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At least 19 recordsLinked to original sources
PubMed1993

Finasteride (MK-906) in the treatment of benign prostatic hyperplasia. The Finasteride Study Group.

The effects of finasteride, a potent 5 alpha-reductase inhibitor, were assessed in 750 patients with benign prostatic hyperplasia (BPH) in a multicenter, double-blind, placebo-controlled study. Patients were randomized to finasteride, 1 or 5 mg, or placebo, daily for 12 months. The following changes were seen with finasteride 5 mg after 12 months: (1) Serum dihydrotestosterone decreased by 62% compared to no change with placebo (P < 0.001); (2) serum prostate-specific antigen (PSA) decreased by 46% compared to no change with placebo (P < 0.001); (3) prostate volume was reduced by 22% compared to a 5% decrease with placebo (P < 0.001); (4) maximum urinary flow rate increased by 1.7 ml/sec compared to a 0.4 ml/sec increase with placebo (P < 0.025); (5) total urinary symptom scores decreased by 3.3 points compared to a 2.0 point decrease with placebo (P = 0.005), and (6) obstructive symptom scores decreased by 2.1 points compared to a 1.4 point decrease with placebo (P = 0.017). The effects of finasteride 1 mg were similar to 5 mg, except in urinary symptoms, where no significant differences between 1 mg and placebo were seen. Patients treated with 5 mg finasteride demonstrated significantly greater improvements in urological status (assessed by the investigator) and the troublesome symptom score, compared to placebo. Treatment with finasteride was well tolerated. We conclude that finasteride is an effective medical therapy for a significant proportion of patients with BPH.

5-alpha Reductase Inhibitors↗
PubMed1992

The clinical effects of a 5 alpha-reductase inhibitor, finasteride, on benign prostatic hyperplasia. The Finasteride Study Group.

Finasteride (Proscar--an orally active 5 alpha-reductase enzyme inhibitor) blocks the conversion of testosterone to dihydrotestosterone. The effects of finasteride in patients with benign prostatic hyperplasia were investigated in 2 double-blind, placebo-controlled studies. In study 1, 86 patients were treated with placebo or finasteride (5 to 80 mg. per day) for 12 weeks, followed by a 12-week drug-free period. After 12 weeks of treatment all doses of finasteride showed significant decreases in prostate volume. However, 12 weeks after discontinuation of finasteride prostate volume returned to near baseline values. In study 2, 104 patients were treated with placebo or finasteride (0.2 to 40 mg. per day) for 24 weeks. After 24 weeks of finasteride treatment prostate volume showed a mean decrease of 24% and 28% (p less than 0.01) in the 1 and 5 mg. groups, respectively. Lower doses had a lesser effect on prostate shrinkage. Maximum urinary flow showed a mean increase of 3.7 cc per second when the 1 and 5 mg. groups were combined. Symptom improvement was observed in the 1 and 5 mg. groups, although this was not statistically different from the placebo group due to the small sample size.

5-alpha Reductase Inhibitors↗
PubMed1994

Maintenance of clinical efficacy with finasteride therapy for 24 months in patients with benign prostatic hyperplasia. The Finasteride Study Group.

BACKGROUND: Finasteride, a 5 alpha-reductase inhibitor, has been shown to have beneficial effects in the treatment of benign prostatic hyperplasia. The long-term safety and efficacy of finasteride in the treatment of benign prostatic hyperplasia was assessed. METHODS: In two multicenter, double-blind, placebo-controlled studies (North American and international), patients with symptomatic benign prostatic hyperplasia were randomly assigned to receive finasteride, 1 or 5 mg, or placebo for 1 year followed by an open-extension study in which all patients were treated with finasteride, 5 mg, regardless of original therapy. Men aged 40 to 80 years, in good physical and mental health, were eligible to enter the study. All patients were to have a maximum urinary flow rate of 15 mL/s or less with a voided volume of 150 mL or more, an enlarged prostate, and symptoms of urinary obstruction. Patients with a prostate-specific antigen level of 40 mg/mL or more or any finding suggestive of prostate cancer were excluded. RESULTS: Two hundred ninety-eight patients received finasteride, 5 mg, continuously for 24 months. At the end of 24 months of finasteride therapy, the median prostate volume was reduced by 25%, and 60% of patients had a 20% or greater reduction in prostate volume. Maximum urinary flow rate was improved by at least 2 mL/s, and symptoms were improved by approximately 3.5 points. Decreased libido and ejaculation disorders were the only drug-related adverse experiences reported in more than 1% of patients. CONCLUSION: These studies support the long-term safety and tolerability of finasteride, while demonstrating its continuing clinical efficacy in the treatment of patients with symptomatic benign prostatic hyperplasia.

