Semin Thromb Hemost 2012; 38(05): 506-514
DOI: 10.1055/s-0032-1305782
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Infection and Inflammation as Risk Factors for Thrombosis and Atherosclerosis

Marcel Levi
1   Department of Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
,
Tom van der Poll
1   Department of Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
2   Laboratory of Experimental Medicine and Center for Infection and Immunity Amsterdam (CINIMA), Amsterdam, The Netherlands
,
Marcus Schultz
3   Laboratory for Experimental Intensive Care and Anesthesiology, Amsterdam, The Netherlands
4   Department of Intensive Care, Academic Medical Center, University of Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Publication Date:
07 March 2012 (online)

Abstract

Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to gross activation of coagulation that may result in localized thrombotic complications or systemic intravascular fibrin deposition. Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Proinflammatory cytokines, immune cells, and the endothelium 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. Similar mechanisms appear to play a role in the development of atherosclerosis and related arterial thrombosis. 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.

 
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