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Factor VII Assay 

  • Author: Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP; Chief Editor: Eric B Staros, MD  more...
 
Updated: Jan 16, 2014
 

Reference Range

Factor VII circulates as a single-chain zymogen of molecular weight of about 50,000 Daltons. It has the shortest half-life of the procoagulant factors, approximately 3-6 hours.[1] The human factor VII gene is located on chromosome 13, very close to the gene for factor X.[1] Embryos deficient in factor VII developed normally without evidence of hemorrhage. Nevertheless, factor VII-deficient newborns sometimes develop fatal intra-abdominal or intracranial hemorrhage.[2]

The reference range for factor VII is 70-150% of normal[3]

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Interpretation

Factor VII is increased in the following:

  • Oral contraceptive use and pregnancy
  • An increase in factor VII has been associated with thrombophilia

A congenital deficiency of factor VII has been linked in the following :

  • Variable hemorrhagic diathesis in homozygotes

Acquired conditions leading to its deficiency include the following:

  • Liver disease
  • Vitamin K deficiency
  • Treatment with vitamin K antagonists
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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.

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Panels

See the list below:

  • Quantitative functional assays of coagulation factors
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Background

Description

Factor VII circulates as a single-chain zymogen of molecular weight of about 50,000 Daltons. It has the shortest half-life of the procoagulant factors, approximately 3-6 hours.[1] The human factor VII gene is located on chromosome 13, very close to the gene for factor X.[1] Embryos deficient in factor VII developed normally without evidence of hemorrhage. Nevertheless, factor VII-deficient newborns sometimes develop fatal intra-abdominal or intracranial hemorrhage.[2]

Factor VII binds to tissue factor. Once bound to its cofactor, factor VII can be activated by a number of different proteases. Carboxylation by vitamin K is necessary to activate this factor. The physiologic activator of factor VII is thought to be factor Xa, although significant auto-activation by factor VIIa can occur.[4] The factor VIIa/TF complex activates both factors IX and X. It is inhibited by tissue factor pathway inhibitor (TFPI) in complex with factor Xa. It is also inhibited by antithrombin (AT), but only in the presence of heparin.

The Food and Drug Administration (FDA) approved recombinant activated factor VIII (synthetic vitamin K -dependent protein) for treatment of bleeding in patients with hemophilia A or B who have developed inhibitors against replacement coagulation factors. Recombinant activated factor VII (rFVIIa) binds to exposed tissue factor at the place of tissue and vascular injury. Thrombin generated by this process activates platelets and the coagulation cascade. It has been used in controlling hemorrhage from surgery, trauma, and other causes with success.[5] It has also been found useful in the treatment of obstetrical hemorrhage in women with or without hemophilia.

Indications/Applications

Factor VII testing is indicated when Factor VII deficiency is suspected.

Considerations

Its shortest half-life of all the clotting factors is reflected in the initial rapid prolongation of prothrombin time (INR) in therapy with vitamin K antagonists.

Recombinant FVIIa has also been used to control severe obstetrical bleeding in women without hemophilia.[6] In that series, bleeding was diminished or arrested in over 80% of patients with no complications due to rFVIIa. However, Lewis et al mention that rFVIIa administration will not be effective if plasma fibrinogen is depleted, particularly if the levels are decreased to 50 mg/dL or less.[7]

Indeed, the specter of thrombosis with rFVIIa use is of concern.[5] In a review of the FDA adverse-event reporting system by O'Connell et al, 185 thrombotic events occurred in off-label use of rFVIIa among 168 nonpregnant patients treated for bleeding.[8] Thrombotic events may affect as many as 7% of treated patients but appear so far to be uncommon in obstetrical patients.[9]

