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Review article: is Helicobacter pylori status relevant in the management of GORD?
S Vigneri1, R Termini, V Savarino
1Institute of Internal Medicine University of Palermo, Italy. vigneri@madeinsicily.com
Insights
Helicobacter pylori (H. pylori) infection
Area of Science:
- Gastroenterology
- Microbiology
- Oncology
Background:
- The relationship between Helicobacter pylori (H. pylori) infection and gastro-oesophageal reflux disease (GORD) is complex and not fully understood.
- H. pylori infection prevalence in GORD patients is often lower than in controls, suggesting a potential protective role.
- Acid-inhibiting therapies for GORD can alter H. pylori behavior and gastritis progression.
Purpose of the Study:
- To explore the intricate relationship between H. pylori infection and GORD.
- To investigate the impact of H. pylori eradication and acid suppressive therapies on GORD development and gastritis.
- To examine the association between H. pylori and Barrett's oesophagus.
Main Methods:
- Literature review and analysis of existing studies on H. pylori and GORD.
- Examination of epidemiological data on H. pylori prevalence in GORD and control groups.
- Discussion of proposed mechanisms for H. pylori's influence on GORD and gastritis progression.
Main Results:
- A negative correlation exists between H. pylori infection and GORD severity.
- H. pylori eradication may precede GORD development, but other factors are involved.
- Proton pump inhibitor (PPI) therapy can exacerbate corpus gastritis and alter H. pylori distribution, potentially influencing acid secretion and reflux.
- H. pylori prevalence in Barrett's oesophagus is similar to controls, and a causal link to adenocarcinoma is unlikely.
Conclusions:
- The interaction between H. pylori and GORD is multifactorial, with H. pylori potentially offering some protection against GORD.
- Long-term GORD treatment in H. pylori-infected individuals may accelerate atrophic gastritis and increase gastric cancer risk.
- H. pylori's impact on gastritis and acid secretion is influenced by acid output levels and therapeutic interventions like PPIs.
Abstract:
There is growing interest in the relationship between H. pylori infection and 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 correlation between H. pylori infection and the severity of GORD. There are many hypothetical mechanisms by which H. pylori infection may protect from the development of GORD. Conversely, there are many possible mechanisms by which H. pylori infection could theoretically foster the GORD. Patients after H. pylori eradication may develop GORD, and this seems to suggest a protective role of H. pylori infection, but other possible explanations include weight gain after H. pylori eradication, changes in dietary habits and smoking, and pre-existing GORD. H. pylori infected patients treated by various acid-inhibiting therapies such as proton pump inhibitors (PPIs), H2-receptors antagonists (H2-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 gastritis intestinal metaplasia and dysplasia, and increase the risk of developing gastric cancer. More recently it has been shown that H. pylori infection may interfere with the acid suppressive therapies used for treating GORD. In our opinion the progression of gastritis depends on the threshold of acid 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 improves in the antrum, but it deteriorates in the body. During proton pump inhibitor 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 secretion 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 not different from that exhibited by controls, roughly one-third of the subjects. Intestinal metaplasia of the gastric cardia seems to be equally frequent in patients with and without GORD. Finally, it appears unlikely that a causal relationship exists between H. pylori infection and Barrett's-associated adenocarcinoma.