Isshak Rouba, Orhun Nagihan, Rajab Islam, Shober Dale, Michael Patrick
Department of Internal Medicine, St. Joseph's University Medical Center, Paterson, New Jersey.
AACE Endocrinol Diabetes. 2025 Apr 10;12(1):57-59. doi: 10.1016/j.aed.2025.02.005. eCollection 2025 May-Jun.
BACKGROUND/OBJECTIVE: Thyrotoxic periodic paralysis is a rare, life-threatening complication of thyrotoxicosis, characterized by hypokalemia, hyperthyroidism, and acute muscle weakness. It often occurs in Graves' disease but is not directly linked to the severity or duration of thyrotoxicosis. The objective of this report is to describe a patient with Graves' disease and thyrotoxic periodic paralysis, emphasizing the importance of achieving an euthyroid state, potassium repletion, and the role of β-blockers in management.
A 23-year-old male with a history of untreated hyperthyroidism presented to the emergency department with palpitations and worsening bilateral lower extremity weakness, culminating in an inability to walk.The patient reported previous episodes of weakness associated with his hyperthyroidism. Physical examination revealed marked muscle weakness and hypertension. Following evaluation, the patient was diagnosed with Graves' disease. He was treated with potassium, magnesium, methimazole, and propranolol, resulting in rapid improvement of his symptoms, and was discharged with outpatient follow-up.
Thyrotoxic periodic paralysis is a rare manifestation of thyrotoxicosis, which can be precipitated by stressors or medication noncompliance. The pathophysiology involves thyroid hormone-induced shifts in potassium, leading to hypokalemia and muscle weakness. Treatment consists of normalizing thyroid function, managing potassium, and using β-blockers to counteract the overstimulation of muscle cells by thyroid hormones and catecholamines. However, the precise role of β-blockers in preventing attacks requires further investigation.
Early diagnosis and treatment of thyrotoxic periodic paralysis, including euthyroid restoration and potassium management, are critical. While β-blockers may be effective in symptom resolution, further studies are needed to clarify their role in preventing attacks.
背景/目的：甲状腺毒症性周期性瘫痪是甲状腺毒症一种罕见的、危及生命的并发症，其特征为低钾血症、甲状腺功能亢进和急性肌无力。它常发生于格雷夫斯病，但与甲状腺毒症的严重程度或病程无直接关联。本报告的目的是描述一名患有格雷夫斯病和甲状腺毒症性周期性瘫痪的患者，强调实现甲状腺功能正常状态、补充钾以及β受体阻滞剂在治疗中的作用的重要性。
一名有未经治疗的甲状腺功能亢进病史的23岁男性因心悸和双侧下肢无力加重就诊于急诊科，最终无法行走。患者报告既往有与甲状腺功能亢进相关的肌无力发作史。体格检查发现明显的肌无力和高血压。经评估，患者被诊断为格雷夫斯病。他接受了钾、镁、甲巯咪唑和普萘洛尔治疗，症状迅速改善，出院后进行门诊随访。
甲状腺毒症性周期性瘫痪是甲状腺毒症的一种罕见表现，可由应激源或药物治疗依从性差引发。其病理生理涉及甲状腺激素诱导的钾离子转移，导致低钾血症和肌无力。治疗包括使甲状腺功能正常化、处理钾离子以及使用β受体阻滞剂来对抗甲状腺激素和儿茶酚胺对肌肉细胞的过度刺激。然而，β受体阻滞剂在预防发作中的确切作用需要进一步研究。
甲状腺毒症性周期性瘫痪的早期诊断和治疗，包括恢复甲状腺功能正常和钾离子管理，至关重要。虽然β受体阻滞剂可能对缓解症状有效，但需要进一步研究以阐明其在预防发作中的作用。
