Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Finasteride”

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 703 records · Page 39Linked to original sources
PubMed2001

Treatment of localized prostate cancer with intermittent triple androgen blockade: preliminary results in 110 consecutive patients.

OBJECTIVES: To determine the effectiveness of triple androgen blockade as an alternative to watchful waiting, radical prostatectomy or radiation therapy in the management of patients with clinical stage T1 to T3 prostate cancer. METHODS: The records of 110 consecutive patients were retrospectively evaluated. Patients were treated with a three-drug androgen blockade regimen, consisting of a luteinizing hormone-releasing hormone agonist (leuprolide or goserelin) plus an antiandrogen (flutamide or bicalutamide) plus finasteride (a 5-alpha-reductase inhibitor), followed by finasteride maintenance therapy, as the sole intervention. All patients refused local therapy and had their prostates intact. Determinants of efficacy included serum prostate-specific antigen (PSA) levels and disease-specific survival. RESULTS: Patients were treated for a median of 13 months with triple androgen blockade. At baseline, mean PSA level was 13.2 +/- 1.2 ng/ml (range, 0.39-100 ng/ml), and mean Gleason score was 6.6 +/- 0.1 (range, 4-10). During treatment, PSA levels declined to < or =0.1 ng/ml in all patients, with a median time of 3 months. After a median follow-up of 36 months since initiation of treatment, PSA levels have remained stable in 105 of 110 patients (95.5%). At a median follow-up of 55 months (range, 38-125 months), the mean PSA level for the first 57 patients treated in this series is 1.88 +/- 0.1 (range, 0-11.0 ng/ml). Only 9 of 110 (8.1%) patients have a PSA level > or =4.0 ng/ml. To date, no patient has received a second cycle of hormone blockade. CONCLUSIONS: Although median follow-up is short, triple androgen blockade therapy followed by finasteride maintenance appears to be a promising alternative for the management of patients with clinically localized or locally advanced prostate cancer. Further study of this approach is warranted.

Adenocarcinoma↗
PubMed1998

Pharmacologic therapy for prostatism.

Although the general approach to management of a sufficient degree of benign prostatic hyperplasia in the past was surgical intervention (transurethral resection of the prostate), the current availability of effective pharmacologic therapy has changed the initial management strategy. At present, two types of drugs are available for treatment of prostatism: (1) selective alpha-adrenergic blocking agents (terazosin, doxazosin, and tamsulosin) and (2) an inhibitor of the 5 alpha-reductase enzyme (finasteride). Pharmacologic blockade of the alpha(1)-adrenoceptors is thought to result in relaxation of the smooth muscle in the prostate and bladder neck, which reduces urethral resistance, improves voiding function, and minimizes the symptoms of prostatism. These effects may be noted by the patient within several weeks after initiation of treatment. The mechanism of action of finasteride is a blocking of the conversion of testosterone to dihydrotestosterone and an associated volume shrinkage of the prostate. On the average, a 25% reduction in prostate volume can be achieved, but a period of 12 months or longer of finasteride therapy is needed for maximal shrinkage and maximal decrease in symptoms of prostatism. The expanding population of middle-aged and elderly men with prostatism of moderate severity will undoubtedly prompt the development of additional pharmacologic options for treatment of prostatism and benign prostatic hyperplasia.

Adrenergic alpha-Antagonists↗
PubMed2002

Stress-induced deoxycorticosterone-derived neurosteroids modulate GABA(A) receptor function and seizure susceptibility.

