病态甲状腺综合征的分子发病机制研究进展

摘要

病态甲状腺综合征(ESS)不但在危重患者中常被检测到,而且ESS的出现常常提示危重患者的预后更差.近年来,临床研究显示ESS与危重患者病程中的心源性猝死风险相关.ESS的分子发病机制研究提示,ESS的发生既与细胞能量代谢及脱碘酶功能异常有关,也与甲状腺结合、转运蛋白异常有关.并通过调控基因表达实现机体在危重症状态下各器官组织的分子水平的调控和反馈.ESS可能不是单纯的机体代偿,而是一个需要进行干预的病理生理过程.%Euthyroid sick syndrome(ESS),is not only often detected in critically ill patients,but also always indicates a worse prognosis of such critically ill patients.Recent clinical studies have shown that ESS is associated with a risk of sudden cardiac death in the course of a critically ill patient.The molecular pathogenesis study of ESS suggests that the mechanism of ESS may include abnormal cell energy metabolism,dysfunction of deiodinases,abnormalities of thyroid combined and transport protein,various activated signaling pathways of proinflammatory cytokines,and regulation as well as feedback of genes in the molecular levels of various organs and tissues in critically ill patients.ESS may not be a simple process of the body compensation,but a pathophysiological process needing intervention.