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Alendronate for Glucocorticoid-Induced Osteoporosis Does Not Reduce Fracture Risk

Article

A recent review of alendronate for the treatment of glucocorticoid-induced osteoporosis (GIO) found that it significantly increased bone mineral density of the lumbar spine and femoral neck in patients with GIO, but does not appear to reduce the risk of fractures.

A recent review of alendronate for the treatment of glucocorticoid-induced osteoporosis (GIO) found that it significantly increased bone mineral density (BMD) of the lumbar spine and femoral neck in patients with GIO, but does not appear to reduce the risk of fractures.

Alendronate, a second-generation bisphosphonate, inhibits osteoclast activity, reduces bone resorption, and maintains the balance of bone resorption and formation. The researchers wrote that it is the first systematic analysis to evaluate the effect of alendronate on GIO as well as its side effects.

Glucocorticoid use for more than 3 months can cause bone loss and decrease BMD, but when the issue has been previously studied, the efficacy of alendronate on BMD as well as the relative risk of fracture in GIO patients has varied.

For the meta-analysis, authors reviewed PubMed, Embase, the Cochrane Controlled Trials Registry, and the China Academic Journal Network Publishing Databases for randomized controlled trials (RCTs) in patients who received alendronate. Outcome measures that were assessed included BMD changes, bone fractures, and adverse reactions.

Overall, 10 studies involving 1002 patients were included. The efficacy of alendronate in treating GIO was evaluated at different time points during treatment. Meta-analysis was performed using a random effect model, which showed that alendronate treatment significantly increased lumbar spine BMD when compared with treatment with calcium during 6 to 24 months. As statistical heterogeneity was observed, the subgroup analyses were used to obtain more robust estimates at 6, 12, 24 months, respectively.

The results indicated that alendronate administration significantly increased BMD of the lumbar spine. In addition, fixed effects model analysis was carried out to evaluate the effects of alendronate after 24 months administration. The same positive result was identified: pooled SMD was 0.82 (95% CI, 0.58 to 1.05, P <.00001, I2 = 38%).

The femoral neck BMD increased significantly when alendronate was taken for 6 months but no statistical difference was observed after 12 or 24 months. As for nonvertebral fracture or vertebral fracture rate, no statistical differences were observed between alendronate and calcium treatments. There were also no significant differences in terms of gastrointestinal or other side effects.

Alendronate treatment did not significantly change fracture risk nor induce significant differences in adverse gastrointestinal effects. The authors said more RCTs are needed to determine the efficacy of alendronate in the prevention of GIO fracture.

Reference

Wang YK, Zhang Ym, Qin SQ, et al. Effects of alendronate for treatment of glucocorticoid-induced osteoporosis: A meta-analysis of randomized controlled trials. Medicine. 2018;97(42):e12691. doi: 10.1097/MD.0000000000012691.

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