Adult↗
PubMed1994

Clinical experience of the detection of prostate cancer in patients with benign prostate hyperplasia treated with finasteride. The Finasteride Study Group.

The clinical experience relating to the detection of prostate cancer in patients participating in 2 large multicenter clinical trials of finasteride in the treatment of benign prostatic hyperplasia is reviewed. A total of 1,645 patients 40 to 83 years old with benign prostatic hyperplasia was randomized to receive 1 or 5 mg finasteride or placebo once a day for 12 months in a double-blind fashion followed by an open extension study in which all patients were treated with 5 mg finasteride daily. At entry, all patients were to have a maximum urinary flow rate of 15 ml per second or less with a voided volume of 150 ml or more, an enlarged prostate and symptoms of urinary obstruction. Patients with a prostate specific antigen level of 40 ng/ml or more, or any finding suggestive of prostate cancer were excluded. During the study period 32 cases of prostate cancer were diagnosed: 12 were detected during the 12 months of the controlled study and were evenly distributed among the treatment groups (4 on placebo, and 3 on 1 mg and 5 on 5 mg finasteride) and 20 cases were detected in the extension study. From these results we conclude that finasteride-treated patients should be evaluated periodically by digital rectal examination, careful monitoring of prostate specific antigen levels and appropriate investigation of any suspicious findings.

Aged↗
PubMed1992

The effect of finasteride in men with benign prostatic hyperplasia. The Finasteride Study Group.

BACKGROUND: Benign prostatic hyperplasia is a progressive, androgen-dependent disease resulting in enlargement of the prostate gland and urinary obstruction. Preventing the conversion of testosterone to its tissue-active form, dihydrotestosterone, by inhibiting the enzyme 5 alpha-reductase could decrease the action of androgens in their target tissues; in the prostate the result might be a decrease in prostatic hyperplasia and therefore in symptoms of urinary obstruction. METHODS: In a double-blind study, we evaluated the effect of two doses of finasteride (1 mg and 5 mg) and placebo, each given once daily for 12 months, in 895 men with prostatic hyperplasia. Urinary symptoms, urinary flow, prostatic volume, and serum concentrations of dihydrotestosterone and prostate-specific antigen were determined periodically during the treatment period. RESULTS: As compared with the men in the placebo group, the men treated with 5 mg of finasteride per day had a significant decrease in total urinary-symptom scores (P less than 0.001), an increase of 1.6 ml per second (22 percent, P less than 0.001) in the maximal urinary-flow rate, and a 19 percent decrease in prostatic volume (P less than 0.001). The men treated with 1 mg of finasteride per day did not have a significant decrease in total urinary-symptom scores, but had an increase of 1.4 ml per second (23 percent) in the maximal urinary-flow rate, and an 18 percent decrease in prostatic volume. The men given placebo had no changes in total urinary-symptom scores, an increase of 0.2 ml per second (8 percent) in the maximal urinary-flow rate, and a 3 percent decrease in prostatic volume. The frequency of adverse effects in the three groups was similar, except for a higher incidence of decreased libido, impotence, and ejaculatory disorders in the finasteride-treated groups. CONCLUSIONS: The treatment of benign prostatic hyperplasia with 5 mg of finasteride per day results in a significant decrease in symptoms of obstruction, an increase in urinary flow, and a decrease in prostatic volume, but at a slightly increased risk of sexual dysfunction.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

One-year experience in the treatment of benign prostatic hyperplasia with finasteride. The MK-906 (Finasteride) Study Group.

