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PubMed1996

The safety of finasteride used in benign prostatic hypertrophy: a non-interventional observational cohort study in 14,772 patients.

OBJECTIVE: To examine the safety of finasteride as used in general medical practice to treat benign prostatic hypertrophy (BPH). PATIENTS AND METHODS: Information was collected on 14,772 patients who were included in an observational cohort study conducted using Prescription-Event Monitoring. RESULTS: Finasteride was reported to have been effective in 60% of the patients in whom an opinion on efficacy was recorded. Impotence or ejaculatory failure was reported in 2.1% of the patients, decreased libido in 1% and gynaecomastia and related conditions in 0.4%. Impotence was the most frequent reason for stopping treatment with finasteride and was the most commonly reported adverse reaction to the drug. Of the patients included in the elderly cohort involved in this study, 819 (5.5%) died; none of these deaths was attributed to finasteride. CONCLUSION: Impotence or ejaculatory failure, decreased libido and gynaecomastia in a small proportion of patients were associated with the use of finasteride. The results of this study strongly suggest that this drug is acceptably safe when used in accordance with the current prescribing information.

Adolescent↗
PubMed2002

Possible autocrine loop of the epidermal growth factor system in patients with benign prostatic hyperplasia treated with finasteride: a placebo-controlled randomized study.

OBJECTIVE: To analyse the expression of the epidermal growth factor (EGF) system in prostate tissue and secretions obtained from patients with benign prostatic hyperplasia (BPH) treated with or without finasteride (which primarily targets the androgen-sensitive secretory epithelial cells in the prostate, with little effect on basal epithelial and stromal cells). PATIENTS AND METHODS: The expression of the EGF system was evaluated by enzyme-linked immunosorbent assay and immunohistochemistry in samples of prostate tissue and secretions from patients with BPH randomized for treatment with finasteride or placebo for 3 months before surgery. RESULTS: Prostate tissue expressed the EGF receptor (HER1) and HER2, and the ligands EGF, transforming growth factor alpha (TGFalpha), heparin-binding (HB) EGF, betacellulin and amphiregulin. Treatment with finasteride produced greater concentrations of amphiregulin (P < 0.05) than did placebo, did not change the level of TGFalpha, HER1 and HER2, and tended to decrease the concentration of EGF, betacellulin and HB-EGF in prostate tissue. Using immunohistochemistry, HER1 and TGFalpha were both localized to the basal epithelial cells, and there was a strong positive correlation among the tissue concentrations of HER1, HER2 and TGFalpha. Amphiregulin localized to the luminal secretory epithelium. Prostate secretions contained only EGF, which was at levels approximately 150 times higher than in prostate tissue; treatment with finasteride did not affect the concentration of EGF in prostate secretion. CONCLUSIONS: There were only minor changes in the expression of TGFalpha, HER1 and HER2 after finasteride treatment. This may represent an important system for the continuous growth and homeostasis of the androgen-independent basal epithelial cells in the prostate.

Amphiregulin↗
PubMed2003

Use of finasteride in the treatment of men with androgenetic alopecia (male pattern hair loss).

Finasteride, a type 2-selective 5alpha-reductase inhibitor, was approved in 1997 as the first oral pharmacologic therapy for the treatment of men with androgenetic alopecia (AGA; male pattern hair loss). Originally developed for the treatment of men with benign prostatic hyperplasia (BPH) at a dose of 5 mg/day, finasteride has a well-established, excellent safety profile. Subsequent studies demonstrated that finasteride was an effective treatment for men with AGA at an optimal dose of 1 mg/day. This report summarizes the published peer-reviewed literature on the use of finasteride in the treatment of men with AGA, including the data on long-term (5 years) use of finasteride in a placebo-controlled clinical trial environment.

Alopecia↗
PubMed1995

Case report: finasteride-induced gynecomastia in a 62-year-old man.

