Urinary immunoreactive TXB2 is elevated in patients with acute cerebral ischemia, particularly in males and those with severe or cardiogenic stroke, suggesting a role for increased platelet activation.
Elevated urinary TXB2 may signal platelet activation in acute ischemia; hypothesis-generating and should not yet change practice.
Thromboxane B2 (TXB2) is the stable metabolite of thromboxane A2 (TXA2), a potent vasoconstrictor which induces irreversible platelet aggregation. The inhibition of TXA2 by aspirin and other agents has been associated with improved outcome following cerebral ischemia in clinical and laboratory studies. To investigate the relation of TXA2 production to cerebral ischemia, we measured the urinary excretion of TXA2 metabolites in 30 patients with acute cerebral ischemia. Urinary immunoreactive TXB2 for this group of ischemic patients was elevated compared to normals, 1818 +/- 344 pg/mg Cr (mean +/- SE) vs 880 +/- 122 pg/mg Cr (p less than .05). Among various subsets of the ischemic patients, those with severe stroke (2108 +/- 536 pg/mg Cr), large vessel disease (1646 +/- 335 pg/mg Cr), and cardiogenic stroke (2712 +/- 1045 pg/mg Cr) were all significantly elevated. Of the stroke patients, only the males demonstrated this significant elevation. These elevations of urinary immunoreactive TXB2 are consistent with a role for increased platelet activation in the pathogenesis of some forms of cerebral ischemia and suggest that gender differences in arachidonate metabolism may exist for stroke patients.
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Fisher et al. (1985) studied this question.
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