Gastritis and the Effect of Eradicating H pylori on GERD
Gastritis and the Effect of Eradicating H pylori on GERD
Background: The effect of Helicobacter pylori eradication on the development of gastro-oesophageal reflux disease is controversial.
Aim: To determine the incidence of symptoms of reflux disease and of erosive oesophagitis, and the relationship to changes in histological gastritis, in patients with non-ulcer dyspepsia over 12 months.
Methods: Six hundred and ninety-three patients in two similar randomized placebo controlled trials of H. pylori eradication in non-ulcer dyspepsia were studied. Symptoms were assessed using the validated Gastrointestinal Symptom Rating Scale during a 1-week run-in period, at 6 months and 12 months. Endoscopy was performed at baseline to exclude patients with pathology and at 3 months and 12 months to determine if oesophagitis was present. Gastric biopsies were scored using the modified Sydney Classification.
Results: Patients without predominant heartburn, oesophagitis or ulcers at endoscopy were randomized to active (n = 297, omeprazole, amoxicillin and clarithromycin) treatment or to placebo/omeprazole (n = 306) for 1 week. The eradication rate was 82% in the active treatment group. Antrum-predominant gastritis (55%) was more frequently found than corpus-predominant gastritis (6%). In patients with antrum-predominant gastritis, heartburn and regurgitation scores improved significantly 12 months after eradication. Erosive oesophagitis developed in 15/232 patients in the eradication group (7%) compared with 2/227 (2%) in the control group, but there was no significant difference when adjusted for oesophagitis present at baseline.
Conclusions: Antrum-predominant gastritis is the most common pattern of gastritis seen in non-ulcer dyspepsia in Western populations. Heartburn and regurgitation improve after eradication therapy or placebo in patients with non-ulcer dyspepsia; the development of oesophagitis is uncommon.
The relationship between eradication of Helicobacter pylori infection and the development of gastro-oesophageal reflux disease (GERD) is highly controversial. In a 3-year follow-up study of 450 patients with duodenal ulcer, Labenz et al. reported that oesophagitis developed in 26% of patients cured of H. pylori infection compared with 13% of those who had persistent infection. The incidence of symptomatic or endoscopic GERD developing in ulcer patients cured of the infection, however, has ranged widely in other reports.
The results of H. pylori eradication in non-ulcer dyspepsia have been mixed, with some studies showing no benefit and others demonstrating improvement in symptoms and prevention of future ulcer disease. A recent meta-analysis demonstrated modest efficacy for H. pylori eradication in alleviating dyspeptic symptoms with a number needed to treat of 19. A subsequent meta-analysis using individual patient data suggested that the benefit of eradication was similar whether patients with predominant epigastric pain or predominant heartburn were studied.
With the declining rates of peptic ulcer disease in most Western countries, H. pylori treatment is being frequently administered in non-ulcer dyspepsia. A reasonable consideration in these patients is whether eradication therapy increases the risk for developing GERD. A recent study has suggested that dyspeptic patients in Western countries are more likely to have oesophagitis than their counterparts in Asia and that the absence of H. pylori is an independent predictor of the presence of oesophagitis. The presence of chronic active H. pylori gastritis has been shown to be associated with milder forms of reflux disease and eradication therapy in patients with corpus-predominant gastritis increases the risk of developing GERD in patients with ulcer disease. There is little information on the pattern of gastritis in Caucasian subjects with dyspepsia and on the development of GERD after H. pylori eradication in non-ulcer dyspepsia. The aim of our study was to determine the incidence of GERD in patients with documented non-ulcer dyspepsia who received eradication therapy and were followed-up for 1 year. We hypothesized that the incidence of GERD at 12 months would be increased in patients with corpus-predominant H. pylori gastritis who had successful eradication compared with the control group without successful eradication.
Summary and Introduction
Summary
Background: The effect of Helicobacter pylori eradication on the development of gastro-oesophageal reflux disease is controversial.
Aim: To determine the incidence of symptoms of reflux disease and of erosive oesophagitis, and the relationship to changes in histological gastritis, in patients with non-ulcer dyspepsia over 12 months.
Methods: Six hundred and ninety-three patients in two similar randomized placebo controlled trials of H. pylori eradication in non-ulcer dyspepsia were studied. Symptoms were assessed using the validated Gastrointestinal Symptom Rating Scale during a 1-week run-in period, at 6 months and 12 months. Endoscopy was performed at baseline to exclude patients with pathology and at 3 months and 12 months to determine if oesophagitis was present. Gastric biopsies were scored using the modified Sydney Classification.
Results: Patients without predominant heartburn, oesophagitis or ulcers at endoscopy were randomized to active (n = 297, omeprazole, amoxicillin and clarithromycin) treatment or to placebo/omeprazole (n = 306) for 1 week. The eradication rate was 82% in the active treatment group. Antrum-predominant gastritis (55%) was more frequently found than corpus-predominant gastritis (6%). In patients with antrum-predominant gastritis, heartburn and regurgitation scores improved significantly 12 months after eradication. Erosive oesophagitis developed in 15/232 patients in the eradication group (7%) compared with 2/227 (2%) in the control group, but there was no significant difference when adjusted for oesophagitis present at baseline.
Conclusions: Antrum-predominant gastritis is the most common pattern of gastritis seen in non-ulcer dyspepsia in Western populations. Heartburn and regurgitation improve after eradication therapy or placebo in patients with non-ulcer dyspepsia; the development of oesophagitis is uncommon.
Introduction
The relationship between eradication of Helicobacter pylori infection and the development of gastro-oesophageal reflux disease (GERD) is highly controversial. In a 3-year follow-up study of 450 patients with duodenal ulcer, Labenz et al. reported that oesophagitis developed in 26% of patients cured of H. pylori infection compared with 13% of those who had persistent infection. The incidence of symptomatic or endoscopic GERD developing in ulcer patients cured of the infection, however, has ranged widely in other reports.
The results of H. pylori eradication in non-ulcer dyspepsia have been mixed, with some studies showing no benefit and others demonstrating improvement in symptoms and prevention of future ulcer disease. A recent meta-analysis demonstrated modest efficacy for H. pylori eradication in alleviating dyspeptic symptoms with a number needed to treat of 19. A subsequent meta-analysis using individual patient data suggested that the benefit of eradication was similar whether patients with predominant epigastric pain or predominant heartburn were studied.
With the declining rates of peptic ulcer disease in most Western countries, H. pylori treatment is being frequently administered in non-ulcer dyspepsia. A reasonable consideration in these patients is whether eradication therapy increases the risk for developing GERD. A recent study has suggested that dyspeptic patients in Western countries are more likely to have oesophagitis than their counterparts in Asia and that the absence of H. pylori is an independent predictor of the presence of oesophagitis. The presence of chronic active H. pylori gastritis has been shown to be associated with milder forms of reflux disease and eradication therapy in patients with corpus-predominant gastritis increases the risk of developing GERD in patients with ulcer disease. There is little information on the pattern of gastritis in Caucasian subjects with dyspepsia and on the development of GERD after H. pylori eradication in non-ulcer dyspepsia. The aim of our study was to determine the incidence of GERD in patients with documented non-ulcer dyspepsia who received eradication therapy and were followed-up for 1 year. We hypothesized that the incidence of GERD at 12 months would be increased in patients with corpus-predominant H. pylori gastritis who had successful eradication compared with the control group without successful eradication.
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