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 271 records · Page 15Linked to original sources

[Pathophysiology of benign prostatic hyperplasia].

Benign prostatic hyperplasia (BPH) is primarily a anatomical diagnosis. The prepubertal weight of the gland is about 1.6 g and at the end of the third decade around 20 g. With histological evidence for BPH there is an increase of weight and volume with aging. The human prostate is divided into zones which form, however, a fairly regular gland. The prostate is organized similar to a grape, these parts are surrounded with the epithelial cells which express different compounds and proteins and finally disappear by apoptosis. The stromal compartment is kind of a skeleton, both compartments (epithelial and stromal part) present manifold interactions based on androgens, androgen receptors and growth factors.

Adolescent↗

Worldwide patterns of prevalence and mortality from benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) can be found in 88% of autopsies in men > or = 80 years, with compatible symptomatology reported in nearly 50% of men aged > or = 50 years in the general population. Despite such a common occurrence, little is known with any certainty about the epidemiology of BPH (for which "prostatism" is a commonly, and wrongly, used synonym). Knowledge of risk factors is sparse: analytic epidemiologic studies of BPH are difficult to conduct. It is essential to establish an epidemiologic definition of BPH for these reasons. Both BPH and prostatism are the problems that seem set to increase in absolute terms. They are clearly identified as priority areas for research into their causes and treatment. However, it is clear that there is a great need for more epidemiologic information, particularly regarding prostatism, whose occurrence is unknown in many parts of the world.

Global Health↗

Terazosin. A pharmacoeconomic evaluation of its use in benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common disorder in elderly men which carries a substantial economic burden. Urinary symptoms associated with moderate to severe disease can significantly interfere with daily activities and reduce quality of life. Obstruction of urine flow in men with BPH can result from nonmalignant enlargement of the prostate gland (static component of BPH) and from alpha 1 receptor-mediated increased smooth muscle tone of the bladder neck and prostate (dynamic component of BPH). Transurethral resection of the prostate (TURP) is generally very effective and has traditionally been the standard treatment for men with moderate to severe BPH. However, response to therapy with TURP is not universal and the procedure is associated with a number of potential complications. Moreover, many men prefer to avoid or are not suitable candidates for this invasive procedure. Thus, there is an increasing role for less invasive treatment, including drug therapy, in men with moderate to severe BPH. Terazosin is an alpha 1 receptor antagonist which has been shown in placebo-controlled trials to significantly improve American Urology Association (AUA) symptom and quality-of-life scores and symptom problem index ('bother' score), as well as increase peak urinary flow rate, in men with BPH. In a recent large randomised US trial, treatment for 1 year with terazosin titrated to 10 mg/day improved mean AUA symptom score and peak urinary flow rate to a significantly greater extent than finasteride 5 mg/day in men with moderate to severe BPH. The most frequently reported adverse events associated with terazosin include dizziness, asthenia, postural hypotension, somnolence, headache, peripheral oedema, nasal congestion/rhinitis and syncope. Approximately 5% of men with BPH discontinue terazosin because of adverse events. Results of an economic evaluation of terazosin, in which both clinical and economic data were collected prospectively in a randomised placebo-controlled study design, showed similar total direct treatment costs per 1000 patients associated with 1 year of therapy with terazosin ($US3.57 million) and placebo ($US3.78 million) in men with moderate to severe BPH (1992 dollars). The analysis, which was conducted from the perspective of a managed care organisation in the US, demonstrated that the lower medication costs in the placebo group relative to the terazosin group were offset by increased inpatient care costs. Thus, terazosin (titrated to response up to a maximum of 10 mg/day) was significantly more effective than placebo in improving disease-specific symptoms and quality of life, but at a similar overall cost to placebo. Another economic analysis, also conducted from a third-party payer perspective in the US, modelled direct treatment costs associated with terazosin, finasteride and TURP during the first 2 years after initiating therapy in men with moderate to severe BPH. Results of the study favoured terazosin; the private insurance cost per patient undergoing primary treatment with TURP was $US6411, compared with $US2860 with finasteride (45% of the cost of TURP) and $US2422 with terazosin (38% of the cost of TURP). Medicare costs were lower for all 3 treatment groups but the relative comparisons were similar; corresponding costs per patient were $US3874, $US2161 and $US1820 (1992 dollars). A companion break-even cost analysis used a hypothetical cohort of men with BPH starting treatment at age 67 years. Private insurance costs associated with terazosin remained lower then those associated with TURP for approximately 15 years (the corresponding break-even point was 10 years for finasteride vs TRUP). Medicare costs associated with terazosin would not exceed those of TURP for approximately 7 years (5.5 years for finasteride vs TURP). In conclusion, a limited number of detailed pharmacoeconomic analysis of terazosin have been conducted to date, although it has not been compared with other a1 receptor antagonists.

