood vessels. Common locations for aneurysms are the aorta, which is the main artery from the heart; the arteries in your brain, legs, and intestines; and the artery leading to your spleen. - blood vessels in your kidneys to narrow, which can cause kidney failure. - blood vessels in your eyes to burst or bleed, which can cause vision changes and can result in blindness. - arteries throughout your body to "harden" faster, especially those in your heart, brain, kidneys, and legs. This can cause a heart attack, stroke, or kidney failure. your heart to work too hard and become larger or weaker, which can lead to heart failure. small bulges (aneurysms) to worsen in your blood vessels. Common locations for aneurysms are the aorta, which is the main artery from the heart; the arteries in your brain, legs, and intestines; and the artery leading to your spleen. blood vessels in your kidneys to narrow, which can cause kidney failure. blood vessels in your eyes to burst or bleed, which can cause vision changes and can result in blindness. arteries throughout your body to "harden" faster, especially those in your heart, brain, kidneys, and legs. This can cause a heart attack, stroke, or kidney failure.
|
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] |
How to diagnose Greig cephalopolysyndactyly syndrome ?
|
Is genetic testing available for Greig cephalopolysyndactyly syndrome? Yes. GLI3 is the only gene known to be associated with Greig cephalopolysyndactyly syndrome (GCPS). Genetic testing is available to analyze the GLI3 gene for mutations. Mutations involving GLI3 can be identified in greater than 75% of people with GCPS. How is Greig cephalopolysyndactyly syndrome diagnosed? Greig cephalopolysyndactyly syndrome (GCPS) is diagnosed based on clinical findings and family history. Major findings of GCPS include: an abnormally large head size (macrocephaly) greater than the 97th percentile widely spaced eyes (ocular hypertelorism) limb anomalies including extra fingers or toes (polydactyly) fused skin between the fingers and toes (cutaneous syndactyly) A diagnosis is established in a first degree relative of a known affected individual if that person has polydactyly with or without syndactyly or craniofacial features (macrocephaly, widely spaced eyes). A diagnosis is additionally established in a person who has features of GCPS and a mutation in the GLI3 gene.
|
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] |
How to diagnose Cowden syndrome ?
|
How is Cowden syndrome diagnosed? A diagnosis of Cowden syndrome is based on the presence of characteristic signs and symptoms. Genetic testing for a change (mutation) in the PTEN gene can then be ordered to confirm the diagnosis. If a mutation in PTEN is not identified, genetic testing for the other genes known to cause Cowden syndrome can be considered. GeneReviews offers more detailed information regarding the diagnosis of Cowden syndrome including the clinical diagnostic criteria. Click here to view this resource. The PTEN Cleveland Clinic Risk Calculator can be used to estimate the chance of finding a PTEN mutation in children and adults with signs and symptoms of Cowden syndrome. Is genetic testing available for Cowden syndrome? Yes, genetic testing is available for many of the genes known to cause Cowden syndrome. Carrier testing for at-risk relatives and prenatal testing are possible if the disease-causing mutation in the family is known. The Genetic Testing Registry (GTR) is a centralized online resource for information about genetic tests. The intended audience for the GTR is health care providers and researchers. Patients and consumers with specific questions about a genetic test should contact a health care provider or a genetics professional.
|
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] |
What is (are) Myelofibrosis ?
|
Myelofibrosis is a disorder of the bone marrow, in which the marrow is replaced by fibrous (scar) tissue. Scarring of the bone marrow causes anemia, which can lead to fatigue and weakness, as well as pooling of the blood in abnormal sites like the liver and spleen, causing these organs to swell. Although myelofibrosis can occur at any age, it typically develops after the age of 50. In most cases, myelofibrosis gets progressively worse. Treatment is aimed at relieving signs and symptoms and may include medications, blood transfusions, chemotherapy, radiation therapy and surgery.
|
[
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What are the symptoms of Diabetes ?
