Coagulation Factor VIII Activity Assay, Plasma
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
Factor VIII is synthesized in the liver, and perhaps in other tissues. It is a coagulation cofactor which circulates bound to von Willebrand factor and is part of the intrinsic coagulation pathway. The biological half-life is 9 to 18 hours (average is 12 hours).
Congenital factor VIII decrease is the cause of hemophilia A which has an incidence of 1 in 10,000 and is inherited in a recessive sex-linked manner on the X chromosome. Severe deficiency (<1%) characteristically demonstrates as hemarthrosis, deep-tissue bleeding, excessive bleeding with trauma and ecchymoses.
Factor VIII may be decreased in von Willebrand disease. Acquired deficiency states also occur.
Antibodies specific for factor VIII are the most commonly occurring specific inhibitors of coagulation factors and can produce serious bleeding disorders (acquired hemophilia).
Factor VIII is highly susceptible to proteolytic inactivation, with the potential for spuriously decreased assay results.
Diagnosing hemophilia A
Diagnosing von Willebrand disease when measured with the von Willebrand factor (VWF) antigen and VWF activity
Diagnosing acquired deficiency states
Investigation of prolonged activated partial thromboplastin time
Mild hemophilia A: 5% to 50%
Moderate hemophilia A: 1% to 5%
Severe hemophilia A: <1%
Congenital deficiency may also occur in combined association with factor V deficiency.
Liver disease usually causes an increase of factor VIII activity.
Acquired deficiencies of factor VIII have been associated with myeloproliferative or lymphoproliferative disorders (acquired von Willebrand disease; VWD), inhibitors of factor VIII (autoantibodies, post-partum conditions, etc.), and intravascular coagulation and fibrinolysis.
May be decreased with von Willebrand factor in VWD
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
Factor VIII is a labile protein. Improper handling of a specimen may give a false result.
Factor VIII is highly susceptible to proteolytic inactivation, with the potential for spuriously decreased assay results. Normal results can be regarded as reliable, but decreased result needs to be correlated with other clinical and laboratory information. Repeat testing may be necessary.
Factor VIII activity in frozen-thawed plasma specimens may be 10% to 20% lower than if assayed in fresh specimens, even under optimum conditions of processing and transportation, or maybe even lower if these conditions are suboptimal.
Factor VIII rises in response to a number of factors, including pregnancy, estrogen therapy, stress, disease, etc.
Not useful for inferring carrier status in suspected female carriers of hemophilia A, unless it is below 50% of normal.
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 or healthy premature infants usually have normal or elevated factor VIII.*
*See Pediatric Hemostasis References in Coagulation Studies in Special Instructions.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Spreafico M, Peyvandi F: Combined FV and FVIII deficiency. Haemophilia 2008 Nov;14(6):1201-1208
2. Barrowcliffe TW, Raut S, Sands D, Hubbard AR: Coagulation and chromogenic assays of factor VIII activity: general aspects, standardization, and recommendations. Semin Thromb Hemost 2002 Jun;28(3):247-256
3. Franchini M, Lippi G, Favaloro EJ: Acquired inhibitors of coagulation factors: part II. Semin Thromb Hemost 2012 Jul;38(5):447-453
4. Carcao MD: The diagnosis and management of congenital hemophilia. Semin Thromb Hemost 2012 Oct;38(7):727-734