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LabCorp

Factor X Activity (Stuart Prower Factor)

$182.00
5172
086306
Only 100 units of this product remain
Phlebotomy (IV Blood Draw)

Evaluate an isolated, prolonged PT, evaluate prolongation of both the aPTT and PT, and to document factor X deficiency.6-8

Direct Xa or thrombin inhibitor therapy may cause factitiously low results.

To evaluate an isolated prolonged PT or to evaluate prolongation of both the APTT and PT and to document factor X deficiency.6-8 Factor X is a 54.8 kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.6 Normal factor X's plasma concentration is approximately 10 mg/mL and half-life is about 40 hours.6 Factor X activation occurs by both the extrinsic and intrinsic pathways. Factor X deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). The dilute Russell viper venom (dRVVT) measures the activation of factor X and will be prolonged in patients with deficiency.7,8 Congenital factor X deficiency is rare and is inherited as an autosomal recessive trait.6 This condition affects both males and females.6 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.6

Acquired deficiencies occur with significant hepatic dysfunction, with vitamin K antagonist (warfarin) therapy, and in individuals with vitamin K deficiency.6,7 Factor X deficiency may be associated with primary systemic amyloidosis.6,8 Isolated factor X deficiency may also occur in patients with respiratory infections, acute myeloid leukemia, amyloidosis, and with other malignancies.7 Acquired specific factor X inhibitors are rare in patients without congenital deficiency.6,7 Symptoms (homozygotes) include hematoma formation, postsurgical hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.6,7 Factor X 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

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.

Van Cott EM, Laposata M. Coagulation. In: Jacobs DS, DeMott WR, Oxley DK eds. Laboratory Test Handbook With Key Word Index. Hudson, Ohio: Lexi-Comp; 2001:327-358.

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