The authors describe a case of bilateral (with left prevalence) gynecomastia in a 62-year-old man after finasteride treatment because of benign prostatic hypertrophy. Finasteride is an inhibitor of 5 alpha-reductase, the enzyme responsible for testosterone metabolism to dihydrotestosterone. In this patient, nonspecific endocrine alterations were found, except for a significant decrease in dihydrotestosterone levels. In addition, there were no pathologic conditions affecting other organs or pharmacologic treatments that could be responsible for gynecomastia. Drug withdrawal started a progressive reduction of the lumps until complete their disappearance. It is possible that gynecomastia was caused by alterations of estrogen/androgen ratio because of a finasteride-induced decrease in circulating dihydrotestosterone levels. In this article, the authors confirm finasteride antiandrogenic activity and recommend a close follow-up of long-term treatments with finasteride to find out other possible side effects.

Dihydrotestosterone↗
PubMed1995

The effect of finasteride on prostate volume, urinary flow rate and symptom score in men with benign prostatic hyperplasia.

This study was designed to determine the efficacy of the 5 alpha-reductase inhibitor finasteride (Proscar, MK-906) in men with reduced urinary flow rates and symptoms of urinary outflow obstruction secondary to benign prostatic hyperplasia. Forty-five men were randomized to one of three groups receiving either placebo, 1 mg/day or 5 mg/day finasteride for the first 12 months of the study period. At the end of this period all men received 5 mg/day finasteride for a further 2 years. Efficacy was determined by measurement of prostate volume, maximum urinary flow rate, and symptom score using a modified Boyarsky assessment. Prostate volume reduced by 20 and 27%, respectively, for those on 1 and 5 mg after the first year. At 3 years the volume had reduced by 43%. This reduction in prostate volume was associated with an improvement in maximum urinary flow rate by 50% (1 mg), and 35% (5 mg) at 1 year, and 36% at 3 years. The total, obstructive and non-obstructive symptom scores decreased (improved) for patients on 1 and 5 mg finasteride, with the total score reducing by 33% from baseline at year 3. The results demonstrate that finasteride causes a modest but significant clinical improvement in men with urinary outflow obstruction secondary to benign prostatic hyperplasia.

Aged↗
PubMed1998

Effects of the anti-androgen finasteride on 5alpha-reductase activity in human gingival fibroblasts in response to minocycline.

In addition to their antimicrobial properties, tetracyclines have antiinflammatory and pro-anabolic effects on the reparatory potential of connective tissue and bone. The physiologically active androgen 5alpha-dihydrotestosterone (DHT) implicated in matrix synthesis is formed in gingivae from androgen substrates. The aim of this investigation is to study the androgen metabolic response of gingivae to minocycline, in the presence or absence of the anti-androgen finasteride. Chronically inflamed gingival tissue derived from 12 subjects aged 30-50 years and passaged fibroblasts derived from this source, were used for the experiments. Duplicate incubations were performed in Eagle's MEM with 14C-testosterone/14C-4-androstenedione in the presence or absence of minocycline (5-60 microg/ml) or finasteride for 24 h. The androgen substrate 14C-testosterone was metabolised mainly to DHT and 4-androstenedione, while 14C-4-androstenedione was converted mainly to DHT and testosterone. Minocycline at 20-30 microg/ml stimulated the formation of these metabolites from both substrates by 13-25%. In the tissue incubations there were 3- and 2-fold increases in DHT and 4-androstenedione formation (n=12; p<0.01). The anti-androgen finasteride caused significant inhibition of 5alpha-reductase activity on both substrates at 0.1 & 1.0 microg/ml with total inhibition at 10 & 50 microg/ml (n=3; p<0.01). Minocycline-induced stimulation of 5alpha-reductase activity was also inhibited by finasteride (n=4; p<0.02). Since finasteride inhibition of 5alpha-reductase activity is specific for the type 2 isoenzyme associated with anabolic functions of target tissue, this enzyme activity may contribute to some of the cited anabolic tissue responses to minocycline.