Stress affects seizure susceptibility in animals and humans, but the underlying mechanisms are obscure. Here, we provide evidence that GABA(A) receptor-modulating neurosteroids derived from deoxycorticosterone (DOC) play a role in stress-related changes in seizure control. DOC, an adrenal steroid whose synthesis is enhanced during stress, undergoes sequential metabolic reduction by 5alpha-reductase and 3alpha-hydroxysteroid oxidoreductase to form 5alpha-dihydrodeoxycorticosterone (DHDOC) and allotetrahydrodeoxycorticosterone (THDOC), a GABA(A) receptor-modulating neurosteroid with anticonvulsant properties. Acute swim stress in rats significantly elevated plasma THDOC concentrations and raised the pentylenetetrazol (PTZ) seizure threshold. Small systemic doses of DOC produced comparable increases in THDOC and PTZ seizure threshold. Pretreatment with finasteride, a 5alpha-reductase inhibitor that blocks the conversion of DOC to DHDOC, reversed the antiseizure effects of stress. DOC also elevated plasma THDOC levels and protected mice against PTZ, methyl-6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate, picrotoxin, and amygdala-kindled seizures in mice (ED50 values, 84-97 mg/kg). Finasteride reversed the antiseizure activity of DOC (ED50, 7.2 mg/kg); partial antagonism was also obtained with indomethacin (100 mg/kg), an inhibitor of 3alpha-hydroxysteroid oxidoreductase. Finasteride had no effect on seizure protection by DHDOC and THDOC, whereas indomethacin partially reversed DHDOC but not THDOC. DHDOC, like THDOC, potentiated GABA-activated Cl- currents in cultured hippocampal neurons (< or =1 microm) and directly activated GABA(A) receptor currents (> or =1 microm), compatible with a role for DHDOC in the antiseizure activity of DOC. DOC is a mediator of the physiological effects of acute stress that could contribute to stress-induced changes in seizure susceptibility through its conversion to neurosteroids with modulatory actions on GABA(A) receptors including THDOC and possibly also DHDOC.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

Evidence for the regulation of prostatic oxytocin by gonadal steroids in the rat.

Oxytocin and its receptor are present in the mammalian prostate, and the peptide has been shown to increase prostatic growth, 5alpha-reductase activity, and contractility. This study was performed to investigate whether local concentrations of the peptide were regulated by gonadal steroids in order to establish whether oxytocin has a physiological role in the prostate. Both intact and castrated adult Wistar rats were treated daily for 7 days with either testosterone propionate or the antiandrogen cyproterone acetate. Animals were then killed, and plasma hormone and prostatic oxytocin concentrations were measured. A separate group of rats was treated with the 5alpha-reductase inhibitor finasteride to investigate whether testosterone or dihydrotestosterone (DHT) was involved in regulating oxytocin concentrations. In a further series of experiments, rats were treated with diethylstilbestrol (DES) or the antiestrogen tamoxifen. Treatment with testosterone significantly decreased prostatic oxytocin, whereas reduction of androgens by castration or by administration of cyproterone acetate increased prostatic peptide concentrations without altering circulating levels of the peptide. Treatment with finasteride increased plasma testosterone but decreased DHT concentrations. Prostatic oxytocin concentrations were higher in finasteride-treated animals than in control animals with comparable testosterone levels. The data suggest that both testosterone and DHT are capable of decreasing prostatic oxytocin concentrations. Treatment with DES did not significantly alter prostatic oxytocin, but administration of tamoxifen decreased concentrations of the peptide, suggesting that low levels of estrogen may be necessary for oxytocin production. These data provide evidence that oxytocin is regulated by androgens, and we hypothesize that this regulatory mechanism may be involved in controlling prostatic growth.

5-alpha Reductase Inhibitors↗
PubMed2000

Neuroactive steroid 3alpha-hydroxy-5alpha-pregnan-20-one modulates electrophysiological and behavioral actions of ethanol.

Neuroactive steroids are synthesized de novo in brain, yet their physiological significance remains elusive. We provide biochemical, electrophysiological, and behavioral evidence that several specific actions of alcohol (ethanol) are mediated by the neurosteroid 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP; allopregnanolone). Systemic alcohol administration elevates 3alpha, 5alpha-THP levels in the cerebral cortex to pharmacologically relevant concentrations. The elevation of 3alpha,5alpha-THP is dose- and time-dependent. Furthermore, there is a significant correlation between 3alpha,5alpha-THP levels in cerebral cortex and the hypnotic effect of ethanol. Blockade of de novo biosynthesis of 5alpha-reduced steroids using the 5alpha-reductase inhibitor finasteride prevents several effects of ethanol. Pretreatment with finasteride causes no changes in baseline bicuculline-induced seizure threshold but reverses the anticonvulsant effect of ethanol. Finasteride pretreatment also reverses ethanol inhibition of spontaneous neural activity in medial septal/diagonal band of Broca neurons while having no direct effect on spontaneous firing rates. Thus, elevation of 3alpha,5alpha-THP levels by acute ethanol administration represents a novel mechanism of ethanol action as well as an important modulatory role for neurosteroids in the CNS.

Animals↗
PubMed2000

Male pattern baldness.

