ASSESSMENT OF THROMBOPHILIC STATUS IN TYPE 2 DIABETIC PATIENTS: THE LINK BETWEEN PAI-1 POLYMORPHISM AND THE ONSET OF COMPLICATIONS

Diabetes is a very common disease characterized by a prothrombotic status involving both the chronic activation of the clotting system and a decrease in the endogenous fibrinolytic capacity. The existing data regarding the hemostatic alterations in diabetic patients are insufficient and contradictory due to the heterogeneity of the studied population, the presence of cardiovascular complications, glycemic status, other associated risk factors, and the type of treatment. The metabolic changes found in diabetic patients cause disturbances in platelet activity, hemostasis, endogenous fibrinolysis and rheology favoring a prothrombotic status. These systemic changes may lead to an extensive atherosclerotic process derived from the thrombophilic status, thus partially explaining the frequent coronary atherosclerosis in type 2 diabetic patients. Moreover, the hemostatic alterations seen in diabetic patients seem to be responsible for the microvascular localization of coronary atherosclerosis. Recent studies indicate that increased PAI-1 levels are correlated with an increase in the incidence of diabetes mellitus and its complications, such as diabetic neuropathy, diabetic retinopathy and ischemic cardiomyopathy. PAI-1 is synthesized both by endothelial cells and hepatocytes. Endothelial cell activation causes an increase in tissue thromboplastin secretion, a decrease in thrombomodulin expression, a diminished tissue plasminogen activator synthesis and an increase in PAI-1 production. Despite all this, the data regarding the association between PAI-1 levels and the incidence of diabetes mellitus remain unclear.