Coagulation Factor XIII in Cerebral Venous Thrombosis

Abstract

Coagulation factor XIII (FXIII) is activated in the last stage of the coagulation cascade in the presence of thrombin and Ca 2 þ by cleavage and release of the activation peptide (FXIII activation peptide, AP-FXIII) from the A-subunit and disso-ciation of the carrier B-subunits. Activated FXIII then cross-links fi brin fi bers and incorporates anti fi brinolytic proteins into the clot. Therefore, FXIII has a crucial role in stabilizing fi brin: it determines clot properties and fi brinolysis, and contributes to clot formation in every acute thrombotic event. 1 Consequently, FXIII is consumed during acute thrombotic events leading to a reduction in systemic circulating FXIII plasma levels which are also associated with outcome, e.g., in acute myocardial infarction, 2 stroke, 3 – 5 and venous thromboembolism. 6 – 9 In patients with acute stroke, we could detect circulating free AP-FXIII