Endothelial hemostatic markers in type 2 diabetes and without diabetes in patients with advanced peripheral arterial disease

Background. Type 2 diabetes (DM2) plays an important role as a risk factor for peripheral arterial disease (PAD). Metabolic abnormalities in DM2, as insulin resistance and hyperglycemia cause overproduction of reactive oxygen species, which via inflammation and endothelial dysfunction lead to atherothrombosis. The injured arterial wall releases hemostatic endothelial markers. The aim of the study was to determine: tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombomodulin (TM), von Willebrand factor (vWF), tissue plasminogen activator (t-PA) and plasminogen activators inhibitor type 1 (PAI-1) in type 2 diabetes and without diabetes in patients with advanced PAD. Material and methods. Endothelial markers were examined in 91 patients with PAD and DM2; 37 women and 54 men - aged 65.2 +/- 9.0 years. Control group concluded 59 PAD patients without DM2. Both groups of patients were in similar compartments of sex and age with similar risk factors and coexisting diseases. Only in patients with DM2 more frequently appeared dyslipidemia (p < 0.022). Blood was collected in the morning to 3.2% sodium citrate in proportion 9:1. Endothelial hemostatic markers were determined with enzyme immunoassay ELISA using commercial tests of American Diagnostica. Results. The levels of endothelial markers: TF, TFPI, TM, vWF, t-PA and PAI-1 in patients with PAD and DM2 were similar compared to patients without DM2. But patients with DM2 had the concentration of TF and vWF significant higher (p < 0.005, p < 0.0001) and TM lower (p < 0.001) in comparison with reference group of healthy patients. But levels of TFPI, t-PA and PAI-1 were almost equal in all three groups of patients with DM2, without DM2 and of healthy persons. Conclusion. DM2 coexisting in PAD patients did not change the release of endothelial hemostatic markers from arterial wall. This confirms the view of "endothelial dysfunction" as common etiology of both diseases PAD and DM2.