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Finasteride

An Update of its Use in the Management of Symptomatic Benign Prostatic Hyperplasia

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Summary

Abstract

Finasteride inhibits type 25α-reductase activity, significantly reducing dihydrotestosterone levels. Consequent reductions in prostate volume, increases in urinary flow rates and improvements in symptoms compared with placebo have been observed in trials of up to 4 years’ duration and in noncomparative extensions (for up to 6 years).

Results from the 4-year placebo-controlled PLESS trial show finasteride to significantly reduce the risk of benign prostatic hypertrophy (BPH)-related acute urinary retention and the requirement for surgical intervention.

Finasteride has significantly greater efficacy in patients with a large prostate (≥40ml) than in patients with a small prostate. However, the predictive value of prostate size has been questioned.

Results of an earlier comparative 1-year trial show terazosin monotherapy and terazosin plus finasteride therapy to be significantly more effective than both finasteride monotherapy and placebo in reducing symptom scores and improving maximum urinary flow rates. Prostatic volume was significantly reduced by finasteride monotherapy and combination therapy only.

The overall efficacy of finasteride in patients with mild to moderate symptomatic BPH tended to be greater than that of serenoa repens (Permixon®)1 in a 6-month trial.

A US cost analysis model indicates that finasteride and terazosin are less expensive than transurethral resection of the prostate (TURP) during the first 2 years of initiation. Canadian cost-effectiveness and cost-utility analyses using decision analysis modelling have shown primary intervention with finasteride to provide more quality-adjusted life years (QALYs) at lesser cost than watchful waiting or TURP in patients with moderate symptoms who receive the drug for ≤3 years and ≤14 years, respectively, but fewer QALYs at a higher cost in patients with severe symptoms needing therapy for ≥4 years. Confirmatory prospective economic studies are required.

Finasteride appears to improve overall quality of life to a similar extent to serenoa repens; patient satisfaction appears similar with finasteride and TURP.

Finasteride is generally well tolerated. Most commonly reported adverse effects are sexually related (1 to 2.1%). Gynaecomastia has been reported in 0.4% of patients.

Conclusions: Despite modest improvements in maximum urinary flow rates and symptom scores, finasteride is a first-line treatment option in those with moderate uncomplicated BPH, especially in patients with a large prostate (≥40ml). It is also an option in patients with more severe symptoms who are unable or unwilling to undergo surgery and in those awaiting surgery. Importantly, finasteride appears to reduce disease progression, significantly decreasing the incidence of acute urinary retention and the requirement for surgical intervention; to date, no other pharmacological agent has been shown to reduce these outcomes.

Pharmacodynamic Properties

Finasteride is a 4-azasteroid which selectively and competitively inhibits the activity of 5α-reductase. This nicotinamide adenine dinucleotide phosphate (NADPH)-dependent enzyme is necessary for converting testosterone to dihydrotestosterone. The drug specifically inhibits the type 2 isoenzyme of 5α-reductase, the predominant form in prostatic tissue. Dose-dependent inhibition of 5α-reductase results in significant reductions in prostatic (by up to >90%) and circulating (by up to 60 to 80%) dihydrotestosterone levels.

Prostatic testosterone levels are increased by finasteride (by approximately 85%) in patients with benign prostatic hypertrophy (BPH); however, these levels do not appear to affect prostatic growth or morphology. The drug has no significant affinity for the androgen receptor.

Finasteride significantly reduces serum prostate-specific antigen (PSA) levels by 41 to 71% in patients with symptomatic BPH. However, the mean free-to-total PSA ratio is unaffected by the drug (see also Dosage and Administration summary).

Prostate size is reduced by finasteride by a combination of atrophy and apoptosis. Drug-induced histological changes have been observed after 6 months’ treatment; glandular elements of prostatic tissue are the most sensitive to finasteride. Finasteride reduces detrusor pressure in patients with bladder outlet obstruction due to BPH.

Pharmacokinetic Properties

Finasteride is well absorbed from the gastrointestinal tract, with food slowing the rate but not the extent of absorption. The drug appears to accumulate after multiple doses. Time to steady state appears to be longer than 17 days; the exact time is unknown.

The volume of distribution of finasteride is large (76Lat steady state); the drug crosses the blood-brain barrier and small amounts are found in semen. The drug may be absorbed through the skin on contact with crushed tablets (see Dosage and Administration summary).

Finasteride is extensively metabolised in the liver to essentially inactive metabolites. Elimination is mainly via the faeces and bile and, to a lesser extent, in the urine.

The overall pharmacokinetic profile of the drug appears generally unaffected by increased age or renal impairment (see also Dosage and Administration summary). The effects of hepatic impairment on the pharmacokinetics of finasteride are not known.

Clinical Efficacy

In a 4-year placebo-controlled trial of patients with moderate to severe disease (PLESS study), finasteride 5 mg/day had significantly superior effects on maximum urinary flow rates (Qmax), prostate volume and symptom scores to those of placebo. Between-treatment differences were usually observed within 4 months of treatment initiation. These findings confirm those of previous trials of up to 2 years’ duration, in which finasteride 5 mg/day, compared with placebo, significantly reduced total symptom scores (by 13 to 23%), increased Qmax(by 12.5 to 22%) and decreased prostate volume (by 15 to 47%) in patients with mild to moderate symptomatic BPH. More finasteride than placebo recipients were classified as responders.

