Benign Nodular Prostatic Hyperplasia Research Articles

Spectrum of prostate gland lesions: a clinico-pathologic study in south-western Bihar, India

Background: Prostate gland is an endocrine dependent organ in males and age-related lesions involve it. Inflammation, benign nodular hyperplasia and tumours are the commonest to involve it worldwide. Occasionally some other pathological changes can also involve it. The study was carried out for the first time to know the spectrum and prevalence of prostate lesions which will be of help to the clinicians in this location.Methods: Retrospective study was carried out for a period of four years and out of surgical cases of males which underwent operative procedure, prostate cases were retrieved and in the department of pathology, haematoxylin and eosin stained slides were evaluated and diagnosed.Results: A total of 138 cases were included and five cases were excluded from this series. Benign nodular hyperplasia (73.9%) was the commonest finding followed by chronic prostatitis associated with hyperplasia (15.2%), atypical glandular hyperplasia (2.9%) and prostatic intraepithelial neoplasia (2.1%). Malignant tumours were 5.8% constituting adenocarcinoma prostate as the most common (62.5%). A case of hemangiopericytoma was also diagnosed.Conclusions: Benign nodular hyperplasia of prostate is the most common affliction among males starting at age 45 years. Early consultation and screening will be of immense value. Adenocarcinoma prostate may involve at age around 58 years.

SOME CHARACTERISTICS OF AGE, ULTRASOUND AND THE RELATION BETWEEN THE PSA DENSITY AND THE HISTOPATHOLOGY OF BENIGN NODULAR PROSTATIC HYPERPLASIA AND PROSTATIC CARCINOMA

Background: PSA density by the ratio of tPSA/prostatic volume plays a meaningful role for the orientation of diagnosis and the screening of the prostatic diseases, especially for the prostatic carcinoma and benign nodular hyperplasia. Objectives: - To describe some characteristics of the age, ultrasound of the patient with the prostatic carcinoma and benign nodular hyperplasia; - To determine the relation between PSA density and the histopathology of the patient with the prostatic carcinoma and benign nodular hyperplasia. Materials and Method: cross-sectional study on 70 patients including 35 cases with benign nodular prostatic hyperplasia and 35 ones with carcinoma of the prostate. Results: The average age was the same between 2 groups of the diseases, 73 for prostatic carcinoma and 75 for benign nodular hyperplasia. 100% of the lesions was discovered by ultrasound, the average weight of the carcinoma and benign nodular hyperplasia was 57.3g and 46.9g respectively. The tPSA density was higher in carcinoma than in benign nodular hyperplasia (1.22 vs 0.10); With the tPSA density threshold >0.15, the prostatic carcinoma accounting for 78.4%, then the benign group only 21.6%; the Sensitivity and the Specificity were 82.9% and 77.1% respectively. Conclusions: PSA density should be applied for the diagnosis and the screening of the prostatic tumors beside the tPSA test. Key words: tPSA (total PSA), PSA density, ultrasound, prostatic carcinoma, benign nodular prostatic hyperplasia.

Phenotypic characterization of the infiltrating immune cells in normal prostate, benign nodular prostatic hyperplasia and prostatic adenocarcinoma

Background Immune cell infiltrate is a constant feature in normal prostate, benign nodular prostatic hyperplasia and prostatic adenocarcinoma. This study elaborates on the cells of the immune system present in normal prostate, benign nodular prostatic hyperplasia and prostatic adenocarcinoma. Hypothesis Here, we hypothesized that “the development of benign nodular prostatic hyperplasia and prostatic adenocarcinoma is associated with numeric alterations of the immune cell infiltrate”. Materials and methods A total of 50 transurethral prostatic resection specimens, each entailing normal prostate, benign nodular prostatic hyperplasia and high grade prostatic adenocarcinoma were evaluated for the density and phenotype of the immune cells using immunohistological methods and mouse monoclonal antibodies decorating T cells (CD3), histiocytes (CD68) and B lymphocytes (CD20). Results Immune cell infiltrate was composed of T cells, histiocytes and B-lymphocytes. CD +3 T lymphocytes and CD68 + cells were the predominant cell populations. We observed variations in the density of the immune cells among the normal prostate, benign nodular prostatic hyperplasia and high grade prostatic adenocarcinoma. Compared with normal prostate, benign nodular prostatic hyperplasia had a statistically significant high density of immune cells (3.4 ± 0.4versus 13.5 ± 1.0, P < 0.00). In contrast, a significant decrease in the counts of these cells was observed in high-grade prostatic adenocarcinoma compared to benign nodular prostatic hyperplasia (13.5 ± 1.0 versus 5.2 ± 0.3, P < 0.01). Conclusions The increased density of immune cells (predominantly CD +3 T cells) in benign nodular prostatic hyperplasia suggests that the initial response to cellular damage is mediated by cell-mediated immunity. The decreased density of immune cells in high-grade prostatic adenocarcinoma may reflect immunosuppression. The underlying mechanisms of these numeric variations are open for further investigations.

Metabolism of testosterone in the human prostate and seminal vesicles.