|
Diabetes is often called a "silent" disease because it can cause serious complications even before you have symptoms. Symptoms can also be so mild that you dont notice them. An estimated 8 million people in the United States have type 2 diabetes and dont know it, according to 2012 estimates by the Centers for Disease Control and Prevention (CDC). Common Signs Some common symptoms of diabetes are: - being very thirsty - frequent urination - feeling very hungry or tired - losing weight without trying - having sores that heal slowly - having dry, itchy skin - loss of feeling or tingling in the feet - having blurry eyesight. being very thirsty frequent urination feeling very hungry or tired losing weight without trying having sores that heal slowly having dry, itchy skin loss of feeling or tingling in the feet having blurry eyesight. Signs of type 1 diabetes usually develop over a short period of time. The signs for type 2 diabetes develop more gradually. Tests for Diabetes The following tests are used to diagnose diabetes or prediabetes. - An A1C test measures your average blood glucose levels over the past 3 months. It can be used to diagnose type 2 diabetes and prediabetes. It does not require fasting and blood can be drawn for the test any time of the day. An A1C test measures your average blood glucose levels over the past 3 months. It can be used to diagnose type 2 diabetes and prediabetes. It does not require fasting and blood can be drawn for the test any time of the day. - A fasting plasma glucose, or FPG test, measures your blood glucose after you have gone at least 8 hours without eating. Doctors use this test to detect diabetes or prediabetes. A fasting plasma glucose, or FPG test, measures your blood glucose after you have gone at least 8 hours without eating. Doctors use this test to detect diabetes or prediabetes. - In a random plasma glucose test, your doctor checks your blood glucose without regard to when you ate your last meal. This test, along with an assessment of symptoms, is used to diagnose diabetes but not prediabetes. In a random plasma glucose test, your doctor checks your blood glucose without regard to when you ate your last meal. This test, along with an assessment of symptoms, is used to diagnose diabetes but not prediabetes. - An oral glucose tolerance test, or OGTT, measures your blood glucose after you have gone at least 8 hours without eating and 2 hours after you drink a sweet beverage. Doctors also use the oral glucose tolerance test to diagnose gestational diabetes in pregnant women. An oral glucose tolerance test, or OGTT, measures your blood glucose after you have gone at least 8 hours without eating and 2 hours after you drink a sweet beverage. Doctors also use the oral glucose tolerance test to diagnose gestational diabetes in pregnant women. If any of these tests show that you might have diabetes, your doctor will need to repeat the test with a second measurement unless there are clear symptoms of diabetes. Get more details about tests for diabetes. Who Should Get Tested? Because type 2 diabetes is more common in older people, anyone who is 45 or older should consider getting tested. If you are 45 or older and overweight, getting tested is strongly recommended. If you are younger than 45, overweight, and have one or more risk factors, you also should talk with your doctor about being tested. See risk factors for type 2 diabetes. Why Early Detection is Important Diabetes is a serious disease that can lead to a number of health problems such as heart disease, stroke, vision problems, kidney disease and even death. Sometimes people have symptoms but do not suspect diabetes. They delay scheduling a checkup because they do not feel sick. Many people do not find out they have the disease until they have diabetes complications, such as a heart attack or stroke. Finding out early if you have diabetes is important because treatment can prevent or delay the complications of the disease.
|
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15
] |
Who is at risk for Stroke? ?
|
Stroke occurs in all age groups, in both sexes, and in all races in every country. It can even occur before birth, when the fetus is still in the womb. Studies show the risk of stroke doubles for each decade between the ages of 55 and 85. However, a recent study found that stroke rates are on the rise for people under 55.
|
[
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] |
[
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1
] |
[
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253,
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323,
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762,
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15
] |
What are the genetic changes related to alpha thalassemia ?
|
Alpha thalassemia typically results from deletions involving the HBA1 and HBA2 genes. Both of these genes provide instructions for making a protein called alpha-globin, which is a component (subunit) of hemoglobin. People have two copies of the HBA1 gene and two copies of the HBA2 gene in each cell. Each copy is called an allele. For each gene, one allele is inherited from a person's father, and the other is inherited from a person's mother. As a result, there are four alleles that produce alpha-globin. The different types of alpha thalassemia result from the loss of some or all of these alleles. Hb Bart syndrome, the most severe form of alpha thalassemia, results from the loss of all four alpha-globin alleles. HbH disease is caused by a loss of three of the four alpha-globin alleles. In these two conditions, a shortage of alpha-globin prevents cells from making normal hemoglobin. Instead, cells produce abnormal forms of hemoglobin called hemoglobin Bart (Hb Bart) or hemoglobin H (HbH). These abnormal hemoglobin molecules cannot effectively carry oxygen to the body's tissues. The substitution of Hb Bart or HbH for normal hemoglobin causes anemia and the other serious health problems associated with alpha thalassemia. Two additional variants of alpha thalassemia are related to a reduced amount of alpha-globin. Because cells still produce some normal hemoglobin, these variants tend to cause few or no health problems. A loss of two of the four alpha-globin alleles results in alpha thalassemia trait. People with alpha thalassemia trait may have unusually small, pale red blood cells and mild anemia. A loss of one alpha-globin allele is found in alpha thalassemia silent carriers. These individuals typically have no thalassemia-related signs or symptoms.
|
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How many people are affected by Behet disease ?
|
Behet disease is most common in Mediterranean countries, the Middle East, Japan, and other parts of Asia. However, it has been found in populations worldwide. The highest prevalence of Behet disease has been reported in Turkey, where the disorder affects up to 420 in 100,000 people. The disorder is much less common in northern European countries and the United States, where it generally affects fewer than 1 in 100,000 people.
|
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What are the symptoms of Dwarfism, low-birth-weight type with unresponsiveness to growth hormone ?
|
What are the signs and symptoms of Dwarfism, low-birth-weight type with unresponsiveness to growth hormone? The Human Phenotype Ontology provides the following list of signs and symptoms for Dwarfism, low-birth-weight type with unresponsiveness to growth hormone. 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) Hearing impairment - Hypoglycemia - Intellectual disability - Intrauterine growth retardation - Severe short stature - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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What are the treatments for 22q11.2 duplication ?
|
These resources address the diagnosis or management of 22q11.2 duplication: - Gene Review: Gene Review: 22q11.2 Duplication - Genetic Testing Registry: 22q11.2 duplication syndrome These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What is (are) Hearing Problems in Children ?
|
Most children hear and listen from the moment they are born. They learn to talk by imitating the sounds around them and the voices of their parents and caregivers. But about 2 or 3 out of every 1,000 children in the United States are born deaf or hard-of-hearing. More lose their hearing later during childhood. Babies should have a hearing screening before they are a month old. If your child has a hearing loss, it is important to consider the use of hearing devices and other communication options by age 6 months. That's because children start learning speech and language long before they talk. Hearing problems can be temporary or permanent. Sometimes, ear infections, injuries or diseases affect hearing. If your child does not hear well, get help. NIH: National Institute on Deafness and Other Communication Disorders
|
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] |
What is (are) aromatic l-amino acid decarboxylase deficiency ?
