Decreased Urinary 5a-Androstane-3α,17β-Diol Glucuronide Excretion in Patients with Benign Prostatic Hyperplasia*

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Abstract
Urinary testosterone and 3α-androstanediol (3adiol G) glucuronides together with plasma testosterone, 5adihydrotestosterone(DHT), and Δ4-androstenedione (Δ4) weremeasured in 43 normal young men (18−36 yr old), 23 elderlymen without clinically evident prostatic pathology (54−89 yrold), 68 elderly men with benign prostatic hyperplasia (BPHgroup; 54−91 yr old), and 26 elderly men with well differentiatedcancer of the prostate (K group; 63−97 yr old). Plasma testosteronedecreased slightly with age in all 3 elderly groups (from 591 to 438, 479, and 444 ng/100 ml, respectively). Plasma DHT,on the contrary, was significantly (P< 0.01) higher in the BPHgroup than in the other three groups (68 vs. 30, 37, and 32 ng/100 ml, respectively). Plasma 4 was significantly lower (P <0.01) in the elderly K group than in all other groups (59 vs. 109,83, and 78 ng/100 ml, respectively). Urinary testosterone glucuronidedecreased with age in all 3 elderly groups (from 109 to55, 38, and 44 <g/24 h, respectively) as a result of decreasedandrogen production rates with age. All 3 elderly groups alsohad decreased urinary 3a diol G, from 194 to 123, 55, and 118 <g/24 h, respectively. The group of elderly patients with BPHhad the lowest mean urinary 3α diol G excretion together withthe highest mean plasma DHT. This low urinary 3α diol G excretion, which reflects a decreasein both androgen production and DHT metabolism, suggests a decrease in 3α-hydroxysteroid dehydrogenase activity, which, inturn, could explain the increased DHT availability and tissueretention in most target organs. Moreover, the extent of thesemodifications in androgen metabolism specific to the BPH conditionraises the question of an overall alteration of androgenmetabolism in patients with BPH which could be the cause ofthe disease.