Finasteride 5 mg/day was significantly more effective in reducing symptoms and improving Qmax in patients with a large prostate (≥40ml and >30ml, respectively) than in patients with a smaller prostate, in a pooled analysis of data from 6 placebo-controlled trials.

Evidence suggests that finasteride may halt and begin to reverse the natural progression of BPH. In contrast to placebo recipients, finasteride-treated patients showed sustained or continued improvements over the study periods. The observed improvements with finasteride in placebo-controlled trials have been at least sustained in noncomparative extensions of several of these trials (for up to 6 years). Furthermore, data from large placebo-controlled trials have shown finasteride 5 mg/day, administered for up to 4 years, to significantly decrease the risk of acute urinary retention and BPH-related surgical intervention compared with placebo.

Symptom scores and Qmax were improved to a significantly greater extent with both terazosin monotherapy and terazosin plus finasteride therapy compared with either finasteride monotherapy or placebo in a trial of >1200 patients with symptomatic BPH. No significant differences between the effects of terazosin monotherapy and combination therapy or between finasteride monotherapy and placebo were observed. Prostate volume was significantly reduced by finasteride and combination therapy; nonsignificant increases occurred with both terazosin monotherapy and placebo. This study was limited by failure to stratify patients according to mean baseline prostate volumes. However, superior effects of terazosin over finasteride and placebo were seen in a subsequent subanalysis of patients with prostate volumes greater than 50ml (data presented in abstract form). In contrast to other findings, there was no evidence of a linear relationship between prostate volume and clinical response.

The overall efficacy of finasteride in patients with mild to moderate symptomatic BPH tended to be greater than that of serenoa repens (Permixon®)1 in a 6-month trial. Longer term trials are needed to confirm these findings.

Tolerability and Drug Interactions

During postmarketing surveillance, the most common adverse events with finasteride therapy in patients with symptomatic BPH were sexually related, namely impotence or ejaculatory failure (2.1%) and decreased libido (1%). Gynaecomastia was reported in 0.4% of patients.

The incidence of adverse events related to sexual dysfunction was significantly greater with finasteride than with placebo (2.1 to 19 vs 0.6 to 10%) in 2-year placebo-controlled trials involving a total of more than 7600 patients with symptomatic BPH. Adverse events were usually mild and transient. The overall incidence of adverse events and the overall percentage of patients withdrawing because of adverse effects was similar in the finasteride and placebo groups. A 4-year placebo-controlled trial showed the incidence of decreased libido and impotence to be more frequent with finasteride than with placebo only in the first year of therapy.

There is no evidence that the incidence of sexually related adverse effects with finasteride increases with increased duration of therapy, according to the results of noncomparative extensions (for up to 6 years) of placebo-controlled trials. Up to 62% of finasteride-related sexual adverse events resolved with continued treatment. A reduced ejaculate volume, observed in some finasteride recipients, did not interfere with normal sexual function.

Other adverse events that have been probably or possibly associated (in case reports) with finasteride administration include exfoliative dermatitis, perioral numbness, lymphadenopathy, ataxia and wheeziness. Hypersensitivity reactions and lip swelling have also been observed.

A significantly higher incidence of impotence and decreased libido has been observed with finasteride (9 and 5%, respectively) than with terazosin (6 and 3%) monotherapy. In contrast, the incidences of dizziness and asthenia were significantly lower with finasteride (8 and 7%, respectively) than with terazosin (26 and 14%) therapy. Ejaculatory abnormalities occurred in significantly more finasteride plus terazosin recipients than in finasteride monotherapy, terazosin monotherapy or placebo recipients (7 vs 0.3 to 2%). The incidence of impotence and decreased libido with finasteride tended to be greater than that with serenoa repens.

There is no evidence that finasteride masks the detection of prostate cancer through its effects on serum PSA levels (see also Pharmacodynamic Properties and Dosage and Administration summaries).

No pharmacodynamic interactions have been reported between finasteride and terazosin (coadministration with terazosin increased finasteride maximum plasma concentration and area under the plasma concentration-time curve values in healthy volunteers), and no pharmacokinetic interactions have been observed between finasteride and doxazosin. In vitro evidence suggests that agents which inhibit CYP3A activity are likely to inhibit the metabolism of finasteride. No clinically significant interactions between finasteride and warfarin, theophylline, digoxin or propranolol have been observed.

Pharmacoeconomic and Quality-of-Life Considerations

Both finasteride and terazosin were less expensive than transurethral resection of the prostate (TURP), from a US third-party payer perspective, according to a decision analytic modelling study in which direct treatment costs were assessed during the first 2 years. Overall treatment costs with finasteride tended to be higher than those with terazosin. Break-even points for medical versus surgical treatment were longer with terazosin than with finasteride.

