Influence of Metabolic Control on Thromboxane Biosynthesis and Plasma Plasminogen Activator Inhibitor Type-1 in Non-insulin-dependent Diabetes mellitus

Giovanni Davì; Mario Belvedere; Sergio Vingneri; Isabella Catalano; Carlo Giammarresi; Salvatore Roccaforte; Agostino Consoil; Andrea Mezzetti

doi:10.1055/s-0038-1650518

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1996; 76(01): 034-037
DOI: 10.1055/s-0038-1650518

Original Article

Schattauer GmbH Stuttgart

Influence of Metabolic Control on Thromboxane Biosynthesis and Plasma Plasminogen Activator Inhibitor Type-1 in Non-insulin-dependent Diabetes mellitus

Giovanni Davì

The Department of Internal Medicine, University of Chieti and Palermo, Italy

,

Mario Belvedere

¹The Department of Internal Medicine, University of Palermo, Italy

,

Sergio Vingneri

¹The Department of Internal Medicine, University of Palermo, Italy

,

Isabella Catalano

¹The Department of Internal Medicine, University of Palermo, Italy

,

Carlo Giammarresi

¹The Department of Internal Medicine, University of Palermo, Italy

,

Salvatore Roccaforte

The Department of Internal Medicine, University of Chieti and Palermo, Italy

,

Agostino Consoil

The Department of Internal Medicine, University of Chieti and Palermo, Italy

,

Andrea Mezzetti

The Department of Internal Medicine, University of Chieti and Palermo, Italy

› Author Affiliations

Abstract

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Summary

We have previously shown that tight metabolic control by insulin therapy reduced thromboxane-dependent platelet activation in noninsulin-dependent diabetes mellitus (NIDDM) patients. The present study was undertaken to determine whether a similar effect could be obtained without switching diabetics in secondary failure to insulin treatment. For this purpose, we gave strict diet and exercise advise program and adjusted on a weekly basis the oral antidiabetic therapy (glipizide) that 26 patients with NIDDM had been given over the previous months.

Basal measurements of urinary ll-dehydro-TXB₂ and PAI-1 confirmed previous findings of enhanced levels of these parameters in NIDDM patients with macrovascular disease in comparison to age-and sex-matched controls. After 2-6 weeks, 16 patients achieved tight metabolic control associated with significant reduction of both thromboxane biosynthesis and PAI-1 levels; 10 patients remained in poor control and no significant decrease of both parameters was observed.

We conclude that reduction of in-vivo platelet activation and PAI-1 antigen levels after metabolic improvement obtained by frequent reassessment of sulphonylurea therapy together with strict diet and exercise programs may have beneficial effects on the progression of diabetic micro- and macrovascular disease.

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References

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