Synergic inhibitory effects of the aromatase inhibitor 1‐methyl‐androsta‐1, 4‐diene‐3, 17‐dione and the antiandrogen cyproterone acetate on androstenedione‐ induced hyperplastic effects in the prostates of castrated dogs

Habenicht, U.‐F.; Etreby, M. F. El

doi:10.1002/pros.2990110205

Cited by 27 publications

(8 citation statements)

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“…Krawice and Heflin reported [9] that prostatic diseases are observed in 43.5% of male dogs brought to veterinary hospitals and BPH is the most prevalent age-related disease among intact male dogs. In treatment of BPH, because the prostate is an androgen (A)-dependent organ, orchidectomy [11] or treatment with anti-A agents [1,3] is performed. We previously showed that oral administration of chlormadinone acetate (CMA), which is a commercially available anti-A agent for human use, improved clincial symptoms during the early phase of BPH [4,10].…”

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confidence: 99%

“…Therefore, to inhibit BPH for a prolonged period, concurrent use of a CMA implant in addition to oral CMA administration may be recommended [6,12]. It has been shown recently that osaterone acetate (OSA), which is being developed as a therapeutic drug for canine BPH, inhibits BPH better than CMA [3,15]. To dogs with BPH, 0.1, 0.2, 0.5, 1.0 mg/kg of OSA was orally administered for one week, and the regression rate was observed.…”

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Effect of Osaterone Acetate Administration on Prostatic Regression Rate, Peripheral Blood Hormone Levels and Semen Quality in Dogs with Benign Prostatic Hypertrophy.

Tsutsui

Hori

Shimizu

et al. 2001

The Journal of Veterinary Medical Science

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ABSTRACT. The effects of osaterone acetate (OSA), which is an anti-androgen agent being developed as a therapeutic drug for benign prostatic hypertrophy (BPH) in dogs, on the degree of prostatic regression and semen qualities were investigated. Prostatic regression was compared between dogs with and without orchidectomy. Five male beagles aged 5-9 years were used in the experiment. OSA was orally administered at doses of 0.2 mg/kg and 0.5 mg/kg for one week. The prostatic regression rate one week after the end of administration was 62.6% on average. In the orchidectomized group, the mean regression rate one week after orchidectomy was 60.1%. However, the prostate became enlarged 6 months after administration, compared to the size prior to administration. The above findings suggested that OSA is clinically applicable as a therapeutic drug for BPH in dogs, and inhibits prostatic hypertrophy during the early phase. KEY WORDS: canine BPH, osaterone acetate, prostatic volume.

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Effect of Osaterone Acetate Administration on Prostatic Regression Rate, Peripheral Blood Hormone Levels and Semen Quality in Dogs with Benign Prostatic Hypertrophy.

Tsutsui

Hori

Shimizu

et al. 2001

The Journal of Veterinary Medical Science

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“…Treatment with CMA by injection or oral administration, however, was followed by relapses of BPH and required repeated medication. It was found that the effect of treatment with some anti-androgens on the canine prostate is equivalent to that of orchidectomy (O'Shea, 1962;Habenicht & Etreby, 1987). In this study it Was shown that the prostate-shrinking effect of CMAimplantation beginning 12 weeks after treatment is histologically equivalent to orchidectomy, and that the prostate is maintained at half of its pretreatment size.…”

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confidence: 56%

Comparison of the effects of chlormadinone acetate‐pellet implantation and orchidectomy on benign prostatic hypertrophy in the dog