5-alpha Reductase Inhibitors↗
PubMed1994

Biotransformation of finasteride (MK-0906) by Selenastrum capricornutum (green algae).

Finasteride (MK-0906), a drug used for the treatment of benign prostatic hyperplasia, is a highly specific inhibitor of steroid 5 alpha-reductase, an enzyme that converts testosterone (T) to dihydrotestosterone (DHT) in animals and humans. In a study to evaluate the effect of finasteride on the growth of green alga, Selenastrum capricornutum, the parent drug was not detected by HPLC in the posttreatment (14 day) samples, suggesting complete biotransformation. Thermospray LC/MS, followed by NMR analysis, indicated that the major algal metabolite was 11 alpha-hydroxy-finasteride. This metabolite has negligible in vitro bioactivity against human prostatic 5 alpha-reductase; its potency is only 2% that of finasteride. The primary metabolite of finasteride produced by the green alga involved a biotransformation not previously observed in mammalian and human studies. The green alga effectively deactivates the drug, thereby mitigating any potential environmental impact.

5-alpha Reductase Inhibitors↗
PubMed2000

Urinary retention in patients with BPH treated with finasteride or placebo over 4 years. Characterization of patients and ultimate outcomes. The PLESS Study Group.

OBJECTIVES: Knowledge regarding the incidence and prevalence of acute urinary retention and the ultimate outcome is very limited. The purpose of the present analysis was to document the natural history and outcomes of acute urinary retention (AUR) further specified as being either precipitated or spontaneous, and to evaluate the potential benefit of finasteride therapy. MATERIALS AND METHODS: Three thousand and forty men with moderate to severe symptoms of BPH and enlarged prostate glands by digital rectal examination were enrolled into the 4-year placebo-controlled PLESS trial and were evaluated for occurrences of AUR and BPH-related surgery. Men in the study were seen every 4 months; discontinued patients were followed up 6 months after discontinuation and again at the end of the 4-year trial. Complete 4-year data on outcomes (occurrence of AUR or BPH-related surgery) was available for 92% of the enrolled subjects in each treatment group. An endpoint committee, blinded to treatment group and center, reviewed and categorized all study-related documentation relating to retention and surgery. RESULTS: Over the 4-year period, 99 of 1,503 placebo-treated patients (6.6%) experienced one or more episodes of AUR in comparison with 42 or 1,513 finasteride-treated patients (2.8%; p<0. 001). Approximately half of the episodes of retention were spontaneous and clearly BPH-related, while the other episodes were precipitated by another factor (PAUR). After spontaneous AUR, subsequent surgery was performed in 39 of 52 (75%) placebo-treated patients versus 8 of 20 (40%) finasteride-treated patients (p = 0. 01). BPH-related surgery was less common in men who had a prior episode of PAUR (26% in the placebo group and 14% in the finasteride group). CONCLUSION: There is a continual risk of spontaneous and precipitated acute urinary retention in men with moderate to severe lower urinary tract symptoms and an enlarged prostate gland. Fewer patients who developed precipitated AUR than spontaneous AUR go on to need subsequent BPH-related surgery. Significantly fewer finasteride-than placebo-treated patients developed AUR, and among those men, fewer ultimately needed BPH-related surgery.

Finasteride↗
PubMed2001

Discontinuation of alpha-blockade after initial treatment with finasteride and doxazosin for bladder outlet obstruction.