According to the results of cost-effectiveness and cost-utility analyses (using retrospective data and decision analysis modelling), primary intervention with finasteride, from the perspective of Canadian provincial/territorial healthcare systems, provides more quality-adjusted life years (QALYs) at lesser cost than watchful waiting or TURP in patients with moderate symptoms who receive the drug for ≤3 years and ≤14 years, respectively. Conversely, it provides fewer QALYs at a higher cost than these options in patients with severe symptoms needing therapy for ≥4 years.

In a 36-month decision-tree model, initial treatment of patients with BPH with α-adrenoceptor antagonists was more cost effective than initial treatment with finasteride, from the perspective of the US military.

Finasteride 5 mg/day appeared to produce greater improvements in disease-specific quality-of-life measures than placebo in pooled data from 2 placebo-controlled trials of more than 1600 patients with symptomatic BPH; however, sexual functioning was reduced in finasteride recipients. Similarly, health-related quality of life (as assessed by the BPH Impact Index) was greater in finasteride than placebo recipients in a 1-year placebo-controlled trial of 2342 men with moderate to severe symptomatic BPH.

Improvements in overall quality of life were similar in finasteride and serenoa repens recipients in the 1 available comparative trial. However, sexual function was significantly better in serenoa repens than finasteride recipients. Patient satisfaction has been reported to be similar with finasteride therapy and TURP.

Dosage and Administration

Finasteride is indicated for use in men with symptomatic BPH. The recommended dosage of finasteride is 5 mg/day orally administered with or without food. A minimum of 6 months’ treatment may be required to determine a response. The optimal duration of therapy has not been determined.

The presence of prostate cancer must be excluded before administering finasteride and all patients who receive finasteride should undergo periodic monitoring for the presence of prostate cancer. The presence of other conditions which may mimic BPH should also be excluded. Because of finasteride-induced reductions in serum PSA levels and the potential to mask the detection of prostate cancer, serum PSA values obtained after 6 months’ therapy should be doubled before interpreting results.

Patients with renal impairment and the elderly do not appear to require reduced dosages of finasteride. Caution is recommended in patients with hepatic impairment; specific dosage recommendations are not available at present.

Finasteride use should be avoided in women and children. Pregnant women or those who may become pregnant should avoid contact with crushed finasteride tablets.

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References

  1. Tewari A, Shinohara K, Narayan P. Transition zone volume and transition zone ratio; predictor of uroflow response to finasteride therapy in benign prostatic hyperplasia patients. Urology 1995 Feb; 45: 258–65

    Article  PubMed  CAS  Google Scholar 

  2. McConnell JD, Barry MJ, Bruskewitz RC, et al. Benign prostatic hyperplasia: diagnosis and treatment. Clinical practice guidelines. v. Number 8. Rockville (MD): US Department of Health and Human Services Public Health Service Agency for Health Care Policy and Research, 1994

    Google Scholar 

  3. Din KEE, Kiemeney LALM, De Wildt MJAM, et al. Correlation between uroflowmetry, prostate volume, postvoid residue, and lower urinary tract symptoms as measured by the international prostate symptom score. Urology 1996; 48: 393–7

    Article  Google Scholar 

  4. Girman CJ, Jacobsen SJ, Guess HA, et al. Natural history of prostatism: relationship among symptoms, prostate volume and peak urinary flow rate. J Urol 1995; 153: 1510–5

    Article  PubMed  CAS  Google Scholar 

  5. Hald T, Nordling J. Reflections on lower urinary tract symptoms in search of a definition of clinical BPH. (Data on file)

  6. Abrams P. New words for old: lower urinary tract symptoms for “prostatism”. BMJ 1994; 308: 929–30

    Article  PubMed  CAS  Google Scholar 

  7. Andersen JT. α-1-Blockers vs 5-α-reductase inhibitors in benign prostatic hyperplasia: a comparative review. Drugs Aging 1995 May; 6: 388–96

    Article  PubMed  CAS  Google Scholar 

  8. Caine M. The present role of alpha-adrenergic blockers in the treatment of benign prostatic hypertrophy. J Urol 1986; 136: 1–4

    PubMed  CAS  Google Scholar 

  9. Christmas TJ, Kirby RS. Alpha-adrenoceptor blockers in the treatment of benign prostatic hyperplasia. World J Urol 1991; 9: 36–40

    Article  Google Scholar 

  10. Peters DH, Sorkin EM. Finasteride: a review of its potential in the treatment of benign prostatic hyperplasia. Drugs 1993 Jul; 46: 177–208

    Article  PubMed  CAS  Google Scholar 

  11. Weisser H, Tunn S, Debus M, et al. 5 Alpha-deductase inhibition by finasteride (Proscar Rm) in epithelium and stroma of human benign prostatic hyperplasia. Steroids 1994 Nov; 59: 616–20

    Article  PubMed  CAS  Google Scholar 

  12. Faller B, Farley D, Nick H. Finasteride: a slow-binding 5α-reductase inhibitor. Biochemistry 1993 Jun 1; 32: 5705–10

    Article  PubMed  CAS  Google Scholar 

  13. Steiner JF. Clinical pharmacokinetics and pharmacodynamics of finasteride. Clin Pharmacokinet 1996 Jan; 30: 16–27

    Article  PubMed  CAS  Google Scholar 

  14. Boudon C, Lobaccaro JM, Lumbroso S, et al. 5α-reductase activity in cultured epithelial and stromal cells from normal and hyperplastic human prostates —effect of finasteride (Proscar), a 5α-reductase inhibitor. Cell Mol Biol 1995 Dec; 41: 1007–15

