The impact of Helicobacter pylori on the presence of Barrett's esophagus in Azerbaijan, a high-prevalence area of infection

There is a strong evidence that Helicobacter pylori infection is inversely associated with Barrett's esophagus. In a high-prevalence region of H. pylori, low rates of esophageal cancer and its precursor BE may indicate its preventive effect. The aim of this study is to determine the impact of H. pylori on characteristics of Barrett's esophagus. A total of 3317 outpatient upper endoscopy reports from 2013 to 2015 from an urban center in Azerbaijan from all patients with dyspepsia were retrospectively analyzed for patients with Barrett's esophagus. This was matched in a 1:2 ratio to age and gender matched control patients without Barrett's esophagus. The prevalence of H. pylori on Barrett's esophagus and the randomly selected control group were compared. There were 83 patients with BE and 167 control group cases. Biopsy-proven BE was diagnosed in 83 patients: 39 (47%) females, with mean age 43.1 ± 13.3 years. Of these, 13 (15.7%) had long segment and 70 (84.3%) had short segment Barrett's esophagus. A control group included 167 patients: 78 (46.7%) females, with mean age (45.8 ± 13.9). All patients were Caucasians. The rates of gastric inflammation, the presence of atrophy, and intestinal metaplasia in gastric specimens did not differ in patients versus controls. The prevalence of H. pylori was determined as 63.2% in male and 61.5 in female groups (odd ratio (OR) = 0.99 95%CI 0.97, 1.01; P = 0.22). Inflammation of gastric mucosa was strongly associated with the infection (67% vs. 33%; OR = 4.46 95% CI: 2.01, 9.92, P < 0.001). Atrophy was noted in majority of H. pylori-positive cases (OR = 1.43, 95% CI: 0.36, 5.65; P = 0.61). Gastric intestinal metaplasia was observed in 55.6% of H. pylori-positive patients and in 44.4% of negative individuals (OR = 0.74, 95% CI: 0.28, 1.94; P = 0.54). There was not a significant difference in the prevalence of HP in BE and control groups; 63.9% were positive for infection in BE cases and 61.7% of controls (OR = 1.10, 95% CI: 0.64, 1.90; P = 0.74). We found that neither presence of erosive esophagitis, length of BE nor dysplasia (45.5% of H. pylori-positive group, whereas 54.5%) was associated with the presence of the H. pylori infection (Table 1). In a predominantly Caucasian nation with a high prevalence of H. pylori gastritis, the presence of H. pylori was not inversely associated with the presence of Barrett's esophagus. These data challenge the mechanistic implications of this association.