Pathogenesis Of BPH Research Articles

The Role of Inflammation and Immune Dysregulation in the Pathogenesis of BPH

The Role of Inflammation and Immune Dysregulation in the Pathogenesis of BPH

PO-150 Modulation of the expression of casein kinase i isoform alpha in the initiation and progression of prostate cancer

IntroductionProstate cancer (PC) is the first cause of fatality related to the reproductive system in men. One out of seven men encounter this pathology once in their lifetime. Prostate Specific Antigen along with digital rectal exam are the first line of screening for prostate pathologies but numerous studies showed that these techniques lack specificity and in sometimes validity for screening. From this notion comes the need to find new biomarkers and molecular players that help get an early detection and effective treatment of PC. Casein Kinase 1 Alpha (CSNK1A1) is an enzyme involved in multiple cellular processes such as the regulation of the oncogenic Wnt/beta-catenin signalling pathway. Its implication in carcinogenesis and cancer progression is still unclear. In this study, we aim to establish a CSNK1A1 expression profile in BPH and in differently advanced PC grades and to investigate the localization of the enzyme compared to beta catenin in the different samples.Material and methodsFormalin-fixed paraffin-embedded human prostatic tissues were collected as follows: 85 BPH, 64 PC and 3 controls. Gene expression was assessed by quantitative RT-PCR of cellular transcripts. Protein localization was monitored by tissue immunostaining for CSNK1A1 and Beta-Catenin. Further in-vitro validation of the results is to be made on normal prostate epithelial cell line and PC cell lines using RT-PCR and western blotting.Results and discussionsWe were able to identify a continuous increase in the CSNK1A1 expression between controls, BPH and PC. These results are being validated in vitro. Preliminary immunostaining results showed membranous beta catenin in BPH and that seemed to be more heterogeneous in PC sections. A correlation with CSNK1A1 localization and amount is still to be achieved. Our results suggest a role of CSNK1A1 in the pathogenesis of BPH and PC by working on the proliferation induction axis, and malignant behaviour of cells. Our staining results suggest a minor role of beta catenin and Wnt pathway in these axes from which emerges the need to deeply investigate the pathways in which CSNK1A1 is implicated in BPH and PC initiation and progression.ConclusionOur results suggest an increase in CSNK1A1 in BPH and PC, which flags this protein as a potential marker in the progression of PC. More investigation is needed to verify whether this protein is involved in cancer initiation or in the direct inhibition of the oncogenic Wnt/beta-catenin signalling pathway and other pathways.

MP04-20 INCREASED RISK OF BPH, LOWER URINARY TRACT SYNDROMES, PROSTATITIS, AND KELOIDS IN MEN WITH PEYRONIE'S DISEASE: ANALYSIS OF UNITED STATES CLAIMS DATA

You have accessJournal of UrologyBenign Prostatic Hyperplasia: Epidemiology & Evaluation1 Apr 2018MP04-20 INCREASED RISK OF BPH, LOWER URINARY TRACT SYNDROMES, PROSTATITIS, AND KELOIDS IN MEN WITH PEYRONIE'S DISEASE: ANALYSIS OF UNITED STATES CLAIMS DATA Alexander W. Pastuszak, Katherine M. Rodriguez, Taylor P. Kohn, Larry I. Lipshultz, and Michael L. Eisenberg Alexander W. PastuszakAlexander W. Pastuszak More articles by this author , Katherine M. RodriguezKatherine M. Rodriguez More articles by this author , Taylor P. KohnTaylor P. Kohn More articles by this author , Larry I. LipshultzLarry I. Lipshultz More articles by this author , and Michael L. EisenbergMichael L. Eisenberg More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2018.02.170AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES The subsequent health risks associated with a diagnosis of Peyronie's Disease (PD) are unknown. This cohort study determines the risk of developing urologic disease, chronic health conditions, and autoimmune disease after a diagnosis of PD. METHODS We assessed the incidence of 25 common chronic conditions and 13 autoimmune diseases in a cohort of men using data from the Truven Health MarketScan database between 2007-2013. The cohort included men with one of three exposures: (1) men with PD, (2) men with erectile dysfunction (ED) but not PD, and (3) men without PD or ED, matched on age and follow-up duration. Men with a diagnosis of a co-prevalent condition at the time or within 1 year of PD diagnosis were excluded. Disease incidence was assessed utilizing a Cox regression model adjusted for age, smoking, obesity, visits per year, and years of follow-up. RESULTS We included 8,728 men with PD, 204,147 men with ED, and 87,280 controls. Men with PD had an increased risk of developing BPH (HR 1.21, 95% CI 1.16-1.27), prostatitis (1.21, 1.12-1.31), and lower urinary tract symptoms (LUTS) (1.10, 1.05-1.16) when compared to both men with ED and age-matched controls without ED or PD. Compared to controls, men with PD also had an increased risk of developing keloids (1.56, 1.16-2.11). No significantly increased risk for any autoimmune disorders was observed. Of note, the pathogenesis of PD, BPH and keloids is dependent in part on myofibroblast activity, suggesting a common etiology for these conditions. CONCLUSIONS Men with PD have an increased risk of developing BPH, LUTS, prostatitis and keloids. This may be related to myofibroblast activity, and these findings support a common etiology for these conditions that may manifest at different points during the male life cycle. © 2018FiguresReferencesRelatedDetails Volume 199Issue 4SApril 2018Page: e41 Advertisement Copyright & Permissions© 2018MetricsAuthor Information Alexander W. Pastuszak More articles by this author Katherine M. Rodriguez More articles by this author Taylor P. Kohn More articles by this author Larry I. Lipshultz More articles by this author Michael L. Eisenberg More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...

