title: 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.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Centre for Clinical and Population Sciences, Queen's University Belfast, Mulhouse Building, Grosvenor Road, Belfast BT12 6BJ, UK. l.anderson@qub.ac.uk
authors.forename: L A
authors.initials: LA
authors.lastname: Anderson
authors.forename: S J
authors.initials: SJ
authors.lastname: Murphy
authors.forename: B T
authors.initials: BT
authors.lastname: Johnston
authors.forename: R G P
authors.initials: RG
authors.lastname: Watson
authors.forename: H R
authors.initials: HR
authors.lastname: Ferguson
authors.forename: K B
authors.initials: KB
authors.lastname: Bamford
authors.forename: A
authors.initials: A
authors.lastname: Ghazy
authors.forename: P
authors.initials: P
authors.lastname: McCarron
authors.forename: J
authors.initials: J
authors.lastname: McGuigan
authors.forename: J V
authors.initials: JV
authors.lastname: Reynolds
authors.forename: H
authors.initials: H
authors.lastname: Comber
authors.forename: L J
authors.initials: LJ
authors.lastname: Murray
mesh_terms: D000230:Adenocarcinoma / Q000150:complications*; D000368:Aged; D000907:Antibodies, Bacterial / Q000097:blood; D000942:Antigens, Bacterial / Q000097:blood; D001426:Bacterial Proteins / Q000097:blood; D001471:Barrett Esophagus / Q000150:complications; D016022:Case-Control Studies; D004938:Esophageal Neoplasms / Q000150:complications*; D004942:Esophagitis, Peptic / Q000150:complications; D005260:Female; D005757:Gastritis, Atrophic / Q000150:complications*; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000276:immunology / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011230:Precancerous Conditions / Q000150:complications; D018570:Risk Assessment
chemical_list: D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001426:Bacterial Proteins; C080866:cagA protein, Helicobacter pylori