scholarly journals The Interplay Between the Immune System, the Renin‐Angiotensin‐Aldosterone System (RAAS), and RAAS Inhibitors May Modulate the Outcome of COVID‐19: A Systematic Review

Author(s):  
Hiba Naveed ◽  
Abdallah Elshafeey ◽  
Dana Al‐Ali ◽  
Emmad Janjua ◽  
Areej Nauman ◽  
...  
2020 ◽  
Author(s):  
Tamirat Bekele Beressa ◽  
Tamiru Sahilu ◽  
Serawit Deyno

Objective: This research aimed to systematically review and summarize the influence of Renin-Angiotensin-Aldosterone System (RAAS) inhibitors on the outcome of COVID_19 patients with hypertension. Methods: Electronic databases; PubMed/Medline, CINAHL, the Cochrane Central Register of Controlled Trials, clinical trial.gov, and Google Scholar were searched from 2019 to June 1, 2020. Additionally, the references of identified articles were also searched. Results: A total of 9 articles comprising 3,823 patients were incorporated; 1416 patients on RAAS inhibitors and 3469 on non-RAAS inhibitors. The study demonstrated that the taking of RAAS inhibitors in COVID_19 patients with hypertension significantly reduced mortality where patients on RAAS inhibitors had a 27% decrease of mortality (RR= 0.73 [95% CI: 0.63- 0.85, p<0.0001, I2=0%, random-effects model]) compared to those not taking ACEI/ARB. No significant association were observed in disease severity (RR= 0.92 (95% CI: 0.74- 1.14) and hospitalization (WMD= -2.33[95% CI: -5.60, 0.75]), random-effects model. Conclusion: This study supports RAAS inhibitors safe use among COVID_19 patients with hypertension. Keywords: COVID_19, ACEI, ARB, Hypertension, Coronavirus


Author(s):  
Davide Ventura ◽  
Amy L Carr ◽  
R Duane Davis ◽  
Scott Silvestry ◽  
Linda Bogar ◽  
...  

Abstract It has been established SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), a membrane-bound regulatory peptide, for host cell entry. Renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to increase ACE2 in type 2 pneumocytes pulmonary tissue. Controversy exists for the continuation of ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) in the current pandemic. ACE2 serves as regulatory enzyme in maintaining homeostasis between proinflammatory Angiotensin II and anti-inflammatory Angiotensin 1,7 peptides. Derangements in these peptides are associated with cardiovascular disease and are implicated in the progression of acute respiratory distress syndrome (ARDS). Augmentation of the ACE2/Ang1,7 axis represent a critical target in the supportive management of COVID-19 associated lung disease. Observational data describing the use of RAAS inhibitors in the setting of SARS-CoV-2 have not borne signals of harm to date. However, equipoise persists requiring an analysis of novel agents including recombinant human-ACE2 and existing RAAS inhibitors while balancing ongoing controversies associated with increased coronavirus infectivity and virulence.


2021 ◽  
Vol 4 (Special2) ◽  
pp. 389-394
Author(s):  
Angela Madalina Lazar

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.


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