Guyétant S, Rousselet M C, Wion-Barbot N, Bigorgne J C, Victor J, Dupré F, Saint André J P
Services d'Anatomie Pathologique, CHU, Angers.
Ann Pathol. 1995;15(6):431-7.
Amiodarone is a widely-used anti-arythmic drug that induces an iodine overload and, in 1 to 23% of the patients, a thyrotoxicosis. In a few cases, the thyrotoxicosis may be refractory to conventional pharmacological therapy, thus leading to thyroidectomy. We report the thyroid gland pathology in 5 thyroidectomies that were performed for uncontrolled thyrotoxicosis, induced by amiodarone (4 cases) and by Colchimax, another iodine-rich drug (1 case). Two cases have been studied by electron microscopy. Pathologic findings were: [1] colloid transformation of the parenchyma, [2] areas of follicular disruption with numerous foamy macrophages in the colloid, [3] regenerative areas and [4] a moderate T lymphocytic infiltration. No lysosomal lamellar inclusion body was found by electron microscopy. These lesions may be rather specific of an iodine toxicity. The pathogeny is still misunderstood, and probably complex. It may essentially involve toxic mechanisms, as well as immunologic or allergic mechanisms.
胺碘酮是一种广泛使用的抗心律失常药物,可导致碘负荷过量,在1%至23%的患者中会引起甲状腺毒症。在少数情况下,甲状腺毒症可能对传统药物治疗无效,从而导致甲状腺切除术。我们报告了5例因胺碘酮(4例)和另一种富含碘的药物秋水仙酰胺(1例)引起的无法控制的甲状腺毒症而进行甲状腺切除术的甲状腺病理情况。对其中2例进行了电子显微镜研究。病理结果为:[1]实质胶体转化;[2]滤泡破裂区域,胶体中有大量泡沫巨噬细胞;[3]再生区域;[4]中等程度的T淋巴细胞浸润。电子显微镜检查未发现溶酶体层状包涵体。这些病变可能是碘毒性相当特异的表现。其发病机制仍未完全明了,可能很复杂。它可能主要涉及毒性机制以及免疫或过敏机制。