BACKGROUND: The role of Helicobacter pylori in the pathogenesis and evolution of gastro-oesophageal reflux disease is still debated. AIM: To investigate the impact of Helicobacter pylori infection on the oesophageal function and on intra-gastric and intra-oesophageal pH in patients with gastro-oesophageal reflux. METHODS: Fifty patients with non-complicated-gastro-oesophageal reflux disease classified according to Savary-Miller in: grade O, n=24; grade 1, n=19; grade 2, n=6; grade 3, n=1. Of these patients, 24 were Helicobacter pylori positive and 26 negative. Patients underwent, on two different days, stationary oesophageal manometry and 24-hour gastro-oesophageal pH-metry. RESULTS: No difference was observed between Helicobacter pylori infected and non-infected individuals with regard to lower oesophageal sphincter function, oesophageal peristalsis and gastrooesophageal reflux. These parameters were more impaired in individuals with erosive gastro-oesophageal reflux disease but this result was not dependent on the Helicobacter pylori status. Helicobacter pylori did not influence the pattern of gastric pH; however, considering only individuals with non-erosive gastro-oesophageal reflux disease, gastric pH was significantly higher in infected individuals, who, histologically, also showed a corpus predominant gastritis. CONCLUSIONS: In patients with gastro-oesophageal reflux disease, Helicobacter pylori does not affect the oesophageal motility or the gastro-oesophageal reflux. These parameters are strictly related to the severity of gastro-oesophageal reflux disease as assessed at endoscopy. In patients with non-erosive gastro-oesophageal reflux disease, a corpus predominant Helicobacter pylori gastritis could be responsible for the less severe gastro-oesophageal reflux.
BACKGROUND: The role of Helicobacter pylori in the pathogenesis and evolution of gastro-oesophageal reflux disease is still debated. AIM: To investigate the impact of Helicobacter pylori infection on the oesophageal function and on intra-gastric and intra-oesophageal pH in patients with gastro-oesophageal reflux. METHODS: Fifty patients with non-complicated-gastro-oesophageal reflux disease classified according to Savary-Miller in: grade O, n=24; grade 1, n=19; grade 2, n=6; grade 3, n=1. Of these patients, 24 were Helicobacter pylori positive and 26 negative. Patients underwent, on two different days, stationary oesophageal manometry and 24-hour gastro-oesophageal pH-metry. RESULTS: No difference was observed between Helicobacter pylori infected and non-infected individuals with regard to lower oesophageal sphincter function, oesophageal peristalsis and gastrooesophageal reflux. These parameters were more impaired in individuals with erosive gastro-oesophageal reflux disease but this result was not dependent on the Helicobacter pylori status. Helicobacter pylori did not influence the pattern of gastric pH; however, considering only individuals with non-erosive gastro-oesophageal reflux disease, gastric pH was significantly higher in infected individuals, who, histologically, also showed a corpus predominant gastritis. CONCLUSIONS: In patients with gastro-oesophageal reflux disease, Helicobacter pylori does not affect the oesophageal motility or the gastro-oesophageal reflux. These parameters are strictly related to the severity of gastro-oesophageal reflux disease as assessed at endoscopy. In patients with non-erosive gastro-oesophageal reflux disease, a corpus predominant Helicobacter pylorigastritis could be responsible for the less severe gastro-oesophageal reflux.