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 91 records · Page 5Linked to original sources
PubMed2000

Combined sabal and urtica extract compared with finasteride in men with benign prostatic hyperplasia: analysis of prostate volume and therapeutic outcome.

OBJECTIVE: To test the hypothesis that in patients with benign prostatic hyperplasia (BPH), the outcome of drug therapy with finasteride may be predictable from the baseline prostate volume and that positive clinical effects might be expected only in patients with prostate volumes of > 40 mL, using a subgroup analysis of results from a previously reported clinical trial of finasteride and phytotherapy. PATIENTS AND METHODS: A subgroup of 431 patients was analysed from a randomized, multicentre, double-blind clinical trial involving 543 patients with the early stages of BPH. Patients received a fixed combination of extracts of saw palmetto fruit (Serenoa repens) and nettle root (Urtica dioica) (PRO 160/120) or the synthetic 5alpha-reductase inhibitor finasteride. The patients assessed had valid ultrasonographic measurements and baseline prostate volumes of either </= 40 mL or > 40 mL. All 516 patients were included in the safety analysis. The results of the original trial showed equivalent efficacy for both treatments. RESULTS: The mean (SD) maximum urinary flow (the main outcome variable) increased (from baseline values) after 24 weeks by 1.9 (5.6) mL/s with PRO 160/120 and by 2.4 (6.3) mL/s with finasteride. There were no statistically significant group differences (P = 0.52). The subgroups with small prostates (</= 40 mL) showed similar improvements, with mean values of 1.8 (5.2) mL/s with PRO 160/120 and 2.7 (7.4) mL/s with finasteride. The mean values for the subgroups with prostates of > 40 mL were similar, at 2.3 (6.1) and 2. 2 (5.3) mL/s, respectively. There were improvements in the International Prostate Symptom Score in both treatment groups, with no statistically significant differences. The subgroup analysis showed slightly better results for voiding symptoms in the patients with prostates of > 40 mL, but there were also improvements in the subgroup with smaller prostates. The safety analysis showed that more patients in the finasteride group reported adverse events and also there were more adverse events in this group than in patients treated with PRO 160/120. CONCLUSION: The present analysis showed that the efficacy of both PRO 160/120 and finasteride was equivalent and unrelated to prostate volume. However, PRO 160/120 had better tolerability than finasteride.

Aged↗
PubMed2003

The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia.

BACKGROUND: Benign prostatic hyperplasia is commonly treated with alpha-adrenergic-receptor antagonists (alpha-blockers) or 5alpha-reductase inhibitors. The long-term effect of these drugs, singly or combined, on the risk of clinical progression is unknown. METHODS: We conducted a long-term, double-blind trial (mean follow-up, 4.5 years) involving 3047 men to compare the effects of placebo, doxazosin, finasteride, and combination therapy on measures of the clinical progression of benign prostatic hyperplasia. RESULTS: The risk of overall clinical progression--defined as an increase above base line of at least 4 points in the American Urological Association symptom score, acute urinary retention, urinary incontinence, renal insufficiency, or recurrent urinary tract infection--was significantly reduced by doxazosin (39 percent risk reduction, P<0.001) and finasteride (34 percent risk reduction, P=0.002), as compared with placebo. The reduction in risk associated with combination therapy (66 percent for the comparison with placebo, P<0.001) was significantly greater than that associated with doxazosin (P<0.001) or finasteride (P<0.001) alone. The risks of acute urinary retention and the need for invasive therapy were significantly reduced by combination therapy (P<0.001) and finasteride (P<0.001) but not by doxazosin. Doxazosin (P<0.001), finasteride (P=0.001), and combination therapy (P<0.001) each resulted in significant improvement in symptom scores, with combination therapy being superior to both doxazosin (P=0.006) and finasteride (P<0.001) alone. CONCLUSIONS: Long-term combination therapy with doxazosin and finasteride was safe and reduced the risk of overall clinical progression of benign prostatic hyperplasia significantly more than did treatment with either drug alone. Combination therapy and finasteride alone reduced the long-term risk of acute urinary retention and the need for invasive therapy.

