Endocrine Abstracts

Background: Hypokalemic Thyrotoxic Periodic Paralysis (HTPP) is a rare acquired muscular channelopathy that develops in the context of thyrotoxicosis. It consists of episodes of painless muscle weakness, precipitated by exercise, fasting, or high-carbohydrate meals. Men among ages 20-40 are more frequently affected than woman. Thyrotoxicosis (and its subsequent beta-adrenergic stimulation) increases the activation of the Sodium-Potassium ATPase channels, which leads to hyperpolarization of the muscle membrane and relative inexcitability of the muscle fibers. Peripheric insulin resistance and testosterone have also been described as contributors to the phenomenon, although the complete pathogenesis remains unclear. The degree of hypokalemia usually corresponds with the severity of clinical manifestations. We present one case of Thyrotoxic Periodic Paralysis with severe hypokalemia in the context of thyrotoxicosis.

Case description: A 23-year-old male attends the ER complaining of acute muscle weakness after an extenuating work-out prior to the visit. The symptoms progressively worsen during the night, leading to the development of tetraparesia and generalized paraesthesia. The patient refers at least three previous episodes in the last two years. Neurologic examination confirms proximal weakness in the four limbs, predominantly in lower extremities, with preserved consciousness and normal breathing pattern. Urgent laboratory test reports serum Potassium (K+) of 1.1 mEq/l. EKG shows sinus tachycardia, ST depression and frequent SV extrasystoles. Due to life-threatening risk, continuum cardiologic monitorization and intensive intravenous K+ repletion through central line is initiated in the Intensive Care Unit. After stabilization, patient confirms that he has been suffering from tachycardia, sweating, heat intolerance and distal tremor for several months. The anamnesis was negative for other symptoms or signs of hyperthyroidism. However, lab test shows supressed serum TSH (<0.005 µlU/ml) and elevated Free T4 (5.97 ng/dl), Free T3 (13.75 pg/ml) and positive Thyroid-Stimulating Immunoglobulin (TSI) (7.36 IU/l), confirming the diagnosis of Graves-Basedow Disease. Anti-thyroid medication and beta-blockers are initiated. During the evolution in hospitalization, the clinical manifestations eventually subside, accompanied by progressive normokalemia and overall clinical stability in a period of 5 days.

Conclusion: In the context of Periodic Paralysis, finding of hypokalemia must be an alert about a case of HTPP. Therefore, thyrotoxicosis should be evaluated, particularly in the absence of a family history of periodic paralysis. Monitorization and K+ supplementation must not be delayed. Restoration of euthyroidism is the only preventive measure to eliminate attacks of HTPP.