Roger J Bedimo1, Lesley S Park2, Fatima M Shebl3, Keith Sigel4, Christopher T Rentsch5, Kristina Crothers6, Maria C Rodriguez-Barradas7, Matthew Bidwell Goetz8, Adeel A Butt9,10,11, Sheldon T Brown12,13, Cynthia Gibert14, Amy C Justice15,16, Janet P Tate15,16. 1. Veterans Affairs North Texas Healthcare System, University of Texas Southwestern Medical Center, Dallas, Texas. 2. Stanford University School of Medicine, Palo Alto, California. 3. Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. 4. Icahn School of Medicine at Mt. Sinai, New York, New York, USA. 5. London School of Hygiene and Tropical Medicine, London, UK. 6. VA Puget Sound Healthcare System, University of Washington School of Medicine, Seattle, Washington. 7. Michael E. DeBakey Veterans Affairs Medical Center, Baylor College of Medicine, Houston, Texas. 8. Veterans Affairs Greater Los Angeles Healthcare System, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California. 9. VA Pittsburgh Healthcare System, Pittsburgh, Pennsylvamia. 10. Weill Cornell Medical College, New York, New York, USA. 11. Weill Cornell Medical College, Doha, Qatar. 12. James J. Peters Veterans Affairs Medical Center, Bronx. 13. Icahn School of Medicine at Mt. Sinai, New York, New York. 14. Washington DC Veterans Affairs Medical Center, George Washington University School of Medicine and Health Sciences, Washington, DC. 15. VA Connecticut Healthcare System, West Haven. 16. Yale School of Medicine, New Haven, Connecticut, USA.
Abstract
OBJECTIVE: To determine whether statin exposure is associated with decreased cancer and mortality risk among persons with HIV (PWH) and uninfected persons. Statins appear to have immunomodulatory and anti-inflammatory effects and may reduce cancer risk, particularly among PWH as they experience chronic inflammation and immune activation. DESIGN: Propensity score-matched cohort of statin-exposed and unexposed patients from 2002 to 2017 in the Veterans Aging Cohort Study (VACS), a large cohort with cancer registry linkage and detailed pharmacy data. METHODS: We calculated Cox regression hazard ratios (HRs) and 95% confidence intervals (CI) associated with statin use for all cancers, microbial cancers (associated with bacterial or oncovirus coinfection), nonmicrobial cancers, and mortality. RESULTS: :The propensity score-matched sample (N = 47 940) included 23 970 statin initiators (31% PWH). Incident cancers were diagnosed in 1160 PWH and 2116 uninfected patients. Death was reported in 1667 (7.0%) statin-exposed, and 2215 (9.2%) unexposed patients. Statin use was associated with 24% decreased risk of microbial-associated cancers (hazard ratio 0.76; 95% CI 0.69-0.85), but was not associated with nonmicrobial cancer risk (hazard ratio 1.00; 95% CI 0.92-1.09). Statin use was associated with 33% lower risk of death overall (hazard ratio 0.67; 95% CI 0.63-0.72). Results were similar in analyses stratified by HIV status, except for non-Hodgkin lymphoma where statin use was associated with reduced risk (hazard ratio 0.56; 95% CI 0.38-0.83) for PWH, but not for uninfected (P interaction = 0.012). CONCLUSION: In both PWH and uninfected, statin exposure was associated with lower risk of microbial, but not nonmicrobial cancer incidence, and with decreased mortality.
OBJECTIVE: To determine whether statin exposure is associated with decreased cancer and mortality risk among persons with HIV (PWH) and uninfected persons. Statins appear to have immunomodulatory and anti-inflammatory effects and may reduce cancer risk, particularly among PWH as they experience chronic inflammation and immune activation. DESIGN: Propensity score-matched cohort of statin-exposed and unexposed patients from 2002 to 2017 in the Veterans Aging Cohort Study (VACS), a large cohort with cancer registry linkage and detailed pharmacy data. METHODS: We calculated Cox regression hazard ratios (HRs) and 95% confidence intervals (CI) associated with statin use for all cancers, microbial cancers (associated with bacterial or oncovirus coinfection), nonmicrobial cancers, and mortality. RESULTS: :The propensity score-matched sample (N = 47 940) included 23 970 statin initiators (31% PWH). Incident cancers were diagnosed in 1160 PWH and 2116 uninfected patients. Death was reported in 1667 (7.0%) statin-exposed, and 2215 (9.2%) unexposed patients. Statin use was associated with 24% decreased risk of microbial-associated cancers (hazard ratio 0.76; 95% CI 0.69-0.85), but was not associated with nonmicrobial cancer risk (hazard ratio 1.00; 95% CI 0.92-1.09). Statin use was associated with 33% lower risk of death overall (hazard ratio 0.67; 95% CI 0.63-0.72). Results were similar in analyses stratified by HIV status, except for non-Hodgkin lymphoma where statin use was associated with reduced risk (hazard ratio 0.56; 95% CI 0.38-0.83) for PWH, but not for uninfected (P interaction = 0.012). CONCLUSION: In both PWH and uninfected, statin exposure was associated with lower risk of microbial, but not nonmicrobial cancer incidence, and with decreased mortality.
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Authors: Jonathan R Emberson; Patricia M Kearney; Lisa Blackwell; Connie Newman; Christina Reith; Neeraj Bhala; Lisa Holland; Richard Peto; Anthony Keech; Rory Collins; John Simes; Colin Baigent Journal: PLoS One Date: 2012-01-19 Impact factor: 3.240