title: Influence of finasteride on free and total serum prostate specific antigen levels in men with benign prostatic hyperplasia.
abstract: OBJECTIVE
  Finasteride therapy for benign prostatic hyperplasia (BPH) results in a marked lowering of serum prostate specific antigen (PSA) levels. However, little is known about the effect of finasteride on unbound or free serum levels of PSA. Such information would be important since percent free PSA may substantially improve the cancer specificity of PSA testing. Thus, we prospectively studied the effect of finasteride therapy on total and free serum PSA levels.
  
  
  METHODS
  In a randomized, placebo controlled, double-blind trial 40 men with histologically confirmed BPH (age range 52 to 78 years) were treated with either 5 mg. finasteride daily (26 patients) for 9 months or placebo (14) for 6 months. Prostate volume was assessed by transrectal ultrasound. Serum levels of free and total PSA were measured from archived serum samples stored at -70C at baseline and for as long as 9 months of treatment.
  
  
  RESULTS
  In the finasteride group mean total PSA levels declined from 3.0 ng./ml. at baseline to 1.5 ng./ml. after 6 months of treatment (50% decrease, p <0.01). In the placebo group, with similar baseline levels, no significant change was observed. PSA density declined significantly in finasteride treated men (p <0.01) but not in men receiving placebo. The mean percent free PSA (13 to 17% at baseline) was not altered significantly by finasteride or placebo.
  
  
  CONCLUSIONS
  Total PSA serum levels decreased by an average of 50% during finasteride therapy but percent free PSA did not change significantly. This information is potentially useful in the interpretation of PSA data used for early detection of prostate cancer in men receiving finasteride. However, further studies are required to demonstrate the use of percent free PSA to detect the development of cancer.
authors.affiliation: James Buchanan Brady Urological Institute and the Department of Clinical Chemistry, Johns Hopkins Medical Institution, Baltimore, Maryland, USA.
authors.forename: J
authors.initials: J
authors.lastname: Pannek
authors.forename: L S
authors.initials: LS
authors.lastname: Marks
authors.forename: J D
authors.initials: JD
authors.lastname: Pearson
authors.forename: H G
authors.initials: HG
authors.lastname: Rittenhouse
authors.forename: D W
authors.initials: DW
authors.lastname: Chan
authors.forename: E D
authors.initials: ED
authors.lastname: Shery
authors.forename: G J
authors.initials: GJ
authors.lastname: Gormley
authors.forename: E N
authors.initials: EN
authors.lastname: Subong
authors.forename: C A
authors.initials: CA
authors.lastname: Kelley
authors.forename: E
authors.initials: E
authors.lastname: Stoner
authors.forename: A W
authors.initials: AW
authors.lastname: Partin
mesh_terms: D000368:Aged; D004311:Double-Blind Method; D018120:Finasteride / Q000494:pharmacology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D017430:Prostate-Specific Antigen / Q000097:blood* / Q000187:drug effects*; D011470:Prostatic Hyperplasia / Q000097:blood* / Q000188:drug therapy*
chemical_list: D018120:Finasteride; D017430:Prostate-Specific Antigen