Thyrotoxic hypokalemic periodic paralysis due to Graves’ disease in 2 adolescents

Abstract

Thyrotoxic periodic paralysis (TPP) is a notable and potentially lethal complication of thyrotoxicosis, and Graves’ disease is the most common cause of TPP. TPP is commonly reported in Asian males between 20–40 years of age, but it is rare in children and adolescents. We report 2 Korean adolescents (a 16-year-old male and a 14-year-old female) with episodes of TPP who were previously diagnosed with Graves’ disease. These 2 patients presented with lower leg weakness in the morning after waking up. They were diagnosed with TPP-associated with thyrotoxicosis due to Graves’ disease. After they were initially treated with potassium chloride and antithyroid drugs, muscle paralysis improved and an euthyroid state without muscle paralytic events was maintained during follow-up. Therefore, clinicians should consider TPP when patients have sudden paralysis and thyrotoxic symptoms such as goiter, tachycardia, and hypertension.

Stroke Mimic: A Case of Unilateral Thyrotoxic Hypokalemic Periodic Paralysis

“…1,2,4 As a result, the cell sequesters K + intracellularly, leading to the common pathway for many acquired paralysis syndromes: hypokalemia. 6 Thyrotoxicosis alone, however, does not result in episodic paralysis, nor do free T4 levels correlate to symptoms. 7 Rather, certain genetic factors in combination with a trigger such as thyrotoxicosis lead to clinical manifestation of the disease.…”

“…3 Males are more susceptible than females, with reported ratios ranging from 17:1 to 70:1. 6 THPP is thought to be mediated through the Na + /K + pump. Studies suggest that androgen-mediated promotion of the Na + /K + pump and a larger muscle-to-body ratio lead to greater risk of THPP episodes.…”

“…8 The potassium inwardly-rectifying channel subfamily J member 2 gene (KCNJ2) and potassium inwardlyrectifying channel subfamily J member 18 gene (KCNJ18) are the two most prominent genes with mutations that predispose individuals to THPP in Asians and Caucasians, respectively. 6 These genes are inward-rectifying K + channels, which counteract the Na + /K + pump by channeling K + extracellularly. 8 In mutated genes, excess thyroid hormone, excess catecholamines or excess insulin may all inhibit efflux of potassium from the cell, further sequestering K + and contributing to intravascular hypokalemia.…”

“…15 Treatment for THPP involves correction of K + and returning the patient to a euthyroid state. 1,2,6,14 Care must be taken when correcting K + as the patient has relative hypokalemia, in which the potassium is merely shifted into the cell instead of being depleted in the body. 1,2 In Clinical Practice and Cases in Emergency Medicine Lajeunesse et al…”

“…Thus, potassium supplementation in the ED must be performed with care as 70-80% of patients treated with potassium have rebound hyperkalemia. 6,14 Providers must also consider management of associated electrolytes such as magnesium when repleting potassium. Close cardiac monitoring is also essential since patients are at risk of both hypo and hyperkalemic-induced dysrhythmias.…”