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PubMed1979

Electron microscopic stereological analysis of the normal human prostate and of benign prostatic hyperplasia.

Normal and benign hyperplastic prostatic tissue was studied by quantitative electron microscopic measurements. Quantitative morphological procedures provide values for volume, surface, number of tissue and cellular components within human prostatic tissue. When a comparison is made of the stereological data of the glandular cell of benign prostatic hyperplasia to that of the normal human prostate no statistically significant difference in the relative volumetric amount of the cell organelles is indicated. An attempt was made to characterize the fine structure of the smooth muscle cells of the stromal area (fibromuscular) in normal and benign hyperplastic prostatic tissue. In benign prostatic hyperplasia a significant increase in the relative amount of organelles in the smooth muscle cell was found, indicating an activation of these cells. Light microscopic analysis has revealed that benign prostatic hyperplasia is primarily a stromal disease.

Cytological Techniques↗
PubMed2006

Prevention of benign prostatic hyperplasia disease.

PURPOSE: We reviewed the evidence that benign prostatic hyperplasia is a progressive condition and men at risk for benign prostatic hyperplasia disease can be identified, treated and protected to a meaningful extent regardless of symptom status. MATERIALS AND METHODS: The MEDLINE database was searched in 4 areas of interest relating to benign prostatic hyperplasia, including 1) progression of clinical manifestations with age, especially in regard to baseline symptom status, 2) the incidence of complications due to disease progression, 3) the use of predictive factors that may help identify men at risk for disease progression and 4) the prevention of benign prostatic hyperplasia disease with medical therapy. RESULTS: Tissue changes in the prostate (benign prostatic hyperplasia) are inevitable consequences of aging. However, benign prostatic hyperplasia disease, which we define as a life altering urinary condition requiring medical intervention, is predictable and preventable. Benign prostatic hyperplasia disease progression is associated with increasing prostate volume, decreasing urinary flow, symptomatic deterioration often to the point of major life-style interference and serious complications, eg acute urinary retention and the need for surgery. The risk of benign prostatic hyperplasia disease progression was found to be directly related to prostate volume and its surrogate marker, serum prostate specific antigen, after prostate cancer is excluded. Other factors, eg baseline symptoms and the flow rate, were found to be less relevant compared with prostate specific antigen greater than 1.5 ng/ml for predicting benign prostatic hyperplasia disease morbidity. CONCLUSIONS: Men at risk for benign prostatic hyperplasia disease can be identified using prostate specific antigen greater than 1.5 ng/ml as a surrogate marker of prostate volume. In men at risk with prostate specific antigen greater than 1.5 ng/ml 5alpha-reductase inhibitors have potential value for benign prostatic hyperplasia disease prevention regardless of symptom status.

Adult↗
PubMed1997

Prostatic volume and ratio of free-to-total prostate specific antigen in patients with prostatic cancer or benign prostatic hyperplasia.

