ABSTRACT
Background. Thyrotoxic periodic paralysis (TPP) is characterized by episodes of neuromuscular weakness occurring in the context of hypokalemia and hyperthyroidism and has been predominantly described in Oriental populations. Whereas it is uncommon in Caucasians and Blacks, TPP does occur in individuals of Native American descent. The objective was to analyze the clinical, biochemical, and HLA characteristics of group of Mexican mestizo patients with TPP. Methods. The sample was comprised of 14 men with TPP diagnosed since january 1990, based on one or more episodes of flaccid paralysis, accompanied by hypokalemia and occurring in the context of clinical and biochemical hyperthyroidism. Eight were available HLA testing. Results. Hyperthyroidsm was diagnosed before the development of periodic paralysis in five of the patients, whereas in six it occurred afterward. The severity of paralysis did not correlate with the degree of either hypokalemia or hyperthyroidism. An increased frequency of HLA-DR3 was found in Graves' patients without paralysis but not in those with paralysis, as compared to the general population. Conclusions. TPP is more common than previously thoought in Mexicans, in whom it behaves as in other Native American groups. The lack of HLA-DR3 association in Graves' patients with TPP is interesting, but at the moment has no pathophysiological implications
Subject(s)
Humans , Male , Adult , Middle Aged , HLA Antigens/analysis , Ethnicity , Gene Frequency , Graves Disease/complications , White People/genetics , Hypokalemia/ethnology , Paralysis/ethnology , Thyrotoxicosis/ethnology , /analysis , HLA Antigens/genetics , Gene Frequency , Graves Disease/immunology , Hypokalemia/blood , Indians, North American/genetics , Paralysis/blood , Potassium/blood , Thyroid Hormones/blood , Thyrotoxicosis/etiologyABSTRACT
Nonfamilial hypokalemic thyrotoxic periodic paralysis is rarely diagnosed among Caucasians and blacks in the western world but it is relatively common among Asiatics. Sudden paralysis occurring while at rest after a large carbohydrate meal or strenuous exercise in an undiagnosed mild thyrotoxic patient is a common presentation. A case illustrating such presentation is reported. Intracellular shifts of potassium triggered or facilitated by hyperthyroidism and hyperinsulinemia are the biochemical features. Correction of the thyrotoxic state is the definitive treatment for this disorder. Judicious administration of potassium is indicated during the hypokalemic episode to prevent life-threatening arrhythmias