Wolff J
Laboratory of Biochemical Pharmacology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Pharmacol Rev. 1998 Mar;50(1):89-105.
Perchlorate competitively blocks iodide from entering the thyroid by an effect on the Na+/I- symporter thus preventing the further synthesis of thyroid hormone but has no effect on the iodination process itself. It is concentrated by thyroid tissue in a manner similar to iodide but is not significantly metabolized in the gland or peripherally. What is not settled is whether there are additional perchlorate effects on iodide transport. Perchlorate has a fast turnover in the body and requires frequent daily doses for therapy of thyrotoxicosis. Perchlorate appears to be substantially more effective against large iodide loads than the thionamides, and, with long-term iodide contamination, combined therapy of perchlorate (with < or = 1 g/day) and thionamides is recommended for the more severe cases of thyrotoxicosis that may result from excess iodide or iodide-generating organic compounds, as for example with amiodarone. After approximately 30 days, the perchlorate dosage can be tapered or stopped, continuing with thionamides alone. This markedly increases its safe use. Despite serious side effects during its early use, lower dosages and shorter treatment periods appear to have prevented such reactions in its recent reintroduction, mostly for amiodarone-induced thyroid dysfunction. Perchlorate can also protect against inhibition of thyroid function and the resulting hypothyroidism caused by excess iodide, presumably by reducing the formation of an iodinated inhibitor. The reduction of the iodide pool by perchlorate thus has dual effects--reduction of excess hormone synthesis and hyperthyroidism, on the one hand, and reduction of thyroid inhibitor synthesis and hypothyroidism on the other. Perchlorate remains very useful also as a single dose application in tests measuring the discharge of radioiodide accumulated in the thyroid as a result of many different disruptions in the further metabolism of iodide in the thyroid gland.
高氯酸盐通过影响钠/碘同向转运体竞争性地阻止碘进入甲状腺，从而防止甲状腺激素的进一步合成，但对碘化过程本身没有影响。它以类似于碘的方式被甲状腺组织摄取，但在甲状腺或外周组织中不会被显著代谢。目前尚未确定的是高氯酸盐对碘转运是否还有其他影响。高氯酸盐在体内代谢迅速，治疗甲状腺毒症需要每日频繁给药。高氯酸盐似乎对大量碘负荷的作用比对硫代酰胺类药物更有效，对于因过量碘或产碘有机化合物（如胺碘酮）导致的更严重甲状腺毒症病例，建议长期碘污染时联合使用高氯酸盐（≤1克/天）和硫代酰胺类药物。大约30天后，可以逐渐减少或停用高氯酸盐剂量，仅继续使用硫代酰胺类药物。这显著增加了其安全使用性。尽管在早期使用时有严重副作用，但较低剂量和较短治疗期似乎在最近重新使用时预防了此类反应，主要是针对胺碘酮引起的甲状腺功能障碍。高氯酸盐还可以预防因过量碘导致的甲状腺功能抑制及由此引起的甲状腺功能减退，可能是通过减少碘化抑制剂的形成。高氯酸盐使碘池减少因此具有双重作用——一方面减少过量激素合成和甲状腺功能亢进，另一方面减少甲状腺抑制剂合成和甲状腺功能减退。高氯酸盐作为单剂量应用在测量因甲状腺内碘进一步代谢的许多不同干扰而在甲状腺中积累的放射性碘排出的试验中仍然非常有用。
