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PubMed1997

Role of finasteride in the treatment of recurrent hematuria secondary to benign prostatic hyperplasia.

OBJECTIVES: We evaluated the efficacy of finasteride for the treatment of gross hematuria secondary to benign prostatic hyperplasia in a prospective fashion. METHODS: Twelve patients with recurrent episodes of gross hematuria secondary to benign prostatic hyperplasia were treated with finasteride 5 mg/day. Before initiating treatment, we excluded other sources of hematuria using intravenous urography, cystoscopy, and urine culture. RESULTS: Bleeding subsided within 2 weeks of treatment in all 12 patients. Minimum follow-up was 6 months. Finasteride was well tolerated by all 12 patients. CONCLUSIONS: Finasteride appears to be effective in treating recurrent gross hematuria secondary to benign prostatic hyperplasia. This therapy should be considered an alternative to transurethral resection of the prostate or hormonal ablation in patients with recurrent hematuria and no significant obstructive uropathy or adenocarcinoma of the prostate.

Enzyme Inhibitors↗
PubMed1998

Insulin-like growth factor binding protein 5 is associated with involution of the ventral prostate in castrated and finasteride-treated rats.

BACKGROUND: Insulin-like growth factor binding protein (IGFBP)-5 has been proposed as a signal for apoptosis in the ovary. To determine the relationship between IGFBP-5 and apoptosis during regression of the androgen-deprived prostate, rats were castrated or treated with the 5alpha-reductase inhibitor finasteride for 4, 9, 14, 21, and 28 days. METHODS: Ventral prostate tissue was immunostained for IGFBP-5, and apoptotic cells were identified by in situ end-labeling of fragmented DNA (TUNEL). To compare the distribution of IGFBP-5 with the distribution of apoptotic cells, mirror-image serial sections of prostate tissues from normal and day 4 finasteride-treated rats were examined. RESULTS: In normal rats, 4+/-1% of prostate epithelial cells stained positively for IGFBP-5, and 0.1+/-0.03% demonstrated DNA fragmentation. IGFBP-5 staining peaked at day 9 with 93 +/-2% and 64+/-13% of epithelial cells staining positively in castrated and finasteride-treated rats, respectively. In contrast, DNA fragmentation peaked at day 4 in tissues from both castrated and finasteride-treated rats with 7+/-1% and 0.7+/-0.3% of epithelial cells, respectively, staining. In the serial sections, TUNEL and IGFBP-5 staining were not usually expressed in the same cells. CONCLUSIONS: Prostatic involution involves both programmed cell death and inhibition of cell growth. Because of the distribution of staining and the delayed expression of IGFBP-5 relative to initiation of apoptosis, we postulate that IGFBP-5 functions as an inhibitor of cell proliferation rather than as a signal for apoptosis.

Animals↗
PubMed1998

Regressive changes in finasteride-treated human hyperplastic prostates correlate with an upregulation of TGF-beta receptor expression.

BACKGROUND: Prostatic atrophy has been documented histologically as a consequence of finasteride action on human hyperplastic prostates. An increase in apoptotic rates has also been reported in androgen-deprived hyperplastic prostates. Transforming growth factor beta (TGF-beta) signaling is implicated in apoptotic cell death. TGF-betas have been detected in normal and diseased human prostate. In the normal prostate, TGF-beta acts as a predominantly negative growth regulator. TGF-beta signaling receptors TbetaRI and TbetaRII have been shown to be negatively regulated by androgens. METHODS: We studied the histological changes in 9 selected finasteride-treated patients with benign prostatic hyperplasia (BPH), and analyzed the levels of expression and localization of TGF-beta receptor types TbetaRI and TbetaRII in these patients as compared to selected BPH controls. RESULTS: The prostatic epithelial compartment seemed to be a primary target site for finasteride action, since we observed moderate to severe glandular atrophy after 4-6 months of treatment. TGF-beta receptors were upregulated in treated cases. We assessed a twofold increase in TbetaRII mRNA levels in treated cases as compared to controls. An increase in both TbetaRI and TbetaRII at the protein level by immunostaining was observed, which also provided a helpful means for detecting glands undergoing regression. CONCLUSIONS: We conclude that finasteride may modulate the TGF-beta signaling system to promote changes leading to apoptosis of epithelial cells and prostatic glandular atrophy.

