Alpha-2 Plasmin Inhibitor, Plasma
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
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
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.
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.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
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
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
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