Adrenergic alpha-Antagonists↗

Role of growth factors in benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common condition among older men. Although surgery is the most effective treatment for patients with severe symptoms of bladder outlet obstruction, many patients with less severe symptoms will benefit from pharmacological intervention. Traditional medical therapies have involved hormonal manipulation. However, evidence has now emerged that prostate growth is under the immediate control of specific growth factors and only indirectly modulated by steroids. In this review we present a hypothesis of the mechanism of action of these growth factors in the developmental of BPH. Many of the more bothersome symptoms of BPH are not directly caused by the outlet obstruction, but only the resulting bladder hypertrophy. The development of the rabbit model of partial bladder outlet obstruction has allowed investigation of the bladder changes likely to occur in BPH. These studies have revealed the important role of growth factors in the development of bladder hypertrophy. Therefore, targeting growth factors potentially represents a direct therapeutic approach to the regulation of abnormal enlargement of the prostate and the amelioration of other symptoms associated with BPH.

Animals↗

Benign prostatic hyperplasia.

Benign prostatic hyperplasia is a common problem in men over 50, causing unpleasant symptoms. This Update examines the range of treatments now available, including traditional interventions and modern techniques.

Humans↗

Induction of apoptosis in human prostate stromal cells by 4-hydroxytamoxifen: an alternative therapy for benign prostate hyperplasia.

Benign prostate hyperplasia (BPH) is a disease of the aging male. In BPH, the imbalance of cell proliferation and programmed cell death (apoptosis) leads to continuous stromal growth. Common medication interrupts stromal cell proliferation but has only little effect on inducing stromal cell apoptosis. In this study, we investigated tamoxifen (TAM) and 4-hydroxytamoxifen (OHT) for their ability to induce apoptosis in human prostate stromal cells (PrSC) in vitro. After the incubation of PrSC with different concentrations of TAM or OHT, the cytotoxic effect was measured using an MTT-assay. The induction of apoptosis after OHT treatment was investigated by FACS-analysis (annexin V FITC staining) and Western blot (PARP-1 cleavage, BCL-2 and BAX-alpha expression). The administration of TAM at concentrations of 0-20 microM had very little effect on cell viability as measured by MTT assay. In contrast, the use of 10-20 microM OHT led to a significant decrease in cell viability. The binding of annexin V FITC to apoptotic cells was demonstrated by FACS-analysis. The induction of apoptosis was further proven by Western blot of PARP-1 protein cleavage and the expression of the anti-apoptotic BCL-2 and the pro-apoptotic BAX-alpha proteins. In conclusion, our data clearly demonstrate, that the administration of OHT at concentrations from 10-20 microM induced apoptosis in human PrSC. The more effective induction of apoptosis with OHT compared with TAM could very well explain the results of clinical studies showing no clinical effect of TAM treatment on BPH. Furthermore, our results, if reproducible in vivo, could open new avenues for the treatment of BPH by local administration of OHT in apoptosis-inducing concentrations.

Apoptosis↗

Future implications for the management of benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a growing medical problem in terms of morbidity, mortality, and health care costs. Renewed research has highlighted the lack of standardized parameters available with which to define and evaluate BPH and its treatment. The many treatments available, ranging from surgery to watchful waiting, point to the complex pathophysiology of BPH and the subjectivity of the treatment decisions. Workup of patients with micturition disorders, coupled with use of the International Prostate Symptom Score evaluation, permits the development of criteria for evaluating treatment efficacy and acceptable treatment options. Based on double-blind, placebo-controlled trials, a-blockers and finasteride have been accepted as treatment options. The former produce relaxation of the smooth muscle by inhibiting adrenergically induced increases in intracellular calcium. The latter blocks the 5a-reductase system, which effectively stops the conversion of testosterone to dihydrotestosterone. a-Blockers improve symptoms and flow immediately while finasteride diminishes the prostate volume, specifically of glandular tissue, leading to improved symptoms and flow. All other medical and nonmedical treatments require further evaluation by randomized, prospective trials to determine their safety profile and efficacy.

