Prolonged treatment with finasteride (a 5α-reductase inhibitor) does not affect bone density and metabolism

OBJECTIVE Since it is not clear whether testosterone or dihydrotestosterone is the active hormone in bone metabolism, we wished to assess the effect of finasteride, a 5α-reductase inhibitor, on vertebral bone mineral density and parameters of bone and mineral metabolism. DESIGN Patients were treated in a randomized, double-blind controlled study with either placebo, 1 or 5 mg/day finasteride. PATIENTS Twenty-three men with benign prostatic hyper-plasla (BPH) were included in this study; eight received placebo, seven were allocated to treatment with 1 mg/day, and eight to 5 mg/day finasteride for 12 months. MEASUREMENTS Vertebral bone mineral density was measured at the lumbar spine by dual energy X-ray bone densltometry. Serum calcium, phosphorus, parathyroid hormone, osteocalcln and vitamin D metabolites were measured regularly. Urinary calcium and creatinlne excretion were monitored as well. RESULTS Finasteride caused a significant decrease in serum dlhydrotestosterone after 6 and 12 months, but no effect on serum testosterone. Vertebral bone mineral density remained unaltered. None of the other parameters monitored were affected except for a small unexplained increase in 1,25-dihydroxyvitamin D in the group receiving 5 mg finasteride/day. CONCLUSIONS Testosterone is probably the active hormone in bone metabolism. However, oestradiol, the product of testosterone aromatization (which remains unaltered under finasteride) may yet be another possible responsible steroid in the maintenance of bone density. We can also not rule out that the small amount of dihydrotestosterone remaining under finasteride administration is sufficient for maintaining normal bone metabolism.