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FACTOR II 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.
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.
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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.
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Test Code
86231
Alias/See Also
Prothrombin
CPT Codes
85210
Preferred Specimen
"Plasma
2 mL
"
2 mL
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Minimum Volume
"1 mL
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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.
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Please print and use the Volume Guide for Coagulation Testing to ensure proper draw volume.
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Transport Container
"Blue-top (sodium citrate) tube
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Transport Temperature
Frozen
Specimen Stability
frozen
Reject Criteria (Eg, hemolysis? Lipemia? Thaw/Other?)
"Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling
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Methodology
"Factor II activity is determined utilizing a prothrombin time (PT)-based one-stage clotting time assay. Factor II-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
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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-------41-69
Day 3-----50-73
1 mo to 1 y------62-103
1-5 y----
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-------41-69
Day 3-----50-73
1 mo to 1 y------62-103
1-5 y----
Clinical Significance
"Document specific factor II deficiency6
Factor II is a 72-kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.6 Normal factor II's plasma concentration is approximately 100 mg/mL and half-life is about 60 hours.6 Factor II activation occurs by both the extrinsic and intrinsic pathways. Factor II deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). The dilute Russell's viper venom time (dRVVT) will be prolonged in patients with factor II deficiency.7,8
Congenital factor II deficiency is rare (fewer than 100 cases have been reported) and is inherited as an autosomal recessive trait.6,7 This condition affects both males and females, and the prevalence of factor II deficiency is equal in all ethnic groups.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 oral anticoagulant (coumarin) therapy, and in individuals with vitamin K deficiency.7,8 Diminished levels that can be associated with bleeding can be observed in some patients with lupus anticoagulants due to enhanced clearance of prothrombin/antibody complexes.6,7
Symptoms of factor II deficiency include easy bruising, hematoma formation, postsurgical hemorrhage, menorrhagia, epistaxis, and umbilical cord hemorrhage.6,7 Heterozygous individuals typically have factor II activities near 50% and are asymptomatic or have minor bleeding complications associated with trauma or surgery.7 Factor II plasma activity <30%, as can be observed in individuals with homozygous deficiency, may result in excessive bleeding following a traumatic event.6,8 Spontaneous bleeding or hemarthroses are rare but may occur in homozygotes with very low activity.6-8
Factor II activity in excess of 115% has been associated with an increased risk of thrombosis.6 The G20210A mutation in the prothrombin gene can be associated with increased plasma prothrombin levels.6,9 This polymorphism can be identified in 1% to 2% of the US population, but is highly race dependent. This mutation is relatively uncommon in blacks, Asians, and native Americans.9 A recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia concluded that the prothrombin G20210A mutation is a significant risk factor of venous thromboembolism and should be considered in the initial evaluation of potential inherited thrombophilia.9
"
Factor II is a 72-kilodalton vitamin K-dependent glycoprotein coagulation factor that is produced by the liver.6 Normal factor II's plasma concentration is approximately 100 mg/mL and half-life is about 60 hours.6 Factor II activation occurs by both the extrinsic and intrinsic pathways. Factor II deficiency should be considered when a patient with bleeding history has both extended protime (PT) and activated partial thromboplastin time (aPTT). The dilute Russell's viper venom time (dRVVT) will be prolonged in patients with factor II deficiency.7,8
Congenital factor II deficiency is rare (fewer than 100 cases have been reported) and is inherited as an autosomal recessive trait.6,7 This condition affects both males and females, and the prevalence of factor II deficiency is equal in all ethnic groups.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 oral anticoagulant (coumarin) therapy, and in individuals with vitamin K deficiency.7,8 Diminished levels that can be associated with bleeding can be observed in some patients with lupus anticoagulants due to enhanced clearance of prothrombin/antibody complexes.6,7
Symptoms of factor II deficiency include easy bruising, hematoma formation, postsurgical hemorrhage, menorrhagia, epistaxis, and umbilical cord hemorrhage.6,7 Heterozygous individuals typically have factor II activities near 50% and are asymptomatic or have minor bleeding complications associated with trauma or surgery.7 Factor II plasma activity <30%, as can be observed in individuals with homozygous deficiency, may result in excessive bleeding following a traumatic event.6,8 Spontaneous bleeding or hemarthroses are rare but may occur in homozygotes with very low activity.6-8
Factor II activity in excess of 115% has been associated with an increased risk of thrombosis.6 The G20210A mutation in the prothrombin gene can be associated with increased plasma prothrombin levels.6,9 This polymorphism can be identified in 1% to 2% of the US population, but is highly race dependent. This mutation is relatively uncommon in blacks, Asians, and native Americans.9 A recent consensus conference of the College of American Pathologists on diagnostic issues in thrombophilia concluded that the prothrombin G20210A mutation is a significant risk factor of venous thromboembolism and should be considered in the initial evaluation of potential inherited thrombophilia.9
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