Semeraro N, Colucci M
Dipartimento di Scienze Biomediche e Oncologia Umana, University of Bari, Italy.
Int J Clin Lab Res. 1992;21(3):214-20. doi: 10.1007/BF02591649.
Over the last few years, evidence has accumulated that the pathogenetic mechanism of disseminated intravascular coagulation encountered in patients with infectious diseases is extraordinarily complex and involves multiple interactions between the microorganism itself and/or a number of mediators, both microorganism derived and host manufactured, and multifunctional cellular systems, namely endothelial cells and mononuclear phagocytes. In particular, infectious agents and mediators shift the coagulation-fibrinolysis equilibrium of these cells towards fibrin formation and accumulation, via enhancement of procoagulant properties and reduction of both anticoagulant and fibrinolytic capacities. New insights into the pathogenetic mechanism may have important implications for the management of infected patients with disseminated intravascular coagulation.
在过去几年中，越来越多的证据表明，传染病患者中出现的弥散性血管内凝血的发病机制极其复杂，涉及微生物自身和/或多种介质（包括微生物衍生的和宿主产生的）以及多功能细胞系统（即内皮细胞和单核吞噬细胞）之间的多种相互作用。特别是，感染因子和介质通过增强促凝特性以及降低抗凝和纤溶能力，使这些细胞的凝血-纤溶平衡朝着纤维蛋白形成和积累的方向转变。对发病机制的新见解可能对弥散性血管内凝血感染患者的管理具有重要意义。
