Background/aim: Helicobacter pylori infection is associated with the development of atrophic gastritis and increased gastric epithelial proliferation that is important in developing gastric carcinoma. Some countries with a high prevalence of H. pylori infection have high gastric cancer rates, whereas in others these rates are low. Several theories have been advanced to explain this phenomenon. One of these explanations is that the concurrent parasitic infection that is common in the African population might alter the immune response to H. pylori infection and reduce the incidence of atrophic gastritis. The aim of the present study was to assess whether concurrent Schistosoma mansoni infection with H. pylori has an effect on gastric mucosal injury in view of cell proliferation, apoptosis, pathological changes, nitric oxide (NO), oxyradicals and antioxidant capacity status.
Patients/methods: Between April 2001 and March 2002, 73 patients were subjected to upper gastrointestinal endoscopy for dyspepsia and liver cirrhosis in the National Liver Institute, Menoufiya University. Biopsies were obtained from any lesion as well as from apparently healthy mucosa. Specimens were preserved in RNA later solution, and then kept at -80 degrees C until utilized for estimation of DNA-flow cytometric assay, reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), NO and lipid peroxidation (LPO) product--malondialdehyde (MDA). Diagnosis of bilharziasis was done by stool analysis, or by sigmoidoscopy and rectal snip.
Results: Of the 73 patients, 48 were H. pylori-positive, 34 of them were positive and 14 were negative for S. mansoni. Of the 25 H. pylori-negative cases, 18 were positive and 7 were negative for S. mansoni. Concurrent infection with S. mansoni occurred in 34 patients and they had reduced DNA S-phase (7.57 +/- 4.99 vs. 14.5 +/- 3.11, P = 0.001), reduced proliferation activity (9.95 +/- 3.95 vs. 16.78, P < 0.004) and reduced apoptosis (21.83 +/- 11.64 vs. 26.0 +/- 8.31, P > 0.05) compared with H. pylori infected patients alone.
Conclusions: The results demonstrate that concurrent helminthes infection may modify the inflammatory response to gastric H. pylori infection manifested by the reduction of oxyradical-induced DNA-damage, apoptosis and cellular proliferation activity, and the increase in antioxidant production. Concurrent S. mansoni infection may have a protective effect against the possible progression of H. pylori-induced gastritis towards gastric carcinoma.