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凝血功能紊乱是急性重症胰腺炎常见现象,轻者仅表现为亚临床凝血功能紊乱,而严重者可出现弥散性血管内凝血(DIC)伴凝血酶及纤维蛋白形成。实验室指标包括PT、APTT延长或缩短、血小板数量减少、D-Dimmer升高及纤维蛋白原异常等。由于重度感染、感染性休克等因素,急性重症胰腺炎患者容易出现血管内皮损伤、炎性反应失控,进而凝血系统激活致各重要脏器纤维蛋白沉积,引起各脏器缺血、坏死,导致重要脏器功能衰竭、MODS等。另外,白细胞活化刺激血管内皮产生炎症介质,这些炎症介质可提高凝血和纤维蛋白形成,系统性炎症反应引起凝血功能紊乱、微血栓形成。本文就急性重症胰腺炎病理过程中各凝血因子的作用机制相关研究进展进行简单概述。
Coagulation disorders are common in patients with acute severe pancreatitis, mild manifestations of subclinical coagulation disorders only, and in severe cases there may be disseminated intravascular coagulation (DIC) with thrombin and fibrin formation. Laboratory indicators include prolongation or shortening of PT, reduction of platelet count, increase of D-Dimmer and abnormality of fibrinogen. Due to severe infection, septic shock and other factors, patients with acute severe pancreatitis prone to vascular endothelial injury, inflammatory reaction out of control, and then the coagulation system activation of fibrin deposition of various important organs, causing various organs ischemia and necrosis, leading to important Organ failure, MODS and so on. In addition, leukocyte activation stimulates the production of inflammatory mediators in the vascular endothelium. These inflammatory mediators increase coagulation and fibrin formation. Systematic inflammatory reactions cause coagulation disorders and microthrombus formation. In this paper, the pathogenesis of acute pancreatitis in the mechanism of action of various coagulation factors related to a brief overview of the research progress.