Abstract

CRP is a marker of inflammation and infection of the gastric mucosa with Helicobacter pylori, which causes an inflammatory reaction. It has been reported that CagA(+) H. pylori strains induce more severe gastric inflammation and are also associated with higher risks of peptic ulcer and gastric cancer. The purpose of this study was to compare serum concentrations of hs-CRP in H. pylori-infected peptic ulcer (PU) patients, H. pylori infected asymptomatic (AS) carriers, and a healthy control group, and their association with bacterial virulence factor CagA. A total of 60 H. pylori infected PU patients (30 patients were positive for anti-CagA antibody and 30 were negative for anti-CagA antibody), 53 H. pylori-infected AS carriers (25 subjects were positive for anti-CagA antibody and 28 were negative for anti-CagA antibody), and 22 healthy H. pylori-negative subjects (as a control group) were enrolled in the study. Serum concentrations of hs-CRP were measured by use of an ELISA method. The mean serum level of hs-CRP in all PU patients (124.9±32.4 μg/dl) was significantly higher than that in all AS subjects (18.6±2.6 μg/dl; P<0.001) and the healthy uninfected control group (10.7±2.9 μg/dl; P<0.0001). Moreover, the mean serum level of hs-CRP in the AS group was significantly higher than that observed in the uninfected control group (P<0.04). No significant difference was observed between mean serum levels of hs-CRP of PU patients with positive test for anti-CagA antibody (132.6±49.4 μg/dl) and PU patients with negative test for anti-CagA antibody (117.1±42.9 μg/dl). Moreover, mean serum levels of hs-CRP were similar in AS subjects with positive test for anti-CagA (18.4±3.1 μg/dl) and in those who were negative for anti-CagA antibody (18.9±4.1 μg/dl). The results of this study showed that mean serum concentrations of hs-CRP in PU patients and in H. pylori infected AS carriers were higher than in a healthy control group. Although H. pylori infection is associated with higher serum levels of hs-CRP, serum concentrations of this inflammatory marker were not affected by expression of bacterial CagA virulence factor.

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