U.O. di Diagnostica Ematochimica, Dipartimento di Patologia e Medicina di Laboratorio, Azienda Ospedaliero-Universitaria di Parma, Italy.
Clin Chem Lab Med. 2010 Dec;48(12):1693-701. doi: 10.1515/CCLM.2010.335. Epub 2010 Aug 13.
The plasma concentration of C-reactive protein (CRP), the first acute-phase protein to be identified, increases dramatically following tissue injury or inflammation. Although the physiological role of CRP is still not fully known, it has been suggested that concentrations might increase as part of the acute-phase response for facilitating non-specific immune functions, defense against bacterial pathogens, clearance of apoptotic and necrotic cells to prevent immunization against autoantigens and acceleration of the repair process. In agreement with the evidence that inflammation plays a pivotal role in the pathogenesis of atherosclerosis, CRP concentrations have been associated with cardiovascular disease, and measurement of CRP has therefore been proposed as a valuable aid to predict and stratify the risk of myocardial infarction and stroke. Recently, some clinical and biological evidence in support of the hypothesis that CRP might be also involved in the onset of venous thrombosis have emerged. Native and monomeric CRP exert several prothrombotic activities, including activation of blood coagulation, impairment of the endogenous fibrinolytic capacity, and stimulation or enhancement of platelet adhesiveness and responsiveness. Epidemiological investigations have also shown that CRP concentrations are associated with increased risk of venous thromboembolism and, even more interestingly, that statins might be effective in reducing the risk of this pathology. Although there is increasing emphasis that CRP might not only be a marker but also an active player in the development of venous thrombosis, further evidence is needed to establish which event comes first--thrombosis or inflammation.
C-反应蛋白（CRP）是最早被发现的急性期蛋白之一，其在组织损伤或炎症后会急剧增加。虽然 CRP 的生理作用仍不完全清楚，但有人认为，CRP 浓度的增加可能是急性期反应的一部分，以促进非特异性免疫功能、防御细菌病原体、清除凋亡和坏死细胞，以防止针对自身抗原的免疫和加速修复过程。与炎症在动脉粥样硬化发病机制中起关键作用的证据一致，CRP 浓度与心血管疾病相关，因此测量 CRP 已被提议作为预测和分层心肌梗死和中风风险的有价值的辅助手段。最近，一些支持 CRP 可能也参与静脉血栓形成发生的假设的临床和生物学证据已经出现。天然和单体 CRP 具有多种促血栓形成活性，包括激活血液凝固、损害内源性纤维蛋白溶解能力，以及刺激或增强血小板黏附和反应性。流行病学研究还表明，CRP 浓度与静脉血栓栓塞风险增加相关，更有趣的是，他汀类药物可能有效降低这种病理的风险。尽管越来越强调 CRP 可能不仅是一个标志物，而且是静脉血栓形成发展的一个活跃参与者，但需要进一步的证据来确定哪个事件是首先发生的——血栓形成还是炎症。
