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.
【저자키워드】 COVID-19, Inflammation, ACE2, Biomarker, Endothelial cell, 【초록키워드】 SARS-CoV-2, coronavirus, Biomarkers, severe COVID-19, Prognosis, SARS-COV-2 infection, Infection, ferritin, E-selectin, angiotensin-converting enzyme 2, viral entry, Endothelium, clinical status, serum, Critically ill, Patient, disease, expression, Critical, acute respiratory distress, COVID-19 patient, IL-6 levels, intravenous, target cells, protective mechanism, acute respiratory syndrome, Activation, subject, syndrome, effective therapy, circulating, Express, recombinant ACE2, MONITOR, main receptor, Cell, Course, reported, promote, upregulated, nonspecific, 【제목키워드】 serum, Critically ill, COVID-19 patient,