Finasteride (MK-906) is a 5 alpha-reductase inhibitor that reduces circulating dihydrotestosterone (DHT) levels without lowering testosterone levels. The goal of this study was to evaluate the effects of long-term (12 months) treatment with finasteride in 67 men with benign prostatic hyperplasia to determine if previously reported short-term efficacy was maintained with chronic therapy. Treatment with 10 mg of finasteride resulted in a 78% to 80% reduction in DHT levels (P less than 0.001) levels, and a small but significant increase in testosterone levels (P less than 0.05) that were maintained over the 12-month period. Significant reduction in prostate volume was observed after 6 months of treatment and maintained at month 12 (P less than 0.05). In patients with baseline maximum flow rates less than or equal to 15 ml/second, maximum urinary flow significantly increased by a mean of 4 ml/second (P less than 0.01), with at least a 3 ml/second improvement observed in up to 70% of the patients at month 12. These results indicate that finasteride can reduce prostate size and improve maximum urinary flow with no loss of efficacy after 1 year of treatment. It is concluded that finasteride has the potential to be an effective chronic therapy for benign prostatic hyperplasia.

5-alpha Reductase Inhibitors↗
PubMed1994

Finasteride for the treatment and control of benign prostatic hyperplasia: summary of phase III controlled studies. The Finasteride Study Group.

The efficacy and safety profiles of finasteride were tested in 1,645 patients with benign prostatic hyperplasia (BPH) over a 12-month period. The following effects were observed: (1) a 60-80% reduction in serum dihydrotestosterone levels; (2) a 20% reduction in prostate volume; (3) significant increases in the maximum urinary flow rate compared with placebo; and (4) significant improvement in urinary symptoms, particularly obstructive symptoms. All effects were well maintained for the entire duration of the study. Finasteride had a good safety profile and was well tolerated.

Aged↗
PubMed1993

Finasteride: a 5 alpha-reductase inhibitor.

The pharmacology and pharmacokinetics of finasteride are reviewed, and finasteride's clinical efficacy, adverse effects, and dosage in patients with benign prostatic hyperplasia (BPH) are described. Finasteride is a member of a new class of medications, the azasteroids, that have antiandrogenic activity limited to certain tissues, including the prostate gland. Finasteride inhibits the activity of 5 alpha-reductase, the enzyme necessary for converting testosterone to dihydrotestosterone in the prostate and other tissues. BPH is androgen dependent, and dihydrotestosterone is necessary for the hyperplasia to occur. Finasteride is well absorbed after oral administration; peak plasma concentration is reached in as little as one hour. Finasteride is approximately 90% bound to plasma proteins, is widely distributed, and is extensively metabolized by the liver. In clinical studies, finasteride has been effective in decreasing prostatic volume, increasing urinary flow rate, and decreasing the obstructive and irritative symptoms of BPH. Because of the heterogeneity of BPH, however, treatment is successful in only one third to one half of patients. Finasteride's adverse effects include decreased libido, ejaculatory disorders, and effects on prostate-specific antigen. The recommended dosage of finasteride is 5 mg/day orally. Therapy should be continued for at least six months before the clinical response is evaluated. Finasteride provides a pharmacologic alternative to surgery in patients with BPH.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

In vitro biotransformation of finasteride in rat hepatic microsomes. Isolation and characterization of metabolites.

Metabolism of finasteride ([N-(1,1-dimethylethyl)-3-oxo-4-aza-5 alpha-androst-1-ene-17 beta- carboxamide]; MK-906), a new type of specific inhibitor of testosterone 5 alpha-reductase, was investigated using rat hepatic microsomes. The metabolism of finasteride by rat hepatic microsomes was oxygen- and NADPH-dependent, and addition of metyrapone, 7,8-benzoflavone, and cytochrome c to the incubation mixture inhibited the metabolism of finasteride. It is suggested that the metabolic reaction of finasteride was mediated by a mixed function oxidase involving P-450. Four major metabolites were detected in vitro on incubating finasteride with hepatic microsomes of rats treated with phenobarbital (PB-Ms), whereas two major metabolites were found in the incubation mixture with microsomes of untreated rats (UT-Ms). These metabolites were isolated and purified by solvent extraction and semi-preparative HPLC, and identified by MS spectrometry and NMR spectroscopy. The metabolites consisted of omega-hydroxy finasteride (M-1), finasteride-omega-al (M-2), finasteride-omega-oic acid (M-3), and 6 alpha-OH finasteride (M-4). M-1 and M-4 are the major metabolites in UT-Ms, and M-1 and M-3 in PB-Ms. These studies revealed that hydroxylation of the t-butyl group and ring hydroxylation at the 6-position were key steps in the metabolism of finasteride in the rat hepatic microsomes. Further, the major metabolite M-4 was hydroxylated at the 6 alpha-position, but not at the 6 beta-position of the drug. This finding suggests the existence of a novel enzyme that catalyzes the 6 alpha-hydroxylation of the 4-azasteroid.

