PubMed · 16817478
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Takehiko Ogawa. 2006-06-28. [Micropenis].. https://pubmed.ncbi.nlm.nih.gov/16817478/
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PURPOSE: We reviewed the effects of 5alpha-reductase inhibitors on prostate specific antigen and clarified the adjustments that should be made to compensate for these effects to ensure that the usefulness of prostate specific antigen for detecting prostate cancer is maintained. MATERIALS AND METHODS: We reviewed articles published in the scientific literature with relevance to the effects of 5alpha-reductase inhibitors on the usefulness of prostate specific antigen for detecting prostate cancer. RESULTS: A total serum prostate specific antigen of 4.0 ng/ml has traditionally been used as the threshold for triggering prostate biopsy. However, clinical trials of finasteride and dutasteride have shown that 5alpha-reductase inhibitors decrease serum prostate specific antigen in patients with and without prostate cancer. To compensate, the doubling rule has been applied in clinical trials and clinical practice. However, doubling serum prostate specific antigen may overestimate actual prostate specific antigen in some patients receiving 5alpha-reductase inhibitors for up to 6 to 9 months, accurately estimate prostate specific antigen from 1 to 3 years and underestimate it thereafter. An increase in prostate specific antigen of 0.3 ng/ml from nadir as a trigger for biopsy maintains 71% sensitivity for prostate cancer in men receiving dutasteride with 60% specificity, similar to the 4.0 ng/ml prostate specific antigen cutoff using placebo. CONCLUSIONS: We propose that a prostate specific antigen increase from nadir of 0.3 ng/ml or greater could represent an alternative to the doubling rule for monitoring prostate specific antigen in patients on 5alpha-reductase inhibitors. The prostate specific antigen increase from nadir appears to be a more accurate cancer indicator than a doubled value in some patients.
The description of 5alpha-reductase deficiency in male pseudohermaphroditism, characterization of type-1 and type-2 isoenzymes of 5alpha-reductase, and development of 4-aza steroid competitive inhibitors of 5alpha-reductase were milestones in the development of 5alpha-reductase inhibitors, a class of drugs approved for the treatment of symptomatic benign prostatic hyperplasia (BPH). Stromal and epithelial hyperplasia in the region of the prostate that surrounds the urethra begins in the fourth decade of life and by the sixth decade, the prevalence is 50%. Benign prostatic hyperplasia is a frequent cause of lower urinary tract symptoms, urinary tract infection, and acute urinary retention requiring surgical intervention. Medical options for treatment of symptomatic BPH include 1) the 5alpha-reductase inhibitors finasteride and dutasteride, 2) the alpha1-adrenergic antagonists doxazocin, terazosin, tamsulosin, and alfuzosin, and 3) the combination of a 5alpha-reductase inhibitor and a alpha1-adrenergic antagonist. By inhibiting the production of dihydrotestosterone (DHT) locally within the prostate gland, 5alpha-reductase inhibitors have the effect of reducing prostate volume, improving lower urinary tract symptoms, increasing peak urinary flow, and decreasing the risk of acute urinary retention and need for surgical intervention. Alpha-1 adrenergic antagonists relax the smooth muscle of the bladder neck and prostate, thereby decreasing the resistance to urine flow and increasing peak urinary flow and improving lower urinary tract symptoms. The alpha1-adrenergic antagonists are effective in the short-term, and reduce clinical progression of BPH, but do not reduce the long-term risk of urinary retention or need for surgical intervention. The 5alpha-reductase inhibitors are effective in the long-term, especially in men with large prostates, and reduce the clinical progression of BPH, and further reduce the long-term risk of urinary retention and need for surgical intervention. The combination of a 5alpha-reductase inhibitor and a alpha1-adrenergic antagonist significantly reduces the clinical progression of BPH over either drug class alone.
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