Reith P E, Granner D K
Arch Intern Med. 1985 Feb;145(2):355-6.
In a 63-year-old woman with a multinodular goiter who was receiving suppressive therapy with levothyroxine sodium, iodine-induced thyrotoxicosis developed after povidone-iodine was applied to the surface of a granulating hip wound. Signs and symptoms of apathetic thyrotoxicosis developed on two occasions, once within a week after exposure of the wound to povidone-iodine soaks and again following repeated Hubbard tank debridement with added povidone-iodine. Iodine-induced thyrotoxicosis was confirmed by markedly elevated serum thyroxine and serum and urine iodine levels. On eliminating the sources of exogenous iodine and inhibiting thyroxine biosynthesis with propylthiouracil, the process was gradually controlled. A year later the patient was taking no medication and was clinically and chemically euthyroid. Apparently, iodine-induced thyrotoxicosis can result from passive diffusion of iodine into autonomous thyroid tissue. Iodine-containing preparations given to patients with multinodular goiters may result in thyrotoxicosis even if thyrotropin is suppressed with exogenous thyroxine.
一名63岁患有多结节性甲状腺肿的女性正在接受左甲状腺素钠抑制治疗，在聚维酮碘应用于肉芽形成的髋部伤口表面后发生了碘致甲状腺毒症。淡漠型甲状腺毒症的体征和症状出现了两次，一次是在伤口接触聚维酮碘浸泡液一周内，另一次是在使用添加了聚维酮碘的哈伯德槽反复清创后。血清甲状腺素以及血清和尿碘水平显著升高证实了碘致甲状腺毒症。在消除外源性碘来源并用丙硫氧嘧啶抑制甲状腺素生物合成后，病情逐渐得到控制。一年后，患者未服用任何药物，临床和化学检查均显示甲状腺功能正常。显然，碘致甲状腺毒症可能是由于碘被动扩散进入自主性甲状腺组织所致。即使使用外源性甲状腺素抑制促甲状腺素，给予多结节性甲状腺肿患者含碘制剂仍可能导致甲状腺毒症。
