Yanfei Mao1, Bo Xu1, Wenbin Guan2, Dunfeng Xu1, Feng Li3, Rongrong Ren1, Xiaoyan Zhu4, Yuan Gao5, Lai Jiang1. 1. Department of Anesthesiology and Surgical Intensive Care Unit, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. 2. Department of Pathology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. 3. Department of Respiratory and Critical Care Medicine, Shanghai Public Health Clinical Center Affiliated to Fudan University, Shanghai, China. 4. Department of Physiology, Navy Medical University, Shanghai, China. 5. Department of Critical Care Medicine, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Abstract
Background: The majority of the critically ill patients may have critical illness-related corticosteroid insufficiency (CIRCI). The therapeutic effect of dexamethasone may be related to its ability to improve cortical function. Recent study showed that dexamethasone can reduce COVID-19 deaths by up to one third in critically ill patients. The aim of this article is to investigate whether SARS-CoV-2 can attack the adrenal cortex to aggravate the relative adrenal insufficiency. Methods: We summarized the clinical features of COVID-19 reported in currently available observational studies. ACE2 and TMPRSS2 expression was examined in human adrenal glands by immunohistochemical staining. We retrospectively analyzed serum cortisol levels in critically ill patients with or without COVID-19. Results: High percentage of critically ill patients with SARS-COV-2 infection in the study were treated with vasopressors. ACE2 receptor and TMPRSS2 serine protease were colocalized in adrenocortical cells in zona fasciculata and zona reticularis. We collected plasma cortisol concentrations in nine critically ill patients with COVID-19. The cortisol levels of critically ill patients with COVID-19 were lower than those in non-COVID-19 critically ill group. Six of the nine COVID-19 critically ill patients had random plasma cortisol concentrations below 10 µg/dl, which met the criteria for the diagnosis of CIRCI. Conclusion: We demonstrate that ACE2 and TMPRSS2 are colocalized in adrenocortical cells, and that the cortisol levels are lower in critically ill patients with COVID-19 as compared to those of non-COVID-19 critically ill patients. Based on our findings, we recommend measuring plasma cortisol level to guide hormonal therapy.
Background: The majority of the critically illpatients may have critical illness-related corticosteroid insufficiency (CIRCI). The therapeutic effect of dexamethasone may be related to its ability to improve cortical function. Recent study showed that dexamethasone can reduce COVID-19deaths by up to one third in critically illpatients. The aim of this article is to investigate whether SARS-CoV-2 can attack the adrenal cortex to aggravate the relative adrenal insufficiency. Methods: We summarized the clinical features of COVID-19 reported in currently available observational studies. ACE2 and TMPRSS2 expression was examined in human adrenal glands by immunohistochemical staining. We retrospectively analyzed serum cortisol levels in critically illpatients with or without COVID-19. Results: High percentage of critically illpatients with SARS-COV-2 infection in the study were treated with vasopressors. ACE2 receptor and TMPRSS2serine protease were colocalized in adrenocortical cells in zona fasciculata and zona reticularis. We collected plasma cortisol concentrations in nine critically illpatients with COVID-19. The cortisol levels of critically illpatients with COVID-19 were lower than those in non-COVID-19critically ill group. Six of the nine COVID-19critically illpatients had random plasma cortisol concentrations below 10 µg/dl, which met the criteria for the diagnosis of CIRCI. Conclusion: We demonstrate that ACE2 and TMPRSS2 are colocalized in adrenocortical cells, and that the cortisol levels are lower in critically illpatients with COVID-19 as compared to those of non-COVID-19critically illpatients. Based on our findings, we recommend measuring plasma cortisol level to guide hormonal therapy.
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