A dramatic rise in serum ACE2 activity in a critically ill COVID-19 patient

• Published in: International journal of infectious diseases Vol. 103; pp. 412 - 414
• Main Authors: Nagy, Béla, Fejes, Zsolt, Szentkereszty, Zoltán, Sütő, Renáta, Várkonyi, István, Ajzner, Éva, Kappelmayer, János, Papp, Zoltán, Tóth, Attila, Fagyas, Miklós
• Format: Journal Article
• Language: English
• Published: Canada Elsevier Ltd 01.02.2021; The Author(s). Published by Elsevier Ltd on behalf of International Society for Infectious Diseases; Elsevier
• Subjects: ACE2; Aged; Angiotensin-Converting Enzyme 2 - blood; Biomarker; Case Report; COVID-19; COVID-19 - blood; COVID-19 - enzymology; COVID-19 - physiopathology; Critical Illness; Endothelial cell; Endothelial Cells - metabolism; Humans; Inflammation; Male; Renin-Angiotensin System - physiology; SARS-CoV-2; COVID-19; ACE2; Endothelial cell; Biomarker; Inflammation
• ISSN: 1201-9712; 1878-3511; 1878-3511
• DOI: 10.1016/j.ijid.2020.11.184

•The upregulated expression of ACE2 was recently reported in bronchoalveolar lavage fluid samples from COVID-19 patients.•We have first analyzed serum ACE2 activity in COVID-19 that increased about 40-fold over the normal range in the presence of two- to threefold higher levels of endothelium biomarkers.•Soluble E-selectin followed the clinical status of our patient similarly to ferritin and IL-6 levels.•Based on the distinct time course of circulating ACE2, its dramatic rise may act as an endogenous nonspecific protective mechanism against SARS-CoV-2 infection that preceded the recovery of the patient. Endothelial cells express surface angiotensin-converting enzyme 2 (ACE2), the main receptor for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that promotes the infection of endothelial cells showing activation and damage. Bronchoalveolar lavage fluid from coronavirus disease-2019 (COVID-19) subjects showed a critical imbalance in the renin-angiotensin-aldosterone system with the upregulated expression of ACE2. Recently, intravenous recombinant ACE2 was reported as an effective therapy in severe COVID-19 by blocking the viral entry to target cells. Here, we present a case of a critically ill COVID-19 patient with acute respiratory distress syndrome where circulating ACE2 was first measured to monitor disease prognosis. ACE2 activity increased about 40-fold over the normal range and showed a distinct time course as compared to 2-3-fold higher levels of endothelium biomarkers. Although the level of soluble E-selectin followed the clinical status of our patient similar to ferritin and IL-6 levels, the dramatic rise in serum ACE2 activity may act as an endogenous nonspecific protective mechanism against SARS-CoV-2 infection that preceded the recovery of our patient.