Khanderia U, Jaffe C A, Theisen V
College of Pharmacy, University of Michigan, Ann Arbor.
Clin Pharm. 1993 Oct;12(10):774-9.
Cases of hypothyroidism and hyperthyroidism associated with amiodarone therapy are described, and the mechanisms, clinical appearance, and management of amiodarone-induced thyroid dysfunction are discussed. A 72-year-old man with a history of recurrent ventricular tachycardia unresponsive to conventional antiarrhythmic drugs was started on amiodarone therapy. Initially he responded well, but after three months he began to have fatigue, dry skin, and intolerance of cold. His serum thyroid-stimulating hormone (TSH) concentration had risen from 4.4 microU/mL before amiodarone therapy began to 20 microU/mL, consistent with hypothyroidism. He was started on sodium levothyroxine for thyroid hormone replacement; the dosage was adjusted in accordance with subsequent TSH measurements. His hospital course was complicated by congestive heart failure. The second patient was a 43-year-old man with a history of atrial fibrillation who developed hyperthyroidism when placed on amiodarone therapy. He had persistent sweating, intolerance of heat, restlessness, and tachycardia. Thyroid function tests confirmed the presence of hyperthyroidism. The patient was treated with propylthiouracil and propranolol, and amiodarone was discontinued. He remained unresponsive to the propylthiouracil, which was discontinued, and was scheduled for radioactive iodine treatment. The mechanism of amiodarone-induced thyroid dysfunction may involve the large iodine content of the drug. Amiodarone-induced hypothyroidism may range in severity from mild symptoms to severe myxedema; the skin, hair, and nails are particularly affected. Persons with clinical hyperthyroidism secondary to amiodarone treatment show the signs and symptoms of a hypermetabolic state resulting from thyroid hormone excess. Amiodarone-induced hypothyroidism is treated with levothyroxine and hyperthyroidism with antithyroid drugs. Amiodarone can cause thyroid dysfunction, which can have serious consequences.
本文描述了与胺碘酮治疗相关的甲状腺功能减退和甲状腺功能亢进病例，并讨论了胺碘酮所致甲状腺功能障碍的机制、临床表现及治疗方法。一名72岁男性，有复发性室性心动过速病史，对传统抗心律失常药物无效，开始接受胺碘酮治疗。最初他反应良好，但三个月后开始出现疲劳、皮肤干燥和不耐寒。他的血清促甲状腺激素（TSH）浓度从胺碘酮治疗开始前的4.4微单位/毫升升至20微单位/毫升，符合甲状腺功能减退。他开始服用左甲状腺素钠进行甲状腺激素替代治疗；剂量根据随后的TSH测量结果进行调整。他的住院过程因充血性心力衰竭而复杂化。第二名患者是一名43岁男性，有房颤病史，在接受胺碘酮治疗时出现甲状腺功能亢进。他持续出汗、不耐热、烦躁不安和心动过速。甲状腺功能检查证实存在甲状腺功能亢进。该患者接受丙硫氧嘧啶和普萘洛尔治疗，胺碘酮停药。他对丙硫氧嘧啶无反应，丙硫氧嘧啶停药，计划进行放射性碘治疗。胺碘酮所致甲状腺功能障碍的机制可能与药物中大量的碘含量有关。胺碘酮所致甲状腺功能减退的严重程度可从轻微症状到严重黏液性水肿不等；皮肤、头发和指甲尤其受影响。胺碘酮治疗继发临床甲状腺功能亢进的患者表现出甲状腺激素过量导致的高代谢状态的体征和症状。胺碘酮所致甲状腺功能减退用左甲状腺素治疗，甲状腺功能亢进用抗甲状腺药物治疗。胺碘酮可导致甲状腺功能障碍，这可能会产生严重后果。
