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目前已公认肝硬化时可发现一定程度的潜在性甲状腺机能减退。可提出几种假设,其中包括某些蛋白载体[甲状腺素结合前白蛋白(TBPA)、甲状腺素结合白蛋白(TBA)]的减少(与肝脏合成蛋白障碍有关)和T_4周围性转化障碍伴有代谢性廓清的减少。最近Vagenakis的研究指出了营养缺乏对甲状腺素周围性代谢的影响:这种代谢偏离表现为3,5,3′-三碘甲状腺原氨酸(L-T_3)的合成减少,而使生物学上无活性的3,5′,3′-三碘甲状腺原氨酸或反T_3(T_3r)增高。这种情况可在正常饮食恢复后完全逆转,这点可进一步阐明肝硬化时确有甲状腺功能障碍。
It has been recognized that cirrhosis can be found to some extent potential hypothyroidism. Several hypotheses can be made, including the reduction of certain protein carriers [thyroid hormone prealbumin (TBPA), thyroxine-binding albumin (TBA)] (associated with liver synthetic protein disorders) and T4 peripheral metastasis Reduction of metabolic clearance. A recent study by Vagenakis points out the effect of nutritional deficits on thyroid hormone metabotropic metabolism: this metabolic bias shows a decrease in the synthesis of 3,5,3’-triiodothyronine (L-T_3) Inactive 3,5 ’, 3’-triiodothyronine or anti-T_3 (T_3r) increased. This situation can be reversed completely after the normal diet, which further clarifies that cirrhosis does have thyroid dysfunction.