PURPOSE: We correlated prostatic volume with the ratio of free-to-total prostate specific antigen (PSA) in serum from patients with prostatic cancer or benign prostatic hyperplasia (BPH) to evaluate how prostatic volume influences the ratio. MATERIALS AND METHODS: We evaluated sera from 395 patients (mean age 65 years, range 45 to 88) with prostate cancer (239) or BPH (156) for total PSA, free PSA and ratio of free-to-total PSA. For detection of total and free PSA we used an Immulite free and total PSA assay. Prostatic volume was determined with transrectal ultrasonography. Prostatic volume in BPH and prostate cancer patients was divided into 10 ml. groups, and mean ratio of free-to-total PSA was calculated for each volume group and both diseases. For statistical analysis Mann-Whitney U and Kruskal-Wallis tests were performed in addition to calculation of sensitivity and specificity, and receiver operator curves for prostates 60 ml. or less and greater than 60 ml. RESULTS: For BPH patients the mean ratio of free-to-total PSA was 14.64 to 25.14% without a close relation to prostatic volume. In prostate cancer patients a proportional increase from 8.45 to 19.37% in the ratio of free-to-total PSA with volume was found. Mann-Whitney U analysis revealed significant differences in prostate cancer versus BPH only in patients with prostates of 60 ml. or smaller (p = 0.0008 to 0.029). No significant differences were seen when prostate cancer and BPH patients with prostates larger than 60 ml. were compared (p = 0.082 to 0.868). Kruskal-Wallis test confirmed independence of the ratio of free-to-total PSA from prostatic volume in BPH patients (p = 0.285) but dependence in prostate cancer patients (p <0.0001). Sensitivity was higher in patients with prostates 60 ml. or smaller (86.72%) than in patients with prostates larger than 60 ml. (66%), and specificity was lower at 45.78 and 56.16%, respectively. CONCLUSIONS: We have shown that the ratio of free-to-total PSA is influenced by prostatic volume in patients with prostate cancer. The ratio of free-to-total PSA provides useful information for differentiate BPH from prostate cancer in patients with small prostates but it is less useful in patients with larger prostates, probably because of the larger proportion of benign hypertrophic tissue.

Aged↗
PubMed1999

Prostate specific antigen density for discriminating prostate cancer from benign prostatic hyperplasia in the gray zone of prostate-specific antigen.

Serum prostate specific antigen (PSA) is currently the best blood marker for prostate cancer. However, low specificity for detection of prostate cancer, especially in the gray zone of PSA, is a problem. We evaluated the clinical significance of PSA density (PSAD) in gray zone PSA cases with conversion of serum PSA to a Stanford reference value. In a series of histologically confirmed 63 benign prostatic hyperplasia (BPH) patients and 234 prostate cancer patients, 36 BPH patients and 25 prostate cancer patients had gray zone PSA levels. Serum PSA was measured with the Markit-F or Markit-M PA assay. All data were converted to Stanford reference values. We used transabdominal ultrasound to determine prostate volume. PSAD was determined as the serum PSA/prostate volume ratio. The mean PSA values for BPH and prostate cancer were 6.42 +/- 1.80 and 7.80 +/- 2.15 ng/ml (p = 0.0116), respectively, and prostate volume was 33.4 +/- 14.1 ml and 17.1 +/- 8.2 ml, respectively (p < 0.0001). The mean PSAD for prostate cancer was 0.572 +/- 0.363 while that for BPH was 0.218 +/- 0.085 (p = 0.0001). Cut-off values with sensitivity > 90% were 0.218 for PSAD and 30 ml for prostate volume. At these cut-off values, specificity reached 56% for each marker. In discriminating prostate cancer from BPH in the gray zone of PSA, PSAD demonstrated better performance than PSA.

Aged↗
PubMed1980

The pathogenesis of benign prostatic hyperplasia.

Development of prostatic hyperplasia is an almost universal feature of the aging man and dog, and in both species the process develops only in males with intact testes. As the result of studies of plasma hormone levels as a function of age, measurements of the concentration of androgen and of androgen receptor proteins within the prostate, and studies of the effects of the administration of various hormones on growth of the prostate in the castrated dog, it is possible to provide a working hypothesis as to the pathogenesis. Dihydrotestosterone accumulation within the gland serves as the hormonal mediator for the hyperplasia in both species; the accumulation probably occurs in part because of decreased catabolism of the molecule and in part because of enhanced intracellular binding of the molecule. The process is accelerated by estrogen, which enhances the level of the androgen receptor in the gland; increase in the androgen receptor allows for androgen-mediated growth even in the face of declining androgen production in advanced age. On theoretic grounds the therapeutic implications of this model are exciting; several potential medical treatments may be feasible that do not involve a chemical castration.

Adolescent↗
PubMed2006

Relationship among serum testosterone, sexual function, and response to treatment in men receiving dutasteride for benign prostatic hyperplasia.

