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PubMed2026

High-Throughput Proteomic and Glycoproteomic Analyses in Benign Prostatic Hyperplasia.

Benign prostatic hyperplasia (BPH) is a disease affecting the majority of aging men; 90% of men develop histological BPH by the time they reach their eighties. BPH can lead to bothersome lower urinary tract symptoms (LUTS), which may reduce quality of life. Many patients fail current treatment options and may progress to surgical intervention. Furthermore, diagnosis is reliant on symptom questionnaires and the cause of LUTS can be difficult to distinguish. Currently, BPH can only be definitively diagnosed through histological analysis of prostate tissue, which is not the standard of care. The resulting lack of clinical tissue samples is a major limitation in investigating disease pathology. Improved understanding of disease development and progression, along with objective biomarkers of disease, is needed for BPH. This investigation uses mass spectrometry (MS)-based proteomics and glycoproteomics to compare healthy prostate tissue with prostate tissue affected by BPH to address this gap in knowledge. By integrating proteomics and glycoproteomics, we identified 206 proteins and 44 glycopeptides that were significantly altered between BPH and control samples. These findings provide deeper insight into disease-associated pathways and may facilitate the identification of clinically relevant targets for further investigation.

Male↗

PubMed1992

[Epidemiology and natural course of benign prostatic hyperplasia].

Benign prostatic hyperplasia (BPH) is a frequent condition in men over 50 years of age. At autopsy the histological characteristics of BPH are seen in 80% of all men older than 80 years. Although BPH is so frequent, its precise etiology is still unknown. Each of the various sources from which epidemiological data on BPH can be obtained has its own specific problems in terms of potential errors and biases, which have to be taken into account in interpretation of the data from these sources. There are clear differences in the incidence of BPH in various races. In negroids BPH is more frequent than in Caucasians, while in Asiatic races BPH is less frequent. However, in Asiatics BPH occurs more frequently in men who have immigrated into western countries. Age and hormonal status are well known to be involved in the development of BPH. Other factors, such as marital status, socioeconomic class, smoking, diet, diabetes, hypertension, and liver cir-rhosis have been implicated, but their relation with the risk of developing BPH has never been proven. The natural history of BPH is characterized by an age-dependent increase in histological changes and an increase in prostate size. The histological changes compatible with BPH are found in men below the age of 30 with an incidence of less than 10%. During the 6th decade, 42% of prostatic specimens have histological signs of BPH and during the 8th decade of life more than 80% of prostatic specimens. The histological changes of BPH precede prostatic enlargement by roughly 1 decade. There is an initial spurt of prostate growth during the period of maturation and puberty.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

Epidemiology and natural history of benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) afflicts the majority of elderly men, and if current rates of surgery persist, the average 40-year-old man in the United States will have a 30 to 40 per cent chance of undergoing a prostatectomy if he survives to age 80. Age is by the far the most important determinant of BPH occurrence. Symptomatic BPH has a waxing and waning course, and a few men may have long-term remission. Surprisingly, the natural history of BPH is poorly defined, particularly with regard to the magnitude of the risks of its complications.

Aging↗

PubMed1992

The clinical assessment of benign prostatic hyperplasia.

BACKGROUND: Benign prostatic hyperplasia (BPH) is the most common pathologic condition to afflict the aging male and the second most common cause of surgical intervention in men older than 60 years of age. Unfortunately, many men currently undergo prostatectomy without rigorous evaluation of their condition in terms of either transition zone hyperplasia or the extent to which this is causing bladder outflow obstruction. METHODS: In this review, the importance of symptoms and symptom scoring systems associated with bladder outflow obstruction due to BPH were considered as well as the use of prostate specific antigen (PBS), uroflowometry, and abdominal and transrectal ultrasound studies in addition to magnetic resonance imaging (MRI). CONCLUSION: Patients undergoing surgical or non-surgical treatment for BPH should be studied by means of a formal symptom score, as well as repeated uroflowometry and abdominal ultrasound. PSA determination should also be made and those patients with values above 4 mg/ml should undergo transrectal ultrasound study and biopsy. Patients with values greater than 10 mg/ml should be considered for systematic biopsy whatever this reveals. MRI, with or without the new endorectal coil, is a promising tool for evaluation of the prostate, but more in a research than routine clinical context.

