| A B C D E F G H I J K L M N O P Q R S T U V W X Y Z # |
FACTOR X ACTIVITY
Message"Avoid warfarin (Coumadin®) therapy for two weeks and heparin therapy for two days prior to the test. Do not draw from an arm with a heparin lock or heparinized catheter
"
"
Test Code
86306
Alias/See Also
"Stuart Factor
Stuart Prower Factor
"
Stuart Prower Factor
"
CPT Codes
85260
Preferred Specimen
"Plasma
2 mL"
2 mL"
Minimum Volume
1 mL
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 evacutated 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. To avoid delays in turnaround time when requesting multiple tests on frozen samples, please submit separate frozen specimens for each test requested.
Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
"
Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
"
Transport Container
Blue-top (sodium citrate) tube
Transport Temperature
Frozen
Specimen Stability
frozen
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
"Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling
"
"
Methodology
"Factor X activity is determined utilizing a PT-based one-stage clotting time assay. Factor X-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. "
Reference Range
"
Age----Range (%)
From Monagle P, Barnes C, Ignjatovic V, et al, ""Developmental Haemostasis. Impact for Clinical Haemostasis Laboratories,"" Thromb Haemost, 2006, 95(2):362-72.
Day 1------46-67
Day 3-----46-75
1 mo to 1 y-----77-122
1-5 y-----72-
Age----Range (%)
From Monagle P, Barnes C, Ignjatovic V, et al, ""Developmental Haemostasis. Impact for Clinical Haemostasis Laboratories,"" Thromb Haemost, 2006, 95(2):362-72.
Day 1------46-67
Day 3-----46-75
1 mo to 1 y-----77-122
1-5 y-----72-
Clinical Significance
"Document factor X deficiency7
Factor X is a 54.8 kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.7 Normal factor X's plasma concentration is approximately 10 mg/mL and half-life is about 40 hours.7 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.8,9 Congenital factor X deficiency is rare and is inherited as an autosomal recessive trait.7 This condition affects both males and females.7 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.7
Acquired deficiencies occur with significant hepatic dysfunction, with vitamin K antagonist (warfarin) therapy, and in individuals with vitamin K deficiency.7,8 Factor X deficiency may be associated with primary systemic amyloidosis.7,9 Isolated factor X deficiency may also occur in patients with respiratory infections, acute myeloid leukemia, amyloidosis, and with other malignancies.8 Acquired specific factor X inhibitors are rare in patients without congenital deficiency.7,8 Symptoms (homozygotes) include hematoma formation, postsurgical hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.7,8 Factor X plasma activity <30% may result in excessive bleeding following a traumatic event.7 Spontaneous bleeding similar to that observed in severe hemophilia may occur when the activity is <1%.
"
Factor X is a 54.8 kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.7 Normal factor X's plasma concentration is approximately 10 mg/mL and half-life is about 40 hours.7 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.8,9 Congenital factor X deficiency is rare and is inherited as an autosomal recessive trait.7 This condition affects both males and females.7 A few cases of combined congenital factor II, VII, IX, and X factor deficiencies have been reported.7
Acquired deficiencies occur with significant hepatic dysfunction, with vitamin K antagonist (warfarin) therapy, and in individuals with vitamin K deficiency.7,8 Factor X deficiency may be associated with primary systemic amyloidosis.7,9 Isolated factor X deficiency may also occur in patients with respiratory infections, acute myeloid leukemia, amyloidosis, and with other malignancies.8 Acquired specific factor X inhibitors are rare in patients without congenital deficiency.7,8 Symptoms (homozygotes) include hematoma formation, postsurgical hemorrhage, menorrhagia, hematuria, and umbilical cord hemorrhage.7,8 Factor X plasma activity <30% may result in excessive bleeding following a traumatic event.7 Spontaneous bleeding similar to that observed in severe hemophilia may occur when the activity is <1%.
"
