Abstract
BackgroundTo explore the clinical significance of serum angiotensin-converting enzyme (ACE) activity in coronavirus disease 2019 (COVID-19).MethodsIn 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.ResultsOf 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.ConclusionSerum 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.
Highlights
To explore the clinical significance of serum angiotensin-converting enzyme (ACE) activity in coronavirus disease 2019 (COVID-19)
The severity of disease was related to older age (57.50 ± 11.70 years vs 49.19 ± 15.98 years, P = 0.047), higher body mass index (BMI) (26.04 ± 5.63 kg/ m2 vs 23.60 ± 3.33 kg/m2, P = 0.018), and higher proportion of hypertension (8 [50%] vs 25 [20.83%], P = 0.011)
We found that the baseline serum ACE activity in the severe group and nonsevere group were both decreased, with the lowest level in the severe group
Summary
To explore the clinical significance of serum angiotensin-converting enzyme (ACE) activity in coronavirus disease 2019 (COVID-19). The renin–angiotensin system (RAS) is well known for its ability to maintain blood pressure and electrolyte balance. It has been implicated in the pathogenesis of ARDS [2]. RAS has two axes, classic RAS: the ACE/ Angiotensin (Ang) II/Ang II type 1 (AT1) receptor axis; and nonclassic RAS: the ACE2/Ang 1–7/Mas receptor (MasR) axis. The former deteriorates the impaired respiratory conditions, while the latter plays a protective role in ARDS [2, 3].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
