title: The differential effects of statins on the risk of developing pancreatic cancer: a case-control study in two centres in the United Kingdom.
abstract: BACKGROUND
  There are plausible biological mechanisms for how statins may prevent pancreatic cancer, although the evidence from epidemiological studies in the general population is conflicting. This study aims to clarify whether statins exert their effects in specific sub-groups, namely, gender, smoking status and diabetes.
  
  
  METHODS
  A matched case-control study was conducted in patients diagnosed with pancreatic cancer, and a group of dermatology patients of similar ages and gender, diagnosed with basal cell carcinoma. Participants' medical records were reviewed for information on statin use prior to diagnosis. Odds ratios and 95 % CIs for the development of pancreatic cancer were estimated using conditional logistic regression. Subgroup analysis was performed in men, women, smokers and those with type 2 diabetes.
  
  
  RESULTS
  Two hundred fifty-two cases (median age 71 years, range 48-73 years, 51 % women) and 504 controls were identified, of which 23 % of cases were regular statin users versus 21 % of controls. In the general study population there was no association between pancreatic cancer and regular statin use (OR 0.82, 95 % CI 0.53-1.23, p = 0.33). However, in male smokers, regular statin use was associated with significantly reduced odds of pancreatic cancer compared to male smokers not prescribed a statin (OR 0.11, 95 % CI 0.01-0.96, p = 0.05). In patients with type 2 diabetes statins use was not associated with reduced odds (OR 0.92, 95 % CI 0.35-2.45, p = 0.80), with no gender effects.
  
  
  CONCLUSIONS
  In male smokers, statins may reduce the odds of pancreatic cancer. Statin use should be measured in aetiological studies of pancreatic cancer but analysed in specific sub-groups. Future work should investigate statins as chemopreventative agents in this high risk sub-group.
authors.affiliation: Norfolk and Norwich University Hospital, Norwich, UK, f.carey@uea.ac.uk.
authors.forename: F J
authors.initials: FJ
authors.lastname: Carey
authors.forename: M W
authors.initials: MW
authors.lastname: Little
authors.forename: T F G
authors.initials: TF
authors.lastname: Pugh
authors.forename: R
authors.initials: R
authors.lastname: Ndokera
authors.forename: H
authors.initials: H
authors.lastname: Ing
authors.forename: A
authors.initials: A
authors.lastname: Clark
authors.forename: A
authors.initials: A
authors.lastname: Dennison
authors.forename: M S
authors.initials: MS
authors.lastname: Metcalfe
authors.forename: R J
authors.initials: RJ
authors.lastname: Robinson
authors.forename: A R
authors.initials: AR
authors.lastname: Hart
mesh_terms: D000328:Adult; D000368:Aged; D002280:Basal Cell Carcinoma / Q000175:diagnosis / Q000209:etiology; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000009:adverse effects*; D006937:Hypercholesterolemia / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010190:Pancreatic Neoplasms / Q000139:chemically induced* / Q000453:epidemiology; D012307:Risk Factors; D012878:Skin Neoplasms / Q000175:diagnosis / Q000209:etiology; D006113:United Kingdom / Q000453:epidemiology
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors