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From the Departments of Vascular Medicine (R.J.B., J.J.P.K., J.H.M.L., B.v.d.B., J.C.M.M., M.L., E.S.G.S.), Hematology (J.J.Z.), and Experimental Medicine (P.H.R.), Academic Medical Center, Amsterdam, the Netherlands; and Pfizer Global Research and Development (D.H.), Ann Arbor, Mich.
Correspondence to Erik S. Stroes, MD, PhD, Department of Vascular Medicine, Rm F4.275, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. E-mail e.s.stroes{at}amc.uva.nl
C-reactive protein (CRP) has been postulated to play a causal part in atherosclerosis and its acute complications. We assessed the effects of CRP-infusion on coagulation and inflammatory pathways to determine its role in atherothrombotic disease. Seven male volunteers received an infusion on two occasions, containing 1.25 mg/kg recombinant human CRP (rhCRP) or diluent, respectively. CRP-concentrations rose after rhCRP-infusion from 1.9 (0.3 to 8.5) to 23.9 (20.5 to 28.1) mg/L, and subsequently both inflammation and coagulation were activated. This sequence of events suggests that CRP is not only a well known marker of cardiovascular disease, but is also probably a mediator of atherothrombotic disease.
Key Words: inflammation endothelium atherosclerosis thrombosis
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