Apoptosis↗
PubMed2000

Pharmacological effects of the lipidosterolic extract of Serenoa repens (Permixon) on rat prostate hyperplasia induced by hyperprolactinemia: comparison with finasteride.

BACKGROUND: The growth of the prostate gland is mainly dependent on androgens. Other hormones, like prolactin (PRL), also influence prostate development. Our purpose was to analyze and compare the effects of two drugs (5alpha-reductase inhibitor) used in the therapy of benign prostatic hyperplasia: lipidosterolic extract of Serenoa repens (LSESR), and finasteride in an in vivo model of rat prostate hyperplasia induced by hyperprolactinemia. METHODS: Hyperprolactinemia was induced by 30 daily injections of sulpiride. Wistar rats received daily gavages of LSESR or finasteride. We used the following groups: control, castrated, castrated with a substitute testosterone (T), or 5alpha-dihydrotestosterone (DHT) implant. RESULTS: Hyperprolactinemia increases the wet weight and induces hyperplasia in the lateral prostate (LP). Unlike finasteride, LSESR significantly reduced LP growth and hyperplasia in castrated, DHT-implanted, and sulpiride-treated rats. CONCLUSIONS: Finasteride was only capable of inhibiting the effect of androgens on rat prostate enlargement. LSESR inhibited not only the androgenic but also the trophic effect of PRL in rat LP hyperplasia.

Androgen Antagonists↗
PubMed1998

Androgen-independent basal cell re-epithelialization, c-erbB-2 mRNA expression and androgen-dependent EGFr mRNA expression in benign prostatic hyperplasia explant cultures treated with finasteride.

We have analyzed the effects of the 5alpha-reductase inhibitor, finasteride (MK906), on the mRNA expression of the epidermal growth factor receptor and c-erbB-2 genes, in benign prostatic hyperplasia explant cultures treated with testosterone and with testosterone plus finasteride. A decrease of the epithelial cell content and an androgen-independent basal cell re-epithelialization was observed during the first 10 days of culture, suggesting a role of basal cells as stem cells involved in androgen-independent epithelial regeneration. Using a semi-quantitative reverse transcription polymerase chain reaction technique, we observed a significant decrease in expression of the epidermal growth factor receptor in the cultures treated with finasteride whereas no effect of finasteride on c-erbB-2 transcription was detected, although the expression of both genes was increased by dihydrotestosterone.

Cholestenone 5 alpha-Reductase↗
PubMed2001

Combined effect of terazosin and finasteride on apoptosis, cell proliferation, and transforming growth factor-beta expression in benign prostatic hyperplasia.

BACKGROUND: Medical treatment of benign prostatic hyperplasia (BPH) targets relief of symptoms by causing either relaxation of the prostatic smooth muscle with alpha1 adrenergic blockade, or shrinkage of the gland with 5alpha-reductase inhibitors. We recently demonstrated that alpha1-blockers, such as terazosin, induce apoptosis in prostatic cells. In this study, we examined the combined effect of finasteride and terazosin on the rate of apoptosis and cellular proliferation to investigate their potential synergy at the cellular level. METHODS: Prostate specimens were obtained from men who were treated with either finasteride (n = 24), terazosin (n = 42), or combination therapy (n = 10) for varying time periods (1 week to 36 months) for the relief of the symptoms of BPH. The proliferative and apoptotic indices of both stromal and epithelial prostatic cell populations were determined. Antibodies against TGF-beta1 and TbetaRII were used to examine the immunoreactivity of TGF-beta1 and TbetaRII, respectively, in all prostate tissue sections. RESULTS: The apoptotic index in both prostate cell populations was significantly higher following the combination treatment compared to terazosin or finasteride alone. There were no significant changes in the rate of cellular proliferation with any treatment. Furthermore, there was a significant increase in TGF-beta1 expression in the prostates of patients treated with terazosin or combination therapy, while there was no change in TbetaRII expression. CONCLUSIONS: These results support the concept that induction of prostate apoptosis is a potential molecular mechanism underlying the combination effect of alpha1 blockade with 5alpha-reductase inhibitors in the effective treatment of BPH. The upregulation of TGF-beta1 implies a role for this ligand as an effector of apoptosis induction in response to alpha1-blockade or finasteride therapy of BPH patients.

