Abstract
Introduction Dysfunction in the renin-angiotensin-aldosterone system (RAAS) has been observed in patients with coronavirus disease 2019 (COVID-19). It is presumed that the effect of reducing interleukin-6 (IL-6) levels by angiotensin II receptor blockers (ARBs) by RAAS modulation. We investigated changes in angiotensin II and IL-6 levels in four COVID-19 patients treated with ARBs. Case Presentation. Cases 1 and 2 were who had not received ARBs before and were newly administered ARBs. Case 3 restarted ARBs after discontinuation for 7 days, and case 4 received an increased dose of ARBs. The mean in angiotensin II levels (607.5 pg/mL, range: 488–850 pg/mL, reference range < 100 pg/mL), C-reactive protein (CRP) (10.58 mg/dL, range 4.45-18.05 mg/dL), and IL-6 (55.78 pg/mL, range: 12.86–144.82 pg/mL, reference range < 7 pg/mL) was observed at the admission in all patients. Upon clinical improvement, the mean decrease in CRP (1.02 mg/dL, range 0.06-3.78 mg/dL) and IL-6 (5.63 pg/mL, range 0.17-20.87 pg/mL) was observed in all patients. Conversely, angiotensin II levels gradually increased. Conclusion This report supports the potential benefit of ARBs to improve the clinical outcomes of COVID-19 patients by controlling RAAS dysfunction.
Highlights
Dysfunction in the renin-angiotensin-aldosterone system (RAAS) has been observed in patients with coronavirus disease 2019 (COVID-19)
Some experts suggest that angiotensinconverting enzyme 2 (ACE2)-stimulating drugs increase the risk of severe coronavirus disease 2019 (COVID-19) [1], others recommend that patients should continue antihypertensive therapy because there is no clinical evidence to suggest that treatment with ACE inhibitors (ACEi) or angiotensin II receptor blockers (ARBs) should be discontinued in cases of COVID-19 infection [2]
We evaluated changes in angiotensin II, IL-6, and C-reactive protein (CRP) levels in four patients who were administered ARBs to determine the change of angiotensin II due to ARBs in COVID-19 patients
Summary
Severe acute respiratory syndrome coronavirus 2 (SARSCoV-2) binds to target cells through the angiotensinconverting enzyme 2 (ACE2), which is expressed by the epithelial cells of the lungs, intestine, kidney, and blood vessels [1, 2]. Previous studies propose that ARBs and ACEi may help attenuate lung injury caused by a cytokine storm [3, 4]. It was observed that severe COVID-19 patients had increased levels of angiotensin II and IL-6 [7, 8]. This can be potentially explained by the fact that the ACE2 that is occupied and downregulated by SARSCoV-2 is incapable of hydrolyzing angiotensin II [9]. Sex Age (y) Weight (kg) Incubation period Interval between symptom onset and admission (days)
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