English

dc.contributor.authorSekuri, C
dc.contributor.authorCam, FS
dc.contributor.authorSagcan, A
dc.contributor.authorErcan, E
dc.contributor.authorTengiz, I
dc.contributor.authorAlioglu, E
dc.contributor.authorBerdeli, A
dc.date.accessioned2024-07-18T11:57:43Z
dc.date.available2024-07-18T11:57:43Z
dc.description.abstractLIPPINCOTT WILLIAMS & WILKINS
dc.identifier.urihttp://akademikarsiv.cbu.edu.tr:4000/handle/123456789/7136
dc.language.isoArticle
dc.publisher0954-6928
dc.subjectObjectives Interleukin (IL-6) may contribute to the inflammatory response by activating endothelial cells and stimulating the synthesis of fibrinogen. It might thus be important in the pathogenesis of inflammation associated with coronary artery disease (CAD). Several studies suggested that the -174 C allele was associated with an increased prevalence of coronary heart disease. The aim of this study was to investigate further the association of the IL-6 -174 G/C allele status with premature CAD. Methods A total of 120 patients and 105 controls were included in the study. The IL-6 -174 G/C polymorphism was genotyped using PCR-restriction fragment length polymorphism. Results The genotype distribution of the -174 G/C polymorphism was not different in premature CAD patients (GG: 53%; GC: 42.6%; CC: 4.3%) and controls (GG: 54.3%; GC: 39%; CC: 6.7%) (P=0.72). The prevalence of the C allele was 25.6% in patients and 26.1% in controls. By multiple regression analysis, family history, smoking, diabetes, and hypertension were independent risk factors of premature CAD, but not IL-6 genotype. Conclusions We conclude that the IL-6 -174 G/C polymorphism is not associated with the risk of premature CAD, and does not contribute to cardiovascular risk stratification.
dc.titleEnglish
dc.typeACUTE MYOCARDIAL-INFARCTION
dc.typeG/C PROMOTER POLYMORPHISM
dc.typeC-REACTIVE PROTEIN
dc.typeCARDIOVASCULAR-DISEASE
dc.typeHEART-DISEASE
dc.typeRECEPTOR ANTAGONIST
dc.typeBYPASS-SURGERY
dc.typeINCREASED RISK
dc.typePLASMA-LEVELS
dc.typeIL-6 GENE

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