Tereshchenko I V, Tsepelev V V
Klin Med (Mosk). 1995;73(1):22-4.
Thyroid function has been assessed in 56 patients with arrhythmic coronary heart disease (CHD) prior to and in the course of cordaron treatment. TTH level made up initially 1.39 +/- 0.27 IU/ml which was normal. T3 blood concentration was low--1.28 +/- 0.06 nmol/l; T4 was normal--128.26 +/- 4.9 nmol/l. It is stated that CHD patients with arrhythmia develop latent hypothyrosis of T3-low-syndrome type. Arrhythmia treatment with cordaron aggravates T3 deficiency as the drug inhibits T4 conversion into T3 in peripheral tissues. It also causes toxic damage to thyroid parenchyma resulting in higher TH levels in the blood. CHD patients receiving long-term cordaron (1 to 8 years) have clinical picture of manifest hypothyrosis. Cordaron molecules includes iodine macro-doses, but these fail to initiate autoimmune thyroid process.
对56例心律失常型冠心病(CHD)患者在使用胺碘酮治疗前及治疗过程中进行了甲状腺功能评估。促甲状腺激素(TSH)水平初始为1.39±0.27IU/ml,属正常范围。血三碘甲状腺原氨酸(T3)浓度较低,为1.28±0.06nmol/l;甲状腺素(T4)正常,为128.26±4.9nmol/l。研究表明,心律失常型冠心病患者会出现T3降低综合征型的潜在甲状腺功能减退。用胺碘酮治疗心律失常会加重T3缺乏,因为该药物会抑制外周组织中T4向T3的转化。它还会对甲状腺实质造成毒性损害,导致血液中甲状腺激素(TH)水平升高。长期(1至8年)使用胺碘酮的冠心病患者会出现明显甲状腺功能减退的临床表现。胺碘酮分子含有大剂量碘,但这些碘并不会引发自身免疫性甲状腺疾病。