Lowe Gordon D O, Pepys Mark B
Centre for Amyloidosis and Acute Phase Proteins, Department of Medicine, University College London, Rowland Hill Street, London NW3 2PF, United Kingdom.
Curr Atheroscler Rep. 2006 Sep;8(5):421-8. doi: 10.1007/s11883-006-0040-x.
C-reactive protein (CRP) has been widely promoted as a strong, independent predictor of cardiovascular events and metabolic syndrome, both in general populations and in patients with clinical cardiovascular disease, and as a causal player in atherothrombosis. However, recent evidence shows that the association of CRP with cardiovascular events is weaker than previously thought, that it may be largely attributed to confounding by established causal risk factors, and that CRP is, therefore, probably not a clinically useful risk predictor. The lack of association of noncoding CRP gene polymorphisms (which determine different baseline CRP values) with coronary events or metabolic syndrome does not support a causal role for CRP, and most of the putatively proatherothrombotic in vitro effects claimed for CRP were caused by contaminants in commercial CRP preparations and not by CRP. Future clinical trials of specific CRP inhibitors now in development could directly test the contribution of CRP to pathogenesis of cardiovascular disease.
C反应蛋白（CRP）在普通人群和临床心血管疾病患者中，已被广泛宣传为心血管事件和代谢综合征的有力独立预测指标，以及动脉粥样硬化血栓形成的致病因素。然而，最近的证据表明，CRP与心血管事件的关联比之前认为的要弱，这可能很大程度上归因于既定因果风险因素的混杂作用，因此，CRP可能不是一个临床有用的风险预测指标。非编码CRP基因多态性（决定不同的基线CRP值）与冠状动脉事件或代谢综合征缺乏关联，不支持CRP的致病作用，并且大多数声称的CRP在体外的促动脉粥样硬化血栓形成作用是由商业CRP制剂中的污染物引起的，而非CRP本身。目前正在研发的特定CRP抑制剂的未来临床试验可以直接测试CRP对心血管疾病发病机制的作用。
