|Values are valid only on day of printing.|
Evaluating patients with incident or recurrent thromboembolic events
Evaluating individuals with a family history of thrombophilia (venous or arterial)
Evaluating patients with ligneous conjunctivitis (strong association with homozygous plasminogen deficiency)
Evaluating fibrinolysis, in combination with other components of the fibrinolytic system (fibrinogen, tPa-inhibitor, and d-dimers)
During the formation of a hemostatic (fibrin) plug, biochemical mechanisms are initiated to limit the extent of the hemostatic process at the site of injury and maintain vascular patency. This process of fibrinolysis is defined as the plasmin-mediated degradation of fibrin. Plasmin limits the extent of the hemostatic process at the site of vessel injury.
Plasmin is generated from its precursor, plasminogen, by plasminogen activators (ie, tissue plasminogen-activator [tPa], urokinase-type plasminogen activator [uPa]). Plasminogen is a single-chain glycoprotein that is synthesized in the liver and has a biologic half-life of approximately 2 days.(1) Deficiency of plasminogen may be inherited or acquired. Persons with congenital plasminogen deficiency may have an increased risk for thrombosis. Homozygous deficiency has been associated with thromboembolic disease and ligneous conjunctivitis. The risk of thrombosis for heterozygous plasminogen deficiency is uncertain. This risk likely is compounded when combined with other inherited or acquired thrombophilias. Congenital deficiency of plasminogen is autosomally transmitted and rare, both in the general population and thrombosis patients, with a prevalence of approximately 0.4% and 1% to 3%, respectively.(2)
Based on the results of functional and immunologic (antigenic) assays, 2 types of plasminogen deficiency have been identified:
-Quantitative deficiency (type I)-defined by a corresponding decrease in both plasminogen activity and antigen level
-Functional deficiency (type II)-caused by a normally synthesized but dysfunctional plasminogen
This plasminogen activity assay will identify both types of deficiency.
Acquired causes of plasminogen deficiency include consumption such as with thrombolytic therapy (urokinase, tPa) or disseminated intravascular coagulation and fibrinolysis (DIC/ICF), or decreased synthesis (liver disease).(1)
Plasminogen activity <75% may represent a congenital deficiency state, if acquired deficiency can be excluded.
Hereditary abnormalities of plasminogen (deficiency or dysfunction) are very uncommon.
Acquired causes of plasminogen deficiency are much more common and may be the result of consumption due to thrombolytic therapy or intravascular coagulation and fibrinolysis or decreased synthesis (ie, liver disease).
Plasminogen levels are low at birth (approximately 50% of adult normal level) and reach adult levels at 6 months of age.
Proper preparation of the blood (plasma) specimen is extremely important to help insure accuracy of results and interpretation.
Plasminogen results are potentially affected by:
-Elevated levels of fibrinogen
-Heparin (unfractionated or low-molecular-weight) >4 U/mL
-Fibrin degradation products (FDP) >30 mg/dL
-Hemoglobin >200 mg/dL
-Bilirubin >20 mg/dL
-Triglycerides >1,000 mg/dL
Although this test can be performed in the absence of other coagulation tests and clinical information, it is most helpful when performed in conjunction with a consultative coagulation test panel with interpretive reporting. When the assay is performed to evaluate for thrombophilia, appropriate testing for other more common thrombophilic states should be performed, if not already done. THRMP / Thrombophilia Profile includes the appropriate panel of assays for an evaluation of an acquired or familial thrombophilia.
1. Bachman F: Plasminogen-plasmin enzyme system. In Homeostasis and Thrombosis. Edited by RW Coman, J Hirsh, VJ Marder, et al. Lippencott, 2001, pp 275-320
2. Demarmels BF, Sulzer I, Stucki B, et al: Is plasminogen deficiency a thrombotic risk factor? Thromb Haemost 1998;80:167-170
3. Andrews M: The hemostatic system in the infant. In Hematology of Infancy and Childhood. Vol 1. Fourth edition. Edited by DG Nathan, FA Oski. WB Saunders Company, 1993, pp 115-153