A systematic review of CXCL13 as a biomarker of disease and treatment response in rheumatoid arthritis.
A systematic review of CXCL13 as a biomarker of disease and treatment response in rheumatoid arthritis.
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DOI：
10.1186/s41927-020-00154-3
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发表时间：
2020-11-02
期刊：
影响因子：
2.2
通讯作者：
Galloway JB
中科院分区：
文献类型：
--
作者：
Bechman K;Dalrymple A;Southey-Bassols C;Cope AP;Galloway JB
B细胞趋化剂CXCL13是类风湿性关节炎（RA）的一种有前景的生物标志物，在支持诊断、监测疾病活动和作为预后价值方面具有合理的作用。它是一个关键的趋化因子驱动形成淋巴样卵泡在发炎的滑膜。本系统综述的目的是评估CXCL13作为RA中可行的生物标志物的作用。我们对所有已发表的评估CXCL13在RA中的作用的队列和随机对照试验进行了系统的文献综述。主要结局是；i)与健康对照组比较RA患者CXCL13水平，ii) CXCL13与疾病活动标志物之间的相关性，以及iii) CXCL13与治疗反应之间的相关性。检索产生278篇文章，其中31篇符合纳入标准。在评估早期或确诊类风湿性关节炎患者CXCL13表达的12项研究中，均报告其表达水平高于健康对照组。16项研究中有12项报告了CXCL13与疾病活动性标志物（包括DAS28和肿胀关节计数）之间的弱正相关，rho值在0.20-0.67之间。在2项研究中，CXCL13水平与滑膜炎的超声证据相关。18项研究评估了CXCL13对治疗干预的反应。大多数表明对包括生物制剂和Janus激酶（JAK）抑制在内的治疗的反应水平下降。在某些情况下，这种减少只出现在治疗反应者身上。高CXCL13水平预示csdmard患者无法实现疾病缓解。生物制剂治疗预测的证据是相互矛盾的。尽管有证据表明它在诊断类风湿性关节炎和检测滑膜炎中起作用，但本综述中纳入的研究的异质性限制了我们得出可靠结论的能力。目前没有足够的结果来证明在RA常规临床实践中常规使用CXCL13作为生物标志物是合理的。
The B cell chemoattractant CXCL13 is a promising biomarker in rheumatoid arthritis (RA), with a plausible role in supporting diagnosis, monitoring disease activity and as a prognostic value. It is a key chemokine driving the formation of lymphoid follicles within the inflamed synovium. The objective of this systematic review was to evaluate the role of CXCL13 as a viable biomarker in RA. We conducted a systematic literature review of all published cohort and randomised controlled trials evaluating the role of CXCL13 in RA. The primary outcomes were; i) CXCL13 levels in RA patients compared to healthy controls, ii) the correlation between CXCL13 and markers of disease activity, and iii) the association between CXCL13 and treatment response. The search produced 278 articles, of which 31 met the inclusion criteria. Of the 12 studies evaluating CXCL13 expression in early or established RA, all reported higher levels than that seen in healthy controls. Twelve of sixteen studies reported a weakly positive correlation between CXCL13 and markers of disease activity including DAS28 and swollen joint count, with rho values between 0.20–0.67. In 2 studies, CXCL13 levels correlated with ultrasonographic evidence of synovitis. Eighteen studies assessed CXCL13 in response to therapeutic intervention. The majority signified a fall in levels in response to treatment including biologics and Janus kinase (JAK) inhibition. In some, this reduction was only seen in treatment responders. High CXCL13 levels predicted failure to achieve disease remission with csDMARDs. The evidence for treatment prediction with biologics was conflicting. Despite evidence to suggest a role in diagnosing RA and in detecting synovitis, the heterogeneity of studies included in this review limit our ability to draw robust conclusions. At present there are inadequate results to justify the routine use of CXCL13 as a biomarker in RA routine clinical practice.