Thyrotoxic periodic paralysis (TPP) is an uncommon but dangerous complication seen in thyrotoxic patients. It is characterized by hypokalemia associated with acute proximal symmetrical lower limb weakness and can progress to involve all four limbs and the respiratory musculature. The mechanisms of hypokalemia are not completely understood. The prevailing theories include increased Na-K ATPase pump activity and mutations in genes encoding inward-rectifier potassium channels in skeletal muscle. It is often confused with familial periodic paralysis (FPP) due to the similarity in presentation but can be differentiated based on the presence of thyrotoxic features and biochemical testing. Commonly recorded and described in East Asian males, the incidence of TPP has been rising in the West and other parts of the world. Knowledge regarding identification, early treatment, and prevention of future episodes of TPP is essential in mitigating this potentially lethal complication.
TPP can be caused by mutations on the KCNJ18 gene. Any cause of hyperthyroidism can lead to thyrotoxic periodic paralysis. They include Graves disease (most common), toxic nodular goiter, solitary toxic nodule, iodine-induced thyrotoxicosis, excess exogenous thyroxine use, thyroiditis, thyrotropin-secreting pituitary adenoma, and amiodarone-induced thyrotoxicosis.
Common factors triggering attacks of periodic paralysis include the consumption of carbohydrate-rich foods, strenuous physical activity, high salt/sodium intake, stresses (surgical, infectious, psychological), trauma, and medications (diuretics, estrogens, acetazolamide, epinephrine, laxatives, corticosteroids, non-steroidal anti-inflammatory drugs, licorice, fluoroquinolones, aminoglycosides, and ecstasy).