Maréchaud R
Service de médecine interne-endocrinologie, Centre hospitalier de La Milétrie, Poitiers.
Rev Prat. 1998 Nov 15;48(18):2018-22.
Many nonthyroidal illnesses are associated with reduced serum T3 and, in more severe conditions, T4 concentrations, without increased serum TSH secretion. The term euthyroid sick syndrome (ESS) identifies these low T3 and low T3-T4 states. It may be difficult to exclude central hypothyroidism in patients admitted to medical intensive care units. The mortality rate has been found to be inversely correlated with the serum T4 concentration. These abnormalities are a consequence of altered hepatic T3 production from T4 (through type 1 5'-desiodase inhibition), T4 serum protein binding and hepatic transport, and TSH secretion. Many mediators and drugs are involved in the pathogenesis of ESS. The role of cytokines has recently been emphasized. It remains unclear whether ESS represents a physiological protective mechanism, or a damaging maladaptative response and whether early thyroid hormones administration might improve survival in severe non thyroidal conditions.
许多非甲状腺疾病都与血清T3降低有关,在病情更严重时还会伴有T4浓度降低,而血清促甲状腺激素(TSH)分泌并未增加。“正常甲状腺病态综合征”(ESS)这一术语用于描述这些低T3和低T3-T4状态。对于入住医疗重症监护病房的患者,可能难以排除中枢性甲状腺功能减退。研究发现死亡率与血清T4浓度呈负相关。这些异常是由于肝脏从T4生成T3的过程发生改变(通过抑制1型5'-脱碘酶)、T4与血清蛋白的结合及肝脏转运以及TSH分泌异常所致。许多介质和药物都参与了ESS的发病机制。细胞因子的作用最近受到了重视。目前尚不清楚ESS是一种生理保护机制,还是一种有害的适应不良反应,以及早期给予甲状腺激素是否能改善严重非甲状腺疾病患者的生存率。