Michael S Simon1,2, Pinkal Desai3, Robert Wallace4, Chunyuan Wu5, Barbara V Howard6, Lisa W Martin7, Nicolas Schlecht8, Simin Liu9, Allison Jay10, Erin S LeBlanc11, Thomas Rohan8, JoAnn Manson12. 1. Department of Oncology, Karmanos Cancer Institute, Wayne State University, Detroit, MI, USA. simonm@karmanos.org. 2. Barbara Ann Karmanos Cancer Institute, 4100 John R, 4221 HWCRC, Detroit, MI, USA. simonm@karmanos.org. 3. Weill Cornell Medical College, New York, NY, USA. 4. Department of Epidemiology, University of Iowa College of Public Health, Iowa City, IA, USA. 5. Fred Hutchinson Cancer Research Center, Seattle, WA, USA. 6. MedStar Health Research Institute and Georgetown/Howard Universities Center for Clinical and Translational Sciences, Washington, DC, USA. 7. George Washington University, Washington, DC, USA. 8. Albert Einstein College of Medicine, Bronx, NY, USA. 9. UCLA School of Public Health, Los Angeles, CA, USA. 10. St John's Hospital and Medical Center, Detroit, MI, USA. 11. Center for Health Research, Kaiser Permanente NW, Portland, OR, USA. 12. Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.
Abstract
PURPOSE: To determine whether HMG-CoA reductase inhibitors (statins) are associated with a lower risk of pancreatic cancer. METHODS: The population included 160,578 postmenopausal women enrolled in the Women's Health Initiative (WHI) in which 385 incident cases of pancreatic cancer were identified over an average of 8.69 (SD ±4.59) years. All diagnoses were confirmed by medical record and pathology review. Information on statin use and other risk factors was collected at baseline and during follow-up. Multivariable-adjusted hazards ratios (HRs) and 95 % confidence intervals (CIs) evaluating the relationship between prior statin use (at baseline only as well as in a time-dependent manner) and risk of pancreatic cancer were computed from Cox proportional hazards regression analyses after adjusting for appropriate confounders. We also evaluated the effect of statin type, potency, lipophilic status, and duration of use. All statistical tests were two-sided. RESULTS: Statins were used at baseline by 12,243 (7.5 %) women. The annualized rate of pancreatic cancer in statin users and nonusers, respectively, was 0.0298 versus 0.0271 %. The multivariable-adjusted HR for statin users versus nonusers at baseline was 0.92 and 95 % CI 0.57-1.48. In a time-dependent model, the HR for low-potency statins was 0.46, 95 % CI 0.20-1.04. There was no significant effect seen by statin lipophilicity or duration of use. CONCLUSIONS: There was no significant relationship between statins and pancreatic cancer risk in the WHI; however, there was a marginal inverse association noted for low-potency statins. Analyses of larger numbers of cases are needed to further explore this relationship.
PURPOSE: To determine whether HMG-CoA reductase inhibitors (statins) are associated with a lower risk of pancreatic cancer. METHODS: The population included 160,578 postmenopausal women enrolled in the Women's Health Initiative (WHI) in which 385 incident cases of pancreatic cancer were identified over an average of 8.69 (SD ±4.59) years. All diagnoses were confirmed by medical record and pathology review. Information on statin use and other risk factors was collected at baseline and during follow-up. Multivariable-adjusted hazards ratios (HRs) and 95 % confidence intervals (CIs) evaluating the relationship between prior statin use (at baseline only as well as in a time-dependent manner) and risk of pancreatic cancer were computed from Cox proportional hazards regression analyses after adjusting for appropriate confounders. We also evaluated the effect of statin type, potency, lipophilic status, and duration of use. All statistical tests were two-sided. RESULTS:Statins were used at baseline by 12,243 (7.5 %) women. The annualized rate of pancreatic cancer in statin users and nonusers, respectively, was 0.0298 versus 0.0271 %. The multivariable-adjusted HR for statin users versus nonusers at baseline was 0.92 and 95 % CI 0.57-1.48. In a time-dependent model, the HR for low-potency statins was 0.46, 95 % CI 0.20-1.04. There was no significant effect seen by statin lipophilicity or duration of use. CONCLUSIONS: There was no significant relationship between statins and pancreatic cancer risk in the WHI; however, there was a marginal inverse association noted for low-potency statins. Analyses of larger numbers of cases are needed to further explore this relationship.
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