Tissue from the normal, hyperplastic and the cancerous human prostate as well as tissue from the human seminal vesicles are capable of metabolizing testosterone in vitro. By incubating minced tissue with 3H-testosterone for 2 hours at 37 degrees C the following radioactive metabolites were identified: testosterone (17 beta-hydroxyl-4-androsten-3-one), androstenedione (4-androstene-3,17-dione), androstanedione (5alpha-androstane-3,17-dione), 5alpha-dihydrostestosterone (17 beta-hydroxy-5alpha-androstane-3-one, DHT), 3alpha-androstanediol (5alpha-androstane-3alpha,17beta-diol), 3beta-androstanediol (5alpha-androstane-3beta-17beta-diol) and androsterone (3alpha-hydroxy-5alpha-androstane-17-one). When normal human prostatic tissue was incubated with 3H-testosterone approximately 40% of the hormone was metabolized and 30-35% of the metabolites were identified as DHT. There were apparently no differences in testosterone metabolism between the dorsal and lateral prostatic lobes. A much lower conversion of 3H-testosterone was observed in the seminal vesicles (24%). The same metabolites were formed by prostatic carcinoma tissue, although distinctive quantitative differences from the normal prostate were observed. Thus, only 23% of the testosterone was metabolized by cancerous tissue of which 15% was present as DHT. The formation of 17-keto metabolites and androstanediols in the prostatic carcinoma tissue was approximately the same as in the normal prostatic tissue. The most extensive metabolism of testosterone was found by incubation of tissue from benign nodular prostatic hyperplasia. About 65% of the testosterone was metabolized, and 40% of the metabolites were identified as DHT. Hyperplastic prostatic tissue also showed a significantly higher formation of 5alpha-androstanedoils and the other tissues examined. The high formation of DHT and 5alpha-androstanediols in benign nodular prostatic hyperplasia in comparison with normal and cancerous prostatic tissue and seminal vesicle tissue might indicate that these metabolites should be studied more closely as possible aetiological factors for prostatic hyperplasia. The very low metabolism of testosterone in prostatic carcinoma tissue should be examined further in relation to tumour differentiation and clinical effect of endocrine therapy.

Effect of anti-androgens on the uptake and binding of androgen by human benign nodular prostatic hyperplasia in vitro.

ABSTRACT The effect of anti-androgenic compounds on the uptake and binding of androgen in human benign nodular prostatic hyperplasia was studied in vitro. The two anti-androgenic compounds, Cyproterone (1,2α-methylene-6-chloro-4,6-pregnadien-17α-ol-3,20-dione) and 17α-methyl-β-nortestosterone (SK &amp; F 7690) were both capable of reducing the uptake of 3H-labelled testeosterone. In four patients, the average reduction caused by Cyproterone was 27 per cent and by 17α-methyl-β-nortestosterone 38 per cent. These two compounds were also capable of reducing the formation of androgen-macromolecular complexes both in the cytosol and in nuclei obtained from prostatic homogenates.

Medical Treatment of Benign Nodular Prostatic Hyperplasia with Cyproterone Acetate

Medical Treatment of Benign Nodular Prostatic Hyperplasia with Cyproterone Acetate

A Search for Inhibitors of Prostate Growth Stimulators

No AccessJournal of Urology1 Apr 1957A Search for Inhibitors of Prostate Growth Stimulators William Wallace Scott, William J. Hopkins, Wendell M. Lucas, and Charles Tesar William Wallace ScottWilliam Wallace Scott More articles by this author , William J. HopkinsWilliam J. Hopkins Present address: Henry Ford Hospital, Detroit, Mich. More articles by this author , Wendell M. LucasWendell M. Lucas American Cancer Society Clinical Fellow. Present address: Howard University School of Medicine, Washington, D. C. More articles by this author , and Charles TesarCharles Tesar More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)66615-1AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1957 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited ByScott W and Wade J (2018) Medical Treatment of Benign Nodular Prostatic Hyperplasia with Cyproterone AcetateJournal of Urology, VOL. 101, NO. 1, (81-85), Online publication date: 1-Jan-1969.Woodruff M and Perez-Mesa C (2018) The Effect of Hormonal Modification on Prostatic MorphologyJournal of Urology, VOL. 88, NO. 2, (273-280), Online publication date: 1-Aug-1962.Woodruff M and Umiker W (2018) The Effect of Estrogen and Androgen on the Rat Prostate Gland and TestesJournal of Urology, VOL. 84, NO. 1, (162-166), Online publication date: 1-Jul-1960.Marden H, Moon K and Milner W (2018) Inhibition of Endogenous Androgenic Response in the Rat By 19-nor-17-ethyl TestosteroneJournal of Urology, VOL. 82, NO. 5, (617-618), Online publication date: 1-Nov-1959. Volume 77Issue 4April 1957Page: 652-659 Advertisement Copyright & Permissions© 1957 by The American Urological Association Education and Research, Inc.MetricsAuthor Information William Wallace Scott More articles by this author William J. Hopkins Present address: Henry Ford Hospital, Detroit, Mich. More articles by this author Wendell M. Lucas American Cancer Society Clinical Fellow. Present address: Howard University School of Medicine, Washington, D. C. More articles by this author Charles Tesar More articles by this author Expand All Advertisement PDF DownloadLoading ...