Platelet Isoprostane Overproduction in Diabetic Patients Treated With Aspirin

Diabetes, 03/22/2012

The findings suggest that in aspirin–treated diabetic patients, oxidative stress–mediated platelet isoprostane overproduction is associated with enhanced platelet recruitment, an effect that mitigates aspirin–mediated TxA2 inhibition.


  • A cross–sectional study was performed comparing T2DM patients, treated (n = 50) or not treated (n = 50) with 100 mg/day aspirin, with 100 nondiabetic patients, matched for age, sex, atherosclerosis risk factors, and aspirin treatment.
  • A short–term (7 days) treatment with 100 mg/day aspirin also was performed in 36 aspirin–free diabetic and nondiabetic patients.


  • Higher platelet recruitment, platelet isoprostane, and NOX2 activation was found in diabetic versus nondiabetic patients and in aspirin–treated diabetic patients versus nontreated patients (P < 0.001).
  • Platelet thromboxane (Tx) A2 (P < 0.001) was inhibited in all aspirin–treated patients.
  • In the interventional study, aspirin similarly inhibited platelet TxA2 in diabetic and nondiabetic patients (P < 0.001).
  • Platelet recruitment, isoprostane levels, and NOX2 activation showed a parallel increase in diabetic patients (P < 0.001) and no changes in nondiabetic patients.

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