Helicobacter pylori infection is now widely accepted to be an important risk factor for a number of gastric and duodenal disorders. It is the major aetiological factor for gastric and duodenal ulcers unrelated to NSAID or aspirin-usage. In addition, it plays an essential role in the aetiology of most cases of non-cardia gastric cancer as well as low-grade gastric MALTomas. Such is the importance of H pylori infection in disorders of the stomach and duodenum that pathology distal to the gastro-oesophageal junction is rarely encountered when endoscoping H pylori naive subjects.

Over the past few years, interest in H pylori has extended from its role in the aetiology of diseases of the stomach and duodenum to its possible role in the aetiology of diseases of the oesophagus. This has focused largely on the possibility that H pylori infection may protect against the development of gastro-oesophageal reflux disease and its complications of Barrett’s oesophagus and oesophageal adenocarcinoma.

Most epidemiological studies have demonstrated a negative association between H pylori infection and gastro-oesophageal reflux disease or its complications. The prevalence of H pylori infection is lower in reflux patients than in controls.^1–,³ There is also some evidence that reflux disease in H. pylori-negative patients tends to be more severe than in H. pylori-positive patients.⁴ In addition, more virulent, cytotoxin-associated gene A (cag A)-positive strains of H pylori are associated with less severe reflux disease.^5,6 Numerous studies have now reported a strong negative association between H pylori infection and risk of adenocarcinoma of the oesophagus or gastro-oesophageal junction.^{7,8,9,10,11 …}