Weaver D K, Nishiyama R H, Batsakis J G
Ann Clin Lab Sci. 1976 Nov-Dec;6(6):545-50.
Although iodine prevents goiter, enlarged thyroid glands continue to be detected in subjects, especially children, in spite of adequate iodine ingestion. Iodine may cause goiter in susceptible individuals by inhibiting the organic binding of iodine as is seen in adult asthmatics, neonates born of iodine ingesting mothers and in subjects residing along the littoral of Japan. Myxedema, especially in treated Graves' disease and Hashimoto's disease, may also be precipitated by iodine. On the other hand, iodine given to euthyroid subjects in areas of endemic goiter and to subjects with nontoxic nodular goiter may induce thyrotoxicosis by disclosing diffuse autonomously functioning thyroid tissue. An indirect adverse effect of iodine upon the thyroid gland may be manifested by lymphocyte glandular infiltrates and chronic thyroiditis which were sparse or absent in thyroid glands removed from subjects living in iodine deficient areas before iodine prophylaxis and therapy. Not only has the incidence of thyroiditis increased, but the histologic and clinical distinctions between treated Graves' disease and chronic thyroiditis have become indistinct. Experimentally, chronic thyroiditis has been produced in animals following large doses of iodine. Accumulated evidence supports the concept that iodine contributes to the genesis of chronic thyroiditis.
尽管碘可预防甲状腺肿，但即便摄入了充足的碘，仍可在一些人群尤其是儿童中检测到甲状腺肿大。碘可能会在易感个体中引发甲状腺肿，比如成年哮喘患者、母亲摄入碘的新生儿以及居住在日本沿海地区的人群，这是由于碘抑制了碘的有机结合。黏液性水肿，特别是在接受治疗的格雷夫斯病和桥本氏病患者中，也可能由碘诱发。另一方面，在地方性甲状腺肿地区给予甲状腺功能正常的受试者以及患有非毒性结节性甲状腺肿的受试者碘时，可能会因暴露弥漫性自主功能性甲状腺组织而诱发甲状腺毒症。碘对甲状腺的间接不良影响可能表现为淋巴细胞性腺体浸润和慢性甲状腺炎，在碘预防和治疗之前，从生活在碘缺乏地区的受试者切除的甲状腺中，这些情况很少见或不存在。不仅甲状腺炎的发病率增加了，而且接受治疗的格雷夫斯病和慢性甲状腺炎之间的组织学和临床区别也变得不明显了。在实验中，给动物大剂量碘后会引发慢性甲状腺炎。越来越多的证据支持碘促成慢性甲状腺炎发生的观点。