Antigens, Neoplasm↗

PubMedDate not supplied

The pathophysiology of benign prostatic hyperplasia.

Although benign prostatic hyperplasia (BPH) is one of the most common disease processes affecting the aging male, surprisingly little is known about its pathophysiology. Cause-and-effect relationships have not been established, despite intense research efforts in the last four or five decades aimed at elucidating the underlying etiology of prostatic growth in older men. Previously held notions that the clinical symptoms of BPH (prostatism) are due simply to a mass-related increase in urethral resistance are too simplistic. It is now clear that a significant portion of the symptoms are due to obstruction-induced detrusor dysfunction. Moreover, obstruction may induce a variety of neural alterations in the bladder and prostate that contribute to symptomatology. Undoubtedly, the constellation of cellular pathologies that give rise to the symptoms of BPH will be far more complex than we currently realize. Only by unraveling these complexities, however, will we be able successfully to design alternative strategies to treat, and possibly prevent BPH.

Humans↗

PubMed1989

Alpha-adrenoceptor inhibitors in the treatment of benign prostatic hyperplasia.

Although benign prostatic hypertrophy is the most common cause of urinary tract symptoms in men, the cause is still unclear. Recently it has been suggested that treatment with alpha-adrenoceptor inhibitors may be helpful in this condition. Eighty patients with prostatic obstruction were entered into a double-blind parallel study of prazosin versus placebo. There were 25 withdrawals or exclusions, leaving 55 patients for analysis. Mean maximal flow rates increased significantly more in patients treated with prazosin than in patients treated with placebo (p less than 0.005), but there was no significant reduction in maximal voiding pressure. The mean number of voids, recorded on diary cards, was reduced from an initial 10.0/24 hours by 2.1 in the final week, a significantly greater reduction than in the placebo group (p less than 0.01). However, there were no statistically significant changes in the filling cystometrograms. When patients were classified as responders or nonresponders in terms of bladder filling, urine flow, bladder emptying, weekly average of voids/24 hours, and nocturia, the proportion of patients responding to prazosin was significantly greater in all categories except bladder filling and emptying. It was concluded that prazosin at a dose of 2 mg twice daily is a safe and effective treatment for prostatic obstruction and may be used in patients awaiting surgery and in those who are unfit for operation.

Adrenergic alpha-Antagonists↗

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↗

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↗

PubMed1979

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

Normal prostate glands from 6 men less than 30 years old and enucleated tissue of benign prostatic hyperplasia were analyzed by stereological methods. Studies on the relative volumetric amount of fibromuscular (stromal) and glandular areas of the gland reveal no statistically significant difference between the inner and outer parts of the normal prostate and between the inner part of the normal prostate and benign prostatic hyperplasia. However, in benign prostatic hyperplasia there is a significant increase in the volumetric amount of the fibromuscular tissue and a decrease in the glandular area compared to the outer part of the normal prostate and the whole normal prostate (sum of the inner and the outer parts). These stereological data are discussed with respect to the pathogenesis of benign prostatic hyperplasia.

Adult↗

PubMed1989

[Prognosis of the prostatectomy of benign prostatic hyperplasia].

Surgery of benign prostatic hyperplasia has been performed in 484 cases during a period of 10 years from January 1978 to December 1987; these 484 cases comprised 345 to transurethral resection, 130 of subcapsular extirpation and 9 of cryosurgery. Their period of prognosis was examined; 10-year survival rate was 88.9, 95.7, 60.4, 55.8 and 42.8% for 55-59, 60-64, 65-69, 70-74 and 75-79 years, respectively, 8-year and 7-year survival rates being 31.7 and 66.7% for 80-84 85-89 years, respectively. Survival rate by age bracket was compared in terms terms of electrocardiogram (ECG), pulmonary function and possible anomalies and operative blood transfusion. The group of patients with abnormal ECG and pulmonary function showed a significant decreasing survival rate with aging. The aged patients showed no difference in survival rate according to possible blood transfusion. Examination of the cause of death revealed predominant involvement of cardiopathy and cerebrovascular disorder, with comparatively less due to cancers. In terms of postoperative conditions of life of these patients and a long period prognosis of their urination, more 75% of them are living in good condition and 70% are in a state of satisfactory urination.

