Clinical Information

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/intravascular coagulation and fibrinolysis (DIC/ICF), or decreased synthesis (liver disease).(1)