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Cortisol metabolism in critical illness: Implications for clinical care

机译:严重疾病中的皮质醇代谢:对临床护理的意义

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摘要

Purpose of review: Critical illness is uniformly characterized by elevated plasma cortisol concentrations, traditionally attributed exclusively to increased cortisol production driven by an activated hypothalamic pituitary adrenal axis. However, as plasma adrenocorticotropic hormone (ACTH) concentrations are often not elevated or even low during critical illness, alternative mechanisms must contribute. Recent findings: Recent investigations revealed that plasma clearance of cortisol is markedly reduced during critical illness, explained by suppressed expression and activity of the main cortisol metabolizing enzymes in liver and kidney. Furthermore, unlike previously inferred, cortisol production rate in critically ill patients was only moderately increased to less than double that of matched healthy subjects. In the face of low-plasma ACTH concentrations, these data suggest that other factors drive hypercortisolism during critical illness, which may suppress ACTH by feedback inhibition. These new insights add to the limitations of the current diagnostic tools to identify patients at risk of failing adrenal function during critical illness. They also urge to investigate the impact of lower hydrocortisone doses than those hitherto used. Summary: Recent novel insights reshape the current understanding of the hormonal stress response to critical illness and further underline the need for more studies to unravel the pathophysiology of adrenal (dys)functioning during critical illness.
机译:审查目的:危重病的特征通常是血浆皮质醇浓度升高,传统上仅归因于激活的下丘脑垂体肾上腺轴驱动皮质醇产生增加。但是,由于在危重病期间血浆促肾上腺皮质激素(ACTH)浓度通常不会升高甚至更低,因此必须采用其他机制。最新发现:最近的研究表明,危重病期间皮质醇的血浆清除率明显降低,这可以通过抑制肝脏和肾脏中主要皮质醇代谢酶的表达和活性来解释。此外,与先前推断的不同,危重患者的皮质醇生成率仅适度增加,不到匹配健康受试者的两倍。面对血浆血浆ACTH浓度低的情况,这些数据表明在危重病期间其他因素也会导致皮质醇过多,这可能通过反馈抑制作用抑制ACTH。这些新见解增加了当前诊断工具的局限性,这些工具可用来识别在危重病期间可能存在肾上腺功能衰竭的风险的患者。他们还敦促研究比以往所用剂量低的氢化可的松剂量的影响。简介:最近的新颖见解重塑了对危重疾病荷尔蒙应激反应的当前理解,并进一步强调了需要开展更多研究以揭示危重疾病期间肾上腺功能障碍的病理生理学的需求。

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