Helicobacter pylori infection is associated with milder gastro‐oesophageal reflux disease

Abstract

Background: We have previously demonstrated a negative relationship between the prevalence of Helicobacter pylori and gastro‐oesophageal reflux disease (GERD). Aim: To study the effects of H. pylori infection on the severity of GERD. Methods: Ethnic Chinese patients with frequent heartburn and/or endoscopic oesophagitis were studied. Endoscopic examination was performed to assess the severity of oesophagitis (modified Savary–Miller grading) and the presence of hiatus hernia. Biopsies were taken for rapid urease testing and confirmation of Barrett’s oesophagus. Risk factors which may affect the severity of oesophagitis (age, sex, smoking, drinking, diabetes mellitus, hiatus hernia, H. pylori status and body mass index) were evaluated by a multiple regression model. The cagA status of H. pylori infected GERD and age‐and‐sex matched controls were determined by Western blot. Age‐and‐sex matched non‐reflux patients were recruited as controls for comparison. Results: Two hundred and twenty‐five patients with GERD were studied, of whom 77 (34%) were infected with H. pylori. Oesophagitis and Barrett’s oesophagus were found in 140 patients (62%) and six patients (3%), respectively. H. pylori infected patients had significantly less severe oesophagitis compared to the uninfected group (P=0.022). All patients with Barrett’s oesophagus were uninfected. Factors that predicted severe oesophagitis included age over 60 years (P < 0.001) and hiatus hernia (P < 0.001). H. pylori infection was the only factor that showed a negative correlation with severe oesophagitis (P=0.011). The prevalence of the cagA positive strain in endoscopy‐negative GERD, erosive oesophagitis and control subjects was 70, 76 and 78%, respectively (P=0.75). Conclusions: H. pylori infection is associated with milder GERD.

Effect of H. pylori infection on gastrin, ghrelin, motilin, and gastroesophageal reflux

“…In our study, we observed neither a change in the gastrin level nor in GERD occurrence between H. pylori-infected and non-infected state. In contrast to these hypotheses, we could not demonstrate any relationship between gastrin and GERD, which was comparable with a few studies in the literature (18)(19)(20)(21)(22)(23)(24). One of the reasons for this difference can be the predominant corpoantral infection in our patients.…”

Symptoms in patients on long‐term proton pump inhibitors: prevalence and predictors

“…32 However, our finding is consistent with a subsequent trial of H. pylori positive patients from this cohort, where eradication reduced overall dyspepsia scores (measured by the LDQ), but not reflux scores (measured by the CDRQ) and consequently, reflux was more likely to be the residual predominant symptom. 8 Helicobacter pylori negative patients may have worse oesophagitis than those who are H. pylori positive 33,34 and this may be especially important in relation to cagA status. 35 This study was unable to capture H. pylori strain as this is not a routinely available laboratory test.…”

Patterns of gastritis and the effect of eradicating Helicobacter pylori on gastro‐oesophageal reflux disease in Western patients with non‐ulcer dyspepsia

“…13 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. 2,14 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.…”