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PubMed2003

The expression of insulin-like growth factor 1 in follicular dermal papillae correlates with therapeutic efficacy of finasteride in androgenetic alopecia.

BACKGROUND: It is generally believed that dihydrotestosterone is one of the pivotal mediators of hair loss in androgenetic alopecia (AGA). Finasteride, which blocks the conversion of testosterone to dihydrotestosterone, has now become an integral part of the current treatment approaches for male AGA. Several lines of evidence support the notion that dermal papilla (DP) cells represent the androgen target within the hair follicle. The specific molecular regulators modulated by androgens within hair follicles in the balding scalp are unknown. OBJECTIVE: The purpose of this study was to identify and quantify changes in expression of specific molecular hair growth regulators in DP of men with AGA treated with finasteride and correlate these findings to clinical efficacy. METHODS: Biopsy specimens were collected from 9 male patients from both the balding area and nonbalding occipital area before and after 4 months of finasteride therapy. DP were microdissected and total RNA was extracted from an equal number of DP from each biopsy specimen. The expression of various cytokines, including insulin-like growth factor (IGF)-1, was determined by reverse transcription polymerase chain reaction. The signals were detected by autoradiography. All 9 patients were given finasteride for 1 year and evaluated for efficacy at month 12. Efficacy was graded on a 7-point scale on the basis of comparison with initial baseline photography. RESULTS: IGF-1 was up-regulated by finasteride treatment in 4 of 9 patients. Among the patients with increased IGF-1 expression, 3 of them showed moderate clinical improvement after 12 months of treatment and another patient remained unchanged. In contrast, 3 patients with decreased IGF-1 expression in the balding scalp showed clinical worsening after 12 months. The other 2 patients without noticeable change in IGF-1 expression showed either slight improvement or no change in their hair condition. CONCLUSION: In a small uncontrolled study of 9 patients with AGA, an increased expression of IGF-1 messenger RNA levels in the DP was associated with patient response to finasteride.

Adult↗
PubMed2002

Effects of finasteride on vascular endothelial growth factor.

OBJECTIVE: Finasteride has been shown to reduce prostate bleeding in patients with benign prostatic hyperplasia (BPH). The mechanisms behind this are not known, but it has been suggested that finasteride reduces bleeding by inhibiting angiogenesis in the prostate. Studies in animals have shown that castration rapidly induces involution of the prostate vasculature, and androgen-stimulated prostate growth may be angiogenesis dependent. The objective of this study was to explore the response to finasteride on the vasculature and the expression of vascular endothelial growth factor (VEGF), a potent regulatory factor of angiogenesis in human prostate tissue. MATERIAL AND METHODS: Patients with BPH were randomly assigned to 3 months of treatment either with finasteride (5 mg/day) or placebo before undergoing transurethral resection of the prostate (TURP). Prostate tissue VEGF expression was quantified by Western blot and the vascular density determined in Factor VIII immunostained tissue sections. Serum concentrations of VEGF were measured with ELISA technique. RESULTS: Patients treated with finasteride (n = 15) showed a decrease in prostate tissue VEGF(165) expression compared with placebo (n = 13) treated patients (p < 0.05), but the vascular density and the serum VEGF levels were unaffected. CONCLUSIONS: This study shows that finasteride treatment decreases VEGF expression in the human prostate.

5-alpha Reductase Inhibitors↗
PubMed2004

Risk of acute pancreatitis in users of finasteride: a population-based case-control study.

GOALS: To examine the risk of acute pancreatitis in > or = 60-year-old male users of finasteride in a case-control study from a population of 490,000 persons in North Jutland County, Denmark, from 1993 to 2000. STUDY: We identified all men age 60 and over with incident acute pancreatitis from the County Hospital Discharge Registry in North Jutland, 1993 to 2000, and selected 10 age-matched controls per case from the Danish Civil Registration System based on incidence density sampling. All prescriptions for finasteride within 90 days prior to admission with acute pancreatitis were identified from the population-based North Jutland Prescription Database. Data on potential confounding factors were also extracted from registries. We used conditional logistic regression to estimate the relative risk of acute pancreatitis, adjusted for these potential confounders. RESULTS: There were 302 men age 60 and older with incident acute pancreatitis, of whom 3 were exposed to finasteride, and 2994 controls, of whom 37 were exposed to finasteride. The crude odds ratio for having reimbursed prescriptions for finasteride was 0.8 (95% confidence interval, 0.2-2.6). After adjustment for alcohol-related diseases, gallstone disease, hyperlipidemia, hypercalcemia, and hyperparathyroidism, the odds ratio was slightly decreased to 0.5 (95% confidence interval, 0.1-2.5). CONCLUSION: We did not find any increased risk of acute pancreatitis in users of finasteride.

