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 145 records · Page 8Linked to original sources
PubMed1996

Effect of MK-386, a novel inhibitor of type 1 5 alpha-reductase, alone and in combination with finasteride, on serum dihydrotestosterone concentrations in men.

Two isozymes (types 1 and 2) of 5 alpha-reductase (5 alpha R; EC 1.3.99.5), with differential tissue distribution, have been identified in humans. These enzymes catalyze the reduction of testosterone (T) to dihydrotestosterone (DHT). The contributions of each of these isozymes to serum and tissue concentrations of DHT remain to be fully defined. Finasteride, a selective inhibitor of type 2 5 alpha R, lowers circulating DHT levels by approximately 70% in men after treatment with 5 mg daily. MK-386 (4,7 beta-dimethyl-4-aza-5 alpha-cholestan-3-one) is a new selective inhibitor of type 1 5 alpha R. A single rising dose, alternating panel, trial in 16 healthy males (age range, 21-25 yr) studied the effect of 0.1-100 mg MK-386. DHT was maximally reduced by 20-30% relative to placebo at MK-386 doses of 10 mg or more, orally, by 24 h posttreatment (P < 0.01 vs. placebo). No consistent effect on T concentrations was evident. In a second trial, finasteride (5 mg) was given for 19 days to 10 healthy young men (age range, 24-47 yr); a 25-mg dose of MK-386 was added for 2 days of combination therapy after at least 10 days of finasteride treatment. Withdrawal of MK-386 was followed by 5-6 days of finasteride follow-up treatment. Finasteride alone reduced DHT, on the average, by 68.7% (SE = 3.4%). Addition of MK-386 suppressed DHT by 89.5% (SE = 1.4%) relative to baseline (P < 0.01 vs. effect of finasteride alone). Small increases in serum T were observed with finasteride alone and in combination with MK-386 (approximately 10% and 19%, respectively). These data are consistent with selective 5 alpha R type 1 inhibition in man by MK-386 and the prediction that types 1 and 2 5 alpha R account for all, or nearly all, of circulating DHT. Further clinical trials are needed to assess the therapeutic utility of type 1 5 alpha R inhibition as well as that of combined inhibition of types 1 and 2 5 alpha R.

Adult↗
PubMed2004

Relative safety and efficacy of finasteride for treatment of hirsutism.

OBJECTIVE: To evaluate the relative safety and efficacy of finasteride for treatment of hirsutism related to hyperandrogenism in women. DATA SOURCES: Literature retrieval was accessed through MEDLINE (1966-March 2003) using the terms finasteride and hirsutism. Additional information was obtained from the drug manufacturer. DATA SYNTHESIS: Finasteride has been evaluated for treatment of hirsutism in multiple observational and randomized trials. Finasteride lowered hirsutism scores by 30-60% in most trials, as well as decreasing average hair diameter. In comparative trials, finasteride demonstrated efficacy similar to that of other antiandrogens, with fewer adverse effects. CONCLUSIONS: Finasteride does reduce the overall hair diameter and number in androgen-sensitive areas. Reported adverse effects have been minimal. Concern over potential teratogenicity and lack of long-term safety information leave finasteride a secondary treatment option for hirsutism.

5-alpha Reductase Inhibitors↗
PubMed2004

Reduction of rat prostate weight by combined quercetin-finasteride treatment is associated with cell cycle deregulation.

Benign prostate hyperplasia and prostate cancer are major public health problems. We report herein that daily treatment of male rats with 50, 100 or 150 mg quercetin per kg body weight resulted in serum concentrations of quercetin equivalent to 25.3 microM, 43.3 microM and 54.3 microM respectively. Concomitantly, serum testosterone levels were increased by 1.79-, 1.83- and 3.48-fold, while serum dihydrotestosterone (DHT) levels were 125%, 92% and 73% of the control. A slight increase in prostate weight coupled with dilated prostate lumens full of secretory materials were observed. Finasteride alone caused a significant decrease in serum DHT level and prostate weight. Co-administration of quercetin with finasteride prevented the finasteride-induced decrease in serum DHT levels but significantly enhanced the reduction in wet prostate weight, which was reduced by 26.9% in finasteride-treated animals to 31.8%, 40.0% and 48.2% after finasteride given together with the three doses of quercetin. The combined treatment altered cell cycle-regulated proteins in a wide spectrum. The expressions of cyclin D1, CDK-4, cdc-2 and phospho-cdc-2 at tyrosine 15, phospho-MEK1/2, phospho-MAP kinase, phospho-pRb at serine 780 and serine 807/811 were significantly inhibited, while the levels of p15, p21 and p27 were increased. In conclusion, quercetin-finasteride treatments caused wide cell cycle deregulation in rat prostates, which, in turn, decreased the proliferation rate, changed the secretion activities of epithelial cells and resulted in a marked reduction in wet prostate weight. The results suggest that quercetin synergizes with finasteride to reduce the wet prostate weight through a cell cycle-related pathway, which may be androgen independent.

