OBJECTIVE: Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Interleukin (IL) 6 has many inflammatory functions, and the IL-6 -174 G/C promoter polymorphism appears to influence IL-6 levels. Findings of previous studies on the relation between this polymorphism and risk of cardiovascular diseases are inconsistent. We investigated this polymorphism in relation to risk of coronary heart disease (CHD) in a population-based study and meta-analysis. METHODS AND RESULTS: Participants (6434) of the Rotterdam Study were genotyped. Analyses on the relation between genotype and CHD were performed using Cox proportional hazards tests, and the association between genotype and plasma levels of IL-6 and C-reactive protein was investigated. All of the analyses were adjusted for age, sex, and common cardiovascular risk factors. A meta-analysis was performed, using a random effects model. No association between genotype and risk of CHD was observed. The polymorphism was not associated with IL-6 levels, but the C-allele was associated with higher C-reactive protein levels (P<0.01). Our meta-analysis did not show a significant association between the genotype and risk of CHD. CONCLUSIONS: We conclude that the polymorphism is not a suitable genetic marker for increased risk of CHD in subjects > or =55 years of age.
OBJECTIVE: Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Interleukin (IL) 6 has many inflammatory functions, and the IL-6-174 G/C promoter polymorphism appears to influence IL-6 levels. Findings of previous studies on the relation between this polymorphism and risk of cardiovascular diseases are inconsistent. We investigated this polymorphism in relation to risk of coronary heart disease (CHD) in a population-based study and meta-analysis. METHODS AND RESULTS:Participants (6434) of the Rotterdam Study were genotyped. Analyses on the relation between genotype and CHD were performed using Cox proportional hazards tests, and the association between genotype and plasma levels of IL-6 and C-reactive protein was investigated. All of the analyses were adjusted for age, sex, and common cardiovascular risk factors. A meta-analysis was performed, using a random effects model. No association between genotype and risk of CHD was observed. The polymorphism was not associated with IL-6 levels, but the C-allele was associated with higher C-reactive protein levels (P<0.01). Our meta-analysis did not show a significant association between the genotype and risk of CHD. CONCLUSIONS: We conclude that the polymorphism is not a suitable genetic marker for increased risk of CHD in subjects > or =55 years of age.
Authors: Christopher S Carlson; Patrick J Heagerty; Alex S Nord; David K Pritchard; Jane Ranchalis; Joshua M Boguch; Hangjun Duan; Thomas S Hatsukami; Stephen M Schwartz; Mark J Rieder; Deborah A Nickerson; Gail P Jarvik Journal: Hum Genet Date: 2006-11-18 Impact factor: 4.132
Authors: Maria José Santos; Diana Fernandes; Susana Capela; Jose Canas da Silva; João Eurico Fonseca Journal: Clin Rheumatol Date: 2010-12-14 Impact factor: 2.980
Authors: Jeremy D Walston; M Daniele Fallin; Mary Cushman; Leslie Lange; Bruce Psaty; Nancy Jenny; Warren Browner; Russell Tracy; Peter Durda; Alex Reiner Journal: Hum Genet Date: 2007-09-13 Impact factor: 4.132