|
Aromatic l-amino acid decarboxylase (AADC) deficiency is an inherited disorder that affects the way signals are passed between certain cells in the nervous system. Signs and symptoms of AADC deficiency generally appear in the first year of life. Affected infants may have severe developmental delay, weak muscle tone (hypotonia), muscle stiffness, difficulty moving, and involuntary writhing movements of the limbs (athetosis). They may be lacking in energy (lethargic), feed poorly, startle easily, and have sleep disturbances. People with AADC deficiency may also experience episodes called oculogyric crises that involve abnormal rotation of the eyeballs; extreme irritability and agitation; and pain, muscle spasms, and uncontrolled movements, especially of the head and neck. AADC deficiency may affect the autonomic nervous system, which controls involuntary body processes such as the regulation of blood pressure and body temperature. Resulting signs and symptoms can include droopy eyelids (ptosis), constriction of the pupils of the eyes (miosis), inappropriate or impaired sweating, nasal congestion, drooling, reduced ability to control body temperature, low blood pressure (hypotension), backflow of acidic stomach contents into the esophagus (gastroesophageal reflux), low blood sugar (hypoglycemia), fainting (syncope), and cardiac arrest. Signs and symptoms of AADC deficiency tend to worsen late in the day or when the individual is tired, and improve after sleep.
|
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What are the genetic changes related to galactosialidosis ?
|
Mutations in the CTSA gene cause all forms of galactosialidosis. The CTSA gene provides instructions for making a protein called cathepsin A, which is active in cellular compartments called lysosomes. These compartments contain enzymes that digest and recycle materials when they are no longer needed. Cathepsin A works together with two enzymes, neuraminidase 1 and beta-galactosidase, to form a protein complex. This complex breaks down sugar molecules (oligosaccharides) attached to certain proteins (glycoproteins) or fats (glycolipids). Cathepsin A is also found on the cell surface, where it forms a complex with neuraminidase 1 and a protein called elastin binding protein. Elastin binding protein plays a role in the formation of elastic fibers, a component of the connective tissues that form the body's supportive framework. CTSA mutations interfere with the normal function of cathepsin A. Most mutations disrupt the protein structure of cathepsin A, impairing its ability to form complexes with neuraminidase 1, beta-galactosidase, and elastin binding protein. As a result, these other enzymes are not functional, or they break down prematurely. Galactosialidosis belongs to a large family of lysosomal storage disorders, each caused by the deficiency of a specific lysosomal enzyme or protein. In galactosialidosis, impaired functioning of cathepsin A and other enzymes causes certain substances to accumulate in the lysosomes.
|
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What is (are) familial thoracic aortic aneurysm and dissection ?
|
Familial thoracic aortic aneurysm and dissection (familial TAAD) involves problems with the aorta, which is the large blood vessel that distributes blood from the heart to the rest of the body. Familial TAAD affects the upper part of the aorta, near the heart. This part of the aorta is called the thoracic aorta because it is located in the chest (thorax). Other vessels that carry blood from the heart to the rest of the body (arteries) can also be affected. In familial TAAD, the aorta can become weakened and stretched (aortic dilatation), which can lead to a bulge in the blood vessel wall (an aneurysm). Aortic dilatation may also lead to a sudden tearing of the layers in the aorta wall (aortic dissection), allowing blood to flow abnormally between the layers. These aortic abnormalities are potentially life-threatening because they can decrease blood flow to other parts of the body such as the brain or other vital organs, or cause the aorta to break open (rupture). The occurrence and timing of these aortic abnormalities vary, even within the same affected family. They can begin in childhood or not occur until late in life. Aortic dilatation is generally the first feature of familial TAAD to develop, although in some affected individuals dissection occurs with little or no aortic dilatation. Aortic aneurysms usually have no symptoms. However, depending on the size, growth rate, and location of these abnormalities, they can cause pain in the jaw, neck, chest, or back; swelling in the arms, neck, or head; difficult or painful swallowing; hoarseness; shortness of breath; wheezing; a chronic cough; or coughing up blood. Aortic dissections usually cause severe, sudden chest or back pain, and may also result in unusually pale skin (pallor), a very faint pulse, numbness or tingling (paresthesias) in one or more limbs, or paralysis. Familial TAAD may not be associated with other signs and symptoms. However, some individuals in affected families show mild features of related conditions called Marfan syndrome or Loeys-Dietz syndrome. These features include tall stature, stretch marks on the skin, an unusually large range of joint movement (joint hypermobility), and either a sunken or protruding chest. Occasionally, people with familial TAAD develop aneurysms in the brain or in the section of the aorta located in the abdomen (abdominal aorta). Some people with familial TAAD have heart abnormalities that are present from birth (congenital). Affected individuals may also have a soft out-pouching in the lower abdomen (inguinal hernia), an abnormal curvature of the spine (scoliosis), or a purplish skin discoloration (livedo reticularis) caused by abnormalities in the tiny blood vessels of the skin (dermal capillaries). However, these conditions are also common in the general population. Depending on the genetic cause of familial TAAD in particular families, they may have an increased risk of developing blockages in smaller arteries, which can lead to heart attack and stroke.
|
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Is Glioblastoma inherited ?
