Jacobsen SJ et al. (2008) Association between 5-α reductase inhibition and risk of hip fracture. JAMA 300: 1660–1664

The effect of 5-α reductase inhibitors such as finasteride—a first-line therapy for benign prostatic hyperplasia—on long-term bone health is unclear. These agents inhibit conversion of testosterone to dihydrotestosterone, a compound thought to have a role in bone metabolism. Jacobsen et al. carried out a case–control study of hip fracture in men in order to evaluate the role of 5-α reductase inhibition in bone metabolism.

Data were collected from Kaiser Permanente Southern California, an integrated managed-care organization. Jacobsen and colleagues assessed medical records from 7,076 men who had a first hip fracture (mean age at diagnosis 77 years) during 1997–2006, and 7,076 control men without hip fracture matched by age and medical center. Benign prostatic hyperplasia was diagnosed in 2,547 (36%) of patients with hip fracture and 2,488 (35%) of controls, respectively. Use of 5-α reductase inhibitors from 1991 onward was identified from electronic data on prescriptions. In total, 109 (1.5%) of patients with hip fracture and 141 (2.0%) of controls had previously used finasteride or dutasteride.

No direct association between 5-α reductase inhibitor therapy and hip fracture was observed. Indeed, Jacobsen and colleagues' findings suggest that 5-α reductase inhibitors might even reduce the risk of hip fracture. The authors attribute the apparent risk reduction to hormonal mechanisms, but recommend further studies to identify the biological mechanisms involved. Such studies could reveal new insights that could be exploited for fracture prevention.