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胺碘酮相关性甲状腺毒症患者的处理方法。

Approach to the patient with amiodarone-induced thyrotoxicosis.

机构信息

Department of Endocrinology, University of Pisa, Ospedale Cisanello, Via Paradisa, 2, 56124 Pisa, Italy.

出版信息

J Clin Endocrinol Metab. 2010 Jun;95(6):2529-35. doi: 10.1210/jc.2010-0180.

DOI:10.1210/jc.2010-0180
PMID:20525904
Abstract

Amiodarone, a benzofuranic iodine-rich antiarrhythmic drug, causes thyroid dysfunction in 15-20% of cases. Although amiodarone-induced hypothyroidism poses no particular problem, amiodarone-induced thyrotoxicosis (AIT) is a diagnostic and therapeutic challenge. There are two main forms of AIT: type 1, a form of iodine-induced hyperthyroidism, and type 2, a drug-induced destructive thyroiditis. However, mixed/indefinite forms exist that may be caused by both pathogenic mechanisms. Type 1 AIT usually occurs in abnormal thyroid glands, whereas type 2 AIT develops in apparently normal thyroid glands (or small goiters). Diagnosis of thyrotoxicosis is easy, based on the finding of increased free thyroid hormone concentrations and suppressed TSH levels. Thyroid radioactive iodine (RAI) uptake values are usually very low/suppressed in type 2 AIT, most commonly low or low-normal, but sometimes normal or increased in type 1 AIT despite the iodine load. Color flow Doppler sonography shows absent hypervascularity in type 2 and increased vascularity in type 1 AIT. Mixed/indefinite forms may have features of both AIT types. Thionamides represent the first-line treatment for type 1 AIT, but the iodine-replete gland is not very responsive; potassium perchlorate, by inhibiting thyroid iodine uptake, may increase the response to thionamides. Type 2 AIT is best treated by oral glucocorticoids. The response very much depends on the thyroid volume and the severity of thyrotoxicosis. Mixed/indefinite forms may require a combination of thionamides, potassium perchlorate, and steroids. RAI is usually not feasible in AIT due to low RAI uptake values. Thyroidectomy represents a valid option in cases resistant to medical therapy.

摘要

胺碘酮是一种苯并呋喃类富碘抗心律失常药物,在 15-20%的病例中会引起甲状腺功能障碍。虽然胺碘酮引起的甲状腺功能减退症没有特别的问题,但胺碘酮引起的甲状腺功能亢进症(AIT)是一个诊断和治疗的挑战。AIT 有两种主要形式:1 型,碘诱导的甲状腺功能亢进症形式,和 2 型,药物诱导的破坏性甲状腺炎。然而,存在混合/不确定的形式,可能由两种致病机制引起。1 型 AIT 通常发生在异常的甲状腺中,而 2 型 AIT 发生在明显正常的甲状腺中(或小甲状腺肿)。甲状腺功能亢进症的诊断很容易,基于发现游离甲状腺激素浓度增加和 TSH 水平抑制。2 型 AIT 的甲状腺放射性碘(RAI)摄取值通常非常低/受抑制,最常见的是低或低正常,但有时 1 型 AIT 中尽管存在碘负荷,仍正常或增加。彩色多普勒超声显示 2 型 AIT 中不存在高血管性,而 1 型 AIT 中增加了血管性。混合/不确定的形式可能具有两种 AIT 类型的特征。硫脲类药物是 1 型 AIT 的一线治疗药物,但碘充足的腺体反应不佳;高氯酸钾通过抑制甲状腺碘摄取,可能增加硫脲类药物的反应。2 型 AIT 最好通过口服糖皮质激素治疗。反应很大程度上取决于甲状腺体积和甲状腺功能亢进症的严重程度。混合/不确定的形式可能需要硫脲类药物、高氯酸钾和类固醇的联合治疗。由于 RAI 摄取值低,RAI 通常不适用于 AIT。甲状腺切除术是对药物治疗有抗性的病例的有效选择。

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