ALIMENTARY TRACT WEST LlUER Ills 2002;34:542-6 Helicobacter py/o+induced duodenal ulcer frequently coincides with gastro-oesophageal reflux disease D. MC Namara M. Buckley C. O’Morain Background. The relationship between Helicobacter pylori infection and gastro-oesophageal reflux disease is complicated. Evidence does not support a causal link. There have been reports, which have impli- cated successful eradication of Helicobacter pylori, in patients with a duodenal ulcer, with the subsequent development of gastro-oe- sophageal reflux disease. Howevec eradication of Halicobacter pylori in these patients with improvement in their condition and a return to not= ma/ lifestyle, weight gain and discontinuation of antacids may unmask pre-existing gastro-oesophageal reflux disease. Aims. To determine the true prevalence of gastro-oesophageal reflux disease in patients with Helicobacter pylori-related duodenal ulceration. Method. Dyspeptic patients undergoing endoscopy were prospectively screened for the presence of a duodenal ulcer Concomitant oe- sophagitis, when present, was recorded. All subjects with a Heli- cobacter pylori-related duodenal ulcer without endoscopic evidence of gas&o-oesophageal reflux disease were invited to undergo a 24-hr ambulatory oesophageal pH assessment prior to receiving treatment. Results. A total of 97 patients with a duodenal ulcer were identified and 83.5% were Helicobacter pylori positive. Overall, 27.8% had as- sociated endoscopic evidence of oesophagitis, 70% grade I-II and 30% grade ill-l\/1 Of those without evidence of oesophagitis at endoscopy, 68% underwent a 24-hr pH assessment. An additional 7 7% were identified by this means as having gastro-oesophageal reflux disease. Overall, 44% of symptomatic subjects with Helicobacter pylori and a duodenal ulcer were found to have coexistent gas&o-oesophageal re- flux disease. Conclusion. Gastro-oesophageal reflux disease is frequently found to coexist with Helicobacter pylori-related duodenal ulcer. In addition, al- most 20% of symptomatic patients without endoscopic evidence of oe- sophagitis will have an abnormal oesophageal pH exposure. It is plau- sible that the development of gastro-oesophageal reflux disease fol- /owing successful eradication of Helicobacter pylori represents un- masking of existing disease rather than de novo development. Digest Liver Dis 2002;34:542-6 Key words: duodenal ulcer; gastro-oesophageal reflux; Helicobacterpylori Introduction The aetiology of gastro-oesophageal reflux disease (GERD) is multi-facto- rial and the relationship between GERD and Hdicobacterpylori (H. pylori) infection is complicated. Epidemiological studies do not support a causal link lW4. There is evidence to show that there is a lower prevalence of H. py- Zori infection in subjects with GERD and also that the severity of oe- sophagitis is inversely related to H. pylori infection. These reports have led to the suggestion that H. pylori infection may protect against the develop- 542