Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients: clinical assessment

P. E. Jennings, N. A. Scott, A. R. Saniabadi, J. J. F. Belch

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    Abstract

    In vitro studies have demonstrated that gliclazide has free radical scavenging and antiplatelet activities. To assess this clinically, we studied gliclazide in a blinded, randomized, glibenclamide-controlled trial in 30 type II diabetic patients with retinopathy. All patients had been taking glibenclamide for more than 12 months before being randomized to receive either an equipotent dose of gliclazide or to continue on glibenclamide. Diabetic control was not modified. The patients were well matched at randomization (mean age, 58 years; duration of diabetes, 8 years; 20 males; mean hemoglobin A1 [HbA1], 8.6%) and their degree of diabetic control was not altered during the trial. Free radical activity was assessed as oxidative status by plasma thiols (PSH), lipid peroxides (MDA-LM), and red blood cell superoxide dismutase activity (SOD). Platelet aggregation in whole blood to collagen (Plt-ag) was used as the measure of platelet reactivity. There were no differences between these measurements at baseline. At 3 months, the oxidative status and platelet aggregation in the gliclazide group had improved significantly compared with baseline and had also showed significant differences in all parameters when compared with the glibenclamide group. Therefore, comparing gliclazide with glibenclamide-treated patients at 3 months, we found: PSH, 458 ± 38 versus 414 ± 34 µmol/L, P < .004; MDA-LM, 7.0 ± 0.6 versus 8.3 ± 0.8 µmol/L, P < .0002; SOD, 152 ± 36 versus 123 ± 15 µg/mL, P < .016; Plt-ag, 50.8 ± 24 versus 72.3% ± 15%, P < .006. These changes were maintained at 6 months. These results confirm in a clinical study that gliclazide is a powerful general free radical scavenger. The effects on platelets may be secondary to this, and the free radical scavenger effect appears to be independent of diabetic control.
    Original languageEnglish
    Pages (from-to)36-39
    Number of pages4
    JournalMetabolism: Clinical and Experimental
    Volume41
    Issue number5, Supplement 1
    DOIs
    Publication statusPublished - May 1992

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    Gliclazide
    Glyburide
    Free Radicals
    Blood Platelets
    Free Radical Scavengers
    Platelet Aggregation
    Sulfhydryl Compounds
    Superoxide Dismutase
    Lipid Peroxides
    Random Allocation
    Hemoglobins
    Collagen
    Randomized Controlled Trials
    Erythrocytes

    Cite this

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    title = "Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients: clinical assessment",
    abstract = "In vitro studies have demonstrated that gliclazide has free radical scavenging and antiplatelet activities. To assess this clinically, we studied gliclazide in a blinded, randomized, glibenclamide-controlled trial in 30 type II diabetic patients with retinopathy. All patients had been taking glibenclamide for more than 12 months before being randomized to receive either an equipotent dose of gliclazide or to continue on glibenclamide. Diabetic control was not modified. The patients were well matched at randomization (mean age, 58 years; duration of diabetes, 8 years; 20 males; mean hemoglobin A1 [HbA1], 8.6{\%}) and their degree of diabetic control was not altered during the trial. Free radical activity was assessed as oxidative status by plasma thiols (PSH), lipid peroxides (MDA-LM), and red blood cell superoxide dismutase activity (SOD). Platelet aggregation in whole blood to collagen (Plt-ag) was used as the measure of platelet reactivity. There were no differences between these measurements at baseline. At 3 months, the oxidative status and platelet aggregation in the gliclazide group had improved significantly compared with baseline and had also showed significant differences in all parameters when compared with the glibenclamide group. Therefore, comparing gliclazide with glibenclamide-treated patients at 3 months, we found: PSH, 458 ± 38 versus 414 ± 34 µmol/L, P < .004; MDA-LM, 7.0 ± 0.6 versus 8.3 ± 0.8 µmol/L, P < .0002; SOD, 152 ± 36 versus 123 ± 15 µg/mL, P < .016; Plt-ag, 50.8 ± 24 versus 72.3{\%} ± 15{\%}, P < .006. These changes were maintained at 6 months. These results confirm in a clinical study that gliclazide is a powerful general free radical scavenger. The effects on platelets may be secondary to this, and the free radical scavenger effect appears to be independent of diabetic control.",
    author = "Jennings, {P. E.} and Scott, {N. A.} and Saniabadi, {A. R.} and Belch, {J. J. F.}",
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    Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients : clinical assessment. / Jennings, P. E.; Scott, N. A.; Saniabadi, A. R.; Belch, J. J. F.

