Case of Thyrotoxic Periodic Paralysis in a Caucasian Male and Review of Literature

Abstract

Objective. Thyrotoxic periodic paralysis (TPP), a known condition in Asian men, is becoming increasingly common in men from Western countries. Since suspicion for TPP as a differential in diagnosis is of utmost importance to avoid overcorrection of hypokalemia and other complications, we are reporting a case of TPP in a 25-year-old Caucasian male. Methods. The patient presented with intermittent lower extremity weakness after consumption of a large high-carbohydrate meal. Clinical examination revealed diffusely enlarged thyroid gland, no muscle power in lower extremities, tremors, and brisk deep tendon reflexes. Results. Clinical and laboratory findings were consistent with Graves' disease and the patient had hypokalemia. The patient responded to potassium repletion and was treated with propylthiouracil and propranolol. After treatment with radioactive iodine, the patient developed postablative hypothyroidism for which he was treated with levothyroxine. Conclusion. Since this condition is overlooked by physicians in Western countries, we present a case of TPP in a Caucasian male thus showing the importance of consideration of TPP in Caucasians despite its rare occurrence and the need for prompt diagnosis to avoid the danger of hyperkalemia in management of the paralytic attack in TPP patients.

Thyrotoxic Periodic Paralysis—A Misleading Challenge in the Emergency Department

“…If thyrotoxicosis is confirmed, then measurement of thyroid antibodies including TRAb should be carried out, especially as Graves' disease is the most common cause of TPP [1]. Although predominantly encountered in young Asian males, we together with other authors [3,16] have shown that TPP can appear irrespective of age, sex, and race, and thus, one should stay alert when facing hypokalemic paralysis. [5,15].…”

“…The usually subtle presentation of thyrotoxicosis accompanying TPP challenges the diagnosis [14]. Increased and elevated BP are more sensitive indicators of TPP than other hyperthyroid signs (fever, moist skin, exophthalmos, and goiter) [3]. In the ED, one should think of TPP if in front of the following criteria: (1) clinical and/or biochemical signs of thyrotoxicosis: a tachycardic patient with systolic hypertension and abnormal ECG (AV block) and/or low TSH together with high FT4 and FT3, (2) hypokalemia with low urinary K + excretion and normal blood acid-base status (hypophosphatemia and mild hypomagnesemia can also be encountered), and (3) negative family history for periodic paralysis [1,5,15].…”

“…Primary hypokalemic periodic paralysis is caused by familial or de novo mutations in the CACNA1S gene (responsible for the synthesis of calcium channels) or SCN4A gene (encodes a critical part of sodium channels); it is characterized by hypokalemic muscle weakness episodes lasting from hours to days, usually appears under the age of 20 and is in most cases accompanied by positive family history (autosomal dominant transmission) [3,15]. Primary normo-and hyperkalemic periodic paralysis are caused by pathogenic variants in SCN4A, have similar clinical features as the hypokalemic form, but the age of onset is even lower, have normal or elevated serum K + levels, and both exhibit myotonic discharges between attacks [15,17].…”

“…The highest incidence (approximately 2%) is seen in the Asian population [2]. In contrast, the very low incidence of 0.1-0.2% in American Caucasians [3] makes the differential diagnosis a struggle: in Caucasians, primary forms (channelopathies) come first in the etiology of hypokalemic periodic paralysis, while other possible secondary causes besides TPP include gastrointestinal and renal pathologies, use of diuretics, etc. [2].…”

Thyrotoxic Periodic Paralysis- An Uncommon Disease in the Western World: A Case Report

“…During this disease, findings include QT-U that is prolonged, a prolonged PR, and resting sinus tachycardia. Although nerve stimulation studies are not necessary for diagnosis, if performed during the paralytic episode, there is a decrease in both compound muscle action potential and the amplitude of the evoked muscle action potential [12].…”