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Contribution of genotypes in Prothrombin and Factor V Leiden to COVID-19 and disease severity in patients at high risk for hereditary thrombophilia

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dc.contributor.authorGEÇKİNLİ, BİLGEN BİLGE
dc.contributor.authorALAVANDA, CEREN
dc.contributor.authorsKiraz A., Sezer O., ALEMDAR A., Canbek S., Duman N., BİŞGİN A., Cora T., Ruhi H. I., Ergoren M. C., GEÇKİNLİ B. B., et al.
dc.date.accessioned2023-03-07T11:16:42Z
dc.date.available2023-03-07T11:16:42Z
dc.date.issued2023-02-01
dc.description.abstractThrombotic and microangiopathic effects have been reported in COVID-19 patients. This study examined the contribution of the hereditary thrombophilia factors Prothrombin (FII) and Factor V Leiden (FVL) genotypes to the severity of COVID-19 disease and the development of thrombosis. This study investigated FII and FVL alleles in a cohort of 9508 patients (2606 male and 6902 female) with thrombophilia. It was observed that 930 of these patients had been infected by SARS-CoV-2 causing COVID-19. The demographic characteristics of the patients and their COVID-19 medical history were recorded. Detailed clinical manifestations were analyzed in a group of cases (n = 4092). This subgroup was age and gender-matched. FII and FVL frequency data of healthy populations without thrombophilia risk were obtained from Bursa Uludag University Medical Genetic Department\"s Exome Databank. The ratio of males (31.08%; 27.01%) and the mean age (36.85 ± 15.20; 33.89 ± 14.14) were higher among COVID-19 patients compared to non-COVID-19 patients. The prevalence of FVL and computerized tomography (CT) positivity in COVID-19 patients was statistically significant in the thrombotic subgroup (p < 0.05). FVL prevalence, CT positivity rate, history of thrombosis, and pulmonary thromboembolism complication were found to be higher in deceased COVID-19 patients (p < 0.05). Disease severity was mainly affected by FVL and not related to genotypes at the Prothrombin mutations. Overall, disease severity and development of thrombosis in COVID-19 are mainly affected by the variation within the FVL gene. Possible FVL mutation should be investigated in COVID-19 patients and appropriate treatment should be started earlier in FVL-positive patients.
dc.identifier.citationKiraz A., Sezer O., ALEMDAR A., Canbek S., Duman N., BİŞGİN A., Cora T., Ruhi H. I., Ergoren M. C., GEÇKİNLİ B. B., et al., "Contribution of genotypes in Prothrombin and Factor V Leiden to COVID-19 and disease severity in patients at high risk for hereditary thrombophilia", Journal of Medical Virology, cilt.95, sa.2, 2023
dc.identifier.doi10.1002/jmv.28457
dc.identifier.issn0146-6615
dc.identifier.issue2
dc.identifier.urihttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85148657613&origin=inward
dc.identifier.urihttps://hdl.handle.net/11424/287280
dc.identifier.volume95
dc.language.isoeng
dc.relation.ispartofJournal of Medical Virology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectTıp
dc.subjectMikrobiyoloji ve Klinik Mikrobiyoloji
dc.subjectViroloji
dc.subjectYaşam Bilimleri
dc.subjectSağlık Bilimleri
dc.subjectTemel Tıp Bilimleri
dc.subjectTemel Bilimler
dc.subjectMedicine
dc.subjectMicrobiology and Clinical Microbiology
dc.subjectVirology
dc.subjectLife Sciences
dc.subjectHealth Sciences
dc.subjectFundamental Medical Sciences
dc.subjectNatural Sciences
dc.subjectYaşam Bilimleri (LIFE)
dc.subjectİmmünoloji
dc.subjectVİROLOJİ
dc.subjectBULAŞICI HASTALIKLAR
dc.subjectLife Sciences (LIFE)
dc.subjectIMMUNOLOGY
dc.subjectVIROLOGY
dc.subjectINFECTIOUS DISEASES
dc.subjectBulaşıcı hastalıklar
dc.subjectInfectious Diseases
dc.subjectCOVID-19
dc.subjectFactor V Leiden
dc.subjectProthrombin
dc.subjectthrombophilia
dc.subjectcOVID‐19
dc.subjectFactor V Leiden
dc.subjectProthrombin
dc.subjectthrombophilia
dc.titleContribution of genotypes in Prothrombin and Factor V Leiden to COVID-19 and disease severity in patients at high risk for hereditary thrombophilia
dc.typearticle
dspace.entity.typePublication
local.avesis.idae2138d8-a112-45a4-a3f2-e1e402d8c618
local.indexed.atPUBMED
local.indexed.atSCOPUS
relation.isAuthorOfPublication5f812a34-2d87-4040-b76f-0b90c1c695ae
relation.isAuthorOfPublication2ad76025-5a7e-429e-8f0a-3da70e4561a5
relation.isAuthorOfPublication.latestForDiscovery5f812a34-2d87-4040-b76f-0b90c1c695ae

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