Markou K, Georgopoulos N, Kyriazopoulou V, Vagenakis A G
Department of Medicine, University of Patras Medical School, Greece.
Thyroid. 2001 May;11(5):501-10. doi: 10.1089/105072501300176462.
Iodine is an essential element for thyroid hormone synthesis. The thyroid gland has the capacity and holds the machinery to handle the iodine efficiently when the availability of iodine becomes scarce, as well as when iodine is available in excessive quantities. The latter situation is handled by the thyroid by acutely inhibiting the organification of iodine, the so-called acute Wolff-Chaikoff effect, by a mechanism not well understood 52 years after the original description. It is proposed that iodopeptide(s) are formed that temporarily inhibit thyroid peroxidase (TPO) mRNA and protein synthesis and, therefore, thyroglobulin iodinations. The Wolff-Chaikoff effect is an effective means of rejecting the large quantities of iodide and therefore preventing the thyroid from synthesizing large quantities of thyroid hormones. The acute Wolff-Chaikoff effect lasts for few a days and then, through the so-called "escape" phenomenon, the organification of intrathyroidal iodide resumes and the normal synthesis of thyroxine (T4) and triiodothyronine (T3) returns. This is achieved by decreasing the intrathyroidal inorganic iodine concentration by down regulation of the sodium iodine symporter (NIS) and therefore permits the TPO-H202 system to resume normal activity. However, in a few apparently normal individuals, in newborns and fetuses, in some patients with chronic systemic diseases, euthyroid patients with autoimmune thyroiditis, and Graves' disease patients previously treated with radioimmunoassay (RAI), surgery or antithyroid drugs, the escape from the inhibitory effect of large doses of iodides is not achieved and clinical or subclinical hypothyroidism ensues. Iodide-induced hypothyroidism has also been observed in patients with a history of postpartum thyroiditis, in euthyroid patients after a previous episode of subacute thyroiditis, and in patients treated with recombinant interferon-alpha who developed transient thyroid dysfunction during interferon-a treatment. The hypothyroidism is transient and thyroid function returns to normal in 2 to 3 weeks after iodide withdrawal, but transient T4 replacement therapy may be required in some patients. The patients who develop transient iodine-induced hypothyroidism must be followed long term thereafter because many will develop permanent primary hypothyroidism.
碘是甲状腺激素合成所必需的元素。甲状腺具备在碘供应稀缺以及碘过量时有效处理碘的能力和机制。后一种情况由甲状腺通过急性抑制碘的有机化来处理，即所谓的急性沃夫-柴可夫效应，自最初描述以来52年，其机制仍未完全明了。有人提出会形成碘肽，它会暂时抑制甲状腺过氧化物酶（TPO）的mRNA和蛋白质合成，进而抑制甲状腺球蛋白碘化。沃夫-柴可夫效应是排出大量碘化物、从而防止甲状腺合成大量甲状腺激素的有效手段。急性沃夫-柴可夫效应持续数天，然后通过所谓的“逃逸”现象，甲状腺内碘化物的有机化恢复，甲状腺素（T4）和三碘甲状腺原氨酸（T3）的正常合成恢复。这是通过下调钠碘同向转运体（NIS）来降低甲状腺内无机碘浓度实现的，从而使TPO-H2O2系统恢复正常活性。然而，在一些看似正常的个体、新生儿和胎儿、一些患有慢性全身性疾病的患者、患有自身免疫性甲状腺炎的甲状腺功能正常患者以及先前接受过放射免疫分析（RAI）、手术或抗甲状腺药物治疗的格雷夫斯病患者中，无法从大剂量碘化物的抑制作用中“逃逸”，继而出现临床或亚临床甲状腺功能减退。在有产后甲状腺炎病史的患者、先前有亚急性甲状腺炎发作史的甲状腺功能正常患者以及接受重组干扰素-α治疗且在干扰素-α治疗期间出现短暂甲状腺功能障碍的患者中也观察到碘化物诱发的甲状腺功能减退。甲状腺功能减退是短暂的，碘化物停用后2至3周甲状腺功能恢复正常，但部分患者可能需要短暂的T4替代治疗。此后，发生短暂碘诱发甲状腺功能减退的患者必须长期随访，因为许多人会发展为永久性原发性甲状腺功能减退。
