goserelin and Prostatic-Hyperplasia

Topics: Adrenergic alpha-Antagonists; Cholestenone 5 alpha-Reductase; Clinical Trials as Topic; Drug Therapy, Combination; Finasteride; Gonadotropin-Releasing Hormone; Goserelin; Humans; Leuprolide; Male; Oxidoreductases; Prazosin; Prostatic Hyperplasia; Sulfonamides; Tamsulosin

The purpose of this study is to describe the benefits afforded by treatment with LH-RH analogues to patients with physical or mental disorders that consult for acute urinary retention or urinary symptomatology secondary to benign prostatic hypertrophy (BPH).. 52 patients with BPH in whom surgery was contraindicated due to poor mental or physical condition were treated with LH-RH analogue for six consecutive months a year for a period of three years. Thirty-eight patients had acute urinary retention and 14 had prostatic symptomatology.. Serum testosterone fell below 11 nmol/l. No significant changes in PSA levels were observed. Assessment of the prostate by DRE and US showed prostatic size had diminished. Voiding and postvoid residual urine improved and the bladder catheter could be withdrawn.. Our results show that treatment with LH-RH analogue can reduce the urinary symptoms and improve the quality of life of patients with BPH in whom surgery is contraindicated.

Topics: Contraindications; Follow-Up Studies; Gonadotropin-Releasing Hormone; Goserelin; Humans; Male; Prostatic Hyperplasia; Surgical Procedures, Operative; Time Factors; Urinary Bladder Neck Obstruction

Nineteen patients seen for AUR secondary to benign prostate hypertrophy and with high surgical risk, were treated with an LH-RH agonist (GOSERELIN). After six months of treatment a 43.28% decrease in the prostate volume was seen, Improvement, i.e., spontaneous miction, was achieved in 46.6% patients, although post-mictional volumes remained high.

Topics: Acute Disease; Aged; Aged, 80 and over; Goserelin; Humans; Male; Prostatic Hyperplasia; Urinary Retention

Gonadotropin-releasing hormone receptors (GnRHR) have been found in extrapituitary tissues, including the prostate, where they might exert a local effect on tissue growth. Degarelix is a GnRHR antagonist approved for use in patients with prostate cancer (PCa) who need androgen deprivation therapy. The slowing of prostate cell growth is a common goal shared by PCa and benign prostate hyperplasia (BPH) patients, and the effect of degarelix on BPH cells has not yet been investigated. We wanted to evaluate the direct effect of degarelix on human BPH primary cell growth. Gene expression studies performed with BPH (n=11), stage 0 (n=15), and PCa (n=65) human specimens demonstrated the presence of GNRHR1 and GNRHR2 and their respective endogenous peptide ligands. BPH-isolated epithelial and stromal cells were either cultured alone or co-cultured (1:4 or 4:1 ratio of epithelial to stromal cells) and subsequently treated with increasing concentrations of degarelix. Degarelix treatment induced a decrease in cell viability and cell proliferation rates, which occurred in parallel to an increase in apoptosis. Both epithelial and stromal BPH cells are sensitive to degarelix treatment and, interestingly, degarelix is also effective when the cells were growing in a co-culture microenvironment. In contrast to degarelix, the GnRHR agonists, leuprolide and goserelin, exerted no effect on the viability of BPH epithelial or stromal cells. In conclusion, (i) prostate tissues express GNRHR and are a potential target for degarelix; and (ii) degarelix directly inhibits BPH cell growth through a decrease in cell proliferation and an increase in apoptosis. Supporting information for this article is available online at http://www.thieme-connect.de/products.

