Beck-Peccoz P, Volpi A, Maggioni A P, Cattaneo M G, Piscitelli G, Giani P, Landolina M, Tognoni G, Faglia G
Horm Metab Res. 1986 Jun;18(6):411-4. doi: 10.1055/s-2007-1012329.
The effects of chronic amiodarone treatment on several thyroid and cardiac function parameters were studied in 50 euthyroid patients with refractory ventricular arrhythmias, divided in responders and nonresponders according to their sensitivity to the antiarrhythmic action of the drug. No differences in the severity of cardiac disease and blood amiodarone concentrations were found in the two groups. Amiodarone induced a significant inhibition of peripheral T4 monodeiodination, more pronounced in responders compared to nonresponders. On the contrary, only in responsive patients, elevated basal and TRH-stimulated TSH levels were observed (despite serum T3 levels were not different from those in nonresponders) and the indirect indices of cardiac performance, particularly the systolic time intervals, fell in a range usually observed in the hypothyroid states. These findings suggest that amiodarone, besides the well-known inhibition of T4 to T3 conversion, also induces a partial resistance to the thyroid hormones, which is probably involved in the therapeutical effectiveness of the drug.
在50例甲状腺功能正常的难治性室性心律失常患者中，研究了慢性胺碘酮治疗对若干甲状腺和心脏功能参数的影响。根据患者对该药抗心律失常作用的敏感性，将其分为反应者和无反应者。两组在心脏病严重程度和血液胺碘酮浓度方面未发现差异。胺碘酮可显著抑制外周T4单脱碘作用，反应者比无反应者更明显。相反，仅在有反应的患者中，观察到基础和促甲状腺激素释放激素（TRH）刺激后的促甲状腺激素（TSH）水平升高（尽管血清T3水平与无反应者无差异），且心脏功能的间接指标，尤其是收缩时间间期，降至甲状腺功能减退状态通常观察到的范围内。这些发现表明，胺碘酮除了众所周知的抑制T4向T3转化外，还诱导了对甲状腺激素的部分抵抗，这可能与该药的治疗效果有关。
