Platelet Isoprostane Overproduction in Diabetic Patients Treated With Aspirin
Diabetes, 03/22/2012Cangemi R et al.
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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