A2-Antiplasmin (or otherwise A2 Plasmin Inhibitor) is synthesized in the liver and has a biological half-life of approximately 3 days. Its main role is to inactivate plasmin, the major fibrinolytic enzyme responsible for remodeling the fibrin clot and binding fibrin with Factor XIIIa, making clot lysis more difficult. The absence of A2-Antiplasmin results in an uncontrolled lysis of the fibrin clot by plasmin, which is associated with an increased risk of bleeding.
A2-Antiplasmin is measured to diagnose congenital deficiencies (rare condition).
Patients with congenital homozygous A2-Antiplasmin deficiency (<10% levels), show clinical symptoms (bleeding). Heterozygotes have 30% - 60% levels of average physiological activity and are usually asymptomatic.
Measurement of A2-Antiplasmin provides a more complete assessment of diffuse intravascular coagulation, intravascular coagulation, fibrinolysis and hyperinolysis (primary fibrinolysis), when measured in combination with fibrinogen, D-dimers, and fibrinolysis products.
A2-Antiplasmin is also measured to evaluate liver disease and the effectiveness of thrombolytic or antifibrinolytic therapy.
Lower than normal levels may indicate consumption of plasminogen activation and inhibition by A2-Antiplasmin. The clinical significance of high levels of A2-Antiplasmin is unknown.