Increased urokinase and consumption of α₂ -antiplasmin as an explanation for the loss of benefit of tranexamic acid after treatment delay.

ABSTRACT: Essentials Delayed treatment with tranexamic acid results in loss of efficacy and poor outcomes. Increasing urokinase activity may account for adverse effects of late tranexamic acid treatment. Urokinase + tranexamic acid produces plasmin in plasma or blood and disrupts clotting. α₂ -Antiplasmin consumption with ongoing fibrinolysis increases plasmin-induced coagulopathy. SUMMARY: Background Tranexamic acid (TXA) is an effective antifibrinolytic agent with a proven safety record. However, large clinical trials show TXA becomes ineffective or harmful if treatment is delayed beyond 3 h. The mechanism is unknown but urokinase plasminogen activator (uPA) has been implicated. Methods Inhibitory mechanisms of TXA were explored in a variety of clot lysis systems using plasma and whole

SUBMITTER: Longstaff C 

PROVIDER: S-EPMC6334274 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature