Thyrotoxic hypokalaemic periodic paralysis

Abstract

Lazarus (Feb 1, p 339)1Lazarus JH Hyperthyroidism.Lancet. 1997; 349: 339-343Summary Full Text Full Text PDF PubMed Scopus (49) Google Scholar notes that a high index of suspicion is often required in the diagnosis of hyperthyroidism, but he neglects to mention one presentation in which the disorder may not be readily apparent, or not considered by most physicians: hypokalaemic periodic paralysis. We recently treated a 26-year-old white man in whom hypokalaemic lower extremity paralysis was the presenting symptom of thyrotoxicosis. During the previous month the patient had had four similar episodes that resolved spontaneously. There was no family history of hypokalaemic paralysis. Physical findings were normal, apart from proximal muscle paralysis of the legs and hypoactive deep tendon reflexes. There were no other signs of hyperthyroidism. His serum potassium was 2·5 mmol/L. He was treated with intravenous potassium, and within 6 h he was symptom free (potassium 3·2 mmol/L). As part of the evaluation of hypokalaemic periodic paralysis, thyroid function tests were done. Thyroid stimulating hormone was low (0·01 mU/L) and concentrations of free thyroxine and total triiodothyronine were high. Radioactive technetium uptake of the thyroid gland was high and uniform. Because of recurrent attacks of paralysis, the patient was also initially treated with propranolol. 2 weeks after presentation he was given 370 mBq of 131I. 1 week after this ablation, he had yet another episode of hypokalaemic paralysis. His T3 and T4 concentrations were still high. Potassium was given, and within a few days thyroid function tests became normal. There have been no further episodes of muscle paralysis during 8 months of follow-up. Thyrotoxic hypokalaemic periodic paralysis occurs predominantly in Asian populations and is a complication rarely encountered in western countries.2Ober KP Thyrotoxic periodic paralysis in the United States. Report of seven cases and review of the literature.Medicine (Baltimore). 1992; 71: 109-120Crossref PubMed Scopus (247) Google Scholar The clinical and biochemical features of this paralysis are identical to those of familial periodic paralysis. In both disorders, patients—usually male—have recurrent flaccid weakness, mainly of the lower limbs. The hypokalaemia results from an intracellular shift of potassium. The symptoms resolve over a few hours as potassium moves out of the cells into the extracellular space. However, patients with thyrotoxic hypokalaemic periodic paralysis have attacks only when they are hyperthyroid. Graves' disease is the commonest cause of hyperthyroidism but any cause of thyrotoxicosis (including administration of exogenous thyroxine) may trigger attacks. Since clinical features of hyperthyroidism may be very subtle or absent in thyrotoxic hypokalaemic periodic paralysis, physicians should be alert to the existence of this entity.