Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Prostatic Hyperplasia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 217 records · Page 12Linked to original sources
PubMed1993

Benign prostatic hyperplasia and normal prostate aging: differences in types I and II 5 alpha-reductase and steroid hormone receptor messenger ribonucleic acid (mRNA) levels, but not in insulin-like growth factor mRNA levels.

Benign prostatic hyperplasia (BPH) is so common in elderly men that the development of adenomatous nodules in this organ can be seen as a normal age-dependent process. In this work, we used Northern blotting to compare the levels of androgen, estrogen, and insulin-like growth factor-I (IGF-I) receptor in young (age range, 23-33; n = 3), old normal (age range, 52-80; n = 3), and BPH-affected subjects (age range, 66-87; n = 15). We have also investigated in these groups the expression of genes coding for the two 5 alpha-reductases (types I and II), aromatase, IGF-I, and IGF-II. Our results show significantly increased levels of IGF mRNA in old healthy and BPH-affected subjects; the respective rises for IGF-I, IGF-II, and IGF-I receptor mRNAs were 3.0-, 2.9-, and 1.5-fold (BPH) and 2.7-, 2.4-, and 1.8-fold (old normal controls). For estrogen receptor, androgen receptor, and type I and II 5 alpha-reductase mRNAs, a marked but opposite effect was observed in adenomatous tissues only; the respective levels were 2.2-, 1.8-, 3.9-, and 1.7-fold lower than those in young adult subjects, whereas no significant differences were recorded between the two normal groups. Morphometric analysis of each tissue specimen confirmed the significantly lower epithelium/stroma ratio in adenomas compared to young or old healthy tissues. Together, these observations suggest that prostatic adenomas may result from at least two conjugate processes: one characterized by a drop in the mRNA levels of steroid hormone receptors, which might be associated with a lower epithelium/stroma ratio, and another characterized by normal aging phenomena, of which the increased production of IGFs and IGF-I receptor transcripts could be biochemical markers.

Adult↗
PubMed1990

Morphometric evaluation of benign prostatic hyperplasia.

Resected prostate tissue from 9 patients with benign prostatic hyperplasia was subjected to a morphometric analysis. The relative volume density of 4 prostatic tissue components was determined: fibrous (47%), muscular (8%), vascular (3%), and glandular (18%). The resolution of the stromal portion of the hyperplastic prostate into 3 subcomponents represents a finer level of resolution than that previously reported. This enhanced precision in the determination of tissue composition lends new insight into the etiology of benign prostatic hyperplasia, and provides a basis for the evaluation of novel approaches to its treatment.

Aged↗
PubMed2005

Juvenile prostatic hyperplasia.

Benign prostatic hyperplasia is common in aging men, but rare in childhood. We report a case of juvenile prostatic hyperplasia in a 10-year-old boy, who visited our clinic for hematuria and voiding symptoms. Radiologic studies revealed a huge prostate protruding into the bladder. The prostate was 33 g. The prostate biopsy showed no evidence of cancer. At 13 years of age, he was seen again because of general weakness, fever, and voiding difficulty. Bilateral hydroureteronephrosis was found on radiologic studies, and his serum creatinine was elevated. The prostate was 55 g. Suprapubic prostatectomy was performed.

Age Factors↗
PubMed1991

Characterization of prostate cancer, benign prostatic hyperplasia and normal prostates using transrectal 31phosphorus magnetic resonance spectroscopy: a preliminary report.

We assessed the ability of 31phosphorus (31P) transrectal magnetic resonance spectroscopy to characterize normal human prostates as well as prostates with benign and malignant neoplasms. With a transrectal probe that we devised for surface coil spectroscopy we studied 15 individuals with normal (5), benign hyperplastic (4) and malignant (6) prostates. Digital rectal examination, transrectal ultrasonography and magnetic resonance imaging were used to aid in accurate positioning of the transrectal probe against the region of interest within the prostate. The major findings of the in vivo studies were that normal prostates had phosphocreatine-to-adenosine triphosphate (ATP) ratios of 1.2 +/- 0.2, phosphomonoester-to-beta-ATP ratios of 1.1 +/- 0.1 and phosphomonoester-to-phosphocreatine ratios of 0.9 +/- 0.1. Malignant prostates had phosphocreatine-to-beta-ATP ratios that were lower (0.7 +/- 0.1) than those of normal prostates (p less than 0.02) or prostates with benign hyperplasia (1.1 +/- 0.2, p less than 0.01). Malignant prostates had phosphomonoester-to-beta-ATP ratios (1.8 +/- 0.2) that were higher than that of normal prostates (p less than 0.02). Using the phosphomonoester-to-phosphocreatine ratio, it was possible to differentiate metabolically malignant (2.7 +/- 0.3) from normal prostates (p less than 0.001), with no overlap of individual ratios. The mean phosphomonoester-to-phosphocreatine ratio (1.5 +/- 0.5) of prostates with benign hyperplasia was midway between the normal and malignant ratios, and there was overlap between individual phosphomonoester-to-phosphocreatine ratios of benign prostatic hyperplasia glands with that of normal and malignant glands. To verify the in vivo results, we performed high resolution magnetic resonance spectroscopy on perchloric acid extracts of benign prostatic hyperplasia tissue obtained at operation and on a human prostatic cancer cell line DU145. The extract results confirmed the differences in metabolite ratios observed in vivo. We conclude that transrectal 31P magnetic resonance spectroscopy can characterize metabolic differences between the normal and malignant prostate.

