International Council for the Control of Iodine Deficiency Disorders (ICCIDD), CH-4500 Solothurn, Switzerland.
Best Pract Res Clin Endocrinol Metab. 2010 Feb;24(1):107-15. doi: 10.1016/j.beem.2009.08.010.
Several mechanisms are involved in the maintenance of normal thyroid hormone secretion, even when iodine intake exceeds physiologic needs by a factor of 100. The sodium-iodide symporter system contributes most to this stability. Faced with an iodine excess, it throttles the transport of iodide into the thyroid cells, the rate-limiting step of hormone synthesis. Even before the iodine symporter reacts, a sudden iodine overload paradoxically blocks the second step of hormone synthesis, the organification of iodide. This so-called Wolff-Chaikoff effect requires a high (>or=10(-3) molar) intracellular concentration of iodide. The block does not last long, because after a while the sodium-iodide symporter shuts down; this allows intracellular iodide to drop below 10(-3) molar and the near-normal secretion to resume. In some susceptible individuals (e.g., after radio-iodine treatment of Graves' disease or in autoimmune thyroiditis), the sodium-iodide symporter fails to shut down, the intracellular concentration of iodide remains high and chronic hypothyroidism ensues. To complicate matters, iodine excess may also cause hyperthyroidism. The current explanation is that this happens in persons with goitres, for example, after long-standing iodine deficiency. These goitres may contain nodules carrying a somatic mutation that confers a 'constitutive' activation of the TSH receptor. Being no more under pituitary control, these nodules overproduce thyroid hormone and cause iodine-induced hyperthyroidism, when they are presented with sufficient iodine. These autonomous nodules gradually disappear from the population after iodine deficiency has been properly corrected. More recent studies suggest that chronic high iodine intake furthers classical thyroid autoimmunity (hypothyroidism and thyroiditis) and that iodine-induced hyperthyroidism may also have an autoimmune pathogenesis.
几种机制参与维持正常的甲状腺激素分泌，即使碘的摄入量超过生理需求的 100 倍。钠碘转运体系统对此稳定性的贡献最大。面对碘过量，它会限制碘进入甲状腺细胞的转运，这是激素合成的限速步骤。甚至在碘转运体反应之前，突然的碘过载会反常地阻断激素合成的第二步，即碘的有机化。这种所谓的 Wolff-Chaikoff 效应需要高（>或=10(-3) 摩尔）细胞内碘浓度。该阻断不会持续很长时间，因为过一段时间后，钠碘转运体就会关闭；这使得细胞内碘浓度降至 10(-3) 摩尔以下，正常的分泌功能得以恢复。在一些易感个体中（例如，在 Graves 病的放射性碘治疗后或自身免疫性甲状腺炎中），钠碘转运体无法关闭，细胞内碘浓度仍然很高，随后会发生慢性甲状腺功能减退。使情况变得复杂的是，碘过量也可能导致甲亢。目前的解释是，这种情况发生在甲状腺肿患者中，例如，在长期碘缺乏后。这些甲状腺肿可能含有携带体细胞突变的结节，该突变赋予 TSH 受体“组成型”激活。这些结节不再受垂体控制，因此当它们接触到足够的碘时，会过度产生甲状腺激素并导致碘诱导的甲亢。在碘缺乏得到适当纠正后，这些自主结节会逐渐从人群中消失。最近的研究表明，慢性高碘摄入会进一步促进经典的甲状腺自身免疫（甲状腺功能减退和甲状腺炎），而碘诱导的甲亢也可能具有自身免疫发病机制。
