Disseminated intravascular coagulation: What's new?
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Updated: Aug 17, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
1Department of Vascular and Internal Medicine (F-4), Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. m.m.levi@amc.uva.nl
Insights
Disseminated intravascular coagulation (DIC) is a critical condition involving systemic coagulation activation, fibrin deposition, and consumption of clotting factors. Understanding its pathways informs new anticoagulant and pathway restoration therapies.
Area of Science:
- Hematology
- Pathophysiology
- Medical Science
Background:
- Disseminated intravascular coagulation (DIC) is a complex syndrome.
- It involves systemic coagulation activation, leading to fibrin deposition in microvasculature.
- This process consumes coagulation factors and platelets, linking DIC to organ dysfunction.
Purpose of the Study:
- To elucidate the pathogenetic mechanisms of DIC.
- To highlight the role of microvascular thrombosis in organ dysfunction.
- To discuss novel therapeutic strategies for DIC.
Main Methods:
- Review of pathological, experimental, and clinical findings.
- Analysis of pathogenetic pathways including coagulation activation, anticoagulant pathways, and fibrinolysis.
- Evaluation of emerging therapeutic approaches.
Main Results:
- DIC pathogenesis involves tissue factor-dependent coagulation activation.
- Defects in physiological anticoagulant pathways (antithrombin, protein C) contribute to DIC.
- Impaired fibrinolysis, due to elevated plasminogen activator inhibitor type 1, is also implicated.
Conclusions:
- Insights into DIC pathogenesis are driving novel therapeutic strategies.
- Therapeutic approaches include anticoagulation targeting tissue factor.
- Restoring physiological anticoagulant pathways, such as with activated protein C concentrate, is a key strategy.
Abstract:
Disseminated intravascular coagulation (DIC) is a syndrome characterized by a systemic activation of coagulation leading to the intravascular deposition of fibrin in the (micro) vasculature and the simultaneous consumption of coagulation factors and platelets. The occurrence of microvascular thrombosis as a consequence of DIC is underscored by pathological, experimental and clinical findings, demonstrating a link between DIC and organ dysfunction. Pathogenetic pathways that play a role in the development of DIC include tissue factor-dependent activation of coagulation, defective physiological anticoagulant pathways (such as the antithrombin system and the protein C system), and impaired fibrinolysis, caused by elevated levels of plasminogen activator inhibitor type 1. Novel therapeutic strategies are based on current insights into the pathogenesis of DIC, and include anticoagulant strategies (eg, directed at tissue factor) and strategies to restore physiological anticoagulant pathways (such as activated protein C concentrate).
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