title: The use of nonsteroidal anti-inflammatory drugs and the risk of Barrett's oesophagus.
abstract: BACKGROUND
  Epidemiological studies have consistently reported inverse associations between nonsteroidal anti-inflammatory drugs (NSAIDs) and oesophageal adenocarcinoma, but few have investigated associations with the precursor lesion, Barrett's oesophagus.
  
  
  OBJECTIVE
  To investigate the relationship between NSAID use and risk of Barrett's oesophagus.
  
  
  METHODS
  We conducted a large population-based case-control study that collected information on patterns of intake for aspirin and non-aspirin NSAIDs during the past 5 years and other exposures from 285 patients with nondysplastic Barrett's oesophagus, 108 patients with dysplastic Barrett's oesophagus, and two separate control groups: 313 endoscopy patients with acute inflammatory changes ('inflammation controls') and 644 population controls. We calculated odds ratios (ORs) and 95% CIs using unconditional logistic regression.
  
  
  RESULTS
  Use of aspirin was not associated with nondysplastic Barrett's oesophagus when compared with population (OR=1.01, 95% CI 0.71-1.43) or inflammation controls (OR=1.16, 95% CI 0.80-1.68). Whereas we observed significant risk reductions for use of non-aspirin NSAIDs when nondysplastic Barrett's oesophagus cases were compared with population controls (OR=0.69, 95% CI 0.49-0.97), the effect was weaker and nonsignificant when cases were compared with inflammation controls (OR=0.82, 95% CI 0.57-1.18), and no dose-response effects were present in either analysis. We found no evidence that aspirin or non-aspirin NSAID use conferred risk reductions for dysplastic Barrett's oesophagus, regardless of the control series. We excluded effect modification by known risk factors as an explanation for these null findings.
  
  
  CONCLUSIONS
  We found little support for an inverse association between use of NSAIDs and Barrett's oesophagus. The question of whether or not these medications prevent the onset of Barrett's oesophagus remains open.
authors.affiliation: School of Population Health, The University of Queensland, Public Health Building, Herston, Brisbane, Australia.
authors.forename: A P
authors.initials: AP
authors.lastname: Thrift
authors.forename: N
authors.initials: N
authors.lastname: Pandeya
authors.forename: K J
authors.initials: KJ
authors.lastname: Smith
authors.forename: A C
authors.initials: AC
authors.lastname: Green
authors.forename: P M
authors.initials: PM
authors.lastname: Webb
authors.forename: D C
authors.initials: DC
authors.lastname: Whiteman
mesh_terms: D000082:Acetaminophen / Q000009:adverse effects*; D000293:Adolescent; D000328:Adult; D000368:Aged; D018712:Analgesics, Non-Narcotic / Q000009:adverse effects*; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects*; D001241:Aspirin / Q000009:adverse effects*; D001471:Barrett Esophagus / Q000139:chemically induced*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D012307:Risk Factors; D055815:Young Adult
chemical_list: D018712:Analgesics, Non-Narcotic; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000082:Acetaminophen; D001241:Aspirin