Segall-Blank M, Vagenakis A G, Shwachman H, Ingbar S H, Braverman L E
J Pediatr. 1981 Feb;98(2):218-22. doi: 10.1016/s0022-3476(81)80638-5.
In view of the reported enhanced sensitivity to iodide-induced hypothyroidism in patients with cystic fibrosis, studies were carried out to determine the possible mechanism of this abnormality. The intrathyroid organification of iodide, as assessed by the iodide-perchlorate discharge test, was normal in patients with cystic fibrosis, strongly suggesting that an organification defect was not present. The serum TSH response to TRH was not significantly different from the response in normal children and adolescents. Serum T4 concentration was normal whereas that of T3 was decreased in patients with cystic fibrosis, strongly suggesting decreased peripheral conversion of T4 to T3, as commonly occurs in nonthyroid illness. Our findings do not delineate the mechanism whereby patients with cystic fibrosis develop iodide-induced hypothyroidism.
鉴于有报道称囊性纤维化患者对碘诱发的甲状腺功能减退更为敏感，因此开展了研究以确定这种异常情况的可能机制。通过碘 - 过氯酸盐释放试验评估，囊性纤维化患者甲状腺内碘的有机化是正常的，这有力地表明不存在有机化缺陷。血清促甲状腺激素（TSH）对促甲状腺激素释放激素（TRH）的反应与正常儿童和青少年的反应无显著差异。囊性纤维化患者的血清甲状腺素（T4）浓度正常，而三碘甲状腺原氨酸（T3）浓度降低，这有力地表明T4向T3的外周转化减少，这在非甲状腺疾病中很常见。我们的研究结果并未阐明囊性纤维化患者发生碘诱发甲状腺功能减退的机制。
