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A means to assess aspirin effect.
Urine samples that are too dilute will not yield accurate results. Approximately 30% of urinary 11dHTxB2 may be derived from extra platelet sources (eg, monocytes, macrophages), which can generate additional COX-a following aspirin inhibition, whereas platelets cannot. 11dHTxB2 may be elevated with inflammatory conditions resulting in the potential to underestimate the degree of aspirin effect on platelet COX-1.
Thromboxane B2 (TxB2) is the stable, inactive product of prostaglandin metabolism of thromboxane A2, which is renally cleared and, therefore, can be measured in the urine. Studies have shown that thromboxane B2 is a sensitive indicator of platelet activation. Since platelets participate in atherogenesis and contribute to acute, ischemic complications, elevated TxB2 levels may reflect ongoing cardiovascular, peripheral vascular, and cerebrovascular disease processes. TxB levels may also be of interest in conditions with increased platelet turnover, such as disseminated intravascular coagulation or immune thrombocytopenia. Studies of patients with diffuse atherosclerotic disease show that TxB2 may be a more sensitive measure of platelet activation than other platelet-specific proteins. Serum or plasma TxB2 assays are typically limited to a research setting because of the significant in vitro platelet instability.
Urinary TxB2 is of interest in monitoring the anticoagulant response to aspirin therapy since aspirin inhibits the formation of TxB2 in platelets. In patients responsive to aspirin therapy and taking an adequate dose, urinary 11-dehydro TxB2 levels should be reduced below a predetermined cutoff when compared to control values.
Eikelboom JQ, Hirsh J, Weitz JI, et al. Aspirin-resistant thromboxane biosynthesis and the risk of myocardial infarction, stroke, or cardiovascular death in patients at high risk for cardiovascular events. Circulation. 2002; 105(14):1650-1655. PubMed 11940542
Gresele P, Catalano M, Giammarresi C, et al. Platelet activation markers in patients with peripheral arterial disease−a prospective comparison of different platelet function tests. Thromb Haemost. 1997; 78(6):1434-1437. PubMed 9423790
Wu KK. Platelet activation mechanisms and markers in arterial thrombosis. J Intern Med. 1996; 239(1):17-34. PubMed 8551196