CONTEXT: Although benign prostatic hyperplasia (BPH) is an androgen-dependent disorder, little is known regarding the influence of serum testosterone levels on sexual or prostate function or clinical response to dutasteride. OBJECTIVE: The objective of the study was to explore these relationships in a large cohort of men treated with dutasteride for BPH. DESIGN, SETTING, PATIENTS, AND OUTCOME MEASURES: Among 4254 men with BPH participating in 2-yr placebo-controlled dutasteride trials, 27% had a pretreatment serum testosterone less than 300 ng/dl. These 1162 men were divided into seven groups based on their serum testosterone level (<150, 150-174, 175-199, 200-224, 225-249, 250-274, and 275-299 ng/dl) and compared with men with normal baseline serum testosterone (BST; > or = 300 ng/dl). Questionnaires were used to assess sexual function, prostate-specific antigen (PSA), and prostate volume to assess androgenic stimulation of the prostate and the American Urological Association Symptom Index to assess clinical responses. RESULTS: Although lower BST was associated with increased sexual dysfunction, this increase was not seen until BST was less than 225 ng/dl. There was no decrease in baseline PSA and prostate volume at low BST levels. Dutasteride was effective at decreasing PSA and prostate volume and improving BPH symptoms at all BST levels. CONCLUSIONS: In men with BPH, the frequency of sexual dysfunction increases at serum testosterone concentrations less than 225 ng/dl. However, PSA and prostate volume were similar at all testosterone levels, explaining why BPH can occur in men that would otherwise be considered hypogonadal. The fact that dutasteride is also effective in men with normal and low testosterone levels suggests that the high levels of 5alpha-reductase and dihydrotestosterone in the prostate allow the development and progression of prostatic hyperplasia, even at low circulating testosterone levels.

Aged↗
PubMed1997

Effects of age and sex hormones on transition and peripheral zone volumes of prostate and benign prostatic hyperplasia in twins.

Benign prostatic hyperplasia has been shown to increase with age and be influenced by sex hormones. The relationship between aging and hormonal influences on growth of zones of the prostate is unresolved. We studied the relationship of age and sex hormones on volume of prostate zones in 214 male twins between 25 and 75 yr old. Volumes of the total prostate (TV), transition zone (TZ), and peripheral zones (PZ) were measured using transrectal ultrasound, and sex steroid concentrations were measured using RIA. Using transformed data corrected for age, TV (r = 0.54, P < 0.00001), TZ (r = 0.58, P < 0.00001), and PZ (r = 0.39, P < 0.00001) volumes increased with age. However, the PZ volume rose more rapidly than the TZ before age 50, and TZ showed a steeper increase after age 50 yr than the PZ volume. The TZ, PZ, and ratio TZ/PZ correlated significantly (r = 0.87, 0.90, and 0.52, respectively; P < 0.00001). After a TV exceeded 30 g, the rise of the PZ became attenuated, and the slope of the TZ became steeper. Age-adjusted sex hormone concentration was not evaluated in men with larger prostate volumes. Men with American Urological Association symptom scores above 10 had significantly (P < 0.001) larger total prostate volume (TV) and TZ volume, but not PZ volumes, than men with scores below 10. Prostate volumes correlated inversely with age-adjusted serum testosterone (T), dihydrotestosterone, sex hormone binding globulin, and sex hormone binding globulin-bound T concentrations. These results demonstrate that before age 50 yr or before a prostate weight exceeds 30 g, prostate growth may be mainly from enlargement of the PZ and after age 50, the TZ. In addition, elevated T and dihydrotestosterone concentrations do not predispose men to prostate enlargement or symptoms of benign prostatic hyperplasia.

Adult↗
PubMed1996

Androgen and glucocorticoid receptors in the stroma and epithelium of prostatic hyperplasia and carcinoma.

