Finasteride to prevent prostate cancer: Should all men or only a high-risk subgroup be treated? Academic Article uri icon

Overview

MeSH Major

  • Enzyme Inhibitors
  • Finasteride
  • Prostatic Neoplasms

abstract

  • PURPOSE Finasteride has been shown to reduce the incidence of prostate cancer. Yet the use of finasteride remains low, likely because of the risk of adverse effects. We sought to determine whether prostate-specific antigen (PSA) levels could identify a high-risk subgroup for which the benefits of finasteride treatment outweigh the potential harms. PATIENTS AND METHODS Raw data from the Prostate Cancer Prevention Trial were used to model chemopreventive treatment strategies: treat all men, treat no men, or treat a high-risk subgroup based on PSA level. We weighted the benefits (reduction in cancer rate) and harms (treatment rate) of each strategy using numbers-needed-to-treat thresholds-the maximum number of men a clinician would treat with finasteride to prevent one cancer. Results Of 9,058 men, 1,957 were diagnosed with prostate cancer during the 7-year study. For the end point of all cancers, including both for-cause and end-of-study biopsies, the optimal strategy is to treat all or nearly all men. To reduce risk of cancers detected through routine care, treating men with PSA > 1.3 or > 2 ng/mL is optimal. For example, treating only men with PSA > 2 ng/mL reduced the treatment rate by 83% and resulted in a cancer rate only 1.1% higher than treating all men. CONCLUSION Clinicians wishing to reduce the risk of any biopsy-detectable prostate cancer should recommend finasteride to all men. Clinicians who believe that it is unnecessary to prevent all cancers, but that preventing those readily detectable by screening would be desirable, would be best off recommending finasteride only to a high-risk subgroup.

publication date

  • March 2010

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed Central ID

  • PMC2834464

Digital Object Identifier (DOI)

  • 10.1200/JCO.2009.23.5572

PubMed ID

  • 20124185

Additional Document Info

start page

  • 1112

end page

  • 6

volume

  • 28

number

  • 7