Correspondence  |   September 2017
In Reply
Author Notes
  • Queen Mary University of London, London, United Kingdom (R.A.D.).
  • (Accepted for publication June 1, 2017.)
    (Accepted for publication June 1, 2017.)×
Article Information
Correspondence   |   September 2017
In Reply
Anesthesiology 9 2017, Vol.127, 585-586. doi:10.1097/ALN.0000000000001761
Anesthesiology 9 2017, Vol.127, 585-586. doi:10.1097/ALN.0000000000001761
We thank Prof. Tanaka and colleagues for their interest in our article1  and for their thoughts on the interpretation of our findings. We believe that overall they are in agreement with the main thrust of our article, which is that activation of protein C (aPC) is central to the pathogenesis of acute traumatic coagulopathy (ATC). Most of their points address matters of interpretation regarding the relative extent that aPC affects different parts of the coagulation system.
First, they highlight our use of D-dimers rather than a specific fibrin degradation marker and state that the high level of D-dimer must simply be a reflection of high thrombin generation. Our extensive reading of the literature and our understanding of fibrinogen and fibrin cleavage is that these processes are not linear and that no specific test differentiates between the different ways in which they are broken down. Indeed, they themselves say that D-dimers represent ongoing fibrin degradation. In either case, we have shown that products of fibrin/fibrinogen breakdown are dramatically higher in patients with ATC and that blocking aPC (with thrombomodulin knock-in mice) essentially abolishes this response (despite equivalent markers of thrombin generation).
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