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Factor VII Activity

CPT

85230

Synonyms
  • Proconvertin

Test Details

Methodology

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. The assay consists of the measurement of the clotting time in a system in which all the factors are present and in excess except factor VII, which is derived from the sample being tested. Testing coagulation factor activities requires that three dilutions be assayed and analyzed to produce a single result.11,12 The slope of the line created by plotting measured factor concentration against sample dilution is evaluated to discern the presence of inhibitors giving rise to nonparallelism.12 Moreover, samples producing results on initial dilution falling outside the analytic measurement range of the assay are tested at additional dilutions to produce reportable results.12

Result Turnaround Time

2 - 3 days

Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.

Related Documents

For more information, please view the literature below.

Use

This test is used to evaluate an isolated prolonged PT and document factor VII deficiency.6-8

Special Instructions

If the patient's hematocrit exceeds 55%, the volume of citrate in the collection tube must be adjusted. Refer to Coagulation Collection Procedures for directions.

Limitations

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

Custom Additional Information

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

Specimen Requirements

Specimen

Plasma, frozen

Volume

1 mL

Container

Blue-top (sodium citrate) tube

Collection Instructions

Blood should be collected in a blue-top tube containing 3.2% buffered sodium citrate.1 Evacuated collection tubes must be filled to completion to ensure a proper blood-to-anticoagulant ratio.2,3 The sample should be mixed immediately by gentle inversion at least six times to ensure adequate mixing of the anticoagulant with the blood. A discard tube is not required prior to collection of coagulation samples unless the sample is collected using a winged (butterfly) collection system. With a winged blood collection set a discard tube should be drawn first to account for the dead space of the tubing and prevent under-filling of the evacuated tube.4,5 When noncitrate tubes are collected for other tests, collect sterile and nonadditive (red-top) tubes prior to citrate (blue-top) tubes. Any tube containing an alternative anticoagulant should be collected after the blue-top tube. Gel-barrier tubes and serum tubes with clot initiators should also be collected after the citrate tubes.

Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.

Stability Requirements

TemperaturePeriod
Frozen28 days
Freeze/thaw cyclesStable x2

Reference Range

Factor VII Activity13-15
AgeRange
1 d52–88%
3 d67–107%
1 to 11 m83–160%
1 to 5 y72–150%
6 to 10 y70–156%
11 to 16 y69–170%
>16 y55–170%

Storage Instructions

Freeze.

Patient Preparation

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.

Causes for Rejection

Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling

References

Girolami A, Ferrari S, Cosi E, Santarossa C, Randi ML. Vitamin K-Dependent Coagulation Factors That May be Responsible for Both Bleeding and Thrombosis (FII, FVII, and FIX). Clin Appl Thromb Hemost. 2018 Dec;24(9_suppl):42S-47S. PubMed 30428703

Mathews N, Hayward CPM. Vitamin K Deficiency: Diagnosis and Management. Ann Lab Med. 2025 Jul 1;1;45(4):358-366. PubMed 40269655

Napolitano M, Mariani G, Lapecorella M. Hereditary combined deficiency of the vitamin K-dependent clotting factors. Orphanet J Rare Dis. 2010 Jul 14;5:21. PubMed 20630065

Footnotes

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. 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. 9620035
3. Clinical Laboratory Standards Institute (CLSI). Collection, Transport, and Processing of Blood Specimens for Testing Plasma-Based Coagulation Assays. 6th ed. CLSI guideline H21. Clinical and Laboratory Standards Institute; 2024.
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. 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. 10539100
6. Sevenet PO, Kaczor DA, Depasse F. Factor VII Deficiency: From Basics to Clinical Laboratory Diagnosis and Patient Management. Clin Appl Thromb Hemost. 2017 Oct;23(7):703-710. PubMed 27701084
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. 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. 12421150
11. Castellone DD, Castillo R, Depasse F, et al. Determination of Coagulation Factor Activities Using the One-Stage Clotting Assay. CLSI Guideline H48. 2nd ed. Wayne, PA: Clinical and Laboratory Standards Institute (CLSI); 2016.
12. Riley PW, Gallea B, Valcour A. Development and Implementation of a Coagulation Factor Testing Method Utilizing Autoverification in a High-volume Clinical Reference Laboratory Environment. J Pathol Inform. 2017 Jun 19;8:25. PubMed 28706751
13. Monagle P, Barnes C, Ignjatovic V, et al. Developmental haemostasis. Impact for clinical haemostasis laboratories.Thromb Haemost. 2006 Feb;95(2):362-372. PubMed 16493500
14. Summerhayes R, et al. J Thromb Haemost. 2007;5(Supp 2):P-S-397.
15. STA® – Deficient VII Instructions For Use (IFU) [package insert]. April 2017.

LOINC® Map

Order Code Order Code Name Order Loinc Result Code Result Code Name UofM Result LOINC
800599 Factor VII Activity 3198-9 800599 Factor VII Activity % 3198-9
Order Code800599
Order Code NameFactor VII Activity
Order Loinc3198-9
Result Code800599
Result Code NameFactor VII Activity
UofM%
Result LOINC3198-9