5-alpha Reductase Inhibitors↗
PubMed1992

Prolonged treatment with finasteride (a 5 alpha-reductase inhibitor) does not affect bone density and metabolism.

OBJECTIVE: Since it is not clear whether testosterone or dihydrotestosterone is the active hormone in bone metabolism, we wished to assess the effect of finasteride, a 5 alpha-reductase inhibitor, or vertebral bone mineral density and parameters of bone and mineral metabolism. DESIGN: Patients were treated in a randomized, double-blind controlled study with either placebo, 1 or 5 mg/day finasteride. PATIENTS: Twenty-three men with benign prostatic hyperplasia (BPH) were included in this study; eight received placebo, seven were allocated to treatment with 1 mg/day, and eight to 5 mg/day finasteride for 12 months. MEASUREMENTS: Vertebral bone mineral density was measured at the lumbar spine by dual energy X-ray bone densitometry. Serum calcium, phosphorus, parathyroid hormone, osteocalcin and vitamin D metabolites were measured regularly. Urinary calcium and creatinine excretion were monitored as well. RESULTS: Finasteride caused a significant decrease in serum dihydrotestosterone after 6 and 12 months, but no effect on serum testosterone. Vertebral bone mineral density remained unaltered. None of the other parameters monitored were affected except for a small unexplained increase in 1.25-dihydroxyvitamin D in the group receiving 5 mg finasteride/day. CONCLUSIONS: Testosterone is probably the active hormone in bone metabolism. However, oestradiol, the product of testosterone aromatization (which remains unaltered under finasteride) may yet be another possible responsible steroid in the maintenance of bone density. We can also not rule out that the small amount of dihydrotestosterone remaining under finasteride administration is sufficient for maintaining normal bone metabolism.

5-alpha Reductase Inhibitors↗
PubMed2005

Comparison of microvessel densities in rat prostate tissues treated with finasteride, bicalutamide and surgical castration: a preliminary study.

BACKGROUND: A group of anti-androgens with different mechanisms of action and adverse effects have been investigated in patients with gross hematuria related to benign prostate hyperplasia; however, there is not yet any consensus about the standard management of these patients. The present study aims to identify if any one type of the hormonal intervention is superior in terms of the suppression of microvessel formation in the prostate. MATERIALS AND METHODS: A total of 28 mature, healthy male Sprague-Dawley rats (300 +/- 50 g) were used in this study. The rats were randomly assigned to one of four groups (n = 7 per group). The effects of three different hormonal therapies on angiogenesis and microvascularity in rat ventral prostate were compared. Groups 1 and 2 were treated for 28 days with finasteride and bicalutamide, respectively, and rats from Group 3 underwent surgical castration. Following treatment, all rats included in the study underwent dissection of the ventral prostate and immunohistochemical analysis of microvessel density by factor VIII-related antigen. RESULTS: The mean number of microvessels in the finasteride and bicalutamide groups was 24.5 (+/-8.44 SE) and 27 (+/-9.89 SE) respectively. In contrast, the castration and control groups had microvessel numbers of 12.9 (+/-5.35 SE) and 40.3 (+/-5.03 SE) respectively. Differences were statistically significant between all three treatment groups and the controls (P < 0.005); the number of microvessels in rat prostate tissues of the control group was significantly higher than the treatment groups. Mean microvessel densities in the bicalutamide and finasteride groups were significantly higher than microvessel densities in the castration group (P < 0.005). There was no statistically significant difference between mean microvessel number in rat prostate tissue treated with finasteride or bicalutamide (P > 0.05). CONCLUSIONS: Even though finasteride was not as effective as castration in reducing microvessel number, its effect was equal to that of bicalutamide in terms of suppressing the angiogenesis in prostatic tissue. Based on the findings of the present study, finasteride might offer a viable option in the management of macroscopic hematuria by inhibition of microvessel formation within the prostatic tissue. Further clinical studies are warranted.