Animals↗
PubMed1993

Finasteride. A review of its potential in the treatment of benign prostatic hyperplasia.

Finasteride is a novel therapeutic agent that selectively inhibits the enzyme 5 alpha-reductase, thereby reducing prostatic dihydrotestosterone (DHT) levels and prostate size. In men with symptomatic benign prostatic hyperplasia (BPH), these effects have been associated with improvements in peak urinary flow rate and urological symptoms; withdrawal from therapy, however, results in regrowth of the adenoma and long term therapy is therefore necessary. Although the magnitude of clinical improvement seen with finasteride has been perceived to be modest [especially when compared with that associated with transurethral resection of the prostate (TURP)], it has been maintained in the medium term (up to 2 years) and thus may represent significant reversal of disease progression. Such beneficial effects, however, may not become apparent until completion of at least 6 months of therapy. Furthermore, since clinical studies have been unable to proactively identify a responsive subgroup, a trial period of 6 or possibly 12 months is necessary to assess patient responsiveness. Despite these potential shortcomings, the benefits of therapy appear to outweigh the risks. Indeed, finasteride is well tolerated; most adverse events have been related to sexual dysfunction (decreased libido, ejaculation disorders and impotence) and occurred in only a small proportion (about 2 to 3%) of patients. Moreover, although there has been concern that finasteride might mask the detection of prostate cancer through its decremental effects on serum prostate specific antigen (PSA) levels, careful monitoring in clinical trials appears to have avoided this problem. Thorough pretreatment assessment and periodic follow-up examinations for malignancy are therefore required in clinical practice. The role of finasteride in the treatment of patients with BPH is still emerging and will no doubt gain in clarity with further planned investigations. TURP (or other invasive procedures such as the insertion of prostatic stents in patients unsuitable for resection), continues to be the mainstay of therapy for those patients with severe symptomatic BPH. However, available data support a first line role for finasteride in the treatment of patients with uncomplicated symptomatic BPH. Within this setting, finasteride appears to offer a needed additional treatment option for those patients in whom surgery is not indicated, and may be of special benefit to the considerable proportion of patients who opt not to undergo prostatectomy.

Animals↗
PubMedDate not supplied

Finasteride cream in hirsutism.

OBJECTIVE: To determine, in a preliminary study, whether women with hirsutism attributable to various causes would benefit from treatment with finasteride cream. METHODS: Finasteride cream (0.25%) and placebo cream were administered to eight women with various degrees of facial hirsutism. The two creams were used on opposite sides of the face in an area of excessive hair growth. The side chosen for the finasteride cream versus placebo was randomized and blinded. In a 1 cm2 area on each side of the face, hair counts were done every 2 months throughout the 6-month study period. Hair thickness was also measured. RESULTS: Hair follicles respond to testosterone by the conversion of this androgen to dihydrotestosterone through the action of 5a-reductase. Finasteride partially blocks this enzyme. Because of the easy solubility of this medication through the skin, a cream applied to the area of hair growth would be expected to decrease hirsutism locally. After a 6-month period, mean hair counts decreased significantly from 27.5 to 15.5 (P<0.05) in the finasteride-treated sites but showed no significant change from baseline in the placebo-applied sites. Moreover, the mean thickness of the measured hairs (in hundredths of millimeters) was significantly different between the placebo and finasteride-treated sites (4.33 versus 3.11, respectively; P<0.001). CONCLUSION: In this study of women with facial hirsutism, topically applied finasteride significantly decreased hair growth and thickness, and no adverse effects were noted.

