Tissue content of dihydrotestosterone in human prostatic hyperplasis is not supranormal.

Abstract

A B S T R A C T The dihydrotestosterone content of normal peripheral and benign hyperplastic prostates was measured in tissue obtained at open surgical procedures on 29 men of ages 36 to 82 yr. The dihydrotestosterone content in normal prostates (mean±SE, 5.1±0.4 ng/g tissue) and in benign hyperplastic prostates (5.0±0.4) was similar. In 11 patients in whom both normal and hyperplastic prostatic tissue was harvested simultaneously at the same operation, there was no significant difference in the content of dihydrotestosterone in the two types of tissue. These findings fail to confirm the widespread belief that dihydrotestosterone content is elevated in benign hyperplastic prostates. Our data differ from the reported literature in one major respect: the dihydrotestosterone content of normal peripheral prostate in this study is three to four times higher than previously reported. This difference between the present and earlier studies was resolved by experiments performed on cadavers, which were the source of normal prostatic tissue used by other investigators. Dihydrotestosterone content was measured in seven cadavers ranging in age from 19 research into the etiology of BPH has focused on factors that may be responsible for this accumulation of supranormal levels of dihydrotestosterone and the mechanismn by which this induces prostatic hyperplasia. Recently, while investigating the value of dihydrotestosterone content as a marker for the hormonal responsiveness of prostatic cancer, we noted that the content of dihydrotestosterone in normal and benign hyperplastic tissues obtained at open surgical procedures was similar. In reviewing the literature to determine why we were unable to confirm the findings of others, we learned that the "elevated" levels of dihydrotestosterone in BPH which were reported by others were based upon measurements performed on surgically removed specimens, whereas the "low levels" of dihydrotestosterone in normal tissue were based upon measurements performed on tissues obtained at autopsy (4-8). This observation suggested that the conditions of tissue harvesting may have significantly influenced the endogenous levels of androgens within the prostate. To explore this possibility, the present study was undertaken. Dihydrotestosterone content in normal and benign hyperplastic tissue has been measured in tissues removed at open surgical procedures and at autopsy on men of varying ages. These data suggest that the dihydrotestosterone content of prostatic tissue removed at autopsy is abnormally low. This finding was confirmed by in vitro incubations of prostatic tissue at 37°C that demonstrated rapid disappearance of dihydrotestosterone. These data indicate that when prostatic tissue is harvested appropriately, the dihydrotestosterone content of normal peripheral and hyperplastic tissues is the same. This finding should influence future research into the etiology of BPH. carcinoma of the prostate (eight patients), and radical cystoprostatectomy for the treatment of carcinoma of the bladder (15 ...

Serum Testosterone, 17β-Estradiol and PSA Levels in Subjects with Prostate Disorders

“…It has been reported that, 17b-estradiol and DHT work synergistically to promote prostate carcinogenesis [23]. Estrogen renders the prostatic cells susceptible to the action of DHT [24]. This study showed that, there was no significant difference between the serum levels of 17b-estradiol in patients with BPH when compared with controls.…”

Pathology of benign prostatic hyperplasia

“…Thus, the action of testosterone and DHT in the prostate is mediated indirectly through autocrine and paracrine pathways. The prostate, unlike other androgen-dependent organs, maintains its ability to respond to androgens throughout life, and levels of androgen receptors 10,11 as well as DHT 12 in the prostate remain high throughout aging. Two steroid 5a-reductase enzymes have been discovered, each encoded by a separate gene.…”

A role for epithelial-mesenchymal transition in the etiology of benign prostatic hyperplasia

“…Men castrated before puberty do not develop BPH (5) and, in men with genetic disorders that inhibit androgen production or androgen action, prostatic growth is impaired (6). Thus, androgen is thought to play a permissive role in BPH and, although levels of DHT are not elevated in BPH (7,8), 5␣-reductase inhibitors do relieve the symptoms of the disease (6).…”