Helicobacter pylori (H. pylori) is an important risk factor for the development of peptic ulcer disease, gastric adenocarcinoma, and primary B cell lymphoma of the stomach. A possible role for H. pylori in the pathogenesis of gastroesophageal reflux disease (GERD) has also been suggested in a growing number of studies. However, the link between GERD and H. pylori is complex.
This topic review will summarize the available evidence suggesting a role for H. pylori in GERD. The pathophysiology of GERD and the treatment of H. pylori are discussed separately. (See "Pathophysiology of reflux esophagitis" and "Treatment regimens for Helicobacter pylori".)
Suspicion of an interaction between H. pylori and gastrointestinal reflux disease (GERD) stems from epidemiologic data showing that as the prevalence of H. pylori decreased in Western societies, the prevalence of GERD and adenocarcinoma of the esophagus increased . This trend led several investigators to examine the prevalence of H. pylori in patients with GERD.
Several reports have suggested that H. pylori positive patients were less likely to have GERD, and, when present, the severity of esophagitis was decreased compared to those who were H. pylori negative [2-4]. A lower prevalence of Barrett's metaplasia and esophageal adenocarcinoma has also been described in individuals who were H. pylori positive [5,6].
Some studies suggested that H. pylori strains positive for Cag A (strains strongly associated with the development of corpus gastritis) may be particularly protective against the development of esophageal adenocarcinoma [7-9]. Thus, the available data suggest that colonization with H. pylori, particularly Cag A strains, may be protective against the more severe forms of GERD. Unfortunately, Cag A positive strains have also been associated with gastric adenocarcinoma. (See "Association between Helicobacter pylori infection and gastrointestinal malignancy".)