2 - 3 days
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
For more information, please view the literature below.
Blue-top (sodium citrate) tube
Citrated plasma samples should be collected by double centrifugation. Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood to anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples, except when using a winged blood collection device (ie, "butterfly"), in which case a discard tube should be used.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternate anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes. Centrifuge for 10 minutes and carefully remove 2/3 of the plasma using a plastic transfer pipette, being careful not to disturb the cells. Deliver to a plastic transport tube, cap, and recentrifuge for 10 minutes. Use a second plastic pipette to remove the plasma, staying clear of the platelets at the bottom of the tube. Transfer the plasma into a Labcorp PP transpak frozen purple tube with screw cap (Labcorp No. 49482). Freeze immediately and maintain frozen until tested.
Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
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.
Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability
Monitor thrombolytic therapy; evaluate ligneous tissue depositions such as conjunctivitis
Plasminogen levels can be decreased in disseminated intravascular coagulation (DIC), hepatitis, leukemia, and with thrombolytic therapy.
Streptokinase (SK) as mixed with the patient sample and the resulting plasminogen-SK complex converts a chromogenic substrate to produce color.
In newborns, ranges are about 50% of adult levels and even lower concentrations occur in premature infants.6,7 Levels can become markedly increased during the second and third trimesters of pregnancy.6
Plasminogen is a glycoprotein with molecular weight of 92 kilodaltons that is produced by the liver.6-8 The plasma half-life of plasminogen is about two days.6 Plasminogen is converted to the proteolytic enzyme plasmin by cleavage of a single peptide bond.6 Plasmin degrades fibrin clots and intact fibrinogen (ie, fibrinogenolysis).7 Plasmin also inhibits coagulation by inactivating factors Va and VIIIa.7
Plasminogen deficiency is not considered a risk factor for thrombosis.6 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.6 Homozygous plasminogen deficiency can result in ligneous conjunctivitis, a condition in which large amounts of fibrin are deposited in the conjunctiva.7 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.6 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;6 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.6
Plasminogen activator inhibitors (PAI) inhibit plasminogen activation in vivo.6 Measurement of PAI-1 levels has clinical application in the assessment of thrombophilia.6
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