F J Bruinsma1, S Jordan2, J K Bassett3, G Severi4, R J MacInnis3, J Walsh5, T Aitken6, M Jenkins7, R Carroll8, M Jefford9, I D Davis10, K Tucker11, T Dudding-Byth12, D R English13, G G Giles14, I Winship15, R L Milne14. 1. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Australia. Electronic address: fiona.bruinsma@cancervic.org.au. 2. School of Public Health, University of Queensland, Brisbane, Australia; Population Health Department, QIMR Berghofer Medical Research Institute, Brisbane, Australia. 3. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia. 4. University Paris-Saclay, UVSQ, Inserm, Gustave Roussy, "Exposome and Heredity" team, CESP UMR1018, 94805, Villejuif, France; Department of Statistics, Computer Science and Applications (DISIA), University of Florence, Florence, Italy. 5. University of Sydney, New South Wales, Australia. 6. Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria, Australia. 7. Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Australia. 8. University of Adelaide, Royal Adelaide Hospital, South Australia, Australia. 9. Department of Medical Oncology, Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, Australia. 10. Faculty of Medicine, Nursing and Health Sciences, Monash University, Clayton, Victoria, Australia; Eastern Health, Victoria, Australia. 11. Hereditary Cancer Centre, Prince of Wales Hospital, Sydney, Australia / Prince of Wales Clinical School UNSW, Australia. 12. University of Newcastle, Newcastle, Australia. 13. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Australia. 14. Cancer Epidemiology Division, Cancer Council Victoria, Melbourne, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Australia; Precision Medicine, School of Clinical Sciences, Monash Health, Monash University, Clayton, Victoria, Australia. 15. Genomic Medicine, Royal Melbourne Hospital, Parkville, Australia; Department of Medicine, RMH, The University of Melbourne, Australia.
Abstract
PURPOSE: The incidence of renal cell carcinoma (RCC) is rising. Use of analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol may affect renal function. The aim of this study was to assess associations between analgesic use and risk of RCC. METHODS: A population-based case-control family design was used. Cases were recruited via two Australian state cancer registries. Controls were siblings or partners of cases. Analgesic use was captured by self-completed questionnaire. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for RCC risk associated with regular analgesic use (at least 5 times per month for 6 months or more) and duration and frequency of use. RESULTS: The analysis included 1064 cases and 724 controls. Regular use of paracetamol was associated with an increased risk of RCC (OR 1.41, 95%CI 1.13-1.77). Regular use of NSAIDs was associated with increased risk of RCC for women (OR 1.71, 95% CI 1.23-2.39) but not men (OR 0.83, 95% CI 0.58-1.18; p-interaction=0.003). There was no evidence of a dose-response for duration of use of paracetamol (linear trend p = 0.77) and weak evidence for non- aspirin NSAID use by women (linear trend p = 0.054). CONCLUSION: This study found that regular use of paracetamol was associated with increased risk of RCC. NSAID use was associated with increased risk only for women.
PURPOSE: The incidence of renal cell carcinoma (RCC) is rising. Use of analgesics such as non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol may affect renal function. The aim of this study was to assess associations between analgesic use and risk of RCC. METHODS: A population-based case-control family design was used. Cases were recruited via two Australian state cancer registries. Controls were siblings or partners of cases. Analgesic use was captured by self-completed questionnaire. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for RCC risk associated with regular analgesic use (at least 5 times per month for 6 months or more) and duration and frequency of use. RESULTS: The analysis included 1064 cases and 724 controls. Regular use of paracetamol was associated with an increased risk of RCC (OR 1.41, 95%CI 1.13-1.77). Regular use of NSAIDs was associated with increased risk of RCC for women (OR 1.71, 95% CI 1.23-2.39) but not men (OR 0.83, 95% CI 0.58-1.18; p-interaction=0.003). There was no evidence of a dose-response for duration of use of paracetamol (linear trend p = 0.77) and weak evidence for non- aspirin NSAID use by women (linear trend p = 0.054). CONCLUSION: This study found that regular use of paracetamol was associated with increased risk of RCC. NSAID use was associated with increased risk only for women.