    PubMed  CAS  Google Scholar 

  15. Berthaut I, Portais MC, Mestayer C, et al. Finasteride inhibition of androgen metabolism in cultured human prostatic and skin cells distinguishes between type 1 and 2 5α-reductases [abstract]. Eur J Endocrinol 1994 Jun; 130 Suppl. 2: 53

    Google Scholar 

  16. Ko HC, Jusko WJ. Pharmacodynamic modeling of finasteride, a 5α-reductase inhibitor. Pharmacotherapy 1995 Jul–Aug; 15: 509–11

    PubMed  CAS  Google Scholar 

  17. Jaffe A, Matzkin H, Gilad S, et al. Effect of 5-alpha-reductase inhibition on sex-hormone-binding globulin in elderly men. Horm Res 1994; 41(5–6): 215–7

    Article  PubMed  CAS  Google Scholar 

  18. Mocellini AI, Gardiner R, Marshall V, et al. Finasteride (MK-906) in the treatment of benign prostatic hyperplasia. Prostate 1993; 22(4): 291–9

    Article  Google Scholar 

  19. Gormley GJ, Stoner E, Bruskewitz RC, et al. The effect of finasteride in men with benign prostatic hyperplasia. N Engl J Med 1992 Oct 22; 327: 1185–91

    Article  PubMed  CAS  Google Scholar 

  20. Moore E, Bracken B, Bremner W, et al. Proscar: five-year experience. Eur Urol 1995; 28: 304–9

    PubMed  CAS  Google Scholar 

  21. Stoner E, Andriole GL, Boake R, et al. Three-year safety and efficacy data on the use of finasteride in the treatment of benign prostatic hyperplasia. Urology 1994 Mar; 43: 284–94

    Article  PubMed  CAS  Google Scholar 

  22. Di Silverio F, Sciarr A, D’Eramo G, et al. Response of tissue androgen and epidermal growth factor concentrations to the long-term administration of Serenoa repens (Permixon), finasteride and flutamide to BPH patients. Eur Urol 1996; 30 Suppl. 2: 96

    Google Scholar 

  23. Schwartz JI, Van Hecken A, De Schepper PJ, et al. Effect of MK-386, a novel inhibitor of type 1 5α-reductase, alone and in combination with finasteride, on serum dihydrotestosterone concentrations in men. J Clin Endocrinol Metab 1996 Aug; 81: 2942–7

    Article  PubMed  CAS  Google Scholar 

  24. Tollin SR, Rosen HN, Zurowski K, et al. Finasteride therapy does not alter bone turnover in men with benign prostatic hyperplasia —a Clinical Research Center Study. J Clin Endocrinol Metab 1996 Mar; 81: 1031–4

    Article  PubMed  CAS  Google Scholar 

  25. Matzkin H, Chen JZ, Weisman Y, et al. Prolonged treatment with finasteride (a 5α-reductase inhibitor) does not affect bone density and metabolism. Clin Endocrinol 1992 Nov; 37: 432–6

    Article  CAS  Google Scholar 

  26. Matzkin H, Chen J, Lewyshon O, et al. Effects of long term treatment with finasteride (MK-906), a 5-alpha-reductase inhibitor, on circulating LH, FSH, prolactin and estradiol. Horm Metab Res 1992 Oct; 24: 498–9

    Article  PubMed  CAS  Google Scholar 

  27. Rittmaster RS, Antonian L, New MI, et al. Effect of finasteride on adrenal steroidogenesis in men. J Androl 1994 Jul–Aug; 15: 298–301

    PubMed  CAS  Google Scholar 

  28. Nickel JC, Fradet Y, Boake RC, et al. Efficacy and safety of finasteride therapy for benign prostatic hyperplasia: results of a 2-year randomized controlled trial (the PROSPECT Study). Can Med Assoc J 1996 Nov 1; 155: 1251–9

    CAS  Google Scholar 

  29. Carraro JC, Raynaud JP, Koch G, et al. Comparison of phytotherapy (Permixon) with finasteride in the treatment of benign prostate hyperplasia: a randomized international study of 1,098 patients. Prostate 1996 Oct; 29: 231–40

    Article  PubMed  Google Scholar 

  30. Andersen JT, Ekman P, Wolf H, et al. Can finasteride reverse the progress of benign prostatic hyperplasia? A two-year placebo-controlled study. Urology 1995 Nov; 46: 631–7

    Article  PubMed  CAS  Google Scholar 

  31. Guess HA, Gormley GJ, Stoner E, et al. The effect of finasteride on prostate specific antigen: review of available data. J Urol 1996 Jan; 155: 3–9

    Article  PubMed  CAS  Google Scholar 

  32. Ruckle HC, Klee GG, Oesterling JE. Prostate-specific antigen: critical issues for the practicing physician. Mayo Clin Proc 1994 Jan; 69: 59–68

