THE PATHOGENESIS OF BENIGN PROSTATIC HYPERPLASIA - A PROPOSED HYPOTHESIS AND CRITICAL-EVALUATION

Citation
Jt. Grayhack et al., THE PATHOGENESIS OF BENIGN PROSTATIC HYPERPLASIA - A PROPOSED HYPOTHESIS AND CRITICAL-EVALUATION, The Journal of urology, 160(6), 1998, pp. 2375-2380
Citations number
54
Categorie Soggetti
Urology & Nephrology
Journal title
ISSN journal
00225347
Volume
160
Issue
6
Year of publication
1998
Part
2
Pages
2375 - 2380
Database
ISI
SICI code
0022-5347(1998)160:6<2375:TPOBPH>2.0.ZU;2-Q
Abstract
Purpose: We used expanding observations regarding effects of testicula r epididymal plasma and nonandrogenic testis factor(s) (NATF) on prost ate growth to propose and evaluate a hypothesis regarding the developm ent of benign prostatic hyperplasia (BPH) in man. Materials and Method s: Current experimental data regarding the presence of NATF were revie wed. The potential for their exposure to the prostate by various route s was assessed. These observations were coupled with recognized anatom ical, histological and epidemiological characteristics of BPH to const ruct a hypothesis regarding its pathogenesis. Results: In vivo observa tions in man, rats and dogs supported the systemic secretion of NATF. These factors probably are, at least in part, spermatogenesis related. In vitro evaluation of the effect of spermatocele derived testicular epididymal plasma on human prostate stromal cells indicated the presen ce of androgen independent and androgen synergistic stromal growth pro moters. These factors have potential local and systemic access to the prostate. The almost ubiquitous development of a regional, histologica lly variegated nodular growth occurring in the prostate in the androge n diminished environment of the aging man is compatible with local as well as systemic exposure to an age associated secretion of NATF. Conc lusions: We propose that human BPH is an induced phenomenon that is us ually initiated by local episodic exposure of periurethral prostate to mitogens secreted by the testis/epididymis. Once initiated, isolated or complex interacting proliferative stimuli from the testis/epididymi s and a variety of other sources may achieve exposure to the prostate by several routes and simulate prostate growth.