TNFα抑制剂治疗RA依然有突破性进展
2017EULAR热点报道：TNFα抑制剂治疗类风湿关节炎依然有突破性进展
高分辨率外周骨定量CT评估类风湿关节炎患者TNFα抑制剂治疗3个月的骨超微结构改变
背景：
骨侵蚀通常在类风湿关节炎（RA）起病后的头几个月内出现，为不可逆性病变。高分辨率外周骨定量CT（HR-pQCT）的分辨率高达81μm，已经成为评估RA骨质改变的有价值的工具。曾有研究报道RA患者在肿瘤坏死因子α（TNFα）抑制剂治疗1年后的骨侵蚀进展极少，但尚无研究探讨TNFα抑制剂治疗开始后的极早期骨质变化。
目的：
TNFα抑制剂治疗3个月后，利用HR-pQCT、放射X线片和3T MRI检测RA患者掌指关节（MCP）和腕关节在骨超微结构和骨侵蚀进展方面的早期变化。
方法：
26例RA患者在基线和治疗3个月后分别接受腕关节3T MRI和MCP、腕关节的HR-pQCT检测，仅在基线时进行X线检查。在基线和治疗3个月时分别评价28个关节疾病活动度评分（DAS28）。患者被分成两组：TNFα抑制剂组和甲氨蝶呤（MTX）单药组。用既往研发出来的方法在HR-pQCT中计算侵蚀体积、关节体积/宽度和骨微结构等参数。关节破坏则在X线和MRI图像上利用Sharp评分和RAMRIS评分分别计算。
结果：
TNFα抑制剂组的患者相对年轻，基线DAS28评分更高，但性别比例、体重指数和病程长短等指标和MTX单药组相似（表格）。从基线到治疗后3个月，TNFα抑制剂组的DAS评分显著改善（图A）。HR-pQCT在基线时共检出骨侵蚀75处。TNFα抑制剂组的MCH3侵蚀体积从基线到治疗后3个月显著下降（MCH2和腕关节均有下降趋势）。相反，MTX单药组的疾病活动度虽低，但MCH2和腕关节的侵蚀体积显著增加（图B）。TNFα抑制剂组的MCP关节间隙宽度和关节体积从基线到治疗后3个月显著缩小，与侵蚀体积变化呈正相关。TNFα抑制剂组的腕关节和MCP微结构参数基本上没有变化，但侵蚀体积改变与骨小梁骨密度（BMD）变化呈显著负相关（图C）。HR-pQCT参数与RAMRIS评分或DAS评分之间未发现明显的相关性。
结论：
我们发现TNFα抑制剂治疗能在前3个月的治疗中防止骨侵蚀进展和骨超微结构退化。HR-pQCT可作为敏感有效的检测工具，即使在短期内也能量化骨质改变，监测RA的治疗。
原文
ASSESSMENT OF 3-MONTH CHANGES IN BONEMICROSTRUCTURE UNDER ANTI-TNFα THERAPY IN PATIENTSWITH RHEUMATOID ARTHRITIS USING HR-PQCT
T. Shimizu 1 , H.J. Choi 1 , U. Heilmeier 1 , M. Tanaka 1 , A.J. Burghardt 1 , J. Gong 1 ,
N. Chanchek 1 , T.M. Link 1 , J. Graf 2 , J.B. Imboden 2 , X. Li 1 .1 Department of Radiology & Biomedical Imaging, Musculoskeletal Quantitative Imaging Research;
2 Department of Medicine, Division of Rheumatology, University of California San Francisco, San Francisco, United States
Background:
Bone erosions are usually thought to be irreversible and occur in the first few months of RA onset. With its resolution of up to 81 μm, HR-pQCT has emerged as valuable tool to assess bone changes in RA (1,2) . Although one previous study showed minimal erosive progression in patients with RA one year after TNFα inhibition therapy(3) , no studies have investigated yet the very early bone changes after the initiation of anti-TNFα treatment.
Objectives:
To investigate the early changes in bone erosion progression and bone microarchitecture in the MCP joints and wrist of RA patients using HR-pQCT, radiographs, and 3T MRI after 3 months of anti-TNFα treatment.
Methods:
26 RA patients underwent 3T MRI wrist scans and HR-pQCT scans of the MCP and wrist joints at baseline (BL) and at 3 months (3M). Radiographs were obtained at the baseline time point only. DAS28 was assessed at BL and 3M. Patients were divided into two groups: the anti-TNFα group and the MTX-only group.HR-pQCT-derived erosion volume, joint volume/width and bone microarchitectural parameters were computed using methods previously developed (4–6) , and the joint destruction was assessed via Sharp and RAMRIS scorings using radiographs and MR images respectively.
Results:
Patients in the Anti-TNFα group were slightly younger than patients in the MTX only group and had a higher initial DAS28 score,but otherwise displayed similar anthropometerics and demographics (Table).DAS scores significantly improved in the anti-TNFα group from BL to 3M (Fig. A).75 erosions were identified at BL by HR-pQCT. The anti-TNFα group showed a significant decrease of erosion volume from BL to 3M at MCH3 (with decreasing trend at MCH2 and wrist). The MTX-only group in contrast, displayed significant increases in erosion volume at MCH2 and wrist despite low disease activity (Fig. B). In the anti TNFα group, joint space width and volume of the MCP joints decreased significantly from BL to 3M and were positively correlated with erosion volume changes. Although microstructural parameters at the wrist and MCP remained largely unchanged, erosion volume changes were significantly negatively correlated with changes of trabecular BMD in the anti-TNFα group (Fig. C). No significant correlations were observed between HR-pQCT parameters and RAMRIS and DAS scores.
Conclusions:
We found that anti-TNFα treatmentcan prevent erosion progression and deterioration of bone microarchitecture within the first 3 months of treatment. HR-pQCT can serve as a sensitive and powerful tool to quantify bone changes and monitor RA treatment even over short time periods.
References:
[1] Barnabe C et al. Nat Rev Rheumatol. 2015.
[2] Tam LS et al. J Rheumatol. 2016.
[3] Moller U et al. Ann Rheum Dis. 2009.
[4] Srikhum W et al. J Rheumatol. 2013.
[5] Yang H et al. Int J Rheum Dis. 2015.
[6] Burghardt AJ et al. Ann Biomed Eng. 2013.
Acknowledgements: The study was supported by UCB Pharma Inc.
Disclosure of Interest: None declared
DOI: 10.1136/annrheumdis-2017-eular.532
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