Barrett Esophagus Is Associated with a Lower Prevalence of H. pylori Gastritis and a Higher Prevalence of Reactive Gastropathy

Abstract

Purpose: The incidence of adenocarcinoma of the gastroesophageal (GE) junction, believed to originate from Barrett esophagus (BE) in most cases, is increasing in parallel with the decreasing prevalence of H. pylori infection; eradication of H. pylori has been suspected of causing an increase in GE reflux diseases (GERD), the main cause of BE. This nation-wide study was designed to compare the status of the gastric mucosa in a group of patients with histologically confirmed BE with that of a group of patients with a normal esophageal mucosa. Methods: We analyzed electronic data from Caris Diagnostics, a specialized gastrointestinal pathology group receiving specimens from gastroenterologists operating in community-based endoscopy centers in 40 states. For each patient, the database includes demographic and clinical information, endoscopic findings, site of origin, and the histopathologic report for each biopsy. To identify the records for eligible gastric and esophageal specimens, we extracted data from all cases examined from 4/01/07 to 3/31/08. Extracted data were stored in a Microsoft Access database. Statistical calculations were performed using SigmaStat 3.5; chi-square test, Student's t-test and the Mann-Whitney Rank Sum Test for non-parametric data were used as appropriate. A P value < 0.05 was considered significant. Results: A total of 8,605 patients had biopsies from both the stomach and the lower third of the esophagus; from these, we extracted 874 patients with a diagnosis of BE (10.1%); 2,844 patients had a diagnosis of normal esophageal mucosa (NEM). Patients with any type of esophageal inflammation, ulcers, erosions, and focal intestinal metaplasia at the GE junction not specifically diagnosed as BE were excluded. Patients with BE were more likely to be men (51.6% vs. 40.7% for those with NEM, P < 0.001) and considerably older (median age = 63 years) than those with NEM (median age 52, P < 0.001). BE patients had a lower prevalence of H. pylori gastritis (5.8% vs. 9.2%, P= 0.002), but a higher prevalence of reactive gastropathy (30.2% vs. 26.4%, P= 0.031); their greater prevalence of gastric intestinal metaplasia (5.7% vs. 4.6%) did not attain statistical significance. The clinical indication for endoscopy was GERD-related in 48.4% of patients with a diagnosis of NSM, but only in 38.1% of those who had histologically confirmed BE (P < 0.001). Conclusion: This nation-wide study indicates that only a minimal proportion of patients with BE are concurrently infected with H. pylori. In contrast, approximately one third have reactive gastropathy; a portion of these may be related to alkaline pancreato-duodeno-biliary reflux, which might contribute to the pathogenesis of Barrett esophagus.