Abstract
There are several reasons for eradicating Helicobacter pylori in patients with chronic gastroesophageal reflux disease (GERD). Perhaps the most compelling is the evidence that chronic acid suppression therapy can lead to the development of atrophic gastritis, a premalignant condition, in patients with H pylori infection. Epidemiological data that suggest that H pylori is less prevalent in GERD patients than in control subjects may be susceptible to publication bias, and confounding social and environmental factors may also be involved. Although it has been thought that eradication of the organism might lead to increased esophageal acid exposure, this has not been demonstrated in practice. Studies that appeared to show that GERD could be provoked by antimicrobial therapy of duodenal ulcers also have methodological weaknesses. Underlying GERD symptoms might be unmasked after withdrawal of acid-suppression therapy, for reasons that are unrelated to H pylori. In fact, eradication of the organism has been shown to decrease heartburn in patients with peptic ulcer disease. When H pylori is successfully eradicated in patients with GERD, relapse rates are not increased, and the disease-free interval seems to be prolonged. Eradication of the organism is a wise policy in patients who face long term acid-suppression therapy for GERD.
Highlights
RÉSUMÉ : Il y a bien des raisons d’éradiquer Helicobacter pylori chez les patients souffrant de reflux gastro-œsophagien (RGO) chronique
In support of the idea that H pylori infection protects against the development of Gastroesophageal reflux disease (GERD) is that the organism is found less frequently in patients with GERD than in control subjects
AND H PYLORI The strongest argument in favour of eradicating H pylori in patients with GERD is the finding that proton pump inhibitor (PPI) therapy promotes the development of atrophic gastritis, a potentially precancerous lesion, in the body of the stomach, in some H pylori-infected patients
Summary
The H pylori-positive patients, when treated with long term acid inhibition, exhibited non-H pylori bacterial proliferation, increased cytokine levels and a higher risk of atrophic gastritis. GERD AS A CONSEQUENCE OF H PYLORI ERADICATION Labenz et al [14] found that 26% of duodenal ulcer patients developed reflux esophagitis within three years of cure of H pylori infection, compared with 13% of patients with persisting infection, but this study could be criticized on the grounds that the two groups were not comparable. Withdrawal of acid suppression following H pylori eradication could unmask GERD symptoms by a mechanism that is not directly related to the organism The contribution of this potentially important confounder, which would cause a bias toward the appearance of reflux disease, is very difficult to evaluate. There has been a tendency to combine patient groups and discuss the issue in general terms [16]
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