title: Antiandrogen drugs lower serum prostate-specific antigen (PSA) levels in hirsute subjects: evidence that serum PSA is a marker of androgen action in women.
abstract: Assay by ultrasensitive methods of serum prostate-specific antigen (PSA) recently demonstrated that many women have detectable levels of this molecule. Interestingly, serum PSA concentrations were higher in hirsute than in nonhirsute subjects, suggesting that, also in females, PSA may be regulated by androgens. To establish the potential for this assay as a biochemical marker of androgen action in women, we studied 40 hirsute subjects recruited in a double-blind, placebo-controlled, 6-month trial assessing the effects of 3 different antiandrogen drugs: spironolactone, flutamide, or finasteride. In each subject, serum PSA, free testosterone, and 3alpha-androstanediol glucuronide were determined at baseline and at the end of treatments. At baseline, PSA concentrations were higher in these 40 women than in 19 nonhirsute healthy controls (12.9+/-1.5 vs. 4.9+/-0.7 pg/mL, P = 0.03) and significantly correlated with serum free testosterone (r = 0.37, P<0.005). After treatments, the 29 hirsute subjects given active drugs showed significant reduction of serum PSA levels (7.2+/-1.4 vs. 14.7+/-3.0 pg/mL, P = 0.002). This phenomenon was correlated to baseline PSA values. No change was found in the placebo group. In conclusion, serum PSA is increased in many hirsute women. A 6-month course of antiandrogen treatments with spironolactone, flutamide, or finasteride determines a reduction of PSA levels in these subjects. These results suggest that serum PSA is a biochemical marker of androgen action in tissues of female subjects.
authors.affiliation: Division of Endocrinology and Metabolic Diseases, University of Verona, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Negri
authors.forename: F
authors.initials: F
authors.lastname: Tosi
authors.forename: R
authors.initials: R
authors.lastname: Dorizzi
authors.forename: A
authors.initials: A
authors.lastname: Fortunato
authors.forename: G G
authors.initials: GG
authors.lastname: Spiazzi
authors.forename: M
authors.initials: M
authors.lastname: Muggeo
authors.forename: R
authors.initials: R
authors.lastname: Castello
authors.forename: P
authors.initials: P
authors.lastname: Moghetti
mesh_terms: D000328:Adult; D000726:Androgen Antagonists / Q000627:therapeutic use*; D000728:Androgens / Q000502:physiology*; D015113:Androstane-3,17-diol / Q000031:analogs & derivatives / Q000097:blood; D015415:Biomarkers; D004311:Double-Blind Method; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005260:Female; D018120:Finasteride / Q000627:therapeutic use; D005485:Flutamide / Q000627:therapeutic use; D006628:Hirsutism / Q000097:blood* / Q000188:drug therapy*; D006801:Humans; D017430:Prostate-Specific Antigen / Q000097:blood*; D013148:Spironolactone / Q000627:therapeutic use; D013739:Testosterone / Q000097:blood
chemical_list: D000726:Androgen Antagonists; D000728:Androgens; D015415:Biomarkers; D004791:Enzyme Inhibitors; D015113:Androstane-3,17-diol; C028895:androstane-3,17-diol glucuronide; D013148:Spironolactone; D013739:Testosterone; D018120:Finasteride; D005485:Flutamide; D017430:Prostate-Specific Antigen