Factor V Activity
| Factor V Activity | | | |
| Number | | 086249 |
| CPT | | 85220 |
| Related Information | | Hemostasis and Thrombosis Appendix |
| Synonyms | | Proaccelerin |
| Special Instructions | | If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions. |
| Specimen | | Plasma, frozen |
| Volume | | 2 mL |
| Minimum Volume | | 1 mL |
| Container | | Blue-top (sodium citrate) tube |
Collection | | 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.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 and carefully remove the plasma
using a plastic transfer pipette, being careful not to
disturb the cells. Transfer the plasma into a LabCorp PP
transpak frozen purple tube with screw cap (LabCorp
No 49482). Freeze immediately and maintain
frozen until tested. To avoid delays in turnaround time
when requesting multiple tests on frozen samples, please
submit separate frozen specimens for each test requested.
Please print and use the Specimen
Collection Bulletin as a tube-filling guide. |
| Storage Instructions | | Freeze |
| Patient Preparation | | Avoid warfarin (Coumadin®) therapy for 2 weeks and heparin therapy for 2 days prior to the test. Do not draw from an arm with a heparin lock or heparinized catheter. |
| Causes for Rejection | | Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling |
| Reference Interval | | Adults: 60% to 140%. In newborns, levels are lower but levels gradually reach adult ranges by 6 months of age.6 |
| Use | | Assess factor V activity level7,8,9 |
| Limitations | | The test is not used for the diagnosis of factor VLeiden mutation. |
| Methodology | | Factor V activity is determined utilizing a prothrombin time (PT)-based one-stage clotting time assay. Factor V-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. |
| Additional Information | | Factor V is a large (330 kilodalton) single-chain nonenzymatic cofactor that is synthesized in hepatocytes, megakaryocytes, and endothelial cells.7,8,9 Approximately 20% of the total factor V is carried in the alpha granules of platelets and is released when platelets are activated.8 The structure of factor V is similar to that of factor VIII.7 Factor V's plasma concentration is 7 mg/mL and half-life is about 15-36 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.7,8,9 This condition affects both males and females and the prevalence of inherited factor V deficiency is equal in all ethnic groups.7 Factor V levels are decreased both in plasma and platelets.8 A syndrome of combined factor V and VIII deficiencies has been described in over 60 families in and around the Mediterranean basin.10 Symptoms (homozygotes) can include hematoma formation, postsurgical and postpartum hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.7,8 Factor V plasma activity <30% may result in excessive bleeding following a traumatic event.7 Unlike individuals with severe hemophilia, patients with factor V levels <1% do not typically develop spontaneous joint hemarthroses.8 Diminished factor V levels can be seen in liver disease, disseminated intravascular coagulation (DIC) syndromes, and in other consumption coagulopathies.7,11 Specific factor V inhibitors can occur, especially after surgical procedures that involve multiple exposures to bovine topical thrombin.7 Postoperative treatment with aminoglycosides and penicillin has also been associated with development of factor V inhibitors.8,9 Inhibitors do not typically develop in individuals with factor V deficiency.8 One study found that elevated factor V activity may be associated with increased risk for myocardial infarction.12 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.11 |
| Footnotes | | - Adcock DM, Kressin DC, and Marlar RA, “Effect of 3.2% vs 3.8% Sodium Citrate Concentration on Routine Coagulation Testing,” Clin Pathol, 1997, 107(1):105-10.
- Reneke J, Etzell J, Leslie S, et al, “Prolonged Prothrombin Time and Activated Partial Thromboplastin Time Due to Underfilled Specimen Tubes With 109 mmol/L (3.2%) Citrate Anticoagulant,” Am J Clin Pathol, 1998, 109(6):754-7.
- “National Committee for Clinical Laboratory Standardization: Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline,” Third Edition, Villanova: NCCLS Document H21-A3:11(23), 1999.
- Gottfried EL and Adachi MM, “Prothrombin Time and Activated Partial Thromboplastin Time Can Be Performed on the First Tube,” Am J Clin Pathol, 1997, 107(6):681-3.
- McGlasson DL, More L, Best HA, et al, “Drawing Specimens for Coagulation Testing: Is a Second Tube Necessary?” Clin Lab Sci, 1999, 12(3):137-9.
- Van Cott EM and Laposata M, “Coagulation,” Laboratory Test Handbook With Key Word Index, Jacobs DS, DeMott WR, and Oxley DK eds, Hudson, OH: Lexi-Comp, 2001, 327-58.
- Adcock DM, Jensen R, Johns CS, et al, Coagulation Handbook, Esoterix Coagulation, 2002.
- Roberts HR and Escobar MA, “Less Common Congenital Disorders of Hemostasis,” Consultative Hemostasis and Thrombosis, Kitchens CS, Alving BM, and Kessler CM, eds, Philadelphia, PA: WB Saunders Co, 2002, 57-71.
- Triplett DA, “Coagulation Abnormalities,” Clinical Laboratory Medicine, McClatchey KD, ed, 2nd ed, Philadelphia, PA: Lippincott Williams and Wilkins, 2002, 1033-49.
- Ginsburg D, Nichols WC, Zivelin A, et al, “Combined Factors V and VIII Deficiency - The Solution,” Haemophilia, 1998, 4(4):677-82.
- Chandler WL, Rodgers GM, Sprouse JT, et al, “Elevated Hemostatic Factor Levels as Potential Risk Factors for Thrombosis,” Arch Pathol Lab Med, 2002, 126(11):1405-14.
- Redondo M, Watzke HH, Stucki B, et al, “Coagulation Factors II, V, VII, and X, Prothrombin Gene 20210G → A Transition, and Factor VLeiden in Coronary Artery Disease: High Factor V Clotting Activity Is an Independent Risk Factor for Myocardial Infarction,” Arterioscler Thromb Vasc Biol, 1999, 19(4):1020-5
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