Adrenergic alpha-Antagonists↗
PubMed1993

Finasteride, a steroid 5 alpha-reductase inhibitor, does not affect the oxidative metabolism of antipyrine.

A single-blind study was conducted to investigate the effect of multiple doses of finasteride, a 5 alpha-reductase inhibitor for the treatment of benign prostatic hyperplasia, on the single-dose pharmacokinetics of antipyrine. Twelve patients with benign prostatic hyperplasia received a total of four single oral doses of 18 mg/kg antipyrine before, during, and after treatment with 10 mg/day of finasteride for 28 days. Finasteride had no effect on antipyrine concentration profiles. There were also no changes in urinary excretion of three principal antipyrine metabolites. A slight increase in renal clearance of antipyrine was observed; however, this is not considered relevant because excretion of unchanged antipyrine represents a minor fraction of total elimination and is not directly related to oxidative metabolism. These results imply that significant interactions between finasteride and drugs metabolized by these cytochrome P-450 enzymes are unlikely.

Administration, Oral↗
PubMed2004

Effect of finasteride on risk of prostate cancer: how little we really know.

The Prostate Cancer Prevention Trial (PCPT) reported conclusively that finasteride prevents or delays the detection of prostate cancer. One perplexing finding was that more high-grade tumors were detected in the finasteride treated group. It is hard to put this into perspective because of the limited published data on the effects of finasteride on prostate cancer. The strong possibility exists that the increase in high-grade tumors may be due to a treatment effect, which causes intermediate grade cancers to appear to be high-grade or aggressive tumors. Confirmation of a spurious tumor grade "inflation" will make the conclusions of this study clearer and define the benefits of finasteride chemoprevention in a more favorable light.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed2006

Enhancement of intermittent androgen ablation by "off-cycle" maintenance with finasteride in LNCaP prostate cancer xenograft model.

BACKGROUND: Intermittent androgen ablation (IAA) was developed with the intention of delaying progression of prostate cancer to androgen-independence and improving quality of life. Our previous studies suggest that relative to dihydrotestosterone (DHT), testosterone (T) is a weak inducer of proliferation and a more potent inducer of differentiation. We hypothesize that administration of finasteride (F), a type-II 5-alpha-reductase inhibitor that increases T and decreases DHT, during the IAA "off-cycle" would enhance the efficacy. METHODS: After LNCaP tumor establishment, nude mice were castrated and randomized to continuous androgen ablation (CAA), continuous androgen ablation plus finasteride (CAA + F), intermittent androgen ablation (IAA), or intermittent androgen ablation plus finasteride (IAA + F). RESULTS: After one cycle of therapy, mice treated with IAA + F had significantly less tumor growth than the other treatment groups (P = 0.002). Mice treated with IAA + F had the best survival (P = 0.048) and were 3-5 times more likely to be alive 70 days following treatment initiation. CONCLUSIONS: IAA with finasteride provides the most favorable tumor growth kinetics and survival compared to both CAA and standard IAA.

Androgens↗
PubMed1994

Effects of chronic oral administration of a selective 5 alpha-reductase inhibitor, finasteride, on the dog prostate.

