Prevalence of Helicobacter pylori infection in 160 patients with Barrett'soesophagus or Barrett's adenocarcinoma

Background: The role of Helicobacter pylori infection in the development of Barrett's oesophagus and its complications is uncertain. The aim of the pr esent study was to determine the importance of H. pylori infection in this disease by comparing the frequency of oesophageal and gastric H. pylori inf ection in a group of patients with Barrett's oesophagus or adenocarcinoma, with the frequency of infection in a control group without Barrett's diseas e. Methods: The study group included 160 patients (123 male, 37 female; mean a ge: 61.2 years) who were classified (according to the highest grade patholo gical lesion in the oesophagus) as having Barrett's intestinal metaplasia ( IM; 88 patients), Barrett's oesophagus with low-grade dysplasia (LGD; 28 pa tients), high-grade dysplasia (HGD; five patients), Barrett's indefinite fo r dysplasia (n = 4), and Barrett's adenocarcinoma (33 patients). A total of 91 of these patients had gastric antral specimens available For study. The control group consisted of 214 consecutive, prospectively enrolled symptom atic patients (122 male, 92 female, mean age: 57.2 years) who underwent upp er gastrointestinal endoscopy and in whom Barrett's oesophagus or Bal-rett' s adenocarcinoma was not found. A modified Warthin-Starry method was used t o detect H. pylori infection. Results: Oesophageal H. pylori infection was found in eight of 160 (5%,) pa tients with Barrett's oesophagus or Barrett's adenocarcinoma. Helicobacter pylori organisms in the oesophagus were found only on non-intestinalized ca rdiac or oxyntocardiac mucose. An patients with oesophageal H. pylori infec tion and an antral biopsy available for study had antral H. pylori infectio n. Gastric antral H. pylori infection was significantly less prevalent in p atients in the Barrett's study group (15/91, 16.5%) than in the non-Barrett 's control group (67/214, 31.3%; Fisher's exact test, P = 0.01). Patients f rom the control group with an endoscopic diagnosis of duodenal ulcer, gastr ic ulcer, gastritis, or duodenitis had a significantly higher prevalence of infection compared with the Barrett's group, but there was no difference i n the infection prevalence in patients in the Barrett's group and patients with reflux oesophagitis, hiatal hernia, no endoscopic abnormality, or any other diagnosis. Conclusions: Oesophageal H. pylori infection is uncommon in patients with B arrett's IM, dysplasia, or adenocarcinoma, and may he restricted to non-int estinalized columnar epithelium. Gastric H. pylori infection may have a pro tective effect for the development of Barrett's oesophagus.