5-alpha Reductase Inhibitors↗
PubMed1999

The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia.

BACKGROUND: Data suggest that androgenetic alopecia is a process dependent on dihydrotestosterone (DHT) and type 2 5alpha-reductase. Finasteride is a type 2 5alpha-reductase inhibitor that has been shown to slow further hair loss and improve hair growth in men with androgenetic alopecia. OBJECTIVE: We attempted to determine the effect of finasteride on scalp skin and serum androgens. METHODS: Men with androgenetic alopecia (N = 249) underwent scalp biopsies before and after receiving 0.01, 0.05, 0.2, 1, or 5 mg daily of finasteride or placebo for 42 days. RESULTS: Scalp skin DHT levels declined significantly by 13.0% with placebo and by 14.9%, 61.6%, 56. 5%, 64.1%, and 69.4% with 0.01, 0.05, 0.2, 1, and 5 mg doses of finasteride, respectively. Serum DHT levels declined significantly (P <.001) by 49.5%, 68.6%, 71.4%, and 72.2% in the 0.05, 0.2, 1, and 5 mg finasteride treatment groups, respectively. CONCLUSION: In this study, doses of finasteride as low as 0.2 mg per day maximally decreased both scalp skin and serum DHT levels. These data support the rationale used to conduct clinical trials in men with male pattern hair loss at doses of finasteride between 0.2 and 5 mg.

5-alpha Reductase Inhibitors↗
PubMed2002

The long-term effect of specific type II 5alpha-reductase inhibition with finasteride on bone mineral density in men: results of a 4-year placebo controlled trial.

PURPOSE: We determine the effect of long-term suppression of dihydrotestosterone with finasteride, a specific type II 5alpha-reductase inhibitor, on bone mineral density. MATERIALS AND METHODS: As part of a large (3,040 cases) 4-year, double-blind, placebo controlled trial designed to assess the long-term effects of finasteride in men with benign prostatic hyperplasia, 157 men 46 to 76 years old who were randomized to receive either 5 mg. finasteride or placebo underwent dual energy x-ray absorptiometry of the lumbar spine at baseline and at years 2, 3 and 4. RESULTS: Of 117 patients who had a baseline measurement and at least 1 additional measurement during the study baseline mean plus or minus standard deviation bone mineral density values were 1.12 +/- 0.17 gm./cm.2 in the finasteride group (63) and 1.10 +/- 0.17 gm./cm.2 in the placebo group (54). After 4 years bone mineral density was not different between treatment groups (finasteride 1.14 +/- 0.17 gm./cm.2 and placebo 1.13 +/- 0.18 gm./cm.2). Similar results were obtained for the 33 finasteride and 25 placebo treated patients who completed the study with year 4 bone mineral density measurements. CONCLUSIONS: These data demonstrate that long-term inhibition of type II 5alpha-reductase with finasteride does not adversely affect bone mineral density.

5-alpha Reductase Inhibitors↗
PubMed2003

The benefits of finasteride for hirsute women with polycystic ovary syndrome or idiopathic hirsutism.

Finasteride has been used frequently in the treatment of prostate hyperplasia, but this drug inhibits 5alpha-reductase and for this reason could be useful for the treatment of hirsutism. The aim of this study was to evaluate the clinical and hormonal effects of finasteride on hirsute women with idiopathic hirsutism or polycystic ovary syndrome. Twenty-four women were randomly divided into two groups: those given placebo and those given finasteride 5 mg/day. The treatment period was 6 months. All patients were evaluated before the beginning of treatment (baseline) and after 3 and 6 months of treatment using clinical examination through Ferriman-Gallwey score, blood pressure, cardiac frequency and body mass index. Also, we collected blood for hormonal determination of levels of prolactin, 17alpha-hydroxyprogesterone, follicle stimulating hormone, luteinizing hormone, total and free testosterone, dehydroepiandrosterone sulfate, androstenedione and dihydrotestosterone. Furthermore, all patients were asked about their concerns and satisfaction with the treatment. The results showed that the Ferriman-Gallwey score in the 6th month of finasteride treatment was significantly lower than at baseline and the 3rd month of this drug treatment. The dihydrotestosterone level in the finasteride group was also significantly reduced compared to that in the placebo group. The other hormones did not show any statistical difference during the study. All the patients treated with finasteride perceived a reduction in hirsutism after 6 months. In conclusion, our data suggest that finasteride may be effective for the treatment of the hirsute woman with idiopathic hirsutism or polycystic ovary syndrome.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Disposition and pharmacokinetics of [14C]finasteride after oral administration in humans.

