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 163 records · Page 9Linked to original sources
PubMed2004

Differentiation of benign prostatic hyperplasia from prostate cancer using prostate specific antigen dynamic profile after transrectal prostate biopsy.

PURPOSE: Serum prostate specific antigen (PSA) level is increased after needle biopsy (Bx) of the prostate. This study tested the hypothesis that the prostate harboring malignant lesions demonstrates less leakage of PSA after prostate biopsy and this phenomenon can be helpful in discriminating benign from cancer diagnosis. MATERIALS AND METHODS: This prospective study was divided into 3 separate phases. Sextant prostate biopsy was done with transrectal ultrasound guidance, and the change and PSA values after biopsy were evaluated. Phases 1 and 2 had 20 and 41 patients, respectively. PSA dynamic profiles were plotted. We defined the most appropriate timing for blood sampling and the cutoff value of the PSA ratio (post-Bx total PSA-to-pre-Bx total PSA) to be applied for further assessment. Phase 3 recruited 97 cases, of which 66 satisfied the end point criteria in which a diagnosis such as malignancy, or 3 successive benign biopsies or benign transurethral resection of prostate was obtained. RESULTS: From phases 1 and 2 the cutoff value for the PSA ratio was 2.0, and the timing of blood sampling was 60 minutes after the biopsy. In phase 3 of those whose PSA ratio was less than 2.0, 92.6% (25) had cancer. For those whose PSA ratio was greater than 2.0, 82.1% (32) were benign. Of the 4 cases with a PSA ratio less than 2.0 and an initial benign biopsy, 3 (75%) were proven to have cancer later. CONCLUSIONS: Evaluating the 1-hour PSA ratio might be helpful for clinicians to select the high risk patients who might have cancer in the prostate. Repeat biopsy should be suggested for cases with a smaller PSA ratio in spite of initial benign results.

Aged↗
PubMed1999

Prostate-specific membrane antigen levels in sera from healthy men and patients with benign prostate hyperplasia or prostate cancer.

Prostate-specific membrane antigen (PSMA) serum levels have been proposed to be of prognostic significance in patients with advanced prostate disease. The objective of the present study was to confirm PSMA serum expression by Western blot techniques, to determine whether such data could assist in the differentiation of benign from malignant prostatic disease, and to determine the suitability of serum PSMA measurements in predicting recurrent or progressive prostate malignancies. We measured PSMA, a transmembrane glycoprotein identified in prostate epithelial cells, in the sera of 236 normal individuals and cancer patients by Western blot analysis. Within the normal male population, PSMA levels increase with age and were found to be significantly elevated in subjects more than 50 years of age when compared to those of younger men. We did not confirm previous reports that serum PSMA measurements could distinguish late-stage prostate carcinoma from early-stage prostate carcinoma, nor did we find PSMA to be more effective than prostate-specific antigen in monitoring prostate cancer patient prognosis. Furthermore, we found elevated serum PSMA in healthy females, and, similar to the healthy male population, the levels increased with age, with the highest levels found in the sera from breast cancer patients. These latter observations further support that PSMA is not a specific biomarker for prostate cancer and that a variety of normal and diseased tissue may contribute to the serum levels of PSMA.

Adult↗
PubMedDate not supplied

Quantitative analysis of epidermal growth factor in human benign prostatic hyperplasia and prostatic carcinoma and its prognostic significance.

The incidence of prostatic carcinoma (PC) is increasing worldwide. Despite the discovery by Huggins in 1941 of the hormone dependency of this tumour, the overall prognosis and survival for patients with advanced disease has not changed. The prognosis for individual patients with PC cannot be accurately predicted by factors such as clinical stage and histological differentiation of the tumour. There is therefore a need to investigate new prognosis factors to assess their role.

Aged↗
PubMed1993

PSA in benign prostatic hyperplasia and prostatic intraepithelial neoplasia.

Prostate specific antigen has become an important adjunct to the digital rectal examination in screening for prostate cancer. The clinician should be familiar with interpretation of this test. Many men with BPH have elevated serum PSA concentrations; however, the majority of these men will have other pathologic processes such as occult cancer, PIN, or acute inflammation that may account for the elevations in serum PSA. Certainly, serial increases in serum PSA should increase concern that occult carcinoma is present. Patients with PIN may also have elevated PSA concentrations. When PIN is associated with elevated PSA, a high incidence of invasive carcinoma is noted on subsequent biopsy. Further investigation into the associations will further refine the clinical utility of this powerful tumor marker.