An intranasal form of desmopressin is also an option for use in hemophilia and is more frequently used at home than the subcutaneous route. A single spray in a single nostril (150 micrograms total dose) is adequate for children more than 5 years old (< 50 kg). A single spray in each nostril is used (300 micrograms total dose) for adolescents (>50 kg) and adults. This dose of intranasal desmopressin increases the factor VIII level by 2-3 times. This therapy can be repeated every 8-12 hours; however, with repetitive use, the patient's stores of factor VIII will be depleted, and, subsequently, the effect will be reduced significantly. Desmopressin is an antidiuretic agent, and fluid restriction may be needed during use.[10]

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.[3]

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Contributor Information and Disclosures
Author

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP Associate Professor of Medicine, St Louis University School of Medicine

Bishnu Prasad Devkota, MD, MHI, FRCS(Edin), FRCS(Glasg), FACP is a member of the following medical societies: American College of Physicians, American Medical Informatics Association, Royal College of Physicians and Surgeons of Glasgow, Royal College of Surgeons of Edinburgh, Healthcare Information and Management Systems Society

Disclosure: Nothing to disclose.

Chief Editor

Eric B Staros, MD Associate Professor of Pathology, St Louis University School of Medicine; Director of Clinical Laboratories, Director of Cytopathology, Department of Pathology, St Louis University Hospital

Eric B Staros, MD is a member of the following medical societies: American Medical Association, American Society for Clinical Pathology, College of American Pathologists, Association for Molecular Pathology

Disclosure: Nothing to disclose.

References
  1. Monroe DM HM, Roberts HR. Molecular Biology and Biochemistry of the Coagulation Factors and Pathways of Hemostasis. Prchal JT KK, Lichtman MA, Kipps TJ, Seligsohn U, ed. Williams Hematology. 8th ed. New York: McGraw-Hill; 2010.

  2. Rosen ED, Chan JC, Idusogie E, Clotman F, Vlasuk G, Luther T. Mice lacking factor VII develop normally but suffer fatal perinatal bleeding. Nature. 1997 Nov 20. 390(6657):290-4. [Medline].

  3. Williamson MA, Snyder LM, Wallach JB. Wallach's interpretation of diagnostic tests. 9th ed. Wolters Kluwer/Lippincott Williams & Wilkins Health: Philadelphia; 2011.

  4. Hedner U, Kisiel W. Use of human factor VIIa in the treatment of two hemophilia A patients with high-titer inhibitors. J Clin Invest. 1983 Jun. 71(6):1836-41. [Medline].

  5. Mannucci PM, Levi M. Prevention and treatment of major blood loss. N Engl J Med. 2007 May 31. 356(22):2301-11. [Medline].

  6. Alfirevic Z, Elbourne D, Pavord S, Bolte A, Van Geijn H, Mercier F. Use of recombinant activated factor VII in primary postpartum hemorrhage: the Northern European registry 2000-2004. Obstet Gynecol. 2007 Dec. 110(6):1270-8. [Medline].

  7. Lewis NR, Brunker P, Lemire SJ, Kaufman RM. Failure of recombinant factor VIIa to correct the coagulopathy in a case of severe postpartum hemorrhage. Transfusion. 2009 Apr. 49(4):689-95. [Medline].

  8. O'Connell KA, Wood JJ, Wise RP, Lozier JN, Braun MM. Thromboembolic adverse events after use of recombinant human coagulation factor VIIa. JAMA. 2006 Jan 18. 295(3):293-8. [Medline].

  9. Cunningham FG LK, Bloom SL, Hauth JC, Rouse DJ, Spong CY ed. Obstetrical Hemorrhage. Cunningham FG LK, Bloom SL, Hauth JC, Rouse DJ, Spong CY. Williams Obstetrics. 23rd ed. New York: McGraw-Hill; 2010.

  10. Gouw SC, van der Bom JG, Auerswald G, Ettinghausen CE, Tedgard U, van den Berg HM. Recombinant versus plasma-derived factor VIII products and the development of inhibitors in previously untreated patients with severe hemophilia A: the CANAL cohort study. Blood. 2007 Jun 1. 109(11):4693-7. [Medline].

 
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