Humans↗

Efficacy and safety of alfuzosin 10 mg once daily in the treatment of symptomatic benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common disorder in ageing men. Patients with BPH often present with bothersome irritative and obstructive lower urinary tract symptoms -- urgency, frequency, nocturia, feeling of insufficient bladder emptying and weak or intermittent flow. alpha(1)-Blockers are the most frequently prescribed oral medications for the first-line treatment of the symptoms associated with BPH. Alfuzosin is a uroselective alpha(1)-blocker that relaxes the smooth muscle of the bladder neck and prostate gland to alleviate BPH symptoms. A pooled analysis of three phase III trials confirmed that treatment with alfuzosin 10 mg q.d. significantly improves the peak urinary flow rate and symptom severity compared with placebo treatment. Unlike some other alpha(1)-blockers, alfuzosin 10 mg q.d. is associated with a low incidence of sexual and vasodilatory side effects. Based on the clinical trials reviewed, alfuzosin 10 mg q.d. is an effective and well-tolerated treatment for the urinary symptoms associated with BPH.

Adrenergic alpha-Antagonists↗

Localization of angiotensin-converting enzyme in the human prostate: pathological expression in benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is the most common hyperplastic disease in man and it is characterized by increased cellular growth (stromal and epithelial hyperplasia) and enhanced local sympathetic tone, both of which are known to be augmented by activation of the renin-angiotensin system (RAS) in other tissues. Angiotensin-converting enzyme (ACE) is an integral component of the RAS that is responsible for the production of the active peptide angiotensin II from the inactive precursor angiotensin I. The present study was undertaken to map the anatomical localization of ACE protein and messenger ribonucleic acid (mRNA) in the normal human prostate and to establish whether their expression is pathologically altered in BPH. Human prostate samples were obtained at post-mortem and histologically defined as normal or hyperplastic. ACE protein binding/expression was determined by in vitro autoradiography and immunohistochemistry using the ACE-specific radioligand [125I]-MK351A and a mouse anti-ACE polyclonal antibody, respectively, whereas the spatiotemporal distribution of ACE mRNA was determined by in situ hybridization using 35S-labelled oligonucleotide probes. ACE protein was localized to the glandular epithelium in the human prostate. ACE binding and immunostaining were increased in BPH compared with normal (non-hyperplastic) prostate specimens [X-ray film autoradiography: normal 873+/-48 dpm/mm2 (n=8) vs. BPH 1631+/-274 dpm/mm2 (n=6), p<0.05; emulsion autoradiography: normal 3.1+/-0.5 grains/mm2 (n=6) vs. BPH 32.8+/-8.6 grains/mm2 (n=5), p<0.01]. ACE mRNA was also localized to glandular epithelial cells in the human prostate with a significant increase in ACE mRNA expression in BPH compared with the normal prostate [normal 11.04+/-2.03 grains/cell (n=220 cells total) vs. BPH 22.29+/-1.34 grains/cell (n=198 cells total), p<0.05]. The findings of the present study suggest that ACE is localized to the glandular epithelium of the human prostate and that its expression, at both protein and mRNA level, is aberrantly increased in BPH. These data support the concept that hyperactivity of the local RAS in the prostate may be involved in the pathogenesis of BPH.

Autoradiography↗

Clinical features and management of benign prostatic hyperplasia.

Benign prostatic hyperplasia represents the most common benign neoplastic condition afflicting men and has a major impact on the health of the population. It refers to a regional and nodular growth of stromal proliferation which, because of its proximity to the urethra, causes varying degrees of bladder outflow obstruction.

Adrenergic alpha-Antagonists↗

alpha-Adrenoceptor antagonists in the treatment of benign prostate hyperplasia.