|
Is glioblastoma inherited? Most glioblastomas are not inherited. They usually occur sporadically in people with no family history of tumors. However, they can rarely occur in people with certain genetic syndromes such as neurofibromatosis type 1, Turcot syndrome and Li Fraumeni syndrome. All of these conditions are inherited in an autosomal dominant manner.
|
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] |
How many people are affected by achondrogenesis ?
|
Achondrogenesis types 1A and 1B are rare genetic disorders; their incidence is unknown. Combined, achondrogenesis type 2 and hypochondrogenesis (a similar skeletal disorder) occur in 1 in 40,000 to 60,000 newborns.
|
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What is (are) HTLV-1 associated myelopathy/tropical spastic paraparesis ?
|
HTLV-1 associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic, progressive disease of the nervous system that affects less than 2 percent of people with HTLV-1 infection. Signs and symptoms vary but may include progressive weakness, stiff muscles, muscle spasms, backache, a 'weak' bladder, and constipation. The HTLV-1 virus can be transmitted from mother to child via breastfeeding or childbirth, from person to person through sexual contact and through blood contact, either by transfusion or by reuse of injection equipment. HTLV infection is not passed from person to person by coughing, sneezing, kissing, cuddling or daily social contact. Screening of donated blood for HTLV-1 has been done in the United States since 1988.
|
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What are the genetic changes related to Bjrnstad syndrome ?
|
Bjrnstad syndrome is caused by mutations in the BCS1L gene. The protein produced from this gene is found in cell structures called mitochondria, which convert the energy from food into a form that cells can use. In mitochondria, the BCS1L protein plays a role in oxidative phosphorylation, which is a multistep process through which cells derive much of their energy. The BCS1L protein is critical for the formation of a group of proteins known as complex III, which is one of several protein complexes involved in this process. As a byproduct of its action in oxidative phosphorylation, complex III produces reactive oxygen species, which are harmful molecules that can damage DNA and tissues. BCS1L gene mutations involved in Bjrnstad syndrome alter the BCS1L protein and impair its ability to aid in complex III formation. The resulting decrease in complex III activity reduces oxidative phosphorylation. For unknown reasons, overall production of reactive oxygen species is increased, although production by complex III is reduced. Researchers believe that tissues in the inner ears and hair follicles are particularly sensitive to reactive oxygen species and are damaged by the abnormal amount of these molecules, leading to the characteristic features of Bjrnstad syndrome.
|
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What is (are) Chromosome 16p13.3 deletion syndrome ?
|
Chromosome 16p13.3 deletion syndrome is a chromosome abnormality that can affect many parts of the body. People with this condition are missing a small piece (deletion) of chromosome 16 at a location designated p13.3. Although once thought to be a severe form of Rubinstein-Taybi syndrome, it is now emerging as a unique syndrome. Signs and symptoms may include failure to thrive, hypotonia (reduced muscle tone), short stature, microcephaly (unusually small head), characteristic facial features, mild to moderate intellectual disability, serious organ anomalies (i.e. heart and/or kidney problems), and vulnerability to infections. Chromosome testing of both parents can provide more information on whether or not the deletion was inherited. In most cases, parents do not have any chromosomal anomaly. However, sometimes one parent has a balanced translocation where a piece of a chromosome has broken off and attached to another one with no gain or loss of genetic material. The balanced translocation normally does not cause any signs or symptoms, but it increases the risk for having an affected child with a chromosomal anomaly like a deletion. Treatment is based on the signs and symptoms present in each person. To learn more about chromosomal anomalies in general, please visit our GARD webpage on Chromosome Disorders.
|
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What causes Urinary Tract Infections in Children ?
|
Most UTIs are caused by bacteria that live in the bowel. The bacterium Escherichia coli (E. coli) causes the vast majority of UTIs. The urinary tract has several systems to prevent infection. The points where the ureters attach to the bladder act like one-way valves to prevent urine from backing up, or refluxing, toward the kidneys, and urination washes microbes out of the body. Immune defenses also prevent infection. But despite these safeguards, infections still occur. Certain bacteria have a strong ability to attach themselves to the lining of the urinary tract.
Children who often delay urination are more likely to develop UTIs. Regular urination helps keep the urinary tract sterile by flushing away bacteria. Holding in urine allows bacteria to grow. Producing too little urine because of inadequate fluid intake can also increase the risk of developing a UTI. Chronic constipationa condition in which a child has fewer than two bowel movements a weekcan add to the risk of developing a UTI. When the bowel is full of hard stool, it presses against the bladder and bladder neck, blocking the flow of urine and allowing bacteria to grow.
Some children develop UTIs because they are prone to such infections, just as other children are prone to getting coughs, colds, or ear infections.
|
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Is frontometaphyseal dysplasia inherited ?
|
This condition is inherited in an X-linked dominant pattern. The gene associated with this condition is located on the X chromosome, which is one of the two sex chromosomes. In females (who have two X chromosomes), a mutation in one of the two copies of the gene in each cell is sufficient to cause the disorder. In males (who have only one X chromosome), a mutation in the only copy of the gene in each cell causes the disorder. In most cases, males experience more severe symptoms of the disorder than females. A characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
|
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What is (are) Diamond-Blackfan anemia ?