Young mature dogs received finasteride, a selective 5 alpha-reductase inhibitor, orally at 0, 5, 15, and 45 mg/kg/day for 27 or 53 weeks. The effect of finasteride administration on prostatic size and morphology was evaluated macroscopically and microscopically. Changes in glandular and fibromuscular compartments were quantitated by a point counting method on trichrome-stained sections. Finasteride administration induced a decrease of mean prostatic weights and epithelial atrophy in all treated groups. No changes in testicular weights and morphology were observed. The greatest prostatic shrinkage was obtained in the group receiving 45 mg/kg/day for 53 weeks; compared to placebo controls, the percent decreases in absolute volumes occupied by epithelium, lumens, fibrovascular stroma, and smooth muscle were 88, 97, 51 and 72, respectively. These results clearly demonstrate that prostatic shrinkage following finasteride administration results from a decrease in both glandular and fibromuscular compartments.

Administration, Oral↗
PubMed1998

Effect of castration and finasteride on urinary oxalate excretion in male rats.

We investigated the effects of castration and finasteride administration on urinary oxalate (Ox) excretion in a rat ethylene glycol (EG) model of urolithiasis. Male adult SD rats were divided into six groups. Group 1 were normal, untreated rats. The other five groups, all treated with 0.75% EG for 4 weeks; were as follows: group 2, non-castrated (intact) rats; group 3, castrated rats; group 4, castrated rats with a 4-cm testosterone implant; group 5, intact rats treated with high-dose finasteride (7.5 mg%); and group 6, intact rats treated with low-dose finasteride (0.75 mg%). Urinary Ox excretion increased 12.8-fold after 4 weeks of EG treatment (group 2 vs group 1). Both castration (group 3) and finasteride administration (groups 5 and 6) significantly decreased urinary Ox excretion compared with intact rats (group 2). We conclude that dihydrotestosterone is partially responsible for the exaggerated hyperoxaluria observed in the rat EG model of urolithiasis.

Animals↗
PubMed2000

Prostatic expression of human 5alpha-reductase type 2 during finasteride therapy: a randomized, double-blind, placebo-controlled study.

This study was aimed at exploring the effect of finasteride, a non-steroidal competitive inhibitor of the enzyme 5alpha-reductase, on 5alpha-reductase type 2 at the mRNA level in human prostate, using an in situ hybridization technique. After randomization, 10 men with benign prostatic hyperplasia (BPH) received oral finasteride (5 mg daily) and five men with BPH received placebo daily. Careful clinical examination was carried out and 2 biopsy samples were taken transrectally before the treatment and after 3, 6, and 12 months of treatment. In situ hybridization was carried out and expression of 5alpha-reductase type 2 mRNA was measured. The results showed that finasteride treatment had no permanent effect on expression of 5alpha-reductase type 2 in prostatic epithelium, compared with placebo treatment. Expression varied during treatment, but there was no clear tendency in this expression. The signal was localized in the epithelial cells. We conclude that finasteride treatment had no clear effect on human 5alpha-reductase type 2 expression in the prostate.

Aged↗
PubMed1991

Reversible decreases of fertility in male Sprague-Dawley rats treated orally with finasteride, a 5 alpha-reductase inhibitor.

Finasteride, a 5 alpha-reductase inhibitor, was investigated for its effects on fertility in male rats as part of its preclinical safety assessment. Studies were initiated when the male Sprague-Dawley rats were either young (4 to 6 weeks old) or mature (15 weeks old). Treatment duration ranged from 6 to 32 weeks. Each male was cohabited with two untreated females at various periods during and after treatment. Litter parameters were evaluated on either day 14 or 20 of gestation. Males were necropsied at the end of treatment or 7 to 11 weeks following the end of treatment. The major findings of these studies were that 1) young rats given 20 to 80 mg/kg/day of finasteride first showed mild to moderate decreases in fertility after 12 weeks of treatment, whereas mature males (given only 80 mg/kg/day) did not show a similar decrease until 24 weeks of treatment, 2) fewer copulatory plugs and atrophy of prostates and seminal vesicles were associated with finasteride treatment, 3) the decreased fertility was only partial (ie, fertility index did not decrease below 48% of control in any study) and was not due to decreases in mating, 4) formation of copulatory plugs, organ weights, and fertility returned to normal levels after at least 6 weeks of drug withdrawal, and 5) the testes showed no histologic or weight changes that would explain the effect on fertility. These results show that the decreased fertility in male rats was associated with finasteride-induced inhibition of accessory gland secretions, an expected pharmacologic effect.

