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Relationship between Helicobacter pylori infection and gastric atrophy and the stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence: results from the FINBAR case–control study
  1. L A Anderson1,
  2. S J Murphy2,
  3. B T Johnston3,
  4. R G P Watson3,
  5. H R Ferguson1,
  6. K B Bamford4,
  7. A Ghazy4,
  8. P McCarron1,
  9. J McGuigan3,
  10. J V Reynolds5,
  11. H Comber6,
  12. L J Murray1
  1. 1
    Centre for Clinical and Population Sciences, Queen’s University Belfast, UK
  2. 2
    Daisy Hill Hospital, Newry, UK
  3. 3
    Royal Group of Hospitals, Belfast, UK
  4. 4
    Imperial College, London, UK
  5. 5
    St James’s Hospital, Dublin, Ireland
  6. 6
    National Cancer Registry, Cork, Ireland
  1. Dr L A Anderson, Centre for Clinical and Population Sciences, Queen’s University Belfast, Mulhouse Building, Grosvenor Road, Belfast BT12 6BJ, UK; l.anderson{at}qub.ac.uk

Abstract

Objective: A number of studies have shown an inverse association between infection with Helicobacter pylori and oesophageal adenocarcinoma (OAC). The mechanism of the apparent protection against OAC by H pylori infection and, in particular, the role of gastric atrophy is disputed. The relationship between all stages of the oesophageal inflammation, metaplasia, adenocarcinoma sequence and H pylori infection and gastric atrophy was explored.

Methods: A case–control study involving 260 population controls, 227 OAC, 224 Barrett’s oesophagus (BO) and 230 reflux oesophagitis (RO) patients recruited within Ireland was carried out. H pylori and CagA (cytotoxin-associated gene product A) infection was diagnosed serologically by western blot, and pepsinogen I and II levels were measured by enzyme immunoassay. Gastric atrophy was defined as a pepsinogen I/II ratio of <3.

Results: H pylori seropositivity was inversely associated with OAC, BO and RO; adjusted ORs (95% CIs), 0.49 (0.31 to 0.76), 0.35 (0.22 to 0.56) and 0.42 (0.27 to 0.65), respectively. Gastric atrophy was uncommon (5.3% of all subjects), but was inversely associated with non-junctional OAC, BO and RO; adjusted ORs (95% CIs), 0.34 (0.10 to 1.24), 0.23 (0.05 to 0.96) and 0.27 (0.08 to 0.88), respectively. Inverse associations between H pylori and the disease states remained in gastric atrophy-negative patients.

Conclusion: H pylori infection and gastric atrophy are associated with a reduced risk of OAC, BO and RO. While use of the pepsinogen I/II ratio as a marker for gastric atrophy has limitations, these data suggest that although gastric atrophy is involved it may not fully explain the inverse associations observed with H pylori infection.

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Footnotes

  • Funding: The FINBAR study was funded by an Ireland–Northern Ireland Co-operation Research Project Grant sponsored by the Research & Development Office, Belfast, the Health Research Board Dublin and the Ulster Cancer Foundation, Northern Ireland. Further funding was obtained for the oesophagitis study from a Research & Development Office Clinical Fellowship

  • Competing interests: None.

  • Ethics approval: Ethical committee approval was obtained from the Research Ethics Committee of Queen’s University Belfast, the Clinical Research Ethics Committee of the Cork Teaching Hospitals and the Research Ethics Committee Board of St James’s Hospital, Dublin.

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