5-alpha Reductase Inhibitors↗
PubMed2000

Lack of efficacy of finasteride in postmenopausal women with androgenetic alopecia.

BACKGROUND: Finasteride, an inhibitor of type 2 5alpha-reductase, decreases serum and scalp dihydrotestosterone (DHT) by inhibiting conversion of testosterone to DHT and has been shown to be effective in men with androgenetic alopecia (AGA). The effects of finasteride in women with AGA have not been evaluated. OBJECTIVE: The purpose of this study was to evaluate the efficacy of finasteride in postmenopausal women with AGA. METHODS: In this 1-year, double-blind, placebo-controlled, randomized, multicenter trial, 137 postmenopausal women (41-60 years of age) with AGA received finasteride 1 mg/day or placebo. Efficacy was evaluated by scalp hair counts, patient and investigator assessments, assessment of global photographs by a blinded expert panel, and histologic analysis of scalp biopsy specimens. RESULTS: After 1 year of therapy, there was no significant difference in the change in hair count between the finasteride and placebo groups. Both treatment groups had significant decreases in hair count in the frontal/parietal (anterior/mid) scalp during the 1-year study period. Similarly, patient, investigator, and photographic assessments as well as scalp biopsy analysis did not demonstrate any improvement in slowing hair thinning, increasing hair growth, or improving the appearance of the hair in finasteride-treated subjects compared with the placebo group. Finasteride was generally well tolerated. CONCLUSION: In postmenopausal women with AGA, finasteride 1 mg/day taken for 12 months did not not increase hair growth or slow the progression of hair thinning.

Administration, Oral↗
PubMed2004

A prospective, 1-year trial using saw palmetto versus finasteride in the treatment of category III prostatitis/chronic pelvic pain syndrome.

PURPOSE: This study was designed to assess the safety and efficacy of saw palmetto or finasteride in men with category III prostatitis/chronic pelvic pain syndrome (CP/CPPS). MATERIALS AND METHODS: A prospective, randomized, open label, 1-year study was designed to assess the safety and efficacy of saw palmetto and finasteride in the treatment of men diagnosed with CP/CPPS. Patients were randomized to finasteride (5 mg once daily) or saw palmetto (325 mg daily) for 1 year. Patients were evaluated using the National Institutes of Health Chronic Prostatitis Symptom Index, individual domains (pain, urinary symptoms, quality of life and mean pain score) and the American Urological Association Symptom Score at baseline, 3, 6 and 12 months. RESULTS: A total of 64 consecutive men 24 to 58 years old (mean age 43.2) with a diagnosis of CP/CPPS were equally randomized to the 2 treatment arms. All 64 men had previously received antibiotics (duration of 3 to 93 weeks), 52 (82%) had been on alpha-blockade. There were 61, 57 and 56 patients evaluable at 3, 6 and 12 months, respectively. At 1 year mean total National Institutes of Health Chronic Prostatitis Symptom Index score decreased from 23.9 to 18.1 in the finasteride group (p <0.003), and from 24.7 to 24.6 in the saw palmetto arm (p = 0.41). In the finasteride arm the quality of life and pain domains were significantly improved at 1 year; however, urination was not. Adverse events included headache (3 cases) in the saw palmetto group and decreased libido (2 cases) in the finasteride group. At the end of the trial 13 of 32 (41%) and 21 of 32 (66%) opted to continue saw palmetto and finasteride, respectively. CONCLUSIONS: CP/CPPS treated with saw palmetto had no appreciable long-term improvement. In contrast, patients treated with finasteride had significant and durable improvement in all various parameters except voiding. Further studies are warranted to ascertain the mechanism and reproducibility of these effects in a placebo controlled trial.

Adult↗
PubMed2006

Evaluation of androgens in the scalp hair and plasma of patients with male-pattern baldness before and after finasteride administration.

