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American Journal of Clinical Nutrition, Vol 47, 256-261, Copyright © 1988 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
C Colette, N Pares-Herbute, LH Monnier and E Cartry
Department of Metabolism, Hopital Lapeyronie, Montpellier, France.
Nine Type I diabetic patients were randomized to a double-blind therapeutic trial divided into two study periods of 35 d with either 1 g vitamin E/d or a placebo. Platelet function was estimated at baseline and after treatment from ADP-induced platelet aggregation tests and from generation of oxidative products (TXB2, 12 HETE, and malondialdehyde) after platelet stimulation by 14C arachidonic acid. Platelet function, plasma lipids, and apoproteins were similar before both treatment periods. The vitamin E treatment resulted in 1) diminution of platelet aggregation with ADP 2.5 microM (56 +/- 4 vs 47 +/- 4 cm2, p = 0.05) and 5 microM (70 +/- 5 vs 57 +/- 4 cm2, p less than 0.01); 2) diminution of malondialdehyde release from platelets (6.4 +/- 0.5 vs 5.0 +/- 0.7 nmol/10(9) platelets, p less than 0.02); and 3) diminution in the percentage of 14C TXB2 (38.1 +/- 2.8 vs 33.3 +/- 3.0%, p less than 0.05). No significant changes were observed on placebo. Results indicate that high doses of vitamin E diminish ADP- induced platelet aggregation in Type I diabetic patients and suggest that this effect is partly mediated through a diminution of the cyclooxygenase activity.
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