|
Diamond-Blackfan anemia is a disorder of the bone marrow. The major function of bone marrow is to produce new blood cells. In Diamond-Blackfan anemia, the bone marrow malfunctions and fails to make enough red blood cells, which carry oxygen to the body's tissues. The resulting shortage of red blood cells (anemia) usually becomes apparent during the first year of life. Symptoms of anemia include fatigue, weakness, and an abnormally pale appearance (pallor). People with Diamond-Blackfan anemia have an increased risk of several serious complications related to their malfunctioning bone marrow. Specifically, they have a higher-than-average chance of developing myelodysplastic syndrome (MDS), which is a disorder in which immature blood cells fail to develop normally. Affected individuals also have an increased risk of developing certain cancers, including a cancer of blood-forming tissue known as acute myeloid leukemia (AML) and a type of bone cancer called osteosarcoma. Approximately half of individuals with Diamond-Blackfan anemia have physical abnormalities. They may have an unusually small head size (microcephaly) and a low frontal hairline, along with distinctive facial features such as wide-set eyes (hypertelorism); droopy eyelids (ptosis); a broad, flat bridge of the nose; small, low-set ears; and a small lower jaw (micrognathia). Affected individuals may also have an opening in the roof of the mouth (cleft palate) with or without a split in the upper lip (cleft lip). They may have a short, webbed neck; shoulder blades which are smaller and higher than usual; and abnormalities of their hands, most commonly malformed or absent thumbs. About one-third of affected individuals have slow growth leading to short stature. Other features of Diamond-Blackfan anemia may include eye problems such as clouding of the lens of the eyes (cataracts), increased pressure in the eyes (glaucoma), or eyes that do not look in the same direction (strabismus). Affected individuals may also have kidney abnormalities; structural defects of the heart; and, in males, the opening of the urethra on the underside of the penis (hypospadias). The severity of Diamond-Blackfan anemia may vary, even within the same family. Increasingly, individuals with "non-classical" Diamond-Blackfan anemia have been identified. This form of the disorder typically has less severe symptoms that may include mild anemia beginning in adulthood.
|
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Who is at risk for Antiphospholipid Antibody Syndrome? ?
|
Antiphospholipid antibody syndrome (APS) can affect people of any age. The disorder is more common in women than men, but it affects both sexes.
APS also is more common in people who have other autoimmune or rheumatic disorders, such as lupus. ("Rheumatic" refers to disorders that affect the joints, bones, or muscles.)
About 10 percent of all people who have lupus also have APS. About half of all people who have APS also have another autoimmune or rheumatic disorder.
Some people have APS antibodies, but don't ever have signs or symptoms of the disorder. The mere presence of APS antibodies doesn't mean that you have APS. To be diagnosed with APS, you must have APS antibodies and a history of health problems related to the disorder.
However, people who have APS antibodies but no signs or symptoms are at risk of developing APS. Health problems, other than autoimmune disorders, that can trigger blood clots include:
Smoking
Prolonged bed rest
Pregnancy and the postpartum period
Birth control pills and hormone therapy
Cancer and kidney disease
|
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How to prevent Diarrhea ?
|
Two types of diarrhea can be preventedrotavirus diarrhea and travelers diarrhea.
Rotavirus Diarrhea
Two oral vaccines have been approved by the U.S. Food and Drug Administration to protect children from rotavirus infections: rotavirus vaccine, live, oral, pentavalent (RotaTeq); and rotavirus vaccine, live, oral (Rotarix). RotaTeq is given to infants in three doses at 2, 4, and 6 months of age. Rotarix is given in two doses. The first dose is given when infants are 6 weeks old, and the second is given at least 4 weeks later but before infants are 24 weeks old.
Parents of infants should discuss rotavirus vaccination with a health care provider. For more information, parents can visit the Centers for Disease Control and Prevention rotavirus vaccination webpage at www.cdc.gov/vaccines/vpd-vac/rotavirus.
Travelers Diarrhea
To prevent travelers diarrhea, people traveling from the United States to developing countries should avoid
- drinking tap water, using tap water to brush their teeth, or using ice made from tap water - drinking unpasteurized milk or milk products - eating raw fruits and vegetables, including lettuce and fruit salads, unless they peel the fruits or vegetables themselves - eating raw or rare meat and fish - eating meat or shellfish that is not hot when served - eating food from street vendors
Travelers can drink bottled water, soft drinks, and hot drinks such as coffee or tea.
People concerned about travelers diarrhea should talk with a health care provider before traveling. The health care provider may recommend that travelers bring medicine with them in case they develop diarrhea during their trip. Health care providers may advise some peopleespecially people with weakened immune systemsto take antibiotics before and during a trip to help prevent travelers diarrhea. Early treatment with antibiotics can shorten a bout of travelers diarrhea.
|
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] |
What are the treatments for Diabetes ?
