• Ozgur Gunal, Ozlem Sezer, Goksenin Unluguzel Ustun, Cagatay Erman Ozturk, Ahmet Sen, Serbulent Yigit, and Mehmet Derya Demirag.
• From the Department of Infectious Diseases and Clinical Microbiology, Samsun Education and Research Hospital, Samsun, Turkey.
• Ann Saudi Med. 2021 May 1; 41 (3): 141-146.

BackgroundAngiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism may play a role in the pathogenesis of coronavirus-19 disease (COVID-19).ObjectivesInvestigate the relationship between ACE I/D polymorphism and the clinical severity of COVID-19.DesignProspective cohort study.SettingTertiary care hospital.Patients And MethodsThe study included COVID-19 patients with asymptomatic, mild, and severe disease with clinical data and whole blood samples collected from 1 April 2020 to 1 July 2020. ACE I/D genotypes were determined by polymerase chain reaction and agarose gel electrophoresis.Main Outcome MeasureACE DD, DI and II genotypes frequencies.Sample Size90 cases, 30 in each disease severity group.ResultsAge and the frequency of general comorbidity increased significantly from the asymptomatic disease group to the severe disease group. Advanced age, diabetes mellitus and presence of ischemic heart disease were independent risk factors for severe COVID-19 [OR and 95 % CI: 1.052 (1.021-1.083), 5.204 (1.006-26.892) and 5.922 (1.109-31.633), respectively]. The ACE II genotype was the dominant genotype (50%) in asymptomatic patients, while the DD genotype was the dominant genotype (63.3 %) in severe disease. The ACE II geno-type was protective against severe COVID-19 [OR and 95% CI: .323 (.112-.929)]. All nine patients (8.9%) who died had severe disease.ConclusionsThe clinical severity of COVID-19 infection may be associated with the ACE I/D polymorphism.LimitationsSmall sample size and single center.Conflict Of InterestNone.

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