The disposition of [14C]finasteride, a competitive inhibitor of steroid 5 alpha-reductase, was investigated after oral administration of 38.1 mg (18.4 microCi) of drug in six healthy volunteers. Plasma, urine, and feces were collected for 7 days and assayed for total radioactivity. Concentrations of finasteride and its neutral metabolite, omega-hydroxyfinasteride (monohydroxylated on the t-butyl side chain), in plasma and urine were determined by HPLC assay. Mean excretion of radioactivity equivalents in urine and feces equaled 39.1 +/- 4.7% and 56.8 +/- 5.0% of the dose, respectively. The mean peak plasma concentrations reached for total radioactivity (ng equivalents), finasteride, and omega-hydroxyfinasteride were 596.5 +/- 88.3, 313.8 +/- 99.4, and 73.7 +/- 11.8 ng/ml, respectively, at approximately 2 hr; the mean terminal half-life for drug and metabolite was 5.9 +/- 1.3 and 8.4 +/- 1.7 hr, respectively. Of the 24-hr plasma radioactivity, 40.9% was finasteride, 11.8% was the neutral metabolite, and 26.7% was characterized as an acidic fraction of radioactivity. Binding of [14C]finasteride to plasma protein was extensive (91.3 to 89.8%), with a trend suggesting concentration dependency (range 0.02 to 2 micrograms/ml). Little of the dose was excreted in urine as parent (0.04%) or omega-hydroxyfinasteride (0.4%). Urinary excretion of radioactivity was largely in the form of acidic metabolite(s)--18.4 +/- 1.7% of the dose was eliminated as the omega-monocarboxylic acid metabolite. Finasteride was scarcely excreted unchanged in feces. In humans, finasteride is extensively metabolized through oxidative pathways.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed2005

Efficacy of terazosin and finasteride in symptomatic benign prostatic hyperplasia: A comparative study.

Medical treatment for symptomatic Benign Prostatic Hyperplasia (BPH) has become popular for the last few years. This study was designed to find out and compare the efficacy of terazosin, a alpha1 adrenoceptor blocker and finasteride, a 5alpha-reductase inhibitor in symptomatic BPH. A total of 60 patients (30 in terazosin group and 30 finasteride group) of symptomatic BPH were selected. Terazosin group received 1 mg daily at bedtime for 3 days, 2 mg at bedtime for 7 days, thereafter 5 mg at bedtime daily for 6 months. Finasteride group received 5 mg once daily. In terazosin treated patients, improvement after 3 months were as follows, IPSS 3.93 +/- .74 points reduction, Qmax 2.13 +/- .68 ml/s increase, post-voided residual urine volume (PVR) 20.67 +/- 10.56 ml reduction (significant, p<0.001) and prostate volume 0.57 +/- 1.54 ml reduction (not significant). Similar statistical differences were observed at 6 months follow up. In finasteride treated patients, improvements after 3 months were as follows, International Prostate Symptom Score (IPSS) 1.38 +/- .63 points reduction, Qmax 0.55 +/- 0.78 ml/s increase, PVR 5.93 +/- 7.64 ml reduction (significant, p<0.001) and prostate volume 0.17 +/- 5.6 ml reduction (non-significant). At 6 month follow up statistical differences were significant in all parameters including prostate volume 4.57 +/- 5.30 ml reduction (p<0.001). In comparison, statistically significant superiority of terazosin over finasteride was found in improving IPSS, Qmax and PVR in both follow up visits. But terazosin had nonsignificant effect in reducing prostate volume; in contrast, finasteride had significant effect in second visit. It can be concluded from this study that terazosin 5mg once daily is effective in mild to moderate cases of symptomatic BPH. On the other hand, finasteride 5mg once daily may be useful in large prostate and to be given for at least 6 months.

Adrenergic alpha-Antagonists↗
PubMed1996

Effect of long-term administration of finasteride (MK-906), an inhibitor of 5 alpha-reductase, in patients with benign prostatic hyperplasia.

