The safety of testosterone supplementation therapy in prostate cancer

• Published in: Nature reviews. Urology Vol. 11; no. 9; pp. 526 - 530
• Main Authors: Dupree, James M., Langille, Gavin M., Khera, Mohit, Lipshultz, Larry I.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.09.2014; Nature Publishing Group
• Subjects: 692/499; 692/699/2743/1526/1561; 692/699/2768/589/466; 692/700/565/238; Androgens; Biopsy; Care and treatment; Contemporary literature; Health aspects; Humans; Hypogonadism - drug therapy; Hypogonadism - etiology; Male; Medicine & Public Health; Metastasis; opinion-2; Prostate cancer; Prostatic Neoplasms - complications; Receptors, Androgen - physiology; Testosterone; Testosterone - adverse effects; Testosterone - deficiency; Testosterone - therapeutic use; Urology
• ISSN: 1759-4812; 1759-4820; 1759-4820
• DOI: 10.1038/nrurol.2014.163

Historically, the use of testosterone supplementation therapy (TST) for hypogonadism in men with prostate cancer has been limited by concerns that such treatment might cause progression of this androgen-dependent cancer; however, the contemporary literature indicates that TST in men with prostate cancer can be safe and, contrary to traditional thinking, that TST might actually reduce the risk of prostate cancer development. In this opinion piece, Larry Lipshultz and colleagues discuss the evidence supporting TST—in contrast with the lack of evidence against this approach—in hypogonodal men with prostate cancer. Patients with prostate cancer can present with hypogonadism and experience health and quality-of-life declines related to low testosterone levels. Despite generations of urological dogma suggesting that testosterone supplementation therapy (TST) for hypogonadism causes prostate-cancer progression, a review of the contemporary literature provides evidence to the contrary. The prostate saturation model suggests that the androgen receptor (AR) is saturated at serum testosterone levels of 150–200 ng/dl, and that additional serum testosterone above this level has limited, if any, effects within the prostate. Indeed, studies in the modern era of PSA assessments indicate that TST does not affect prostate size, intraprostatic testosterone levels, or prostate-cancer progression, provided the baseline serum testosterone level is greater than this AR saturation point. However, the body of data on this subject comes from a small number of cases, and TST should only be administered to patients with prostate cancer after thorough discussions of the risks and benefits, with subsequent careful monitoring.