Androgen Antagonists↗
PubMed2004

Finasteride treatment of patterned hair loss in normoandrogenic postmenopausal women.

BACKGROUND: Finasteride, an inhibitor of type 2 5alpha-reductase, inhibits conversion of testosterone to dihydrotestosterone, resulting in a decrease in serum and scalp dihydrotestosterone levels believed to be pathogenic in androgenetic alopecia. Oral finasteride has been shown to be effective in the treatment of hair loss in men, while its efficacy in women has remained controversial. METHODS: 5 postmenopausal women without clinical or laboratory signs of hyperandrogenism were given 2.5 or 5 mg/day oral finasteride for the treatment of pattern hair loss. Efficacy was evaluated by patient and investigator assessments, and review of photographs taken at baseline and at months 6, 12 and 18 by an expert panel. RESULTS: Finasteride treatment improved scalp hair by all evaluation techniques. The patients' self-assessment demonstrated that finasteride treatment decreased hair loss, increased hair growth and improved appearance of hair. These improvements were confirmed by investigator assessment and assessments of photographs. No adverse effects were noted. CONCLUSIONS: Oral finasteride in a dosage of 2.5 mg/day or more may be effective for the treatment of pattern hair loss in postmenopausal women in the absence of clinical or laboratory signs of hyperandrogenism.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

Chemoprevention of prostate carcinogenesis by DFMO and/or finasteride treatment in male Wistar rats.

In the present study the chemopreventive activities of DFMO, the irreversible inhibitor of ornithine decarboxylase, and finasteride, the inhibitor of prostatic 5a-reductase, against the development of chemically induced prostate adenocarcinoma by methylnitrosourea/testosterone propionate in male Wistar rats were investigated. According to histological examination, oral administration of DFMO and finasteride, either alone or combined, for two months to MNU/TP-inoculated rats reduced the tumor incidence to 11.11%, 10% and 10%, respectively, compared to tumored controls (64.3%). DFMO and/or finasteride treatment resulted in significant reductions in the wet weight of the prostate gland and seminal vesicles and its ratio relative to the total body weight, as well as the levels of prostate total protein, DNA, RNA and DNA/RNA ratio, compared to tumored controls. However, the effect of the combined treatment was of no statistical significance compared to single DFMO or finasteride treatment, as demonstrated by the non-significant differences between the mean values of most of the studied parameters. The tumor chemopreventive activity and the prostate growth inhibitory effect of DFMO and finasteride were due to suppression of prostate polyamine synthesis. ANOVA test revealed that the relative weight of the prostate as well as blood and tissue polyamine levels could be used as significant endpoint biomarkers for DFMO and finasteride as cancer chemopreventive agents.

Adenocarcinoma↗
PubMed1992

Hair growth effects of oral administration of finasteride, a steroid 5 alpha-reductase inhibitor, alone and in combination with topical minoxidil in the balding stumptail macaque.

A 5 alpha-reductase inhibitor, finasteride, was administered orally at 0.5 mg/day, alone or in combination with topical 2% minoxidil, for 20 weeks to determine the effects on scalp hair growth in balding adult male stumptail macaque monkeys. A 7-day dose-finding study showed that both 0.5- and 2.0-mg doses of the drug produced a similar diminution in serum dihydrotestosterone (DHT) in male stumptails. Hair growth was evaluated by shaving and weighing scalp hair at baseline and at 4-week intervals during treatment to obtain cumulative delta hair weight (sum of the 4-week changes in hair weight from baseline) for the 20-week study. The activity of the 5 alpha-reductase enzyme was assessed by RIA of serum testosterone (T) and DHT at 4-week intervals. The combination of finasteride and minoxidil generated significant augmentation of hair weight (additive effect) compared to either drug alone. Finasteride increased hair weight in four of five monkeys. When the data of the one nonresponsive monkey were excluded, finasteride elicited a significant elevation in hair weight compared to topical vehicle alone. Minoxidil also evoked a significant increase in hair weight compared to vehicle alone. Serum T was unchanged, whereas serum DHT was significantly depressed in monkeys that received either finasteride or the combination of finasteride and minoxidil. These data suggest that inhibition of the conversion of T to DHT by this 5 alpha-reductase inhibitor reverses the balding process and enhances hair regrowth by topical minoxidil in the male balding stumptail macaque.

