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Regulatory role of cytokines in disseminated intravascular coagulation

T van der Poll1, E de Jonge, M Levi

  • 1Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. T.vanderPoll@amc.uva.nl

Seminars in Thrombosis and Hemostasis
|December 12, 2001
PubMed

Insights

Disseminated intravascular coagulation (DIC) during sepsis arises from coagulation system overactivation and inhibited natural anticoagulants. This review highlights key cytokines mediating the procoagulant response in systemic infections.

Area of Science:

  • Hematology
  • Immunology
  • Critical Care Medicine

Background:

  • Disseminated intravascular coagulation (DIC) is a severe complication in various diseases.
  • DIC in sepsis involves robust coagulation activation and impaired fibrinolysis/anticoagulation.
  • Cytokines are recognized as critical mediators of these hemostatic changes.

Purpose of the Study:

  • To review current understanding of cytokine involvement in sepsis-induced DIC.
  • To identify specific cytokines driving the procoagulant state during systemic infection.

Main Methods:

  • Literature review of recent research on cytokines and DIC in sepsis.
  • Analysis of studies investigating hemostatic alterations in systemic infections.

Main Results:

  • Cytokines play a significant role in the procoagulant response to sepsis.
  • Specific pro-inflammatory cytokines are implicated in triggering DIC pathways.
  • Understanding these cytokine-driven mechanisms is crucial for managing sepsis-associated coagulopathy.

Conclusions:

  • Cytokines are key players in the pathogenesis of DIC during sepsis.
  • Targeting specific cytokines may offer novel therapeutic strategies for sepsis-induced coagulopathy.

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