et al. 1995

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Summary Five beagles out of 11 dogs aged 7–10 years with benign prostatic hypertrophy (BPH) were implanted subcutaneously with pellets of the synthetic anti‐androgen chlormadinone acetate (CMA) at a dose of 10 mg/kg bodyweight. The remaining six dogs (one beagle and five mongrel dogs) underwent bilateral orchidectomy. Changes in prostatic volume, histological findings in the prostate and the testis, and peripheral plasma levels of LH, testosterone and oestradiol‐17β (E2) were assessed up until 24 and 4 weeks after CMA‐implantation and orchidectomy, respectively. Measurements of the size of the prostate and biopsies of the prostate were performed by laparotomy. Mean prostatic volume had decreased to 71% and 41%, respectively, of its pretreatment volume, by 4 weeks after CMA‐implantation and orchidectomy, and was 49% and 47%, respectively, of pretreatment volume at 12 and 24 weeks after CMA‐implantation. The clinical signs of BPH, e.g. haematuria, resolved within 2 weeks after either treatment. When the prostate was examined histologically 4 weeks after either treatment, hardly any evidence of active secretion (e.g. glandular epithelium projecting markedly into the lumen), was observed in CMA‐implanted dogs, alveolar diameter and height of the glandular epithelium had decreased markedly and the glandular lumen had become very small in the orchidectomized dogs. By 12 weeks after CMA‐implantation, degenerative and atrophic glands were observed in the prostate nearly the same as at 4 weeks after orchidectomy. In the testis the number of germ cells in the seminiferous tubules decreased markedly after CMA‐implantation. The mean level of plasma LH at 4 weeks after orchidectomy had increased to 14.9 ng/ml, twice the value before operation. The mean levels of plasma testosterone and E2 at 4 weeks after CMA‐implantation had decreased to 0.7 ng/ml and 9 pg/ml from 1.5 ng/ml and 15 pg/ml, the values before treatment, respectively. CMA‐implantation resulted in poor semen quality. The results indicate that CMA‐implantation at a dose of 10 mg/kg results in the same prostate‐shrinking effect as orchidectomy.

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“…Our previous canine studies on this subject had been carried out in castrated animals. Bypassing the pituitary-gonadal axis and treating the animals simultaneously with androstenedione and an aromatase inhibitor, we succeeded in antagonizing the increase in prostate weights that can be induced by the aromatizable androgen androstenedione [9]. In addition, we were able to demonstrate, under the same conditions, that combined treatment with an aromatase inhibitor plus an antiandrogen has a synergic inhibitory effect.…”

Section: Introductionmentioning

confidence: 83%

Selective inhibition of androstenedione‐induced prostate growth in intact beagle dogs by a combined treatment with the antiandrogen cyproterone acetate and the aromatase inhibitor 1‐methyl‐androsta‐1,4‐diene‐3,17‐dione (1‐methyl‐ADD)

Habenicht¹,

Etreby²

1989

The Prostate

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Interference with estrogenic and androgenic actions might result in an inhibitory effect of benign prostatic hyperplasia (BPH). In the present study the effects of the treatment of intact, adult beagle dogs with the antiandrogen cyproterone acetate (CPA) and the aromatase inhibitor 1-methyl-ADD either alone or in combination on androstenedione-induced prostate growth and on testes, epididymides, and the pituitary was investigated. 1-Methyl-ADD induced a marked counterregulatory increase in the serum testosterone and dihydrotestosterone (DHT) concentrations leading to hyperplasia of the glandular part of the prostate. However, the aromatase inhibitor antagonized the androstenedione-induced (estrogen-related) stimulation of the fibromuscular stroma of the prostate. CPA caused a complete atrophy of the prostate that was also present after treatment with both the aromatase inhibitor and CPA in spite of a striking elevation of the serum testosterone and DHT levels and in spite of the antagonization of the inhibition of testes and epididymal weight induced by androstenedione plus CPA. This indicates a selective inhibition of the prostate of intact beagle dogs treated with CPA and 1-methyl-ADD.

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Synergic inhibitory effects of the aromatase inhibitor 1‐methyl‐androsta‐1, 4‐diene‐3, 17‐dione and the antiandrogen cyproterone acetate on androstenedione‐ induced hyperplastic effects in the prostates of castrated dogs

Cited by 27 publications

References 30 publications

Effect of Osaterone Acetate Administration on Prostatic Regression Rate, Peripheral Blood Hormone Levels and Semen Quality in Dogs with Benign Prostatic Hypertrophy.

Effect of Osaterone Acetate Administration on Prostatic Regression Rate, Peripheral Blood Hormone Levels and Semen Quality in Dogs with Benign Prostatic Hypertrophy.

Comparison of the effects of chlormadinone acetate‐pellet implantation and orchidectomy on benign prostatic hypertrophy in the dog

Selective inhibition of androstenedione‐induced prostate growth in intact beagle dogs by a combined treatment with the antiandrogen cyproterone acetate and the aromatase inhibitor 1‐methyl‐androsta‐1,4‐diene‐3,17‐dione (1‐methyl‐ADD)

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