BACKGROUND: Male pattern baldness, or androgenetic alopecia (AGA) in men, occurs with varying severity and age of onset. Two new treatments widely available as alternatives to 2% minoxidil are 1 mg finasteride and topical 5% minoxidil. Finasteride is a 5 alpha-reductase inhibitor available by prescription only; 5% minoxidil is available over the counter. METHODS: We searched MEDLINE to identify all articles on AGA and its pharmacologic therapies. RESULTS: We found limited information on AGA in peer review medical journals. Associated diseases include psychologic disorders and coronary heart disease. Hair growth is unpredictable and limited for all pharmacologic therapies, with the vast majority of treatment studies being industry sponsored. CONCLUSION: AGA is not easy to treat. Finasteride and 5% minoxidil offer new therapeutic options to the balding man. Treatment options may improve as new drugs are further investigated.

5-alpha Reductase Inhibitors↗
PubMed2000

Urethral development in the fetal rabbit and induction of hypospadias: a model for human development.

PURPOSE: To determine whether the development of the rabbit phallus would be an appropriate model of human phallic development, we evaluated the formation of the fetal rabbit phallus and attempted to induce hypospadias pharmacologically. MATERIALS AND METHODS: New Zealand rabbit fetuses were obtained on gestational days 20 to 24, 26, 28 and 31. Sex was determined by gonadal morphology, and 6 fetuses were obtained at each age. The perineum was dissected, fixed, sectioned and stained with hematoxylin and eosin, and monoclonal antibodies against neuronal specific enolase. Two pregnant rabbits were treated with 10 mg./kg. finasteride orally daily between gestational days 19 and 28. The development of the external genitalia was compared in treated and untreated control rabbits. RESULTS: The rabbit phallus contains 2 corpora cavernosa and dorsolateral nerves similar to the human. In male and female fetuses fusion of the urethral folds progressed in a proximal to distal sequence forming a seam at the point of ventromedial fusion. In male fetuses urethral fold and ventral preputial fusion continued more distally toward the glans compared to females. Thus, in mature males the urethral meatus and ventral prepuce extended to the tip of the phallus, whereas in females the urethral meatus opened on the proximal phallus and the prepuce was deficient ventrally forming a dorsal hood. Male offspring had a significantly larger anogenital distance postnatally than female offspring. In male fetuses exposed to finasteride urethral fusion did not extend distally and the prepuce was deficient ventrally. Also, male offspring exposed to finasteride in utero had a significantly shorter anogenital distance than females and untreated control males at all ages (p <0.05). CONCLUSIONS: Fetal development of the rabbit phallus and urethra is homologous to the human. Although the gestational period is significantly shorter, the temporospatial pattern of external genitalia development is analogous in these species. Feminization of the rabbit urethra, hypospadias, can be induced by inhibiting 5alpha-reductase. Use of this animal model will allow further study of molecular mechanisms involved in urethral fusion and the evaluation of the pathophysiological processes of hypospadias.

Animals↗
PubMedDate not supplied

Influence of estrogens on the androgen metabolism in different subunits of human hair follicles.

The molecular pathways involved in estrogen-mediated induction of hair growth in androgenetic alopecia are unknown. Some authors found that estradiol (E) inhibited 5alpha-reductase (5alpha-R) activity and therefore we addressed the question whether 17alpha- or 17beta-E are able to modulate the activity of 5alpha-R, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) or 17beta-hydroxysteroid dehydrogenase (17beta-HSD) in isolated compartments of human hair follicles. For this purpose, scalp biopsies from volunteers were taken and from each biopsy root sheaths, connective tissue sheaths and dermal papillae (DP) were dissected and incubated in the presence of 3H-testosterone (T) and, in addition, either 17alpha-E, 17beta-E, progesterone or finasteride for up to 48 hrs. Thereafter high-performance liquid chromatography analysis of culture supernatants was performed to detect T-metabolites. At the tested concentrations, finasteride was found to be a major inhibitor of dihydrotestosterone (DHT) formation. Even 1 nM finasteride inhibited DHT synthesis in DP by 86% and 1 nM progesterone by 75%. Estrogens were less able to inhibit the synthesis of DHT in DP (e.g. 100 nM 17alpha-E: 20%; 100 nM 17beta-E: 60%). Whether E directly inhibits 5alpha-R in DP's or whether the effect of estrogens might be explained by an increased conversion of T to the weaker androgens such as androstendione (via 17beta-HSD), androstenediol (via 3beta-HSD) or 17beta-E (via aromatase), thereby diminishing the amount of T available for the conversion to DHT, remains to be shown.