OBJECTIVES: Patients with symptomatic bladder outlet obstruction and moderately enlarged prostates can receive durable relief from finasteride. However, the delayed onset of action has led many clinicians to prescribe an alpha-blocker in addition to finasteride early in therapy for more rapid symptom relief. Our goal was to determine when to discontinue the alpha-blocker in this group of patients. METHODS: We enrolled 100 consecutive men with an estimated prostate size of >40 g and an AUA symptom score of > or =20, who reported an initially favorable response to combination therapy with 5 mg finasteride and 2 mg doxazosin daily. The average symptom score reduction at 1 month was 3.3. We discontinued the doxazosin at 3, 6, 9, or 12 months, while continuing finasteride, then reevaluated patients 1 month later to determine if the patients reported any worsening of symptoms. RESULTS: Twenty-five patients discontinued doxazosin at 3 months. Five (20%) were successfully discontinued, reporting no change in symptom score. Twenty reported worsening symptoms. Twenty-five patients discontinued doxazosin at 6 months. Twelve (48%) were successfully discontinued, reporting no change in symptom scores. Thirteen (52%) reported worsening symptoms. Twenty-five patients discontinued doxazosin at 9 months. Twenty-one (84%) were successfully discontinued, reporting no change in symptom scores. Four (16%) reported worsening symptoms. Twenty-five patients discontinued doxazosin at 12 months. Twenty-one (84%) were successfully discontinued, reporting no change in symptom scores. Four (16%) reported worsening symptoms. CONCLUSION: Patients with symptomatic bladder outlet obstruction and moderately enlarged prostates who are placed initially on combination therapy using finasteride and an alpha-blocker are likely to tolerate discontinuation of the alpha-blocker after 9 months of combination therapy.

Adrenergic alpha-Antagonists↗
PubMed2006

Natural scalp hair regression in preclinical stages of male androgenetic alopecia and its reversal by finasteride.

Using contrast-enhanced phototrichogram (CE-PTG) at monthly intervals during 48 months, we measured the duration of the hair cycle, i.e. anagen, catagen and telogen at the exclusion of exogen. Exogen, a recently identified phase of the hair cycle, is characterized by weakening of anchorage of the club hair to the surrounding epithelium. The processing of the club hair terminates at the time of exogen hair release, i.e. hair shedding. We combined a noninvasive exogen sampling before each CE-PTG so that the area contained only anagen, catagen and telogen hair or empty follicular openings. During the first 24 months of this study, natural regression of hair cycling in early i.e. preclinical stages of androgenetic alopecia (AGA) in androgen sensitive areas was documented. Shortening of the hair cycle of thicker hair characterized progression of AGA. During the next 24 months, finasteride (1 mg/day) was introduced into the system. Shortening of the hair cycle was reversed by finasteride in androgen sensitive sites as long as the affected follicle was able to produce a thick hair fiber at the time of treatment initiation. Compared to the baseline period, responding follicles did not produce thicker hair. On average, they initiated active growth more rapidly by reducing the duration of the lag phase by 40%. The duration of the anagen phase of thick hair showed an average 23% increase. In this particular experiment, the already miniaturized follicles producing thinner hair (<40 microm thickness) at the time of finasteride introduction regressed further on treatment. Our results seem to indicate that reversal of 'hair loss' by finasteride probably means that the terminal type follicles that are functionally deficient--a stage of reversible hypotrophy--will be reactivated by two non-mutually exclusive mechanisms: faster regrowth followed by extension of the duration of anagen. In our study, there was no clear evidence in favour of reversal of miniaturized hair into terminal hair. This new interpretation indicates that miniaturized hair follicles may be an important diagnostic marker of AGA in males but also that it might be less contributive to the therapeutic response to finasteride. Our results highlight that precise measurement of terminal type hair follicle functionalities opens up avenues for the selection of 'drug-responsive organs' in the human scalp in vivo and these may possibly serve to predict 'quality of response to treatment'.

Alopecia↗
PubMed1995

Bone density is normal in male rats treated with finasteride.

