Massimo Vicentini1, Paola Ballotari2, Paolo Giorgi Rossi3, Francesco Venturelli4, Claudio Sacchettini5, Marina Greci6, Lucia Mangone7, Annamaria Pezzarossi8, Valeria Manicardi9. 1. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Massimo.Vicentini@ausl.re.it. 2. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: paola.ballotari@ats-valpadana.it. 3. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Paolo.GiorgiRossi@ausl.re.it. 4. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy; Specialization School of Hygiene and Preventive Medicine, Department of Biomedical, Metabolic and Neural Sciences, University of Modena and Reggio Emilia, Modena, Italy; Clinical and Experimental Medicine PhD Program, University of Modena and Reggio Emilia, Modena, Italy. Electronic address: venturelli.dr.francesco@gmail.com. 5. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Claudio.Sacchettini@ausl.re.it. 6. Primary Health Care, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Marina.Greci@ausl.re.it. 7. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Lucia.Mangone@ausl.re.it. 8. Epidemiology Unit, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Annamaria.Pezzarossi@ausl.re.it. 9. Department of Internal Medicine, Hospital of Montecchio, Local Health Authority of Reggio Emilia-IRCCS, Reggio Emilia, Italy. Electronic address: Valeria.Manicardi@ausl.re.it.
Abstract
AIM: To assess the effect of metformin on cancer incidence in type 2 diabetes (T2DM), considering possible interactions with other glucose-lowering drugs and diabetes duration. METHODS: Study cohort included diabetes patients aged 20-84 on December 2009, still alive and resident in Reggio Emilia province as of December 2011. Drug exposure was assessed for 2009-2011; subjects taking metformin continuously, with or without other hypoglycaemic drugs, were compared to subjects on diet-only therapy. The cohort was followed up from 2012 to 2014 through the cancer registry. Age- and sex-adjusted incidence rate ratios (IRRs) were computed using Poisson regression models for all sites, lung, breast, liver, colorectal, prostate and pancreatic cancer. RESULTS: The cohort includes 17,026 people with T2DM, 7460 taking metformin. 887 cancers occurred during follow-up, 348 among metformin users. Cancer risk was similar in T2DM patients using metformin and those on diet-only. The risk for prostate (IRR = 0.65; 95%CI:0.36; 1.17), liver (IRR = 0.82; 95%CI:0.36; 1.85) and breast (IRR = 0.77; 95%CI:0.43; 1.40) cancers only was slightly reduced; for lung (IRR = 1.52; 95%CI:0.92; 2.50), pancreas (IRR = 1.51; 95%CI:0.59:3.89) and colon-rectum (IRR = 1.71; 95%CI:0.94; 3.08) the risk was slightly increased. CONCLUSIONS: There is no evidence of antitumor effect of metformin. A possible decrease only for breast, liver and prostate cancer, is compatible with random fluctuations.
AIM: To assess the effect of metformin on cancer incidence in type 2 diabetes (T2DM), considering possible interactions with other glucose-lowering drugs and diabetes duration. METHODS: Study cohort included diabetespatients aged 20-84 on December 2009, still alive and resident in Reggio Emilia province as of December 2011. Drug exposure was assessed for 2009-2011; subjects taking metformin continuously, with or without other hypoglycaemic drugs, were compared to subjects on diet-only therapy. The cohort was followed up from 2012 to 2014 through the cancer registry. Age- and sex-adjusted incidence rate ratios (IRRs) were computed using Poisson regression models for all sites, lung, breast, liver, colorectal, prostate and pancreatic cancer. RESULTS: The cohort includes 17,026 people with T2DM, 7460 taking metformin. 887 cancers occurred during follow-up, 348 among metformin users. Cancer risk was similar in T2DM patients using metformin and those on diet-only. The risk for prostate (IRR = 0.65; 95%CI:0.36; 1.17), liver (IRR = 0.82; 95%CI:0.36; 1.85) and breast (IRR = 0.77; 95%CI:0.43; 1.40) cancers only was slightly reduced; for lung (IRR = 1.52; 95%CI:0.92; 2.50), pancreas (IRR = 1.51; 95%CI:0.59:3.89) and colon-rectum (IRR = 1.71; 95%CI:0.94; 3.08) the risk was slightly increased. CONCLUSIONS: There is no evidence of antitumor effect of metformin. A possible decrease only for breast, liver and prostate cancer, is compatible with random fluctuations.