Animals↗
PubMed1993

Androgen metabolism in men receiving finasteride before prostatectomy.

Oral administration of finasteride, a 5 alpha-reductase inhibitor, affects intraprostatic androgens by suppressing dihydrotestosterone and increasing testosterone. This study was designed to determine the correlation of these effects of finasteride with changes in serum dihydrotestosterone, testosterone and androstanediol glucuronide. In a double blind, placebo-controlled study, 27 men with symptomatic benign prostatic hyperplasia were treated with placebo or 1 or 5 mg. per day finasteride for 6 to 8 weeks before transurethral resection of the prostate. There was no significant change in serum testosterone in any group, or in serum dihydrotestosterone or androstanediol glucuronide in the placebo group. There was a decrease in serum dihydrotestosterone by 66 +/- 4% and 70 +/- 8% (p = 0.32), and of serum androstanediol glucuronide by 78 +/- 3% and 86 +/- 3% (p = 0.012) in the 1 and 5 mg. finasteride groups, respectively. Intraprostatic dihydrotestosterone in the placebo group decreased from 18.6 +/- 1.4 nmol./kg. to 3.8 +/- 1.0 nmol./kg. and 1.7 +/- 0.7 nmol./kg. with 1 mg. and 5 mg. finasteride, respectively (p = 0.049 between 1 mg. and 5 mg. finasteride). Intraprostatic testosterone in the placebo group increased from 1.1 +/- 0.2 nmol./kg. to 7.6 +/- 1.0 nmol./kg. and 8.3 +/- 0.7 nmol./kg. with 1 mg. and 5 mg. finasteride, respectively (no significant difference between 1 mg. and 5 mg. finasteride). Serum and intraprostatic dihydrotestosterone correlated (p = 0.002). There was no correlation between intraprostatic dihydrotestosterone and serum androstanediol glucuronide. We conclude that 5 mg. of finasteride cause greater inhibition of intraprostatic 5 alpha-reductase than 1 mg. and that serum dihydrotestosterone is a better marker of intraprostatic dihydrotestosterone than androstanediol glucuronide.

Androstane-3,17-diol↗
PubMed1995

Treatment with finasteride following radical prostatectomy for prostate cancer.

OBJECTIVES: The objective of this study was to evaluate the effect of finasteride (10 mg/d) or placebo on serum prostate-specific antigen (PSA) and recurrence rates in men with detectable PSA levels after radical prostatectomy. METHODS: A total of 120 men, 48 to 89 years old, previously treated with radical prostatectomy for prostate cancer within the past 10 years, with serum PSA levels between 0.6 and 10.0 ng/mL, with no evidence of skeletal metastasis on bone scan, and with no previous androgen deprivation therapy, were treated with 10 mg finasteride or placebo in a double-blind fashion for 12 months. After the first year, all patients were treated with finasteride for an additional 12 months. Primary endpoints were serum PSA levels and recurrence rates defined as positive bone scan or positive biopsy. RESULTS: Patients treated with finasteride had a delayed increase in serum PSA compared with placebo of approximately 9 months in the first year and 14 months by the end of the second year. Patients with baseline PSA levels less then 1.0 ng/mL had no significant increase in serum PSA during the 2 years of treatment. Fewer recurrences were observed in the finasteride group, but these differences were not statistically significant. Finasteride was well tolerated, and side effects were balanced between treatment groups. CONCLUSIONS: The results of this study indicate that treatment with finasteride delays but does not prevent the rise in serum PSA observed in untreated patients with detectable PSA levels after radical prostatectomy. The reduction in local and distant recurrences in the finasteride group suggests that the effect on PSA reflects a direct effect on tumor growth without affecting the initial response to subsequent hormonal therapy. These data require confirmation by studies that are longer and larger, focused on demonstrating significant differences in progression rates and survival before the use of finasteride can be considered as an option for men with detectable PSA levels after radical prostatectomy.