    PubMed  CAS  Google Scholar 

  33. Waldstreicher J, Tocker PF, Cheng J, et al. The effects of finasteride on serum prostate specific antigen in men with benign prostatic hyperplasia [abstract]. J Urol 1995 Apr; 153 Suppl.: 396

    Google Scholar 

  34. Brown JA, Peterson DD, Lieber MM, et al. Terazosin and finasteride both lower the serum prostate-specific antigen (PSA) level in men with benign prostatic hyperplasia (BPH) [abstract]. J Urol 1996 May; 155 Suppl.: 424A

    Google Scholar 

  35. Bach MA, Tocker PF, Malice M-P, et al. The effects of finasteride on serum prostate specific antigen (PSA) in men with benign prostatic hyperplasia (BPH) and prostate cancer (PCa) [abstract]. J Urol 1995 Apr; 153 Suppl.: 397

    Article  Google Scholar 

  36. Lepor H, Williford WO, Barry MJ, et al. The efficacy of terazosin, finasteride, or both in benign prostatic hyperplasia. N Engl J Med 1996 Aug 22; 335: 533–9

    Article  PubMed  CAS  Google Scholar 

  37. Matzkin H, Barak M, Braf Z. Effect of finasteride on free and total serum prostate-specific antigen in men with benign prostatic hyperplasia. Br J Urol 1996 Sep; 78: 405–8

    Article  PubMed  CAS  Google Scholar 

  38. Narayan P, Tewari A, Jacob G, et al. Differential suppression of serum prostatic acid phosphatase and prostate-specific antigen by 5-alpha-reductase inhibitor. Br J Urol 1995 May; 75: 642–6

    Article  PubMed  CAS  Google Scholar 

  39. Keetch DW, Andriole GL, Ratliff TL, et al. Comparison of percent free prostate-specific antigen levels in men with benign prostatic hyperplasia treated with finasteride, terazosin, or watchful waiting. Urology 1997; 50: 901–5

    Article  PubMed  CAS  Google Scholar 

  40. Brown JA, Peterson DD, Lieber MM, et al. The effects of terazosin and finasteride on prostate-specific antigen (PSA) in men with benign prostatic hyperplasia (BPH) [abstract]. J Urol 1995 Apr; 153 Suppl.: 320A

    Article  Google Scholar 

  41. Stenman U-H, Alfthan H, Scandinavian BPH Study Group. Effect of long term treatment with finasteride on free and total PSA in serum [abstract]. J Urol 1996 May; 155 Suppl.: 698A

    Google Scholar 

  42. Gormley GJ, Stoner E, Ng J, et al. Effect of finasteride on prostate-specific antigen density. Urology 1994 Jan; 43: 53–9

    Article  PubMed  CAS  Google Scholar 

  43. Oesterling JE, Roy J, Agha A, et al. Biologic variability of prostate-specific antigen and its usefulness as a marker for prostate cancer: effects of finasteride. Urology 1997; 50: 13–8

    Article  PubMed  CAS  Google Scholar 

  44. Andriole GL, Guess HA, Epstein JI, et al. Treatment with finasteride preserves usefulness of prostate-specific antigen in the detection of prostate cancer: results of a randomized, double-blind, placebo-controlled clinical trial. Urology 1998; 52: 195–202

    Article  PubMed  CAS  Google Scholar 

  45. Rittmaster RS, Norman RW, Thomas LN, et al. Evidence for atrophy and apoptosis in the prostates of men given finasteride. J Clin Endocrinol Metab 1996 Feb; 81: 814–9

    Article  PubMed  CAS  Google Scholar 

  46. Krieg M, Weisser H, Tunn S. Potential activities of androgen metabolizing enzymes in human prostate. J Steroid Biochem Mol Biol 1995 Jun; 53: 395–400

    Article  PubMed  CAS  Google Scholar 

  47. Miller PD, Brewster S, Reynard J, et al. Prostatic morphometry following treatment with finasteride [abstract]. J Urol 1993 Apr; 149 Suppl.: 432A

    Google Scholar 

  48. Norman RW, Rittmaster RS, Thomas L, et al. Temporal changes in prostatic histology following treatment with finasteride [abstract]. J Urol 1994 May; 151 Suppl.: 267A

    Google Scholar 

  49. Tempany CMC, Partin AW, Zerhouni EA, et al. The influence of finasteride on the volume of the peripheral and periurethral zones of the prostate in men with benign prostatic hyperplasia. Prostate 1993; 22(1): 39–42

    Article  PubMed  CAS  Google Scholar 

  50. Prahalada SR, Keenan KP, Hertzog PR, et al. Qualitative and quantitative evaluation of prostatic histomorphology in rats following chronic treatment with finasteride, a 5-alpha reductase inhibitor. Urology 1994 May; 43: 680–5

    Article  PubMed  CAS  Google Scholar 

  51. Tammela TLJ, Kontturi MJ. Urodynamic effects of finasteride in the treatment of bladder outlet obstruction due to benign prostatic hyperplasia. J Urol 1993 Feb; 149: 342–4

