Finasteride is a novel therapeutic agent that selectively inhibits the enzyme 5α-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 decrementai 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.
Competitive inhibition of 5α-reductase by finasteride has been demonstrated in a series of in vitro experiments. In animal studies, acute administration of finasteride to the rat or dog resulted in a significant reduction in prostatic dihydrotestosterone (DHT) levels and a significant increase in prostatic testosterone. With longer periods of administration (up to 12 weeks), the decrementai effects of finasteride on canine prostatic DHT levels were maintained and prostate size declined by ≈33 to 47%.
In healthy volunteers administered finasteride as a single dose, maximum suppression of plasma DHT levels (⩾50%) was shown to occur at doses greater than 0.5mg. Little variation in the magnitude of this effect was evident over a wide range of doses above 5mg. In a similar population, plasma DHT was suppressed by >60% following continued administration of finasteride 0.04 to 100 mg/day for 1 to 3 weeks. The ‘no-effect multiple-dosage’ was shown to lie between 5 and 40 μg/day. Although biochemical effects are evident with low finasteride doses, the results of phase II and III investigations suggest that dosage of 1 or 5 mg/day are required to produce clinically significant effects in patients with BPH. In healthy volunteers, no clear overall effect of finasteride on circulating testosterone was demonstrated, and where fluctuations in this parameter were recorded, values remained within the accepted normal range. The ability to detect small changes in testosterone levels, however, was limited by the small numbers of participants and the known assay variability. Other hormones [including follicle stimulating hormone (FSH), luteinizing hormone (LH), cortisol and estradiol] and serum lipids were unaffected by finasteride administration, although at supratherapeutic doses Δ4-androstenedione levels became elevated.
In men with symptomatic BPH treated with finasteride 1 or 5 mg/day for 1 year, the major reduction in prostate volume occurred in the periurethral zone, which is responsible for urethral obstruction. The serum sex hormone profile of patients with BPH administered finasteride confirmed similar findings to those recorded in studies of healthy volunteers. In addition, patients awaiting transurethral resection of the prostate (TURP) administered finasteride 1 to 100 mg/day for 1 week showed a reduction in prostatic DHT levels of more than 90% at all dosage levels with a significant increase in prostatic testosterone.
Finasteride does not appear to have a direct effect on androgenic mechanisms in vivo and had no significant affinity for the androgen receptor in vitro. As expected, at low dosages (⩾0.003 mg/kg/day), it caused dysmorphogenesis of male offspring in animal studies.
The bioavailability of finasteride 5mg is 80% and most absorption occurs within 2 hours. Food does not affect its pharmacokinetic profile. The plasma profile of finasteride showed dose proportionality after single oral doses of 5 to 50mg, although at higher doses conflicting results were reported. Healthy volunteers administered oral finasteride 5mg showed maximum plasma concentrations of 37 to 41 μg/L approximately 2 hours later, while values for the area under the plasma concentration-time curve (AUC) were 349 to 385 μg/L · h and terminal elimination phase half-life ranged from 4.8 to 6.0h.
In elderly (⩾70 years) healthy volunteers, daily administration of finasteride 5mg for 17 days resulted in a plasma pharmacokinetic profile characteristic of slower elimination when compared with that of their younger (45 to 60 years) healthy counterparts. Plasma finasteride concentrations increased with time in both groups, although notably the increases in minimum plasma finasteride concentration (Cmin) and AUC were greater among the elderly. At steady-state, Cmin values of 8.3 and 9.6 μg/L were predicted for younger and elderly volunteers, which were marginally greater than those observed after 17 days.
Finasteride undergoes wide tissue distribution. Plasma protein binding is approximately 90% over a concentration range of 0.02 to 2 μg/L and is not affected by moderate or severe renal impairment. In humans, finasteride is extensively metabolised through oxidative mechanisms and eliminated in the faeces and urine. Patients with moderate to severe renal dysfunction showed a decrease in urinary excretion of radiolabelled finasteride which correlated with the severity of the condition, but was compensated by an increase in faecal elimination. An increase of AUC0–48h of ≈ 35% associated with renal impairment does not appear to warrant dosage adjustment in this patient group as high doses of finasteride are well tolerated.
Therapeutic Potential of Finasteride in Benign Prostatic Hyperplasia
The clinical efficacy of finasteride was first demonstrated in a series of pivotal phase II placebo-controlled, randomised, double-blind clinical investigations in which dosages of 0.2 to 40 mg/day or 5 to 80 mg/day were administered to men with symptomatic BPH for up to 24 weeks. Significant reductions in circulating DHT levels were reflected in significant prostate shrinkage after 24 weeks with dosage levels of 1 mg/day and above; concomitant reductions in prostate specific antigen (PSA) levels were also evident. Peak urinary flow rate improved by at least 3 ml/sec for most finasteride-treated groups, while urological symptoms assessed by evaluating total (obstructive and nonobstructive) and obstructive symptom scores (using an adapted Boyarski scale) showed a trend towards improvement. Cessation of therapy was associated with reversal of the beneficial clinical effects suggesting the need for continual therapy.
