Roti E, Minelli R, Gardini E, Bianconi L, Gavaruzzi G, Ugolotti G, Neri T M, Braverman L E
Centro per lo Studio, Prevenzione, Diagnosi e Cura delle Tireopatie, Universitá di Parma, Italy.
J Clin Endocrinol Metab. 1992 Nov;75(5):1273-7. doi: 10.1210/jcem.75.5.1331165.
Amiodarone-induced thyrotoxicosis (AIT) occurs most frequently in patients with underlying thyroid disease and is generally believed to be due to the iodine contamination of amiodarone and iodine released by the metabolism of the drug. We and others have suggested that the thyrotoxicosis may also be secondary to amiodarone-induced thyroiditis. To further determine the etiology of AIT, we administered large doses of iodides [10 drops saturated solution of potassium iodide (SSKI) daily] to 10 euthyroid patients long after an episode of AIT believed to be due at least in part to amiodarone-induced thyroiditis. Six of these 10 patients had an abnormal iodide-perchlorate discharge test before SSKI administration, indicating a subtle defect in the thyroidal organification of iodide. During SSKI administration, 6 patients developed marked iodine-induced basal and/or TRH-stimulated serum TSH elevations, 2 had suppressed basal and TRH-stimulated TSH values, and 2 had normal TSH responses compared to SSKI-treated euthyroid subjects with no history of amiodarone ingestion or thyroid disease. Serum T4 and T3 concentrations remained normal and unchanged during SSKI administration in both the AIT patients and control subjects. These results strongly suggest that excess iodine may not be the cause of the hyperthyroidism associated with amiodarone therapy, especially in those patients with probable amiodarone-induced thyroiditis. Furthermore, like patients with a previous history of subacute thyroiditis and postpartum thyroiditis, the present results suggest that some patients with a previous history of AIT may be at risk to develop hypothyroidism when given excess iodine.
胺碘酮所致甲状腺毒症（AIT）最常发生于有潜在甲状腺疾病的患者，一般认为是由于胺碘酮的碘污染以及该药物代谢释放的碘所致。我们和其他人曾提出，甲状腺毒症也可能继发于胺碘酮所致的甲状腺炎。为了进一步确定AIT的病因，我们在一次被认为至少部分归因于胺碘酮所致甲状腺炎的AIT发作很久之后，给10名甲状腺功能正常的患者大剂量服用碘化物[每日10滴碘化钾饱和溶液（SSKI）]。这10名患者中有6名在服用SSKI之前碘 - 过氯酸盐释放试验异常，表明甲状腺对碘的有机化存在细微缺陷。在服用SSKI期间，6名患者出现明显的碘诱导的基础和/或促甲状腺激素释放激素（TRH）刺激的血清促甲状腺激素（TSH）升高，2名患者基础和TRH刺激的TSH值被抑制，与未服用胺碘酮或无甲状腺疾病病史的接受SSKI治疗的甲状腺功能正常的受试者相比，另外2名患者的TSH反应正常。在AIT患者和对照受试者服用SSKI期间，血清T4和T3浓度保持正常且未发生变化。这些结果强烈提示，碘过量可能不是胺碘酮治疗相关甲状腺功能亢进的原因，尤其是在那些可能患有胺碘酮所致甲状腺炎的患者中。此外，与有亚急性甲状腺炎和产后甲状腺炎既往史的患者一样，目前的结果提示，一些有AIT既往史的患者在给予过量碘时可能有发生甲状腺功能减退的风险。
