Olguín R, Nungaray L, Reyes P A, Molina L, Cardoso G, Boyer J L, Baltazares E, Posadas C
Departamento de Endocrinología e Inmunología, Instituto Nacional de Cardiología Ignacio Chávez, México, D.F.
Arch Inst Cardiol Mex. 1988 May-Jun;58(3):197-202.
Spontaneous autoimmune thyroid disease (SATD) shows familial aggregation. Some patients receiving amiodarone treatment have been found to develop thyroid dysfunction. Previously, we reported genetic predisposition among this group of patients, now we inform a prospective study which includes the search for autoantibodies and family history to identify risk factors in amiodarone treated patients, 40 of them with amiodarone related thyroid disfunction, and 100 without it; for comparison, 30 patients with SATD and a control group of healthy subjects were also studied. We looked for the presence of autoantibodies against thyroglobulin, smooth muscle, gastric mucosa, myocardium, mitochondria, epithelial intercellular substance, and basal membrane as well as antinuclear antibodies and rheumatoid factors; in addition the history of thyroid disease in first degree relatives was investigated. Organ-specific antibodies anti-thyroglobulin, gastric mucosa and myocardium were found with increased frequency in the three groups of patients compared with controls (p less than 0.05). The frequency of antihydroglobulin antibodies was similar in patients receiving amiodarone with or without thyroid dysfunction. Prognostic stratification revealed that this finding is independent of sex, age, dosage or duration of treatment. A family history of thyroid dysfunction was found more frequently among patients with SATD and amiodarone related dysthyroidism in comparison with patients receiving amiodarone without altered thyroid function (p less than 0.005). The appearance of clinical thyroid disease depends on individual genetical predisposition. In patients with a positive family history, the risk of developing clinical, thyroid disease is 7.6 when treated with amiodarone.
自身免疫性甲状腺疾病（SATD）具有家族聚集性。已发现一些接受胺碘酮治疗的患者会出现甲状腺功能障碍。此前，我们报道了这组患者的遗传易感性，现在我们报告一项前瞻性研究，该研究包括寻找自身抗体和家族史，以确定胺碘酮治疗患者的风险因素，其中40例有胺碘酮相关甲状腺功能障碍，100例无此情况；作为对照，还研究了30例SATD患者和一组健康受试者。我们寻找抗甲状腺球蛋白、平滑肌、胃黏膜、心肌、线粒体、上皮细胞间质和基底膜的自身抗体以及抗核抗体和类风湿因子；此外，还调查了一级亲属的甲状腺疾病史。与对照组相比，三组患者中抗甲状腺球蛋白、胃黏膜和心肌的器官特异性抗体出现频率增加（p小于0.05）。接受胺碘酮治疗的患者中，无论有无甲状腺功能障碍，抗甲状腺球蛋白抗体的频率相似。预后分层显示，这一发现与性别、年龄、治疗剂量或疗程无关。与甲状腺功能未改变的胺碘酮治疗患者相比，SATD患者和胺碘酮相关甲状腺功能减退患者中甲状腺功能障碍家族史更为常见（p小于0.005）。临床甲状腺疾病的出现取决于个体的遗传易感性。有家族史阳性的患者，接受胺碘酮治疗时发生临床甲状腺疾病的风险为7.6。
