Selected article for: "activity mechanism and acute respiratory distress syndrome"

Author: Nagy, Béla; Fejes, Zsolt; Szentkereszty, Zoltán; Suto, Renáta; Várkonyi, István; Ajzner, Éva; Kappelmayer, János; Papp, Zoltán; Tóth, Attila; Fagyas, Miklós
Title: A dramatic rise in serum ACE2 activity in a critically ill COVID-19 patient
  • Cord-id: y69r7gxm
  • Document date: 2020_11_26
  • ID: y69r7gxm
    Snippet: Endothelial cells express surface angiotensin converting enzyme 2 (ACE2), the main receptor for SARS-CoV-2 that promotes the infection of endothelial cells showing activation and damage. Bronchoalveolar lavage fluid from COVID-19 subjects showed a critical imbalance in the renin-angiotensin-aldosterone system with 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 pres
    Document: Endothelial cells express surface angiotensin converting enzyme 2 (ACE2), the main receptor for SARS-CoV-2 that promotes the infection of endothelial cells showing activation and damage. Bronchoalveolar lavage fluid from COVID-19 subjects showed a critical imbalance in the renin-angiotensin-aldosterone system with 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 compared to 2-3-fold higher levels of endothelium biomarkers. Although the level of soluble E-selectin followed the clinical status of our patient similarly 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.

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