    PubMed  CAS  Google Scholar 

  52. Tammela TLJ, Kontturi MJ. Long-term effects of finasteride on invasive urodynamics and symptoms in the treatment of patients with bladder outflow obstruction due to benign prostatic hyperplasia. J Urol 1995 Oct; 154: 1466–9

    Article  PubMed  CAS  Google Scholar 

  53. Kirby RS, Vale J, Bryan J, et al. Long-term urodynamic effects of finasteride in benign prostatic hyperplasia: a pilot study. Eur Urol 1993; 24: 20–6

    PubMed  CAS  Google Scholar 

  54. Carlin JR, Höglund P, Eriksson L-O, et al. Disposition and pharmacokinetics of [14C]finasteride after oral administration in humans. Drug Metab Dispos 1992 Mar–Apr; 20: 148–55

    PubMed  CAS  Google Scholar 

  55. Ohtawa M, Morikawa H, Shimazaki L. Phannacokinetics and biochemical efficacy after single and multiple oral administration of N-(2-methyl-2-propyl)-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide, a new type of specific competitive inhibitor of testosterone 5α-reductase, in volunteers. Eur J Drug Metab Pharmacokinet 1991; 16: 15–21

    Article  PubMed  CAS  Google Scholar 

  56. Huskey S-EW, Dean DC, Miller RR, et al. Identification of human cytochrome P450 isozymes responsible for the in vitro oxidative metabolism of finasteride. Drug Metab Dispos 1995 Oct; 23: 1126–35

    PubMed  CAS  Google Scholar 

  57. Gregoire S, Winchell G, Constanzer M, et al. The effect of renal function on the disposition of finasteride, a new 5α-reductase inhibitor [abstract]. J Clin Pharmacol 1991; 31: 859

    Google Scholar 

  58. McConnell JD, Bruskewitz R, Walsh P, et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. N Engl J Med 1998; 338(9): 557–63

    Article  PubMed  CAS  Google Scholar 

  59. Merck and Co. Inc.The long term effects of finasteride in patients with moderate symptoms of benign prostatic hyperplasia: how to optimize patient management. (Data on file)

  60. Marberger MJ, PROWESS Study Group. Long-term effects of finasteride in patients with benign prostatic hyperplasia: a double-blind, placebo-controlled, multicenter study. Urology 1998; 51: 677–86

    Article  PubMed  CAS  Google Scholar 

  61. Boyle P, Gould AL, Roehrborn CG. Prostate volume predicts outcome of treatment of benign prostatic hyperplasia with finasteride: meta-analysis of randomized clinical trials. Urology 1996 Sep; 48: 398–405

    Article  PubMed  CAS  Google Scholar 

  62. Boyle P, Gould L, Roehrborn CG, et al. Baseline serum prostate specific antigen (PSA) levels predict degree of symptom improvement following therapy of benign prostatic hyperplasia (BPH) with finasteride [abstract no. 524]. J Urol 1997 Apr; 157 Suppl: 134

    Article  Google Scholar 

  63. Lepor H, Williford W. Factors predicting response to medical therapy for BPH: an anlysis of the V.A. study [abstract no. 810]. Urology 1997; 80 Suppl. 2: 207

    Google Scholar 

  64. Lepor H, Williford WO, Barry MJ, et al. The impact of medical therapy on bother due to symptoms, quality of life and global outcome, and factors predicting response. J Urol 1998; 160: 1358–67

    Article  PubMed  CAS  Google Scholar 

  65. US finasteride/doxazosin trial in BPH. Scrip Sep 19; 2061: 21

  66. Plosker GL, Brogden RN. Serenoa repens (Permixon): a review of its pharmacology and therapeutic efficacy in benign prostatic hyperplasia. Drugs Aging 1996; 9(5): 379–95

    Article  PubMed  CAS  Google Scholar 

  67. Fitzpatrick JM, Dreikorn K, Habib F, et al. Medical management of benign prostatic hyperplasia other than with hormones of alpha blockers. Prog Clin Biol Res 1994; 386: 303–9

    PubMed  CAS  Google Scholar 

  68. Hamdy FC, Chopin DK, Authié D, et al. Prostatic volume does not correlate with efficacy of treatment for mild to moderate benign prostatic hyperplasia using either finasteride or phytotherapy (Permixon). Br J Urol 1997; 80 Suppl. 2: 195

    Article  Google Scholar 

  69. Andersen JT, Nickel JC, Marshall VR, et al. Finasteride significantly reduces acute urinary retention and need for surgery in patients with symptomatic benign prostatic hyperplasia. Urology 1997; 49: 839–45

    Article  PubMed  CAS  Google Scholar 

  70. Agha AH, Roy JB, Culkin DJ. The impact of 5-alpha-reductase inhibitors on the number of prostatectomies for benign prostatic hyperplasia. Adv Ther 1995 Nov–Dec; 12: 361–6

    PubMed  CAS  Google Scholar 

  71. Ekman P, Scandinavian Finasteride Study Group. Maximum efficacy of finasteride is obtained within 6 months and maintained over 6 years. Eur Urol 1998; 33: 312–7

