Ticlopidine does not reduce in vivo platelet thromboxane biosynthesis and metabolism in diabetic patients.

Diabetic patients are at higher risk of development of cardiovascular complications than the general population. The role of platelets in the pathogenesis of these complications is still controversial, it being difficult to ascertain whether altered platelet function is a cause or consequence of vascular complications of diabetes. Measurement of urinary 11-dehydro-thromboxane has been proposed as a reliable index of in vivo platelet activation and has been reported to be significantly higher in non insulin-dependent diabetic patients with micro- or macrovascular complications. We therefore studied the effect of ticlopidine, an antiplatelet drug acting through mechanisms different from cyclo-oxygenase inhibition, on urinary 11-dehydro-TXB(2) excretion in diabetic patients with macrovascular complications. The results indicate that urinary excretion of 11-dehydro-TXB(2) after ticlopidine treatment is not different from pre-treatment values, suggesting that the chosen parameter might not be reliable for monitoring the antiplatelet activity of ticlopidine and possibly of other drugs which do not directly affect arachidonic acid metabolism.