Adult↗
PubMed1997

Benign prostatic hyperplasia.

Benign prostatic hyperplasia is a common and costly disease that affects older men. This article reviews the underlying histopathologic changes that cause benign prostatic hyperplasia. The symptoms and systematic evaluation of the patient are described, along with the current therapeutic options for treatment.

Adrenergic alpha-Antagonists↗
PubMed1997

Decreased expression of Wilms' tumor gene WT-1 and elevated expression of insulin growth factor-II (IGF-II) and type 1 IGF receptor genes in prostatic stromal cells from patients with benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common proliferative disorder of unknown etiology. We have previously documented that the insulin-like growth factor (IGF) axis is critical for prostate cell growth and is abnormal in BPH. The type 1 IGF receptor (IGF-1R) is constitutively expressed by most body tissues and plays a significant role in regulating cell proliferation, consistent with the role of its ligands (IGF-I and IGF-II) as important mitogenic factors. The Wilms' tumor gene product (WT-1) is a tumor suppressor that has been shown to be altered in rare kidney tumors and is known to regulate IGF-II and IGF-1R. We investigated the possibility that the expression of prostatic WT-1, IGF-1R, and IGF-II genes is altered in patients with BPH. We utilized primary cultures of prostatic stromal cells grown from normal (n = 9) and hyperplastic (n = 9) surgical specimens and analyzed WT-1, IGF-1R, and IGF-II messenger RNA levels. In all of the BPH cell strains, WT-1 expression (measured by RT-PCR and RNase protection assays) was strikingly lower than that found in normal strains (0-20% of normal, mean 14% of normal, P < 0.01). The expression of both the IGF-1R (300% of normal, P < 0.05) and IGF-II (1000% of normal, P < 0.01) messenger RNAs was higher in BPH strains as compared with normal strains. No changes were seen in stromal cell strains derived from prostatic adenocarcinoma. Thus, in cultured human prostatic stromal cell strains from patients with BPH, decreased WT-1 gene expression is associated with increases in the expression of the IGF-1R and IGF-II genes that are known transcriptional targets of WT-1. These findings indicate that reduced expression of the WT-1 tumor suppressor gene and elevated IGF-1R and IGF-II gene expression may be involved in the pathophysiology of prostatic hyperplasia, implying a new role for the Wilms' tumor gene in nonmalignant states.

Aged↗
PubMed2005

[Evalution of benign prostatic hyperplasia].

Benign prostatic hyperplasia is a disorder of aging men and according to reasons for consultation its incidence is continually increasing in parallel with the constant increase in life expectancy. Recommendations about its management have been made by numerous national and international, scientific authorities and those responsible for public health. However, despite a rationale based on regularly published data, there are many disparities between them and they are only partially followed up in routine practice. The purpose of a working group during the "2nd Interfaces in Urology" was to make a new assessment on this disorder with regard to the most recent data and existing recommendations, in order to offer clinicians a clearer attitude for the prescription of the initial evaluation of benign prostatic hyperplasia.

Humans↗
PubMed1991

Effect of LH-RH analogue in patients with benign prostatic hyperplasia.

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.

Aged↗
PubMed1994

New insights into the epidemiology and natural history of benign prostatic hyperplasia.

