Factor VII Activity

Plasma, frozen

1 mL

Blue-top (sodium citrate) tube

Ideally, the patient should not be on anticoagulant therapy. Avoid warfarin (Coumadin®) therapy for two weeks prior to the test and heparin, direct Xa, and thrombin inhibitor therapies for about three days prior to testing. Do not draw from an arm with a heparin lock or heparinized catheter.

Evaluate an isolated prolonged PT and document factor VII deficiency^6-8

Direct Xa or thrombin inhibitor therapy may cause factitiously low results. Artifactual elevations in factor VII can occur as the result of cold activation of factor VII in the collection tube prior to analysis.⁶ Refrigerating or placing on ice for an extended period prior to freezing the plasma can result in the conversion of factor VII to activated factor VIIa.⁶

Factor VII activity is determined utilizing a prothrombin time (PT)-based one-stage clotting time assay. Factor VII-depleted plasma is used as the substrate, and the clotting time with the patient plasma is compared to the clotting time of normal pooled plasma.

Factor VII is a 48 kilodalton single-chain nonenzymatic cofactor that is synthesized in the liver.⁶ Factor VII is a vitamin K-dependent protein with a plasma concentration of 0.5 mg/mL.⁶

The plasma half-life of factor VII is short at about four to six hours.⁶ Factor VII deficiency should be considered when a patient with excessive bleeding has an extended protime (PT) and a normal activated partial thromboplastin time (aPTT). Congenital factor VII deficiency is rare (less than one case per 500,000 individuals) and is inherited as an autosomal recessive trait.^6,7 This condition affects both males and females and the prevalence of factor VII deficiency is equal in all ethnic groups.^6,7 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.⁶

Symptoms (homozygotes and double heterozygotes) can include mucosal bleeding, epistaxis, postsurgical and postpartum hemorrhage, menorrhagia, gastrointestinal bleeding, and umbilical cord hemorrhage.^6-8 Heterozygotes are usually asymptomatic.⁸ Factor VII plasma activity <30% may result in excessive bleeding following a traumatic event.⁶ Spontaneous bleeding similar to that observed in severe hemophilia may occur when the activity is <1%;^6,7 however, symptomatology does not always correlate with the degree of factor VII deficiency and some patients with low levels may have no bleeding symptoms at all.^6,7

Diminished factor VII levels can be seen in patients with significant hepatic dysfunction, with oral anticoagulant (coumarin) therapy, and in individuals with vitamin K deficiency.^6,7 Low levels can also be observed in patients with specific factor VII inhibitors and in association with homocystinuria and aplastic anemia.⁷

High levels of factor VII activity were found to be associated with increased risk for ischemic heart disease events by the Northwick Park Heart Study in 1986;⁹ however, more recent studies have failed to identify factor VII levels as an independent risk factor for thrombosis.¹⁰ A recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia did not recommend measurement of factor VII levels for the assessment of thrombotic risk.¹⁰