Ideally, the patient should not be on anticoagulant therapy. Avoid warfarin (Coumadin®) therapy for two weeks prior to the test and heparin, direct Xa, and thrombin inhibitor therapies for about three days prior to testing. Do not draw from an arm with a heparin lock or heparinized catheter.

Lt blue Sodium citrate (Na Cit) - 2.7mL

• Do not over or under fill tube as the ratio of anticoagulant to whole blood is critical

Coag – tube fill guidelines

• Immediatley following collection, mix sample thoroughly by gentle inverting 8 - 10 times, to prevent clotting

• Process Platelet Poor Plasma (P.P.P)
  • Coag – how to prepare a specimen for special coagulation testing
• Transfer plasma into an aliquot tube using a spot label "NaCit Plasma P.P.P" to label as platelet poor plasma
• Freeze immediately

Screw-cap polypropylene frozen transport vial/tube - 4 mL (LabCorp)

Frozen - 28 days

Freeze/thaw cycles - stable x3

• Severe hemolysis
• Improper labeling
• Clotted specimen
• Specimen diluted with IV fluids
• Samples thawed in transit
• Improper sample type
• Sample out of stability

Streptokinase (SK) as mixed with the patient sample and the resulting plasminogen-SK complex converts a chromogenic substrate to produce color.

70 - 150%

Plasminogen is a glycoprotein with molecular weight of 92 kilodaltons that is produced by the liver. The plasma half-life of plasminogen is about two days. Plasminogen is converted to the proteolytic enzyme plasmin by cleavage of a single peptide bond. Plasmin degrades fibrin clots and intact fibrinogen (ie, fibrinogenolysis). Plasmin also inhibits coagulation by inactivating factors Va and VIIIa.

Plasminogen deficiency is not considered a risk factor for thrombosis. Hereditary deficiencies in plasminogen activity are rare and include type 1 deficiency, characterized by decreased plasminogen protein levels, and type II deficiency, characterized 

by normal levels of dysfunctional plasminogen production. Plasminogen deficiency is usually transmitted as an autosomal recessive defect. Homozygous plasminogen deficiency can result in ligneous conjunctivitis, a condition in which large amounts of fibrin are deposited in the conjunctiva. Fibrin deposits can occur in other tissues as well, leading to a variety of disorders.

There are two physiologic activators of plasminogen, tissue plasminogen activator (TPA), and urinary-type plasminogen activator (UPA). Thrombin generated during coagulation stimulates the release of TPA from the endothelial cells. TPA release also occurs as the result of exercise or stress. Treatment with desmopressin (DDAVP) also causes the release of TPA. TPA forms a complex with fibrin, which, in turn, converts plasminogen to plasmin. Kallikrein, a protein component of the contact system, stimulates the release of UPA from the kidneys; however, in healthy individuals, the majority of this released UPA is bound to the endothelial tissue urokinase plasminogen activator receptor (uPAR). Streptokinase (SK) produced by β-hemolytic streptococci can also activate plasminogen. All three of these activators have been used therapeutically to dissolve pathologic clots. Plasminogen levels drop in patients undergoing thrombolytic therapy with TPA, UPA, or SK and measurement of plasminogen activity can be used to monitor the therapeutic efficacy of this treatment.

Plasminogen activator inhibitors (PAI) inhibit plasminogen activation in vivo. Measurement of PAI-1 levels has clinical application in the assessment of thrombophilia.