BACKGROUND: Finasteride, a competitive inhibitor of the enzyme 5alpha-reductase II, is widely used as a medical treatment for patients with male-pattern baldness (MPB), which is affected by the distribution of androgenic steroids. It is also notable that the androgenic effect in MPB is different for each region of the head. OBJECTIVES: To study the effect of the drug finasteride, we quantified androgenic steroids in the vertex and occipital scalp hair and in the plasma of patients with MPB. METHODS: The patients with MPB, aged 23-52 years, were treated with finasteride 1 mg daily for 5 months. The hair and plasma samples were hydrolysed, extracted with n-pentane, and derivatized with MSTFA:NH4I:DTE (1000:4:5, v/w/w). We analysed the concentrations of dihydrotestosterone (DHT) and testosterone (T) in the hair and plasma using gas chromatography-mass spectrometry (GC-MS). RESULTS: In the hair, the ratio of DHT/T was decreased in the vertex scalp hair after the individual received finasteride (P < 0.005). However, we found no significant difference in the ratio of DHT/T in the occipital scalp hair before and after individuals received finasteride. Like the results in the vertex scalp hair, the ratio of DHT/T in the plasma was remarkably decreased after finasteride administration (P < 0.001). CONCLUSIONS: This study supports the effect of finasteride in patients with MPB by examining the decreased level of DHT/T in scalp hair and in plasma. Thus, in view of the androgenic effect in the different hair regions, the vertex scalp hair plays a more important role for patients with MPB treated with finasteride than does the occipital hair.

5-alpha Reductase Inhibitors↗
PubMed2005

Gleason grade remains an important prognostic predictor in men diagnosed with prostate cancer while on finasteride therapy.

OBJECTIVE: To evaluate men treated with finasteride for lower urinary tract symptoms, who subsequently were diagnosed with prostate cancer and had a radical prostatectomy (RP) at our institution, to determine if finasteride therapy prevented accurate Gleason grade assignment and prediction of biochemical recurrence. PATIENTS AND METHODS: Between May 1996 and July 2003, 45 men were identified who had RP and had previously been treated with finasteride for > or = 6 months before the diagnosis of prostate cancer. Clinical and pathological information was gathered from a RP database. Serum prostate-specific antigen (PSA) level, duration of finasteride therapy, biopsy Gleason grade, clinical stage, RP Gleason grade and pathological stage were reviewed. Freedom from recurrence was predicted using validated nomograms before and after RP, and compared against actuarial 5-year freedom from recurrence using the Kaplan-Meier method. RESULTS The mean duration of finasteride therapy before diagnosis was 23.6 months, the mean serum PSA (doubled to account for finasteride use) 11.02 ng/mL and mean biopsy Gleason score 6. When comparing the biopsy and RP specimen Gleason score, it was downgraded by 1 point in six men, upgraded by 1 point in eight, and upgraded by 2 points in one. The Gleason score was constant in 30 patients. The nomograms predicted freedom from recurrence in 83% and 85%, respectively; the 5-year actuarial freedom from recurrence was 86%. CONCLUSION: Finasteride does not appear to compromise the assignment of Gleason grade for use in prediction tools before or after RP in men undergoing prostate biopsy or RP. The actuarial 5-year freedom from recurrence was similar to that predicted by the validated nomograms. Gleason grade remains an important prognostic predictor in men treated with finasteride and undergoing RP for clinically localized prostate cancer.

Enzyme Inhibitors↗
PubMed2002

Finasteride in the treatment of clinical benign prostatic hyperplasia: a systematic review of randomised trials.