3-Hydroxysteroid Dehydrogenases↗
PubMed2002

5 alpha-reductase inhibition by a new synthetic steroid (PM-9) in cultures of Penicillium crustosum.

The conversion of testosterone (T) to 5 alpha-dihydrotestosterone (DHT), plus the presence of 5 alpha-reductase enzyme, which is responsible for this reduction, had been demonstrated in P. crustosum broth. This enzyme is also present in androgen-dependent animal and human tissues such as prostate and seminal vesicles. The increase in the conversion of T to DHT has been implicated in androgen-dependent diseases such as benign prostate hyperplasia and prostate cancer. The use of 5 alpha-reductase inhibitors could mitigate these illnesses by inhibiting the DHT-receptor complex formation. The purpose of this study is to determine the inhibition pattern of 5 alpha-reductase by finasteride and PM-9 in P. crustosum broth. Km and Vmax values were determined in the broth by Lineweaver-Burk plots using different testosterone concentrations. The Km value was 0.22 microM and Vmax 0.833 pmol of DHT/mg of mycelium/day. The inhibition pattern of finasteride and PM-9 was also determined by Lineweaver-Burk plot, using different concentrations of T and inhibitors. The results of this study show that both finasteride and PM-9 inhibit 5 alpha-reductase in a competitive manner.

5-alpha Reductase Inhibitors↗
PubMed2004

Morphology of the testis and the epididymis in rats with dihydrotestosterone (DHT) deficiency.

The aim of the study was to estimate morphology in the testis and epididymis of adult rats, treated with finasteride for 28 days (the time period of two seminiferous epithelium cycles) and 56 days (the time period of one spermatogenesis). A 28 days long DHT deficiency did not significantly influence the structure of seminiferous epithelium. After 56 days of treatment, finasteride induced sloughing of immature genninal cells (spermatids and rarely pachytene spermatocytes) into the lumen of the seminiferous tubules. A reduced content of spermatozoa was observed in the lumen of rat epididymis in rats with 56-day-long deficiency. The results indicated that 5alpha-reductase 2 activity is important for the maintenance of spermatogenesis. The decreased content of spermatozoa in the epididymal lumen of rats, treated with finasteride during one course of spermatogenesis, could reflect seminiferous epithelium condition.

Animals↗
PubMedDate not supplied

Effective treatment of female androgenic alopecia with dutasteride.

Dihydrotestosterone is the main molecule responsible for androgenic alopecia. Finasteride, which reduces transformation of testosterone into dihydrotestosterone and decreases dihydrotestosterone activity, is approved for treatment of androgenic alopecia in men. We describe the case of a 46-year-old woman with androgenic alopecia, non-responsive to minoxidil, who initially benefited from finasteride. Due to only limited improvement after finasteride and persisting profound psychological distress resulting from androgenic alopecia, another 5-reductase inhibitor, dutasteride, was introduced. Clinical evaluation and trichogram were applied for assessment of dutasteride efficacy in this patient. Additionally, mean hair diameter was monitored by means of computer dermoscopy. After 6 months of therapy, significant improvement was observed and after 9 months the clinical diagnosis of androgenic alopecia could no longer be made in this patient. No side effects were observed. In conclusion, theoretical data and our experience in this case show that dutasteride might develop into a true alternative in treatment of androgenic alopecia.

5-alpha Reductase Inhibitors↗
PubMed2005

Immunolocalization of androgen receptor in the epididymis of rats with dihydrotestosterone deficiency.

Dihydrotestosterone (DHT), 5alpha-reduced metabolite of testosterone, is the most potent androgen in the epididymis. The conversion of T into DHT is carried out by 5alpha-reductase. The activity of 5alpha-reductase type 2, preferentially expressed in the epididymis can be inhibited by a finasteride (a steroid-based specific inhibitor of 5alpha-reductase type 2) which results in DHT deficiency. The aim of the study was to examine the morphology of epididymis and the immunolocalization of an androgen receptor (AR) in the initial segment, caput and cauda epididymis of rats treated with finasteride for 56 days. There were no morphological changes in the morphology of epididymal epithelium in the experimental rats. Immunostainable AR was localized in nuclei of epithelial cells, smooth muscle cells and mainly in the cytoplasm of interstitial cells in the epididymis of control rats. In the epididymis of experimental rats, AR immunostaining was noticed mainly in the cytoplasm of epithelial cells and interstitial cells. The single cells of the initial segment epithelium, basal cells and smooth muscle cells of cauda epididymis showed nuclear AR staining. In conclusion, finasteride affected the expression of the AR in the rat epididymis without changing the morphology of epididymal epithelium. Altered AR expression reflected the hormonal status within the epididymis.