Aged↗
PubMed1994

Effects of finasteride, a 5 alpha-reductase inhibitor, on circulating androgens and gonadotropin secretion in hirsute women.

An oral 5-mg dose of finasteride, a 5 alpha-reductase inhibitor, was administered for 3 months to 10 hirsute women to determine the effect on gonadotropin secretion, on basal and stimulated androgen secretion, and on hair growth. Hair growth was assessed by the Ferriman-Gallwey score. All of the above determinations were evaluated before and after 1 and/or 3 months of finasteride treatment. Basal and GnRH-stimulated gonadotropin secretions were not affected. Indeed, finasteride did not modify the pulsatility of LH secretion. No change was seen in estradiol, PRL, free testosterone, androstenedione, dehydroepiandrosterone sulfate, and sex hormone-binding globulin concentrations. Serum concentrations of cortisol (F) were significantly reduced after 1 month of finasteride treatment. The F levels returned to pretreatment levels after 3 months. Plasma levels of dihydrotestosterone and 3 alpha-androstanediol glucuronide significantly decreased during finasteride treatment. A significant increase in testosterone concentrations was observed after 3 months. Finasteride did not modify the responses of testosterone, androstenedione, and dehydroepiandrosterone sulfate to ACTH-(1-24) injection. Conversely, finasteride blunted the F response to corticotropin stimulation. Three months of finasteride treatment significantly decreased the Ferriman-Gallwey score. In conclusion, finasteride significantly decreased dihydrotestosterone and hair growth in hirsute women without negatively affecting gonadotropin secretion.

5-alpha Reductase Inhibitors↗
PubMed1994

5 alpha-reductase inhibition by finasteride (Proscar) in epithelium and stroma of human benign prostatic hyperplasia.

Finasteride is a specific 5 alpha-reductase inhibitor that has been shown to reduce the size of human benign prostatic hyperplasia (BPH) by inhibiting the intraprostatic conversion of testosterone to 5 alpha-dihydrotestosterone. The aim of the present in vitro study was to describe in more detail the inhibitory effect of finasteride on 5 alpha-reductase in epithelium and stroma of human BPH. 5 alpha-Reductase activity in epithelium and stroma was inhibited dose-dependently by finasteride. The mean IC50 (50% inhibitory concentration) values, determined in the presence of various testosterone concentrations, were generally 2- to 4-fold lower in epithelium than in stroma. With finasteride concentrations greater than 5 nM, competitive inhibition of 5 alpha-reductase occurred both in epithelium and stroma. The mean inhibition constant Ki[nM +/- SEM] was 7 +/- 3 and 31 +/- 3 in epithelium and stroma, respectively. In the presence of finasteride concentrations < or = 5 nM, the epithelial 5 alpha-reductase seems to be inhibited in an uncompetitive manner, whereas such low finasteride concentrations cause either no inhibition (1-2 nM) or competitive inhibition (5 nM) in stroma. Our present study provides evidence that the inhibitory effect of finasteride on 5 alpha-reductase is much stronger in epithelium than in stroma. Therefore, it is conceivable that the global size-reduction of BPH under finasteride treatment is primarily due to the regression of BPH epithelium.

5-alpha Reductase Inhibitors↗
PubMed1994

Three-year safety and efficacy data on the use of finasteride in the treatment of benign prostatic hyperplasia.

