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Evaluate an isolated prolonged PT or for evaluation when both the aPTT and PT are prolonged and to assess factor V activity level.6-8
This test is not used for the diagnosis of factor V Leiden mutation. Direct Xa or thrombin inhibitor therapy may cause factitiously low results.
Factor V is a large (330 kilodalton) single-chain nonenzymatic cofactor that is synthesized in hepatocytes, megakaryocytes, and endothelial cells.6,7,9 Approximately 20% of the total factor V is carried in the α granules of platelets and is released when platelets are activated.6 The structure of factor V is similar to that of factor VIII.9 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.6,7,9 This condition affects both males and females and the prevalence of inherited factor V deficiency is equal in all ethnic groups.9 Factor V levels are decreased both in plasma and platelets.6 A syndrome of combined factor V and VIII deficiencies has been described in over 60 families in and around the Mediterranean basin.8
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.9 Unlike individuals with severe hemophilia, patients with factor V levels <1% do not typically develop spontaneous joint hemarthroses.6
Diminished factor V levels can be seen in liver disease, disseminated intravascular coagulation (DIC) syndromes, and in other consumption coagulopathies.9,10 Specific factor V inhibitors can occur, especially after surgical procedures that involve multiple exposures to bovine topical thrombin.9 Postoperative treatment with aminoglycosides and penicillin has also been associated with development of factor V inhibitors.6,7 Inhibitors do not typically develop in individuals with factor V deficiency.6 One study found that elevated factor V activity may be associated with increased risk for myocardial infarction;11 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.10
1. Adcock DM, Kressin DC, Marlar RA. Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing. Am J Clin Pathol. 1997 Jan; 107(1):105-110. PubMed 8980376
2. Reneke J, Etzell J, Leslie S, Ng VL, Gottfried EL. 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 Jun; 109(6):754-757. PubMed 9620035
3. National Committee for Clinical Laboratory Standardization. Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline. 5th ed. Villanova, Pa: NCCLS; 2008. Document H21-A5:28(5).
4. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997 Jun; 107(6):681-683. PubMed 9169665
5. McGlasson DL, More L, Best HA, Norris WL, Doe RH, Ray H. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999 May-Jun; 12(3):137-139. PubMed 10539100
6. Roberts HR, Escobar MA. Less common congenital disorders of hemostasis. In: Kitchens CS, Alving BM, Kessler CM, eds. Consultative Hemostasis and Thrombosis. Philadelphia, Pa: WB Saunders Co; 2002: 57-71.
7. Triplett DA. Coagulation abnormalities. In: McClatchey KD, ed. Clinical Laboratory Medicine. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2002:1033-1049.
8. Ginsburg D, Nichols WC, Zivelin A, Kaufman RJ, Seligsohn U. Combined factors V and VIII deficiency-the solution. Haemophilia. 1998 Jul; 4(4):677-682. PubMed 9873813
9. Adcock DM, Bethel MA, Macy PA. Coagulation Handbook. Aurora, Colo: Esoterix-Colorado Coagulation; 2006.
10. Chandler WL, Rodgers GM, Sprouse JT, Thompson AR. Elevated hemostatic factor levels as potential risk factors for thrombosis. Arch Pathol Lab Med. 2002 Nov; 126(11):1405-1414. PubMed 12421150
11. Redondo M, Watzke HH, Stucki B, et al. Coagulation factors II, V, VII, and X, prothrombin gene 20210G ? A transition, and factor V Leiden in coronary artery disease: High factor V clotting activity is an independent risk factor for myocardial infarction. Arterioscler Thromb Vasc Biol. 1999 Apr; 19(4):1020-1025. PubMed 10195931
Adcock DM, Gosselin R. Direct oral anticoagulants (DOACs) in the laboratory: 2015 review. Thromb Res. 2015 Jul; 136(1):7-12. PubMed 25981138