Regulatory network analysis of hypertension and hypotension microarray data from mouse model

ABSTRACTWe aimed to identify the potential genes related to blood pressure regulation and screen target genes for high blood pressure (BPH) and low blood pressure (BPL) treatment. The GSE19817 microarray dataset, which included the aorta, liver, heart, and kidney samples from BPH, BPL, and normotensive mice, was downloaded from the Gene Expression Omnibus. Principal component analysis (PCA) was performed based on the entire expression profile. Differentially expressed genes (DEGs) were screened, followed by pathway enrichment analysis. Finally, gene regulatory networks were constructed based on BPH-related and BPL-related DEGs in the aorta, liver, heart, and kidney samples. As a result, DEGs were screened within their respective tissues due to high heterogeneity of different tissues. Totally, 2,726 BPH-related DEGs and 2,472 BPL-related DEGs were screened, which were mainly enriched in pathways such as immune response. The topology data of gene regulatory networks constructed by DEGs in the heart, kidney, and liver were similar than that in aorta. Finally, among BPH-related DEGs, Sept6 and Pigx were found in the top 10 differentially regulated DEGs by comparing the BPH-related DEGs of the aorta with the DEGs of the other 3 tissues in the regulatory network. Although among the top 10 differentially regulated BPL-related DEGs, no common differentially regulated DEGs were found, Wif1, Urb2, and Gtf2ird1 were found among the top ten DEGs in the three tissues other than the kidney tissue. Sept6 and Pigx might participate in the pathogenesis of BPH, whereas Gtf2ird1, Urb2, and Wif1 might be critical target genes for BPL treatment.

Metabolic syndrome and prostatic disease: potentially role of polyphenols in preventive strategies. A review.

ABSTRACTBenign prostatic hyperplasia and prostate cancer are two common urological diseases of the elderly. Scientific community has always looked for a link that could explain the correlation between the two diseases and the role of chronic inflammation in the pathogenesis of BPH and PCa. As shown by the reports of the two diseases relationship with oxidative stress and metabolic syndrome, the use of compounds with antioxidant action could therefore affect both the symptoms and their onset. Polyphenols appear to act not only against oxidative stress but also at different levels. The aim of this review is to evaluate the role of the most important polyphenols on these two urological diseases. As antioxidants these compounds seems to have a direct action on the cell cycle and hormone function, important for both prostate cancer and BPH. Despite a large number of articles about the relationship of the polyphenols with prostate cancer, very little evidence exists for BPH. Additional clinical trials or meta-analysis are necessary on this topic.

HORMONAL DISTURBANCES IN PATIENTS WITH BENIGN PROSTATE HYPERPLASIA

Ihsan S Sahi*, Mukhallad A Ramadhan@ & Sadiq U Khadim# *CABS, Head, Dept. of Surgery. @#MSc, Department of Pathology, University of Missan, College of Medicine, Missan, IRAQ. Abstract Benign prostatic hyperplasia (BPH, benign prostatic hypertrophy), a non-malignant abnormal growth of the prostate gland, affects almost all men in some degree as they age and can cause a significant disruption of lifestyle due to urinary outflow obstructive and irritative symptoms. The present study was performed on patients with BPH and other group of normal persons (40 person for each) to evaluate some of hormonal changes that result in BPH. The blood samples were collected from the groups of study those were of ages 45 and more and serum levels of both estrogen and testosterone were evaluated, as well as tissue of prostate were collected from some of the patients after surgery and estrogen receptors were estimated by immunohistochemisitry. The results shows significant reduction of the testosterone with elevation of the estradiol levels with marked expression of estrogen receptors in both epithelial and stromal cells of the prostate in patients. In conclusion, the present study found that sex hormonal disturbances associated with increase age of the person was implicated in the pathogenesis of BPH.

