Postprandial hyperglycemia is a determinant of platelet activation in early type 2 diabetes mellitus

Background: Chronic hyperglycemia is a major contributor to in vivo platelet activation in diabetes mellitus. Objectives: To evaluate the effects of acarbose, an α‐glucosidase inhibitor, on platelet activation and its determinants in newly diagnosed type 2 diabetic patients. Methods: Forty‐eight sub...

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Veröffentlicht in:Journal of thrombosis and haemostasis 2010-04, Vol.8 (4), p.828-837
Hauptverfasser: SANTILLI, F., FORMOSO, G., SBRACCIA, P., AVERNA, M., MICCOLI, R., DI FULVIO, P., GANCI, A., PULIZZI, N., LATTANZIO, S., CIABATTONI, G., CONSOLI, A., LAURO, R., PATRONO, C., DAVÌ, G.
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Sprache:eng
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Zusammenfassung:Background: Chronic hyperglycemia is a major contributor to in vivo platelet activation in diabetes mellitus. Objectives: To evaluate the effects of acarbose, an α‐glucosidase inhibitor, on platelet activation and its determinants in newly diagnosed type 2 diabetic patients. Methods: Forty‐eight subjects (26 males, aged 61 ± 8 years) with early type 2 diabetes (baseline hemoglobin A1c ≤ 7% and no previous hypoglycemic treatment) were randomly assigned to acarbose up to 100 mg three times a day or placebo, and evaluated every 4 weeks for 20 weeks. The main outcome measures were urinary 11‐dehydro‐thromboxane (TX)B2 (marker of in vivo platelet activation) and 8‐iso‐prostaglandin (PG)F2α (marker of in vivo lipid peroxidation) excretion rate, 2‐h postprandial plasma glucose (PPG) after a test meal, and assessment of glucose fluctuations by mean amplitude of glycemic excursions (MAGE). Results: Baseline measurements revealed biochemical evidence of enhanced lipid peroxidation and platelet activation. As compared with the placebo group, patients treated with acarbose had statistically significant reductions in urinary 11‐dehydro‐TXB2 and 8‐iso‐PGF2α excretion rate as early as after 8 weeks and at each subsequent time point (between‐group P 
ISSN:1538-7933
1538-7836
1538-7836
DOI:10.1111/j.1538-7836.2010.03742.x