Bone is an androgen-dependent tissue. It is not known whether normal bony growth and mineralization in males is dependent on testosterone alone, or whether its metabolite, dihydrotestosterone (DHT), also is required. To answer this question, we examined the effect of finasteride, an inhibitor of DHT synthesis, on bone in rats. Three-month-old male rats were treated with placebo, finasteride, or orchidectomy. The bone mineral densities (BMD) of the spine and whole body were measured in vivo by dual x-ray absorptiometry at weeks 0 and 11, and the BMD of the femur and tibia were measured ex vivo at week 11. Histomorphometric analysis was performed on the proximal tibia at week 11. The increase in spine and whole body BMD in finasteride-treated rats did not differ from that in controls, whereas these values were significantly lower in orchidectomized rats. Similarly, the BMD of the femur and tibia and the cancellous bone volume of the proximal tibia in finasteride-treated rats did not differ from those in controls, whereas these values were significantly lower in orchidectomized rats. In summary, bone development and density were normal in rats treated with finasteride. We conclude that selective DHT deficiency is not deleterious to the male rat skeleton.

Alkaline Phosphatase↗
PubMed1997

Androgen metabolism in the prostate of the finasteride-treated, adult rat: a possible explanation for the differential action of testosterone and 5 alpha-dihydrotestosterone during development of the male urogenital tract.

Previous work has clearly demonstrated that inhibition of 5 alpha-dihydrotestosterone (DHT) formation in vivo is not as effective as total androgen ablation (castration) in causing involution of the prostate. It is likely that this is due to the fact that testosterone is partially effective in maintaining androgen action. To provide insight into this observation, the androgenic metabolites of testosterone, androstenedione, and 5 alpha-DHT, were measured in prostate tissue and in blood of 5 alpha-reductase inhibitor (finasteride)-treated adult male rats. Finasteride treatment caused a significant decrease in prostatic DHT levels and a profound increase in prostatic testosterone and androstenedione levels. Similarly, circulating DHT levels were decreased in finasteride-treated rats (0.02 ng/ml compared with 0.05 ng/ml seen in control rats); and circulating androstenedione and testosterone levels were significantly elevated in finasteride-treated animals compared with controls. The in vitro effects of finasteride were assessed on the metabolism of [3H]testosterone in a tissue-slice assays. In the prostate, the inhibition of 5 alpha-reductase activity resulted not only in the decreased formation of 5 alpha-reduced metabolites (primarily DHT and 5 alpha-androstanedione), but also an increase in the 17-oxo metabolite androstenedione. In contrast, the tissues derived from the embryonic wolffian duct (seminal vesicle and epididymis) formed relatively low amounts of 17-keto steroids. Because DHT is a high affinity ligand for the androgen receptor and androstenedione shows very little, if any, affinity for the receptor, these studies suggest that 5 alpha-reduction of testosterone may be a mechanism to amplify androgen action in urogenital tissues such as the prostate by preventing catabolism of testosterone to the inactive androgen, androstenedione, at the site of hormone action.

Androgens↗
PubMed2005

Pharmacogenetic analysis of human steroid 5 alpha reductase type II: comparison of finasteride and dutasteride.

Human steroid 5 alpha-reductase type II is a prostate-specific, membrane-associated enzyme that catalyzes the conversion of testosterone to dihydrotestosterone, the most potent androgen in the prostate gland. Genetic variants of this enzyme have been associated with both the development and the progression of prostate cancer. Both finasteride and dutasteride are competitive inhibitors of the type II steroid 5 alpha-reductase that have been effectively used for the treatment of benign prostatic hyperplasia. Finasteride has also been successfully utilized for prostate cancer chemoprevention. We here investigate 5 alpha-reductase inhibition assays in vitro to measure the effect of incubation time on the apparent inhibition constant (Ki) for both constitutional and somatic (prostate cancer) enzyme variants. Our systematic pharmacogenetic analysis shows that both finasteride and dutasteride are slow, time-dependent inhibitors of steroid 5 alpha-reductase type II, and that the inhibition kinetics depend on the 5 alpha-reductase genotype. We also show that, overall, dutasteride is a more efficient steroid 5 alpha-reductase inhibitor than finasteride. Based on our data, we are able to map areas of the enzyme that are responsible for this time-dependent inhibition for either (or both) enzyme inhibitor(s). This comprehensive pharmacogenetic analysis of steroid 5 alpha-reductase variants unveiled significant pharmacogenetic variation for both finasteride and dutasteride and thus should be taken into account when designing protocols for treatment and/or chemoprevention of prostatic diseases with either one of these 5 alpha-reductase inhibitors since there is considerable pharmacogenetic variation for both drugs.