An introduction to acinar pressures in BPH and prostate cancer

Intra-acinar and peri-acinar pressures in the prostate might be key factors in the evolution of its zonal morphology and the pathogenesis of BPH and cancer. Herein, I hypothesize that intra-acinar pressures lead to a decrease in apoptosis by distending or stretching acinar epithelium and its surrounding stroma. Increased prostatic smooth muscle content and tone might generate peri-acinar pressures, which could, in the long-term, counteract intra-acinar pressures and decrease epithelial stretch. Thus, it is proposed that BPH (characterized by increased prostatic smooth muscle and, therefore, raised peri-acinar pressures) might decrease the risk of prostate cancer progression by counteracting intra-acinar pressures. In the context of this theory, the transition zone might have evolved as a specialized region within the prostate that can mount a concerted stromal-epithelial response to increased urethral and intra-acinar pressures (BPH), and the urethral angulation, anterior stroma and the prostatic capsule have an adjunctive evolutionary role in this phenomenon.

Lower urinary tract symptoms and depression

Study Type--Symptom prevalence (cohort) Level of Evidence 2b. What's known on the subject? and What does the study add? Depression plays an important role in pathogenesis of BPH. Our study shows that prostatic symptoms can be helpful in the screening for depression. • To evaluate the relationship between lower urinary tract symptoms (LUTS) and depression in men through validated questionnaires. • Healthy male workers (n = 673) were invited to a free health check-up. • Patients underwent a detailed medical examination. • All participants completed the International Prostate Symptom Score (IPSS) questionnaire and the Beck Depression Inventory (BDI). • Under multiple logistic regression analysis (adjusted for total testosterone and age), a significant effect of IPSS on BDI score was observed: mild depression (BDI score >9): odds ratio (OR) 1.092, 95% confidence interval (CI) 1.056-1.129; P < 0.001; moderate-to-severe depression (BDI score >19): OR 1.093, 95% CI 1.031-1.159; P = 0.003; and severe depression (BDI score >29): OR 1.176, 95% CI 1.048-1.320; P = 0.006. • In healthy men, LUTS are significantly associated with depression. • The treatment of LUTS is very important for the mental health of older men.

1978 EFFECTS OF SERENOA REPENS, SELENIUM AND LYCOPENE ON CHRONIC INFLAMMATION ASSOCIATED WITH BPH: RESULTS OF A MULTICENTRE ITALIAN STUDY “FLOG” (FLOGOSIS AND PROFLUSS IN PROSTATIC AND GENITAL DISEASE)

1978 EFFECTS OF SERENOA REPENS, SELENIUM AND LYCOPENE ON CHRONIC INFLAMMATION ASSOCIATED WITH BPH: RESULTS OF A MULTICENTRE ITALIAN STUDY “FLOG” (FLOGOSIS AND PROFLUSS IN PROSTATIC AND GENITAL DISEASE)

Does intraprostatic inflammation have a role in the pathogenesis and progression of benign prostatic hyperplasia?

To compare the incidence of acute and/or chronic intraprostatic inflammation (ACI) in men undergoing transurethral resection of the prostate (TURP) for urinary retention and lower urinary tract symptoms (LUTS), as recently a role was suggested for ACI in the pathogenesis and progression of BPH, and urinary retention is considered an endpoint in the natural history of this condition. Details of TURPs done between January 2003 and December 2005 at one institution were obtained from the operating theatre database. Patients were divided by indication (retention/LUTS). Clinical data and histology reports were then reviewed and bivariate and logistic regression used to compare the pathological features between these groups. Of 406 patients, 374 had evaluable data; 70% of men with urinary retention had ACI, vs 45% of those with LUTS (P < 0.001). On logistic regression, the pathological factors associated with TURP for acute retention compared to that for LUTS were ACI, old age, and resection weight to a lesser degree. Inflammation appears to be important in the pathogenesis and progression of BPH. In this study, the risk of urinary retention due to BPH was significantly greater in men with ACI than in those without, and the association of TURP for retention with ACI was stronger than that with prostate weight. This finding might offer new avenues for the medical treatment of men with LUTS due to BPH.

