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,17β-Diol Glucuronide Excretion in Patients with Benign Prostatic Hyperplasia*
Service de Biochimie, CHU Pitié-Salpêtrière (F.W., R.P., M.B., F.B., A.D.),75634 Paris Cedex 13 75634 Paris Cedex 13
Departement dEndocrinologie de la Reproduction, Hopital Necker (PM.-J 75730 Paris Cedex 15, France
Urinary testosterone and 3
-androstanediol (3adiol G) glucuronides together with plasma testosterone, 5adihydrotestosterone(DHT), and
4-androstenedione (
4) 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 3
diol G excretion together withthe highest mean plasma DHT.
This low urinary 3
diol G excretion, which reflects a decreasein both androgen production and DHT metabolism, suggests a decrease in 3
-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.
* Results presented in part at the 65th Annual meeting of The Endocrine Society, San Antonio, TX, 1983 (Abstract 667).
Received July 6, 1984.
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M. H. Choi, J. N. Kim, and B. C. Chung Rapid HPLC-Electrospray Tandem Mass Spectrometric Assay for Urinary Testosterone and Dihydrotestosterone Glucuronides from Patients with Benign Prostate Hyperplasia Clin. Chem., February 1, 2003; 49(2): 322 - 325. [Full Text] [PDF] |
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