3-Oxo-5-alpha-Steroid 4-Dehydrogenase↗
PubMed1996

An economic evaluation of finasteride for treatment of benign prostatic hyperplasia.

This evaluation was conducted at the request of a Canadian provincial government considering finasteride for formulary inclusion. The comparator therapies, in accordance with Canadian pharmacoeconomic guidelines, were the most prevalent treatment [transurethral resection of the prostate (TURP)] and the lowest cost treatment (watchful waiting). All costs were measured in 1994 Canadian dollars ($Can), and both costs and outcomes were discounted at 5% per annum. Cost-effectiveness and cost-utility ratios were calculated, and were found to be dependent on initial symptom severity and the anticipated duration of treatment with finasteride. The drug was shown to be the dominant alternative compared with both TURP and watchful waiting for patients with moderate symptoms, when the duration of drug therapy is 3 years or less. However, finasteride is a weak alternative for patients with severe symptoms who are treated for 4 years or more. For other groups of patients (i.e. moderate symptoms and on finasteride for 4 years or more; severe symptoms and on treatment for 3 years or less), the drug can improve health-related quality of life, but at a cost of between $Can3000 and $Can97,000 per incremental quality-adjusted life year (1994 dollars). Our study also indicated that it would cost between $Can2.7 million and $Can5.6 million, depending on the severity mix of the patients, to treat cohort of 10,000 men aged 60 years or older with finasteride.

Aged↗
PubMed2002

Finasteride-induced prostatic involution by apoptosis in dogs with benign prostatic hypertrophy.

OBJECTIVE: To determine the effect of finasteride on programmed cell death (apoptosis) of prostatic cells during prostatic involution in dogs with benign prostatic hypertrophy (BPH). ANIMALS: 9 dogs with BPH. PROCEDURE: Dogs were randomly assigned to treatment or control groups. Treatment dogs (n = 5) were administered finasteride (0.1 to 0.5 mg/kg, PO, q 24 h) for 16 weeks, whereas the 4 control dogs were administered an inert compound. Prostatic cells from the prostatic fluid portion of the ejaculate of treatment and control dogs were obtained before and 1, 2, 3, 4, 8, and 16 weeks after initiation of treatment. Cells were concentrated by use of centrifugation. Prostatic cells were examined for indications of apoptosis by use of a terminal deoxyribonucleotidyl transferase-mediated deoxyuracil triphosphate nick-end labeling technique. After receiving the inert compound for 16 weeks, the 4 control dogs were administered finasteride for 16 weeks, and evaluations were repeated. RESULTS: Percentage of apoptotic prostatic cells in ejaculated prostatic fluid of treatment dogs increased significantly (from 9% before treatment to 33, 31, 26, and 27% after 1, 2, 3, and 8 weeks of treatment, respectively). There was no significant change in percentage of apoptotic prostatic cells in the ejaculated prostatic fluid of control dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Finasteride-induced prostatic involution appears to be via apoptosis in dogs with BPH. Finasteride treatment of dogs with BPH causes prostatic involution by apoptosis rather than necrosis.

Animals↗
PubMed2004

[Effect of finasteride on intraoperative bleeding and irrigating fluid absorption during transurethral resection of prostate: a quantitative study].