Age Factors↗

PubMed1987

Relationship between echogram and histology of benign prostatic hyperplasia.

Echograms of benign hyperplastic prostates by means of transrectal ultrasonography were evaluated according to their ability to distinguish between internal and external glands. Of the 112 benign prostatic hyperplasia (BPH) cases, we could distinguish between internal and external glands in 43 cases (38.4%). In 24 of all BPH cases, their preoperative echograms and postoperative histologies were compared. The result was that it was difficult to distinguish between internal and external glands in the many chronic-inflammatory infiltrates.

Humans↗

PubMed1992

Measuring the quality of life of patients with benign prostatic hyperplasia. Assessment of the usefulness of a new quality of life questionnaire specially adapted to benign prostatic hyperplasia patients.

A questionnaire consisting of 36 questions based on a visual analogue scale for measuring the quality of life (QOL) of benign prostatic hyperplasia (BPH) patients is presented and assessed. The sensitivity of the questionnaire is demonstrated by its ability to register a statistically significant (p less than 0.01) improvement of QOL after prostate surgery (transurethral resection of the prostate). Its reliability is shown by its ability to give reproducible results in a nonoperated BPH patient group. Patient compliance has been excellent. It is discussed to what extent questions directly concerning symptoms from prostatism should be included in QOL questionnaires for BPH patients. Nonparametric statistics are applied. It is concluded that questionnaires like this are useful tools in the assessment of BPH patients, irrespective of the treatment modality. They will probably be of particular value in studies of drug therapy of BPH, complementing methods of assessment like symptom score and urodynamic parameters.

Humans↗

PubMed1987

Comparative study of plasma steroid and steroid glucuronide levels in normal men and in men with benign prostatic hyperplasia.

Plasma steroids were analyzed in 16 normal men and in 10 men with prostatic benign hyperplasia (BPH). The steroids measured by radioimmunoassay include pregnenolone, 17-OH-pregnenolone, dehydroepiandrosterone, androst-5-ene-3 beta, 17 beta-diol, testosterone, dihydrotestosterone, androstane-3 alpha, 17 beta-diol, androstane-3 beta, 17 beta-diol, estrone, and estradiol as well as their glucuronide derivatives. In addition, cortisol and the sulphoconjugated form of dehydroepiandrosterone were determined. Whereas the levels of pregnenolone, pregnenolone glucuronide and 17-OH-pregnenolone glucuronide are not different in the two groups, the levels of 17-OH-pregnenolone in the BPH group (0.87 +/- 0.07 ng/ml) exceed by two-fold (p less than 0.01) those observed in normal men. Plasma dehydroepiandrosterone and androst-5-ene-3 beta, 17 beta-diol concentrations are markedly elevated in the BPH group (1.49 +/- 0.23 and 0.55 +/- 0.08 ng/ml vs the control groups 0.43 +/- 0.11 and 0.31 +/- 0.05 ng/ml, respectively). Since the plasma cortisol and pregnenolone levels are comparable in these two groups, our data suggest that the elevation of plasma 17-OH-pregnenolone, dehydroepiandrosterone, and androst-5-ene-3 beta, 17 beta-diol reflects an increase of adrenal 17-hydroxylase activity in patients with BPH. A slight increase of the plasma dihydrotestosterone and androsterone glucuronide concentration is also observed in men with BPH, indicating an increase of 5 alpha-reduced androgen formation. We have also observed, in the BPH group, a 50% decrease (p less than 0.01) of plasma glucuronidated androst-5-ene-3 beta, 17 beta-diol, estrone, and estradiol levels, suggesting that the transformation of unconjugated estrogenic steroids into glucuronide derivative is inhibited in BPH patients. In summary, our data indicate that adrenal C-19 steroids might be involved in the process of BPH. Furthermore, whereas the estrogen glucuronide formation is diminished in men with BPH, the prostatic androgen metabolism as reflected by plasma dihydrotestosterone and androsterone glucuronide concentrations seems to be increased.

