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Alpha-2 plasmin inhibitor (antiplasmin) is synthesized in the liver with a biological half-life of approximately 3 days. It inactivates plasmin, the primary fibrinolytic enzyme responsible for remodeling the fibrin thrombus, and binds fibrin, together with factor XIIIa, making the clot more difficult to lyse. Absence of alpha-2 plasmin inhibitor results in uncontrolled plasmin-mediated breakdown of the fibrin clot and is associated with increased risk of bleeding.
Diagnosing congenital alpha-2 plasmin inhibitor deficiencies (rare)
Providing a more complete assessment of disseminated intravascular coagulation, intravascular coagulation and fibrinolysis, or hyperfibrinolysis (primary fibrinolysis), when measured in conjunction with fibrinogen, fibrin D-dimer, fibrin degradation products, soluble fibrin monomer complex, and plasminogen
Evaluating liver disease
Evaluating the effects of fibrinolytic or antifibrinolytic therapy
Patients with congenital homozygous deficiency (with levels of <10%) are clinically affected (bleeding). Heterozygotes having levels of 30% to 60% of mean normal activity are usually asymptomatic.
Lower than normal levels may be suggestive of consumption due to activation of plasminogen and its inhibition by alpha-2 plasmin inhibitor.
The clinical significance of high levels of alpha-2 plasmin inhibitor is unknown.
Alpha-2 plasmin inhibitor results are potentially affected by:
-Heparin, unfractionated or low-molecular-weight >4 U/mL
-Alpha-2-macroglobulin >7 mg/mL; potentially leading to a falsely-increased result
-Hemoglobin >200 mg/dL
-Bilirubin >20 mg/dL
-Triglycerides >1,000 mg/dL
Normal, full-term newborn infants may have borderline low or mildly decreased levels (> or =50%) which reach adult levels within 5 to 7 days postnatal.*
Healthy, premature infants (30-36 weeks gestation) may have mildly decreased levels which reach adult levels in < or =90 days postnatal.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
1. Lijnen HR, Collen D: Congenital and acquired deficiencies of components of the fibrinolytic system and their relation to bleeding or thrombosis. Blood Coagul Fibrinolysis 1989;3:67-77
2. Francis RB Jr: Clinical disorders of fibrinolysis: A critical review. Blut 1989;59:1-14
3. Aoki N: Hemostasis associated with abnormalities of fibrinolysis. Blood Rev 1989;3:11-17