5-alpha Reductase Inhibitors↗
PubMed1994

The effect of finasteride, a 5 alpha-reductase inhibitor, on scalp skin testosterone and dihydrotestosterone concentrations in patients with male pattern baldness.

The effects of the 5 alpha-reductase inhibitor, finasteride, on scalp skin testosterone (T) and dihydrotestosterone (DHT) levels were studied in patients with male pattern baldness. In a double blind study, male patients undergoing hair transplantation were treated with oral finasteride (5 mg/day) or placebo for 28 days. Scalp skin biopsies were obtained before and after treatment for measurement of T and DHT by high pressure liquid chromatography-RIA. In 10 male subjects studied at baseline, mean (+/- SEM) DHT levels were significantly higher in bald (7.37 +/- 1.24 pmol/g) compared to hair-containing (4.20 +/- 0.65 pmol/g) scalp, whereas there was no difference in mean T levels at baseline. In bald scalp from 8 patients treated with finasteride, the mean DHT concentration decreased from 6.40 +/- 1.07 pmol/g at baseline to 3.62 +/- 0.38 pmol/g on day 28. Scalp T levels increased in 6 of 8 subjects treated with finasteride. Finasteride decreased the mean serum DHT concentration from 1.36 +/- 0.18 nmol/L (n = 8) at baseline to 0.46 +/- 0.10 nmol/L on day 28 and had no effect on serum T. There were no significant changes in scalp or serum T or DHT in placebo-treated patients. In this study, male subjects treated with 5 mg/day finasteride for 4 weeks had significantly decreased concentrations of DHT in bald scalp, resulting in a mean level similar to the baseline levels found in hair-containing scalp.

5-alpha Reductase Inhibitors↗
PubMed1995

A prospective randomized trial comparing finasteride to spironolactone in the treatment of hirsute women.

Enhanced 5 alpha-reductase activity has been found in the skin of the majority of women with hirsutism. Finasteride is a specific competitive inhibitor of 5 alpha-reductase, preferentially inhibiting the type 2 isoenzyme. Therefore, we randomly assigned 14 hirsute women in a 2:1 ratio to 1 of 2 treatment arms: 1) finasteride (F) treatment (n = 9; 5 mg, orally, daily), or 2) spironolactone (S) treatment (n = 5; 100 mg, orally, daily). Each group was treated for 6 months. Patients were evaluated at baseline and after 3 and 6 months of treatment. The 2 groups were similar in age, weight, hip/waist ratio, baseline Ferriman-Gallwey score (F, 19 +/- 2; S, 19 +/- 2), and baseline androgen levels. Finasteride treatment resulted in a significant increase in testosterone (T; P < 0.01) and the T/dihydrotestosterone ratio (P < 0.01). Finasteride caused a significant decrease in 5 alpha-androstane-3 alpha,17 beta-diol glucuronide (3 alpha-diolG; P < 0.05), the 3 alpha-diolG/T ratio (P < 0.01), and the 3 alpha-diolG/androstenedione ratio (P < 0.05). All changes were consistent with 5 alpha-reductase inhibition. In contrast, spironolactone treatment did not result in significant changes in serum hormone levels. Both treatments produced a significant decrease in anagen hair diameters [F, -14.0 +/- 6.7% (P < 0.05); S, -13.4 +/- 3.8% (P < 0.05)] and Ferriman-Gallwey scores [F, -2.1 +/- 0.4 (P < 0.05); S, -2.5 +/- 0.7 (P < 0.05)]. In conclusion, despite significantly different effects on androgen levels, finasteride and spironolactone treatment resulted in a similar clinical effect on hirsutism. Both caused significant, but limited, improvement in hirsutism. Although promising, further studies with finasteride are needed to verify its effectiveness as a treatment for hirsutism. Such studies will also provide a better understanding of the relative contribution of 5 alpha-reductase isoenzymes to hirsutism.