BACKGROUND: Benign prostatic hyperplasia affects older men. This systematic review determined efficacy and adverse effects of finasteride. REVIEW METHODS: PubMed, the Cochrane Library, reference lists of reports, and reviews were searched for randomised, double-blind trials of finasteride in benign prostatic hyperplasia. Outcomes included symptom score, urinary flow rate, prostate volume, discontinuation, and adverse effects. Relative risk and NNT or NNH were calculated for dichotomous data. Sensitivity analyses assessed influences of baseline symptom severity, initial prostate volume, a dominating trial, and previous interventions. RESULTS: Three trials had active controls and 19 had placebo. In placebo-controlled trials, 8820 patients received finasteride 5 mg and 5909 placebo over 3-48 months. Over 48 months finasteride produced greater improvements in total symptom score, maximum urinary flow rate, and prostate volume. Significantly more sexual dysfunction, impotence, ejaculation disorder and decreased libido occurred with finasteride at 12 months; the NNH for any sexual dysfunction at 12 months was 14. Significantly fewer men treated with finasteride experienced acute retention or had surgery at 24 or 48 months than with placebo; at 12 months the NNT was 49 (31 to 112) to avoid one acute urinary retention and 31 (21 to 61) to avoid one surgery. Sensitivity analyses showed benefit with finasteride 5 mg to be constant irrespective of the initial prostate volume. CONCLUSIONS: Information from many patients in studies of high quality showed beneficial effects of finasteride in terms of symptoms, flow rate and prostate volume. More utility would result if patient centred outcomes were reported in dichotomous form.

Enzyme Inhibitors↗
PubMed1993

Effect of combination treatment with zanoterone (WIN 49596), a steroidal androgen receptor antagonist, and finasteride (MK-906), a steroidal 5 alpha-reductase inhibitor, on the prostate and testes of beagle dogs.

The effects of the steroidal androgen receptor antagonist zanoterone (WIN 49596) and the steroidal 5 alpha-reductase inhibitor finasteride (MK-906) either alone or in combination on prostatic size, histomorphology, and biochemistry were determined in the intact male dog. Additionally, the effects of treatment with zanoterone and/or finasteride on testicular size, serum testosterone and LH levels, and spermatogenesis were determined in the same dogs. Daily oral treatment for 16 weeks with either zanoterone alone at 10 mg/kg.day or finasteride alone at 1.0 mg/kg.day reduced (P < 0.05) the size of the prostate, resulted in mild to moderate diffuse glandular atrophy of the prostate, and decreased prostatic DNA and prostatic arginine esterase (the primary canine prostatic protein) levels compared to those in intact controls. These changes occurred with no effect on testicular weight, testicular histomorphology, daily sperm production, or serum LH levels. Serum testosterone concentrations were increased (P < 0.05) approximately 3-fold in the 10 mg/kg.day zanoterone treatment group compared to those in intact controls. Combination treatment of male dogs for 16 weeks with zanoterone (10 mg/kg.day) plus finasteride (1.0 mg/kg.day) orally also reduced (P < 0.05) prostate size, resulted in moderate to marked diffuse prostatic glandular atrophy, and decreased prostatic DNA and arginine esterase levels more than either drug alone, without affecting testicular size, testicular histomorphology, serum LH concentrations, or serum testosterone concentrations compared to those in intact controls. The effects of combination treatment with zanoterone and finasteride on prostatic size; histomorphology; and DNA, arginine esterase protein, and arginine esterase mRNA levels were similar to those observed in castrate controls. In addition, in situ estimates of prostatic size using transrectal ultrasonography indicated that the median time to 70% prostatic regression in dogs administered combination zanoterone plus finasteride was similar to that in castrate controls (9.6 and 9.3 weeks, respectively), indicating that the combination was more effective in causing prostatic regression than either drug alone. Finally, at the dosages used, no adverse effects of combination treatment with zanoterone plus finasteride on testicular or other major body organ weights were observed. Based on these results, combination therapy using zanoterone and finasteride for the treatment of human androgen-dependent disorders such as benign prostatic hyperplasia and prostate cancer has potential utility.

Androstenes↗
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↗
PubMed1996

Evidence for atrophy and apoptosis in the prostates of men given finasteride.

