Quantitative platelet agglutination with ristocetin
1 - 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.
For more information, please view the literature below.
Plasma (platelet poor), frozen
Blue-top (sodium citrate) tube
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.
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.
Gross hemolysis; clotted specimen; frozen specimen thawed in transit; improper labeling
Screen and diagnose von Willebrand factor (vWF) deficiency6,8-10
vWF ristocetin cofactor activity may be spuriously low in individuals with certain polymorphisms in the vWF gene (eg, Asp1472His) that alter the binding of ristocetin to vWF. These polymorphisms have been reported in 17% of whites and 63% of African Americans without a history of a bleeding disorder.11 A number of transient clinical conditions can raise the vWF levels of individuals with congenital deficiency into the normal range.8 vWF is an acute phase reactant and levels can increase due to stress, inflammation, acute infection, physical exercise, and following surgery.8 Levels can also increase with estrogen administration for contraception or hormone replacement.8 vWF levels are increased two- to threefold in the second and third trimesters of pregnancy.10 Individuals with type O blood tend to have approximately 30% lower vWF levels than those with other blood types.10
In this ristocetin cofactor assay, the patient plasma is mixed with formalin-fixed platelets in the presence of ristocetin.12 The extent of platelet agglutination detected photo-optically is proportional to the vWF activity of the sample.
50% to 150%. Average vWF levels tend to vary by blood type.6 One study found the mean vWF levels by blood type to be as follows:7
• Type O: 74.8%
• Type A: 105.6%
• Type B: 116.9%
• Type AB: 123.3%
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|164509||vWF Activity||6014-5||164509||vWF Activity||%||6014-5|
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