Review article: is Helicobacter pylori status relevant in the management of GORD?

There is growing interest in the relationship between H. pylori infection a nd gastro-oesophageal reflux disease (GORD). However, this relationship is complex, as yet not fully elucidated, and probably based on a multiplicity of factors. The prevalence of H. pylori infection in patients with GORD is similar, more often lower than in matched controls. There is a negative cor relation between H. pylori infection and the severity of GORD. There are ma ny hypothetical mechanisms by which H. pylori infection may protect from th e development of GORD. Conversely, there are many possible mechanisms by wh ich H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protec tive role of H. pylori infection, but other possible explanations include w eight gain after H. pylori eradication, changes in dietary habits and smoki ng, and pre-existing GORD. H. pylori infected patients treated by various acid-inhibiting therapies su ch as proton pump inhibitors (PPIs). H-2-receptors antagonists (H-2-RA) or vagotomy, have an increase of their corpus gastritis severity. both in the activity of inflammation and in the density of organisms. Long-term therapy of GORD in H. pylori infected may lead to rapid progression of atrophic ga stritis intestinal metaplasia and dysplasia, and increase the risk of devel oping gastric cancer. More recently it has been shown that H. pylori infect ion may interfere with the acid suppressive therapies used for treating GOR D. In our opinion the progression of gastritis depends on the threshold of aci d output at which H. pylori can 'flourish'. Recently interest is growing on gastric transitional zones and Helicobacter ecology. Any decrease of acid secretion changes the behaviour of H. pylori: the activity of gastritis imp roves in the antrum, but it deteriorates in the body. During proton pump in hibitor treatment, H. pylori redistribution occurs within the stomach, from an antral to a corpus or fundus prevalent pattern: corpus-fundus gastritis , exacerbated by PPI therapy, may result both in a diminished acid secretio n and gastro-oesophageal reflux. The interest in Barrett's oesophagus is growing due to the associated risk of adenocarcinoma. The literature seems to demonstrate that the prevalence of H. pylori infection of the stomach in Barrett's oesophagus patients is n ot different from that exhibited by controls, roughly one-third of the subj ects. Intestinal metaplasia of the gastric cardia seems to be equally frequ ent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's-associ ated adenocarcinoma.