Benign prostate hyperplasia (BPH) is a common malady affecting elderly men throughout the world, and it is the most common cause of voiding dysfunctions in man. The disease becomes prevalent, as the mean age of the population increases. In BPH the glandular cells and myofibroblasts of periurethral and transition zones proliferate excessively. This excessive growth of tissue mass physically compresses the urethra, leading to urinary obstruction and lower urinary tract symptoms (LUTS). Another major factor that contributes to LUTS in BPH is the increase in smooth muscle tone, a dynamic component. Contraction of the prostate gland is mainly under the control of the autonomic system and is mediated through alpha-adrenoceptors. In addition to alpha1-adrenoceptors, there are many other components that influence growth and contraction of the prostate gland, resulting in the development of BPH and LUTS. The prostate gland is contracted on stimulating 5-HT, endothelin, tachykinin, and muscarinic cholinergic receptors. Growth of the prostate gland is under the control of androgens, endothelin growth factor, vasoactive intestinal peptide, nerve growth factor, and growth hormone. The combination of excessive growth and the tone produced by different components results in LUTS and BPH. alpha1-Adrenoceptor antagonists were successfully used in the treatment of BPH to relieve the LUTS. The high selectivity of alpha1A-adrenoceptor antagonists reflects the uroselectivity. The uroselective compounds like terazosin, doxazosin, tamsulosin, and alfuzosin are in clinical use. Other new potent uroselective compounds, which are analogs of nigulidipine, 5-methyl-urapidil, or naftopidil, are in clinical trials. In addition to alpha-antagonists, antiandrogens (5alpha-reductase inhibitors) and polyherbal formulations are used to treat BPH. The success of BPH treatment lies in the development of new chemical entities which are efficacious as well as more uroselective and hence have least side effects.

Adrenergic alpha-Antagonists↗

Benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is the most common cause of bladder outlet obstruction and voiding symptoms in elderly men. The pathogenesis is not fully determined but a combination of androgens and age are needed for development of BPH. Symptoms of BPH are divided into obstructive and irritative symptoms but large interpersonal variability is found and no specific BPH symptom exists. Treatment modalities include surgery (TURP, TUIP, open prostatectomy, laser ablation, balloon dilatation, hyperthermia and thermotherapy, and urethral stents) and medical therapy. TURP is the gold standard treatment and TUIP is a safe and effective alternative to TURP in patients with smaller prostates. Laser ablation, hyperthermia and thermotherapy, and urethral stents are at the present time under investigation. Balloon dilatation is FDA-approved but not often used because of low efficacy and poor long-term results. Medical treatment includes alpha-blocker or finasteride treatment and is indicated in patients with moderate to severe symptoms of BPH without a strong indication for surgery.

Humans↗

Management of benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common cause of morbidity among older men. Primary care physicians need to develop expertise in its management. The causes of BPH are unknown; aging and the presence of male androgens are the dominant risk factors. Obtaining a medical history is a key step in assessing whether lower urinary tract symptoms are due to BPH or to some other process. A reliable and valid seven-item questionnaire has been developed to objectively assess symptom severity. A focused physical examination including a digital rectal exam should be performed, as well as a urinalysis and serum creatinine. Optional tests include uroflowmetry, post-void residual urine, and prostate-specific antigen measurements. BPH is treated primarily to improve the quality, rather than increase the quantity, of life. Optimal decisions about treatment are best made by a clinician and an informed patient working together.

Humans↗

Etiology of benign prostatic hyperplasia.

Benign Prostatic Hyperplasia (BPH) is the most common neoplastic condition that afflicts men, and it constitutes a major factor impacting the health of the American male. This article reviews voiding dysfunction and the role of aging, the testis, and androgen in the development of BPH. Emphasis is placed on new concepts in the basic aspects of BPH etiology as a result of recent investigations.

Aging↗

Results of deep prostatic hyperthermia applied with Thermex II in 525 benign prostatic hyperplasias.

Deep prostatic hyperthermia (DPH) with radiofrequency waves has been found to be of considerable beneficial value in benign prostatic hyperplasia. This study was performed on 525 patients. Madsen's criteria were used for symptom scoring. All the treatments were performed at 44.5 degrees C. Mean follow-up was 18 months. DPH is well tolerated and no severe complications were noted. Statistically meaningful changes of improvement were seen in mean flow rate and residual volume in 51% of the patients.

Adult↗

Medical therapy for benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common clinical entity in elderly men. We review the epidemiology of BPH and the mechanisms by which it causes bladder outlet obstruction. The currently available medical therapies are examined with respect to mechanism of action, effectiveness, side effects, and cost. They are briefly compared with the more traditional treatment options of watchful waiting and transurethral prostatectomy. A logical approach to the treatment of symptomatic BPH is discussed.

Adrenergic alpha-Antagonists↗

Benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) is a common condition, which increases with increasing age. Although not a life-threatening condition, BPH can significantly affect quality of life. BPH manifests clinically with lower urinary tract symptoms (LUTS) and may be associated with sexual dysfunction. As many as 60% of men aged 60 years have some degree of clinical BPH. With the projected increases in the distribution of people over the age of 60, BPH isset to become an even greater problem in men's health.

Age Factors↗

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↗