RESUMO
OBJECTIVE: Platelet hyper-reactivity is one of the most important causes of accelerated atherosclerosis and increased risk of thrombotic vascular events associated with type 2 diabetes mellitus (T2DM). This study aimed to investigate the effects of different add-on anti-diabetic therapies on platelet function in T2DM patients. PATIENTS AND METHODS: A three-group parallel study was conducted in 120 patients with T2DM (HbA1c > 7%) undergoing treatment with metformin. Patients were randomly assigned to receive add-on therapy with glipizide or pioglitazone. Markers of PF (platelet PAC-1 binding, p-selectin expression and adenosine diphosphate-induced platelet aggregation) were measured at weeks 0, 4 and 24. Primary outcome was effects of pioglitazone and glipizide on platelet aggregation. Secondary outcome was the related influencing factors of platelet aggregation. RESULTS: There were no significant differences in baseline characteristics between glipizide and pioglitazone groups. After 24 weeks, fasting blood glucose (p < 0.01) and HbA1c (p < 0.01) were higher in pioglitazone group than those in glipizide group. Fasting insulin (p < 0.01) and HOMA-IR (p < 0.01) were lower in pioglitazone group than that in glipizide group. Markers of platelet function were significantly decreased in both groups at 24 weeks (PAC-1: pioglitazone: -63.3%; glipizide: -45.9%; p-selectin: pioglitazone: -73.9%; glipizide: -54.9%; platelet aggregation: pioglitazone: -24.1%; glipizide: -13.4%; all p < 0.01 vs. baseline), but the decrease in platelet function was more significant in pioglitazone group (p < 0.05). Multiple linear regression analyses showed that platelet aggregation was independently associated with treatment groups (p < 0.001), Triglyceride (p = 0.009) and HDL-C (p = 0.015). CONCLUSIONS: Add-on therapy with pioglitazone may be more effective than glipizide for inhibiting platelet activation in T2DM.