Factor V Activity
Evaluate an isolated prolonged PT or for evaluation when both the aPTT and PT are prolonged and to assess factor V activity level.
Factor V is a large (330 kilodalton) single-chain nonenzymatic cofactor that is synthesized in hepatocytes, megakaryocytes, and endothelial cells. Approximately 20% of the total factor V is carried in the α granules of platelets and is released when platelets are activated. The structure of factor V is similar to that of factor VIII. Factor V’s plasma concentration is 7 mg/mL and half-life is about 15 to 36 hours. Factor V activation occurs by both the extrinsic and intrinsic pathways. Factor V deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT).
Congenital factor V deficiency, sometimes referred to as parahemophilia, is rare (less than one case per million individuals) and is inherited as an autosomal recessive trait. This condition affects both males and females and the prevalence of inherited factor V deficiency is equal in all ethnic groups. Factor V levels are decreased both in plasma and platelets. A syndrome of combined factor V and VIII deficiencies has been described in over 60 families in and around the Mediterranean basin.
Symptoms (homozygotes) can include hematoma formation, postsurgical and postpartum hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.6,9 Factor V plasma activity <30% may result in excessive bleeding following a traumatic event. Unlike individuals with severe hemophilia, patients with factor V levels <1% do not typically develop spontaneous joint hemarthroses.
Diminished factor V levels can be seen in liver disease, disseminated intravascular coagulation (DIC) syndromes, and in other consumption coagulopathies.0 Specific factor V inhibitors can occur, especially after surgical procedures that involve multiple exposures to bovine topical thrombin. Postoperative treatment with aminoglycosides and penicillin has also been associated with development of factor V inhibitors. Inhibitors do not typically develop in individuals with factor V deficiency. One study found that elevated factor V activity may be associated with increased risk for myocardial infarction however, a recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia did not recommend measurement of factor V levels for the assessment of thrombotic risk.
Blue-top (sodium citrate) tube
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.
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.
Severe hemolysis; improper labeling; clotted specimen; specimen diluted with IV fluids; samples thawed in transit; improper sample type; sample out of stability