Aged↗
PubMed1995

Prostate specific antigen in the expressed prostatic fluid of men with benign prostatic hyperplasia and prostate carcinoma.

PURPOSE: We tested the hypothesis that the histochemically demonstrated prostate specific antigen (PSA) content of prostate carcinoma cells does not necessarily reflect PSA production and secretion by evaluating expressed prostatic fluid. MATERIALS AND METHODS: Expressed prostatic fluid and serum from 152 men with clinical benign prostatic hypertrophy (BPH), 132 with histologically proved BPH and 46 with prostate carcinoma were analyzed with the Hybritech PSA assay. RESULTS: Expressed prostatic fluid PSA levels from carcinoma patients (median 1.70 mg./ml., mean 2.25) were significantly higher than in the histologically proved BPH group (median 1.28 mg./ml., mean 1.42, p < 0.05). CONCLUSIONS: PSA concentration is increased in the expressed prostatic fluid of prostates of men with carcinoma compared to those with histological BPH. This finding may be a functional manifestation of a field change or paracrine effects within the prostate.

Aged↗
PubMed1997

Predictors of general quality of life in patients with benign prostate hyperplasia or prostate cancer.

PURPOSE: Studies in disease specific populations have emphasized disease specific quality of life with little study of general quality of life. Furthermore, studies of general quality of life in disease specific populations have mostly examined the importance of disease specific variables, and have generally yielded poor correlations of such variables and general quality of life. We attempted to model the emotional component of general quality of life in patients with prostate disease. MATERIALS AND METHODS: We integrated prospectively collected disease specific and nonspecific clinical and self-reported patient data. We also applied neural network and more conventional statistical tools to examine the relative use of various available analytical methodologies in modeling general quality of life. RESULTS: Neural networks created reasonably good models of the emotional component of general quality of life. Logistic regression analysis also created reasonably good models and, given current computational schemes, allowed for identification of significant inputs in the models more readily than did the feed-forward, back propagation neural networks. All models of general quality of life relied primarily on disease nonspecific inputs, including social support, activities of daily living and coping. CONCLUSIONS: Our observations suggested that efforts to optimize general quality of life in patients with prostate disease must integrate disease nonspecific variables.

Humans↗
PubMedDate not supplied

Comparative pathology of benign prostatic hyperplasia and prostate cancer.

Basic studies on the pathogenesis of prostate disease including hypertrophy and cancer have been difficult due to the lack of suitable animal models. Much effort has been directed to the development of appropriate animal models, and yet many obstacles still remain. Rodents do not develop spontaneous hypertrophy of the prostate, in fact the prostate atrophies with advancing age. Guinea pigs appear to be a good model to study the effect of hormones on the prostate gland. Microinvasive prostatic adenocarcinoma occurs spontaneously in various species of rodents, and can be induced by radiation, hormones and chemical carcinogens. The man and dog appear to be the only mammals which suffer naturally from the pathological processes of the prostate gland associated with aging. We review the currently available models for the study of benign, and malignant prostate disease and assess the strengths and weaknesses each for preclinical investigations.

Adenocarcinoma↗
PubMed1988

Expression of basic fibroblast growth factor mRNA in benign prostatic hyperplasia and prostatic carcinoma.

In our previous work we demonstrated that prostate-derived growth factor (PrGF) is homologous to basic fibroblast growth factor (bFGF), not acidic fibroblast growth factor (aFGF). Using Northern blot analysis we now show that the messenger RNA for bFGF but not aFGF is expressed in benign prostatic hyperplastic (BPH) tissue as well as in carcinoma of the prostate (CAP). This not only corroborates our previous results, but suggests that PrGF is produced locally and not merely stored in the prostate. The demonstration of local production of bFGF by prostate tissue may indicate that this growth factor plays a role, either alone or in conjunction with other factors, in the etiology of benign hyperplasia or prostatic cancer.

Animals↗
PubMed1998

Relationship between prostate specific antigen density, microvessel density and prostatic volume in benign prostatic hyperplasia and advanced prostatic carcinoma.

