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[类风湿关节炎关节破坏的早期预测]

[Early prediction of joint destruction in rheumatoid arthritis].

作者信息

Eguchi Katsumi

机构信息

Nagasaki University, Graduate School of Biomedical Sciences, First Department of Internal Medicine.

出版信息

Clin Calcium. 2007 Apr;17(4):517-25.

Abstract

It is proposed by hypothesis that early intervention in rheumatoid arthritis might result in remission or cure. It was undertaken to classify rheumatoid arthritis (RA) in early stage from undifferentiated arthritis (UA) and predict the progression of joint destruction at the first visit using by serological markers and magnetic resonance imaging (MRI) . Logistic regression analysis using the statistical analysis system software demonstrated that the presence of anti-cyclic citrullinated peptide (CCP) antibody and/or immunoglobulin M-rheumatoid factor (IgM-RF) , symmetric synovitis and bone marrow edema and/or bone erosion at entry could discriminate patients with RA from UA or other than RA. A total score of two or more of the three objective measures allowed the prediction for RA with 83% sensitivity and 85% specificity, respectively. The presence of bone marrow edema and/or bone erosion determined by MRI is a forerunner of bone erosion on plain radiography. Both presences of anti-CCP antibody and/or IgM-RF and bone marrow edema determined by MRI may predict the early-stage of RA and the progression of articular destruction. From the above findings, it was recommended that early intervention of anti-rheumatic drugs and/or TNF blocker should be started the UA patients with both autoantibody (anti-CCP antibody and/or IgM-RF) and bone marrow edema determined by MRI.

摘要

假设提出,类风湿关节炎的早期干预可能会导致缓解或治愈。本研究旨在从未分化关节炎(UA)中对早期类风湿关节炎(RA)进行分类,并使用血清学标志物和磁共振成像(MRI)在首次就诊时预测关节破坏的进展。使用统计分析系统软件进行的逻辑回归分析表明,抗环瓜氨酸肽(CCP)抗体和/或免疫球蛋白M类风湿因子(IgM-RF)的存在、对称性滑膜炎以及初诊时的骨髓水肿和/或骨质侵蚀可将RA患者与UA或非RA患者区分开来。三项客观指标中两项或以上的总分分别以83%的敏感性和85%的特异性预测RA。MRI确定的骨髓水肿和/或骨质侵蚀是X线平片骨质侵蚀的先兆。抗CCP抗体和/或IgM-RF的存在以及MRI确定的骨髓水肿均可预测RA的早期阶段和关节破坏的进展。根据上述研究结果,建议对MRI确定同时存在自身抗体(抗CCP抗体和/或IgM-RF)和骨髓水肿的UA患者尽早开始抗风湿药物和/或肿瘤坏死因子阻滞剂干预。

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