Coagulation Factor V Activity Assay, Plasma
Diagnosing congenital deficiencies (rare) of coagulation factor V
Evaluating acquired deficiencies associated with liver disease, factor V inhibitors, myeloproliferative disorders, and intravascular coagulation and fibrinolysis
Investigation of prolonged prothrombin time or activated partial thromboplastin time
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Factor V is a vitamin K-independent protein synthesized in the liver and in other tissues (endothelium, megakaryocytes/platelets). In its thrombin-activated form (factor Va), it serves as an essential cofactor in the prothrombinase enzyme complex which converts prothrombin to thrombin (the prothrombinase complex consists of the enzyme, activated factor X, factor Va cofactor, a phospholipid surface, and calcium).
Deficiency of factor V may cause prolonged prothrombin time and activated partial thromboplastin time. Deficiency may result in a bleeding diathesis. Plasma biological half-life varies from 12 to 36 hours.
Platelets contain 20% to 25% of the factor V in blood. Factor V (also known as labile factor) is highly susceptible to proteolytic inactivation, with the potential for spuriously decreased assay results.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Normal, full-term newborn infants may have borderline low or mildly decreased levels (> or =30% to 35%) which reach adult levels within 21 days postnatal. Healthy premature infants (30-36 weeks gestation) may have borderline low or mildly decreased levels.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
Acquired deficiencies are much more common than congenital (see Useful For).
Congenitally deficient homozygotes generally have levels < or =10% to 20%.
Congenitally deficient heterozygotes generally have levels < or =50%.
Congenital deficiency may occur in combined association with factor VIII deficiency.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Factor V (labile factor) is highly susceptible to proteolytic inactivation, with the potential for spuriously decreased assay results. In normal individuals, after freeze-thaw of citrate plasma, factor V activity typically may be 10% to 20% less than observed in a fresh plasma specimen, and in occasional individuals, a more marked decrease of factor V activity occurs. Normal results can be regarded as reliable, but decreased factor V activity results need to be correlated with other clinical and laboratory information. Repeat testing may be necessary.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Girolami A, Scandellari R, Scapin M, Vettore S: Congenital bleeding disorders of the vitamin K-dependent clotting factors. Vitam Horm 2008;78:281-374
2. Brenner B, Kuperman AA, Watzka M, Oldenburg J: Vitamin K-dependent coagulation factors deficiency. Semin Thromb Hemost 2009 Jun;35(4):439-446
3. Asselta R, Peyvandi F: Factor V deficiency. Semin Thromb Hemost 2009 Jun;35(4):382-389
4. Lippi G, Favaloro EJ, Montagnana M, et al: Inherited and acquired factor V deficiency. Blood Coagul Fibrinolysis 2011;22(3):160-166
5. Spreafico M, Peyvandi F: Combined FV and FVIII deficiency. Haemophilia 2008 Nov;14(6):1201-1208