title: CagA-positive strains of Helicobacter pylori may protect against Barrett's esophagus.
abstract: OBJECTIVE
  Helicobacter pylori (H. pylori) colonization is associated with chronic gastritis, peptic ulcer disease, and adenocarcinoma of the distal stomach. However, the role of H. pylori strain variation in complicated gastroesophageal reflux disease, especially Barrett's esophagus, is unknown. Therefore, the aim of this study was to evaluate the prevalence of colonization by cagA+ and cagA- H. pylori strains in the spectrum of gastroesophageal reflux disease, including Barrett's esophagus.
  
  
  METHODS
  A total of 251 patients undergoing endoscopy were categorized into four groups: controls, patients with gastroesophageal reflux disease alone, and patients with short- and long-segment Barrett's esophagus. All patients underwent upper endoscopies with biopsies and serum collections. H. pylori and degree of mucosal inflammation in gastric biopsies were assessed and serological assessment made for H. pylori and cagA status.
  
  
  RESULTS
  The overall prevalence of H. pylori colonization in the study population was 35% (95% confidence interval = 29.5-41.4%) which did not differ significantly among the groups. However, colonization by cagA+ H. pylori strains was significantly more prevalent among controls (11/25; 44%) and patients with gastroesophageal reflux disease (13/36; 36%) than in patients with short-segment (2/10; 20%) or long-segment Barrett's esophagus (0/18; 0%). Patients with Barrett's esophagus were less likely to be colonized by cagA+ H. pylori strains than reflux patients without Barrett's esophagus (odds ratio = 0.27, 95% confidence interval = 0.11-0.67, p = 0.004).
  
  
  CONCLUSIONS
  Colonization by cagA+ H. pylori strains may be protective against the formation of short- and long-segment Barrett's esophagus and its malignant complications.
authors.affiliation: Center for Swallowing and Esophageal Disorders, Department of Gastroenterology, The Cleveland Clinic Foundation, Ohio 44195, USA.
authors.forename: M F
authors.initials: MF
authors.lastname: Vaezi
authors.forename: G W
authors.initials: GW
authors.lastname: Falk
authors.forename: R M
authors.initials: RM
authors.lastname: Peek
authors.forename: J J
authors.initials: JJ
authors.lastname: Vicari
authors.forename: J R
authors.initials: JR
authors.lastname: Goldblum
authors.forename: G I
authors.initials: GI
authors.lastname: Perez-Perez
authors.forename: T W
authors.initials: TW
authors.lastname: Rice
authors.forename: M J
authors.initials: MJ
authors.lastname: Blaser
authors.forename: J E
authors.initials: JE
authors.lastname: Richter
mesh_terms: D000907:Antibodies, Bacterial / Q000032:analysis; D001471:Barrett Esophagus / Q000382:microbiology* / Q000473:pathology; D001706:Biopsy; D003030:Coagulase / Q000276:immunology / Q000378:metabolism*; D015169:Colony Count, Microbial; D016145:Endoscopy, Digestive System; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005753:Gastric Mucosa / Q000382:microbiology* / Q000473:pathology; D005756:Gastritis / Q000150:complications / Q000382:microbiology* / Q000473:pathology; D005764:Gastroesophageal Reflux / Q000382:microbiology* / Q000473:pathology; D016481:Helicobacter Infections / Q000150:complications / Q000382:microbiology* / Q000473:pathology; D016480:Helicobacter pylori / Q000201:enzymology* / Q000254:growth & development / Q000276:immunology; D006801:Humans; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D015995:Prevalence; D011379:Prognosis; D012189:Retrospective Studies
chemical_list: D000907:Antibodies, Bacterial; D003030:Coagulase