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oai:ebyu-rdlopen.rawdatalibrary.net:ebyu/111112026-10-18T21:13:16Zopenairedrivercom_ebyu_10000col_ebyu_10001

Association between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infectionPolat, SeherŞimşek, Zühal ÖzerbiomarkercomorbiditiesCovid-19genetic susceptibilityrisk assessmentAdultAgedFemaleGenetic Predisposition to DiseaseHumansIntensive Care UnitsMaleMiddle AgedPeptidyl-Dipeptidase APlasminogen Activator Inhibitor 1Polymorphism, Single NucleotideReceptor, Angiotensin, Type 1SARS-CoV-2Severity of Illness Indexangiotensin receptorangiotensin receptor type 1biological markerC reactive proteincreatinineD dimerdipeptidyl carboxypeptidaseferritinfibrinogengenomic DNAglucoseObjective: It is necessary to identify appropriate clinical, biochemical, epidemiological and genetic biomarkers to elucidate the underlying mechanisms of the coronavirus disease-2019 (COVID-19) disease. The study focused on not only the link between disease severity (non-intense unit care (non-ICU) versus intensive unit care (ICU) and genetic susceptibility in COVID-19 patients but also the connection between comorbidity and genetic susceptibility affecting the severity of COVID-19. Subject and methods: One hundred and sixty-two COVID-19 patients treated in the non-ICU and ICU in Kayseri City Hospital were included. All volunteers underwent a physical examination and biochemical evaluation. Angiotensin-converting enzyme (ACE p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (AGTR1) c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (PAI-1-844 G > A (rs2227631) polymorphisms were analysed as well. Results: To have ACE “ID” genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41–2.1, p = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1–7.0, p = 0.03). In PAI-1-844 G > A, having the “AA” genotype in the “A” recessive model increased the risk of the diabetes mellitus (DM) 2.3-fold (OR: 2.3 95%, CI: 1.16–4.66, p = 0.018). In the “G” recessive model, to have the GG genotype increased the risk of chronic kidney disease (CKD) 4.8-fold (OR:4.8, 95% CI: 1.5–15.5, p = 0.008). “GG” genotype in the DM group had a higher fibrinogen level compared to those with the “AG” genotype (AG:4847.2 mg/L (1704.3) versus GG:6444.67 mg/L (1861.62) p = 0.019) and “AA” genotype in the CKD group had lower platelet levels and those with “GG” had higher platelet levels (AA:149 µL (18–159) versus GG: 228 µL (146–357) p = 0.022). Conclusion: This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19. © 2024 Taylor & Francis Group, LLC.Taylor and Francis Ltd.2025Articlehttps://rdlopen.rawdatalibrary.net/r/ebyu/11111https://doi.org/10.1080/15257770.2024.23870331525-7770enNucleosides, Nucleotides and Nucleic Acidsinfo:eu-repo/semantics/openAccessinfo:eu-repo/semantics/articlehttps://ebyu-rdlopen.rawdatalibrary.net/tr/items/ebyu/11111