Yoshida Hideo, Granger D Neil
Department of Molecular & Cellular Physiology, LSU Health Sciences Center, Shreveport, Louisiana 71130-3932, USA.
Inflamm Bowel Dis. 2009 Aug;15(8):1245-55. doi: 10.1002/ibd.20896.
Inflammatory bowel diseases (IBDs) are associated with platelet activation and an increased risk for thromboembolism. While the mechanisms that underlie the altered platelet function and hypercoagulable state in IBD remain poorly understood, emerging evidence indicates that inflammation and coagulation are interdependent processes that can initiate a vicious cycle wherein each process propagates and intensifies the other. This review addresses the mechanisms that may account for the mutual activation of coagulation and inflammation during inflammation and summarizes evidence that implicates a role for platelets and the coagulation system in the pathogenesis of human and experimental IBD. The proposed link between inflammation and coagulation raises the possibility of targeting the inflammation-coagulation interface to reduce the morbidity and mortality associated with IBD.
炎症性肠病（IBD）与血小板活化及血栓栓塞风险增加相关。虽然IBD中血小板功能改变和高凝状态的潜在机制仍知之甚少，但新出现的证据表明，炎症和凝血是相互依存的过程，可引发恶性循环，其中每个过程都会促进和加剧另一个过程。本综述探讨了可能解释炎症期间凝血与炎症相互激活的机制，并总结了表明血小板和凝血系统在人类及实验性IBD发病机制中起作用的证据。炎症与凝血之间的潜在联系增加了针对炎症-凝血界面以降低IBD相关发病率和死亡率的可能性。
