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Cardiovascular Research 2003 60(1):26-39; doi:10.1016/S0008-6363(02)00857-X
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Infection and inflammation and the coagulation system

Marcel Levia,*, Tymen T Kellera, Eric van Gorpb and Hugo ten Catec

aDepartment of Vascular Medicine and Internal Medicine (F-4), Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands
bDepartment of Internal Medicine, Slotervaart Ziekenhuis, Amsterdam, The Netherlands
cDepartment of Internal Medicine, Academic Hospital Maastricht, Maastricht, The Netherlands

*Corresponding author. Tel.: +31-20-566-2171; fax: +31-20-691-9658. Email address: m.m.levi{at}amc.uva.nl

Severe infection and inflammation almost invariably lead to hemostatic abnormalities, ranging from insignificant laboratory changes to severe disseminated intravascular coagulation (DIC). Systemic inflammation results in activation of coagulation, due to tissue factor-mediated thrombin generation, downregulation of physiological anticoagulant mechanisms, and inhibition of fibrinolysis. Pro-inflammatory 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 promising results in the treatment of severe systemic infection with modulators of coagulation and inflammation.

KEYWORDS Cytokines; Hemostasis; Infection/inflammation

* For this manuscript Dr. F. Calabrese acted as Guest Editor.

Time for primary review 28 days.


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