Adolescent↗
PubMed2004

Activation of caspases-3, -6, and -9 during finasteride treatment of benign prostatic hyperplasia.

Benign prostatic hyperplasia (BPH) results from an increase in both epithelial and stromal compartments of the human prostate. Although inhibitors of 5alpha-reductase such as finasteride have been shown to reduce the size of BPH tissues by inducing apoptosis, their mechanisms of action still remain unknown. The present study supports that such a process triggered by finasteride is caspase dependent with a possible involvement of two effector caspases (caspase-3 and 6) and two initiator caspases (caspase-8 and 9). Indeed, by using tissues from patients affected by BPH and treated by finasteride (5 mg/d) for 2-3, 6-8, or 27-32 d, we observed that the 5alpha-reductase inhibitor induced apoptosis in epithelial cells (evaluated through cell number positive for terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling) as early as 2-3 d of treatment, with a maximal activity (250-fold increase, P < 0.0001) at 6-8 d of treatment. However, after 27-32 d of treatment, the number of apoptotic cells was reduced and was close to control. Caspases-3, -6, -8, and -9 were immunolocalized to (basal and secretory) epithelial cells and to a lesser extent to stromal cells. Activated caspase-3 immunoexpression was restricted to epithelial secretory cells, and its immunostaining intensity appeared to be higher in BPH tissues from patients treated for 2-3 or 6-8 d. Consistently, in Western blotting analyses, activated caspases-3 and -6 were detected as early as 2-3 d of treatment in BPH tissues, and their levels were increased after 6-8 d of treatment. In real time quantitative PCR experiments, caspase-3 and -6 mRNA levels were found to be unchanged after finasteride treatment. Activated caspase-8 was not detected in the different conditions tested, whereas activated caspase-9 protein levels were maximally enhanced after 2-3 d of finasteride treatment. In conclusion, we report here that finasteride treatment of BPH tissues induced a caspase-dependent apoptotic process restricted to epithelial cells by activating effector caspases-3 and -6 and exhibited a transient action because the apoptotic process was no longer observed after 27-32 d of treatment.

Aged↗
PubMed2000

Increased levels of clusterin (SGP-2) mRNA and protein accompany rat ventral prostate involution following finasteride treatment.

Finasteride is a well-known inhibitor of the prostatic enzyme 5 alpha-reductase type 2 which prevents conversion of testosterone into 5 alpha-dihydrotestosterone, the active intraprostatic androgen, which causes prostate involution through a combination of cell atrophy and cell death. The drug is widely used to improve symptoms of benign prostatic hyperplasia in man. Clusterin, a glycoprotein which is generally up-regulated under conditions inducing cell atrophy or organ involution, is produced at a high level in the regressing rat ventral prostate following androgen ablation. According to several authors, clusterin does not respond to finasteride treatment, suggesting a different action of testosterone and 5 alpha-dihydrotestosterone. We show here that, under our conditions, finasteride was capable of inducing production of both clusterin mRNA and protein in the rat ventral prostate. In fact, by using different and converging techniques, such as Northern hybridization, in situ hybridization histochemistry and immunohistochemistry, we were able to show a strong induction of the clusterin gene in the epithelial cell population of the gland. The response to finasteride, which was similar to that seen with castration, occurred with a delay of a few days. In situ and immunohistochemistry experiments indicated that both orchidectomy and finasteride administration resulted in increased transition of the epithelial cells from the columnar to the cuboidal (atrophic) shape, and this was accompanied by an increased intensity of the signal for clusterin. Thus, it appears that induction of clusterin is part of the molecular process leading to prostate involution caused by either orchidectomy or finasteride administration.

5-alpha Reductase Inhibitors↗
PubMed2001

Co-administration of finasteride and the pure anti-oestrogen ICI 182,780 act synergistically in modulating the IGF system in rat prostate.