Finasteride, a 5 alpha-reductase inhibitor, decreases prostate size and improves symptoms in men with benign prostatic hyperplasia. However, little is known about prostate histopathology in men taking finasteride. To determine the mechanism by which finasteride reduces prostate size, tissue was collected at the time of prostatectomy from men taking either no medication (n = 10) or 5 mg finasteride daily for 6-18 days (n = 6; group 1), 23-73 days (n = 5; group 2), or 3 months to 4 yr (n = 5; group 3). To assess whether finasteride causes epithelial atrophy, morphometric measurement of epithelial cell and duct width was used. The mean epithelial cell width in control prostates (mean +/- SEM, 21 +/- 0.7 microns) decreased with duration of treatment to 19 +/- 1 microns in group 1, 15 +/- 2 microns in group 2, and 8 +/- 0.3 microns in group 3. Mean duct width decreased from 135 +/- 6 microns in the control prostates to 128 +/- 10 microns in group 1, 103 +/- 3 microns in group 2, and 63 +/- 6 microns in group 3. To assess whether prostate cell death was occurring, sections were in situ end labeled for DNA breaks and immunostained for tissue transglutaminase (tTG), a marker of apoptosis (programmed cell death). The percentage of epithelial cells staining for DNA breaks was 0.4 +/- 0.2 in control prostates, 2.8 +/- 0.9 in group 1, 1.7 +/- 0.5 in group 2, and 0.7 +/- 0.3 microns in group 3. Anti-tTG staining of epithelial cells was graded on a scale of 0-4. In control prostates, 3 +/- 1% of the ducts were grade 3 or 4 (> 50% of epithelial cells staining). In finasteride-treated prostates, 2 +/- 2% of the prostates in group 1, 13 +/- 4% of the prostates in group 2, and 0.5 +/- 0.5% of the prostates in group 3 were grade 3-4. These results indicate that a progressive decrease in epithelial cell size and function occurs during the first several months in the prostates of men treated with finasteride. The staining for DNA breaks and the tTG staining also indicate that an increased rate of apoptosis is occurring transiently in these prostates. We conclude that finasteride causes prostate involution through a combination of atrophy and cell death.

5-alpha Reductase Inhibitors↗
PubMed1999

A prospective randomized trial comparing low dose flutamide, finasteride, ketoconazole, and cyproterone acetate-estrogen regimens in the treatment of hirsutism.

Sixty-six hirsute women were randomized and treated with 1) flutamide (n = 15), 250 mg/day; 2) finasteride (n = 15), 5 mg/day; 3) ketoconazole (n = 16), 300 mg/day; and 4) ethinyl estradiol (EE)-cyproterone acetate (CPA; n = 20), 0.01 mg EE/day for the first week, 0.02 mg EE/day for the second week, and 0.01 mg EE/day for the third week, followed by a pause of 7 days, then 12.5 mg CPA/day added during the first 10 days of every month for 12 months. Hirsutism was evaluated by the Ferriman-Gallwey score, and hair diameter and hair growth rate were determined by a special image analysis processor in basal conditions and after 90, 180, 270, and 360 days of treatment. All treatments produced a significant decrease in the hirsutism score, hair diameter, and daily hair growth rate: flutamide, -55 +/- 13%, -21 +/- 14%, and -37 +/- 18%; finasteride, -44 +/- 13%, -16 +/- 12%, and -27 +/- 14%; ketoconazole, -53 +/- 18%, -14 +/- 12%, and -30 +/- 21%; and EE-CPA, -60 +/- 18%, -20 +/- 11%, and -28 +/- 21%. Some differences existed among treatments with regard to effectiveness; EE-CPA and flutamide seem to be the most efficacious in improving hirsutism. For the hirsutism score, a greater decrease was seen with EE-CPA (-60 +/- 18%) than with finasteride (-44 +/- 13%; P < 0.01) and a greater decrease was seen with flutamide (-58 +/- 18%) than with finasteride (-44 +/- 13%; P < 0.05). Flutamide is the fastest in decreasing hair diameter; EE-CPA is the fastest in slowing down hair growth, even though at the end of the treatment there was a significant difference between flutamide and finasteride only (-41 +/- 18% vs. -27 +/- 14%; P < 0.05). Flutamide, ketoconazole, and EE-CPA induced a significant decrease in total and free testosterone, 5alpha-dihydrotestosterone, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and androstenedione plasma levels. During the EE-CPA treatment, gonadotropins were suppressed, and the sex hormone-binding globulin level increased. Finasteride induced a decrease in dehydroepiandrosterone sulfate and 5alpha-dihydrotestosterone and an increase in testosterone levels. Very few side-effects were observed during treatment with low doses of flutamide, EE-CPA, and particularly finasteride. Flutamide induced a decrease whereas EE-CPA induced an increase in triglycerides and cholesterol, showing higher values within the normal range. Ketoconazole induced several side-effects and complications, and several people dropped out of the study. Despite different modalities of action and significantly different effects on androgen levels, low doses of flutamide, finasteride, and EE-CPA constitute very satisfactory alternative therapeutic regimens in the treatment of hirsutism.