Differences in stromal and epithelial cell staining for androgen and glucocorticoid receptors (ARs and GRs) were investigated in 20 patients with clinically localized prostatic carcinoma treated by radical prostatectomy. Sections of benign prostatic hyperplasia and prostatic carcinoma from each patient were stained with antibodies to AR and GR using an avidin-biotin peroxidase technique. The specificity of the GR immunoreactivity was established in benign prostatic hyperplasia and prostatic carcinoma by immunohistochemistry using the GR antibody absorbed with synthetic peptide and Western blotting. Nuclear staining intensity and percentage of nuclei stained were summed to obtain AR and GR immunostaining scores. AR staining of prostatic carcinoma epithelial [103 +/- 58 (SD)] and stromal (126 +/- 48) nuclei was less than in benign prostatic hyperplasia (142 +/- 47 and 169 +/- 56; paired Student's t tests, P = 0.02 and P = 0.01); however, no difference in staining intensity occurred between stroma and epithelium in either tissue type. GR stained intensely in stromal cells from benign prostatic hyperplasia (189 +/- 50) and prostatic carcinoma (163 +/- 60). However, prostatic carcinoma epithelial cells (34 +/- 57) had low levels of glucocorticoid receptor staining (P < 10(-7)), and benign prostatic hyperplasia epithelium (74 +/- 51) was intermediate. In most patients, GR could not be detected in nuclei of prostatic carcinoma epithelial cells but was undiminished in stromal cell nuclei. There was no relationship by multivariate regression analysis between AR or GR staining and age, serum prostate-specific antigen, Gleason grade, or pathological stage. In comparison with AR, the greater variability of GR staining in epithelium versus stroma of prostatic carcinoma warrants further study of GR, particularly in the area of stromal-epithelial interaction.

Aged↗
PubMedDate not supplied

[Long-term results of proscar (finasteride, MSD) treatment of patients with benign prostatic hyperplasia].

Patients with benign prostatic hyperplasia (BPH) received proscar (finasteride) in daily dose 5 mg for: at least 6 months (n = 206, 20.4%), 12 months (n = 513, 50.9%), 24 months (n = 164, 16.3%), 3-4 years (n = 125, 12.4%). Because the size of the prostatic gland reduced significantly (by 22%) only after one year of proscar treatment, the duration of this treatment should be continued for at least 12 months, in some patients as long as the whole life. The duration of the treatment should be decided for each individual patient. The improvement after the proscar treatment was observed in 95% of the patients treated for benign prostatic hyperplasia.

Aged↗
PubMed1987

Observations with Bazoton in the management of prostatic hyperplasia.

Thirty patients with prostatic hyperplasia stages I and II were administered Bazoton capsules (extract of Radix Urticae) for an average period of 3.5 months. Residual urine, mean and maximal flow were measured before and after treatment. A significant decrease in the volume of residual urine was found. Increase in mean urinary flow was also significant. Maximal urinary flow increased in 50% of the cases. A marked subjective relief was reported by the patients. Bazoton is regarded as suitable for the conservative treatment of prostatic hyperplasia stages I and II.

Humans↗
PubMed2006

Central obesity as a risk factor for prostatic hyperplasia.

