Benign prostatic hyperplasia: etiological considerations.

P C Walsh

Home/Archive/PubMed

PubMed · 66685

Benign prostatic hyperplasia: etiological considerations.

P C Walsh

View original source ↗Export metadata ↓

Abstract

The evidence for a hormonal etiology of BPH in man and the dog has been reviewed. Experimentally, although the administration of testosterone or dihydrotestosterone or dihydrotestosterone plus estradiol failed to produce BPH in the dog, treatment with androstanediol or androstanediol plus estradiol produces many of the features characteristic of canine prostatic hyperplasia. This development may provide an experimental model for exploration of the pathogenesis of prostatic hyperplasia.

Explore related subjects

Androstane-3,17-diol Animals Castration Dihydrotestosterone Estradiol Humans Male Organ Size Prostate Prostatic Hyperplasia Testosterone Journal Article

Keep this discovery

Explore connections, maps & timelines

BibTeX RIS

P C Walsh. 1976. Benign prostatic hyperplasia: etiological considerations.. https://pubmed.ncbi.nlm.nih.gov/66685/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed1979

Coupling between steroid oxidoreductions in vivo. Deuterium transfer from [17alpha-2H]estradiol to C19 steroids.

Explore the source record for details and available documents.

Androstane-3,17-diol↗

PubMed1979

[Evidence of 5 alpha-androstane-3 beta, 6 alpha, 17 beta-triol and of 5 alpha-androstane-3 beta, 7 alpha, 17 beta-triol in the anterior pituitary of the prepuberal male rate].

Incubation of 3H-5 alpha-androstane-3 beta, 17 beta-diol with anterior pituitaries from immature male Rats led to the major production of polar radio-metabolites. Of these, 53 and 27% were identified with 5 alpha-androstane-3 beta, 6 alpha, 17 beta-triol and 5 alpha-androstane-3 beta, 7 alpha, 17 beta-triol, respectively. The formation of these trihydroxysteroids may be involved in the intracellular regulation of 5 alpha-androstane-3 beta, 17 beta-diol levels.

Androstane-3,17-diol↗

PubMed1979

Role of the pituitary gland in experimental hormonal induction and prevention of benign prostatic hyperplasia in the dog.

The antiandrogen, cyproterone acetate (CPA), prevents development of prostatic hyperplasia, induced in castrated dogs by a 6 month-treatment with 5 alpha-androstane-3 alpha, 17 beta-diol (A)alone or in combination with 17 beta-oestradiol (E2). The immunoperoxidase technique was used to study functional cell types in the pars distalis of the pituitary gland and to detect growth hormone (GH) and prolactin (PRL) target sites in the prostate gland. Homologous radioimmunoassays for estimation of serum canine GH and PRL concentrations were also performed. Treatment with the combinations A + E2 and A + E2 + CPA resulted in morphological indications of stimulated GH and PRL cells and depressed gonadotrophs. This correlates well with an increase in PRL-dependent staining in glandular epithelium and fibromuscular tissue of the prostate gland. However, basal serum PRL and GH levels were not significantly affected. Treatment with A and A + E2 stimulated, while additional treatment with CPA clearly suppressed adrenocorticotrophin/melanotrophin (ACTH/MSH) cells. These findings indicate that an endocrine imbalance in hypothalamic-pituitary-adrenal function may be involved in induction and prevention of prostatic hyperplasia in the dog.

Androstane-3,17-diol↗