We evaluated the effect of long-term administration of finasteride (MK-906), a potent inhibitor of 5 alpha-reductase in patients with benign prostatic hyperplasia (BPH). The effect of an increase in dose was also assessed. Finasteride was administered to 61 patients with BPH at the dose of 1 mg/day for 48 weeks. Thirty three of these patients subsequently received finasteride at the dose of 5 mg/day for further 24 weeks in an open extension study. Urinary symptoms, urinary flow rate, residual urinary volume, prostatic volume and serum concentrations of dihydrotestosterone and prostate-specific antigen were examined periodically during the treatment. The size of the prostate and total urinary symptom scores decreased progressively during the first 16 weeks of treatment. The patients who received finasteride had a significant increase in the maximal urinary flow rate and a significant decrease in residual urinary volume. After 72 weeks of treatment, finasteride at an increased dose of 5 mg did not provide additional benefit to patients, although the effects of the drug at a dose of 1 mg were well maintained. Treatment with finasteride was well tolerated at both doses. In conclusion, the treatment of BPH with 1 mg of finasteride per day for 48 weeks results in a significant increase in maximal urinary flow rate, and a decrease in prostatic volume, symptoms of obstruction and residual urinary volume, with minimal toxicity.

5-alpha Reductase Inhibitors↗
PubMed1997

Prostate tissue composition and response to finasteride in men with symptomatic benign prostatic hyperplasia.

PURPOSE: We sought to quantify prostate tissue changes induced by finasteride and to identify a predictor of finasteride response in men with symptomatic benign prostatic hyperplasia (BPH) via a randomized, placebo controlled, double-blind clinical trial. MATERIALS AND METHODS: Men with symptomatic BPH (52 to 78 years old) were randomly assigned to 6 months of treatment with finasteride (26) or placebo (15). Outcome measures were clinical (urinary symptom score and flow rate), chemical (serum prostate specific antigen and dihydrotestosterone levels), volumetric (transrectal ultrasound, and magnetic resonance imaging for whole and zonal prostate volumes) and histological (morphometry of prostate sextant biopsies, separated into inner and outer gland segments, to measure the percent epithelium, stroma and glandular lumen). RESULTS: In the finasteride group we found a suggestion of decreasing symptom scores and increasing flow rates (not significant) with significant decreases (p < 0.01) in prostate specific antigen (48%), dihydrotestosterone (74%) and prostate volume (21%). Finasteride treatment induced a 55% decrease in inner gland epithelium (p < 0.01) with little effect on stroma or lumina. We also found a linear correlation between pretreatment inner gland epithelial content and prostate volume decrease induced by the drug (tau = 0.58, p = 0.01). CONCLUSIONS: Finasteride treatment results in a major suppression of prostate epithelium, which is most pronounced in the inner gland. Moreover, a finasteride induced prostate volume decrease was predictable by quantification of epithelial tissues of the inner gland. These data lend additional support to the emerging concept of transition zone primacy in symptomatic BPH.

Aged↗
PubMedDate not supplied

[Effect of finasteride on the percentage of free PSA: implications in the early diagnosis of prostatic cancer].

OBJECTIVE: To analyze the behaviour of free PSA percentage in finasteride-treated patients and to evaluate whether this ratio allows an increased PSA specificity in the early diagnosis of prostate cancer. MATERIAL AND METHODS: Evaluation of PSA serum levels and free PSA ratio in 336 patients initially diagnosed with prostate benign hyperplasia (PBH). A group of 82 patients were treated with finasteride for 14 to 58 months. A second group of 254 patients received no treatment. All patients were within the same age range and had similar PSA serum levels. In total, 141 prostate biopsies were performed: 19.5 (16/82) and 49.1 (125/254) respectively. RESULTS: Median PSA level in PBH patients was 1.6 ng/mL for the finasteride-treated group and 3.5 for the untreated group, p < 0.0001. Free PSA ratio was 18.6 and 18.8%, respectively, p > 0.05. Carcinoma detection rate was 25% (4/16) for the finasteride group and 27.2% (34/125) for the untreated group. If biopsy had been requested when PSA percentage was below 25%, 17.7 and 19.8% respectively would have been prevented and all carcinoma detected. CONCLUSION: Long-term treatment with finasteride reduces PSA serum concentration about 50% without changing the free PSA ratio. Carcinoma detection rate was similar in finasteride-treated and untreated patients. Free PSA ratio allows to increase PSA specificity and avoid unnecessary biopsied also in finasteride-treated patients.

