Abstract

Background: High levels of adhesion molecules are known to result in inflammation of the vascular cells through endothelial dysfunction and thus atherogenesis. To this end, this trial was performed to investigate whether a cause of the accelerated atherogenesis in cases with non-alcholic fatty liver disease (NAFLD) was the increase in the levels of the adhesion molecules. Material and Methods: 53 cases with NAFLD diagnosed using ultrasonography and biopsy and 46 control cases were enrolled in the trial. Soluble intercellular adhesion molecule (sICAM-1), Vascular adhesion molecule (sVCAM) and sE-selectinconcentrations were determined by using an enzyme linked immunosorbent assay (ELISA) kit from Biosource (Bender MedSystems GmbH, Vienna Austria) according to the manufacturer’s instructions. Results: The levels of these adhesion molecules in patients with NAFLD were higher than those in the control subjects but only a significant difference in sE-selectin levels between the NAFLD and control groups was observed (p<0.05). However, there were no statistically significant differences in sICAM-1 and sVCAM-1 levels between the two groups (p>0.05). Conclusions: The high levels of adhesion molecules and particularly of the sE-selectin statistically suggest that endothelial dysfunction and inflammation occur, which may represent a major factor in accelerating the atherogenesis process. We believe that detection of a high sE-selectin level would be leading the way when developing new therapeutical modalities for cases with NAFLD.

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