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Address for correspondence: Mirko Barone, MD. Department of General and Oncological Surgery, SS. Annunziata Hospital, Via dei Vestini n.1, 66100 Chieti, Italy Phone: +39 0871 358326 E-mail: mir87mb@libero.it Submitted Date: March 01, 2020 Accepted Date: March 14, 2020 Available Online Date: April 15, 2020 ©Copyright 2020 by Eurasian Journal of Medicine and Oncology Available online at www.ejmo.org OPEN ACCESS This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License. Coronavirus disease 2019 (COVID-19) is a respiratory tract infection caused by a newly emergent betacoronavirus closely linked to SARS virus, characterized by interstitial lung infiltrate, whose intensive care unit related admission rate is of 5%. Its natural history can be complicated by mild to severe respiratory failure till the onset of a fearsome life-treatening acute respiratory distress syndrome (ARDS). Given the interaction with host ACE2 type II pneumocytes receptors, dysregulation of the renin-angiotensin system may serve a central role both in the onset and progression of lung injury.[1, 2] The complex SARS-CoV-2 Spike (S) glycoprotein and ACE2 receptor primed by the cellular protease TMPRSS2 is a critical step for ectodomain virion entry by suppressing ACE2 activity and altering the ACE/ACE2 balance to a predominant ACE/AngII axis with a reduction of Ang(1-7)-Mas complex and subsequent vasoconstriction, cytokines-bradykinin inflammatory response, Fas-induced apoptosis, fibrogenesis and oxidative damage. [3] As reported by Liu et al.,[4] in a small monocentric case series including twelve patients, serum Ang II levels in COVID-19 patients were significantly higher than in non-infected individuals with a linear association with both viremia and lung severity injury. Since ACE2 exerts cytoprotective effects on pulmonary parenchyma by an antagonistic action of Ang II, we speculated about both direct (restorative of the renin angiotensin system) and indirect (chimeric receptor effect) therapeutic effects in the treatment of COVID-19 related ARDS. Khan A et al.,[5] in a double-blind two-part phase II trial comparing the effect of the administration of a recombinant form of human angiotensin-converting enzyme 2 (GSK2586881) in forty-six patients with acute respiratory distress syndrome, reported a significant reduction of Ang II levels after scalar infusion with a long standing 48-hours plateau phase. Moreover, surfactant protein D increased as far as interleukin-6 concentrations decreased. The authors reported no significant differences in either peak or plateau pressures between recombinant human angiotensin-converting enzyme 2 (rhACE2) and placebo group in the first 72 hours, but an equally increase at the end of the five-day observation period. No adverse haemodynamic effects were reported; however, hypernatremia, rush and dysphagia were noted. However, some Mirko Barone,1 Claudio Ucciferri,2,5 Giuseppe Cipollone,3,4 Felice Mucilli3,4

Recombinant Human Angiotensin-Converting Enzyme 2 and COVID-19 Acute Respiratory Distress Syndrome: A Theoretical or a Real Resource?