Abstract

BACKGROUND: Endothelial dysfunction is one of the early stages of vascular diseases. OBJECTIVE: The aim of this study was to investigate the endothelial dysfunction markers in patients with chronic gastritis associated with Helicobacter pylori (H. pylori) infection. METHODS: By a cross sectional study, basic and clinical information of 120 participants (40 patients with positive H. pylori infection, 40 patients with negative H. pylori infection and 40 healthy people) were analyzed. Carotid intima media thickness and fl ow-mediated dilation levels were measured in all patients and controls. Soluble vascular cell adhesion molecule-1 (sVCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured with Elisa for all subjects. IgG level was assessed in chronic gastritis patients. RESULTS: The fl ow-mediated dilation level in patients with positive H. pylori infection (0.17+/-0.09) was significantly lower than those with negative H. pylori infection (0.21 +/-0.10, P<0.05) and compared to the control group (0.27 +/-0.11, P<0.05). Carotid intima media thickness level in patients with positive H. pylori infection (0.58+/-0.13 mm) was significantly higher than those with negative H. pylori infection (0.48+/-0.32 mm, P<0.05) and compared to the control group (0.36+/-0.44mm, P<0.05). The mean level of sICAM-1 in positive H. pylori infection group (352.16+/-7.54 pg/mL) was higher than negative H. pylori infection group (332.64+/-8.75 pg/mL =0.75) and compared to the control group (236.32+/-12.43 pg/mL, P<0.05). A direct relationship was revealed between fl ow-mediated dilation and carotid intima media thickness changes and between sICAM-1 and sVCAM-1 associated with the level of H. pylori IgG in chronic gastritis. CONCLUSION: The levels of fl ow-mediated dilation, carotid intima media thickness and sICAM-1 were higher among patients with positive H. pylori infection. Patients with chronic gastritis associated with H. pylori infection are at risk of endothelial dysfunction due to fl ow-mediated dilation and carotid intima media thickness abnormalities and increased level of sICAM-1 and sVCAM-1.