Estimation of Coagulation Factor XIII Activity Based on the Initial Plasma Fibrinogen Level in Trauma

Overview

Coagulation factor XIII (FXIII), a plasma transglutaminase, is known as the final enzyme of the coagulation cascade, responsible for a cross-linking of fibrin to strengthen blood clot. It also minimizes fibrin degradation by its cross-linking it with alfa2-antiplasmin molecules. It has been found that similar to plasma fibrinogen level, FXIII activity can be reduced in the early phase of severe trauma. Therefore, its immediate substitution is of potential therapeutic interest in trauma-induced coagulopathy. However, unlike plasma fibrinogen level evaluation, measurement of the FXIII activity is not routinely available. Therefore, targeted substitution of FXIII is practically impossible. The plasma fibrinogen level is routinely measured in severe trauma patients. Based on pathophysiologic assumptions and a limited number of published data we hypothesize that the FXIII activity correlates with fibrinogen level. In such case, indirect FXIII activity prediction by fibrinogen level measurement would be a convenient approach to enable FXIII targeted substitution. Therefore we decided to perform a prospective observational clinical trial to determine whether the low plasma fibrinogen level in severe trauma correlates with decreased FXIII activity.

Coagulation factor XIII (FXIII), a plasma transglutaminase, is known as the final enzyme of the coagulation cascade, responsible for a cross-linking of fibrin to strengthen blood clot. It also minimizes fibrin degradation by its cross-linking it with alfa2-antiplasmin molecules. It has been found that similar to plasma fibrinogen level, FXIII activity can be reduced in the early phase of severe trauma. Therefore, its immediate substitution is of potential therapeutic interest in trauma-induced coagulopathy. However, unlike plasma fibrinogen level evaluation, measurement of the FXIII activity is not routinely available. Therefore, targeted substitution of FXIII is practically impossible. The plasma fibrinogen level is routinely measured in severe trauma patients. Based on pathophysiologic assumptions and a limited number of published data we hypothesize that the FXIII activity correlates with fibrinogen level. In such case, indirect FXIII activity prediction by fibrinogen level measurement would be a convenient approach to enable FXIII targeted substitution. Therefore we decided to perform a prospective observational clinical trial to determine whether the low plasma fibrinogen level in severe trauma correlates with decreased FXIII activity.