Endocrine Abstracts

The benign prostatic hyperplasia (BPH) represents an enlargement of the epithelial and fibromuscular parts of the prostate. Although androgens per se do not cause BPH, an intact androgen metabolism is a prerequisite for the normal fetal and pubertal development of the prostate. Furthermore, growth factors play a role in the development of BPH. Animal experiments have shown that the prostate – similar to other organs of the reproductive tract – undergoes a neonatal steroid imprinting. In the present study the role of this neonatal steroid imprinting as well as the role of a peripubertal growth hormone excess for the development of the prostatic size and for the development of the tissue features with special regard to the ratio epithelium:stroma is investigated with the aim to create an animal model for human BPH. Newborn rats were injected with estradiol benzoate, dihydrotestosterone, testosterone propionate, finasteride, fadrozole or solvent. From day 45–59 of life part of the animals received 1IU/d human growth hormone. At day 60 all animals were sacrificed for investigation of prostatic histology. Pronounced fibromuscular hypertrophy, comparable to that seen in human BPH, was observed in neonatally androgen+GH treated rats, especially in the dorsal part of the prostate, but not in animals which had only received neonatal steroid treatment without additional peripubertal GH. Neonatal adrogens appear to increase the susceptibility of the rat prostate to growth factor stimuli as provided by GH. Furthermore, with the administration of peripubertal GH in neonatally androgen treated male rats for the first time an animal model was elaborated which is histologically comparable to human BPH.