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Factor V Assay 

  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 16, 2014
 

Reference Range

Factor V is a large glycoprotein with a molecular weight of 330,000 Daltons and has a plasma half-life of about 12 hours, with some reports of a half-life of up to 36 hours.[1] It functions as a cofactor in converting factor II to active factor II. It is proteolyzed by protein C/S complex.[2]

The reference range for factor V is as follows:

  • 70-150% of normal [2]
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Interpretation

Factor V is decreased in the following congenital conditions:

  • Inherited autosomal deficiency
  • Bleeding in homozygotes

Factor V is also decreased in the following acquired conditions:

  • Liver disease
  • Pathological fibrinolysis
  • Disseminated intravascular coagulation (DIC)
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Collection and Panels

See the list below:

  • Specimen: Plasma
  • Container: Blue-top vacuum tube
  • Collection method: Routine venipuncture

All samples must be sent in a sealed, leak-proof container marked with a biohazard sticker to comply with Occupational Safety and Health Administration (OSHA) safety standards.

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Panels

See the list below:

  • Quantitative functional assays of coagulation factors
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Background

Description

Factor V is a large glycoprotein with a molecular weight of 330,000 Daltons and has a plasma half-life of about 12 hours, with some reports of a half-life of up to 36 hours.[1] It functions as a cofactor in converting factor II to active factor II. It is proteolyzed by protein C/S complex.[2]

Factor V deficiency has been called parahemophilia because hemarthrosis may occur with severe deficiency of factor V. This also increases the bleeding time.[3] It is also called Owren disease after Dr Paul Owren, who identified the defect first and published it in Lancet in 1947.[4]

The gene for factor V is located on chromosome 1. Factor V circulates in plasma as a single-chain molecule. Platelets contribute approximately 20% of the factor V present in whole blood, with nearly all of it in granules.[5] Activated platelet factor V is also more resistant to inactivation by activated protein C.[6, 7] Platelet factor V appears to be sufficient for hemostatic function, at least in mice.[8]

Factor V is believed to be primarily activated by thrombin in vivo, although it can be activated by factor Xa as well.[9] Factor Xa appears to be the preferred activator of factor V released from platelet granules.[6] A common Arg 506 Gln mutation in factor V leads to resistance to inactivation by activated protein C (factor V Leiden) and is associated with an increased risk of venous thromboembolism.[10] Disruption of the factor V gene leads to either intrauterine death or death from massive bleeding within 2 hours of birth in experimental animals (mice).[11]

Factor V has anticoagulant and procoagulant properties. It enhances the anticoagulant action of activated protein C against factor VIIIa in a reaction in which protein S acts synergistically with factor V.[12, 13] Evidence from patients with inhibitors and deficiencies of plasma and platelet factor V indicates that platelet-derived factor V has an important role in hemostasis.[14, 15] Platelets undergo microvesiculation when activated, and the microvesicles, which are rich in factor V, are potent promoters of coagulation.[14]

Indications/Applications

When deficiency of factor V is suspected

Considerations

Factor V Leiden is a completely different inherited disorder in which factor V is mutated in a specific gene, which results in a hypercoagulable state. The mutation is very common, occurring in 5% of the US population. Factor V activity levels in patients with factor V Leiden are usually normal.[16]

Limitations of the test include partially clotted specimens due to poor mixture of anticoagulant (3:2 sodium citrate as per manufacturer’s blue topped tube), overfilled or underfilled test tubes altering the ratio of blood to anticoagulant (9:1), improperly stored plasma, contamination with heparin or dilution of collected sample if indwelling catheters are used or analytical errors such as lipemic, icteric, or hemolyzed plasma, which may interfere with photoelectric measuring instruments.[2]

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Contributor Information and Disclosures
Author

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Associate Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Healthcare Information and Management Systems Society

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Ortel T KF, Kane W. Factor V. New York: M. Dekker; 1995.

  2. Williamson MA, Snyder LM, Wallach JB. Wallach's interpretation of diagnostic tests. 9th ed. Wolters Kluwer/Lippincott Williams & Wilkins Health: Philadelphia; 2011.

  3. Duckers C, Simioni P, Rosing J, Castoldi E. Advances in understanding the bleeding diathesis in factor V deficiency. Br J Haematol. 2009 Jun. 146(1):17-26. [Medline].

  4. Owren PA. Parahaemophilia; haemorrhagic diathesis due to absence of a previously unknown clotting factor. Lancet. 1947 Apr 5. 1(6449):446-8. [Medline].

  5. Gould WR, Simioni P, Silveira JR, Tormene D, Kalafatis M, Tracy PB. Megakaryocytes endocytose and subsequently modify human factor V in vivo to form the entire pool of a unique platelet-derived cofactor. J Thromb Haemost. 2005 Mar. 3(3):450-6. [Medline].

  6. Gould WR, Silveira JR, Tracy PB. Unique in vivo modifications of coagulation factor V produce a physically and functionally distinct platelet-derived cofactor: characterization of purified platelet-derived factor V/Va. J Biol Chem. 2004 Jan 23. 279(4):2383-93. [Medline].

  7. Oliver JA, Monroe DM, Church FC, Roberts HR, Hoffman M. Activated protein C cleaves factor Va more efficiently on endothelium than on platelet surfaces. Blood. 2002 Jul 15. 100(2):539-46. [Medline].

  8. Sun H, Yang TL, Yang A, Wang X, Ginsburg D. The murine platelet and plasma factor V pools are biosynthetically distinct and sufficient for minimal hemostasis. Blood. 2003 Oct 15. 102(8):2856-61. [Medline].

  9. Monkovic DD, Tracy PB. Activation of human factor V by factor Xa and thrombin. Biochemistry. 1990 Feb 6. 29(5):1118-28. [Medline].

  10. Bertina RM, Koeleman BP, Koster T, Rosendaal FR, Dirven RJ, de Ronde H. Mutation in blood coagulation factor V associated with resistance to activated protein C. Nature. 1994 May 5. 369(6475):64-7. [Medline].

  11. Cui J, O'Shea KS, Purkayastha A, Saunders TL, Ginsburg D. Fatal haemorrhage and incomplete block to embryogenesis in mice lacking coagulation factor V. Nature. 1996 Nov 7. 384(6604):66-8. [Medline].

  12. Shen L, Dahlback B. Factor V and protein S as synergistic cofactors to activated protein C in degradation of factor VIIIa. J Biol Chem. 1994 Jul 22. 269(29):18735-8. [Medline].

  13. JH G. Control of Coagulation Reaction. Prchal JT KK, Lichtman MA, Kipps TJ, Seligsohn U,, ed. Williams Hematology. New York: McGraw-Hill; 2010.

  14. Smyth SS WS, Italiano JE, Coller BS. Platelet Morphology, Biochemistry, and Function. Prchal JT KK, Lichtman MA, Kipps TJ, Seligsohn U, ed. Williams Hematology. 8th ed. New York: McGraw-Hill; 2010.

  15. Bouchard BA BS, Mann KG, et al. Interactions between platelets and the coagulation system. Michelson AD, ed. Platelets. San Diego. London: Academic Press; 2002. 956.

  16. Hamedani AG, Cole JW, Cheng Y, Sparks MJ, O'Connell JR, Stine OC. Factor V Leiden and Ischemic Stroke Risk: The Genetics of Early Onset Stroke (GEOS) Study. J Stroke Cerebrovasc Dis. 2011 Nov 17. [Medline].

 
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