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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
BACKGROUND: Although pathways associated with hemostasis and thrombosis are well documented to have an impact on venous thromboembolism (VTE), whether the inflammatory cascade also influences VTE risk is uncertain.METHODS AND RESULTS: We evaluated 51 polymorphisms from 32 inflammation-related genes (and an additional 19 polymorphisms from 15 thrombosis-related genes) as potential determinants of VTE in a prospective cohort of 22 413 white women followed over a 10-year period.Hazard ratios (HRs) for incident VTE according to the different genotypes were assessed by Cox proportional-hazards models.The false discovery rate (FDR) was used for correction for multiple testing with a 0.20 cut point.During follow-up, 158 idiopathic and 180 secondary VTE events occurred.As anticipated, factor V Leiden (HR, 3.22; 95% CI, 1.92 to 5.40; P<0.0001; FDR=0.004) and the prothrombin mutation (HR, 2.57; 95% CI, 1.64 to 4.02; P<0.0001; FDR=0.004) were both strongly associated with incident idiopathic VTE, as was the rs6046 polymorphism in the factor VII gene (HR, 0.54; 95% CI, 0.35 to 0.86; P=0.008; FDR, 0.12).With regard to polymorphism in the inflammatory genes, variation at rs1143634 in the IL-1beta gene was associated with a reduced risk of idiopathic VTE (HR, 0.59; 95% CI, 0.44 to 0.80; P=0.0007; FDR=0.02), whereas variation at rs1800872 in the IL-10 gene was associated with increased risk (HR, 1.42; 95% CI, 1.12 to 1.80; P=0.004; FDR=0.07).By contrast, no significant associations were found for secondary VTE events.CONCLUSIONS: In addition to previously reported polymorphisms associated with hemostasis and thrombosis, these prospective cohort data suggest that genetic variation in IL-1 beta and IL-10 genes may also influence the risk of idiopathic VTE.[1]
