25464 Plasminogen Activity, Plasma (PSGN)

Plasminogen, Functional, Plasma

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)

1. Spin down, remove plasma, and spin plasma again.
2. Freeze specimen immediately at < or =-40 degrees C, if possible.

Additional Information:
1. Double-centrifuged specimen is critical for accurate results as platelet contamination may cause spurious results.
2. Each coagulation assay requested should have its own vial.

​Hemolysis	​Gross
​Lipemia	​Gross
​Icterus	​Gross

 

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. 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. 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).

75-140%

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.