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[Thyrotoxic hypokalemic periodic paralysis in a black African man in Abidjan (Côte d'Ivoire)].

Med Trop Sante Int

December 2024

Service de neurologie, Centre hospitalier universitaire (CHU) de Cocody, Université Félix Houphouët Boigny, UFR des sciences médicales d'Abidjan, Cote d'Ivoire.

Introduction: Thyrotoxic hypokalemic periodic paralysis (THPP) is a sporadic form of hypokalemic periodic paralysis (HPP). It is a diagnostic and therapeutic emergency rarely described in the black population. We report a case in a black subject from Côte d'Ivoire.

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Insulin-induced severe thyrotoxic periodic paralysis: A case report.

World J Clin Cases

March 2025

Department of Endocrinology and Metabolism, Zigong First People's Hospital, Zigong 643000, Sichuan Province, China.

Background: Thyrotoxic periodic paralysis (TPP) is an endocrine emergency caused by thyrotoxicosis, manifesting mainly as periodic myasthenia and hypokalemia, and posing a serious threat to the patient's health. Fatigue, strenuous exercise, alcohol abuse, high carbohydrate intake and insulin injections are common triggers of paralysis. This article reports a case of severe TPP induced by insulin injection, elucidates the characteristics and pathogenesis of the disease, analyses the risk factors for triggering TPP, and hopefully provides more clinical data for TPP patients.

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Introduction: Hypokalemic periodic paralysis (HPP) presents a diagnostic challenge due to the painless muscle weakness it causes. This case discusses a patient with HPP along with electrocardiogram (ECG) findings of Brugada phenocopies (BrP) in the setting of hypokalemia. A review of the literature showed that it is the seventh documented example of BrP induced by hypokalemia alongside HPP.

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-associated triadopathy presenting with myalgia, muscle weakness, and asymptomatic hyperCKemia.

Ther Adv Neurol Disord

February 2025

Department of Neurology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Yong Wai Zheng Street 17#, Nanchang 330006, China.

variants can alter the structure and function of the calcium channel, resulting in abnormal calcium influx and homeostasis. It is well established that pathogenic variants in can lead to hypokalemic periodic paralysis, malignant hyperthermia, and congenital myopathy. Nevertheless, the clinical presentations and disease progression of exertional myalgia and weakness associated with variants remain elusive.

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