Woeber K A
Mount Zion Medical Center, University of California, San Francisco.
Med Clin North Am. 1991 Jan;75(1):169-78. doi: 10.1016/s0025-7125(16)30477-1.
Iodine is a requisite substrate for the synthesis of the thyroid hormones, the minimum daily requirement being about 50 micrograms. An autoregulatory mechanism within the thyroid serves as the first line of defense against fluctuations in the supply of iodine and also permits escape from the inhibition of hormone synthesis that a very large quantity of iodine induces (Wolff-Chaikoff effect and escape therefrom). Environmental iodine deficiency continues to be a significant public health problem worldwide, compounded in some geographic regions by the presence of other goitrogens in some staple foods. The pathologic consequences of severe iodine deficiency include endemic goiter, endemic cretinism, increased fetal and infant mortality, and an increased prevalence in the community of cognitive and neuromotor disabilities. The implementation of an iodization program prevents endemic cretinism and reduces the frequency of the other pathologic consequences of iodine deficiency. Iodine excess results principally from the use of iodine-containing medicinal preparations or radiographic contrast media. The pathologic consequences of iodine excess will ensue only when thyroid autoregulation is defective, in that escape from the Wolff-Chaikoff effect cannot occur, or when autoregulation is absent. Defective autoregulation characterizes the fetal and neonatal thyroid, Hashimoto's thyroiditis, radioiodine or surgically treated Graves' hyperthyroidism, the thyroid of patients with cystic fibrosis, and the thyroid that has been exposed to weak inhibitors of the organic binding of iodine. In these circumstances, the provision of excess iodine may lead to iodide goiter with or without hypothyroidism. Absent autoregulation may be a feature of longstanding multinodular goiter, and the provision of excess iodine in this circumstance may induce thyrotoxicosis (Jod-Basedow disease). The pathologic consequences of iodine excess will resolve when the source of iodine has been dissipated. In addition to its role in reversing iodine deficiency, iodine is used as adjunctive therapy for hyperthyroidism. By inhibiting the proteolytic release of iodothyronines from thyroglobulin, it induces a prompt slowing of thyroid hormone secretion. This effect is exploited in the treatment of thyrotoxic crisis or severe thyrocardiac disease. Iodine also reduces thyroid cellularity and vascularity and therefore is used in the preparation of the patient for thyroidectomy. Finally, by exploiting the failure of escape from the Wolff-Chaikoff effect, iodine may also be used in the early management of radioiodine-treated Graves' hyperthyroidism.
碘是合成甲状腺激素的必需底物，每日最低需求量约为50微克。甲状腺内的一种自动调节机制是抵御碘供应波动的第一道防线，并且还能避免因大量碘诱导的激素合成抑制（沃尔夫 - 柴可夫效应及其解除）。环境碘缺乏在全球范围内仍然是一个重大的公共卫生问题，在一些地理区域，某些主食中存在其他致甲状腺肿物质使情况更加复杂。严重碘缺乏的病理后果包括地方性甲状腺肿、地方性克汀病、胎儿和婴儿死亡率增加，以及社区中认知和神经运动障碍患病率上升。实施碘强化计划可预防地方性克汀病，并减少碘缺乏的其他病理后果的发生频率。碘过量主要源于含碘药物制剂或放射造影剂的使用。只有当甲状腺自动调节功能缺陷（即无法解除沃尔夫 - 柴可夫效应）或不存在自动调节功能时，碘过量才会产生病理后果。自动调节功能缺陷见于胎儿和新生儿甲状腺、桥本甲状腺炎、放射性碘治疗或手术治疗的格雷夫斯甲亢、囊性纤维化患者的甲状腺以及接触碘有机结合弱抑制剂的甲状腺。在这些情况下，摄入过量碘可能导致伴有或不伴有甲状腺功能减退的碘致甲状腺肿。自动调节功能缺失可能是长期多结节性甲状腺肿的一个特征，并在这种情况下摄入过量碘可能诱发甲状腺毒症（约德 - 巴塞多病）。当碘源消除后，碘过量的病理后果将会消失。除了在纠正碘缺乏方面的作用外，碘还用作甲亢的辅助治疗。通过抑制甲状腺球蛋白中碘甲状腺原氨酸的蛋白水解释放，它可使甲状腺激素分泌迅速减慢。这种作用被用于治疗甲状腺毒症危象或严重甲状腺心脏病。碘还可减少甲状腺细胞数量和血管分布，因此用于甲状腺切除术前患者的准备。最后，通过利用无法解除沃尔夫 - 柴可夫效应，碘也可用于放射性碘治疗的格雷夫斯甲亢的早期处理。