OBJECTIVE: To assess the long-term safety and efficacy of finasteride in the treatment of symptomatic benign prostatic hyperplasia in patients treated with finasteride 5 mg for thirty-six months. METHODS: Two large multicenter studies were used. Patients were randomly assigned to treatment with finasteride, 1 or 5 mg, or placebo for twelve months. After completing twelve months of therapy, patients were invited to enter an open extension to the study in which all patients received finasteride 5 mg. Urinary symptoms, urinary flow rate, prostate volume, and serum concentrations of prostate-specific antigen and dihydrotestosterone were measured periodically during the study. RESULTS: After thirty-six months of treatment with finasteride 5 mg, prostate volume was reduced from baseline by approximately 27 percent, maximum urinary flow rate improved by approximately 2.3 mL/second, and symptom scores improved by 3.6 points. Forty-two percent of patients had a 30 percent or greater decrease in prostate volume, 40 percent of patients showed an increase of 3 mL/second or more in maximum urinary flow rate, and 48 percent of patients experienced a 50 percent or greater improvement in symptom scores. Finasteride was well tolerated and there was no evidence of increased adverse experiences with increased duration of treatment. CONCLUSIONS: The excellent safety profile and sustained clinical efficacy, over thirty-six months, of daily treatment with finasteride 5 mg recommend finasteride as a low-risk medical option for the treatment of symptomatic benign prostatic hyperplasia.

Adult↗
PubMed1995

Can finasteride reverse the progress of benign prostatic hyperplasia? A two-year placebo-controlled study. The Scandinavian BPH Study Group.

OBJECTIVES: To study if placebo-induced improvement in men with symptomatic benign prostatic hyperplasia (BPH) is maintained over 2 years, and to study the efficacy and safety from intervention with finasteride 5 mg for 24 months. METHODS: This was a multicenter, double-blind, placebo-controlled study involving 707 patients with moderate symptoms of BPH enrolled at 59 centers in five Scandinavian countries. Following enrollment and a 4-week single-blind placebo run-in period, patients were randomized to receive finasteride 5 mg once daily or placebo for 24 months. Urinary symptoms, urinary flow rate, prostate volume, postvoiding residual urinary volume, and serum concentrations of prostate-specific antigen together with laboratory safety parameters were measured at entry and at months 12 and 24. Interim physical and laboratory examinations were performed when indicated clinically. RESULTS: In finasteride-treated patients the total symptom score improved throughout the study, with a significant difference between the two groups at 24 months (P < or = 0.01), whereas in placebo-treated patients, there was an initial improvement in the symptom score but no change from baseline at 24 months. The maximum urinary flow rate decreased in the placebo group, but improved in the finasteride group, resulting in a between-group difference of 1.8 mL/s at 24 months (P < or = 0.01). The mean change in prostate volume was +12% in the placebo group versus -19% in the finasteride-treated group (P < 0.01). Finasteride was generally well tolerated throughout the 2-year study period. CONCLUSIONS: The efficacy of therapy with finasteride 5 mg in improving both symptoms and maximum urinary flow rate and reducing prostate volume has been shown to be maintained during 24 months while patients receiving placebo experienced a return to baseline or deterioration of these parameters during the study. These results demonstrate that finasteride can reverse the natural progression of BPH.

Aged↗
PubMed1995

Evidence for atrophy and apoptosis in the ventral prostate of rats given the 5 alpha-reductase inhibitor finasteride.