Increased growth factor production in a human prostatic stromal cell culture model caused by hypoxia.

Local hypoxia may be one of the triggers of embryonic reawakening of the stroma and subsequent hyperplastic growth in the prostate. Using a cell culture model of human prostatic stromal cells, we investigated the effects of hypoxia on activation of hypoxia-inducible factor 1 (HIF 1) and on the production of growth factors. Primary prostatic stromal cells were grown in normal and hypoxic (1% O(2)) atmosphere. Activation of HIF 1 was evaluated after different time intervals by Western blot. Induced secretion of growth factors VEGF, FGF-7, TGF-beta, IL 8, and FGF-2 were analyzed by ELISA. To confirm the in vitro findings we also performed immunohistochemistry of HIF 1alpha as well as pro-collagen I, collagens I, III, and IV in the benign tissue of radical prostatectomy specimens. HIF 1 is activated in a time-dependent manner, already starting 1 hr after exposure of stromal cells to hypoxic conditions. Secretion of VEGF, FGF-7, TGF-beta, FGF-2, and IL 8 is increased under hypoxic in vitro conditions in comparison to normoxia. Levels of TGF-beta, VEGF, and IL 8 were rapidly and statistically significantly increased in the supernatant of hypoxic cells. Consistent with the in vitro findings, immunohistochemistry of HIF 1alpha in (benign prostatic hyperplasia) BPH tissue revealed strong HIF 1alpha nuclear staining in hyperplastic areas. No difference was observed in the collagen pattern between hyperplastic and normal prostate tissue. Prostatic stromal cells respond to hypoxia by upregulation of secretion of several growth factors suggesting that hypoxia can trigger prostatic growth. Therefore, hypoxia might be a key factor contributing to the pathogenesis of BPH.

Norepinephrine activates P44 and P42 MAPK in human prostate stromal and smooth muscle cells but not in epithelial cells.

In vascular smooth muscle cells, alpha1-adrenergic stimulation increases DNA synthesis and cell proliferation via activation of p44/42 (ERK1/2) MAPK. We examined whether norepinephrine (NE) activates MAPK and stimulates the proliferation of prostatic epithelial and non-epithelial cells. Human prostatic epithelial cells, stromal cells, and smooth muscle cells were purchased from BioWhittaker (Walkersville, MD). After reaching a semi-confluent condition, the cells were cultured in RPMI-1640 without serum for 1 day. At 10 min after adding NE (10(-6) or 10(-7) M) to the medium, the cells were collected. Cell lysate was analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) followed by Western blot using anti-phospho-p44/42 and anti-p44/42 antibodies. The activation of p44/42 was estimated by the ratio of phospho-p44/42 to total p44/42. Cell proliferation was evaluated by (3)H-thymidine uptake assay. After reaching a semi-confluent condition, the cells were cultured in RPMI-1640 containing 0.5% FCS with or without NE (10(-6) or 10(-7) M) for 16 hr followed by a (3)H-thymidine uptake period (24 hr). P44/42 MAPK was significantly activated by NE in non-epithelial cells (stromal cells and smooth muscle cells) while not in epithelial cells. The uptake of (3)H-thymidine was significantly increased by NE in both non-epithelial cells, which was inhibited by alpha1-adrenoceptor antagonists. These results suggest that NE may stimulate the proliferation of non-epithelial prostatic cells, which may be involved in the pathogenesis of BPH.

Life-Style in Patients with LUTS Suggestive of BPH

Background: Owing to the existing controversy about the role of life-style in the pathogenesis of BPH, the possible associations of LUTS and prostate enlargement with alcohol intake, coffee consumption, smoking, physical activity, body mass index (BMI) and concomitant diseases were studied in the large series of patients of the QUIBUS study. Results: Among concomitant diseases, essential hypertension was the most represented. However no apparent additive or synergistic influence on symptoms was recorded in this subset of the population. Coffee consumption was not associated with prostate volume or LUTS. Alcohol consumption was associated with urgency and intermittence and with an overall higher IPSS. No major influence on symptoms was found in smokers. Physical activity was associated with a lower frequency of incomplete bladder emptying, repeated urination, intermittence and urgency. The postulated existence of an association between BMI and BPH was not confirmed in this study. When a prediction of the IPSS scores was tempted by entering the life-style factors in a multiple regression model, they were able to explain at best 5% of the variance of the dependent variable. Conclusion: Life-style patterns bear a greater influence on individual symptoms than on total scores. This difference is sometimes high enough to recommend specific life-style measures to patients with LUTS and prostate enlargement.

