Urinary 11-Dehydrothromoboxane B2: A Quantitative Index of Platelet Activation in Cerebral Infarction.

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Abstract
Thromboxane A2 (TXA2) biosynthesis was studied in healthy subjects, patients with chronic cerebral infarction, patients under chronic aspirin treatment and patients with atrial fibrillation. Urinary 11-dehydro-TXB2, as a major metabolite of TXA2, was measured by radio-immunoassay. The extent of carotid atherosclerosis was determined by B-mode ultrasonography. The mean ± SD urinary excretion in patients with cerebral infarction and distinct carotidatherosclerotic lesions (1, 725 ± 239ng/g creatinine, n = 6) was significantly higher (p < 0.01) than in healthy subjects (911 ± 239 ng/g creatinine, n = 44) and patients with cerebral infarction who had no distinct carotid lesion (1, 050 ± 191 ng/g creatinine, n = 6). The urinary excretion of healthy subjects was higher (p < 0.01) in smokers (1, 063 ± 244 ng/g creatinine, n = 17) than in non-smokers (815 ± 183 ng/g creatinine, n = 27). Aspirin largely suppressed 11-dehydro-TXB2 excretion (266 ± 114 ng/g creatinine, n = 7). Three of 5 patients with atrial fibrillation showed very high values. Our results indicated that platelet activation occurs in the atherosclerotic lesions, and that urinary 11-dehydro-TXB2 is the appropriate analytic target for detecting platelet activation. (Internal Medicine 31 : 735-739, 1992)

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