|
People with type 1 diabetes control their blood sugar with insulin -- either with shots or an insulin pen. Many people with type 2 diabetes can control blood glucose levels with diet and exercise alone. Others require oral medications or insulin, and some people may need to take both, along with lifestyle modification. (Watch the video to learn how one woman manages her type 2 diabetes. To enlarge the video, click the brackets in the lower right-hand corner. To reduce the video, press the Escape (Esc) button on your keyboard.) To manage your diabetes, here are things to do every day. - Take your medicines for diabetes and for any other health problems, even when you feel good. Take your medicines for diabetes and for any other health problems, even when you feel good. - Keep track of your blood glucose (blood sugar). You may want to check it one or more times a day. Be sure to talk about it with your health care team. Keep track of your blood glucose (blood sugar). You may want to check it one or more times a day. Be sure to talk about it with your health care team. - Check your blood pressure if your doctor advises and keep a record of it. Check your blood pressure if your doctor advises and keep a record of it. - Check your feet every day for cuts, blisters, red spots and swelling. Call your health care team right away about any sores that do not go away. Check your feet every day for cuts, blisters, red spots and swelling. Call your health care team right away about any sores that do not go away. - Brush your teeth and floss every day to keep your mouth, teeth and gums healthy. Brush your teeth and floss every day to keep your mouth, teeth and gums healthy. - Stop smoking. Ask for help to quit. Call 1-800 QUIT NOW ( 1-800-784-8669) Stop smoking. Ask for help to quit. Call 1-800 QUIT NOW ( 1-800-784-8669) - Eat well. Ask your doctor to give you the name of someone trained to help you create a healthy eating plan, such as a dietitian. See small steps for eating healthy foods. Eat well. Ask your doctor to give you the name of someone trained to help you create a healthy eating plan, such as a dietitian. See small steps for eating healthy foods. - Be active. Try to exercise almost every day for a total of about 30 minutes. If you haven't exercised lately, begin slowly. To learn more, see Exercise: How To Get Started, or visit Go4Life, the exercise and physical activity campaign for older adults from the National Institute on Aging. Be active. Try to exercise almost every day for a total of about 30 minutes. If you haven't exercised lately, begin slowly. To learn more, see Exercise: How To Get Started, or visit Go4Life, the exercise and physical activity campaign for older adults from the National Institute on Aging.
|
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] |
What is (are) Obsessive-Compulsive Disorder ?
|
Obsessive-compulsive disorder (OCD) is a type of anxiety disorder. If you have OCD, you have frequent, upsetting thoughts called obsessions. To try to control the thoughts, you feel an overwhelming urge to repeat certain rituals or behaviors. These are called compulsions. Examples of obsessions are a fear of germs or a fear of being hurt. Compulsions include washing your hands, counting, checking on things, or cleaning. With OCD, the thoughts and rituals cause distress and get in the way of your daily life. Researchers think brain circuits may not work properly in people who have OCD. It tends to run in families. The symptoms often begin in children or teens. Treatments include therapy, medicines, or both. One type of therapy, cognitive behavioral therapy, is useful for treating OCD. NIH: National Institute of Mental Health
|
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How many people are affected by alpha thalassemia ?
|
Alpha thalassemia is a fairly common blood disorder worldwide. Thousands of infants with Hb Bart syndrome and HbH disease are born each year, particularly in Southeast Asia. Alpha thalassemia also occurs frequently in people from Mediterranean countries, North Africa, the Middle East, India, and Central Asia.
|
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What are the treatments for Alport syndrome ?
|
These resources address the diagnosis or management of Alport syndrome: - Gene Review: Gene Review: Alport Syndrome and Thin Basement Membrane Nephropathy - Genetic Testing Registry: Alport syndrome - Genetic Testing Registry: Alport syndrome, X-linked recessive - Genetic Testing Registry: Alport syndrome, autosomal dominant - Genetic Testing Registry: Alport syndrome, autosomal recessive - MedlinePlus Encyclopedia: Alport Syndrome - MedlinePlus Encyclopedia: End-Stage Kidney Disease These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What is (are) Unverricht-Lundborg disease ?
|
Unverricht-Lundborg disease is an inherited form of progressive myoclonus epilepsy that is characterized by episodes of involuntary muscle jerking or twitching (myoclonus) that increase in frequency and severity over time. Episodes of myoclonus may be brought on by physical exertion, stress, light, or other stimuli. Affected individuals usually begin showing signs and symptoms of the disorder between the ages of 6 and 15. Over time, the myoclonic episodes may become severe enough to interfere with walking and other everyday activities. Other features include seizures involving loss of consciousness, muscle rigidity, and convulsions (tonic-clonic or grand mal seizures). Like the myoclonic episodes, these may increase in frequency over several years but may be controlled with treatment. After several years of progression, the frequency of seizures may stabilize or decrease. Unverricht-Lundborg disease is caused by mutation in the CSTB gene. It is inherited in an autosomal recessive pattern.
|
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Is Familial exudative vitreoretinopathy inherited ?
|
How is familial exudative vitreoretinopathy inherited? FEVR has different inheritance patterns depending on the gene involved. Most individuals have the autosomal dominant form of this condition, caused by mutations in the FZD4 or LRP5 gene. FEVR caused by LRP5 gene mutations can also have an autosomal recessive inheritance. When this condition is caused by mutations in the NDP gene, it has an X-linked pattern of inheritance.
|
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How many people are affected by adenylosuccinate lyase deficiency ?
|
Adenylosuccinate lyase deficiency is a rare disorder; fewer than 100 cases have been reported. The condition is most common in the Netherlands and Belgium, but it has been found worldwide.
|
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What are the symptoms of Anti-plasmin deficiency, congenital ?
|
What are the signs and symptoms of Anti-plasmin deficiency, congenital? The Human Phenotype Ontology provides the following list of signs and symptoms for Anti-plasmin deficiency, congenital. If the information is available, the table below includes how often the symptom is seen in people with this condition. You can use the MedlinePlus Medical Dictionary to look up the definitions for these medical terms. Signs and Symptoms Approximate number of patients (when available) Autosomal recessive inheritance - Bruising susceptibility - Hemothorax - Joint hemorrhage - Persistent bleeding after trauma - The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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How many people are affected by SOST-related sclerosing bone dysplasia ?