    Article  PubMed  CAS  Google Scholar 

  72. Beisland HO, Binkowitz B, Brekkan E, et al. Scandinavian clinical study of finasteride in the treatment of benign prostatic hyperplasia. Eur Urol 1992; 22: 271–7

    PubMed  CAS  Google Scholar 

  73. Wilton L, Pearce G, Edet E, et al. The safety of finasteride used in benign prostatic hypertrophy: a non-interventional observational cohort study in 14,772 patients. Br J Urol 1996 Sep; 78: 379–84

    Article  PubMed  CAS  Google Scholar 

  74. Merck. Proscar 5mg (finasteride once daily) prescribing information. Philadelphia (PA): Merck

  75. Green L, Wysowski DK, Fourcroy JL. Gynecomastia and breast cancer during finasteride therapy [letter]. N Engl J Med 1996 Sep 12; 335: 823

    Article  PubMed  CAS  Google Scholar 

  76. Kirby KA. Gynecomastia after finasteride therapy. South Med J 1995 Oct; 88: S136

    Article  Google Scholar 

  77. Cook T, Stoner E, Shapiro D, et al. Efficacy is maintained with long term use of finasteride, with no increase in adverse experiences [abstract]. J Urol 1993 Apr; 149 Suppl.: 431A

    Google Scholar 

  78. Haan J, Hollander JMR, van Duinen SG, et al. Reversible severe myopathy during treatment with finasteride. Muscle Nerve 1997; 20: 502–4

    Article  PubMed  CAS  Google Scholar 

  79. Stoner E, Round E, Ferguson D, et al. Clinical experience of the detection of prostate cancer in patients with benign prostate hyperplasia treated with finasteride. J Urol 1994 May; 151: 1296–300

    PubMed  CAS  Google Scholar 

  80. Berry SJ, Coffey DS, Walsh PC, et al. The development of human benign prostatic hyperplasia with age. J Urol 1984; 132: 474–9

    PubMed  CAS  Google Scholar 

  81. Drummond MF, McGuire AJ, Black NA, et al. Economic burden of treated benign prostatic hyperplasia in the United Kingdom. Br J Urol 1993; 71: 290–6

    Article  PubMed  CAS  Google Scholar 

  82. Goluboff ET, Olsson CA. Urologists on a tightrope: coping with a changing economy. J Urol 1994; 151: 1–4

    PubMed  CAS  Google Scholar 

  83. Holtgrewe HL. Economic issues and the management of benign prostatic hyperplasia. Urology 1995 Sep; 46 Suppl. 3A: 23–5

    Article  PubMed  CAS  Google Scholar 

  84. Lowe FC, McDaniel RL, Chmiel JJ. Economic modeling to assess the costs of treatment with finasteride, terazosin, and transurethral resection of the prostate for men with moderate to severe symptoms of benign prostatic hyperplasia. Urology 1995 Oct; 46: 477–83

    Article  PubMed  CAS  Google Scholar 

  85. Baladi J-F, Menon D, Otten N. An economic evaluation of finasteride for treatment of benign prostatic hyperplasia. Pharmacoeconomics 1996 May; 9: 443–54

    Article  PubMed  CAS  Google Scholar 

  86. Cockrum PC, Finder SF, Ries AJ, et al. A pharmacoeconomic analysis of patients with symptoms of benign prostatic hyperplasia. Pharmacoeconomics 1997 Jun; 11(6): 550–65

    Article  PubMed  CAS  Google Scholar 

  87. Girman CJ, Kolman C, Liss CL, et al. Effects of finasteride on health-related quality of life in men with symptomatic benign prostatic hyperplasia. Prostate 1996 Aug; 29: 83–90

    Article  PubMed  CAS  Google Scholar 

  88. Byrnes CA, Morton AS, Liss CL, et al. Efficacy, tolerability, and effect on health-related quality of life of finasteride versus placebo in men with symptomatic benign prostatic hyperplasia: a community-based study. Clin Ther 1995 Sep–Oct; 17: 956–69

    Article  PubMed  CAS  Google Scholar 

  89. Kaplan SA, Olsson CA. Patient satisfaction with finasteride in the treatment of symptomatic benign prostatic hyperplasia. Clin Ther 1996 Jan–Feb; 18: 73–83

    Article  PubMed  CAS  Google Scholar 

  90. Vashi V, Chung M, Hilbert J, et al. Pharmacokinetic interaction potential between doxazosin or terazosin and finasteride in healthy volunteers [abstract no. 10]. J Clin Pharmacol 1997; 37: 860

    Google Scholar 

  91. Cavanaugh J, Samara E, Eason C, et al. Lack of adverse pharmacokinetic and pharmacodynamic interactions between terazosin and finasteride [abstract]. Clin Pharmacol Ther 1995 Feb; 57: 171

    Google Scholar 

  92. Winchell GA, Grégoire S, Taylor AM, et al. Finasteride, a steroid 5α-reductase inhibitor, does not affect the oxidative metabolism of antipyrine. J Clin Pharmacol 1993 Oct; 33: 967–70

    PubMed  CAS  Google Scholar 

  93. Clark RL, Anderson CA, Prahalada S, et al. Critical developmental periods for effects on male rat genitalia induced by finasteride, a 5α-reductase inhibitor. Toxicol Appl Pharmacol 1993 Mar; 119: 34–40