Benign Prostatic Hyperplasia (BPH) has undoubtedly been an important cause of the urinary difficulties observed in elderly men for many centuries although the condition was only recognised as such during the last century. Benign Prostatic Hyperplasia is a very common condition (88 per cent of autopsy specimens in men aged over 80 have histological BPH) and the cause of the commonest surgical procedure in elderly men (three men in ten ultimately may require surgery for this condition). A common cause of death in elderly men just 20-30 years ago, improved medical care has seen dramatic declines in this aspect of BPH and today treatment choices in BPH are largely determined by considerations of quality-of-life. Despite such a common occurrence, little is known with any certainty about the epidemiology of BPH. The incidence, even the population prevalence, is difficult to determine for a variety of reasons associated with difficulties surrounding the diagnosis of BPH and the identification of a source population to provide a denominator to calculate rates. Knowledge of risk factors is sparse: analytical epidemiologic studies of BPH are difficult to conduct. Case-control studies, the most commonly employed design in epidemiology, are problematic in that a control group may be difficult to define in view of the likelihood that a large proportion of these may have undiagnosed BPH. Against this background, knowledge of the prostate in the general population was sought in an international survey and found to be poor: although most men are aware of its existence, very few could correctly identify the function of the gland. Men tended to discuss urination problems with their doctors not when a symptom develops but when that symptom becomes bothersome. A 10-fold variation in frequency of rectal examination was identified between men in Germany and Italy which could not be explained by potential confounding variables. Given the large increases in the number of males reaching older ages, it is clear that BPH will continue to have substantial and increasing influence in terms of morbidity, mortality and health costs. Before the end of the present century, the life expectancy of a male at birth will exceed 80 years in many of the developed countries. Put put another way, one man in every two born can expect to reach an at which he has an 88 per cent chance of having a prostate with morphological BPH. Clearly, the need for high quality epidemiological information and consequent increased prospects for prevention is obvious.

Age Factors↗
PubMed2006

How do patients with familial benign prostatic hyperplasia differ clinically from those with sporadic benign prostatic hyperplasia?

INTRODUCTION: The aim of this study was to compare age, prostatic volume, International Prostate Symptom Score (IPSS), maximal flow rate, serum total prostate-specific antigen (PSA), serum free PSA, free/total PSA ratio and PSA density values of familial and sporadic benign prostatic hyperplasia (BPH) patients suffering moderate or severe lower urinary tract symptoms. MATERIALS AND METHODS: Between September 1999 and August 2004, 511 patients with moderate or severe lower urinary tract symptoms (IPSS > or =8) due to BPH were included in the study. Patients with at least 2 first-degree relatives who had undergone surgery or received medication for BPH were classified as having the familial form of the disease, while the remaining patients were taken as sporadic cases. Mean age, prostatic volume, symptom score, maximal flow rate, PSA, free PSA, free/total PSA ratio and PSA density values of the familial and sporadic groups were compared using student's t test. RESULTS: Thirty-eight patients had a positive family history and formed the familial group, while the remaining 473 made up the sporadic group. No significant difference was observed in the parameters studied, except that mean prostate volume of the familial group was found to be greater and the mean age to be lower than those of sporadic patients in accordance with the literature. CONCLUSIONS: Patients with familial BPH need treatment significantly earlier and have larger prostates than those with sporadic BPH.

Aged↗
PubMed2002

Current concepts in the pharmacotherapy of benign prostatic hyperplasia.

Benign prostatic hyperplasia is a major men's health issue, with approximately 80% of all men developing this condition within their lifetime. A variety of oral treatments is available, including alpha-adrenoceptor antagonists (alpha-blockers), 5alpha reductase inhibitors, aromatase inhibitors and phytotherapy. A large number of alpha-blockers can be administered, but no single agent has demonstrated a clear superiority over the other drugs. 5alpha Reductase inhibitors have demonstrated similar efficacy in larger volume prostates but most evidence suggests that there is no benefit in combining them with alpha-blockers. The use of phytotherapy is not entirely novel but requires further long-term evaluation before it can be endorsed for clinical use in benign prostatic hyperplasia.

Adrenergic alpha-Antagonists↗
PubMed2005

Establishment of a pregnancy following intravaginal insemination with epididymal semen from a dog castrated due to benign prostatic hyperplasia.