5-alpha Reductase Inhibitors↗
PubMed2006

Development and validation of a new gas flame ionization detector method for the determination of finasteride in tablets.

A simple, rapid, and sensitive method based on gas chromatography with flame ionization detection is described for the determination of finasteride in tablets. The method is based on the derivatization of finasteride with N,O-bis(trimethylsilyl)trifluoroacetamide-1% trimethylchlorosilane at 60 degrees C for 30 min. The method was validated for specificity, linearity, precision, accuracy, robustness, and limit of quantification. The degree of linearity of the calibration curves, the percentage recoveries of finasteride, and the limit of detection (LOD) and limit of quantification (LOQ) for the gas chromatographic method were determined. The assay was linear over the concentration range of 10 to 50 microg ml(-1) (R approximately 0.999). LOQ and LOD (signal/noise ratio = 10) were found to be 10 and 2 microg ml(-1), respectively. The method was found to be simple, specific, precise, accurate, and reproducible. All of the validation parameters were within the acceptance range. The developed method was applied successfully to estimate the amount of finasteride in tablets. The results were compared statistically with those obtained by the official method using t and F tests. There was no significant difference between the two methods with respect to mean values and standard deviations at the 95% confidence level.

Chromatography, Gas↗
PubMed2006

Finasteride effects on hypoxia and angiogenetic markers in benign prostatic hyperplasia.

OBJECTIVES: To assess the effects of finasteride on angiogenetic and hypoxia markers in benign prostatic hyperplasia. METHODS: A total of 178 patients aged 51 to 85 years (mean 68.7) with benign prostatic hyperplasia and awaiting transurethral prostate resection were prospectively randomized into a group of patients receiving finasteride (group 1; 88 patients) and a group of patients who received no medication until transurethral prostate resection (group 2; 90 patients). Tissue specimens were immunohistochemically stained with monoclonal antibodies against CD34 for microvessel density (MVD), vascular endothelial growth factor (VEGF), and hypoxia inducible factor-1alpha (HIF-1alpha). RESULTS: Blood loss during transurethral prostate resection was significantly higher in group 2 compared with group 1 (P <0.001). The distribution of CD34 immunostaining was mainly at the suburethral prostate. MVD, VEGF, and HIF-1alpha values were significantly lower statistically (P <0.001) in group 1 compared with group 2. In the finasteride group (group 1), the positive correlation of the immunoreactivity of CD34 and HIF-1alpha, VEGF and HIF-1alpha, and VEGF and CD34 was statistically significant (P <0.001). In the same group, MVD and VEGF and HIF-1alpha expression correlated statistically with the treatment duration. CONCLUSIONS: Finasteride administration in benign prostatic hyperplasia results in statistically significant suppression of MVD, VEGF, and HIF-1alpha in a time-dependent manner.

Aged↗
PubMed2006

Can effect of finasteride on prostate-specific antigen be used to decrease repeat prostate biopsy?