OBJECTIVE: To evaluate the effect of pretreatment with finasteride in decreasing intraoperative bleeding and irrigating fluid absorption during transurethral resection of prostate (TURP). METHODS: Eighty patients with benign prostate hypertrophy undergoing TURP were divided into two groups: 40 patients were pretreated with finasteride for 7 to 14 days before TURP and 40 patients without pretreatment. Absorption of irrigating fluid was quantified by analyzing the serum concentration of gentamycin. Intraoperative blood loss was calculated based on hemoglobin concentrations before and after operation. RESULT: The whole blood loss, hemoglobin concentration of irrigating fluid used, blood loss per minute, blood loss per gram tissue resected, whole irrigation absorption, irrigation absorption per minute and per gram tissue resected in patients pretreated with finasteride were significantly less than those in patients without pretreatment (P<0.05). The blood transfusion volume, the incidence of hypotension and hyponatremia in patients pretreated with finasteride were significantly less than those in patients without pretreatment (P<0.05). CONCLUSION: Pretreatment with finasteride is of value in reducing intraoperative bleeding, irrigation absorption and perioperative complication during TURP.

Absorption↗
PubMed2000

Cytologic atypia in a 53-year-old man with finasteride-induced gynecomastia.

Finasteride has been associated with the development of gynecomastia. Although cytoplasmic vacuolization has been noted in prostatic epithelium in men taking this drug, we found no documentation of the cytologic changes in finasteride-associated gynecomastia. We present the case of a 53-year-old man who developed unilateral gynecomastia following finasteride therapy for alopecia. A fine-needle aspiration biopsy of the mass was diagnosed as adenocarcinoma on the basis of nuclear atypia and particularly because of cytoplasmic vacuolization. Subsequent excisional biopsy revealed benign gynecomastia with no evidence of malignant change. The ductal epithelium did exhibit cytoplasmic vacuolization similar to that described in the prostate following finasteride therapy. We believe this is the first reported case documenting the cytologic changes seen in gynecomastia secondary to finasteride therapy. Cytoplasmic vacuolization in this setting should not be considered evidence of malignancy in men with gynecomastia. As with gynecomastia in general, extreme caution should be used before rendering a cytologic diagnosis of malignancy.

Alopecia↗
PubMed1999

Long-term effects of finasteride on prostate tissue composition.

OBJECTIVES: To determine the long-term effects of finasteride treatment on prostate tissue composition; to relate these effects to clinical outcomes; and to test the hypothesis that finasteride exerts a selective or preferential action on the transition zone. METHODS: Nineteen men with symptomatic benign prostatic hyperplasia (BPH) who completed a 6-month double-blind trial of finasteride were enrolled in a 24-month open-label extension study of drug responders. Magnetic resonance imaging and prostate biopsy for morphometric analysis were performed together 70 times: at baseline (n = 19), after treatment periods of intermediate duration (6 to 18 months, n = 32), and after long-term drug treatment (24 to 30 months, n = 19). At baseline, prostate volume averaged 51 cc, of which 57% was transition zone. RESULTS: Decreases in symptom score, dihydrotestosterone and prostate-specific antigen levels, and prostate volume occurred at 6 months (P <0.01), stabilized, and were maintained without further long-term decreases. Prostate epithelium contracted progressively from baseline (19.2% tissue composition; 6.0-cc volume; 3.2 stroma/epithelial ratio) to intermediate (12.5%, 3.3 cc, and 5.6, respectively) to long-term treatment (6.4%, 2.0 cc, and 17.4, respectively, P <0.01 for all). Percent epithelial contraction was similar in the peripheral and transition zones (P = NS). The transition zone remained a relatively constant proportion (53% to 58%) of whole-prostate volume from baseline to long-term observation. CONCLUSIONS: Long-term finasteride treatment (24 to 30 months) results in a marked involution of the prostate epithelium, which continues to progress for many months after clinical effects stabilize. The effect on the epithelium is similar in the peripheral and transition zones for both morphometric and volumetric changes. Progressive contraction of the prostate epithelium appears to constitute the underlying mechanism for sustained action of finasteride.

Double-Blind Method↗