OBJECTIVE: Obesity-related metabolic diseases may influence prostatic hyperplasia. This study examined the impact of obesity on prostate volume in men without overt obesity-related metabolic diseases. RESEARCH METHODS AND PROCEDURES: We recruited 146 men over the age of 40 years who did not have overt obesity-related diseases, such as diabetes, impaired fasting glucose, hypertension, or dyslipidemia. Transrectal ultrasonography was performed on all subjects. The subjects were divided into three groups according to their BMI: normal (18.5 to 22.9 kg/m2), overweight (23 to 24.9 kg/m2), and obese (> or = 25 kg/m2), and two groups according to their waist circumference: normal waist (< or = 90 cm) and central obesity (> 90 cm). The classification of the subgroups was based on the Asia-Pacific criteria of obesity. We compared the prostate volume among subgroups and assessed factors related to prostatic hyperplasia. RESULTS: Mean prostate volume was 18.8 +/- 5.0, 21.8 +/- 7.2, and 21.8 +/- 5.6 mL in the normal, overweight, and obese groups, respectively, and was 20.0 +/- 5.9 and 23.7 +/- 5.3 mL in the normal waist and central obesity group, respectively. Prostate volume was significantly greater in the obese group than in the normal group (P = 0.03) and in the central obesity group compared with the normal waist group (P = 0.002). Prostate volume was positively correlated with BMI and waist circumference after adjustment for age. After adjusting for confounding factors, central obesity was an independent factor affecting prostatic hyperplasia, which was defined as a prostate volume > 20 mL (odds ratio = 3.37, p = 0.037). Relative to men with both low BMI (18.5 to 22.9 kg/m2) and normal waist circumference, those with high BMI (> or = 25 kg/m2) and central obesity were at significantly increased risk of prostatic hyperplasia (odds ratio = 4.88, p = 0.008). However, those with high BMI (> or = 25 kg/m2) and normal waist circumference were not at significantly increased risk. DISCUSSION: Prostate volume was greater in the obese and central obesity groups than in the normal group after patients with overt obesity-related metabolic diseases were excluded. Although both BMI and waist circumference were positively correlated with prostate volume, central obesity was the only independent factor affecting prostate hyperplasia. We suggest that central obesity is an important risk factor for prostatic hyperplasia.

Abdominal Fat↗
PubMed1991

[Hyperthermic treatment of benign prostatic hyperplasia by a prostathermer].

Prostate thermotherapy consisting of 6 sessions of intrarectal 60 min irradiation of 915 MHz microwave generated by a prostathermer (Blodan, Isreal) was performed once or twice a week on 30 patients with benign prostatic hyperplasia. Excluding 2 cases who refused further therapy at the first session because of rectal discomfort, 28 cases were evaluated for the efficacy of the treatment. Good or fair improvement in subjective symptoms was observed in 24 (85.7%) of the cases. Nocturia was significantly relieved from 2.9 to 2.0 a night. Among the objective responses, no improvement was achieved as to residual urine or prostate size, while a significant increase of maximum or average flow rate on uroflowmetry was observed. Adverse effects were minor or moderate, including 2 cases of urethral bleeding and rectal discomfort, 2 cases of lower urinary tract infection and 1 case of hypotension, which occurred at the 5th session. The scoring criteria taking into account of both subjective and objective responses showed that the efficacy is good in 10 cases (33.3%) and fair or good in 20 cases (66.7%). These results indicated the usefulness of the prostathermer as one of non-surgical therapies for benign prostatic hyperplasia.

Aged↗
PubMed1993

[Immunohistochemical study of the prostatic tissues with monoclonal antibody against gamma-seminoprotein. Analyses of benign prostatic hyperplasia, metastatic foci from adenocarcinoma of the prostate and malignant neoplasms other than adenocarcinoma of the prostate].

The immunohistochemical specificity of the monoclonal antibody (43-21-1-1) against gamma-seminoprotein (gamma-Sm) in the prostatic tissues was evaluated by avidin-biotin peroxidase complex method. The normal tissues of various organs, other than male genitourinary organs already examined in the previous study, the brain, skin, spinal cord, tongue, esophagus, stomach, small intestine, rectum, trachea, lung, pleura, diaphragm, liver, spleen, pancreas, mesentery, kidney, lymph node, bone, bone marrow and striated muscle were examined for control study. The prostatic tissues obtained by surgery or biopsy, benign prostatic hyperplasia (BPH; 72) urethral polyp with prostatic-type epithelium (1), bone (3) or testicular (2) metastases from adenocarcinoma of the prostate and malignant neoplasms other than adenocarcinoma of the prostate, including primary small-cell carcinoma (1), secondary embryonal carcinoma (1) and secondary mucinous adenocarcinoma (1) of the prostate were then examined. Since all but 2 (97%) specimens of BPH were obtained by transurethral resection (TUR), which might cause non-specific staining due to electro-mechanical effects, the tissue of BPH obtained by suprapubic prostatectomy were examined simultaneously, serving as a control for immunostaining. The normal tissues of various organs were never stained positively for gamma-Sm. Positive reactions of gamma Sm with this monoclonal antibody were recognized in the cytoplasms of urethral polyp with prostatic-type epithelium, bone or testicular metastases from adenocarcinoma of the prostate. The malignant neoplasms other than adenocarcinoma of the prostate examined in this study, were never stained positively. There was obviously evidence of non-specific staining in the TUR tissues of BPH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed2005