    In: Metabolism: Clinical and Experimental, Vol. 41, No. 5, Supplement 1, 05.1992, p. 36-39.

    Research output: Contribution to journalArticle

    TY - JOUR

    T1 - Effects of gliclazide on platelet reactivity and free radicals in type II diabetic patients

    T2 - clinical assessment

    AU - Jennings, P. E.

    AU - Scott, N. A.

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    AU - Belch, J. J. F.

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    N2 - In vitro studies have demonstrated that gliclazide has free radical scavenging and antiplatelet activities. To assess this clinically, we studied gliclazide in a blinded, randomized, glibenclamide-controlled trial in 30 type II diabetic patients with retinopathy. All patients had been taking glibenclamide for more than 12 months before being randomized to receive either an equipotent dose of gliclazide or to continue on glibenclamide. Diabetic control was not modified. The patients were well matched at randomization (mean age, 58 years; duration of diabetes, 8 years; 20 males; mean hemoglobin A1 [HbA1], 8.6%) and their degree of diabetic control was not altered during the trial. Free radical activity was assessed as oxidative status by plasma thiols (PSH), lipid peroxides (MDA-LM), and red blood cell superoxide dismutase activity (SOD). Platelet aggregation in whole blood to collagen (Plt-ag) was used as the measure of platelet reactivity. There were no differences between these measurements at baseline. At 3 months, the oxidative status and platelet aggregation in the gliclazide group had improved significantly compared with baseline and had also showed significant differences in all parameters when compared with the glibenclamide group. Therefore, comparing gliclazide with glibenclamide-treated patients at 3 months, we found: PSH, 458 ± 38 versus 414 ± 34 µmol/L, P < .004; MDA-LM, 7.0 ± 0.6 versus 8.3 ± 0.8 µmol/L, P < .0002; SOD, 152 ± 36 versus 123 ± 15 µg/mL, P < .016; Plt-ag, 50.8 ± 24 versus 72.3% ± 15%, P < .006. These changes were maintained at 6 months. These results confirm in a clinical study that gliclazide is a powerful general free radical scavenger. The effects on platelets may be secondary to this, and the free radical scavenger effect appears to be independent of diabetic control.

    AB - In vitro studies have demonstrated that gliclazide has free radical scavenging and antiplatelet activities. To assess this clinically, we studied gliclazide in a blinded, randomized, glibenclamide-controlled trial in 30 type II diabetic patients with retinopathy. All patients had been taking glibenclamide for more than 12 months before being randomized to receive either an equipotent dose of gliclazide or to continue on glibenclamide. Diabetic control was not modified. The patients were well matched at randomization (mean age, 58 years; duration of diabetes, 8 years; 20 males; mean hemoglobin A1 [HbA1], 8.6%) and their degree of diabetic control was not altered during the trial. Free radical activity was assessed as oxidative status by plasma thiols (PSH), lipid peroxides (MDA-LM), and red blood cell superoxide dismutase activity (SOD). Platelet aggregation in whole blood to collagen (Plt-ag) was used as the measure of platelet reactivity. There were no differences between these measurements at baseline. At 3 months, the oxidative status and platelet aggregation in the gliclazide group had improved significantly compared with baseline and had also showed significant differences in all parameters when compared with the glibenclamide group. Therefore, comparing gliclazide with glibenclamide-treated patients at 3 months, we found: PSH, 458 ± 38 versus 414 ± 34 µmol/L, P < .004; MDA-LM, 7.0 ± 0.6 versus 8.3 ± 0.8 µmol/L, P < .0002; SOD, 152 ± 36 versus 123 ± 15 µg/mL, P < .016; Plt-ag, 50.8 ± 24 versus 72.3% ± 15%, P < .006. These changes were maintained at 6 months. These results confirm in a clinical study that gliclazide is a powerful general free radical scavenger. The effects on platelets may be secondary to this, and the free radical scavenger effect appears to be independent of diabetic control.

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