Arne Kandulski1, Peter Malfertheiner. 1. Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Abstract
PURPOSE OF REVIEW: The purpose of the review is to discuss key studies conducted on the intriguing relationship between Helicobacter pylori and gastroesophageal reflux disease. RECENT FINDINGS: Epidemiological studies have repeatedly described a negative association between H. pylori infection and erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma, but not between H. pylori and gastroesophageal reflux disease symptoms. Especially, infection with CagA-positive strains appears to protect the distal esophagus by causing fundic gland atrophy and impaired gastric acid secretion. Although earlier reports suggested the development of erosive esophagitis after H. pylori eradication, more recent studies discuss that H. pylori eradication usually does not have an important clinical impact on gastroesophageal reflux disease. SUMMARY: Gastric atrophy is the most widely accepted mechanism by which the distal esophagus is protected from abnormal acid exposure in patients with H. pylori infection. The clinical impact of H. pylori infection on the prevalence of erosive esophagitis and Barrett's esophagus remains a matter of debate. In areas with a high prevalence of H. pylori-induced atrophic gastritis, the protection that this infection may afford against gastroesophageal reflux disease is not comparable to the risk that H. pylori poses for the development of gastric cancer.
PURPOSE OF REVIEW: The purpose of the review is to discuss key studies conducted on the intriguing relationship between Helicobacter pylori and gastroesophageal reflux disease. RECENT FINDINGS: Epidemiological studies have repeatedly described a negative association between H. pyloriinfection and erosive esophagitis, Barrett's esophagus, and esophageal adenocarcinoma, but not between H. pylori and gastroesophageal reflux disease symptoms. Especially, infection with CagA-positive strains appears to protect the distal esophagus by causing fundic gland atrophy and impaired gastric acid secretion. Although earlier reports suggested the development of erosive esophagitis after H. pylori eradication, more recent studies discuss that H. pylori eradication usually does not have an important clinical impact on gastroesophageal reflux disease. SUMMARY: Gastric atrophy is the most widely accepted mechanism by which the distal esophagus is protected from abnormal acid exposure in patients with H. pyloriinfection. The clinical impact of H. pyloriinfection on the prevalence of erosive esophagitis and Barrett's esophagus remains a matter of debate. In areas with a high prevalence of H. pylori-induced atrophic gastritis, the protection that this infection may afford against gastroesophageal reflux disease is not comparable to the risk that H. pylori poses for the development of gastric cancer.
Authors: Serena Scida; Michele Russo; Chiara Miraglia; Gioacchino Leandro; Lorella Franzoni; Tiziana Meschi; Gian Luigi De' Angelis; Francesco Di Mario Journal: Acta Biomed Date: 2018-12-17