Effect of TNF-α Inhibitor Therapy on Growth of the Prostate Gland

Abstract

Background: Inflammation has been linked to the development of benign prostatic hyperplasia (BPH). SRD5A2 is a pivotal enzyme in the development and growth of the prostate gland and a critical target for BPH therapy. TNF-α regulates epigenetic changes in SRD5A2, leading to suppression of SRD5A2 gene and protein expression. It is unknown whether TNF-α inhibitor therapy affects prostate growth.

Objective: To evaluate the effect of TNF-α inhibitor therapy on prostate growth via analysis of measurements on serial pelvic imaging scans.

Design, setting, and participants: In this retrospective cohort study, we analyzed serial pelvic cross-sectional imaging (magnetic resonance imaging or computed tomography scans) for men aged ≥18 yr receiving TNF-α inhibitors. Our inclusion/exclusion criteria yielded a treatment cohort of 99 men. An age-matched cohort was constructed with the same inclusion/exclusion criteria but without TNF-α therapy (n = 99).

Outcome measurements and statistical analysis: Prostate growth on serial pelvic cross-sectional imaging was the primary outcome measure.

Results and limitations: There was no significant difference in total prostate volume (TPV) at baseline between the two groups. The TNF-α treatment group had a lower mean TPV on follow-up (26.21 ± 9.43 vs 32.71 ± 18.89 cm³; p = 0.002) and a lower median prostate growth rate (-0.01 vs 0.68 cm³/yr; p = 0.001). A multivariable linear regression model adjusted for age, race, initial TPV, and body mass index also revealed a significantly lower growth rate for men in the treatment group.

Conclusion: TNF-α inhibitor use was negatively correlated with the prostate growth rate, suggesting that inflammatory mediators regulate prostate growth.

Patient summary: We examined prostate growth rates in men taking TNF-α inhibitors and found that these drugs have a shrinking effect on the prostate. We conclude that TNF-α inhibitors may impede prostate growth.

Keywords: Benign prostatic hyperplasia; Epigenetics; Inflammation; Prostate; TNF-α.