The aim of this study was to investigate the relationship between prostate specific antigen density and prostate volume with microvessel density in patients with benign prostatic hyperplasia and advanced prostatic carcinoma. Sixty-eight patients with benign prostatic hyperplasia and 11 patients with advanced prostatic carcinoma participated in the study. The paraffin blocks of all patients were stained with CD34 by the standard immunohistochemical technique and microvessel density, prostate specific antigen density and prostatic volume were determined. In patients with benign prostatic hyperplasia the mean microvessel density, mean prostate specific antigen density and mean prostatic volume were 74+/-89+/-22.73, 0.12+/-0.10 and 59.97+/-27.0 ml, respectively. There was no correlation between prostate specific antigen density and mean prostatic volume or microvessel density (r = 0.079 and -0.095, respectively). In patients with advanced prostatic carcinoma the mean microvessel density, mean prostate specific antigen density and mean prostatic volume were 147.90+/-47.55, 0.63+/-0.41 and 54.00+/-22.42 ml, respectively. In this group, while there was a good correlation between prostate specific antigen density and microvessel density (r = 0.785), no significant correlation was found between prostatic volume and microvessel density (r = -0.07). There was significant statistical difference in patients with advanced prostatic carcinoma compared to patients with benign prostatic hyperplasia in terms of mean microvessel density (p<0.0001). The findings that there was no correlation between prostatic volume and MVD either in benign prostatic hyperplasia or in prostatic carcinoma suggest that microvessel development is not correlated with prostatic volume but may be correlated with morphology.

Aged↗
PubMed1989

Monoclonal antibody Ki-67 defined growth fraction in benign prostatic hyperplasia and prostatic cancer.

Growth fractions were assessed immunohistochemically in prostatic tissues with benign glandular hyperplasia (BPH) and in specimens of prostatic cancer using the monoclonal antibody Ki-67. This antibody is specific for a proliferation-associated nuclear antigen. In BPH tissues about 0.3% of nuclei of epithelial cells was reactive with Ki-67. The Ki-67 positive nuclei were distributed equally among the basal and luminal cells of the hyperplastic prostatic acini. In prostatic cancer the Ki-67 defined growth fraction ranged from 0.4% to 9.1% (mean value 2.9%). Cancers with a cribriform growth pattern and tumors composed of solid areas of undifferentiated cancer cells showed the highest growth fraction (average values 4.0%, respectively 7.6%). The investigated four tumors composed of undifferentiated solitary tumor cells with diffuse infiltration of the stroma demonstrated an unexpectedly low growth activity (average 1.2%). In cancers with a glandular growth pattern the Ki-67 defined growth fraction of tumor cells varied from 2.2% to 5%. Compared with other epithelial tumors these values are low, but they are in agreement with the earlier findings on prostatic cancer obtained with 3H-thymidine labeling and bromodeoxyuridine incorporation. The observed variation in the level of Ki-67 defined growth activity partly related to the histological tumor pattern suggests that Ki-67 labeling may serve as a prognostic factor additional to the current histopathological grading criteria of prostatic cancer.

Adenocarcinoma↗
PubMed1995

A unifying hypothesis that links benign prostatic hyperplasia and prostatic intraepithelial neoplasia with prostate cancer. Invited comments.

Prostatic Intraepithelial Neoplasia (PIN) and prostatic cancer (PCA) are not caused by infection, allergic reaction, inadequate immunological response, ischemia, ageing, systemic hormones, carcinogens, nor prostatic ductal contents. PIN and PCA are apparently caused by increased inner acinar pressure due to partially blocked draining ducts. Only this explanation can account for all the observations about PIN and PCA. All other possible causes are disproved by specific observations. In order to further clarify the cause of PIN and PCA, it is important to discover if peripheral zone lesions cluster around ducts or blood vessels. PIN patterns are the morphological precursors of both PCA and prostatic cysts. Different PIN patterns represent different adaptive stages to increasing inner acinar pressure. The immediate tissue cause of PCA is PIN disruption seeding the stroma with high-grade PIN (HGPIN) cells. These cells, programmed for adaptive proliferation and mobility in PIN, are sufficient in the stroma to cause all stages and patterns of invasive PCA. No mutated cells are necessary. For reasons given, the primary cause of the initial ductal blockage that results in PIN and PCA cannot be inflammation, stones, proteineous plugs, infarction, venus thrombosis, ductal hyperplasia, nor a constricted penis at ejaculation. Only benign prostatic hyperplasia (BPH) can explain all the facts and is thus the primary cause of the ductal blockage resulting in cysts, PIN and PCA. The main causes of BPH are apparently disuse atrophy of sexual and abdominal muscles, and atherosclerosis of the capsular branch of the prostatic artery, causes atypical adenomatous hyperplasia (AAH) in the transition zone. The resulting muscular and glandular atrophy decreases local and general growth inhibitors. New growth in the adult prostate is abnormal because epithelial cells grow into ducts rather into the stroma. In such ducts, the growths cannot receive stromal growth inhibitory signals, and thus continue to grow indefinitely and result in BPH, AAH-adenosis, blockage of ducts, cysts, PIN and PCA.

Adult↗