Consequences of switching 5alpha-reductase inhibitors on prostate specific antigen velocity.
OBJECTIVE
The 5alpha-reductase inhibitors improve urinary symptoms related to benign prostatic hyperplasia, deter benign prostatic hyperplasia progression and provide prostate cancer chemoprevention. Currently there are a number of 5alpha-reductase inhibitor formularies, including Proscar, generic finasteride and dutasteride. While all formularies decrease serum prostate specific antigen (a proxy for prostate volume), they may not accomplish this to the same degree, which may have dramatic effects on prostate specific antigen kinetics in men changing 5alpha-reductase inhibitor formularies. We examined prostate specific antigen velocity after changes in 5alpha-reductase inhibitor formularies.


METHODS
We identified patients treated with 2 or more 5alpha-reductase inhibitor formularies who had sufficient prostate specific antigen values to calculate prostate specific antigen velocity during each 5alpha-reductase inhibitor treatment. Patient data were grouped depending on the formularies received. Statistical analysis was done to compare prostate specific antigen velocity at various time points while on different 5alpha-reductase inhibitors.


RESULTS
Eight men changed from dutasteride to generic finasteride (group 1), 21 changed from dutasteride to Proscar (group 2), 49 changed from Proscar to dutasteride (group 3) and 77 changed from Proscar to generic finasteride (group 4). We noted a significant increase in prostate specific antigen velocity in groups 1 and 2 (p <0.05), and 4 (p <0.005). The increase was greater than 0.35 ng/ml per year, the common cutoff for prostate biopsy recommendations, in more than a third of patients.


CONCLUSIONS
Results confirm that changing 5alpha-reductase inhibitors drugs can be associated with a clinically significant change in prostate specific antigen velocity. These prostate specific antigen velocity changes could place patients at risk for unnecessary prostate biopsy. Additional prospective studies are warranted.
Helfand
Brian T
BT
Department of Urology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Blackwell
Robert H
RH
McVary
Kevin T
KT
D000368:Aged; D001378:Azasteroids / Q000008:administration & dosage*; D016009:Chi-Square Distribution; D042944:Cholestenone 5 alpha-Reductase / Q000037:antagonists & inhibitors*; D018680:Cholinergic Antagonists / Q000008:administration & dosage; D000068538:Dutasteride; D004791:Enzyme Inhibitors / Q000008:administration & dosage*; D018120:Finasteride / Q000008:administration & dosage*; D006801:Humans; D016014:Linear Models; D008297:Male; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage; D017430:Prostate-Specific Antigen / Q000097:blood* / Q000187:drug effects; D011470:Prostatic Hyperplasia / Q000097:blood / Q000188:drug therapy*; D011471:Prostatic Neoplasms / Q000097:blood; D011788:Quality of Life
D001378:Azasteroids; D018680:Cholinergic Antagonists; D004791:Enzyme Inhibitors; D010726:Phosphodiesterase Inhibitors; D018120:Finasteride; D042944:Cholestenone 5 alpha-Reductase; D017430:Prostate-Specific Antigen; D000068538:Dutasteride