Cell lineage characteristics of human prostatic stromal cells cultured in vitro.

An in vitro model of prostatic stromal cells suitable for experimental studies of the pathogenesis of BPH is still lacking. We therefore standardized the isolation, cultivation, and characterization of human prostatic stromal cell lineages. Stromal cells were isolated from a surgical specimen of BPH. Using antibodies specific for either epithelial or stromal cells of the human prostate, the isolated cells were morphologically and immunohistochemically characterized. Viability and functional activity were assessed by proliferation assays and stimulation experiments. Gene expression was monitored by RT-PCR. In early passages (P8), cells showed a high purity (>/=98%) for stromal markers; about 60% displayed the characteristics of fibroblasts, and the remaining 40% were classified as smooth muscle cells. In late passages (P20), the proportion of muscle cells declined to 10%. Stimulation experiments including basic fibroblast growth factor (bFGF) resulted in enhanced proliferation, whereas dihydrotestosterone (DHT), estrogen, and flutamide did not influence proliferation. Gene expression studies demonstrated a positive signal for androgen receptor and keratinocyte growth factor (KGF). Prostatic stromal cells can be propagated several times and show karyotypic stability for up to 18 subculture experiments. The ratio of myoid and fibroblastic cells can be used for standardization of cell cultures with stable characteristics.

CHARACTERIZATION OF A STROMAL CELL MODEL OF THE HUMAN BENIGN AND MALIGNANT PROSTATE FROM EXPLANT CULTURE

Purpose There is a lack of suitable in vitro models for the human prostate. To study stromal-epithelial interactions, we established stromal cells in cultures from benign and malignant prostate tissue that resemble more closely the in vivo conditions of the human prostate. Materials and Methods Stromal cells were obtained from explant primary culture, established in DU145 cell conditioned medium and maintained in RPMI-fetal bovine serum (FBS) supplemented with insulin, transferrin and selenium (ITS). Proliferation studies to compare different media were performed using a 3 [H]thymidine assay. Stromal cells were characterized by immunocytochemistry using epithelial and mesenchymal markers. Morphology was evaluated by electron microscopy, light and phase-contrast microscopy. Androgen receptor (AR) mRNA expression was measured by polymerase-chain-reaction (PCR). The response to different concentrations of dihydrotestosterone (DHT) and the antihormones flutamide and hydroxyflutamide was tested by 3 [H] thymidine assay. Results Microscopic evaluation revealed typical stromal morphology with elongated cell shapes, cilia, collagen and microfilaments. Immunocytochemical characterization revealed typical fibroblastic and smooth muscle differentiation. ITS supplemented in RPMI-FBS showed the best growth stimulation compared with other serum-free media (p <0.05) and became our basal medium. The presence of DU145 cell conditioned medium in this basal medium showed a significant increase in cell proliferation in stromal cells. Stromal cells maintained AR mRNA expression and significant DHT dose dependent growth stimulation in up to 10 passages. Both the antiandrogens flutamide and hydroxyflutamide counteracted the DHT effect (p <0.05). Conclusions This stromal cell model maintains many cellular and functional properties of the human prostate, which may enable us to study growth factor modulation, drug and hormone metabolism in stromal-epithelial interaction with emphasis on the pathogenesis of BPH and prostate cancer.

LOCALIZATION AND EXPRESSION OF THE alpha 1A-1 , alpha 1B AND alpha 1D-ADRENOCEPTORS IN HYPERPLASTIC AND NON-HYPERPLASTIC HUMAN PROSTATE

To determine the expression and localization of the alpha1A-1, alpha1B and alpha1D-adrenoceptor (AR) subtypes in hyperplastic and non-hyperplastic human prostate tissue. The expression of the alpha1-AR subtypes was examined at the mRNA level by quantitative solution hybridization, and at the protein level by immunohistochemistry using subtype selective antibodies. While the overall level of alpha1-AR mRNA was not significantly different between hyperplastic and non-hyperplastic tissue, there were significant differences in the ratio of the alpha1-AR subtypes expressed in the two tissue types. The most significant finding from these studies was the reduced expression of the alpha1b-AR mRNA in both glandular and stromal hyperplasia. By immunohistochemistry, the alpha1A-1-AR was detected in the stroma and not in the glandular epithelium. The alpha1B-AR was localized predominantly in the epithelium and was weakly present in the stroma. Lower levels of the alpha1B-AR were detected in the hyperplastic prostatic epithelium. The alpha1D-AR was detected in areas of stroma and was abundantly present in blood vessels. The alpha1A-1-, alpha1B- and alpha1D-AR subtypes are differentially localized in human prostate, and the expression levels of all three subtypes are altered in BPH. Alterations in a1-AR subtype expression (particularly the alpha1B-AR) in BPH cannot be solely attributed to changes in tissue morphometry resulting from hyperplasia and may be of significance in the pathogenesis of BPH.

