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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 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
1. Adcock DM, Kressin DC, Marlar RA. Effect of 3.2% vs 3.8% sodium citrate concentration on routine coagulation testing. Am J Clin Pathol. 1997 Jan; 107(1):105-110. PubMed 8980376
2. Reneke J, Etzell J, Leslie S, Ng VL, Gottfried EL. Prolonged prothrombin time and activated partial thromboplastin time due to underfilled specimen tubes with 109 mmol/L (3.2%) citrate anticoagulant. Am J Clin Pathol. 1998 Jun; 109(6):754-757. PubMed 9620035
3. National Committee for Clinical Laboratory Standardization. Collection, Transport, and Processing of Blood Specimens for Coagulation Testing and General Performance of Coagulation Assays; Approved Guideline. 5th ed. Villanova, Pa: NCCLS; 2008. Document H21-A5:28(5).
4. Gottfried EL, Adachi MM. Prothrombin time and activated partial thromboplastin time can be performed on the first tube. Am J Clin Pathol. 1997 Jun; 107(6):681-683. PubMed 9169665
5. McGlasson DL, More L, Best HA, Norris WL, Doe RH, Ray H. Drawing specimens for coagulation testing: Is a second tube necessary? Clin Lab Sci. 1999 May-Jun; 12(3):137-139. PubMed 10539100
6. Adcock DM, Bethel MA, Macy PA. Coagulation Handbook. Aurora, Colo: Esoterix-Colorado Coagulation; 2006.
7. Roberts HR, Escobar MA. Less common congenital disorders of hemostasis. In: Kitchens CS, Alving BM, Kessler CM, eds. Consultative Hemostasis and Thrombosis. Philadelphia, Pa: WB Saunders Co; 2002: 57-71.
8. Triplett DA. Coagulation abnormalities. In: McClatchey KD, ed. Clinical Laboratory Medicine. 2nd ed. Philadelphia, Pa: Lippincott Williams and Wilkins; 2002:1033-1049.
9. Meade TW, Mellows S, Brozovic M, et al. Haemostatic function and ischaemic heart disease: Principal results of the Northwick Park Heart Study. Lancet. 1986 Sep 6; 2(8506):533-537. PubMed 2875280
10. Chandler WL, Rodgers GM, Sprouse JT, Thompson AR. Elevated hemostatic factor levels as potential risk factors for thrombosis. Arch Pathol Lab Med. 2002 Nov; 126(11):1405-1414. PubMed 12421150
Adcock DM, Gosselin R. Direct oral anticoagulants (DOACs) in the laboratory: 2015 review. Thromb Res. 2015 Jul; 136(1):7-12. PubMed 25981138
