Article Text
Abstract
Objectives Investigate potential association between pioglitazone exposure and risk of prostate cancer.
Research design and methods Nested, matched case–control study. UK primary care data (Clinical Practice Research Datalink (CPRD) GOLD) linked to inpatient (Hospital Episode Statistics (HES)) and cancer registry (National Cancer Information Network (NCIN)) data. English men aged ≥40 years diagnosed with type 2 diabetes mellitus, January 1, 2001 to January 5, 2015. Cases, with prostate cancer diagnosis, matched with up to 4 controls by age, cohort entry date and region. ORs for association of exposure to pioglitazone to incident prostate cancer, adjusted for potential confounders.
Results From a cohort of 47 772 men with 243 923 person-years follow-up, 756 definite cases of prostate cancer were identified. Incidence was 309.9/100 000 person-years (95% CI 288.6 to 332.8). Pioglitazone use was not associated with prostate cancer risk; adjusted OR 0.759, 95% CI 0.502 to 1.148. Analyses showed no difference when possible cases, prostate cancer in CPRD GOLD only, included (adjusted OR 0.726, 95% CI 0.510 to 1.034). No association when adjusted for channeling bias (OR 0.778, 95% CI 0.511 to 1.184) or limited to an index date prior to July 1, 2011 (adjusted OR 0.508, 95% CI 0.294 to 0.879), despite prostate-specific antigen screening occurring more frequently among cases than controls (81.6% of 756 definite cases cf. 24.2% of 2942 controls (p<0.01)). No association with duration of pioglitazone use, increasing pioglitazone dose or increasing time since initiation.
Conclusions In this real-world, nested matched case–control study, exposure to pioglitazone was not associated with increased risk of prostate cancer.
- Type 2 Diabetes
- Prostate Cancer
- Thiazolidinediones
- Humans
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Footnotes
Contributors PLT, NB, DB and PD designed the study and provided methodological input. NB, DB and PD participated in the process of application for protocol approval by ISAC. NB, MH and DB contributed to the CPRD GOLD, HES and NCIN data acquisition. MH, NB and PLT processed the data and conducted the statistical analyses. NB wrote the first draft of the manuscript. All authors contributed to discussion, reviewed and interpreted the data, provided critical comments and revised the manuscript.
Funding This study was supported by the Takeda Pharmaceutical Company Limited.
Competing interests All authors have completed the ICMJE form for disclosure of potential conflicts at http://www.icmje.org/coi_disclosure.pdf. PD and DB are employees of Takeda Pharmaceutical Company Limited.
Ethics approval Ethics approval was granted by ISAC. The presented CPRD GOLD, HES and NCIN data are anonymised and, thus, the risk of patient identification is extremely low. The European Network of Centres for Pharmacoepidemiology and Pharmacovigilance (ENCePP) study registration ENCEPP/SDPP/11750.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data are available.