Borowski G D, Garofano C D, Rose L I, Spielman S R, Rotmensch H R, Greenspan A M, Horowitz L N
Am J Med. 1985 Mar;78(3):443-50. doi: 10.1016/0002-9343(85)90336-5.
Both hyperthyroidism and hypothyroidism have been noted to occur in some patients treated with amiodarone for cardiac arrhythmias. To determine the frequency of the development of thyroidal abnormalities in patients receiving amiodarone, 45 euthyroid patients were prospectively evaluated. Serum samples were obtained for measurement of thyroxine, thyrotropin, triiodothyronine, and triiodothyronine resin uptake prior to initiation of amiodarone treatment and serially over a 12- to 27-month period during which amiodarone was administered. The patients were divided into four subgroups as follows: Group I (n = 22) had elevated thyroxine levels, Group IIA (n = 13) had normal thyroxine levels and normal thyrotropin levels, Group IIB (n = 7) had normal thyroxine levels and elevated thyrotropin levels, and Group III (n = 3) had subnormal thyroxine levels. Demographic factors (such as route of administration, cardiac diagnosis, sex of the patient, or indication for amiodarone therapy) and amiodarone levels had no significant effect on the thyroid hormone parameters. However, Group I patients were statistically older than the patients in the other groups. Linear regression analysis revealed a negative correlation for thyroxine levels and a positive correlation with thyrotropin levels with age for the whole group. The various groups were not statistically affected by duration of therapy, but a positive trend existed for increasing thyroxine levels. Although virtually all patients showed changes in their thyroid hormone levels, chemical hyperthyroidism (elevated thyroxine and triiodothyronine levels without symptoms) developed in only two patients (4 percent), and clinical hyperthyroidism (elevated thyroxine and triiodothyronine levels with symptoms) developed in no patients. Four patients (9 percent) became biochemically and clinically hypothyroid. Thus, amiodarone frequently influences thyroid hormonal parameters, but less commonly causes a change in actual thyroid function. However, hyperthyroidism and hypothyroidism do occur in a significant number of patients.
已注意到,在一些接受胺碘酮治疗心律失常的患者中,会同时出现甲状腺功能亢进和甲状腺功能减退。为了确定接受胺碘酮治疗的患者出现甲状腺异常的频率,对45名甲状腺功能正常的患者进行了前瞻性评估。在开始胺碘酮治疗前采集血清样本,以测定甲状腺素、促甲状腺激素、三碘甲状腺原氨酸和三碘甲状腺原氨酸树脂摄取率,并在给予胺碘酮的12至27个月期间连续采样。患者被分为以下四个亚组:第一组(n = 22)甲状腺素水平升高;第二A组(n = 13)甲状腺素水平正常且促甲状腺激素水平正常;第二B组(n = 7)甲状腺素水平正常但促甲状腺激素水平升高;第三组(n = 3)甲状腺素水平低于正常。人口统计学因素(如给药途径、心脏诊断、患者性别或胺碘酮治疗指征)和胺碘酮水平对甲状腺激素参数无显著影响。然而,第一组患者在统计学上比其他组的患者年龄更大。线性回归分析显示,全组甲状腺素水平与年龄呈负相关,促甲状腺激素水平与年龄呈正相关。各亚组未受到治疗持续时间的统计学影响,但甲状腺素水平呈上升趋势。尽管几乎所有患者的甲状腺激素水平都有变化,但仅两名患者(4%)出现了化学性甲状腺功能亢进(甲状腺素和三碘甲状腺原氨酸水平升高但无症状),无患者出现临床甲状腺功能亢进(甲状腺素和三碘甲状腺原氨酸水平升高且有症状)。四名患者(9%)出现了生化和临床甲状腺功能减退。因此,胺碘酮经常影响甲状腺激素参数,但较少导致实际甲状腺功能改变。然而,相当数量的患者确实会出现甲状腺功能亢进和甲状腺功能减退。