• Marcel Levi, Marcus Schultz, and Tom van der Poll.
• Department of Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
• Semin. Thromb. Hemost. 2010 Jun 1; 36 (4): 367-77.

AbstractSevere infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation. Systemic inflammation as a result of severe infection leads to activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Proinflammatory cytokines play a central role in the differential effects on the coagulation and fibrinolysis pathways. Vice versa, activation of the coagulation system may importantly affect inflammatory responses by direct and indirect mechanisms. Apart from the general coagulation response to inflammation associated with severe infection, specific infections may cause distinct features, such as hemorrhagic fever or thrombotic microangiopathy. The relevance of the cross-talk between inflammation and coagulation is underlined by the results of the treatment of severe systemic infection with modulators of coagulation and inflammation.Copyright Thieme Medical Publishers.

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