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Diabetes 51:2840-2845, 2002
© 2002 by the American Diabetes Association, Inc.
Type 1 And Type 2 Diabetic Patients Display Different Patterns of Cellular Microparticles
1 INSERM EMI 0019, Laboratory of Immunology and Hematology, UFR de Pharmacie, Université de la Méditerranée, Marseille, France
2 Federation of Autoimmunity and Thrombosis, AP-HM de la Conception, Marseille, France
3 Department of Endocrinology, Metabolic Diseases and Nutrition, AP-HM Nord, Marseille, France
4 Institute of Hematology and Immunology, Faculty of Medicine, Strasbourg, France
5 Department of Internal Medicine, AP-HM Nord, Marseille, France
The development of vasculopathies in diabetes involves multifactorial processes including pathological activation of vascular cells. Release of microparticles by activated cells has been reported in diseases associated with thrombotic risk, but few data are available in diabetes. The aim of the present work was to explore the number and the procoagulant activity of cell-derived microparticles in type 1 and 2 diabetic patients. Compared with age-matched control subjects, type 1 diabetic patients presented significantly higher numbers of platelet and endothelial microparticles (PMP and EMP), total annexin V-positive blood cell microparticles (TMP), and increased levels of TMP-associated procoagulant activity. In type 2 diabetic patients, only TMP levels were significantly higher without concomitant increase of their procoagulant activity. Interestingly, in type 1 diabetic patients, TMP procoagulant activity was correlated with HbA1c, suggesting that procoagulant activity is associated with glucose imbalance. These results showed that a wide vesiculation process, resulting from activation or apoptosis of several cell types, occurs in diabetes. However, diabetic patients differ by the procoagulant activity and the cellular origin of microparticles. In type 1 diabetic patients, TMP-procoagulant activity could be involved in vascular complications. Moreover, its correlation with HbA1c reinforces the importance of an optimal glycemic control in type 1 diabetes.
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