Pharmacology of Tranexamic Acid: Mechanisms and Applications in Modern Medicine

Abstract

Tranexamic acid (TXA) is a synthetic lysine-analogue antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin, preventing the dissolution and degradation of fibrin clots. TXA has demonstrated efficacy in reducing blood loss and transfusion requirements across various clinical contexts, including cardiac surgery, trauma, liver surgery, and orthopedic procedures. In cardiac surgery, TXA inhibits plasmin-induced platelet activation during cardiopulmonary bypass, attenuates the inflammatory response, and interacts beneficially with desmopressin. Robust evidence supports TXA use in trauma, with the CRASH-2 trial showing reduced all-cause mortality and death due to bleeding. In liver transplantation, TXA exhibits similar efficacy to aprotinin in reducing blood loss and transfusion needs. TXA is also effective in treating menorrhagia and reducing blood loss in obstetric and gynecological surgeries. Topical TXA application achieves lower plasma concentrations while maintaining effectiveness in reducing bleeding. Adverse effects include dose-dependent seizures, particularly in cardiac surgery, potentially due to TXA's inhibition of GABA and glycine receptors. Despite no definitive evidence of increased thromboembolic risk, judicious use is advised, especially with prothrombotic medications. Optimal dosing regimens and the impact on renal-impaired patients require further research. Ongoing trials, such as CRASH-3, WOMAN, and ATACUS, are expected to provide insights into TXA's role in improving morbidity and mortality across diverse clinical settings.