Benign prostatic hyperplasia was diagnosed in an American Staffordshire Terrier of high breeding value presenting concurrent haematuria. Castration as a treatment was synchronized with the oestrus cycle of a bitch selected for insemination. After castration the cauda epididymis was flushed with Gent semen extender and collected spermatozoa were filtered and analysed by Hamilton Thorn computer assisted sperm analysis. A total of 7 ml semen containing 742 x 10(6) spermatozoa with 76.5% mean motility was used for insemination. Intravaginal insemination of the bitch was performed with an insemination catheter for dogs (Kruuse, Marslev, Denmark) on the day when plasma progesterone levels reached 9.9 ng/ml. Normal pregnancy without complications resulted in eight live-born puppies 63 days after insemination. This is the first report of a normal pregnancy and birth of puppies from a bitch inseminated with epididymal semen obtained from a dog affected by benign prostate hyperplasia.

Animals↗
PubMed1993

[The quotient of prostate-specific antigen and prostate volume. Improved differentiation between benign prostatic hyperplasia and locally circumscribed prostate cancer].

Absolute serum prostate-specific antigen (PSA) values are of little help in the identification of locally confined prostatic cancer (PCA), because of a considerable overlap with the PSA values found in benign prostatic hyperplasia (BPH). Prostate gland volumes were estimated sonographically in 112 patients using the product of the three maximal diameters (longitudinal, anterior-posterior, transverse) and the factor 0.52. PSA was determined with a monoclonal immunoenzymetric assay (Tandem-E, Hybritech). The prostates were removed by either transvesical prostatectomy (for BPH) or radical retropubic prostatovesiculectomy (for PCA). In each case the diagnosis was verified by systematic histological examination. The ratio of serum PSA to estimated prostate volume did not exceed 0.4 ng/(ml x ml) in any of the 74 patients with BPH, whereas 23 of the 38 patients with PCA had a ratio above 0.4 ng/(ml x ml). The information provided by the PSA-prostate volume ratio is superior to absolute PSA values in preoperative differentiation between BPH and PCA. With a PSA-prostate volume ratio over 0.4 ng/(ml x ml) patients are at high risk for PCA and should be evaluated by prostate biopsy.

Adult↗
PubMed1998

The precursor form of the human kallikrein 2, a kallikrein homologous to prostate-specific antigen, is present in human sera and is increased in prostate cancer and benign prostatic hyperplasia.

Prostate-specific antigen (PSA, hK3) is a diagnostic marker for prostatic cancer but lacks the specificity to sufficiently distinguish between prostatic cancer and benign prostatic hyperplasia (BPH). Human glandular kallikrein 2 (hK2) has been proposed as a potential diagnostic marker for prostate cancer that could complement the current PSA test. Recently we demonstrated that proPSA is present in prostate cancer sera. This study examines the expression of prohK2 in prostate cells and its presence in human sera. Western blot analysis was used to assess prohK2 expression in the human carcinoma cell line, LNCaP. A highly specific and sensitive dual monoclonal immunoassay for prohK2 was developed and used to assess the presence of prohK2 in human sera. prohK2 was detected in the spent media of LNCaP cells. Furthermore, prohK2 was present at immunodetectable concentrations in human sera, and its concentration was increased in prostatic cancer and BPH. These results indicate for the first time that prohK2 is secreted by human prostate cells and is a major component of uncomplexed (free) hK2 in human sera. In addition, prohK2 in human sera is associated with prostate disease and thus may be a useful marker for prostatic cancer and BPH.

Antibodies, Monoclonal↗
PubMed1993

Platelet derived growth factor (PDGF), androgens and inflammation: possible etiologic factors in the development of prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is characterized by varying degrees of epithelial and stromal hyperplasia in association with inflammation. Although androgens are known to be important for the growth and function of the prostate, their role in the development of BPH is unclear. The release of platelet-derived growth factor (PDGF) in response to inflammation suggests that PDGF may participate in the development of BPH. Cultured prostate cells derived from patients with BPH were examined for the presence of functional PDGF and androgen receptors. The cells expressed PDGF receptors and responded to PDGF stimulation by the activation of the PDGF signal transduction pathway and a dose-dependent stimulation of cell proliferation. Even though the cells expressed androgen receptors, dihydrotestosterone failed to elicit a mitogenic response. While the role of androgens in BPH remains unclear, these results suggest that inflammation and, specifically, PDGF may be important etiologic factors in the development of BPH.

Aged↗
PubMed1994

Comparison of testosterone metabolism in benign prostatic hyperplasia and human prostate cancer cell lines in vitro.

