Factor VII Workup

  • Author: Jeyanthi Ramanarayanan, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: May 19, 2011
 

Laboratory Studies

Routine initial hemostatic tests include an aPTT, a PT, and a platelet count. A normal aPTT and a prolonged PT in a patient with a lifelong history of a tendency for mild or severe bleeding is consistent with the diagnosis of factor VII deficiency or the presence of an inhibitor to factor VII.

Bleeding time is usually within the reference range.

With no significant clinical bleeding but a prolonged PT and a normal aPTT, the patient has either mild factor VII deficiency or is taking oral anticoagulants.

To distinguish between factor VII deficiency and the presence of an inhibitor to factor VII, mixing studies are useful. PT testing is repeated using a 1:1 mixture of the patient's plasma and normal plasma. Normal plasma is a source of factor VII; therefore, when such a mixture normalizes the prolonged PT, the patient likely has a deficiency of factor VII. When the mixture still results in a prolonged PT, an inhibitor to factor VII is probably present.

A specific assay for factor VII, using known factor VII–deficient plasma, is required to confirm the diagnosis. Factor VII antigen can be measured using a radioimmunoassay.

Functional factor VII assays are as follows:

  • To determine the severity, factor VII activity levels (factor VII:c) are measured using a single-stage, PT-based assay.
  • The factor VII:c assay uses the ability of tissue factor to promote the conversion of factor VII to factor VIIa and measures the total clotting activity of factor VII and factor VIIa. Results can vary dramatically depending on the source of tissue factor used in the in vitro assay.

Immunological factor VII assays can be used to measure factor VII:Ag (antigen levels). This can be an enzyme-linked immunosorbent assay or an immunoradiometric assay.

A factor VIIa:c assay is used to evaluate therapeutic factor VIIa levels. This is an enzyme-linked immunosorbent assay using specific antibodies or soluble mutant tissue factor that is insensitive to native factor VII but that serves as a cofactor for factor VIIa catalyzed activation of factor X.

A more definitive approach involves genetic analysis of mutant genes in involved families.

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Imaging Studies

CT scan and ultrasound have been used to localize, quantify, and serially monitor the location and response of bleeding to specific therapy.

Plain radiography is not useful for evaluating soft tissue damage.

MRI can be used to assess soft tissue damage; is a better modality to evaluate joint effusion, synovial hyperplasia, and cartilage loss; and can help localize the bleeding site. MRI is beneficial for evaluating reversible joint changes for earlier intervention in persons with hemophilia A and B.

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Contributor Information and Disclosures
Author

Jeyanthi Ramanarayanan, MD  Assistant Professor, Department of Medicine, Division of Medical Oncology, Roswell Park Cancer Institute

Jeyanthi Ramanarayanan, MD is a member of the following medical societies: American Association of Physicians of Indian Origin and American Society of Hematology

Disclosure: Nothing to disclose.

Coauthor(s)

Ganapathy S Krishnan, MBBS  Fellow, Department of Hematology and Oncology, Michigan State University

Ganapathy S Krishnan, MBBS is a member of the following medical societies: American Society of Hematology

Disclosure: Nothing to disclose.

Francisco J Hernandez-Ilizaliturri, MD  Assistant Professor, Departments of Medicine and Immunology, Roswell Park Cancer Institute, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Francisco J Hernandez-Ilizaliturri, MD is a member of the following medical societies: American Association for Cancer Research and American Society of Hematology

Disclosure: Nothing to disclose.

Specialty Editor Board

Paul Schick, MD  Emeritus Professor, Department of Internal Medicine, Jefferson Medical College of Thomas Jefferson University; Research Professor, Department of Internal Medicine, Drexel University College of Medicine; Adjunct Professor of Medicine, Lankenau Hospital

Paul Schick, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Hematology, International Society on Thrombosis and Haemostasis, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Ronald A Sacher, MB, BCh, MD, FRCPC  Professor, Internal Medicine and Pathology, Director, Hoxworth Blood Center, University of Cincinnati Academic Health Center

Ronald A Sacher, MB, BCh, MD, FRCPC is a member of the following medical societies: American Association for the Advancement of Science, American Association of Blood Banks, American Clinical and Climatological Association, American Society for Clinical Pathology, American Society of Hematology, College of American Pathologists, International Society of Blood Transfusion, International Society on Thrombosis and Haemostasis, and Royal College of Physicians and Surgeons of Canada

Disclosure: Glaxo Smith Kline Honoraria Speaking and teaching; Talecris Honoraria Board membership

Rebecca J Schmidt, DO, FACP, FASN  Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine

Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association

Disclosure: Renal Ventures Ownership interest Other

Chief Editor

Emmanuel C Besa, MD  Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

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Factor VII. Intrinsic and extrinsic pathways of coagulation. Factor VII/tissue factor complex activates factor IX and factor X. Factor IXa along with factor VIIIa results in formation of more factor Xa. Factor Xa along with factor Va converts prothrombin to thrombin.
 
 
 
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