Effect of Helicobacter pylori infection in Barrett's esophagus and the genesis of esophageal adenocarcinoma

The relation between Helicobacter pylori and gastroesophageal reflux disease is unclear. Recent reports have suggested a possible protective role for H. pylori, particularly in preventing the complications of gastroesophageal reflux disease (GERD). The purpose of this article is to present a brief overview of the recent literature regarding the role of H. pylori in the genesis of the complications of GERD, focusing on Barrett's esophagus and esophageal adenocarcinoma. The prevalence of H. pylori infection in the population of the West is around 40% and is not different in cohorts of patients with GERD. When the infection induces pangastritis or corpus-predominant gastritis, there may be concomitant reduced gastric acid secretion. Eradication of the bacteria in this subgroup of patients may enhance gastric acid secretion and provoke reflux symptoms. H. pylori organisms do not colonize the specialized intestinal metaplasia characteristic of Barrett's esophagus. H. pylori infection rates in gastric mucosa of patients with Barrett's esophagus occur at a similar or slightly lower frequency than is found in controls. Gastric infection with cagA-positive strains of H. pylori appears to be uncommon in patients with Barrett's esophagus. Furthermore, epidemiologic studies indicate that cagA-positive strains are protective against esophageal adenocarcinoma. Several investigators have proposed that the decreasing prevalence of H. pylori infection might be an important factor in the rising incidence of this tumor.