title: Post-hoc analysis on the CD14 C(-260)T promoter polymorphism and coronary heart disease.
abstract: Functional C(-260)--> T polymorphism in the promoter of the CD14 gene has been reported to be associated with coronary heart disease (CHD). The functional role of the polymorphism, however, is still a matter of debate, since several studies have not proved its effect on clinical outcomes associated with atherosclerosis. Cardiovascular-related morbidity and mortality was assessed in a post-hoc approach four years after baseline characterization of patients (male/female n = 36/32) with angiographically proven coronary heart disease. CD14 C(-260)--> T promoter genotype was determined at baseline. Seventeen out of 20 CHD patients with non-lethal cardiovascular events carried at least one T-allele. CD14 T-260 allele carriers have a 3.59-fold (95 % confidence interval: 1.11-6.75) increased risk for non-lethal cardiovascular events (Kaplan-Meier plot: log rank test p = 0.029). All patients with lethal outcomes (n = 6) were also T-allele carriers. Multivariate logistic regression analysis among CHD patients including age, established risk factors and the C(-260)--> T polymorphism as covariates and non-lethal events as a dependent variable confirmed the independent prospective effect of the T-allele on cardiovascular outcomes in this subset. Further evidence is provided for the role of CD14 C(-260)--> T promoter polymorphism as a genetic susceptibility marker of atherosclerosis in patients with an advanced clinical course of the disease. Due to the small sample size and post-hoc character of the study large-scale prospective studies that monitor patients with proven CHD are needed to confirm these findings.
authors.affiliation: Institute of Clinical Chemistry and Laboratory Medicine, University of Regensburg, Regensburg, Germany. mail@DrPorsch.de
authors.forename: M
authors.initials: M
authors.lastname: Porsch-Ozcürümez
authors.forename: J
authors.initials: J
authors.lastname: Hucke
authors.forename: S
authors.initials: S
authors.lastname: Westphal
authors.forename: J A
authors.initials: JA
authors.lastname: Hubáček
authors.forename: G
authors.initials: G
authors.lastname: Schmitz
authors.forename: C
authors.initials: C
authors.lastname: Luley
mesh_terms: D000368:Aged; D015415:Biomarkers; D003327:Coronary Disease / Q000453:epidemiology / Q000235:genetics*; D004247:DNA / Q000096:biosynthesis / Q000235:genetics; D005260:Female; D005823:Genetics; D005838:Genotype; D006801:Humans; D008055:Lipids / Q000097:blood; D018950:Lipopolysaccharide Receptors / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics; D011401:Promoter Regions, Genetic / Q000235:genetics*; D012306:Risk
chemical_list: D015415:Biomarkers; D008055:Lipids; D018950:Lipopolysaccharide Receptors; D004247:DNA