Adult↗
PubMed1999

Comparison of finasteride versus flutamide in the treatment of hirsutism.

OBJECTIVE: To compare the effectiveness of finasteride and flutamide in the treatment of hirsutism in patients with polycystic ovary syndrome (PCOS) and with idiopathic hirsutism. DESIGN: Randomized study. PATIENTS: One hundred and ten hirsute patients were selected: 64 women with PCOS and 46 with idiopathic hirsutism. METHODS: Patients were assigned randomly to receive 5mg finasteride once daily or 250mg of flutamide twice daily, for 12 consecutive months. Hirsutism was evaluated at 12 months of therapy, with the Ferriman-Gallwey score and with measurement of the terminal hair diameters (microm) taken from four different body areas. Blood samples were taken for assessment of endocrine and hematochemical parameters. Side effects were monitored during the treatment. RESULTS: Both finasteride and flutamide induced a significant decrease in the hirsutism scores and hair diameters at the end of 12 months. Finasteride reduced the Ferriman-Gallwey score by 31.4% in the PCOS cases and by 34.2% in the idiopathic hirsutism cases, and hair diameter by 27.0-34.1% in PCOS and by 29.6-37.9% in idiopathic hirsutism. Flutamide reduced the Ferriman-Gallwey score by 56.7% in PCOS and by 50.9% in idiopathic hirsutism, and hair diameter by 50. 3-60.0% in PCOS and by 47.7-56.5% in idiopathic hirsutism. Flutamide did not induce hormone variations, while finasteride increased testosterone levels by 40% in PCOS and by 60% in idiopathic hirsutism and decreased 3alpha-androstanediol glucuronide (3alpha-diolG) by 66.7% in PCOS and by 69.5% in idiopathic hirsutism. No important side effects or changes in the hematochemical parameters were observed with finasteride, while two patients (3.6%) in the flutamide group expressed abnormal transaminase levels after 6 months of treatment. Dry skin also appeared significantly more with flutamide (67.3%) than with finasteride (23.6%). CONCLUSIONS: Both drugs are effective in the treatment of hirsutism but flutamide is more effective than finasteride.

Adolescent↗
PubMed2004

Finasteride-associated male infertility.

Finasteride is a potent and specific inhibitor of the 5alpha-reductase enzyme in men. Clinical studies have shown that finasteride 1mg/day is effective for promoting hair growth in men with male pattern hair loss. However, there is a concern about the use of finasteride, especially in young fertile patients, because of its action on testosterone metabolism. This paper describes 3 cases of young patients who had very poor seminal quality during finasteride treatment (1 mg/day), and their seminal quality greatly improved after cessation of finasteride treatment. Two of them presented with a left varicocele and the other was obese. We hypothesize that finasteride may not dramatically change the spermatogenesis process in healthy men, but in patients with conditions related to infertility, an amplification of the negative influence of finasteride could occur. Future studies should be done to clarify the extent of the effect of finasteride in patients fertility problems.