Botulinum toxin type A improves benign prostatic hyperplasia symptoms in patients with small prostates.

OBJECTIVES: To expand the clinical use of botulinum toxin A (BTX-A) in treating patients with small prostates and symptomatic benign prostatic hyperplasia (BPH). BTX-A injection into the prostate in patients with voiding dysfunction and large prostates has been reported. METHODS: Sixteen men with symptomatic BPH, a prostate volume less than 30 cm3, peak flow rate less than 12 mL/s, and with refractory disease after at least 1 month of alpha-blocker treatment received BTX-A 100 U injection into the prostate transperineally under transrectal ultrasound guidance. The clinical effects were evaluated at baseline and after treatment. RESULTS: No significant local or systemic side effects were observed in any of the patients. All patients reported subjective improvement starting at approximately 1 week and achieved a maximal effect after 1 month that was maintained at 3 and 6 months. At 6 to 12 months (mean 10) of follow-up, no patient had symptom recurrence. The mean prostate volume, symptom score, and quality-of-life index were significantly reduced by 13.3% (from 19.6 +/- 1.2 to 17.0 +/- 1.1 cm3), 52.6% (from 18.8 +/- 1.6 to 8.9 +/- 1.9), and 44.7% (from 3.8 +/- 0.3 to 2.1 +/- 0.3), respectively. The maximal flow rate increased significantly by 39.8% (from 7.3 +/- 0.7 to 11.8 +/- 0.8 mL/s). In 2 patients who underwent biopsy 1 month after BTX-A injection, terminal deoxynucleotidyl-mediated deoxyuridine triphosphate nick end labeling staining demonstrated an increase in apoptotic activity, not only in the glandular component, but also in the stromal component of the prostatic tissue. CONCLUSIONS: BTX-A injected into the prostate is a promising treatment for patients with small prostates and symptomatic BPH.

Aged↗
PubMed2004

Treatment of benign prostatic hyperplasia and occurrence of prostatic surgery and acute urinary retention: a population-based cohort study in the Netherlands.

OBJECTIVES: To assess and compare the risk of prostatic surgery in (subsets of) patients with a diagnosis of BPH. We sought to expand on data of an earlier pharmacy-based study by obtaining more information on BPH disease parameters by using a Dutch GP-based research database. METHODS: A retrospective cohort study (1994-mid-year 2002) was conducted among 1430 men aged > or =45 years with > or =6 months of registration with the GP. BPH case identification was based on review of medical records. RESULTS: Overall, we found that there was no difference in the risk of prostatic surgery between patients on medical treatment and watchful waiting. Patients using 5alpha-reductase inhibitors (5-ARIs) at any stage had a statistically significant reduced risk of surgery compared to patients using alpha-blockers only: adjusted hazard ratio 0.35 (95%CI: 0.13-0.96). The routine collection of BPH parameters were insufficient to be useful in the analysis. CONCLUSION: Patients using 5-ARIs seemed to have a reduced risk of prostatic surgery compared to patients using alpha-blockers. However, it was unknown whether the disease profile of 5-ARI users is different compare to non-5-ARI-treated and untreated patients with BPH, as detailed medical information necessary to characterise patients according to the BPH disease severity and development of disease parameters is not routinely recorded by GPs.

Acute Disease↗