Topics: Apoptosis; Cell Proliferation; Cells, Cultured; Gonadotropin-Releasing Hormone; Goserelin; Humans; Leuprolide; Male; Oligopeptides; Prostatic Hyperplasia

Benign prostatic hyperplasia (BPH) is related to advancing age and the presence of androgens and occurs in virtually all older men. BPH causes morbidity, most often by urinary obstruction, in a substantial fraction of men over sixty. Both finasteride and androgen ablation induce partial diminution in BPH that occurs over weeks to months. This is in contrast to the often rapid involution seen in both normal prostatic epithelium and prostatic carcinoma in response to androgen withdrawal. This study was performed to analyze the response of prostatic cells, and in particular BPH, to acute androgen ablation.. We subjected a cohort of 26 men to androgen ablation with goserelin, a gonadotrophin releasing hormone agonist, for 3-4 weeks prior to radical prostatectomy for prostate cancer. Preablation biopsy specimens and prostatectomy specimens were immunohistochemically stained for apoptotic cells and for expression of apoptosis regulatory proteins Bcl-2, Bax, Bcl-x, and Bak.. Normal prostatic epithelial cells and prostate cancer responded to hormone deprivation by undergoing apoptosis, but in 19/26 specimens prostatic hyperplasia had a total absence of apoptosis. In all 26 specimens, benign prostatic hyperplasia demonstrated increased expression of the Bcl-2 protein, but no change in the expression of Bax, Bcl-x, and Bak. In contrast, adjacent normal and malignant prostatic epithelium showed positive staining for apoptosis and did not alter Bcl-2 expression in response to androgen ablation.. BPH demonstrated increased staining for Bcl-2 after androgen deprivation that may render hyperplastic epithelium relatively resistant to apoptosis induced acutely by androgen withdrawal.

Topics: Apoptosis; bcl-2 Homologous Antagonist-Killer Protein; bcl-2-Associated X Protein; bcl-X Protein; Gonadotropin-Releasing Hormone; Goserelin; Humans; Male; Membrane Proteins; Prostatic Hyperplasia; Proto-Oncogene Proteins; Proto-Oncogene Proteins c-bcl-2; Up-Regulation

Twelve prostatic hyperplasia patients with total urine retention and, consequently, a permanent catheter, were treated for six months with luteinizing hormone-releasing hormone (LH-RH) analogue having long-term effect. Seven of the 12 patients no longer needed a permanent catheter after the six-month treatment period. Transurethral resection of the prostate was performed for 3 patients. The remaining 2 patients continued to have a catheter. The mean prostatic volume, which was 83 g at the start of the study, fell by 51 percent, to 41 g. Treatment with LH-RH proved to be safe even for patients in poor physical condition, and it also seemed to improve symptoms of prostatic hyperplasia.

Topics: Aged; Aged, 80 and over; Buserelin; Goserelin; Humans; Male; Middle Aged; Prostatic Hyperplasia; Ultrasonography; Urinary Retention

Topics: 5-alpha Reductase Inhibitors; Adrenergic alpha-Antagonists; Androgen Antagonists; Androstenes; Azasteroids; Buserelin; Finasteride; Goserelin; Humans; Leuprolide; Male; Prostatic Hyperplasia

Topics: Antineoplastic Agents; Buserelin; Gonadotropin-Releasing Hormone; Goserelin; Humans; Male; Prostatic Hyperplasia

We characterized the epidermal growth factor (EGF) receptor in the membrane fraction of prostatic tissue from men with benign prostatic hyperplasia (BPH). The maximum specific binding of [125I]EGF to the BPH membrane fraction was achieved after 30-min incubation at 35 C. Analysis of the binding data revealed two classes of binding sites, one of high affinity [Kd, 2.5 +/- 0.5 (+/- SE) x 10(-11) mol/L] and one of lower affinity (2.2 +/- 0.3 x 10(-9) mol/L). [125I]EGF binding was inhibited by excess EGF, but not by insulin, proinsulin, fibroblast growth factor, or insulin-like growth factors I and II. In prostatic tissue of men with BPH treated for 3 months with the GnRH agonist analog Goserelin (Zoladex, depot formulation), the binding capacities of both sites were significantly higher than those of BPH tissue from untreated men (P less than 0.001). These results demonstrate that prostatic tissue from men with BPH contains two classes of specific binding sites for EGF, and their levels are modulated by chronic GnRH agonists treatment.

Topics: Aged; Binding Sites; Buserelin; Dihydrotestosterone; Epidermal Growth Factor; ErbB Receptors; Goserelin; Humans; Male; Middle Aged; Models, Biological; Prostatic Hyperplasia; Testosterone