Department of Pharmacy, National Cerebral and Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka, Japan.
Division of Clinical Drug Informatics, Kindai University School of Pharmacy, 3-4-1, Kowakae, Higashi-osaka, Osaka, 577-8502, Japan.
Clin Drug Investig. 2018 Jan;38(1):39-48. doi: 10.1007/s40261-017-0582-4.
This retrospective cohort study was performed to examine the association between serum amiodarone (AMD) and N-desethylamiodarone (DEA) concentrations and the development of thyroid dysfunction.
Patients treated with AMD from January 2012 to April 2016 were identified from the computerized hospital information system database at the National Cerebral and Cardiovascular Center. Only patients whose serum AMD and DEA concentrations had been determined at least once were included in the study.
A total of 377 patients were enrolled. Consequently, 54 (14.3%) and 60 (15.9%) patients who developed AMD-induced thyrotoxicosis and hypothyroidism were included. The mean DEA/AMD ratio during the pre-index period in the thyrotoxicosis group (0.86 ± 0.24) was significantly higher than in the hypothyroidism (0.68 ± 0.27) and euthyroidism (0.78 ± 0.30; p < 0.0001) groups. In addition, the mean DEA/AMD ratio during the post-index period in the thyrotoxicosis group (1.05 ± 0.40) was significantly higher than in the hypothyroidism (0.81 ± 0.24) and euthyroidism (0.88 ± 0.22; p < 0.0001) groups. A persistently higher DEA/AMD ratio was observed throughout the study period in the thyrotoxicosis group. In addition, good correlations between the DEA/AMD ratio and the levels of free thyroxine, free triiodothyronine levels, and log (thyroid-stimulating hormone) were observed in the thyrotoxicosis and euthyroidism groups.
Patients with AMD-induced thyrotoxicosis had an increased DEA/AMD ratio and patients with AMD-induced hypothyroidism had a decreased DEA/AMD ratio before the development of thyroid dysfunction. The DEA/AMD ratio may be a predictive marker for AMD-induced thyroid dysfunction.
本回顾性队列研究旨在探讨血清胺碘酮(AMD)和去乙基胺碘酮(DEA)浓度与甲状腺功能障碍发展之间的关系。
从国立循环器病研究中心的计算机医院信息系统数据库中,确定了 2012 年 1 月至 2016 年 4 月期间接受 AMD 治疗的患者。仅纳入了至少有一次血清 AMD 和 DEA 浓度检测结果的患者。
共纳入 377 例患者。因此,包括了 54 例(14.3%)和 60 例(15.9%)发生 AMD 诱导性甲状腺毒症和甲状腺功能减退的患者。甲状腺毒症组的索引前时期平均 DEA/AMD 比值(0.86±0.24)显著高于甲状腺功能减退组(0.68±0.27)和甲状腺功能正常组(0.78±0.30;p<0.0001)。此外,甲状腺毒症组索引后时期的平均 DEA/AMD 比值(1.05±0.40)显著高于甲状腺功能减退组(0.81±0.24)和甲状腺功能正常组(0.88±0.22;p<0.0001)。甲状腺毒症组在整个研究期间持续观察到更高的 DEA/AMD 比值。此外,在甲状腺毒症和甲状腺功能正常组中,DE A/AMD 比值与游离甲状腺素、游离三碘甲状腺原氨酸水平和 log(促甲状腺激素)水平之间存在良好的相关性。
在发生甲状腺功能障碍之前,AMD 诱导性甲状腺毒症患者的 DEA/AMD 比值升高,AMD 诱导性甲状腺功能减退患者的 DEA/AMD 比值降低。DEA/AMD 比值可能是 AMD 诱导性甲状腺功能障碍的预测标志物。