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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
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 unless the sample is collected using a winged (butterfly) collection system. With a winged blood collection set a discard tube should be drawn first to account for the dead space of the tubing and prevent under-filling of the evacuated tube.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 alternative 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.
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.
Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling
Evaluate an isolated prolonged PT and document factor VII deficiency6-8
Direct Xa or thrombin inhibitor therapy may cause factitiously low results. Artifactual elevations in factor VII can occur as the result of cold activation of factor VII in the collection tube prior to analysis.6 Refrigerating or placing on ice for an extended period prior to freezing the plasma can result in the conversion of factor VII to activated factor VIIa.6
Factor VII activity is determined utilizing a prothrombin time (PT)-based one-stage clotting time assay. Factor VII-depleted plasma is used as the substrate, and the clotting time with the patient plasma is compared to the clotting time of normal pooled plasma.
Factor VII is a 48 kilodalton single-chain nonenzymatic cofactor that is synthesized in the liver.6 Factor VII is a vitamin K-dependent protein with a plasma concentration of 0.5 mg/mL.6
The plasma half-life of factor VII is short at about four to six hours.6 Factor VII deficiency should be considered when a patient with excessive bleeding has an extended protime (PT) and a normal activated partial thromboplastin time (aPTT). Congenital factor VII deficiency is rare (less than one case per 500,000 individuals) and is inherited as an autosomal recessive trait.6,7 This condition affects both males and females and the prevalence of factor VII deficiency is equal in all ethnic groups.6,7 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.6
Symptoms (homozygotes and double heterozygotes) can include mucosal bleeding, epistaxis, postsurgical and postpartum hemorrhage, menorrhagia, gastrointestinal bleeding, and umbilical cord hemorrhage.6-8 Heterozygotes are usually asymptomatic.8 Factor VII plasma activity <30% may result in excessive bleeding following a traumatic event.6 Spontaneous bleeding similar to that observed in severe hemophilia may occur when the activity is <1%;6,7 however, symptomatology does not always correlate with the degree of factor VII deficiency and some patients with low levels may have no bleeding symptoms at all.6,7
Diminished factor VII levels can be seen in patients with significant hepatic dysfunction, with oral anticoagulant (coumarin) therapy, and in individuals with vitamin K deficiency.6,7 Low levels can also be observed in patients with specific factor VII inhibitors and in association with homocystinuria and aplastic anemia.7
High levels of factor VII activity were found to be associated with increased risk for ischemic heart disease events by the Northwick Park Heart Study in 1986;9 however, more recent studies have failed to identify factor VII levels as an independent risk factor for thrombosis.10 A recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia did not recommend measurement of factor VII levels for the assessment of thrombotic risk.10
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|800599||Factor VII Activity||3198-9||800599||Factor VII Activity||%||3198-9|
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