The role of Helicobacter pylori in esophageal disease has not been clearly defined. To clarify this issue, we analyzed 120 patients with histologically confirmed esophageal disease. Helicobacter pylori (H. pylori)
causes a long-term infection of the human gastric and duodenal mucosa (1). Mucosal colonisation predisposes for peptic ulcer disease, atrophic gastritis and distal (antral) stomach cancer (2), with various effects on gastric acid secretion. Genetic variability of H. pylori
is high (3). Several genes have been identified that may play a role in the pathogenicity (4, 5). Most important is the cytotoxin- associated gene A (CagA),
which is associated with peptic ulcer disease (6), and intestinal type adenocarcinoma of the stomach (7). Patients with duodenal ulcer often have high basal gastrin levels, high peak acid output and high 24-hour intragastric acidity (8-10).
Materials and methods: This investigation was performed at the RL Jalappa Hospital, Tamaka, Kolar in patients who underwent Upper GI Endoscopy. The time of investigation was from January 2016-December 2018.
Results: This study included 30 patients with BE out of 120 patients with GERD. The average age of patients in BE group was 52.4 years. (SD } 10.8 yr.) In the GERD group average age was 40.8 years. In all groups included in this study, men were more represented than women. In BE group, H. pylori infection was present in 16.0% of patients. In GERD group, H. pylori infection was present in 42.9%.
Conclusion: The prevalence of H. pylori infection in patients with BE was lower in comparison with patients with GERD (p<0.01). The prevalence of H. pylori infection in patients with BE, especially those with Lower Segment BE was very low, which indicates the possible protective role of this microorganism.