Gastro-oesophageal reflux disease and Helicobacter pylori

The interaction between gastro-oesophageal reflux disease (GERD) and Helicobacter pylori (H. pylori) infection has been the subject of intense scrutiny in recent years. Although the evidence base is incomplete it is now sufficient to clarify a number of key questions. H. pylori is not a risk factor for reflux disease. Similarly, H. pylori infection, in most patients, is not 'protective' against the risk of developing reflux and oesophagitis. Furthermore, reflux and oesophagitis are not more likely to develop or to worsen after H. pylori eradication therapy and eradication does not make control of reflux symptoms with proton pump inhibitor (PPI) therapy more difficult. Long term PPI therapy in the presence of H. pylori infection does increase the rate at which gastric mucosal atrophy and intestinal metaplasia develop. Eradication therapy has been shown to reduce this risk. In the uninfected stomach, PPIs are associated with a low likelihood of these adverse histological changes. PPI therapy reduces the accuracy of diagnostic tests for H. pylori. The decision to test for and treat H. pylori infection in the context of reflux must be individualised based on patient factors including co-morbidity, age, gastric histology, family history and informed choice. Distinction must be made between treating symptoms and potentially reducing risks. A decision not to test for and treat H. pylori is now just as active a choice as is the decision to test and treat. Recent international consensus statements recommend eradication of H. pylori prior to long term PPI therapy in reflux disease, although there is not a universal agreement on this. Further research to clarify the risk and benefits of such an approach is required.