Faculty of Pharmacy, University of Montreal, Pavillon Jean-Coutu, 2940 chemin de la polytechnique, Montreal, QC, Canada, H3C 3J7.
Osteoporos Int. 2013 Sep;24(9):2483-92. doi: 10.1007/s00198-013-2321-x. Epub 2013 Mar 16.
Prevention of bone mineral density loss in rheumatoid arthritis (RA) has been associated with use of biologic disease-modifying anti-rheumatic drugs (DMARDs). However, in this study, we could not demonstrate a reduction in the risk of non-vertebral fractures. Additional research is required to clarify the impact of biologic DMARDs on fracture risk in RA.
Small studies have suggested biologic DMARDs preserve bone mineral density at 6-12 months. Our objective was to determine the association between biologic DMARD use and the risk of non-vertebral osteoporotic fractures in RA subjects aged ≥50 years.
A nested case-control study was conducted using Quebec physician billing and hospital discharge data. RA subjects were identified from International Classification of Disease-9/10 codes in billing and hospitalisation data and followed from cohort entry until the earliest of non-vertebral osteoporotic fracture, death, or end of study period. Controls were matched to cases (4:1 ratio) on age, sex, and date of cohort entry. Biologic DMARD exposure was defined as being on treatment for ≥180 days pre-fracture (index). Conditional logistic regression was used, adjusting for indicators of RA severity, comorbidity, drugs influencing fracture risk, and measures of health care utilisation.
Over the study period, 1,515 cases were identified (6,023 controls). The most frequent fracture site was hip/femur (42.3%). In total, 172 subjects (49 cases and 123 controls) were exposed to biologic DMARDs. The median duration of exposure was 735 (interquartile range (IQR), 564) and 645 (IQR, 903) days in cases and controls, respectively. We were unable to demonstrate an association between biologic DMARDs and fracture risk (odds ratio, 1.03; 95% confidence interval, 0.42-2.53). RA duration significantly increased the fracture risk.
Despite the positive impact of biologic DMARDs on bone remodelling observed in small studies, we were unable to demonstrate a reduction in the risk of non-vertebral osteoporotic fractures in older adults with RA.
尽管小型研究表明生物 DMARD 可在 6-12 个月内保持骨密度，但我们仍需确定生物 DMARD 的使用与≥50 岁 RA 患者非椎骨骨质疏松性骨折风险之间的关联。
使用魁北克省医生计费和住院数据进行了嵌套病例对照研究。从计费和住院数据中的国际疾病分类第 9/10 代码中识别出 RA 患者，并从队列入组开始对其进行随访，直至发生非椎骨骨质疏松性骨折、死亡或研究期结束。将对照与病例（4:1 比）按年龄、性别和队列入组日期进行匹配。生物 DMARD 暴露定义为在骨折前（索引）至少接受治疗 180 天。采用条件逻辑回归，调整了 RA 严重程度、合并症、影响骨折风险的药物以及医疗保健利用的指标。
在研究期间，共确定了 1515 例病例（6023 例对照）。最常见的骨折部位是髋部/股骨（42.3%）。共有 172 名患者（49 例病例和 123 例对照）暴露于生物 DMARD。病例和对照中暴露的中位时间分别为 735（四分位距（IQR），564）和 645（IQR，903）天。我们无法证明生物 DMARD 与骨折风险之间存在关联（比值比，1.03；95%置信区间，0.42-2.53）。RA 持续时间显著增加了骨折风险。
尽管小型研究表明生物 DMARD 对骨重塑有积极影响，但我们仍无法证明生物 DMARD 可降低老年 RA 患者非椎骨骨质疏松性骨折的风险。
