Increased urokinase and consumption of α2‐antiplasmin as an explanation for the loss of benefit of tranexamic acid after treatment delay
ConclusionsTXA protects fibrin but stimulates uPA activity and slows inhibition of plasmin by α2‐antiplasmin. Plasmin proteolytic activity digests fibrinogen and disrupts coagulation, exacerbated when α2‐antiplasmin is consumed by ongoing fibrinolysis. Additional direct inhibition of plasmin by aprotinin may prevent development of coagulopathy and extend the useful time window of TXA treatment.This article is protected by copyright. All rights reserved.
Source: Journal of Thrombosis and Haemostasis - Category: Hematology Authors: Colin Longstaff,
Matthew Locke Tags: Original Article ‐ Fibrinolysis Source Type: research