5-alpha Reductase Inhibitors↗
PubMed1995

Benign prostatic hyperplasia. Hormonal treatment.

Androgen withdrawal therapy appears to produce a 20% to 30% decrease in the volume of the hyperplastic prostate after 3 to 6 months of therapy. Longer periods of treatment do not result in further prostatic regression, but further growth of the gland is not apparent in men treated with finasteride for 4 years. Although biopsy studies indicate that epithelial regression occurs to a much more significant degree than stromal regression, this may simply reflect the relatively longer turnover of the stromal cell population. The significant placebo effect of oral medication in patients with BPH makes interpretation of clinical symptomatology and uroflow data difficult. Analysis of symptom improvement is further complicated by the relatively slow improvement of patients on hormonal therapy, as opposed to surgery, where relief is immediate. In addition to limited stromal involution and inadequate treatment duration, other biologic factors may limit the clinical efficacy of androgen withdrawal therapy. Most importantly, partial involution may not necessarily decrease urethral resistance. In addition, obstruction-induced detrusor dysfunction may persist after relief of outflow obstruction in some patients, as it does following surgery. Incomplete blockade of androgen action, as well as compliance issues, may also limit efficacy. Long-term studies validate a modest but significant clinical response rate of finasteride therapy with preservation of sexual function in most men. Of the available hormonal therapeutic agents, only finasteride appears to have an acceptable risk-benefit ratio. Other 5 alpha-reductase inhibitors in the "pipeline," such as episteride, may have similar benefits. In the long term, this class of drugs may have a much larger role in patients who present with the early signs of BPH, to prevent any further progression of the disease. Presently, no form of antiandrogen therapy is as effective as transurethral resection of the prostate in relieving symptomatology. Because of patient preferences, however, medical therapy will play an increasingly important role in the management of patients with BPH.

Androgen Antagonists↗
PubMed1995

Endocrine therapy for benign prostatic hyperplasia in the 90's.

Endocrine therapy by means of castration for benign prostatic hyperplasia was introduced already in the middle of the 19th century. The technique was never popularized and was abandoned following the introduction of safe surgical techniques. In the second half of this century, small series of various endocrine treatments have been reported, mainly using progestational agents. The hormone dependency of the prostate is unique, since testosterone itself is not very active on the prostate cells but has to be converted to 5 alpha-dihydrotestosterone, which is almost ten times as effective an androgen in the prostate cell. By blocking this conversion, highly specific antiandrogenic effect will be obtained in the prostate but not in other organs of the body. The first 5 alpha-reductase inhibitor, finasteride, has proven effective in reducing prostate DHT. In large clinical trials, it has shown to reduce prostate size, improve urinary flow and reduce symptom score, statistically significantly better than placebo. The effect is sustained over at least 3 years. In a double-blind, randomized, placebo-controlled study over 2 years, patients were similarly improved in the finasteride group, whereas they deteriorated in the placebo group. This indicates that finasteride is able to halt the progression of the natural course of benign prostatic hyperplasia. Benign prostatic hyperplasia, generally believed to be a stromal disease, is potentially dependent on estrogens for its development. By blocking aromatization of testosterone to estrogen in the prostate cells, a hypothetical beneficial effect on the disease process should be gained. Results from phase II-studies have been promising. However, in placebo-controlled studies, aromatase inhibitors did not perform better than placebo.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstenedione↗
PubMed1993

Characterization of Chinese hamster ovary cell lines expressing human steroid 5 alpha-reductase isozymes.

Membrane-bound isozymes of steroid 5 alpha-reductase, designated 1 and 2, synthesize the potent androgen, dihydrotestosterone. Isozyme 1 has an alkaline pH optimum (7.0-8.5), whereas isozyme 2 has an acidic pH optimum (5.0). To gain insight into this enigmatic difference, Chinese hamster ovarian cell lines expressing the human 5 alpha-reductase isozymes were established. The half-lives of both proteins are > 30 h and are not altered by the 4-azasteroid inhibitors finasteride and 17 beta-(N,N,-diethyl)carbamoyl-4-methyl-4-aza-5 alpha-androstan-3-one. Nanomolar concentrations of finasteride block immunoprecipitation of isozyme 2 by antipeptide antibodies, which suggests that drug binding alters protein conformation. In contrast, finasteride (50 microM) has no effect on immunoprecipitation of isozyme 1. Both isozymes are localized to the endoplasmic reticulum by immunocytochemistry and have their carboxyl termini exposed to the cytoplasm. In cell lysates, isozyme 2 exhibits a Vmax at pH 5.0 but has a higher substrate affinity at neutral pH. In intact and permeabilized cells, isozyme 2 has an apparent substrate Km similar to that determined in cell lysates at neutral pH. The results suggest that isozyme 2 is more efficient at neutral pH and that the acidic pH optimum determined in lysates is a consequence of cell lysis.

