EDITORIAL

Pulmonary coagulopathy

Pulmonary coagulopathy: a potential therapeutic target in different forms of lung injury

Marcus J Schultz¹ and Marcel Levi²

¹ Department of Intensive Care Medicine and Laboratory of Experimental Intensive Care and Anesthesiology (LEICA), Academic Medical Center - University of Amsterdam, and HERMES Critical Care Group, Amsterdam, The Netherlands
² Department of Internal Medicine, Academic Medical Center - University of Amsterdam, Amsterdam, The Netherlands

Correspondence to:
Correspondence to:
Dr Marcus J Schultz
Department of Intensive Care Medicine, C3-415, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands;m.j.schultz@amc.uva.nl

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The role and source of tissue factor

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The first 150 words of the full text of this article appear below.

A large body of evidence has shown that systemic coagulopathy is a key event in severe systemic inflammation, such as that which occurs in sepsis.¹ Systemic coagulopathy is the net result of activation of coagulation and defective systems of natural inhibition of coagulation, on the one hand, and attenuation of fibrinolysis on the other. Activation of coagulation is primarily driven by the extrinsic coagulation pathway which starts with expression of tissue factor (TF) on mononuclear cells and endothelial cells. TF then binds and activates factor VII which activates downstream coagulation cascades.^2,3 Mechanisms that regulate the coagulation pathway under normal conditions involve natural inhibitors of coagulation, including activated protein C (APC), antithrombin (AT) and tissue factor pathway inhibitor (TFPI). In general, they all interfere with the TF–factor VIIa-induced activation of coagulation, but on different levels. In patients with sepsis, increased coagulant activity is not sufficiently counterbalanced by these natural . . . [Full text of this article]

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