Light-microscopic stereologic analysis of spontaneous and steroid-induced canine prostatic hyperplasia

A combined light-microscopic and stereologic analysis of the canine prostate was performed under the following experimental conditions: intact and castrated dogs, spontaneous benign prostatic hyperplasia, intact and castrated dogs after treatment with testosterone, 5 alpha-dihydrotestosterone or 3 a...

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Published inThe Journal of urology Vol. 137; no. 3; p. 552
Main Authors Bartsch, G, Bruengger, A, de Klerk, D P, Coffey, D S, Rohr, H P
Format Journal Article
LanguageEnglish
Published United States 01.03.1987
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Abstract A combined light-microscopic and stereologic analysis of the canine prostate was performed under the following experimental conditions: intact and castrated dogs, spontaneous benign prostatic hyperplasia, intact and castrated dogs after treatment with testosterone, 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with estradiol. Regarding the absolute amounts of the glandular and stromal parts of the prostate as well as the glandular cells, no difference was found among the testosterone, 3 alpha-androstanediol and 5 alpha-dihydrotestosterone treated castrated dogs. Treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with 17 beta-estradiol induced a four-fold increase in glandular and a two-fold increase in stromal tissue. The glandular to stromal tissue ratio equals that found in spontaneous canine hyperplasia, which is indicative of the glandular type of spontaneous canine hyperplasia. Therefore, it can be stated that treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol combined with 17 beta-estradiol not only induces prostatic overgrowth but also leads to prostatic hyperplasia of the glandular type. However, the stereologic analysis of canine prostates following steroid administration shows that canine hyperplasia is primarily a glandular disease, while human benign prostatic hyperplasia shows more stromal activation.
AbstractList A combined light-microscopic and stereologic analysis of the canine prostate was performed under the following experimental conditions: intact and castrated dogs, spontaneous benign prostatic hyperplasia, intact and castrated dogs after treatment with testosterone, 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with estradiol. Regarding the absolute amounts of the glandular and stromal parts of the prostate as well as the glandular cells, no difference was found among the testosterone, 3 alpha-androstanediol and 5 alpha-dihydrotestosterone treated castrated dogs. Treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol in combination with 17 beta-estradiol induced a four-fold increase in glandular and a two-fold increase in stromal tissue. The glandular to stromal tissue ratio equals that found in spontaneous canine hyperplasia, which is indicative of the glandular type of spontaneous canine hyperplasia. Therefore, it can be stated that treatment with 5 alpha-dihydrotestosterone or 3 alpha-androstanediol combined with 17 beta-estradiol not only induces prostatic overgrowth but also leads to prostatic hyperplasia of the glandular type. However, the stereologic analysis of canine prostates following steroid administration shows that canine hyperplasia is primarily a glandular disease, while human benign prostatic hyperplasia shows more stromal activation.
Author Coffey, D S
Bartsch, G
Bruengger, A
Rohr, H P
de Klerk, D P
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Snippet A combined light-microscopic and stereologic analysis of the canine prostate was performed under the following experimental conditions: intact and castrated...
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StartPage 552
SubjectTerms Androstane-3,17-diol - toxicity
Animals
Castration
Dihydrotestosterone - toxicity
Dogs
Estradiol - toxicity
Male
Microscopy - methods
Prostate - pathology
Prostatic Hyperplasia - chemically induced
Prostatic Hyperplasia - pathology
Testosterone - toxicity
Title Light-microscopic stereologic analysis of spontaneous and steroid-induced canine prostatic hyperplasia
URI https://www.ncbi.nlm.nih.gov/pubmed/2434668
Volume 137
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