title: Aspirin may prevent cholangiocarcinoma: a case-control study from the United kingdom.
abstract: BACKGROUND
  The proliferation of cholangiocarcinoma cells is suppressed in cell culture by nonsteroidal antiinflammatory drugs (NSAIDs) through the inhibition of cyclo-oxygenase-2 enzyme and also by statins which decrease the production of mediators of the cell cycle.
  
  
  OBJECTIVE
  To investigate whether there is an inverse association between NSAIDs, including aspirin, and the development of cholangiocarcinoma and, for the first time in a Western population, between statin use and the development of cholangiocarcinoma.
  
  
  METHODS
  This epidemiological study had a case-control design in which cases of cholangiocarcinoma diagnosed in Norwich between 2004 and 2010 and in Leicester in 2007 were identified from clinical databases. Controls were patients with basal cell carcinomas treated in the respective dermatology departments. The case notes of all subjects were reviewed to confirm diagnoses and obtain information on medication use. The data were analyzed using unconditional logistic regression to calculate odds ratios (OR) with 95 % confidence intervals (CI).
  
  
  RESULTS
  In total, 81 cases of cholangiocarcinoma and 275 controls were identified. For all cases there was radiological evidence of cancer and 86 % of the cases involved the extrahepatic biliary system. Aspirin use was inversely associated with the development of cholangiocarcinoma (OR 0.45, 95 % CI 0.22-0.92), but there were no significant associations between the development of cholangiocarcinoma and NSAIDs (OR 0.39; 95 % CI 0.11-1.42) or statins (OR 0.58; 95 % CI 0.28-1.19).
  
  
  CONCLUSIONS
  The epidemiological data from this study support the biological evidence for aspirin having a protective effect against the development of cholangiocarcinoma. Aspirin use should be measured in future etiological studies and assessed as a chemoprevention agent in those at high risk of developing this type of cancer.
authors.affiliation: Section of Molecular Gastroenterology, Leeds Institute of Molecular Medicine, St James's University Hospital, Leeds, LS9 7TF, UK, n.burr@leedsth.nhs.uk.
authors.forename: N E
authors.initials: NE
authors.lastname: Burr
authors.forename: R J
authors.initials: RJ
authors.lastname: Talboys
authors.forename: S
authors.initials: S
authors.lastname: Savva
authors.forename: A
authors.initials: A
authors.lastname: Clark
authors.forename: M
authors.initials: M
authors.lastname: Phillips
authors.forename: M
authors.initials: M
authors.lastname: Metcalfe
authors.forename: A
authors.initials: A
authors.lastname: Dennison
authors.forename: R
authors.initials: R
authors.lastname: Robinson
authors.forename: M P
authors.initials: MP
authors.lastname: Lewis
authors.forename: M
authors.initials: M
authors.lastname: Rhodes
authors.forename: S
authors.initials: S
authors.lastname: Rushbrook
authors.forename: A R
authors.initials: AR
authors.lastname: Hart
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use*; D001650:Bile Duct Neoplasms / Q000209:etiology / Q000517:prevention & control*; D001653:Bile Ducts, Intrahepatic; D016022:Case-Control Studies; D018281:Cholangiocarcinoma / Q000209:etiology / Q000517:prevention & control*; D016001:Confidence Intervals; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D012307:Risk Factors; D006113:United Kingdom
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D001241:Aspirin