Adult↗
PubMed1998

A risk-benefit assessment of treatment with finasteride in benign prostatic hyperplasia.

As an androgen target organ, the prostate gland has the almost unique characteristic of being less sensitive to testosterone than to its metabolite 5 alpha-dihydrotestosterone (5 alpha-DHT). The conversion of testosterone to 5 alpha-DHT is induced by the enzyme 5 alpha-reductase. By blocking the activity of 5 alpha-reductase, the androgenic stimulation of the prostate gland can be significantly reduced. The first drug with such capacity to be introduced on the market was finasteride. Following the administration of this drug to men, serum 5 alpha-DHT levels were reduced by approximately 80%. Large phase III trials have demonstrated the efficacy of finasteride in treating benign prostatic hyperplasia (BPH). While in some patients the drug was poorly effective, other patients showed significant improvements. The mean reduction in size of the prostate gland was 20 to 25% after 6 months of therapy, and this effect was maintained as long as the patient was on the drug, at least up to the end of a 6-year follow-up period. Prostatic symptom scores were improved by a mean of 30%, while urinary flow was only improved by a mean of 1.5 ml/sec (15%). In a recent double-blind, placebo-controlled study comparing the alpha-blocker terazosin with finasteride, significant improvement was demonstrated for the alpha-blocker, while finasteride produced little improvement overall and was not significantly more effective than placebo in treating moderately symptomatic BPH. However, a subanalysis of this study showed that while finasteride was poorly effective in patients with small prostate glands, a significant improvement was apparent in those with glands larger than 40 ml. There is some evidence that early intervention with finasteride can reduce the number of surgical procedures that are required, at least over a 2-year period. Finasteride is very well tolerated. However, since 5 alpha-DHT potentiates erectile capacity, a 3 to 4% incidence of impotence has been reported, as well as a decreased ejaculatory volume. Gynaecomastia has been noted in a few patients (0.4%). In conclusion, finasteride appears to be a very well tolerated drug to treat outflow obstruction in patients with moderately symptomatic BPH caused by large prostate glands.

Enzyme Inhibitors↗
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↗
PubMed1999

Finasteride following balloon dilatation of the prostate. A double-blind, placebo-controlled, multicenter study.

BACKGROUND AND AIMS: To evaluate the efficacy, safety and tolerability of finasteride administered for 24 months following successful balloon dilatation in patients with benign prostatic hyperplasia (BPH). PATIENTS AND METHODS: 75 patients with moderate to severe symptoms of benign prostatic hyperplasia were first treated with balloon dilatation. After a 4-week placebo runin period, 64 patients with successful dilatation and over 50 % reduction in symptoms were randomized to receive either finasteride (33 pts.) at 5 mg/day or placebo (31 pts.) for 24 months. Altogether 12 patients dropped out at some stage, and the final analysis hence included 27 patients in the finasteride group and 25 patients in the placebo group. RESULTS: The symptom scores increased by an average of 3.2 points in the finasteride group and 4.4 points in the placebo group during two years. The mean maximum flow in the finasteride group remained constant: 13.7 ml/s at baseline and 13.9 ml/s at 24 months. In the placebo group the mean maximum flow decreased from 13.3 ml/sec to 11.2 ml/s. During the two-year study period, neither of the groups displayed any changes in residual urine. The above mentioned changes were not statistically significant, however. Prostate volume and serum PSA were significantly lower in the finasteride group (p < 0.001). The groups did not differ with regard to side-effects. CONCLUSIONS: On the basis of the findings, BPH patients with moderate to severe symptoms can be treated with balloon dilatation. The effect of balloon dilatation is quick, and it alleviates the patients' symptoms immediately. Finasteride treatment maintains the positive effect of balloon dilatation. This combination of treatment is tolerated well and side-effects are rare. The favourable effect of balloon dilatation was maintained for at least two years. Finasteride treatment diminished significantly both prostate volume and serum prostate-specific antigen after balloon dilatation compared to placebo treatment.

