• T Lustenberger, B Relja, B Puttkammer, E C Gabazza, E Geiger, Y Takei, J Morser, and I Marzi.
• Department of Trauma, Hand and Reconstructive Surgery, Goethe University Frankfurt am Main, Frankfurt, Germany. tom.lustenberg@gmail.com
• Thromb. Res. 2013 Jan 1;131(1):e26-30.

IntroductionThe thrombin-activatable fibrinolysis inhibitor (TAFI) is a potent inhibitor of fibrinolysis. However, the time course of TAFI and its activated form (TAFIa) following trauma, in particular in patients suffering trauma-induced coagulopathy, has been poorly examined.MethodsA total of 26 severely injured trauma patients were prospectively enrolled. TAFI and TAFIa levels were measured upon arrival and through hospital days one to 10. Trauma-induced coagulopathy was defined as elevated international normalized ratio (INR), and/or prolonged activated partial thromboplastin time (aPTT) and/or thrombocytopenia within one day of admission.ResultsTAFIa and TAFI levels showed the largest decrease on days one and two, respectively, with a progressive increase thereafter. Overall, 11 patients developed coagulopathy. No statistically significant differences were found for TAFI levels between the two groups. For TAFIa, however, coagulopathic patients experienced significantly lower levels on admission and on days six to eight (all p<0.05). Statistically significant correlations were found between TAFIa level on admission and the amount of packed red blood cells (p=0.011; Spearman's correlation coefficient=-0.5) and fresh frozen plasma (p=0.044; Spearman's correlation coefficient=-0.405) transfused within the initial 24hours.ConclusionDepletion of TAFIa may contribute to the development of trauma-induced coagulopathy.Copyright © 2012 Elsevier Ltd. All rights reserved.

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