Gene Expression and Autoradiographic Localization of Endothelin-1 and its Receptors A and B in the Different Zones of the Normal Human Prostate

Purpose To investigate the gene expression and tissue distribution of prepro Endothelin-1 (ET-1), Endothelin Converting Enzyme (hECE-1), and ET A and ET B receptors in the central (CZ), transition (TZ) and peripheral (PZ) zones of normal human prostates. Materials and Methods Sections of the different zones of histologically normal prostates from 35 year-old men were obtained and autoradiographically studied with 125 I ET-1 with and without the ET A antagonist BQ-123, the ET B agonists sarafotoxin 6C, and excess cold ET-1. Specimens from PZ and CZ and DU145 and PC3 human prostate cancer cell lines were also investigated by reverse transcription (RT)-PCR. Results The mRNAs of all genes were detected in all specimens examined. No ET B expression was found in either cell lines. Specific intense 125 I ET-1 binding with clear-cut differences among zones was found. In the CZ the main subtype in the glandular stroma and epithelium was the ET A and ET B, respectively, in the PZ the opposite was true. In PZ, the ET sub A receptors were detected on the glandular epithelium; in the TZ both receptor subtypes were only in the stroma. Conclusions These receptors' zonal distribution differences may be relevant for the pathogenesis of BPH and prostatic cancer.

Human Cytomegalovirus is not Implicated in Benign Prostatic Hyperplasia

To evaluate whether human cytomegalovirus (CMV) may play a role in the pathogenesis of benign prostatic hyperplasia. We used immunohistochemistry and the polymerase chain reaction (PCR) to evaluate the presence of CMV in normal prostatic tissue (n = 12) and BPH tissue (n = 21). Immunostaining for CMV in prostatic tissue was negative; however, staining was evident in mononuclear cells seen in the tissues of both groups. With nested PCR, CMV genomic material was demonstrated in 1 tissue specimen from each group (p > 0.1). These data suggest that CMV is unlikely to be a significant factor in the pathogenesis of BPH.

Human Cytomegalovirus is not Implicated in Benign Prostatic Hyperplasia: A Study Using Immunohistochemistry and the Polymerase Chain Reaction

Purpose To evaluate whether human cytomegalovirus (CMV) may play a role in the pathogenesis of benign prostatic hyperplasia. Materials and Methods We used immunohistochemistry and the polymerase chain reaction (PCR) to evaluate the presence of CMV in normal prostatic tissue (n=12) and BPH tissue (n=21). Results Immunostaining for CMV in prostatic tissue was negative; however, staining was evident in mononuclear cells seen in the tissues of both groups. With nested PCR, CMV genomic material was demonstrated in 1 tissue specimen from each group (p greater than 0.1). Conclusions These data suggest that CMV is unlikely to be a significant factor in the pathogenesis of BPH.

Effect of obesity on prostatic hyperplasia: its relation to sex steroid levels.

In 68 men with benign prostatic hyperplasia, we evaluated the association between obesity and prostatic enlargement, as well as changes in serum levels of oestradiol, testosterone, dihydroepiandrosterone and dihydroepiandrosterone sulphate. Despite the larger adenomas, no increase in the symptom score for BPH was observed with increasing obesity. Average specimen weights increased with increasingly obesity and increasing host age from 46 to 80 g. We also found the serum oestradiol level significantly elevated in obese men who were 140% or over recommended weight compared to underweight men younger than 60 years (51.3 pg/ml versus 26.8 pg/ml, p < 0.01). This pattern was present in all age groups. These results indicate that obesity is a risk factor for prostatic enlargement but not for obstruction. Also the degree of obesity appears to have a direct effect on oestradiol levels through transformation of androgens in adipose tissue to oestrogens. In conclusion, further studies to evaluate the pathogenesis, pathophysiology, natural history and symptomatology of BPH would be of great interest and should help to define better the associations that we have recognized.