Testosterone Replacement Therapy and BPH/LUTS. What is the Evidence?

Abstract

Contrary to the previous dogma that prostatic growth is directly proportional to testosterone levels, emerging research has suggested a lack of testosterone may be a risk factor for lower urinary tract symptoms (LUTS) and benign prostatic hyperplasia (BPH). Within this review article, we have demonstrated the current understanding of the physiology of hypogonadism and its interplay with prostatic and lower urinary tract physiology. The current evidence suggests that not only does testosterone replacement therapy (TRT) not worsen LUTS, but that hypogonadism itself is an important risk factor for LUTS/BPH.

Systemic effects of the hormonal treatment of male hypogonadism with preliminary indications for the management of COVID-19 patients

“…A number of studies suggest that prostatic receptors for androgens are totally saturated at levels close to castration (50 ng/dl), although the prostate has numerous ARs. 82 In particular, the AR becomes saturated in human prostate tissue at about 8 nmol/l in vivo. Beyond this saturation point (8 nmol/l) T does not appear to further increase prostate volume.…”

“…In line with this theory, although the high T levels reached in young men, they do not develop LUTSs or BPH compared with the norm, contrary to what happens in the elderly with minimal T values. 82 …”

“…T modulates cGMP levels by stimulating high levels of NOS and inhibiting cGMP degradation by phosphodiesterase type 5 (PDE5). 82 The increased NO availability provided by normal serum T levels may positively impact on LUTSs in patients with BPH.…”

How does lower urinary tract dysfunction (LUTD) affect sexual function in men and women? ICI‐RS 2015—Part 2

“…Current evidence suggests that hypogonadism itself is an important risk factor for LUTS, too. 16 In the Hypogonadism in Males (HIM) study of men over 45, the prevalence rates of hypogonadism were 52.4% for obesity (OR 2.38), 50.0% for diabetes (OR 2.09), 42.4% for hypertension (OR 1.84), and 40.4% for hyperlipidemia (OR 1.47), the four criteria of the metabolic syndrome. 17 The more components of the metabolic syndrome are present, the higher is the prevalence of hypogonadism in men with SD.…”

Testosterone replacement therapy and voiding dysfunction

“…Numerous research studies in both animals and humans suggest that these receptors are completely saturated at near castration serum testosterone levels (approximately 50 ng/dL) (36). As such, young men with the maximum T in their lifetime do not develop large prostates and develop LUTS/BPH (47). Instead, prostatic size steadily increases with age despite lowering levels of testosterone (48,49).…”