|
SOST-related sclerosing bone dysplasia is a rare condition; its exact prevalence is unknown. Approximately 100 individuals with sclerosteosis have been reported in the scientific literature. Sclerosteosis is most common in the Afrikaner population of South Africa. Van Buchem disease has been reported in approximately 30 people. Most people with van Buchem disease are of Dutch ancestry.
|
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Do you have information about Biodefense and Bioterrorism
|
Summary : A bioterrorism attack is the deliberate release of viruses, bacteria, or other germs to cause illness or death. These germs are often found in nature. But they can sometimes be made more harmful by increasing their ability to cause disease, spread, or resist medical treatment. Biological agents spread through the air, water, or in food. Some can also spread from person to person. They can be very hard to detect. They don't cause illness for several hours or days. Scientists worry that anthrax, botulism, Ebola and other hemorrhagic fever viruses, plague, or smallpox could be used as biological agents. Biodefense uses medical measures to protect people against bioterrorism. This includes medicines and vaccinations. It also includes medical research and preparations to defend against bioterrorist attacks. Centers for Disease Control and Prevention
|
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] |
What are the treatments for ADCY5-related dyskinesia ?
|
These resources address the diagnosis or management of ADCY5-related dyskinesia: - Gene Review: Gene Review: ADCY5-Related Dyskinesia - Genetic Testing Registry: Dyskinesia, familial, with facial myokymia - National Ataxia Foundation: Movement Disorder Clinics These resources from MedlinePlus offer information about the diagnosis and management of various health conditions: - Diagnostic Tests - Drug Therapy - Surgery and Rehabilitation - Genetic Counseling - Palliative Care
|
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What is (are) What I need to know about Hepatitis C ?
|
The liver is an organ that does many important things. You cannot live without a liver.
*See the Pronunciation Guide for tips on how to say the words in bold type.
The liver
- removes harmful chemicals from your blood - fights infection - helps digest food - stores nutrients and vitamins - stores energy
|
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What is (are) alpha thalassemia ?
|
Alpha thalassemia is a blood disorder that reduces the production of hemoglobin. Hemoglobin is the protein in red blood cells that carries oxygen to cells throughout the body. In people with the characteristic features of alpha thalassemia, a reduction in the amount of hemoglobin prevents enough oxygen from reaching the body's tissues. Affected individuals also have a shortage of red blood cells (anemia), which can cause pale skin, weakness, fatigue, and more serious complications. Two types of alpha thalassemia can cause health problems. The more severe type is known as hemoglobin Bart hydrops fetalis syndrome or Hb Bart syndrome. The milder form is called HbH disease. Hb Bart syndrome is characterized by hydrops fetalis, a condition in which excess fluid builds up in the body before birth. Additional signs and symptoms can include severe anemia, an enlarged liver and spleen (hepatosplenomegaly), heart defects, and abnormalities of the urinary system or genitalia. As a result of these serious health problems, most babies with this condition are stillborn or die soon after birth. Hb Bart syndrome can also cause serious complications for women during pregnancy, including dangerously high blood pressure with swelling (preeclampsia), premature delivery, and abnormal bleeding. HbH disease causes mild to moderate anemia, hepatosplenomegaly, and yellowing of the eyes and skin (jaundice). Some affected individuals also have bone changes such as overgrowth of the upper jaw and an unusually prominent forehead. The features of HbH disease usually appear in early childhood, and affected individuals typically live into adulthood.
|
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What is the outlook for Chronic Myelogenous Leukemia ?
|
Certain factors affect prognosis (chance of recovery) and treatment options. The prognosis (chance of recovery) and treatment options depend on the following: - The patients age. - The phase of CML. - The amount of blasts in the blood or bone marrow. - The size of the spleen at diagnosis. - The patients general health.
|
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What are the genetic changes related to purine nucleoside phosphorylase deficiency ?
|
Purine nucleoside phosphorylase deficiency is caused by mutations in the PNP gene. The PNP gene provides instructions for making an enzyme called purine nucleoside phosphorylase. This enzyme is found throughout the body but is most active in specialized white blood cells called lymphocytes. These cells protect the body against potentially harmful invaders by making immune proteins called antibodies that tag foreign particles and germs for destruction or by directly attacking virus-infected cells. Lymphocytes are produced in specialized lymphoid tissues including the thymus and lymph nodes and then released into the blood. The thymus is a gland located behind the breastbone; lymph nodes are found throughout the body. Lymphocytes in the blood and in lymphoid tissues make up the immune system. Purine nucleoside phosphorylase is known as a housekeeping enzyme because it clears away waste molecules that are generated when DNA is broken down. Mutations in the PNP gene reduce or eliminate the activity of purine nucleoside phosphorylase. The resulting excess of waste molecules and further reactions involving them lead to the buildup of a substance called deoxyguanosine triphosphate (dGTP) to levels that are toxic to lymphocytes. Immature lymphocytes in the thymus are particularly vulnerable to a toxic buildup of dGTP, which damages them and triggers their self-destruction (apoptosis). The number of lymphocytes in other lymphoid tissues is also greatly reduced, resulting in the immune deficiency characteristic of purine nucleoside phosphorylase deficiency.
|
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How many people are affected by iron-refractory iron deficiency anemia ?
