Complete Information on Andersen Tawil syndrome with Treatment and Prevention

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. In some cases, a person with Andersen tawil syndrome inherits the mutation from one affected parent. These cases occur in people with no history of the disorder in their family. There may be several variant mutations, producing similar but slightly different forms of the disorder, as occurs in the other forms of periodic paralysis, where several variants of each type have been identified.

The most common change influence heart is the ventricle heart rate is abnormal, is the severance in the heart lower chamber's rhythm, and long quart comprehensive symptom. The long quart comprehensive symptom is causes the cardic muscle to need for a long time compared to usually to the overcharging between striking heart situation. Perhaps the patient has normo, the hypo or stimulated kalemia, perhaps or the serum potassium is instable in attack period. Perhaps ATS includes the severe heart disease involvement and the skeleton anomaly. ATS in the periodic paralysis or the long quart comprehensive symptom gene which current identifies with other does not connect. Perhaps the trigger changes from the person to the person. This unfortunately is the food trigger other types equally clear is likely not defined the periodicity to be lacking in vigilance, it is the region which possibly said or the sweets triggers the plot in rich potassium food. Common trigger at other periodic paralysis including not lively rest in activity later and period. The sleep is a powerful trigger.

The syndrome of Andersen tawil influences the heart, is the symptoms a verstoring in the rhythm of the lower chambers of the heart beside the symptoms of long QT syndrome. Physical abnormalities associated with Andersen tawil syndrome typically affect the head, face, and limbs. These features often include a very small lower jaw, dental abnormalities, low-set ears, widely spaced eyes, and unusual curving of the fingers or toes (clinodactyly). Some affected people also have short stature and an abnormal curvature of the spine. Partial manifestations of ATS are common. The subtle nature of the cardiac and dysmorphic features may delay diagnosis, but clinical recognition of ATS is vital given the predisposition for dysrhythmias and sudden death.

A variety of tests may be used. If untreated, the irregular heartbeats can lead to discomfort, fainting, or cardiac arrest. Since individuals vary so much it is difficult, if not impossible, to give guidelines which apply to all ATS patients. Treatment for Andersen tawil syndrome remains empirical and is frustrated by a paradoxical response of cardiac and skeletal muscle to changes in potassium levels, unpredictable responses to drugs, and an overall refractoriness to antiarrhythmic agents. Medications which regulate the heart are often prescribed, other treatment depends on the individual and their reaction to potassium. Patients with severe heart rhythm problems may require a pacemaker-like device. In addition to the standard pharmacologic therapies for the periodic paralyses, beta-blockers have been used successfully in some patients. Patients must avoid hypokalemia and drugs that cause prolongation of the QT interval.