Available evidence would suggest that Helicobacter pylori infection does not contribute to the pathogenesis of gastro-oesophageal reflux disease. The prevalence of H pylori infection in patients with reflux disease is no greater than that in control populations. There are some data suggesting that the organism has a protective role: patients with duodenal ulcers develop reflux disease after H pylori eradication, whereas in patients with oesophageal reflux those with H pylori infection have less severe reflux changes. There is also evidence indicating that the presence of H pylori augments the anti-secretory properties of both the H2 receptor antagonists and proton pump inhibitors (PPIs), suggesting that eradication therapy may not be beneficial. However, the considerable recent interest in the association between H pylori and reflux disease has largely been generated by studies outlining the interactions between H pylori infection and acid suppression in the long term. In H pylori positive patients, therapy with PPIs is associated with a proximal extension of the infection and its associated gastritis. In addition long term PPI therapy is reported to be associated with an accelerated development of atrophic gastritis, suggesting that H pylori should be diagnosed and treated. Although these latter findings in particular need confirmation, H pylori eradication therapy should be considered in this patient group, at least until there is evidence to the contrary.
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Lee et al. (1998) studied this question.
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