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Sepsis is a clinical syndrome which symptoms are caused by a systemic host response to infection. Amongst the most prominent features of sepsis are inflammation-induced activation of coagulation with concurrent downregulation of anticoagulant systems and fibrinolysis, in its most severe form leading to disseminated intravascular coagulation, which contributes to multiple organ failure and mortality. Another important hallmark in sepsis is endothelial dysfunction. Under normal conditions the endothelium provides for an anticoagulant surface, a property which is lost in sepsis. Activation of coagulation in turn impacts on inflammation. In this chapter data on the interplay between inflammation and coagulation in sepsis are summarized with a special focus on the role of the endothelium. Tissue factor-induced activation of coagulation is discussed, together with the procoagulant role of microparticles, platelets and von Willebrand factor. Downregulation of the anticoagulants tissue factor pathway inhibitor, antithrombin and the protein C system is discussed, together with the roles of glycosaminoglycans, proteoglycans and heparin. Moreover, inhibition of fibrinolysis in sepsis is described. The influence of coagulation and fibrinolysis in turn on inflammation is discussed with a special focus on protease-activated receptors, a research area that could substantially contribute to our understanding of the interplay between coagulation and inflammation in sepsis.

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Schouten, M., van der Poll, T. (2009). Coagulation Disorders in Sepsis. In: Rello, J., Díaz, E., Rodríguez, A. (eds) Management of Sepsis: The PIRO Approach. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-00479-7_10

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