Factor V Assay

Updated: Aug 03, 2021
  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP, FAMIA; Chief Editor: Eric B Staros, MD  more...
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Reference Range

Factor V is a large glycoprotein with a molecular weight of 330,000 daltons and 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:

  •  50-150% of normal [3]


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

  • Pathologic fibrinolysis

  • Disseminated intravascular coagulation (DIC)

A study by Tinholt et al indicated that the gene for factor V is a prognostic indicator in breast cancer, with high expression of the gene correlating with improved relapse-free patient survival. The investigators reported that greater infiltration with lymphoid cells (T cells, natural killer [NK] cells, B cells) and myeloid cells (macrophages, dendritic cells) occurred in tumors in which the factor V gene was highly expressed, with a negative correlation found between expression of the gene and tumor purity. [4]


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.



See the list below:

  • Quantitative functional assays of coagulation factors




Factor V is a large glycoprotein with a molecular weight of 330,000 daltons and 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. [5] It is also called Owren disease after Dr Paul Owren, who identified the defect first and published it in Lancet in 1947. [6]

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. [7] Activated platelet factor V is also more resistant to inactivation by activated protein C. [8, 9] Platelet factor V appears to be sufficient for hemostatic function, at least in mice. [10]

Factor V is believed to be primarily activated by thrombin in vivo, although it can be activated by factor Xa as well. [11] Factor Xa appears to be the preferred activator of factor V released from platelet granules. [8] 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. [12] 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). [13]

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. [14, 15] 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. [16, 17] Platelets undergo microvesiculation when activated, and the microvesicles, which are rich in factor V, are potent promoters of coagulation. [16]

A study by Ellery et al indicated that in people with hemophilia, decreased factor VIII or IX levels may give rise to a compensatory procoagulant response, including an increase in platelet factor V. The investigators found that plasma protein S, platelet protein S, and plasma tissue factor pathway inhibitor-α were, respectively, one-third, 26%, and 9% lower than in controls, while platelet factor V was 50% higher. [18]

A study by Link et al, using a mathematic model of flow-mediated coagulation, indicated that in patients with hemophilia A, thrombin generation is boosted by low-normal factor V levels. The investigators suggested that a reduction in the level of factor V weakens the protein’s ability to compete with factor VIII for factor Xa on activated platelet surfaces, leading to enhanced factor VIII activation and, consequently, improved thrombin production. [19]

A study by Sridharan et al of patients with factor V inhibitors found that inhibitor titers and/or factor V activity did not correlate with clinical bleeding. In addition, laboratory data suggested that inhibitor effects are not time dependent. [20]


When deficiency of factor V is suspected


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. [21]

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]