Aged↗
PubMed1993

The effect of finasteride on prostate-specific antigen in men with benign prostatic hyperplasia.

Finasteride is a specific 5-alpha-reductase inhibitor that has been shown to reduce prostate size and decrease serum levels of prostate specific antigen (PSA). Among men who received finasteride (5 mg/day) for 12 months in North American clinical trials and in whom prostate cancer was not diagnosed the median percentage change in PSA was -50% (5-95% range: -81% to +20%). At baseline 72% had PSA < or = 4.0 ng/ml and 93% had PSA < or = 10.0 ng/ml. After 12 months on finasteride, 75% had PSA < or = 2.0 ng/ml and 95% had PSA < or = 5.0 ng/ml. Thus, the proportion of BPH patients with PSA levels of 2.0 ng/ml and 5.0 ng/ml after 12 months of treatment was comparable to the proportion with pretreatment PSA levels of 4.0 ng/ml and 10.0 ng/ml. Among the 10 men in these trials subsequently diagnosed with prostate cancer while on long-term finasteride therapy (5 mg/day), the median percentage change in PSA was -26% (range: -48% to +12%). Limited experience with finasteride in men with prostate cancer suggests that the reduction in PSA of malignant origin appears to be no greater than the percentage reduction in PSA of benign origin. These effects on PSA have not been shown to confer any therapeutic benefit. Physicians using finasteride should be aware of its effect on PSA levels.

5-alpha Reductase Inhibitors↗
PubMed1993

Critical developmental periods for effects on male rat genitalia induced by finasteride, a 5 alpha-reductase inhibitor.

The conversion of testosterone to 5 alpha-dihydrotestosterone by the enzyme 5 alpha-reductase is inhibited by finasteride. In a study in which maternal dosing with finasteride commenced on Gestational Day 15 and terminated on Postpartum Day 21, there were 13 and 27% decreases in anogenital distance of male pups on Postnatal Day 1 at 0.03 and 3 mg/kg/day, respectively. These decreases were largely reversed by Postnatal Day 22 even though treatment of the dams continued. Treatment at 3 mg/kg/day also resulted in hypospadias with cleft prepuce and a 5-day delay in the separation of the prepuce from the glans penis in those animals without hypospadias. A second study in which 20 mg/kg/day finasteride was administered on successive 2-day periods during late gestation in rats demonstrated that the period of Gestational Days 16 to 17 was the most sensitive (critical period) for finasteride-induced hypospadias, cleft prepuce, decreased anogenital distance, reduced prostate weight, and nipple formation in F1 male offspring. This critical period is just prior to the appearance on Day 18 of gestation of a midline mesenchymal plate between the urogenital sinus and the rectum in normal male fetuses. This midline plate does not appear in finasteride-exposed fetuses destined to have hypospadias as demonstrated in a previous study. Based on these observations, we hypothesize that finasteride causes hypospadias by preventing the formation of the medial mesenchymal plate which is necessary for assisting the movement of the urogenital sinus from the base to the tip of the genital tubercle.

5-alpha Reductase Inhibitors↗
PubMed1998

Comparison of cyproterone acetate plus ethinyl estradiol and finasteride in the treatment of hirsutism.

