The mechanism by which hyperthyroidism can produce hypokalemic PP is not well understood. Thyroid hormone increases tissue responsiveness to beta-adrenergic stimulation, which, along with thyroid hormone, increases sodium-potassium ATPase activity on the skeletal muscle membrane. This tends to drive potassium into cells, perhaps leading to hyperpolarization of the muscle membrane and relative inexcitability of the muscle fibers. Thyrotoxic patients with PP have been found to have higher sodium pump activity than those without paralytic episodes . In this way, excess thyroid hormone may predispose to paralytic episodes by increasing the susceptibility to the hypokalemic action of epinephrine or insulin .