The pathogenesis of benign prostatic hyperplasia: a proposed hypothesis and critical evaluation.
OBJECTIVE
We used expanding observations regarding effects of testicular epididymal plasma and nonandrogenic testis factor(s) (NATF) on prostate growth to propose and evaluate a hypothesis regarding the development of benign prostatic hyperplasia (BPH) in man.


METHODS
Current experimental data regarding the presence of NATF were reviewed. The potential for their exposure to the prostate by various routes was assessed. These observations were coupled with recognized anatomical, histological and epidemiological characteristics of BPH to construct a hypothesis regarding its pathogenesis.


RESULTS
In vivo observations 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 presence of androgen independent and androgen synergistic stromal growth promoters. These factors have potential local and systemic access to the prostate. The almost ubiquitous development of a regional, histologically variegated nodular growth occurring in the prostate in the androgen diminished environment of the aging man is compatible with local as well as systemic exposure to an age associated secretion of NATF.


CONCLUSIONS
We propose that human BPH is an induced phenomenon that is usually 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/epididymis and a variety of other sources may achieve exposure to the prostate by several routes and simulate prostate growth.
Grayhack
J T
JT
Department of Urology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
Kozlowski
J M
JM
Lee
C
C
D000818:Animals; D004285:Dogs; D004822:Epididymis / Q000378:metabolism; D006133:Growth Substances / Q000378:metabolism*; D006801:Humans; D008297:Male; D011470:Prostatic Hyperplasia / Q000209:etiology* / Q000473:pathology; D051381:Rats; D013737:Testis / Q000378:metabolism
D006133:Growth Substances