Castration causes cell loss in the rat ventral prostate through a process called apoptosis. Although 5 alpha-reductase inhibition also causes prostate cell loss, the mechanisms involved have been debated. To investigate this question further, we have evaluated the histological responses of the rat ventral prostate to both castration and 5 alpha-reductase inhibition. Rats were left intact, castrated, or given the selective 5 alpha-reductase inhibitor finasteride. After 4, 9, 14, and 21 days the prostates were excised, the androgen and DNA content determined, and the tissue was subjected to histological and histomorphometric analysis. Finasteride and castration decreased prostate weight at day 21 by 65% and 93%, respectively. Castration decreased DNA content (micrograms per prostate) by a maximum of 88% at 14 days. Finasteride had no significant effect on DNA content after 4 days and decreased DNA content by a maximum of 52% at 14 days. When castrate prostate sections were stained for tissue transglutaminase, a marker of apoptotic cell death, a maximum of 23% of epithelial cells were stained by day 14 with a return to control levels by day 21. Finasteride caused a less intense increase in staining in which 16% of epithelial cells stained for tissue transglutaminase on day 9 with a return to baseline by day 14. When prostate sections were stained for DNA breaks, another marker of cell death, castration, caused a peak of staining on day 4 with 6% of epithelial cells staining and a return to near control levels by day 21. Finasteride-induced staining was less intense with peak staining at day 4 (0.7% of epithelial cells) and a return to control values by day 9. Morphometrics were used to assess the effect of castration and finasteride on prostate duct size and epithelial cell mass. After 4 days of finasteride treatment, the mean ductal mass decreased by 47%, with no significant change thereafter. The mean epithelial cell mass decreased by 15% on day 4 and 60% on day 9, with no further decrease thereafter. Castration caused a more rapid and greater decrease in both morphometric parameters with a 95% reduction in the mass of prostate ducts and a 93% decrease in epithelial cell mass by day 9. We conclude that castration induces a more profound involution of the rat ventral prostate than does 5 alpha-reductase inhibition. Cell loss occurs in both groups, but the degree of cell loss is less with finasteride.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Metabolism of finasteride in rat hepatic microsomes: age and sex differences and effects of P450 inducers.

1. The age- and sex-related metabolism of finasteride and the effects of P450 inducers and inhibitors were investigated using rat hepatic microsomes. 2. No marked age difference (3-13 weeks) in the rates of finasteride disappearance and the formation of 1 (omega-hydroxyfinasteride) and 4 (6 alpha-OH finasteride) was observed in the male rat. Whereas the rate of 1 formation remained about the same in male rat aged 1 year as compared with rat aged 7 weeks, a 21 and 45% decrease in the rate of finasteride disappearance and 4 formation, respectively, were observed. 3. The rates of finasteride disappearance and metabolite formation 1 and 4 in the female rat decreased with an increase in age (3-7 weeks). Metabolite 4 was hardly formed by the hepatic microsomes from the female rat at 7 weeks of age. 4. Hepatic microsomes from the male rat treated with phenobarbital (PB) and dexamethasone (Dex) increased the rate of the finasteride disappearance (PB, 5.5-fold; Dex, 11.6-fold), whereas no increase in this activity was observed after administration of beta-naphthoflavone (BNF). Similarly, pretreatment of the female rat with PB and Dex resulted in increases of 26.6 and 8.4-fold in the rate of finasteride disappearance, respectively, whereas no inductive effect on this activity was observed in the BNF-treated female rat. 5. These observations suggest that finasteride is metabolized by P4502B, P4502C, and P4503A subfamilies in the male rat and by P4502B and P4502C subfamilies in the female rat.

Aging↗
PubMedDate not supplied

Therapeutic effects of finasteride in benign prostatic hyperplasia: a randomized double-blind controlled trial.

The clinical effects of finasteride, a 5 alpha-reductase inhibitor, in patients with benign prostatic hyperplasia (BPH) were evaluated in a double-blind, placebo-controlled study. Forty-six patients with symptomatic BPH were randomly assigned to 2 groups, the finasteride group and the placebo group. The finasteride group received 5 mg of finasteride daily for 6 months. Prostate volume, urinary flow, urinary symptoms, serum prostate-specific antigen (PSA) and adverse events were determined before and after treatment. After 6 months of treatment the patients treated with 5 mg of finasteride per day had a 30% decrease in their total urinary symptom score, a 14% decrease in prostate volume and a 0.9 ng/dL decrease of PSA. Their maximal urinary flow rate increased by 1.42 mL per second and the mean urinary flow rate increased by 0.64 mL per second. The patients given placebo showed no significant changes in their prostate volume, serum PSA and maximal and mean urinary flow rate. However, the symptom scores in the placebo group also decreased significantly. When compared with the placebo group, those in the finasteride group had significantly lower prostate volume, serum PSA, maximal urinary flow rate and urinary symptoms, but not mean urinary flow rate. The frequency of adverse events was low in both the finasteride and placebo groups. These results show that finasteride may be an effective and safe alternative for the treatment of patients with BPH.

Aged↗