Chopin F, Garnero P, le Henanff A, Debiais F, Daragon A, Roux C, Sany J, Wendling D, Zarnitsky C, Ravaud P, Thomas T
INSERM U890, Rheumatology Department, University Hospital of St-Etienne, France.
Ann Rheum Dis. 2008 Mar;67(3):353-7. doi: 10.1136/ard.2007.076604. Epub 2007 Jul 20.
Rheumatoid arthritis (RA) is associated with systemic bone loss, subchondral bone erosion and cartilage degradation under the control of pro-inflammatory cytokines, including tumour necrosis factor alpha (TNFalpha). Therefore, we tested the hypothesis that administration of infliximab, an anti-TNFalpha drug in the treatment of RA, would modulate systemic and local bone resorption and reduce cartilage degradation.
We performed a prospective study of a multicentric cohort of 48 women, mean (SD) age 54.2 (12.1) years old, with severe RA for 11.4 (7.8) years, who started infliximab after failure of other disease-modifying antirheumatic drugs. At baseline and 6, 22 and 54 weeks after initiating Infliximab therapy we measured the following biochemical markers: pro-collagen serum type I N-terminal propeptide (PINP), a marker of bone formation; serum C-terminal cross-linked telopeptide of type I collagen (CTX-I), a marker of cathepsin K-mediated bone collagen degradation believed to reflect systemic bone resorption; serum C-terminal cross-linked telopeptide of type I collagen (ICTP), an index of matrix metalloprotease (MMP) mediated type I collagen degradation reflecting preferential joint metabolism; and urinary CTX-II a biochemical markers of cartilage degradation. Total hip and lumbar spine bone mineral density (BMD) was assessed at baseline, and after 6 and 12 months by dual-energy x-ray absorptiometry (DXA). No patient received bisphosphonates while 77% were under oral glucocorticoids.
BMD remained stable over 1 year. Serum CTX-I levels rapidly decreased by 19% and 28% at week 6 and week 22, respectively (analysis of variance (ANOVA) p = 0.032) values returning to pre-treatment level at week 54. By contrast, ICTP levels progressively declined with a maximal 25% decrease at week 54 (ANOVA p = 0.028). By contrast, PINP levels remained stable over time, which led to a 30 to 40% improvement in bone remodelling balance, as assessed by the ratios PINP/CTX and PINP/ICTP (p<0.05). There was no significant change of urinary CTX-II in the whole population, but a slight decrease (ANOVA p = 0.041) in those with pre-treatment levels above the upper limit of normal range.
In summary, the improvement in the formation/resorption marker ratio suggests beneficial systemic and local bone effects of infliximab in patients with RA.
类风湿性关节炎(RA)与全身骨质流失、软骨下骨侵蚀以及在包括肿瘤坏死因子α(TNFα)在内的促炎细胞因子控制下的软骨降解有关。因此,我们检验了以下假设:给予英夫利昔单抗(一种用于治疗RA的抗TNFα药物)将调节全身和局部骨吸收并减少软骨降解。
我们对一个多中心队列中的48名女性进行了一项前瞻性研究,这些女性平均(标准差)年龄为54.2(12.1)岁,患有严重RA达11.4(7.8)年,在其他改善病情抗风湿药物治疗失败后开始使用英夫利昔单抗。在开始英夫利昔单抗治疗的基线、第6周、第22周和第54周,我们测量了以下生化标志物:血清I型前胶原N端前肽(PINP),一种骨形成标志物;血清I型胶原C端交联端肽(CTX-I),一种组织蛋白酶K介导的骨胶原降解标志物,被认为反映全身骨吸收;血清I型胶原C端交联端肽(ICTP),一种基质金属蛋白酶(MMP)介导的I型胶原降解指数,反映优先的关节代谢;以及尿CTX-II,一种软骨降解的生化标志物。在基线以及第6个月和第12个月通过双能X线吸收法(DXA)评估全髋和腰椎骨密度(BMD)。没有患者接受双膦酸盐治疗,而77%的患者接受口服糖皮质激素治疗。
BMD在1年内保持稳定。血清CTX-I水平在第6周和第22周分别迅速下降了19%和28%(方差分析(ANOVA)p = 0.032),在第54周时恢复到治疗前水平。相比之下,ICTP水平逐渐下降,在第54周时最大下降了25%(ANOVA p = 0.028)。相比之下,PINP水平随时间保持稳定,这导致通过PINP/CTX和PINP/ICTP比值评估的骨重塑平衡改善了30%至40%(p<0.05)。整个人群中尿CTX-II没有显著变化,但在治疗前水平高于正常范围上限的患者中有轻微下降(ANOVA p = 0.041)。
总之,形成/吸收标志物比值的改善表明英夫利昔单抗对RA患者具有有益的全身和局部骨效应。