Alpha-2 Plasmin Inhibitor, Plasma
CPT CODE:
- 85410
USEFUL FOR:
Diagnosing congenital alpha-2 plasmin inhibitor deficiencies (rare)
Providing a more complete assessment of disseminated intravascularcoagulation, 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 or the effects of fibrinolytic or antifibrinolytic therapy
SPECIMEN REQUIRED:
See "Coagulation Studies" in Special Instructions.
1. Draw blood in a light blue-top (citrate) tube(s). Spin down, remove plasma, spin plasma again, and place 1 mL of platelet-poor plasma in plastic vial. (Glass vial is not acceptable.) Note: Double-centrifuged specimens are critical for accurate results as platelet contamination may cause spurious results.2. Freeze specimen immediately at < or = -40 degrees C if possible.3. Send specimen frozen.Note: 1. Each coagulation assay requested should have its own vial. 2. If ordering electronically, no form is required with the specimen. If not ordering electronically, please complete and submit a "Coagulation Request Form" (Supply T237) with the specimen.
TRANSPORT TEMPERATURE:
Frozen\Refrig NO\Ambient NO
CLINICAL INFORMATION:
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.
CLINICAL INTERPRETATION:
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 toactivation of plasminogen and its inhibition by alpha-2 plasmin inhibitor.
The clinical significance of high levels of alpha-2 plasmin inhibitor is unknown.
REFERENCE VALUES:
Adults: 80-140%
Normal, full-term newborn infants may have borderline low or mildly
decreased levels (> or =50%) which reach adult levels within 5-7 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.








