P187	C-Reactive protein and complement C3: associations with haemostatic and cardiovascular risk factors in the Leeds Family Study.
U.K.Prasad, A.M.Carter, M.S.Freeman, P.J.Grant
Academic Unit of Molecular Vascular Medicine, Leeds, GB.

Background: Elevated CRP and C3 levels are independent cardiovascular risk factors. CRP and C3 correlate with features of the insulin resistance syndrome; however, their relationship with haemostatic factors is unclear. Hypothesis: We tested the hypothesis that CRP and C3 are associated with haemostatic cardiovascular risk factors in addition to features of the insulin resistance syndrome. Method: Plasma CRP, C3, haemostatic factors and measures of insulin resistance were determined in plasma from 508 healthy Caucasian subjects from 89 families. Statistical analyses were carried out to determine associations of CRP and C3 with haemostatic factors and measures of insulin resistance, using SPSS v12.0 and SOLAR v2.1.4. Result: CRP and C3 were correlated (r=0.351, p<0.001). Both CRP and C3 correlated with haemostatic factors fibrinogen, FVII:C, PAI-1 and tPA. CRP and C3 were correlated with: BMI, cholesterol, HOMA, insulin, leptin, LDL, triglycerides, WHR and systolic and diastolic BP, and negatively correlated with HDL. In addition C3, but not CRP, was correlated with fasting glucose and negatively correlated with adiponectin. In quantitative genetic analyses, additive genetic components explained 34% of the variance in plasma CRP; C3, fibrinogen, leptin and triglycerides were independently associated with CRP and together explained 43.7% of the total variance in CRP. The phenotypic correlation between two traits in the same individual comprises an environmental and a genetic component. Environmental correlations were found for CRP with C3, fibrinogen, leptin and triglycerides, whereas genetic correlation was found only between CRP and fibrinogen (rG=0.67, p<0.001). For C3, additive genetic components explained 28.7% of the variance; CRP, adiponectin, leptin, HOMA and triglycerides were independently associated with C3 and together explained 20.4% of the total variance of C3. Environmental correlations were found for C3 with CRP, HOMA, leptin and triglycerides but no significant genetic correlations were found. Conclusion: These data confirm the complex interrelationships between inflammation and atherothrombotic risk clustering in insulin resistance.

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