TICLOPIDINE DOES NOT REDUCE INVIVO PLATELET THROMBOXANE BIOSYNTHESIS AND METABOLISM IN DIABETIC-PATIENTS

Citation
S. Rotondo et al., TICLOPIDINE DOES NOT REDUCE INVIVO PLATELET THROMBOXANE BIOSYNTHESIS AND METABOLISM IN DIABETIC-PATIENTS, Platelets, 4(2), 1993, pp. 97-99
Citations number
5
Categorie Soggetti
Hematology
Journal title
ISSN journal
09537104
Volume
4
Issue
2
Year of publication
1993
Pages
97 - 99
Database
ISI
SICI code
0953-7104(1993)4:2<97:TDNRIP>2.0.ZU;2-1
Abstract
Diabetic patients are at higher risk of development of cardiovascular complications than the general population. The role of platelets in th e pathogenesis of these complications is still controversial, it being difficult to ascertain whether altered platelet function is a cause o r consequence of vascular complications of diabetes. Measurement of ur inary 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 macro vascular complications. We therefore studied the effect of ticlopidine , an antiplatelet drug acting through mechanisms different from cyclo- oxygenase inhibition, on urinary 11-dehydro-TXB2 excretion in diabetic patients with macrovascular complications. The results indicate that urinary excretion of 11-dehydro-TXB2 after ticlopidine treatment is no t different from pre-treatment values, suggesting that the chosen para meter might not be reliable for monitoring the antiplatelet activity o f ticlopidine and possibly of other drugs which do not directly affect arachidonic acid metabolism.