Prostate cancer is the most diagnosed invasive malignancy in males. Androgens and oestrogens have been implicated in the pathogenesis of prostate cancer. We report herein that the pure anti-oestrogen ICI 182,780 (ICI) reduces Ki-67 labelling index and IGF-I receptor levels in rat prostate. Increase of IGF-I mRNA and IGF-binding protein 3 (IGFBP-3) accumulation occur without any effect on prostate weight. Finasteride significantly decreases prostate weight and inhibits IGF-I gene expression. IGFBP-3 mRNA, Akt and phospho-Akt are not affected by finasteride. Co-administration of ICI plus finasteride reduces prostate weight by approximately 50% and causes acinar dilation with decreased luminal epithelial cell thickness. The acinar epithelial cells became atrophic and inactive with minimal cytoplasm. We also demonstrate a synergistic effect of ICI and finasteride on induction of IGFBP-3 accumulation and inhibition of Akt phosphorylation. Because the IGF and IGFBP-3 system plays an important role in prostate epithelial cell proliferation, apoptosis and tumour progression, the inhibitory effects of finasteride and ICI on IGF system may contribute to their anti-proliferative activity. These observations support a potential use of ICI in conjunction with finasteride in the prevention and/or treatment of prostate cancer.

5-alpha Reductase Inhibitors↗
PubMed2001

Effects of finasteride on size of the prostate gland and semen quality in dogs with benign prostatic hypertrophy.

OBJECTIVE: To determine the effect of the 5alpha-reductase inhibitor finasteride on prostatic diameter and volume, semen quality, and serum dihydrotestosterone (DHT) and testosterone concentrations in dogs with spontaneous benign prostatic hypertrophy (BPH). DESIGN: Double-blind placebo-controlled trial. ANIMALS: 9 dogs with BPH. PROCEDURE: Five dogs were treated with finasteride for 16 weeks (0.1 to 0.5 mg/kg [0.05 to 0.23 mg/lb] of body weight, PO, q 24 h); the other 4 received a placebo. Prostatic diameter, measured radiographically, prostatic volume, measured ultrasonographically, semen quality, and serum DHT and testosterone concentrations were evaluated before and during treatment. After receiving the placebo for 16 weeks, the 4 control dogs were treated with finasteride for 16 weeks, and evaluations were repeated. RESULTS: Finasteride significantly decreased prostatic diameter (mean percentage decrease, 20%), prostatic volume (mean percentage decrease, 43%), and serum DHT concentration (mean percentage decrease, 58%). Finasteride decreased semen volume but did not adversely effect semen quality or serum testosterone concentration. No adverse effects were reported by owners of dogs in the study. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that finasteride can be used to reduce prostatic size in dogs with BPH without adversely affecting semen quality or serum testosterone concentration.

Animals↗
PubMed2001

Cost-sharing for prescriptions of sildenafil and finasteride: a case study in veteran patients.

OBJECTIVE: To evaluate patients willingness to share the costs of 2 medications (often described as "lifestyle medications"): sildenafil for erectile dysfunction and finasteride for hair loss, which are not routinely covered by the Department of Veterans Affairs (VA) healthcare system. STUDY DESIGN: Self-administered, anonymous survey. PATIENTS AND METHODS: Adult men (n = 339) were recruited from waiting rooms for primary care or erectile dysfunction clinic appointments at 2 Los Angeles VA facilities. RESULTS: Participants with self-reported need were analyzed separately for finasteride (primary care patients only) and sildenafil (both primary care and erectile dysfunction clinic patients). The mean age of the participants was 56 and 60 years for the finasteride and sildenafil groups, respectively. Mean annual household income for both groups was under $10,000. Respondents reported a mean willingness to cost-share $4.20 for a 30-day prescription of daily finasteride (VA wholesale cost = $27) and $5.40 for 4 sildenafil pills (VA wholesale cost = $20). In the multivariate analysis, higher income (P = .002) and increasing self-reported need for medication (P = .04) were associated with increased willingness to cost-share for finasteride after controlling for age, race/ethnicity, insured status, comorbid conditions, and type of clinic. In addition, younger age (P = .01) was associated with greater willingness to cost-share for sildenafil. CONCLUSIONS: In this low-income veteran population, patients with a self-reported need for sildenafil and finasteride would be willing to make a higher copayment than the current VA maximum copayment of $2.00 per 30-day prescription, if these medicines were made available.