OBJECTIVES: Patients often undergo multiple prostate biopsies for persistently elevated prostate-specific antigen (PSA) levels. Finasteride decreases serum PSA by approximately 50%. We performed a pilot study to examine the correlation among finasteride, PSA, and PSA density (PSAD) to identify patients who could be excluded from repeat prostate biopsy. METHODS: We performed a prospective study from 2001 to 2002 on 25 men with elevated PSA levels. These patients had prior negative prostate biopsy findings. At study onset, the patients' PSA level and PSAD were measured. Patients were instructed to take finasteride 5 mg for 6 months. PSA and PSAD determination and prostate biopsies were repeated at 6 months and the findings compared with the initial results. RESULTS: The mean patient age was 67.2 years (median 62). The median PSA level was 8.3 ng/dL at study entry (mean 9.34) and 4.6 ng/dL (mean 5.09) at 6 months. The median PSAD was 0.18 (mean 0.20) at study entry and 0.09 (mean 0.12) at 6 months. Of the 23 patients who completed the study, 6 (26%) were diagnosed with prostate cancer. At study entry, the median PSA level in those with prostate cancer was 9.6 ng/dL and was 5.8 ng/dL at 6 months. Patients without prostate cancer on repeat biopsy had a 44% decrease in PSAD. Patients with prostate cancer had a 5% decrease in PSAD. CONCLUSIONS: The results of our study have demonstrated that patients without prostate cancer have a greater decrease in PSAD when taking finasteride than those with prostate cancer. This pilot study had a small population with limited power, and a repeat prospective study with a larger population is warranted.

Aged↗
PubMed1996

Finasteride in the treatment of hirsutism: new therapeutic perspectives.

OBJECTIVE: To determine of the clinical and hormonal effects of finasteride (Proscar; Merck, Sharp, and Dohme, Rahway, NJ) in the treatment of idiopathic hirsutism and hirsutism in patients with polycystic ovary syndrome (PCOS). DESIGN: Controlled clinical study. SETTING: Istitute of Obstetrics and Gynecology, University of Naples "Federico II." PATIENTS: Ten women affected by idiopathic hirsutism and 15 women with PCOS. INTERVENTIONS: Finasteride was administered orally at a daily dose of 5 mg for a period of 6 months. MAIN OUTCOME MEASURES: Rating of hirsutism with the Ferriman-Gallwey method; serum androgen assays. RESULTS: Finasteride produced a reduction in the average hirsutism scores ( > 50% in all patients), whereas no change was observed in serum T, androstenedione, and DHEAS levels. A significant reduction was measured in serum dihydrotestosterone and 3 alpha, 17 beta-androstenediol glucuronide levels. CONCLUSIONS: This study demonstrates that symptomatic hirsutism has to be considered as a skin disease associated with the increased activity of the 5 alpha-reductase. It also indicates that the selective 5 alpha-reductase inhibitor, finasteride, is very effective and well tolerated in the treatment of both idiopathic hirsutism and of hirsutism in patients with PCOS.

Adult↗
PubMed1997

Comparison of finasteride versus spironolactone in the treatment of idiopathic hirsutism.

OBJECTIVE: To compare the efficacy of finasteride and spironolactone in the treatment of idiopathic hirsutism. DESIGN: Prospective, randomized, single-blind study. SETTING: A tertiary hirsutism clinic. PATIENT(S): Forty women with idiopathic hirsutism were selected. INTERVENTION(S): Patients were assigned randomly to receive either 5 mg of finasteride or 100 mg of spironolactone for 9 months. MAIN OUTCOME MEASURE(S): Hirsutism scores were measured according to the Ferriman-Gallwey scoring system, and side effects were monitored for 9 months of treatment. Blood samples were taken at each visit for assessment of endocrine, biochemical, and hematologic parameters. RESULT(S): Hirsutism scores were decreased significantly in both groups at the end of 9 months. The mean percent change (+/- SD) in hirsutism scores in the finasteride and spironolactone groups was as follows: 5.91% +/- 7.18% and 20.60% +/- 12.59% at 3 months, 10.61% +/- 12.18% and 32.57% +/- 15.68% at 6 months, and 15.15% +/- 15.38% and 42.36% +/- 12.31% at 9 months, respectively. There was a significantly better response with spironolactone treatment at the end of 9 months. Eleven (55%) of 20 patients in the spironolactone group experienced side effects. However, none of them stopped treatment because of side effects. CONCLUSION(S): The present data suggest that both finasteride and spironolactone are effective in the treatment of idiopathic hirsutism. However, it appears that the spironolactone group responded significantly better.

Adult↗