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Cancer Epidemiol Biomarkers Prev. 2019 Oct 22. pii: cebp.0619.2019. doi: 10.1158/1055-9965.EPI-19-0619. [Epub ahead of print]

Testosterone therapy in relation to prostate cancer in a US commercial insurance claims database.

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Division of Cancer Epidemiology and Genetics, National Cancer Institute
Safety & Epidemiology, HealthCore Inc.
TRAQ, HealthCore Inc.
Department of Biostatistics, Epidemiology and Informatics, University of Pennsylvania School of Medicine.
Consolidated Research, Inc.
Division of Cancer Epidemiology and Genetics, National Cancer Institute.



We conducted a study assess whether testosterone therapy (TT) alters prostate cancer risk using a large US commercial insurance research database.


From the HealthCore Integrated Research Database (HIRDSM), we selected men aged 30 years or greater who were new users of TT during 2007-2015. We selected two comparison groups: 1) unexposed (matched 10:1); 2) new users of phosphodiesterase type 5 inhibitor (PDE5i). Incident prostate cancer was defined as diagnosis of prostate cancer within four-weeks following prostate biopsy. Propensity scores and inverse probability of treatment weights were used in Poisson regression models to estimate adjusted incidence rates, incidence rate ratios (IRRs) and 95% confidence intervals (CI). Subgroup analyses included stratification by prostate cancer screening, hypogonadism, and follow-up time.


The adjusted prostate cancer IRR was 0.77 (95%CI: 0.68, 0.86) when comparing TT with the unexposed group and 0.85 (95%CI: 0.79, 0.91) in comparison with the PDE5i group. Inverse associations between TT and prostate cancer were observed in a majority of subgroup analyses, although in both comparisons estimates generally attenuated with increasing time following initial exposure. Amongst TT users, duration of exposure was not associated with prostate cancer.


Men who received TT did not have a higher rate of prostate cancer compared with the unexposed or PDE5i comparison groups. The inverse association between TT and prostate cancer could be the result of residual confounding, contraindication bias, or undefined biologic effect.


This study suggests that limited TT exposure does not increase risk of prostate cancer in the short-term.

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