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高碘甲肿及碘致甲亢机制新假说:脱碘酶障碍学说 被引量:8

A New Hypothesis about Iodine-induced Goiter and Hyperthyroidism:Deiodinase Activity Decrease Theory
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摘要 基于近年对碘甲腺氨酸脱碘酶的研究进展所获得的大量新知识和高碘甲肿的流行病学、临床和组织学证据 ,提出的高碘或补碘甲肿和甲亢机制新假说 :硒营养缺乏或相对缺乏所造成的脱碘酶活性下降是高碘甲肿和甲亢形成的主要原因 ,从摄入高碘到甲肿、甲亢形成 ,可分为三个阶段 :T4潴留、T4入血增加以代偿T3的不足以及T3毒症发生 ,甲亢形成 ,因此 ,该假说可称为“脱碘酶障碍学说”。 WT5”BZ]Based on a large amount of new knowledge about thyroid hormone metabolism,especially iodothyronine deiodinase construction and regulation mechanism,and epidemiological and clinical and histomorphological evidences,we proposed that the mechanism of iodine induced goiter and hyperthyroidism is related with iodothyronine deiodinase inactivation by selenium deficiency.From taking iodine to iodine induced goiter resulted and to hyperyoridism,there are three phases:1)TH detained in thyroid, 2)incerase of blood T4 compensating for low T3,3) “T3 toxemia” takes place and hyperthyroidism is formed,It can be called “deiodinase activity decrease theory”.
出处 《华西医学》 CAS 2000年第4期405-408,共4页 West China Medical Journal
关键词 高碘性甲状腺肿 机制 碘甲腺氨酸脱碘酶 硒不足 Iodine-induced goiter and hyperthroidism Mechanism Iodothyronine deiodinase Selenium deficiency
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