Finasteride, a specific and competitive inhibitor of 5alpha-reductase
enzyme Type 2, inhibits the conversion of
testosterone to
dihydrotestosterone (DHT). In adults, DHT acts as primary
androgen in prostate and hair follicles. The only FDA-approved dermatological indication of
finasteride is
androgenetic alopecia. But, apprehension regarding sexual dysfunction associated with
finasteride deters dermatologists from prescribing the
drug and patients from taking the
drug for
androgenetic alopecia.
Testosterone, through its humoral endocrine and local paracrine effects is relevant in central and peripheral modulation of sexual function than locally acting DHT. Several large population-based long-term placebo-controlled studies, using International Index of Erectile Function-5 questionnaire and objective method (Nocturnal Penile Tumescence) to assess the erectile function have demonstrated no clear evidence of the negative effect of
finasteride on erectile function. Reduction in ejaculatory volume is the only established causal relationship between
finasteride and sexual dysfunction. Though
finasteride causes significant reduction in all the semen parameters except sperm morphology, they did not fall below the threshold levels to interfere with fertility. Therefore, the sexual adverse effects associated with
finasteride should be viewed in relation to normal prevalence and natural history of
erectile dysfunction in the population, age of the patient, other confounding factors and also nocebo effect. The impact of
finasteride on the prevention of
prostate cancer has been discussed extensively.
Finasteride is found to be effective in significantly reducing the incidence of low-grade
prostate cancer. But the paradoxical increase in high-grade
cancer in the
finasteride group has been attributed to increased sensitivity and improved performance of
prostate specific antigen levels to detect all grades of
prostate cancer.