Does Helicobacter pylori infection contribute to gastroesophageal reflux disease?

Helicobacter pylori organisms that infect the stomach conceivably could contribute to esophageal inflammation in patients with gastroesophageal reflux disease (GERD) through any of at least three potential mechanisms: 1) by causing an increase in gastric acid secretion; 2) by spreading to infect the gastric-type columnar epithelium that occasionally can line the distal esophagus; and/or 3) by secreting noxious bacterial products into the gastric juice. Studies regarding these potential mechanisms are discussed in this report. Most investigations have found no apparent association between H. pylori infection and reflux esophagitis. Presently, infection with H. pylori does not appear to play an important role in the pathogenesis of GERD.

[1]  M. Johnston,et al.  The prevalence and clinical characteristics of short segments of specialized intestinal metaplasia in the distal esophagus on routine endoscopy. , 1996, The American journal of gastroenterology.

[2]  E. Boyd The prevalence of esophagitis in patients with duodenal ulcer or ulcer-like dyspepsia. , 1996, The American journal of gastroenterology.

[3]  R. Logan,et al.  Adherence of Helicobacter pylori , 1996, Alimentary pharmacology & therapeutics.

[4]  W. Peterson Gastrin and acid in relation to Helicobacter pylori. , 1996, Alimentary pharmacology & therapeutics.

[5]  R. Liston,et al.  Reflux oesophagitis and Helicobacter pylori infection in elderly patients. , 1996, Postgraduate medical journal.

[6]  J. Fléjou,et al.  Helicobacter pylori infection in patients with Barrett's oesophagus: a prospective immunohistochemical study. , 1996, Journal of clinical pathology.

[7]  R. Goyal,et al.  The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. , 1996, Gastroenterology.

[8]  A. Blum,et al.  Effect of curing Helicobacter pylori infection on intragastric pH during treatment with omeprazole. , 1995, Gut.

[9]  J. Walsh,et al.  The treatment of Helicobacter pylori infection in the management of peptic ulcer disease. , 1995, The New England journal of medicine.

[10]  Z. Abbas,et al.  Barrett's oesophagus and Helicobacter pylori , 1995, Journal of gastroenterology and hepatology.

[11]  B. Dwyer,et al.  Cytotoxin production by Helicobacter pylori from patients with upper gastrointestinal tract diseases , 1995, Journal of clinical microbiology.

[12]  A. Blum,et al.  Effect of Helicobacter pylori status on intragastric pH during treatment with omeprazole. , 1995, Gut.

[13]  R. Goyal,et al.  Prevalence of metaplasia at the gastro-oesophageal junction , 1994, The Lancet.

[14]  M. Glassman,et al.  Esophagitis and Helicobacter pylori in children: incidence and therapeutic implications. , 1993, The American journal of gastroenterology.

[15]  P. Lundborg,et al.  Effect of once daily intravenous and oral omeprazole on 24-hour intragastric acidity in healthy subjects. , 1993, Scandinavian journal of gastroenterology.

[16]  J. Arends,et al.  Prevalence and significance of Helicobacter pylori in patients with Barrett's esophagus. , 1992, The American journal of gastroenterology.

[17]  M. Blaser,et al.  Association of infection due to Helicobacter pylori with specific upper gastrointestinal pathology. , 1991, Reviews of infectious diseases.

[18]  J. Val-Bernal,et al.  Helicobacter pylori in Barrett's oesophagus , 1991, Histology and histopathology.

[19]  D. Graham,et al.  Inappropriate hypergastrinaemia in asymptomatic healthy subjects infected with Helicobacter pylori. , 1990, Gut.

[20]  A. Zinsmeister,et al.  Campylobacter pylori and Barrett's esophagus. , 1988, Mayo Clinic proceedings.

[21]  G. Paull,et al.  Gastric and esophageal Campylobacter pylori in patients with Barrett's esophagus. , 1988, Gastroenterology.

[22]  J. Zieleński,et al.  Campylobacter pyloridis degrades mucin and undermines gastric mucosal integrity. , 1987, Biochemical and biophysical research communications.

[23]  J. Hayward The lower end of the oesophagus. , 1961, Thorax.

[24]  P. Dítě,et al.  [Barrett's esophagus]. , 2000, Bratislavske lekarske listy.

[25]  R. Genta Recognizing atrophy: another step toward a classification of gastritis. , 1996, The American journal of surgical pathology.

[26]  K. Okazaki,et al.  Lipolytic activity of Campylobacter pylori: effect of sofalcone. , 1989, Digestion.