A2-antiplasmin (or otherwise A2 plasmin inhibitor) is synthesized in the liver.
A2-antiplasmin main role is to inactivate plasmin, the major fibrinolytic enzyme responsible for remodeling the fibrin clot and binding fibrin together with Factor XIIIa, making clot lysis more difficult.
The absence of A2-antiplasmin results in 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 conditions).
Patients with congenital homozygous A2-antiplasmin deficiency (levels < 10%), show clinical symptoms (bleeding). Heterozygotes have 30% to 60% levels of average physiological activity and are usually asymptomatic.
A2-antiplasmin is also measured to evaluate liver disease and the effectiveness of thrombolytic or antifibrinolytic therapy.
Alpha-2-antiplasmin is the major physiologic inhibitor of plasmin. Reductions in alpha-2-antiplasmin have been associated with DIC, severe liver disease, malignancy, nephrotic syndrome and following thrombolytic therapy.
Lower than normal levels may indicate its consumption as a result of plasminogen activation and its inhibition by A2-antiplasmin. The clinical significance of high levels of A2-antiplasmin is unknown.
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