Sauer-Schulz Anja, Müssig Karsten, Kurth Ralf, Fend Falko, Teichmann Reinhard, Schnauder Günter
Abteilung Endokrinologie, Diabetologie, Nephrologie, Angiologie und Klinische Chemie, Medizinische Klinik, Universitätsklinikum Tübingen, Germany.
Dtsch Med Wochenschr. 2010 Sep;135(37):1798. doi: 10.1055/s-0030-1247616. Epub 2010 Sep 7.
Amiodarone-induced thyrotoxicosis (AIT) should be included in differential diagnoses of thyrotoxicosis in presence of a suggestive drug history. Adequate treatment requires knowledge of the underlying type of AIT.
A 68-year-old male was admitted because of progressive dyspnea and tachyarrhythmia. Symptoms of thyrotoxicosis, including agitation, sleep disturbances, and palpitations, had developed 14 days earlier and the patient's condition had worsened despite initiation of antithyroid treatment.
Laboratory values showed manifest hyperthyroidism. Thyroid autoantibodies proved negative. C-reactive protein and erythrocyte sedimentation rate were slightly increased. Ultrasound revealed a moderately increased thyroid without nodules and with normal perfusion.
DIAGNOSIS, TREATMENT AND COURSE: Suspecting AIT type 2, treatment with high-dosed glucocorticoids and antithyroid drugs was initiated. Under additional beta-blockade and heart insufficiency therapy the patient's condition significantly improved. After achievement of euthyreosis, thyroidectomy was performed.
In patients with preexisting thyroid disorders, such as Grave's disease or functional autonomy in multinodular goiter, the high iodine content of amiodarone may cause iodine-induced thyrotoxicosis, also known as AIT type I. Treatment comprises high-dosed antithyroid drugs. In contrast, in patients suffering from AIT type II, toxic effects of amiodarone on a previously healthy thyroid result in destructive thyroiditis. Treatment consists of glucocorticoids in a dosage of 1 mg per kg body weight per day. Antithyroid treatment could be added in cases of equivocal diagnosis. In most cases, thyroidectomy is indicated. Whether amiodarone can be discontinued, should be discussed with the responsible cardiologist. Due to the long half-life time of amiodarone, treatment discontinuation will not result in an immediate improvement.
在有提示性用药史的情况下，胺碘酮诱发的甲状腺毒症（AIT）应纳入甲状腺毒症的鉴别诊断中。充分的治疗需要了解AIT的潜在类型。
一名68岁男性因进行性呼吸困难和快速性心律失常入院。甲状腺毒症症状，包括烦躁、睡眠障碍和心悸，在14天前出现，尽管开始了抗甲状腺治疗，但患者病情仍恶化。
实验室检查结果显示明显的甲状腺功能亢进。甲状腺自身抗体检测为阴性。C反应蛋白和红细胞沉降率略有升高。超声检查显示甲状腺中度增大，无结节，血流灌注正常。
诊断、治疗及病程：怀疑为2型AIT，开始使用大剂量糖皮质激素和抗甲状腺药物治疗。在额外的β受体阻滞剂和心力衰竭治疗下，患者病情明显改善。甲状腺功能正常后，进行了甲状腺切除术。
在患有既往甲状腺疾病的患者中，如格雷夫斯病或多结节性甲状腺肿的功能自主性，胺碘酮的高碘含量可能导致碘诱发的甲状腺毒症，也称为1型AIT。治疗包括大剂量抗甲状腺药物。相比之下，在患有2型AIT的患者中，胺碘酮对先前健康的甲状腺的毒性作用导致破坏性甲状腺炎。治疗包括每天每公斤体重1毫克的糖皮质激素。在诊断不明确的情况下可加用抗甲状腺治疗。在大多数情况下，需要进行甲状腺切除术。是否停用胺碘酮，应与负责的心脏病专家讨论。由于胺碘酮的半衰期长，停药不会立即改善病情。
