The effect of Helicobacter pylori infection on oxidative stress status in erosive reflux disease

Background and Objectives: Helicobacter pylori (H. pylori) infection has been associated with increased production of reactive oxygen species, which leads to oxidative stress in the gastrointestinal mucosa. Nevertheless, the association of H. pylori infection and oxidative stress in erosive reflux disease (ERD) is still unclear. We sought to investigate the association between oxidative stress status and H. pylori infection in ERD. Materials and Methods: Eighty-three ERD patients (45 male/ 38 female; mean age: 40.4 ± 14.3 years) who had heartburn and/or regurgitation and erosion(s)-confirmed by endoscopy-in the distal esophagus were enrolled. Two antral biopsies were taken from the patients for rapid urease test. Blood samples were drawn for measurement of oxidative stress parameters, including malondialdehyde (MDA), ferric reducing antioxidant power (FRAP), superoxide dismutase (SOD) activity, and glutathione peroxidase (GPX) activity. Data were compared among H. pylori(+) and H. pylori(-) patients. Results : The overall prevalence of H. pylori infection was 71% (59/83). There was a significant increase in the levels of MDA in H. pylori(+) patients (0.98 ± 0.28 μmol/l) when compared with H. pylori(-) patients (0.84 ± 0.33 μmol/l; P = 0.048). However, the levels of FRAP in the H. pylori-infected patients were significantly lower than in those without infection (941 ± 211.8 vs. 1060.3 ± 216.6 μmol/l, respectively; P = 0.028). There were no significant differences in SOD activity, GPX activity, age, sex, and body mass index (BMI) of H. pylori(+) vs. H. pylori(-) patients (P > 0.05). Conclusion: Increased levels of MDA in H. pylori(+) patients showed association between oxidative stress and H. pylori infection in EDR patients. Also, considerable changes of antioxidant concentrations indicate a compensatory mechanism to cope with the increased oxidant status in H. pylori(+) patients. It may be concluded that oxidative stress increases in the presence of H. pylori in ERD patients, and antioxidant defense mechanisms, try to minimize oxidative stress damage