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LEADING ARTICLE
Helicobacter pylori in gastro-oesophageal reflux disease: causal agent, independent or protective factor?
  1. JOACHIM LABENZ,
  2. PETER MALFERTHEINER
  1. Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Magdeburg, Germany
  1. Professor P Malfertheiner, Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University, Leipziger Strasse 44, 39120 Magdeburg, Germany.

https://doi.org/10.1136/gut.41.3.277

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    Helicobacter pylori causes chronic gastritis with variable activity and topographic distribution. Patient age at acquisition, expression of gastritis, strain virulence, host factors, and environmental factors determine the outcome of the infection. Well established consequences are peptic ulcer disease (PUD) and gastric neoplasia.1-4

    As duodenal ulcer is often associated with gastro-oesophageal reflux disease (GORD),5 and antral gastritis is a frequent finding in patients with reflux disease,6 H pyloriinfection may be a common cause of both conditions. Our aim was to explore the strength of the postulate that H pyloriis a causal factor in GORD by reviewing publications on epidemiological studies, clinical observations or treatment trials, and identifying possible pathogenic mechanisms.

    Association of H pylori and GORD

    Currently, we have no clear data to show that patients with GORD are more frequently infected by H pylori than controls, neither in adults nor in children.7 Indeed, a recent well designed case control study from Japan showed a significantly lower incidence of H pylori infection in patients with reflux oesophagitis than in age and sex matched controls.8 This finding is supported by one of our own studies.9 The prevalence of both H pylori infection and GORD increases with age.10 ,11 Male sex is a risk factor for GORD,12 but the prevalence of H pylori is equally distributed between men and women.10 ,12

    H pylori is able to colonise Barrett’s epithelium. Many uncontrolled studies showed H pylori prevalence rates similar to those in the background population.7 Also, in a controlled study the prevalence of H pylori infection was similar in patients with Barrett’s oesophagus and controls.13 However, patients with Barrett’s oesophagus and an ulcer within the columnar metaplasia were more frequently infected by H pylori than those without ulcers.14

    The prevalence of H pylori infection …

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