Aged↗

PubMed1977

Rectal invasion by benign prostatic hyperplasia.

Rectal invasion by benign prostatic hyperplasia occurred subsequent to an open transrectal biopsy of the prostate gland. Frequent transrectal resections of the prostate controlled this unusual lesion initially. However, massive intrarectal regrowth of this clinically malignant but histologically proved benign prostatic enlargement required eventual pelvic exenteration.

Humans↗

PubMed1989

Diagnostic assessment of benign prostatic hyperplasia.

Clinical evaluations of benign prostatic hyperplasia (BPH) are based upon careful history taking, uroflowmetry, palpation of the prostate, and diagnosis of urinary infection or possible damage to the kidneys caused by outflow obstruction. Symptom assessment includes scoring by the patient of the four obstructive and five irritative symptoms of prostatic obstruction: a simple questionnaire is used. The scoring system should be reviewed with the urinary flow measurements as part of the workup. The various forms of ultrasound used for diagnosis, although invaluable, may not be assessed out of context, and the combination of digital palpation and endoscopy generally provide most information leading to a decision for operation. When available, perrectal ultrasound scanning should be used to investigate palpable abnormalities and to identify unexpected prostatic cancer.

Humans↗

PubMed1991

Pathogenesis of benign prostatic hyperplasia.

The pathogenesis of benign prostatic hyperplasia (BPH) remains largely unresolved. Three major theories have evolved over the years, each emphasizing a possible causative mechanism. The first theory, the dihydrotestosterone hypothesis, is based on the failure of BPH to develop in men castrated prior to puberty. The second, the embryonic reawakening theory, assumes a reawakening of the embryonic induction potential of prostatic stroma. The third, or stem cell theory, postulates the development of BPH through an increase in the number of stem cells or through an abnormal increase in clonal expansion of amplifying or transit cells. These mechanisms may act in concert.

Androgens↗

PubMed1991

Symptomatology and diagnosis of benign prostatic hyperplasia.

The symptoms of benign prostatic hyperplasia are well known. Diagnosis rests on digital palpation of the enlarged prostate. Objective parameters are laboratory tests, imaging techniques, endoscopy, and urodynamic investigations. Laboratory tests include urinalysis and serum creatinine measurement. Markers are not reliable and the determination of acid phosphatase and prostate-specific antigen is not recommended routinely for patients with prostatism. Imaging techniques are usually restricted to a complete echographic investigation of the entire urinary tract. Endoscopic manipulations are seldom necessary. Uroflow measurements are customarily performed, but the need for a complete urodynamic investigation is still open to debate.

Humans↗

PubMed1991

Steroid hormones and the pathogenesis of benign prostatic hyperplasia.

The pathogenesis of benign prostatic hyperplasia (BPH) is still poorly understood: there is, however, general acceptance that the condition is not premalignant and that it has an etiology distinct from that of cancer. Interest now focuses on the biochemistry of the target prostate cells and the propensity of the gland for uncontrolled growth. Dihydrotestosterone (DHT) is the active intracellular androgen formed from testosterone by 5 alpha-reductase. DHT concentrations appear a little higher in BPH tissue than in normal tissue, and there is no doubt that DHT-receptor complex modulates gene expression. Current studies suggest that DHT is essential but not sufficient for proliferation, and that other regulatory factors, including peptide growth factors, are prerequisite. The growth responsiveness of prostate tissue to androgens may be dependent on the balance between epithelial and stromal tissues, with biologic processes in the epithelium indirectly controlled by androgen-dependent mediators of stromal origin.

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