Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2805446 | Metabolism | 2015 | 7 Pages |
PurposeTo compare denosumab-induced changes in lumbar spine (LS) and femoral neck (FN) bone mineral density (BMD), bone markers and free soluble receptor activator of nuclear factor kappaB ligand (sRANKL) between treatment naïve postmenopausal women with low bone mass (naïve group) and those who were previously treated with a single zoledronic acid infusion (post-Zol group).ProceduresProcollagen type 1 N-terminal propeptide (P1NP), C-terminal cross-linking telopeptide of type 1 collagen (CTx) and sRANKL levels were measured in serum samples obtained at baseline and 3, 6 and 12 months after denosumab initiation. LS and FN BMD were measured at baseline and 12 months.ResultsLS and FN BMD increased significantly in both naïve and post-Zol group (p < 0.001 and p = 0.025 vs. p < 0.001 and p = 0.017, respectively). Despite the higher P1NP and CTx levels in naïve patients at baseline (both p < 0.001), denosumab caused comparable decreases in both groups at month 3, which returned to post-Zol group baseline levels at month 6 and 12 in all patients. Similarly, sRANKL levels decreased significantly at month 3 in both groups and returned to baseline levels at months 6 and 12.ConclusionsIn patients previously treated with zoledronic acid, sequential denosumab treatment is effective in terms of BMD increases and bone turnover suppression. Despite the lower baseline levels in patients pre-treated with zoledronic acid, bone markers are similarly decreased in both groups following denosumab administration and maintain their reversibility. Denosumab reversibly suppresses endogenous free sRANKL levels in both naïve and zoledronic acid pre-treated patients.