    Article  PubMed  CAS  Google Scholar 

  94. Imperato McGinley J, Sanchez RS, Spencer JR, et al. Comparison of the effects of the 5α-reductase inhibitor finasteride and the antiandrogen flutamide on prostate and genital differentiation: dose-response studies. Endocrinology 1992 Sep; 131: 1149–56

    Article  PubMed  CAS  Google Scholar 

  95. Spencer JR, Torrado T, Sanchez RS, et al. Effects of flutamide and finasteride on rat testicular descent. Endocrinology 1991 Aug; 129: 741–8

    Article  PubMed  CAS  Google Scholar 

  96. George FW, Johnson L, Wilson JD. The effect of a 5α-reductase inhibitor on androgen physiology in the immature male rat. Endocrinology 1989; 125: 2434–8

    Article  PubMed  CAS  Google Scholar 

  97. Jonler M, Riehmann M, Bruskewitz RC. Benign prostatic hyperplasia. Current pharmacological treatment. Drugs 1994 Jan; 47: 66–81

    CAS  Google Scholar 

  98. Monda JM, Oesterling JE. Medical treatment of benign prostatic hyperplasia: 5α-reductase inhibitors and α-adrenergic antagonists. Mayo Clin Proc 1993 Jul; 68: 670–9

    PubMed  CAS  Google Scholar 

  99. Amin EA, Amin M. Comparison of the cost-effectiveness of various therapies for common prostatic disorders. Pharmacoeconomics 1992 May; 1: 357–69

    Article  PubMed  CAS  Google Scholar 

  100. Oesterling JE. Benign prostatic hyperplasia: choosing the best therapy for each patient. J Clin Outcome Manage 1996 Jan–Feb; 3: 43–50

    Google Scholar 

  101. Shapiro E, Hartanto V, Lepor H. The response to alpha blockade in benign prostatic hyperplasia is related to the percent area density of prostate smooth muscle. Prostate 1992; 21: 297

    Article  PubMed  CAS  Google Scholar 

  102. Wilde MI, Fitton A, Sorkin EM. Terazosin: a review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential in benign prostatic hyperplasia. Drugs Aging 1993 May–Jun; 3: 258–77

    Article  PubMed  CAS  Google Scholar 

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Authors and Affiliations

  1. Adis International Limited, 41 Centorian Drive, Private Bag 65901, Mairangi Bay, Auckland 10, New Zealand

    Michelle I. Wilde & Karen L. Goa

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  1. Michelle I. Wilde
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  2. Karen L. Goa
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Correspondence to Michelle I. Wilde.

Additional information

Various sections of the manuscript reviewed by: A.H. Agha, Department of Urology, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma, USA; J.T. Andersen, Department of Urology, Frederiksberg Hospital, University of Copenhagen, Frederiksberg, Denmark; J-F. Baladi, Canadian Coordinating Office for Health Technology Assessment, Ottawa, Ontario, Canada; P. Ekman, Department of Urology, Karolinska Hospital, Stockholm, Sweden; F.C. Lowe, Department of Urology, St Luke’s Roosevelt Hospital Center, New York, New York, USA; H. Matzkin, Department of Urology, Tel Aviv Medical Center, Tel Aviv, Israel; K.G. Naber, Department of Urology, Elisabeth Hospital, Straubing, Germany, J. Nacey, Department of Urology, Wellington School of Medicine, Wellington, New Zealand; M.J. Naslund, Division of Urology, Department of Surgery, University of Maryland Medical Systems, Baltimore, Maryland, USA; B. Standaert, Oncology Centre, Antwerp, Belgium; G. Strauch, Institut de Recherche Therapeutique, C.H.U. Cochin-Port Royal, Paris, France; H. Weisser, Institute of Clinical Chemistry and Laboratory Medicine, University Clinic Bergmannsheil, Bochum, Germany.

Data Selection

Sources: Medical literature published in any language since 1966 on finasteride, identified using AdisBase (a proprietary database of Adis International, Auckland, New Zealand), Medline and EMBASE. Additional references were identified from the reference lists of published articles. Bibliographical information, including contributory unpublished data, was also requested from the company developing the drug.

Search strategy: AdisBase search terms were ‘finasteride’ and ‘prostatic hypertrophy’. Medline and EMBASE search terms were ‘finasteride’ and ‘benign prostatic hyperplasia’. Searches were last updated 2 February 1999.

Selection: Studies in patients with benign prostatic hyperplasia who received finasteride. Inclusion of studies was based mainly on the methods section of the trials. When available, large, well controlled trials with appropriate statistical methodology were preferred. Relevant pharmacodynamic and pharmacokinetic data are also included.

Index terms: finasteride, benign prostatic hyperplasia, pharmacodynamics, pharmacokinetics, therapeutic use, tolerability, drug interactions, dosage and administration, pharmacoeconomics, quality of life.

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Wilde, M.I., Goa, K.L. Finasteride. Drugs 57, 557–581 (1999). https://doi.org/10.2165/00003495-199957040-00008

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