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Unlabelled: Cytokines secreted by the monocyte-macrophage system play a key role in the progression of atherosclerotic lesions in Type 2 diabetes. The objectives of this study were to assess the influence of cytokine gene expression in monocytes from patients with Type 2 diabetes on direct markers of endothelial injury with regard to clinically manifest atherosclerosis., Methods: Monocytes from 58 patients with Type 2 diabetes and from 22 age-matched healthy volunteers of a control group were isolated in order to assess expression of tumor necrosis factor alpha (TNFalpha), interleukin (IL)-6, IL-8 and IL-10 cytokines (RTPCR, Applied Biosystems). Thrombomodulin concentration was determined using a Diagnostica Stago Immunoenzymatic assay, and circulating endothelial cell numbers were assayed using immunofluorescence studies with CLB-HEC19 antibodies., Results: In 28 patients, TNFalpha expression in monocytes was observed. In these patients, as compared to those with undetectable levels of this cytokine's expression, higher hemoglobin A(1c) (P=.012) and thrombomodulin (P=.005) concentrations were found. IL-8 expression was determined in 36 patients. Higher expression of TNFalpha (P=.048) and IL-8 (P=.049) was detected in patients with peripheral arterial disease in contrast to those free from this complication., Conclusion: TNFalpha and IL-8 play a significant role in the proatherogenic activity of monocytes in Type 2 diabetes. The TNFalpha-connected activity of monocytes may directly determine endothelial dysfunction and injury. The location of atherosclerosis should be taken into account in the assessment of the proinflammatory activity of peripheral blood monocytes.

Diabetes causes the development of atherosclerotic vascular changes. Leukocytes, thrombocytes and also cytokines are involved in this process via endothelial activation. Estimation of interleukin 1 beta (IL-1 beta) and fibrinogen serum level of patients suffering from diabetes in context of endothelial damage is presented. The stage of vascular endothelium damage is based on the measurement of blood endothelial cells (EC) count and concentration of the plasmatic von Willebrand factor (vWF). Endothelial destruction level was established on the base of selectin L, P and E serum concentration. Activation of inflammatory proliferative mechanisms was indicated by IL-1 beta serum level. Serum haemostasis disorders were indicated by fibrinogen concentration. Patients with diabetes t. 1 and t. 2 differentiated by age and diabetes duration time with normal blood pressure and hypertension were included into the research. We showed that in both types of diabetes endothelium damage goes with significant increase of circulated EC count and vWF concentration. Increased serum level of IL-1 beta and fibrinogen in those patients shoulds significant correlation with vascular wall destruction, visibly marked in patients with diabetes t. 2. Hiperfibrinogenaemia and increased IL-1 beta concentration associate with significant engagement of SL and SE in inflammatory proliferative process of endothelium in young people suffering from diabetes t. 1 over 6 years. Hypertension coexisting with essential disease in both types of diabetes remains important progression factor in atheromatic vascular changes.