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Helicobacter pylori
The significance of cagA + Helicobacter pylori in reflux oesophagitis
  1. V J Warburton-Timmsa,
  2. A Charlettd,
  3. R M Valorib,
  4. J S Uffc,
  5. N A Shepherdc,
  6. H Barrb,
  7. C A M McNultya
  1. aPublic Health Laboratory, Gloucestershire Royal Hospital, Gloucester, UK, bGloucester Gastroenterology Group, Gloucestershire Royal Hospital, Gloucester, UK, cDepartment of Histopathology, Gloucestershire Royal Hospital, Gloucester, UK, dPHLS Statistics Unit, 61 Colindale Avenue, London, UK
  1. Dr C A M McNulty, Public Health Laboratory, Gloucestershire Royal Hospital, Great Western Road, Gloucester GL1 3NN, UK. jwhiting{at}phls.nhs.uk

Abstract

BACKGROUND Helicobacter pylori is a gastroduodenal pathogen associated with ulceration, dyspepsia, and adenocarcinoma. Recent preliminary studies have suggested that H pylori may be protective for oesophageal adenocarcinoma. In addition, strains ofH pylori identified by the presence of the cytotoxin associated gene A (cagA) are shown to have a significant inverse association with oesophageal adenocarcinoma. Given that cagA + H pylori may protect against oesophageal carcinoma, these strains may be protective for oesophagitis, a precursor of oesophageal carcinoma.

AIMS The aim of this study was to investigate the association betweencagA + H pylori and endoscopically proved oesophagitis.

PATIENTS The study group included 1486 patients attending for routine upper gastrointestinal tract endoscopy.

METHODS At endoscopy the oesophagus was assessed for evidence of reflux disease and graded according to standard protocols. Culture and histology of gastric biopsy specimens determined H pylori status. The prevalence of cagA was identified by an antibody specific ELISA (Viva Diagnostika, Germany).

RESULTS H pylori was present in 663/1485 (45%) patients and in 120/312 (38%) patients with oesophagitis. Anti-CagA antibody was found in 499/640 (78%) H pylori positive patients. Similarly, anti-CagA antibody was found in 422/521 (81%) patients with a normal oesophagus and in 42/60 (70%) with mild, 24/35 (69%) with moderate, and 11/24 (46%) with severe oesophagitis. The risk of severe oesophagitis was significantly decreased for patients infected withcagA + H pylori after correction for confounding variables (odds ratio 0.57, 95% confidence interval 0.41–0.80; p=0.001).

CONCLUSIONS These results suggest that infection bycagA + H pylori may be protective for oesophageal disease.

  • Helicobacter pylori
  • cagA +
  • gastro-oesophageal reflux disease
  • oesophagitis
  • oesophageal adenocarcinoma
  • hiatus hernia

  • Abbreviations used in this paper

    cag
    cytotoxin associated gene
    cagA, cytotoxin associated gene A
    PAI, pathogenicity island
    GORD
    gastro-oesophageal reflux disease
    NSAID
    non-steroidal anti-inflammatory drug
    PPI
    proton pump inhibitor
    LOS
    lower oesophageal sphincter

    • https://doi.org/10.1136/gut.49.3.341

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    • Abbreviations used in this paper

      cag
      cytotoxin associated gene
      cagA, cytotoxin associated gene A
      PAI, pathogenicity island
      GORD
      gastro-oesophageal reflux disease
      NSAID
      non-steroidal anti-inflammatory drug
      PPI
      proton pump inhibitor
      LOS
      lower oesophageal sphincter
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