Pathways of testosterone metabolism in tissue slices and cell suspensions of human benign hyperplastic prostate (BPH) tissue and human prostate cancer cell lines (DU145, HPC-36M, PC-3/MA2 and LNCaP) were investigated. Thin layer chromatography analysis was used to identify the following tritiated metabolites: testosterone, 5 alpha-dihydrostestosterone (DHT), 5 alpha-androstane-3 alpha/3 beta-17 beta-diol (androstanediols), 4-androstene-3,17-dione (androstenedione) and 5 alpha-androstanedione. The predominant pathway for testosterone metabolism in BPH was via 5 alpha-reductase producing 5 alpha-dihydrotestosterone (71% and 75% total metabolites in slices and suspensions incubated for 24 h, respectively). The cancer cell lines DU145 and HPC-36M resembled BPH by metabolizing testosterone predominantly to DHT (68% and 82% total metabolites, respectively), although the rate of metabolism was much lower in the cell lines (0.099 and 0.05 pmol testosterone/mg protein/h in DU145 and HPC-36M) compared to the BPH cell suspensions (6.4 pmol testosterone/mg protein/h). In contrast, PC-3/MA2 contained high 17 beta-HSD activity forming large amounts of 4-androstene-3,17-dione (84% total metabolites), converting testosterone at a rate faster (12.8 pmol testosterone/mg protein/h) than the BPH cell suspensions. LNCaP rapidly converted testosterone exclusively to a glucuronide conjugate (7.4 pmol testosterone/mg protein/h), although after incubation with [3H]-4-androstene-3,17-dione, 5 alpha-reductase activity was demonstrated. LNCaP was the only cell line whose growth and colony-forming ability was stimulated by testosterone and DHT. BPH and all the cell lines tested had 5 alpha-reductase activity, but only the prostate tissue and the cell lines DU145 and HPC-36M converted testosterone predominantly to DHT.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1997

Inflammation in benign prostatic hyperplasia: correlation with prostate specific antigen value.

PURPOSE: We attempted to identify morphological parameters of benign prostatic hyperplastic inflammation that correlate with pre-biopsy prostate specific antigen (PSA) concentrations. MATERIALS AND METHODS: Patients undergoing prostate biopsy at our department were prospectively studied between January 1995 and January 1996. preoperative blood and 24-hour urine samples were measured for PSA. Biopsy samples harboring exclusively benign prostatic tissue were graded on a 4-point scale for inflammation (0-no inflammatory cells, 1-scattered inflammatory cell infiltrate, 2-nonconfluent lymphoid nodules and 3-large inflammatory areas with confluence of infiltrate) and aggressiveness (0-no contact between inflammatory cells and glandular epithelium; 1-contact between inflammatory cell infiltrate and glandular epithelium; 2-clear but limited, that is less than 25% of the examined material, glandular epithelium disruption, and 3-glandular epithelium disruption on more than 25% of the examined material). RESULTS: A total of 66 patients with exclusively benign prostatic tissue on prostate biopsies was analyzed. Difference between inflammation graded groups was not significant when considering serum or urinary PSA. There was a significant correlation between aggressiveness grading and serum PSA (rho = 0.51, p < 0.0001), whereas aggressiveness grading and urinary PSA did not correlate (rho = -0.06, p = 0.6). CONCLUSIONS: Prostatic subclinical inflammation is not associated with high urinary PSA. Unless associated with glandular epithelial disruption, density of prostatic interstitial inflammatory cell infiltrate is not significantly correlated with serum PSA concentration. We believe that this issue should be considered when interpreting a prostate biopsy.

Aged↗
PubMed1995

[Characterization of prostate cancer, benign prostatic hyperplasia and normal prostates using endorectal 1H magnetic resonance spectroscopy].

BACKGROUND: We evaluate the usefulness of 1H endorectal resonance spectroscopy to characterize prostate pathology. METHODS: With an endorectal surface coil we have studied 20 individuals with normal (1), benign hyperplastic (9) and malignant (10) prostates. RESULTS: The major findings of our studies were that the patients with cancer have a significantly lower citrate-to-choline ratio (cit/cho) and creatin-to-choline ratio (cre/cho) than the patients with BPH (p < 0.05). There is well correlation between cit/cho and gland-to-stroma ratio of the BPH tissue as well as histological grade of the cancer tissue. 1H spectroscopy offers the advantages of differential diagnosis between benign and malignant prostates. We, however, failed to demonstrate cancer in 2 cases; the lesion was too small in one case, and out of the region of interest in the other. It is necessary that the foci in the prostate is at least 1.5 X 1.5 X 1.5 cm3 of the volume in order to obtain genuine spectrogram of carcinoma. CONCLUSION: Endorectal 1H magnetic resonance spectroscopy can characterize metabolic differences between the normal and malignant prostate.

Adult↗