The effect of 5α-reductase inhibitors on prostate growth in men receiving testosterone replacement therapy: a systematic review and meta-analysis

Androgen replacement therapy is a widely accepted form of treatment worldwide for aging men with late-onset hypogonadism (LOH) syndrome. Urologists have been concerned with the use of androgen supplements due to the possibility of enhancing prostate growth. We performed a systematic review and meta-analysis to assess the effect of 5α-reductase inhibitors on prostate growth in men receiving testosterone replacement therapy.

A literature review was performed to identify all published randomized placebo-controlled trials (RCT) that used exogenous testosterone combined with 5α-reductase inhibitor therapy for the treatment of hypogonadism. The search included the following databases: MEDLINE, EMBASE, and the Cochrane Controlled Trials Register. The reference lists of the retrieved studies were also investigated, and a systematic review and meta-analysis were conducted.

Five publications involving a total of 250 patients were used in the analysis, including 4 RCTs that were short-term (≤6 mo) comparisons of testosterone plus a 5α-reductase inhibitor with testosterone plus placebo and 3 RCTs that were long-term (18–36 mo) comparisons of testosterone plus a 5α-reductase inhibitor with testosterone plus placebo. In our meta-analysis, we found that testosterone plus a 5α-reductase inhibitor may slow the progression of prostate growth. For the comparison of short-term testosterone plus 5α-reductase inhibitor treatment with testosterone plus placebo therapy, the prostate-specific antigen (PSA) level (the standardized mean difference (SMD) = −0.24, 95 % confidence interval (CI) = −0.45 to 0.04, p = 0.02)) and the prostate volume (SMD = −1.66, 95 % CI = −4.54 to 1.22, p = 0.26) indicated that, compared with testosterone plus placebo therapy, the testosterone plus 5α-reductase inhibitor may decrease the PSA level. For the comparison of long-term testosterone plus 5α-reductase inhibitor with testosterone plus placebo, the PSA level (SMD = −0.53, 95 % CI = −0.84 to 0.21, p = 0.001) and the prostate volume (SMD = −8.53, 95 % CI = −15.51 to 1.54, p = 0.02) showed that, compared with testosterone plus placebo therapy, the testosterone plus 5α-reductase inhibitor treatment may slow the progression of prostate growth.

Our meta-analysis indicates that the treatment of LOH patients with short-term testosterone plus 5α-reductase inhibitor therapy does not lead to prostate growth; however, this treatment could effectively decrease the PSA level. Additionally, long-term testosterone plus 5α-reductase inhibitor therapy could slow the progression of prostate growth.