The aim of this study was to compare the clinical efficacy and safety of low dose cyproterone acetate-estrogen combination (Diane) and the 5 alpha-reductase inhibitor finasteride in the treatment of hirsutism. Fourty-two women with hirsutism were included in the study. Twenty-one patients treated with cyproterone acetate (CPA) 2 mg and ethinyl estradiol (E) 35 micrograms daily on days 5-25 of the menstrual cycle, 21 with finasteride 5 mg daily. Hirsutism score, hormone levels, multiscreen blood chemistry and side effects were evaluated at three-monthly intervals for 9 months. A significant decrease in hirsutism score as compared to baseline was observed after 9 months with either CPA + E (Diane) (mean +/- SE, 15.81 +/- 1.19 vs 8.38 +/- 1.21) or finasteride treatment (17.81 +/- 1.05 vs 10.86 +/- 0.91) (p < 0.0005). The reductions in hirsutism scores (mean% +/- SE) were 14.23 +/- 2.29 vs 19.77 +/- 2.22 (p < 0.05) at 3, 40.23 +/- 4.58 vs 29.49 +/- 2.69 (p < 0.02) at 6 and 50.99 +/- 4.13 vs 39.87 +/- 3.30 (p < 0.02) at 9 months in CPA + E and finasteride groups, respectively. No significant changes were observed in hormone levels during finasteride treatment. Serum free testosterone significantly decreased at the third month of treatment, and remained suppressed for the duration of treatment in CPA + E group. DHEAS levels also decreased significantly after 6 and 9 months of therapy with CPA + E. SHBG significantly increased during CPA + E treatment. We conclude that both drugs are effective and well tolerated, but CPA + E appears to be more effective than 5 alpha-reductase inhibitor finasteride in long-term treatment of hirsute women. Diane is also a cost-effective drug.

5-alpha Reductase Inhibitors↗
PubMed1998

Effect of finasteride in idiopathic hirsutism.

Increased 5 alpha-reductase activity has been found in hair follicles of hirsute women, suggesting a pathogenetic role. The aim of the present study was to evaluate the effect of finasteride in the treatment of idiopathic hirsutism. Twenty-seven women with idiopathic hirsutism, aged 16-35 years, were treated for 6 months with finasteride, 5 mg once daily. Fourteen patients were on finasteride alone (group A), while the remaining received in addition an oral contraceptive (group B). Clinical, hormonal and biochemical evaluation were performed before, and after 3 and 6 months of treatment. Clinical evaluation was repeated 6 months after drug discontinuation in seven patients. Treatment was well tolerated by all patients; no side effects or adverse reactions were reported. A significant improvement of hirsutism was obtained by finasteride; clinical score observed at the 6th month of therapy was reduced from 11.71 +/- 2.23 to 7.92 +/- 1.81 (p < 0.05) and from 14.92 +/- 6.13 to 9.3 +/- 2.75 (p < 0.05) in group A and B, respectively. Clinical score in seven patients was still 8.61 +/- 2.28 (p < 0.05) 6 months after the end of therapy. Finasteride treatment alone (group A) induced a slight increase, though not significant, in serum androgens; DHT and SHBG did not change. In group B (finasteride plus oral contraceptive) total testosterone and free testosterone showed no significant decrease; after 6 months of therapy DHT was reduced significantly, while SHBG levels were increased. These data demonstrate that 5 alpha-reductase inhibition may be an effective treatment in women suffering from idiopathic hirsutism. This approach may be attractive due to the absence of adverse reactions, although the necessity of an adequate contraception should be kept in mind.

Adolescent↗
PubMed1991

Decreased fertility in male rats administered the 5 alpha-reductase inhibitor, finasteride, is due to deficits in copulatory plug formation.

Oral administration of 80 mg/kg/day of finasteride, a potent specific inhibitor of 5 alpha-reductase, to sexually mature male Sprague-Dawley rats for 24 to 38 weeks caused an approximate 30% to 40% decrease in fertility. There were no effects on mating indices or implants per pregnant female. From the mating trials, a selected group of treated males with poor reproductive performance was compared to a selected group of control males with good reproductive performance. Observed matings showed no qualitative effects on mating behavior or ejaculation. However, finasteride-treated males did not form or formed small and improperly positioned copulatory plugs, which are required in rats to transport sperm into the uterus. Intrauterine insemination of epididymal sperm from males that were nonfertile by natural mating resulted in similar numbers of embryos and unfertilized oocytes recovered from controls and finasteride-treated males, confirming that there was no effect of finasteride on the ability of sperm to fertilize. Decreased fertility of finasteride-treated males was due to failure to form copulatory plugs and is related to decreased weight of seminal vesicles and prostate, an expected pharmacologic effect. Testes weight was unaffected. Decreased fertility in male rats after finasteride administration is considered a species specific effect. The mechanism of the decrease in rats is not likely to be relevant to species that do not form copulatory plugs.

5-alpha Reductase Inhibitors↗