Bone density threshold and other predictors of vertebral fracture in patients receiving oral glucocorticoid therapy

TLDR

The study aimed to identify predictors of vertebral fractures, including a bone mineral density threshold, in patients on oral glucocorticoids. Using data from two randomized risedronate trials, the authors performed Cox regression to identify fracture predictors in the placebo group and compared 1‑year fracture risk between glucocorticoid users and nonusers to assess a BMD threshold. Baseline lumbar spine BMD and daily glucocorticoid dose were significant predictors of incident fractures, with GC users exhibiting a markedly higher fracture risk (adjusted RR 5.67) than nonusers even when BMD was similar, indicating daily dose—not cumulative dose—drives fracture risk.

Abstract

Abstract Objective To evaluate predictors of vertebral fractures, including a threshold for bone mineral density (BMD), in patients receiving oral glucocorticoids (GCs). Methods Data were obtained from 2 randomized clinical trials (prevention and treatment trials of risedronate) using similar methods, but different inclusion criteria were applied with regard to prior exposure to GCs. Predictors of vertebral fracture in the placebo group were identified using Cox regression with forward selection. The BMD threshold analysis involved a comparison of the 1‐year fracture risk in postmenopausal women receiving placebo in the GC trials with that in postmenopausal women not taking GCs in 3 other trials. Results The study population comprised 306 patients with baseline and 1‐year followup data on vertebral fractures (111 receiving placebo and 195 receiving risedronate). In the placebo group, the statistically significant predictors of incident fracture were the baseline lumbar spine BMD (for each 1‐point decrease in T score, relative risk [RR] 1.85, 95% confidence interval [95% CI] 1.06–3.21) and the daily GC dose (for each 10‐mg dose increase, RR 1.62, 95% CI 1.11–2.36). In the BMD threshold analysis, compared with nonusers of GCs, patients receiving GCs were younger, had a higher BMD at baseline, and had fewer prevalent fractures; nevertheless, the risk of fracture was higher in the GC users compared with nonusers (adjusted RR 5.67, 95% CI 2.57–12.54). The increased risk of fracture was observed in GC users regardless of whether osteoporosis was present. Conclusion The daily, but not cumulative, GC dose was found to be a strong predictor of vertebral fracture in patients receiving GCs. At similar levels of BMD, postmenopausal women taking GCs, as compared with nonusers of GCs, had considerably higher risks of fracture.