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Plasminogen, Antigenic (5164X)
Test Code59915P
CPT Codes
85421
Preferred Specimen
1 mL plasma collected in 3.2% sodium citrate (lt. blue-top) tube
Patient Preparation
Overnight fasting is required
Minimum Volume
0.5 mL
Other Acceptable Specimens
Plasma collected in: EDTA (lavender-top) tube
Instructions
Use 3.2% sodium citrate (light blue-top) anticoagulant tube. Fill tube with venous blood and gently mix without shaking the tube. Centrifuge within 1 hour of blood draw at 1500 g for 10 minutes, preferably at 4° C. Remove plasma using plastic pipette and place into plastic tube and cap. Freeze immediately.
Transport Temperature
Frozen
Specimen Stability
Room temperature: Unacceptable
Refrigerated: 8 days
Frozen: 30 days
Refrigerated: 8 days
Frozen: 30 days
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
Received room temperature
Methodology
Fixed Time Nephelometry
Setup Schedule
P.M. Sets up 2 days a week.
Report Available
Reports in 2 days.
Clinical Significance
This test, in combination with Plasminogen Activity (test code 4458), can help distinguish between 2 rare congenital plasminogen deficiency disorders: type 1 deficiency (hypoplasminogenemia) and type 2 deficiency (dysplasminogenemia) [1].
Type I deficiency is a quantitative deficiency that results in low plasminogen antigenic and activity levels. Type I deficiency may cause ligneous conjunctivitis. Type II deficiency is a functional deficiency that results in normal antigenic levels and low activity levels [1,2].
Plasminogen, a protein synthesized by the liver, is part of the fibrinolysis system. In the body, plasminogen is converted to plasmin in the presence of fibrin and serves to limit the extent of clot formation to preserve blood flow through vessels [1]. Plasminogen also plays an integral role in wound healing [2].
Low levels of plasminogen may be acquired or congenital. Most plasminogen deficiencies are acquired as a result of (1) treatment with thrombolytic agents such as urokinase or tissue plasminogen activator (TPA); (2) consumption from disseminated intravascular coagulation (DIC); or (3) impaired synthesis from liver disease [3].
Type I congenital plasminogen deficiencies have been associated with pseudomembrane formation on mucosal surfaces. Ligneous conjunctivitis is the most well-defined disorder associated with quantitative deficiency of plasminogen [2]. The relationship between plasminogen deficiency and thrombosis is unclear [2,3].
Many conditions may affect results of plasminogen testing, including liver failure; processes that increase fibrin degradation products (FDPs), such as DIC; and interference from elevated hemoglobin, bilirubin, or triglycerides. Exposure to heparin or cryoprecipitate products may also affect results.
Interpretation of the antigenic plasminogen result requires integration with other laboratory and clinical studies. This test should be interpreted in the context of pertinent clinical and family history, and physical examination findings.
References
1. Shaz BH, et al. Transfusion Medicine and Hemostasis Clinical and Laboratory Aspects. 2nd ed. New York, NY: Elsevier; 2013:883-884.
2. Mehta R, et al. Haemophilia. 2008;14:1261-1268.
3. Hedner U, et al. Haemostasis.1988;18(suppl 1):87-92
Type I deficiency is a quantitative deficiency that results in low plasminogen antigenic and activity levels. Type I deficiency may cause ligneous conjunctivitis. Type II deficiency is a functional deficiency that results in normal antigenic levels and low activity levels [1,2].
Plasminogen, a protein synthesized by the liver, is part of the fibrinolysis system. In the body, plasminogen is converted to plasmin in the presence of fibrin and serves to limit the extent of clot formation to preserve blood flow through vessels [1]. Plasminogen also plays an integral role in wound healing [2].
Low levels of plasminogen may be acquired or congenital. Most plasminogen deficiencies are acquired as a result of (1) treatment with thrombolytic agents such as urokinase or tissue plasminogen activator (TPA); (2) consumption from disseminated intravascular coagulation (DIC); or (3) impaired synthesis from liver disease [3].
Type I congenital plasminogen deficiencies have been associated with pseudomembrane formation on mucosal surfaces. Ligneous conjunctivitis is the most well-defined disorder associated with quantitative deficiency of plasminogen [2]. The relationship between plasminogen deficiency and thrombosis is unclear [2,3].
Many conditions may affect results of plasminogen testing, including liver failure; processes that increase fibrin degradation products (FDPs), such as DIC; and interference from elevated hemoglobin, bilirubin, or triglycerides. Exposure to heparin or cryoprecipitate products may also affect results.
Interpretation of the antigenic plasminogen result requires integration with other laboratory and clinical studies. This test should be interpreted in the context of pertinent clinical and family history, and physical examination findings.
References
1. Shaz BH, et al. Transfusion Medicine and Hemostasis Clinical and Laboratory Aspects. 2nd ed. New York, NY: Elsevier; 2013:883-884.
2. Mehta R, et al. Haemophilia. 2008;14:1261-1268.
3. Hedner U, et al. Haemostasis.1988;18(suppl 1):87-92
