• Marcel Levi, Evert de Jonge, and Tom van der Poll.
• Department of Internal Medicine, Academic Medical Center, University of Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
• Blood Rev. 2002 Dec 1;16 Suppl 1:S29-34.

AbstractDisseminated intravascular coagulation (DIC) is a syndrome characterized by systemic intravascular activation of coagulation, leading to widespread deposition of fibrin in the circulation. Recent knowledge on important pathogenetic mechanisms that may lead to DIC has resulted in novel preventive and therapeutic approaches to patients with DIC. Thrombin generation proceeds via the (extrinsic) tissue factor/activated factor VII route and simultaneously occurring depression of inhibitory mechanisms, such as antithrombin and the protein C and protein S system. Also, impaired fibrin degradation, due to high circulating levels of plasminogen activator inhibitor type-I, contributes to enhanced intravascular fibrin deposition. Strategies aimed at the inhibition of coagulation activation may theoretically be justified and have been found beneficial in experimental and initial clinical studies. These strategies comprise inhibition of tissue factor-mediated activation of coagulation or restoration of physiological anticoagulant pathways, by means of the administration of antithrombin concentrate or (activated) protein C.

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