In well designed phase III placebo-controlled, randomised, double-blind trials, 1645 men with mild to severe symptomatic BPH were administered finasteride 1 or 5 mg/day for 1 year. Significant reductions in serum mean DHT levels (45 to 66%) again reflected in prostate shrinkage (median ≈20%) at both dosages, although 6 months of therapy was necessary before the maximum effect on the prostate became evident. Concomitant reductions in serum mean PSA levels (43 to 50%) were also observed. Peak urinary flow rate increased modestly by 1.3 to 1.7 ml/sec, although it may be argued that this degree of improvement represents a reversal of 6.5 to 7.5 years of declining function. Total symptom score decreased slightly by about 3 to 4 points (on a scale of 0 to 36) for patients receiving finasteride 5 mg/day and by about 2 to 4 points for those receiving 1 mg/day. Obstructive symptom scores followed a similar trend. Reductions in prostate size and improvements in urinary flow and symptom scores during finasteride therapy were partially offset by the larger than expected placebo response. There was no correlation between efficacy parameters and disease severity, and subgroup analysis revealed reductions in prostate size and increases in urine flow rate that were similar regardless of baseline values. In noncomparative extensions to phase HI studies the clinical effects of finasteride 5 mg/day were maintained for 2 years.
Available data from 1398 patients treated with finasteride 0.2 to 80 mg/day for periods of up to 1 year in phase II and III investigations show that the drug is well tolerated. Most adverse events were related to sexual dysfunction (decreased libido, ejaculation disorders and impotence) and occurred in only a small proportion of the patient population (2.2 to 3.4% vs 0.8 to 1.6% for placebo); similar findings were observed when only patients recruited to phase III studies were considered. Withdrawal rates were essentially similar for finasteride- and placebo-treated groups in phase III investigations (≈5%), although withdrawal associated with sexual adverse events was higher among finasteride recipients (0.5 to 0.9 vs 0.2%). No fatalities attributable to finasteride were noted. Finasteride did not mask the detection of prostate cancer through its effects on PSA levels. Indeed, the detection rate for prostate cancer was twice that noted for the general population (probably reflecting close patient monitoring) and most patients who developed the disease had elevated PSA levels at baseline. A greater proportion of finasteride-treated patients showed increased neutrophil counts, blood urea nitrogen and glucose levels, but these findings were not corroborated by changes in other parameters or the results of other investigations. Small increases in circulating testosterone and LH levels, and slight changes in other circulating hormone levels associated with finasteride therapy were considered not to be of clinical relevance.
Dosage and Administration
The recommended oral dosage of finasteride is 5mg daily. Dosage adjustment in patients with renal insufficiency or in the elderly appear unwarranted. Finasteride is not indicated for use in women or children. Furthermore, due to the dysmorphogenic effects of finasteride on male offspring, women who are, or who may become, pregnant should avoid exposure to the drug. In this respect, patients should avoid transvaginal exposure via the semen of their sexual partner as a precautionary measure.
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Various sections of the manuscript reviewed by: U. Dunzendorfer, Maingau Krankenhaus, Frankfurt, Federal Republic of Germany; P. Ekman, Department of Urology, Karolinska Hospital, Stockholm, Sweden; J. Geller, Department of Medical Education, Mercy Hospital and Medical Center, San Diego, California, USA; F.W. George, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA; J.C. Gingell, Department of Urology, Southmead Hospital, Westbury-on-Trym, Bristol, England; J.W. Goldzieher, Department of Obstetrics and Gynecology, Baylor College of Medicine, San Antonio, Texas, USA; D. Horii, Kashima Laboratory, Mitsubishi-Kasei Institute of Toxicological and Environmental Sciences, Ibaraki, Japan; H. Matzkin, Department of Urology, Tel Aviv-Elias Sourasky Medical Center, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; J. Nacey, Department of Surgery, Wellington School of Medicine, Wellington, New Zealand; W.B. Peeling, St Woolos Hospital, Newport, Gwent, Wales; R.S. Rittmaster, Department of Medicine and Physiology, Dalhousie University, Halifax, Nova Scotia, Canada; P.J. De Schepper, Department of Pharmacology and Clinical Pharmacology, School of Medicine, University of Leuven, Leuven, Belgium.
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Peters, D.H., Sorkin, E.M. Finasteride. Drugs 46, 177–208 (1993). https://doi.org/10.2165/00003495-199346010-00010
- Benign Prostatic Hyperplasia
- Prostate Specific Antigen Level
- Total Symptom Score
- Symptomatic Benign Prostatic Hyperplasia