A dramatic rise in serum ACE2 activity in a critically ill COVID-19 patient. (February 2021)

• Record Type: Journal Article
• Authors: Nagy, Béla; Fejes, Zsolt; Szentkereszty, Zoltán; Sütő, Renáta; Várkonyi, István; Ajzner, Éva; Kappelmayer, János; Papp, Zoltán; Tóth, Attila; Fagyas, Miklós
• Is Part Of: International journal of infectious diseases. Volume 103(2021)
• Page Start: 412
• Page End: 414
• Publication Date: 2021-02
• Subjects: COVID-19 -- ACE2 -- Endothelial cell -- Inflammation -- Biomarker; Communicable diseases -- Periodicals; Communicable Diseases -- Periodicals; Communicable diseases; Periodicals; Electronic journals; 616.9
• DOI: 10.1016/j.ijid.2020.11.184
• Languages: English
• ISSNs: 1201-9712

Abstract

Highlights: 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. Abstract: 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.