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Test Code TXBU 11-Dehydro-Thromboxane B2, Urine

Reporting Name

11-Dehydro-Thromboxane B2, U

Useful For

Assessing if a patient will derive benefit from aspirin therapy

 

Determining an individual’s risk of coronary heart disease and stroke

 

Identifying the effectiveness of antiplatelet therapies

Additional Tests

Test ID Reporting Name Available Separately Always Performed
AACT Creatinine, U No Yes

Testing Algorithm

When 11-dehydro-thromboxane B2 testing is performed, urine creatinine will always be performed at no additional charge.

Method Name

TXBU: Liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS)

AACT: Enzymatic Colorimetric Assay

Performing Laboratory

Mayo Medical Laboratories in Rochester

Specimen Type

Urine


Specimen Required


Container/Tube: Plastic, 10-mL urine tube (T068)

Specimen Volume: 10 mL

Collection Instructions:

1. Collect a random urine specimen.

2. No preservative.

Additional Information: Patient should not have taken nonsteroidal anti-inflammatory drugs within 72 hours or aspirin within 2 weeks prior to collection of a specimen.


Specimen Minimum Volume

5 mL

Specimen Stability Information

Specimen Type Temperature Time
Urine Refrigerated (preferred) 7 days
  Frozen  90 days
  Ambient  7 days

Reject Due To

Hemolysis

NA

Lipemia

NA

Icterus

NA

Other

NA

Reference Values

≥18 years: 0-2,211 pg/mg creatinine

Reference values have not been established for patients who are <18 years of age.

Reference intervals apply to patients not taking agents known to influence platelet function (aspirin or other nonsteroidal anti-inflammatory drugs, thienopyridines, etc). Healthy individuals taking aspirin typically have 11-dehydro-thromboxane B2 concentrations below 500 pg/mg creatinine using this method.

Day(s) and Time(s) Performed

Wednesday; 8 a.m.

CPT Code Information

84431

LOINC Code Information

Test ID Test Order Name Order LOINC Value
TXBU 11-Dehydro-Thromboxane B2, U In Process

 

Result ID Test Result Name Result LOINC Value
83335 11-Dehydro-Thromboxane B2, U 49734-7

Analytic Time

2 days

Cautions

A variety of tests are available to assess platelet function and interpretation of results from 1 platform to another is confounded by the lack of standardization, because the tests quantitate different aspects of platelet function and use different cutoffs for determining appropriate response to the various antithrombotic therapies. Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit inflammation via the cyclooxygenase 1 pathway, will lower thromboxane B2 concentrations and prevent an accurate baseline assessment of platelet reactivity and response. Patients should not take NSAIDs within 72 hours or aspirin within 2 weeks prior to providing a urine specimen for analysis.

Supportive Data

An enzyme-linked immunosorbent assay (ELISA) for quantitation of urine thromboxane B2 (TxB2) is marketed under the name of AspirinWorks. The ELISA assay has a high correlation with the liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for TxB2, however there is a bias between methods with LC-MS/MS producing concentrations 25% less than the ELISA method.

Method Description

Thromboxane B2 (TxB2) is quantitated with an assay developed using liquid chromatography-tandem mass spectrometry (LC-MS/MS). Urine specimens are vortexed thoroughly to reconstitute all of the native TxB2. Urine samples are adjusted to a pH of 2.0 + or -0.2 and incubated for 3 hours at ambient temperature to force all the urinary thromboxane into the closed ring form that is recognized by the LC-MS/MS method. After addition of d4 internal standard (d4-11-dTxB2) to the sample, it is positive-pressure filtered and the 11-dTxB2 is separated from the urine matrix via turboflow online extraction. A Cyclone MAX anion-exchange column is used for the extraction, while a Waters Xbridge C8 is used for separation from other prostaglandins. From this column, the sample is transferred to an API 5000 MS/MS for instrumental analysis. A calibration curve is included with each batch of samples. This method does not have any cross-reactivity with the 2,3-dinor thromboxane B2 metabolite.(Lueke AJ, Saenger AK: Development and validation of an LC-MS/MS assay for quantitation of urinary prostaglandins. Clin Chem 2011;57:A133)

Interpretation

The normal reference range was derived from an in-house normal donor study with individuals who were self-reported as not taking any aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), or other lipid-lowering therapies. Elevated concentrations of urine thromboxane B2 (TxB2) may indicate an increase in platelet activation and thrombosis resulting from atherosclerotic deposits or other vascular obstructions and may identify those individuals who may be at increased risk for an ischemic cardiovascular event. Elevations of TxB2 in patients already receiving antiplatelet therapies suggest a failure in the suppression of laboratory-assessed platelet function, a continued hypercoagulable state, and alternative antithrombotic or antiplatelet therapies may be considered.

The liquid chromatography-tandem mass spectrometry method is specific for TxB2 and is not subject to interference from the other metabolite of thromboxane A2, the 2,3-dinor-TxB2 component.

Specimen Retention Time

1 week

Clinical Information

Antiplatelet medications are frequently utilized in the prevention of stroke, myocardial infarction, and vascular thrombotic diseases due to the fundamental role of platelet aggregation in a variety of atherothrombotic processes. Modulation of the prostaglandin thromboxane A2 (TxA2) pathway is 1 of the pivotal routes of activation involved in stimulating platelet aggregation. Synthesis of TxA2 is mediated in platelets by the cyclooxygenase 1 (COX-1) enzyme, which must be functional for stimulating the production of TxA2 from arachidonic acid.

 

The importance of TxA2 is demonstrated by the reduction in risk of myocardial infarction (MI) or death in patients with acute coronary syndrome (ACS) following administration of aspirin, which irreversibly inhibits platelet COX-1 and inhibits the production of TxA2. TxA2 has an extremely short half-life, converting to 2 stable, inactive metabolites: 11-dehydro-thromboxane B2 (TxB2) and 2, 3-dinor-11-dehydrothromboxane B2. Excretion of TxB2 in the urine has been shown to reflect in vivo platelet activation. Elevated concentrations of TxB2 have been noted in up to 85% of patients with acute ischemic stroke and demonstrate further diagnostic and prognostic utility in patients with ACS.

 

Aspirin therapy has been reported to reduce cardiovascular events in men and women by up to 40%. However, use of aspirin is not without risk and is associated with higher frequencies of gastrointestinal bleeding and hemorrhagic stroke. Identification of patients most likely to benefit from antiplatelet therapy with aspirin or other pharmaceutical agents has great clinical utility.

 

Quantitation of urinary TxB2 offers an advantage over platelet-activation markers measured in plasma or blood because measurements are not subject to interference from in vitro platelet activation, which commonly occurs as a result of preanalytical variables such as local vein trauma or insufficient anticoagulation during phlebotomy. Measurement of urine TxB2 may be performed in patients to assess the effectiveness of specific inhibition in the TxA2 pathway, along with identification of a patient’s ability to benefit from antiplatelet therapy, and their associated risk for developing future cardiovascular events.

Test Classification

This test was developed and its performance characteristics determined by Mayo Clinic in a manner consistent with CLIA requirements. This test has not been cleared or approved by the U.S. Food and Drug Administration.

Forms

If not ordering electronically, complete, print, and send a Cardiovascular Test Request Form (T724) with the specimen (http://www.mayomedicallaboratories.com/it-mmfiles/cardiovascular-request-form.pdf).