• Helicobacter pylori
• eradication
• gastro-oesophageal reflux disease
• reflux oesophagitis

• GORD, gastro-oesophageal reflux disease
• PPI, proton pump inhibitors

Although the prevalence of Helicobacter pylori is steadily decreasing in industrialised nations, over the same time gastro-oesophageal reflux disease (GORD) and its complications have increased in Western countries.¹ GORD affects 25–40% of the population² and Barrett’s oesophagus and oesophageal adenocarcinoma are being recognised at an increasingly alarming rate.¹ This has led to the suggestion that H pylori is the possible aetiological factor for this changing epidemiology.

Most studies find no evidence that H pylori infection causes GORD.³ Rather, some but not all studies have found a lower prevalence of H pylori infection in patients with reflux symptoms or oesophagitis, suggesting a possible protective effect of this bacteria.^4–7 A recent systematic review of the literature suggests that geography is an important factor complicating this relationship. Raghunath and colleagues⁸ evaluated 20 studies and found that the pooled estimate of the odds ratio for the prevalence of H pylori in patients with GORD was 0.60 (95% confidence intervals (CI) 0.47–0.78). The evidence for this protective relationship in Europe was equivocal, but consistent evidence was found for a lower prevalence of H pylori among both North American (odds ratio 0.70 (95% CI 0.55–0.90)) and Far Eastern (odds ratio 0.24 (95% CI 0.19–0.32)) patients with GORD.

H pylori infection can have a variable effect on acid secretion, depending on the type and distribution of gastritis.⁹ Non-atrophic predominantly antral inflammation results in hypergastrinaemia and acid hypersecretion; this pattern is prevalent in patients with duodenal ulcer disease. In contrast, patients with corpus predominant gastritis have decreased acid secretion, which is the predominant pattern in patients with gastric ulcers or gastric cancer. Eradication of the organism is associated with correction of these abnormalities in both types of gastritis. However, the majority of H pylori infected patients without disease have a mixed pattern of gastritis, whereby the elevated gastrin resulting from antral inflammation fails to cause gastric acid secretion because of corpus inflammation.

The effect of H pylori eradication on 24 hour oesophageal acid exposure is variable. Two studies¹⁰¹¹ in patients with H pylori gastritis found no changes in 24 hour oesophageal acid exposure before and 12 weeks after eradication therapy. On the other hand, Feldman and colleagues¹² found that three of nine asymptomatic gastritis patients developed pathological acid reflux after H pylori eradication. In another study, Wu and colleagues¹³ investigated oesophageal acid exposure in 14 patients with GORD and H pylori infection, who were randomised to receive eradication therapy, and 11 patients randomised to omeprazole alone. There was no difference in per cent time to oesophageal pH <4 before and 26 weeks after treatment between the groups. However, the per cent time pH <2 (p = 0.01) and pH <3 (p = 0.02) was significantly increased in patients receiving H pylori eradication treatment. A small number of patients developed worsening oesophagitis (n = 3). Conclusions from these studies are difficult because sample sizes were small, the type and extent of gastritis was not assessed, and the prevalence and severity of GORD were rarely defined.

H pylori infection may affect the action of proton pump inhibitors (PPI). Intragastric pH is consistently higher during PPI treatment in H pylori infected patients than in either uninfected or eradicated patients.¹⁴ Is this clinically important as we treat our GORD patients with or without H pylori infection? Holtzmann and colleagues¹⁵ showed that patients with H pylori infection treated with pantoprazole had better symptom relief and healing of oesophagitis at four and eight weeks than non-infected reflux patients. The effects were much less pronounced at eight weeks than at four weeks. However, four other studies found that H pylori status did not adversely effect treatment results with PPI. Carlsson and colleagues¹⁶ studied 1350 patients with GORD treated with omeprazole and found that symptom relief and healing rates were similar in patients with H pylori infection and those who were not infected. Vakil and colleagues¹⁷ likewise showed that H pylori infection did not affect healing rates in erosive oesophagitis treated with esomeprazole. Peters and colleagues¹⁸ treated 26 patients with Barrett’s oesophagus (14 H pylori negative, 12 H pylori positive) with omeprazole 40 mg twice daily. Omeprazole resulted in a decrease in 24 acid reflux values from 23.4% (7.9–39.3) to 0% (0.0–2.9) in H pylori negative and from 17.3% (8.9–38.8) to 0.1% (0.0–1.7) in H pylori positive patients. Symptoms were also equally controlled in each group. Finally, Schenk and colleagues¹⁹ showed that the dose of omeprazole required for maintenance after healing of erosive oesophagitis was similar in patients with and without H pylori infection.

In summary, most treatment trials with PPI do not find that H pylori status adversely affects symptom relief, healing of acute oesophagitis, or maintenance treatment of erosive oesophagitis. Therefore, clinicians should continue to eradicate H pylori infection when found and not be concerned about aggravating possible coexisting reflux disease which should easily respond to PPI therapy.