Abstract

Helicobacter pylori infection, a common infection in many countries, is related to the clinical course of upper gastrointestinal diseases. Gastroesophageal reflux disease (GERD) is a common esophageal disease in Western countries and its prevalence is increasing in Asian countries. The pathophysiology of GERD is multifactorial. Although no single factor has been isolated as the cause of GERD, a negative association between the prevalence of H. pylori and the severity of GERD, including Barrett's esophagus, has been demonstrated in epidemiological studies. The high prevalence of H. pylori infection affects the incidence of GERD in Asian countries. In the subjects with East Asian CagA-positive strains, acid injury may be minimized by hypochlorhydria from pangastritis and gastric atrophy. Additionally, host genetic factors may affect the development of GERD. The interactions between genetic factors and the virulence of H. pylori infection may be the reason for the low prevalence of GERD in Asian countries. H. pylori eradication is not considered pivotal in GERD exacerbation based on evidence from Western studies. A recent meta-analysis demonstrated that eradication therapy of H. pylori was related to a higher risk of developing de novo GERD in Asian studies. H. pylori infection remains an inconclusive and important issue in GERD in Asian countries.

Highlights

  • The prevalence of gastroesophageal reflux disease (GERD) in the general population has been estimated to be 10– 20% [1,2,3,4]

  • An increasing prevalence of GERD and decreasing prevalence of H. pylori have been reported in Asian countries [8], which is in agreement with a previous report of no increase in the prevalence of GERD symptoms with age [4]

  • In Asian populations with East Asian cytotoxin-associated gene product- (CagA-)positive strains, acid injury may be minimized by hypochlorhydria from pangastritis and gastric atrophy

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Summary

Introduction

The prevalence of gastroesophageal reflux disease (GERD) in the general population has been estimated to be 10– 20% [1,2,3,4]. This negative association was evident in patients with severe GERD and H. pylori infection with virulent CagA-positive strains in Western countries [36, 37]. Long-term maintenance therapy of proton pump inhibitors (PPIs) for GERD induces gastritis and progression of gastric atrophy and intestinal metaplasia to gastric adenocarcinoma in patients with H. pylori infection [46, 47] These patterns are significantly associated with the CagA-positive strains [48]. The revised version of the Korean guidelines for Helicobacter pylori infection states that H. pylori eradication does not affect the development or clinical course of GERD [58]

Conclusion
Findings
10 RCTs using symptomatic GERD as outcome
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