The potential role of serum angiotensin-converting enzyme in coronavirus disease 2019

Abstract

Background To explore the clinical significance of serum angiotensin-converting enzyme (ACE) activity in coronavirus disease 2019 (COVID-19). Methods In this retrospective study, a total of 136 consecutive patients with confirmed COVID-19 were recruited. Demographic and clinical data were recorded. The serum ACE activity was measured at baseline and during the recovery phase, and its relationship with clinical condition was analyzed. Results Of the 136 patients with confirmed COVID-19, the 16 severe patients were older and had a higher body mass index (BMI) and proportion of hypertension than the 120 nonsevere patients. In comparison to those of normal controls, the baseline serum ACE activities of subjects in the severe group and nonsevere group were decreased, with the lowest level in the severe group. However, the serum ACE activity increased in the recovery phase, and there were no significant differences among the severe group, nonsevere group and normal control group. Conclusion Serum ACE activity could be used as a marker to reflect the clinical condition of COVID-19 since low activity was associated with the severity of COVID-19 at baseline, and the activity increased with the remission of the disease.

Beta‐Adrenergic Blockers as a Potential Treatment for COVID‐19 Patients

“…[ 11 ] It has been suggested that Tocilizumab by the inhibition of IL‐6 receptor may help decrease the mucus secretion in COVID‐19. [ 12 ] As mentioned earlier, beta‐adrenergic blockers decrease IL‐6. It is interesting to note that chronic propranolol administration has been shown to decrease MUC5AC expression and mucus secretion.…”

“…As mentioned earlier, Tocilizumab may help decrease the mucus secretion in COVID‐19. [ 12 ] Recently National Institutes of Health (NIH) had recommended Remdesivir for COVID‐19 patients who are on supplemental oxygen but not for those who are on mechanical ventilation. NIH has also recommended dexamethasone due to their immunomodulatory role for the COVID‐19 patients who are on mechanical ventilation.…”

“…[ 11 ] It has been suggested that Tocilizumab by the inhibition of IL‐6 receptor may help decrease the mucus secretion in COVID‐19. [ 12 ] Postmortem study has shown the presence of hyperplasia of type II alveolar epithelial cells, diffuse alveolar damage, macrophage and neutrophil infiltration, fibrosis, hyaline membrane formation. [ 13 ] It is known that cytokine storm occurs in COVID‐19, as the levels of IL‐1β, IL‐6, TNFα are increased and this leads to multiple organ dysfunction and septic shock.…”

Soluble Angiotensin Converting Enzyme 2 (ACE2) Is Upregulated and Soluble Endothelial Nitric Oxide Synthase (eNOS) Is Downregulated in COVID-19-induced Acute Respiratory Distress Syndrome (ARDS)

“…In a previous study, baseline serum ACE activity of severe and non-severe COVID-19 patients was decreased compared to normal controls; the lowest levels were noted in the severe group. The respective activities, however, increased in the recovery phase, and the authors concluded that serum ACE activity could be potentially used as a marker to reflect severity of COVID-19 at baseline [ 36 ]. In another study, no association was seen between serum ACE activity and COVID-19; furthermore, serum ACE activity on admission did not reflect disease severity [ 37 ].…”

Epithelial-endothelial cross-talk hypothesis explains the early pathobiology of COVID-19 pneumonia

“…High ACE levels in bronchoalveolar lavage (BAL) fluids have been observed in ARDS despite a reduction in serum ACE levels [19]. Though, no study on COVID-19 has actually measured the ACE levels in BAL fluid and ACE protein expression in lungs, a recent study measuring the circulating ACE levels in COVID-19 patients demonstrated decreased circulatory levels of ACE in severe COVID-19 patients that normalizes during the recovery phase [20]. This reduced serum ACE levels may reflect loss of enzyme release from a damaged pulmonary vascular endothelium, but not be the true representative of ACE activity in the lung compartment [20] that may actually be increased [21].…”