Adult↗
PubMedDate not supplied

Advances in the treatment of male androgenetic alopecia: a brief review of finasteride studies.

Finasteride is a type 2 5a-reductase inhibitor and therefore mimics the biochemical profile of inherited type 2 5a-reductase deficiency in men. It was developed to grow hair in androgenetic alopecia and shrink benign prostatic hyperplasia. Various clinical trials of finasteride have confirmed its beneficial effects in androgenetic alopecia in males, but not in females. It can produce visible hair growth in up to 66% of men with mild to moderate alopecia, but importantly can stop hair loss in 91% of patients. In long-term finasteride studies, placebo patients were characterized by significant and progressive hair loss. It can be concluded that finasteride prevents further hair loss by actually continuing to grow enough hair to preserve scalp coverage. This is confirmed by the loss of hair following withdrawal of finasteride in such cases. The proven preservative effect of finasteride, in addition to its restorative effect, is a strong indication for prescribing it in early cases of androgenetic alopecia before much hair has been lost.

5-alpha Reductase Inhibitors↗
PubMedDate not supplied

Finasteride improves male pattern hair loss in a randomized study in identical twins.

OBJECTIVES: This study compared the efficacy of finasteride with placebo in the treatment of male pattern hair loss (androgenetic alopecia) in nine pairs of male identical twins. METHODS: In this randomized, double-blind, placebo-controlled, single-center study, one twin from each identical twin pair received finasteride 1 mg/day for one year while the other received placebo. Hair growth was evaluated from standardized clinical photographs, hair counts and patient self-assessment questionnaires. Serum dihydrotestosterone and testosterone levels were analyzed and adverse events recorded. RESULTS: Finasteride significantly improved hair growth at one year compared to placebo (p < 0.05) based on analysis of photographs of the vertex and superior-frontal scalp. These results were consistent with the hair count change measured in the finasteride group, which was superior (p < 0.05) to the change measured in the placebo group. Patient self-assessment demonstrated that treatment with finasteride, in comparison to placebo, led to improvements in scalp hair growth and patients' satisfaction with appearance of hair. No drug-related adverse events were reported during the study. CONCLUSION: Through the use of identical twins, this study provides further evidence that finasteride significantly reduces hair loss progression and restores hair growth in men with male pattern hair loss.

Adult↗
PubMed1992

Four-amino acid segment in steroid 5 alpha-reductase 1 confers sensitivity to finasteride, a competitive inhibitor.

The 4-azasteroid 17 beta-(N-t-butyl)carbamoyl-4-aza-5 alpha-androst-1-en-3-one (finasteride) is 100-fold more potent as a competitive inhibitor of the rat NADPH:delta 4-3-oxosteroid-5-alpha- oxidoreductase (steroid 5 alpha-reductase) type 1 enzyme (Ki = 3-5 nM) than of the human type 1 enzyme (Ki greater than or equal to 300 nM). In this study, we exploit this differential sensitivity to map a major determinant of finasteride sensitivity in steroid 5 alpha-reductase. Chimeric steroid 5 alpha-reductase cDNAs composed of different combinations of rat and human exon sequences were created by genetic engineering, expressed in human embryonic kidney 293 cells, and assayed for their sensitivity to finasteride. Hybrid proteins containing sequences encoded by rat exon 1 were found to be as sensitive to finasteride as the parental enzyme. The exchange of progressively smaller protein segments encoded within exon 1 identified a tetrapeptide sequence (Val-Ser-Ile-Val) in the rat enzyme that conferred sensitivity to finasteride. The analogous sequence in the human enzyme (Ala-Val-Phe-Ala) conferred partial resistance to the drug. Finasteride was a competitive inhibitor of the native and all chimeric enzymes tested, suggesting that the tetrapeptide segments form a portion of the substrate-binding domain of steroid 5 alpha-reductase.

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