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COVID-19 的内分泌和代谢方面。

Endocrine and metabolic aspects of COVID-19.

机构信息

Professor emeritus, Department of Immunoendocrinology, Medical University of Lodz, Lodz, Poland.

Department of Neuroendocrinology, Medical University of Lodz, Lodz, Poland.

出版信息

Endokrynol Pol. 2021;72(3):256-260. doi: 10.5603/EP.a2021.0023. Epub 2021 May 19.

DOI:10.5603/EP.a2021.0023
PMID:34010445
Abstract

The paper presents the theoretical considerations on the role of endocrine and metabolic alterations accompanying COVID-19 infection. These alterations may be presumed on the basis of the following two observations. Firstly, the virus SARS-CoV-2 responsible for the COVID-19 infection uses an important renin-angiotensin system (RAS) element - angiotensin-converting enzyme 2 (ACE2) - as a receptor protein for entry into target cells and, in consequence, disturbs the function of the main (circulating) renin-angiotensin-aldosterone system (RAAS) and of the local renin-angiotensin system localized in different tissues and organs. The binding of SARS-CoV-2 to ACE2 leads to the downregulation of this enzyme and, in the aftermath, to the excess of angiotensin II and aldosterone. Thus, in the later stage of COVID-19 infection, the beneficial effects of ACEI and ARB could be presumed. It is hypothesized that the local RAS dysregulation in the adipose tissue is the main cause of the negative role of obesity as a risk factor of severe outcome of the COVID-19 infection. Secondly, the outcome of COVID-19 strongly depends on the age of the patient. Age-related hormonal deficiencies, especially those of melatonin and dehydroepiandrosterone, may contribute to morbidity/mortality in older people. The usefulness of melatonin and angiotensin converting enzyme inhibitors/angiotensin receptor 1 blockers (the latter only in later phases of the infection) as adjuvant drugs is probable but needs thorough clinical trials.

摘要

本文提出了关于伴随 COVID-19 感染的内分泌和代谢改变的理论思考。这些改变可以基于以下两个观察结果来推测。首先,导致 COVID-19 感染的病毒 SARS-CoV-2 使用一种重要的肾素-血管紧张素系统(RAS)元件 - 血管紧张素转换酶 2(ACE2) - 作为进入靶细胞的受体蛋白,因此干扰了主要(循环)肾素-血管紧张素-醛固酮系统(RAAS)和局部肾素-血管紧张素系统的功能,局部肾素-血管紧张素系统定位于不同的组织和器官。SARS-CoV-2 与 ACE2 的结合导致该酶下调,随后导致血管紧张素 II 和醛固酮过量。因此,在 COVID-19 感染的后期,可推测 ACEI 和 ARB 的有益作用。据假设,脂肪组织中局部 RAS 失调是肥胖作为 COVID-19 感染严重后果的危险因素的主要原因。其次,COVID-19 的结局强烈取决于患者的年龄。与年龄相关的激素缺乏,尤其是褪黑素和脱氢表雄酮的缺乏,可能导致老年人的发病率/死亡率增加。褪黑素和血管紧张素转换酶抑制剂/血管紧张素受体 1 阻滞剂(仅在感染后期使用)作为辅助药物的用途可能是合理的,但需要进行彻底的临床试验。

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