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

The role of sex steroids in the pathogenesis and maintenance of benign prostatic hyperplasia.

BACKGROUND: It has long been suspected that sex steroids play a key role in the pathogenesis of benign prostatic hyperplasia (BPH). Prostatic diseases do not occur in males castrated before puberty or in males with heritable disorders of androgen production or action. Both estrogens and androgens have been shown to induce BPH in experimental animals. METHODS: Clinical studies utilizing hormonal therapies to treat BPH were reviewed. Studies that used total medical castration therapy via the use of a long-acting gonadotropin-releasing hormone (GnRH agonist), partial androgen blockade via the use of the 5 alpha-reductase inhibitor finasteride, and estrogen blockade (via the use of aromatase inhibitors) were analyzed. RESULTS AND CONCLUSIONS: Both the GnRH agonists and finasteride result in prostatic size reduction and alleviate symptoms in some patients. Both therapies are more effective in men with larger prostates (> 40 cc). Finasteride is less efficacious in terms of size reduction than the GnRH agonists but also has fewer side effects. To date, clinical trials with aromatase inhibitors have not yielded dramatic positive results in the treatment of BPH.

Antineoplastic Agents, Hormonal↗
PubMed1997

Clinical and biological characteristics of familial benign prostatic hyperplasia.

PURPOSE: We attempted to determine the clinical and biological characteristics of familial benign prostatic hyperplasia (BPH). MATERIALS AND METHODS: Urinary flow rate, prostate size, symptom score, serum prostate specific antigen, testosterone and dihydrotestosterone were measured in subjects who participated in the nationwide Merck phase III finasteride clinical trial. Findings in the 69 men with familial BPH (3 or more family members with BPH, including the proband) were compared to those in the 345 with no family history of BPH. Logistic regression was used to detect relationships between familial BPH, and these variables before and after 5 alpha-reductase inhibition with finasteride. RESULTS: Familial BPH was characterized by large prostate size. Mean prostate volume in men with familial and sporadic BPH was 82.7 and 55.5 ml., respectively (p < 0.001). Other clinical findings, including serum androgen levels and response to finasteride, were similar in familial and sporadic BPH. The frequency of familial BPH in patients with prostate size in the largest and smallest deciles was 46 and 13%, respectively. CONCLUSIONS: Familial BPH in this group of patients was associated with large prostate size, normal serum androgen levels and normal response to 5 alpha-reductase inhibition. A genetic factor responsible for familial BPH may exert its influence through androgen independent control of prostatic growth.

5-alpha Reductase Inhibitors↗
PubMed1998

Some remarks on the epidemiology of acute urinary retention.

Acute urinary retention is an unpleasant, painful experience which requires immediate medical, and frequently surgical intervention. Population studies reveal that acute urinary retention is a common event: a 60 year-old man who survives a further 20 years has a 23 per cent probability of experiencing an acute episode of urinary retention. About half of acute retention episodes appear to be linked to general anaesthesia and a further large population due to the natural history of benign prostatic hyperplasia. The risk of acute urinary retention increases with increasing age. There are a number of other risk factors with risk increased in men with moderate and severe urinary symptoms, low peak urinary flow rates (less than 12 ml/sec) and among men with large prostates. Recent placebo-controlled randomised trials reveal that finasteride is associated with a 57 per cent reduction in the hazard ratio of acute urinary retention when used for at least two years. Since finasteride acts in a positive manner on the major risk factors (finasteride use increases peak urinary flow rate, reduces symptom scores in moderately symptomatic men and reduces prostate volume), this result is not too surprising. It remains to be determined what the risk factors for anaesthesia-induced acute retention are and how they can be altered. Nevertheless, the improvement of our knowledge of the epidemiology of acute urinary retention in the past 12 months is impressive.

Acute Disease↗