Plasminogen (PLG) is a glycoprotein (molecular weight 92 kDa) synthesized in the liver, and it circulates in the blood, with a half-life of 2.2 days. Plasminogen is the precursor of plasmin, which lyses fibrin clots to fibrin degradation products (FDP) and D-dimer; the conversion to active protease is mediated by tissue-type (tPA) and urokinase-type (uPA) plasminogen activators. Generated plasmin is quickly inactivated by its main inhibitor alpha2-antiplasmin.[1, 2, 3]
Normal findings: 2.4-4.4 Committee on Thrombolytic Agents (CTA) units/mL[4]
Increased PLG levels are observed in the following clinical situations:
Anabolic steroids treatment
Hypothyroidism
Hormonal contraceptives
After liver/kidney transplantation
Pregnancy
Inherited decreased PLG levels are observed in the following clinical situations:
Type I: Both functional and immunological PLG level is decreased (hypoplasminogenemia).
Type II: Only functional activity is decreased while protein concentration is normal (dysplasminogenemia).
Acquired decreased PLG levels are observed in the following clinical situations:
Disseminated intravascular coagulation
Thrombolytic therapy
Liver disease
Hyperthyroidism
L-asparaginase therapy
Postoperative period
Severe congenital hypoplasminogenemia is associated with pseudomembranous disease (or ligneous inflammation) of mucous membranes (eye, middle ear, mouth, pharynx, duodenum, upper and lower respiratory tract, and female genital tract).
See the list below:
Specimen - Citrated plasma
Collection - Tube with sodium citrate 3.2% citrate, blue top
Centrifugation - 2000-2500 g for 15 min or similar regime to produce platelet-poor plasma
Storage - Up to 24 hours at room temperature, or plasma sample should be frozen; specimen is stable for 1 month at -20 º C, or 6-9 months at -80 º C
A high concentration of hemoglobin, bilirubin, triglycerides and fibrin degradation products might affect PLG measurement. The presence of aprotinin in the sample may lead to underestimation of PLG levels in plasma.
Plasminogen is a glycoprotein (molecular weight 92 kDa) synthesized in the liver, and it circulates in the blood, with a half-life of 2.2 days. Plasminogen is the precursor of plasmin, which lyses fibrin clots to fibrin degradation products (FDP) and D-dimer; the conversion to active protease is mediated by tissue-type (tPA) and urokinase-type (uPA) plasminogen activators. Generated plasmin is quickly inactivated by its main inhibitor alpha2-antiplasmin.[1, 2, 3]
See the list below:
Pseudomembranous disease (eg, ligneous conjunctivitis, gingivitis)
Idiopathic thromboembolic disease (if other causes of thrombophilia are excluded)
No clear association exists between sole plasminogen deficiency and increased risk of thrombosis. PLG testing should not be included in routine thrombophilia workup.