Catheterization↗
PubMed2002

Clinical predictors in the use of finasteride for control of gross hematuria due to benign prostatic hyperplasia.

PURPOSE: We identify predictors of clinical response as well as response time in patients treated with finasteride for gross hematuria due to benign prostatic hyperplasia. MATERIALS AND METHODS: A retrospective chart review was preformed of 53 patients who had been given 5 mg. finasteride daily for the treatment of active bleeding or a recent history of recurrent bleeding. Urological evaluations were negative for tumor in all patients. A history of prostatectomy, anticoagulant status and prostate size was determined. The degree of hematuria was then graded before and after finasteride treatment according to our previously described system. Of the 53 patients who were actively bleeding at initial evaluation 16 were followed to determine time required for complete resolution of hematuria. RESULTS: Hematuria grade improved after finasteride in 50 (94%) patients. Overall 77% of patients (41 of 53) experienced no further bleeding while taking finasteride. Mean followup was 38 months (range 3 to 86). Of the patients 86% (12 of 14) taking coumadin, 77% (10 of 13) taking aspirin and 73% (19 of 26) on no anticoagulants had no further bleeding once on finasteride. Of the patients who had undergone prior transurethral prostatectomy 84% (26 of 31) experienced no further bleeding versus 68% (15 of 22) of those who had not undergone previous surgery. In the 16 patients who began finasteride while actively bleeding the average time to clear urine was 12 days (range 2 to 45). Prostatic volume correlated with the average time needed for resolution of hematuria, which was 2.7 days or longer for small (less than 40 gm.), 10.3 days or longer for large (40 to 100), 19 days or longer for extra large (100 to 150) and 45 days or longer for extra extra large (greater than 150) glands. Hematuria resolved an average of 5.5 days versus 18.6 days in those who had or had not undergone previous prostatectomy, respectively. CONCLUSIONS: Our long-term followup demonstrates finasteride as a useful treatment for benign prostatic hyperplasia related gross hematuria, which is effective in patients who are on anticoagulants. In patients with larger prostatic volumes a longer time to response and higher incidence of recurrent but lower grade bleeding should be anticipated compared to those who have undergone prior prostatectomy or have a smaller prostate.

5-alpha Reductase Inhibitors↗
PubMed2002

Induction of apoptosis in rat ventral prostate by finasteride is associated with alteration in MAP kinase pathways and Bcl-2 related family of proteins.

Finasteride is widely used in treatment of symptomatic benign prostatic hyperplasia. Treatment of rats with finasteride caused a significant decrease in ventral prostate weight and intraprostatic dihydrotestosterone levels while intraprostatic testosterone levels were increased. Finasteride inhibited Akt-1 and MAPK expression while expression of PTEN was significantly increased only at 100 mg dose. Basal phosphorylation of c-Raf, MEK1/2, MAPK and the transcription factor Elk-1 was significantly reduced by finasteride. The rate of prostate epithelial apoptosis is equivalent to 0.1+/-0.03, 0.6+/-0.18%, 0.92+/-0.24% and 1.42+/-0.3% on treatments with 0, 1, 10 and 100 mg finasteride per kg body weight, respectively. Concomitantly, these treatments led to a 2.5-, 4.0- and 4.0-fold increase in Bad while a slight decrease in Bax was observed. Similar elevations were also observed in Bcl-xs levels which increased by 9.8-, 10- and 12-fold respectively in the finasteride treatments as compared to controls. Bcl-xL levels in ventral prostates treated with 1, 10 and 100 mg finasteride were approximately 30, 30 and 26% of control, respectively. Significant reduction in Bcl-2 expression was observed only at the dose of 100 mg/kg body weight. These findings suggest that modulation of MAP kinase and Akt expression, Bcl-xL, Bcl-xs, Bcl-2 and Bad proteins by finasteride may be, in part, responsible for the anti-proliferative and apoptotic effect of this drug seen clinically and in animal models.

Animals↗