|
Although iron deficiency anemia is relatively common, the prevalence of the iron-refractory form of the disease is unknown. At least 50 cases have been described in the medical literature. Researchers suspect that iron-refractory iron deficiency anemia is underdiagnosed because affected individuals with very mild symptoms may never come to medical attention.
|
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What are the symptoms of Epiphyseal dysplasia hearing loss dysmorphism ?
|
What are the signs and symptoms of Epiphyseal dysplasia hearing loss dysmorphism? The Human Phenotype Ontology provides the following list of signs and symptoms for Epiphyseal dysplasia hearing loss dysmorphism. 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 dermatoglyphics 90% Abnormality of the wrist 90% Anteverted nares 90% Behavioral abnormality 90% Cognitive impairment 90% Delayed skeletal maturation 90% Depressed nasal bridge 90% Epicanthus 90% Facial asymmetry 90% Hypertelorism 90% Hypopigmented skin patches 90% Proximal placement of thumb 90% Seizures 90% Sensorineural hearing impairment 90% Short stature 90% Wide mouth 90% Abnormality of the genital system 50% Deep philtrum 50% Finger syndactyly 50% Long philtrum 50% Ptosis 50% Scoliosis 50% Abnormal localization of kidney 7.5% The Human Phenotype Ontology (HPO) has collected information on how often a sign or symptom occurs in a condition. Much of this information comes from Orphanet, a European rare disease database. The frequency of a sign or symptom is usually listed as a rough estimate of the percentage of patients who have that feature. The frequency may also be listed as a fraction. The first number of the fraction is how many people had the symptom, and the second number is the total number of people who were examined in one study. For example, a frequency of 25/25 means that in a study of 25 people all patients were found to have that symptom. Because these frequencies are based on a specific study, the fractions may be different if another group of patients are examined. Sometimes, no information on frequency is available. In these cases, the sign or symptom may be rare or common.
|
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1,
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1,
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1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
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1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
1,
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1,
1,
1,
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1
] |
[
1276,
403,
253,
5917,
273,
10643,
532,
1994,
339,
267,
48723,
4854,
2957,
7915,
78,
28506,
3736,
1276,
403,
253,
7871,
285,
5917,
273,
10643,
532,
1994,
339,
267,
48723,
4854,
2957,
7915,
78,
28506,
32,
380,
8801,
34689,
5174,
15195,
1497,
3400,
253,
1563,
1618,
273,
7871,
285,
5917,
323,
10643,
532,
1994,
339,
267,
48723,
4854,
2957,
7915,
78,
28506,
15,
1310,
253,
1491,
310,
2130,
13,
253,
2829,
2708,
3797,
849,
2223,
253,
19831,
310,
2326,
275,
952,
342,
436,
1617,
15,
1422,
476,
897,
253,
3050,
1282,
25263,
8710,
26372,
281,
1007,
598,
253,
14308,
323,
841,
3739,
2426,
15,
8714,
84,
285,
40561,
3056,
17274,
13954,
1180,
273,
1363,
313,
9453,
2130,
10,
3506,
6320,
29863,
19644,
545,
982,
5091,
6,
3506,
12850,
1319,
273,
253,
20051,
5091,
6,
743,
442,
13083,
295,
4420,
5091,
6,
29475,
267,
43108,
5091,
6,
43419,
15151,
5091,
6,
6304,
19416,
20847,
24988,
5091,
6,
3315,
2079,
23761,
9729,
5091,
6,
39688,
386,
10034,
5091,
6,
16035,
451,
27110,
5091,
6,
8305,
8292,
293,
263,
1204,
5091,
6,
25295,
412,
304,
16390,
4808,
20412,
5091,
6,
1294,
89,
1983,
14663,
273,
17300,
5091,
6,
1023,
478,
980,
5091,
6,
322,
11313,
460,
1546,
4854,
15151,
5091,
6,
14196,
45540,
5091,
6,
36181,
6208,
5091,
6,
3506,
12850,
1319,
273,
253,
34020,
985,
2456,
6,
18147,
30005,
1206,
360,
2456,
6,
401,
4940,
7979,
514,
90,
314,
2456,
6,
8057,
30005,
1206,
360,
2456,
6,
29673,
2433,
2456,
6,
1810,
10424,
2433,
2456,
6,
3506,
6320,
14536,
273,
12333,
818,
15,
22,
6,
380,
8801,
34689,
5174,
15195,
1497,
313,
41,
5964,
10,
556,
5728,
1491,
327,
849,
2223,
247,
861,
390,
19831,
6634,
275,
247,
1617,
15,
18770,
273,
436,
1491,
3249,
432,
2207,
15671,
292,
13,
247,
5284,
7520,
2728,
5447,
15,
380,
4294,
273,
247,
861,
390,
19831,
310,
3798,
7117,
347,
247,
7227,
6642,
273,
253,
7155,
273,
1363,
665,
452,
326,
4735,
15,
380,
4294,
778,
671,
320,
7117,
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247,
6919,
15,
380,
806,
1180,
273,
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574,
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16,
1099,
2097,
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1263,
273,
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952,
512,
1363,
497,
1119,
281,
452,
326,
19831,
15,
4923,
841,
11383,
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1754,
327,
247,
2173,
1263,
13,
253,
17711,
778,
320,
1027,
604,
1529,
1387,
273,
1363,
403,
6730,
15,
13168,
13,
642,
1491,
327,
4294,
310,
2130,
15,
496,
841,
2219,
13,
253,
861,
390,
19831,
778,
320,
7520,
390,
1846,
15
] |
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