Test ID: TXBU
11-Dehydro-Thromboxane B2, Urine

Determining increased risk of coronary heart disease and stroke

Identifying patients most likely to benefit from antiplatelet therapy

Thromboxane A2 is produced by the enzyme cyclo-oxygenase-1 (COX1) of activated platelets and stimulates further platelet activation, platelet aggregation, and vasoconstriction. 11-Dehydro-thromboxane B2 (11-dTXB2) is the stable, inactive metabolite of thromboxane A2. Urinary 11-dTXB2 has been shown to reflect in vivo platelet activation.(1) Elevated values have been seen in up to 85% of patients with acute ischemic stroke.(2,3) This marker also has been shown to have potential use as an aid in the diagnosis of myocardial infarction.(4)  

Aspirin therapy has been reported to reduce cardiovascular events in men and women by 15% to as much as 40%. However, aspirin use 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 agents may be useful. Measurement of urinary 11-dTXB2 concentration may be used to assess an individual's platelet activity and associated risk for developing cardiovascular events, as well as identify individuals most likely to benefit from antiplatelet therapy.

Urinary 11-dTXB2 offers an advantage over platelet-activation markers measured in plasma or blood because it is not subject to interference from in vitro platelet activation, which can easily occur as a result of local vein trauma or insufficient anticoagulation during blood sample collection.

Males > or =18 years: 0-1,089 pg/mg of creatinine

Females > or =18 years: 0-1,811 pg/mg of creatinine

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

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

Elevated baseline levels of 11-dehydro-thromboxane B2 (11-dTXB2) in patients may indicate an increase in platelet activation and thrombosis resulting from atherosclerotic deposits or other vascular obstructions. Patients that exhibit 11-dTXB2 values above the normal reference value may be at increased risk for an ischemic cardiovascular event.

Elevations of 11-dTXB2 in patients already receiving anti-platelet therapy suggest a continued hypercoagulable state and alternative anti-thrombotic or anti-platelet therapies should be considered.

Aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit inflammation via cyclo-oxygenase-1 (COX1) will lower 11-dehydro-thromboxane B2 (11-dTXB2) values. Patients should not have taken NSAIDs within 72 hours or aspirin within 2 weeks prior to providing a specimen.

An enzyme-linked immunosorbent assay (ELISA) for 11-dehydro-thromboxane B2 (11-dTXB2) is marketed under the name of Aspirin Works. That test was set up in our laboratory and compared to our liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay. The 2 methods correlated with each other, but there was a bias between methods, with values from the LC-MS/MS method averaging 66% lower than the values obtained by ELISA.

1. Catella F, Lawson JA, Fitzgerald DJ, et al: Physiological formation of 8-epi-PGF2 alpha in vivo is not affected by cyclooxygenase inhibition. Adv Prostaglandin Thromboxane Leukot Res 1995;23:233-236

2. Koudstaal PJ, Ciabattoni G, van Gijn J, et al: Increased thromboxane biosynthesis in patients with acute cerebral ischemia. Stroke 1993;24(2):219-223

3. McConnell JP, Cheryk LA, Durocher A, et al: Urinary 11-dehydro-thromboxane B(2) and coagulation activation markers measured within 24 h of human acute ischemic stroke. Neurosci Lett 2001;313(1-2):88-92

4. Foegh ML, Zhao Y, Madren L, et al: Urinary thromboxane A2 metabolites in patients presenting in the emergency room with acute chest pain. J Intern Med 1994 ;235(2):153-161