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C-reactive protein and venous thromboembolism

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Issue: 2009: 102/4 (Oct) pp. 611-798
Pages: 615-619

C-reactive protein and venous thromboembolism

A prospective investigation in the ARIC cohort

Aaron R. Folsom 1; Pamela L. Lutsey 1; Brad C. Astor 2; Mary Cushman3

1Division of Epidemiology & Community Health, School of Public Health, University of Minnesota, Minneapolis, Minnesota, USA; 2 Department
of Epidemiology, The Johns Hopkins Bloomberg School of Public Health, The Johns Hopkins University, Baltimore, Maryland, USA;
3Department of Medicine, University of Vermont, Burlington, Vermont, USA; 3 Department of Pathology, University of Vermont, Burlington,
Vermont, USA


Venous thrombosis, C-reactive protein, prospective study, pulmonary embolus


The role of inflammation in the causation of venous thromboembolism (VTE) is uncertain. In 10,505 participants of the Atherosclerosis Risk in Communities (ARIC) Study, we assessed the association of the systemic inflammation marker, elevated C-reactive protein (CRP), with incidence of VTE (n=221) over a median of 8.3 years of follow-up. Adjusted for age, race, and sex, the hazard ratios of VTE across quintiles of CRP were 1.0, 1.61, 1.16, 1.56, and 2.31 (p for trend p<0.0007). For CRP above the upper 10 percentile (≥8.55 mg/L), compared with the lowest 90% of CRP values, the hazard ratio of VTE was 2.07 (95% CI 1.47, 2.94). Further adjustment for baseline hormone replacement therapy, diabetes, and body mass index attenuated the hazard ratios only slightly. For example, the adjusted hazard ratio of VTE was 1.76 (95% CI 1.23, 2.52) for CRP above versus below the 90th percentile. In conclusion, this prospective, populationbased study suggests elevated CRP is independently associated with increased risk of VTE.

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