Hereditary Angioedema (HAE) is a very rare and potentially life threatening genetic condition that occurs in about 1/10,000 to 1/50,000 people. HAE symptoms include episodes of edema (swelling) in various body parts including the hands, feet, face, and airway. In addition, patients often have bouts of excruciating abdominal pain, nausea, and vomiting that is caused by swelling in the intestinal wall. Airway swelling is particularly dangerous and can lead to death by asphyxiation.

Most attacks occur spontaneously with no apparent reason, however anxiety, stress, minor trauma, surgery, and illnesses such as colds and flu have been cited as triggers. Trauma to the oral cavity caused by dental procedures make HAE patients particularly vulnerable to airway attacks. Patients have also reported swelling in extremities following typing, prolonged writing, pushing a lawn mower, hammering, shoveling, and other physical activities.

Most cases of angioedema are not HAE because swelling attacks are typically caused by something other than C1-inhibitor deficiency, usually an allergic reaction. Laboratory analysis of blood samples or genetic testing is required to establish the HAE diagnosis. There are two specific blood tests that confirm HAE: C1-inhibitor functional common form of the disease--Type I--is characterized by low quantitative levels of C1-inhibitor and affects about 85% of patients.

Patients often report tingling or tightness at the site where edema will occur thirty minutes to several hours later. In some cases, this sensation can be present twelve to twenty four hours before the onset of swelling. Approximately one fourth of HAE patients experience a flat, non itching red blotchy rash both before and during an attack. The edema itself usually lasts for twenty four to seventy two hours, but the length of an attack can range from four hours to four or more days.

Swelling of the extremities is uncomfortable and, according to some patients, can be painful and debilitating depending on the location of the edema. Attacks that involve the face and throat must be taken seriously and medical treatment should be sought without delay. Swelling of the throat can close the air passage and cause death by suffocation. The symptoms of an impending airway obstruction include difficulty swallowing and a change in voice pitch.

Treatment of acute attacks Clinicians generally recommend long term therapy for patients who experience more than one attack per month, or who believe that the disease significantly interferes with their life style. The present drugs of choice for long-term therapy are 17 alpha alkylated androgens such as danazol, and oxandrolone (Oxandrin). 17 alpha alkylated androgens produce an increase in C1-inhibitor levels, but the exact mechanism of how they do so has not been precisely defined.

The age of HAE onset varies considerably, however, in one study, half of the patients reported onset of their symptoms by the age of seven, and over two thirds became symptomatic by the age of thirteen. There also seems to be an increased frequency of attacks during puberty or adolescence.

Fortunately, most prepubescent children with HAE do not suffer from frequent attacks and infrequent flares affecting the abdomen can be managed by using pain relievers and anti nausea agents. The small number of severely affected children who experience frequent and severe attacks must be managed on a case by case basis.

this time RPC is not believed to be hereditary, however there are several families with documented and diagnosed RPC in them. Siblings are the most commonly found grouping, although several twins only one twin developed RPC. The next factor seen is parent and child, then grandparent and child.

There appears to be a predisposition based on heredity for some people when they are exposed to loud sounds, but whether or not tinnitus is genetically indicated is not certain. Scientists working on the Human Genome Project, for example, have not discovered a "tinnitus gene," but they have identified genes that are responsible for a few rare varieties of hearing loss, temporomandibular joint (TMJ) dysfunction, Ménière's Disease, and acoustic Neuroma.

Hereditary hemochromatosis is a genetic disease that is the result of inheriting two defective copies of a particular gene, one from each parent. The mutation in this gene causes the intestine to absorb too much iron. Over time, usually several years, this excess iron is deposited in the cells of the liver, heart, pancreas, joints, and pituitary gland. If left untreated, organ damage can result.

Heredity does seem to play a role. Ten percent of lupus patients have a first-degree relative (sister, daughter, son, mother) or a second-degree relative (aunt, uncle, first cousin) with lupus. Therefore, 90 percent of lupus patients DO NOT have relatives with lupus. Even in identical twins, when one sibling has lupus and the other twin does not, it is believed there are environmental factors that play an important role.

Each of us is the result of genes inherited from our parents, and the influence of our environment on the functioning of the genes and body components encoded in our genes. Sometimes an error occurs during replication of genes as part of the reproductive process. Most of the errors are analogous to typos in printed text - a single wrong character appears in an instruction in a gene. The defective gene results in the production of a faulty component for the body.

No, hammertoes and bunions are caused by pathomechanics, although shoe gear can aggravate the symptoms that can cause these problems.

Research indicates that genetic factors may play a part in causing autism in some individuals. Most researchers agree that autism probably results from many separate causes.

There is no proof that Social Phobia is hereditary. Some epidemiologic data suggest it, but there are not enough elements to warrant a conclusion. The same occurrence in one of the parents cannot be regarded as evidence. A person's self-concept, values, and beliefs, as well as many current feelings and emotions, may have their roots in childhood, when the self was being formed.

Yes, heredity plays a role. In one out of five persons with alopecia areata, someone else in the family also has it. Those who develop alopecia areata for the first time after the age of thirty years have less likelihood that another family member will have it. Those who develop their first patch of alopecia areata before the age of thirty have a higher possibility that other family members will also have it.

There is an increase in AMD among children of AMD patients. This is one more reason why your children, after age 40, should have regular eye exams at least every other year.

To some extent, but this does not mean that it is impossible to treat. Environment, stress and even your personality can play a role. Genetics are also said to play a part in baldness. However, Hair Fantastiques success rate with thinning hair and male patter baldness is very high.top

According to estimates, approximately 29.5 million people in the United States suffer from migraine. Four out of five (80 percent) of them report a family history of migraine, but scientists are not sure if this is genetic or a family predisposition. Despite the uncertainty, a child has a 50% chance of having migraine if one parent suffers and a 75% chance if both parents suffer.

It is more correct to say that there is evidence of a strong family history and genetic relationship to bipolar disorder.

CML is chromosomal/genetic but not hereditary. This means it is not caused by a gene being passed on. During the patient's lifetime, they somehow were exposed to something which damaged their genes. This resulted in the translocation of the 9 and 22 chromosome, and led to CML. However, there are familial incidences among 2 or more family members in other myeloproliferative disorders so the answer is not clear.

Hereditary hemochromatosis is an inherited condition. It occurs when a person inherits two copies of a mutation, one from each parent. People with one copy of this mutation are carriers for the condition and usually have little or no excess accumulation of iron. It is estimated that 10% of the population are carriers for hemochromatosis. However, not all people with two genetic mutations develop signs and symptoms of the disorder during their lifetimes.

Some foot problems are hereditary, but the majority of foot problems are a result of lack of proper foot care, ill-fitting shoes, overuse injuries, infection, trauma, systemic diseases (for example diabetes) and general wear and tear.

Hereditary diseases, such as hypothyroidism and other autoimmune diseases are diagnosed in all breeds, and the Bearded Collie is no exception. Hyperthyroidism is the most common and the easiest to treat. Addisons is probably the second most common. There are many other, less common diseases. One reason we hear more about genetic diseases is because they are being diagnosed where previously dogs would die of some unknown cause.

Macular degeneration appears to be hereditary in some families but not in others. Since macular degeneration affects most patients later in life, it is difficult to study successive generations in a family. Recent studies of twins indicate that both genetic and non-genetic factors play important roles in age-related macular degeneration. Yes. It has been demonstrated that the blue rays of the spectrum seem to accelerate macular degeneration more than other rays of the spectrum.