Sorted By Test Name - Mayo Medical Laboratories

FPACT
91760
PSGN
9079
Hemostasis and Thrombosis. Edited by RW Colman, J Hirsh, VJ Marder, et al. Philadelphia, Lippincott,
2001, pp 355-365 3. Vaughn DE, Declerck PJ: Regulation of fibrinolysis. In Thrombosis and
Hemorrhage. Edited by J Loscalzo, AI Schager. Philadelphia, Lippincott, 2003, pp 389-396 4. Goodnight
SH Jr, Hathaway WE: Fibrinolytic defects and thrombosis. In Disorders of Hemostasis and Thrombosis:
A Clinical Guide. New York, McGraw-Hill Book Company, 2001, pp 389-396 5. Kruithof EK, Gudinchet
A, Bachman F: Plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 in various disease
states. Thromb Haemostasis 1988;59(1):7-12 6. Salat C, Holler E, Kolb HJ, et al: Plasminogen activator
inhibitor-1 confirms the diagnosis of hepatic veno-occlusive disease in patients with hyperbilirubinemia
after bone marrow transplantation. Blood 1997;89:2184-2188 7. Fay WP, Shapiro AD, Shih JL, et al:
Brief report: complete deficiency of plasminogen-activator inhibitor Type 1 due to a frame-shift mutation.
N Engl J Med 1992 Dec 10;327(24):1729-1733
Plasminogen Activator Inhibitor-1, 4G/5G Genotyping (PAI-1)
Polymorphism
Reference Values:
A final report will be faxed under separate cover.
Test Performed By: Esoterix Coagulation
8490 Upland Dr.
Suite 100
Englewood, CO 80112
Plasminogen Activity, Plasma
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 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)
Useful For: 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)
Interpretation: Plasminogen activity