Alendronate increased bone mineral density but did not reduce new fractures in glucocorticoid induced osteoporosis

Abstract

Alendronate increased bone mineral density but did not reduce new fractures in glucocorticoid induced osteoporosis Saag KG, Emkey R, Schnitzer TJ, et al, for the Glucocorticoid-Induced Osteoporosis Intervention Study Group. Alendronate for the prevention and treatment of glucocorticoid-induced osteoporosis. N Engl J Med 1998;339:292-9. QuestionIn patients who have osteoporosis that is induced by long term glucocorticoid treatment, is alendronate eVective for increasing bone mineral density (BMD) and reducing new fractures? Design 2 parallel randomised, placebo controlled trials with 48 weeks follow up. Setting centres in the US and 22 centres in other countries.Patients 560 patients who were 17-83 years of age and had rheumatological, pulmonary, dermatological, gastrointestinal, or other diseases that required >1 year of glucocorticoid treatment (daily dose >7.5 mg of prednisone or its equivalent). Exclusion criteria were evidence of metabolic bone disease (other than glucocorticoid induced or postmenopausal osteoporosis), low serum 25-hydroxyvitamin D concentrations, concomitant drug treatments that might aVect bone turnover, pregnancy, lactation, renal insuYciency, severe cardiac disease, or major upper gastrointestinal disease. A 2.5 mg dose of alendronate was used in the multinational study only, and patients allocated to this group (n=83) were not analysed. Patients (n=477, 30% men, 22% premenopausal women, 49% postmenopausal women) were stratified according to duration of glucocorticoid treatment: <4 months (34%), 4-12 months (21%), and >12 months (45%).

Effects of alendronate for treatment of glucocorticoid-induced osteoporosis

“…These results indicate that improvement of BMD of the femoral-neck was not as significant as that of the lumbar spine. [ 20 , 28 ] The reason for this phenomenon may be that the lumbar spine contains more trabecular bone and corticosteroid associated bone loss is greater in bones with higher trabecular bone ratio. [ 32 ] To some extent, similar results were obtained in our study compared with Kan's study.…”

“…Okada concluded that alendronate protects premenopausal women from bone loss and fracture associated with high-dose glucocorticoid therapy. [ 19 ] However, Compston [ 20 ] regarded alendronate as a drug which can increase BMD but could not reduce new fractures along with GIO.…”

Bone health and glucocorticoid‐containing lymphoma therapy — a review of risk factors and preventative measures

“…[38][39][40] Randomized data demonstrate the efficacy of BPs in reducing loss of BMD in GIO, but were not powered to demonstrate reduction in fracture risk in the context of GIO. [41][42][43] More recently denosumab, a fully human anti-RANKL monoclonal antibody, was licensed for prevention of GIO. Randomized data from a study of 795 patients on ≥7.5 mg prednisolone and previous fracture or osteopenia indicate denosumab is superior to risedronate for BMD preservation with a more convenient schedule of a six-monthly subcutaneous injection.…”

“…There are numerous licensed amino‐bisphosphonates, of which the intravenous zoledronic acid (ZA) is the only product specifically licensed for GIO treatment, although oral alendronate (ALN) and risedronate were also licensed for the reduction of fracture risk in postmenopausal women and men at high risk of fracture 38–40 . Randomized data demonstrate the efficacy of BPs in reducing loss of BMD in GIO, but were not powered to demonstrate reduction in fracture risk in the context of GIO 41–43 . More recently denosumab, a fully human anti‐RANKL monoclonal antibody, was licensed for prevention of GIO.…”