Plasminogen Activity, Plasma
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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 are at an increased risk for development of an ocular condition called ligneous conjunctivitis. Congenital deficiency of plasminogen is autosomally transmitted and rare in the general population, with a prevalence of approximately 0.4%.(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)
Evaluating patients with ligneous conjunctivitis (strong association with homozygous plasminogen deficiency)
Evaluating fibrinolysis, in combination with other components of the fibrinolytic system (fibrinogen, tissue plasminogen-activator-inhibitor, and d-dimers)
Plasminogen activity below 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.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
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
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.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
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. Mehta R, Shapiro AD: Plasminogen deficiency. Haemophilia 2008;14:1261-1268
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