Relationship between bone turnover and density with teriparatide, denosumab or both in women in the DATA study.
Relationship between bone turnover and density with teriparatide, denosumab or both in women in the DATA study.
复制标题
数据研究中女性特立帕肽、狄诺塞麦或两者的骨转换和密度之间的关系。
DOI:
10.1016/j.bone.2016.11.009
复制
发表时间:
2017
期刊:
影响因子:
4.1
通讯作者:
Leder,BZ
中科院分区:
文献类型:
--
作者:
Tsai,JN;Burnett-Bowie,SM;Lee,H;Leder,BZ
BackgroundWhile changes in biochemical markers of bone turnover (BTM) have been reported to predict changes in bone mineral density (BMD), the relationship between changes in BMD and BTMs with combined antiresorptive/anabolic therapy is unknown.MethodsIn the DATA study, 94 postmenopausal osteoporotic women (ages 51–91) received either teriparatide 20-mcg SC daily, denosumab 60-mg SC every 6 months, or both for 2 years. Pearson's correlation coefficients (R) were calculated to determine the relationship between baseline and early changes in BTMs (as well as serum sclerostin) and 2-year changes in BMD.ResultsIn women receiving teriparatide, baseline BTMs did not correlate with 2-year BMD changes though 12-month increases in osteocalcin and P1NP were associated with 2-year increases in spine BMD. In women receiving denosumab, spine and hip BMD gains correlated with both baseline and changes in P1NP and C-telopeptide. In women receiving combined teriparatide/denosumab, while both baseline and decreases in P1NP were associated with spine BMD gains, distal radius increases were associated with less CTX suppression. Neither baseline nor changes in serum sclerostin correlated with BMD in any treatment group.Summary and conclusionsIn women treated with teriparatide or denosumab, early BTM changes (increases and decreases, respectively) predict 2-year BMD gains, especially at the spine. In women treated with combined teriparatide/denosumab therapy, BMD increases at the distal radius were associated with less suppression of bone turnover. These results suggest that efficacy of combination therapy at cortical sites such as the radius may depend on residual bone remodeling despite RANKL inhibition.