Impact of hemostatic gene single point mutations in patients with non-diabetic coronary artery disease

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dc.contributor.authorVar A.
dc.contributor.authorÜtük O.
dc.contributor.authorAkçalı S.
dc.contributor.authorŞanlıdağ T.
dc.contributor.authorUyanık B.S.
dc.contributor.authorDinç G.
dc.date.accessioned2024-07-22T08:21:54Z
dc.date.available2024-07-22T08:21:54Z
dc.date.issued2009
dc.description.abstractSingle point mutations in the genes coding for hemostatic factors were shown to be major inherited predisposing factors for venous thromboembolism. However, their contribution in the development of non-diabetic coronary artery disease [nDCAD] remains controversial. Angiographically demonstrated nDCAD patients (n = 86) and healthy controls (n = 90) were included in the study. Genotype analysis of hemostatic gene polymorphisms were assessed by using CVD strip assay, based on allele specific oligonucleotide probes. The carrier frequency of factor V (FV) H1299R, prothrombin G20210A, glycoprotein (Gp) IIIa L33P, plasminogen activator inhibitor-I (PAI-1) 4G/5G, 4G/4G, 5G/5G, methylenetetrahydrofolate reductase (MTHFR) A1298C and β-fibrinogen -455 G > A were similar between patients and controls. In contrast, frequency of FV Leiden was significantly higher among patients (12.5%) than controls (5%, OR: 7.94; 95%CI: 1.9-49.6) and FXIII V34L was significantly lower among patients (23.7%) than controls (40%, OR: 0.24; 95%CI: 0.1-0.89). In addition, the frequency of the MTHFR C677T polymorphism was 32.5% among patients compared with 42.5% in controls, of which the T/T genotype was significantly lower among patients (5%) than controls (17.5%, OR: 0.06; 95%CI: 0.01-0.58). No difference was observed in prevalence of prothrombin G20210A, FV H1299R, Gp IIIa L33P, PAI-1 4G5G, MTHFR A1298C, β fibrinogen 455 G > A mutations between patients and controls. However, lower frequency of FXIII Val34Leu and MTHFR C677T polymorphisms may decrease, while FV Leiden polymorphism may increase development of nDCAD. © 2009 Springer Science+Business Media B.V.
dc.identifier.DOI-ID10.1007/s11033-008-9439-5
dc.identifier.issn03014851
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/18835
dc.language.isoEnglish
dc.publisherSpringer Netherlands
dc.subject5,10 methylenetetrahydrofolate reductase (FADH2)
dc.subjectblood clotting factor 5
dc.subjectblood clotting factor 5 Leiden
dc.subjectfibrinogen
dc.subjectfibrinogen b beta chain
dc.subjectglycoprotein IIIa
dc.subjectleucine
dc.subjectplasminogen activator inhibitor 1
dc.subjectprothrombin
dc.subjectunclassified drug
dc.subjectvaline
dc.subjectadult
dc.subjectarticle
dc.subjectcardiovascular risk
dc.subjectcontrolled study
dc.subjectcoronary artery disease
dc.subjectdisease course
dc.subjectDNA polymorphism
dc.subjectfemale
dc.subjectgene frequency
dc.subjectgenetic variability
dc.subjectheterozygosity
dc.subjecthomozygosity
dc.subjecthuman
dc.subjectmajor clinical study
dc.subjectmale
dc.subjectnon diabetic coronary artery disease
dc.subjectpoint mutation
dc.titleImpact of hemostatic gene single point mutations in patients with non-diabetic coronary artery disease
dc.typeArticle

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