[Eradication of Helicobacter pylori. Is it necessary to eradicate Helicobacter pylori in gastric reflux?]

POTENTIAL PROTECTIVE EFFECT OF H. PYLORI: Epidemiological studies have not demonstrated an association between H. pylori infection and symptoms of gastroesophageal reflux, reflux esophagitis, or Barrett's esophagus with or without dysplasia or esophageal adenocarcinoma. On the contrary, an apparently favorable negative association has been identified suggested a potential protective effect of H. pylori. An inverse association is also observed between the severity of reflux complications and infection by strains of H. pylori expressing certain virulence markers (cogA) associated with the more severe gastric lesions. The prevalence of gastroesophageal reflux-related disease has increased steadily for more than fifty years while the incidence of H. pylori infection has decreased in developed countries. This observation might suggest that H. pylori infection plays a protective role. In addition, eradication of H. pylori could favor he development of gastroesophageal reflux or reflux esophagitis. The degree of risk is unknown. Pangastritis with significant lesions of the gastric body leading to a reversible decrease in the secretion of acid after H. pylori eradication might lower the risk of gastroesophageal reflux.

The relations between H. pylori and gastroesophageal reflux are complex. Reflux associated with duodenal ulcer appears to be improved by eradication of H. pylori suggesting that infection might promote the development of reflux. The causal mechanism would be increased acid secretion induced by antral gastritis predominantly resulting from the H. pylori infection. Further work is needed to determine the exact role of gastritis and perturbed acid secretion.

Data on the role of H. pylori in transient relaxation of the lower esophageal sphincter, implicated in the pathogenesis of gastroesophageal reflux, are lacking. Antisecretion treatments reduce the quantity of gastric acid favoring H. pylori colonization of the fundic mucosa and possibly aggravating fundic gastritis. The risk of progression from H. pylori gastritis to atrophy or intestinal metaplasia of the fundus under prolonged proton pump inhibitor treatment remains to be determined. Eradication of H. pylori reduces the efficacy of antisecretory drugs according to poorly understood mechanisms. The potential effect of gastroesophageal reflux on the transmission of H. pylori infection remains to be established.

Much remains to be learned concerning the beneficial or deleterious effects of eradication of H. pylori on the course of gastroesophageal reflux. In clinical practice, eradication of H. pylori is not useful for patients with gastroesophageal reflux.