Trifănescu Raluca, Fica Simona, Barbu Carmen, Vârtej Ioana, Ursu H, Bunghez Rodica, Coculescu M
C. I. Parhon" Institute of Endocrinology, Bucharest, Romania.
Rom J Intern Med. 2004;42(3):595-605.
Amiodarone via iodine excess can determine thyroid dysfunction.
to assess thyroid dysfunction in patients treated with amiodarone, according to previous daily iodine intake.
63 patients treated with amiodarone were assessed. 11 of 63 were resident in a moderate iodine deficient area. Thyroid stimulating hormone (TSH), free and total thyroxine (T4) and total triiodothyronine (T3) were measured. Thyroid ultrasonography, color flow Doppler sonography (CFDS), radioiodine uptake (RAIU) at 2 and 24 hours were also performed.
Amiodarone-induced thyrotoxicosis developed in 31 patients (49.2%); 17 patients (27%) remained euthyroid. Patients from iodine deficient areas developed more frequent hyperthyroidism (91% vs. 40.4%), at significant lower cumulative doses of amiodarone, and never hypothyroidism. Overt hyperthyroidism prevails (29/31 patients). Frequency of amiodarone-induced thyrotoxicosis type I was 19% (12/63), type II 12.7% (8/63), and of mixed forms 17.5% (11/63), without significant differences between the two geographical areas. There are no peculiar features of amiodarone-induced thyrotoxicosis versus common hyperthyroidism, but there is a tendency at recurrence of tachyarrhythmias at lower levels of T3 than in common hyperthyroidism. Amiodarone-induced hypothyroidism developed in 15 patients (23.8%) and none was from iodine deficient areas, but almost half show high levels of antithyroid peroxidase antibodies (ATPO). Subclinical hypothyroidism prevails (11/15 patients).
a predictor for amiodarone-induced thyroid dysfunction is iodine deficiency in nutrition.
胺碘酮通过碘过量可导致甲状腺功能障碍。
根据既往每日碘摄入量评估接受胺碘酮治疗患者的甲状腺功能障碍情况。
对63例接受胺碘酮治疗的患者进行评估。63例中有11例居住在碘中度缺乏地区。检测促甲状腺激素（TSH）、游离甲状腺素和总甲状腺素（T4）以及总三碘甲状腺原氨酸（T3）。还进行了甲状腺超声检查、彩色多普勒超声检查（CFDS）、2小时和24小时放射性碘摄取（RAIU）检查。
31例患者（49.2%）发生胺碘酮所致甲状腺毒症；17例患者（27%）甲状腺功能正常。来自碘缺乏地区的患者甲状腺功能亢进更为常见（91%对40.4%），胺碘酮累积剂量显著更低，且从未发生甲状腺功能减退。显性甲状腺功能亢进占主导（29/31例患者）。I型胺碘酮所致甲状腺毒症的发生率为19%（12/63），II型为12.7%（8/63），混合型为17.5%（11/63），两个地理区域之间无显著差异。胺碘酮所致甲状腺毒症与普通甲状腺功能亢进相比无特殊特征，但与普通甲状腺功能亢进相比，在T3水平较低时快速心律失常复发有一定倾向。15例患者（23.8%）发生胺碘酮所致甲状腺功能减退，且无一例来自碘缺乏地区，但几乎一半患者抗甲状腺过氧化物酶抗体（ATPO）水平较高。亚临床甲状腺功能减退占主导（11/15例患者）。
营养性碘缺乏是胺碘酮所致甲状腺功能障碍的一个预测因素。
