CXC ligand 13 in rheumatoid arthritis and its relation to secondary Sjögren’s syndrome

Sherif, Nahed Mounir; Arafa, Mostafa A.; Ibrahim, Saad M.; Galal, Salwa

doi:10.1016/j.ejr.2013.03.004

Cited by 7 publications

(3 citation statements)

References 23 publications

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“…Correlation RF in ERA (r = 0.54) & EstRA (0.45) Sellam et al (2013) [ 27 ] N = 278. ERA Serum by ELISA ERA > HC Correlation: DAS28-CRP ( r = 0.20) Sherif et al (2013) [ 28 ] N = 30. ERA Serum by ELISA ERA > HC RA + sSS: 137(±63), RA -sSS: 165(±91), HC: 12 (±2.2) Correlation: DAS28-ESR ( r = 0.68), disease duration ( r = 0.41) Ahmed et al (2013) [ 29 ] N = 30.…”

Section: Resultsmentioning

confidence: 99%

“…For the most part, these were weakly positive correlations, with rho values between 0.20–0.67. The strongest correlation was reported in association with DAS28-ESR [ 28 ]. Correlations were also noted with DAS28-CRP [ 17 , 26 , 27 ].…”

Section: Resultsmentioning

confidence: 99%

“…Levels are significantly higher than seen in healthy controls, present in very early RA (even in cases of less than 6 weeks disease duration) [ 25 ] and in both seropositive and seronegative disease, signifying a promising role as a diagnostic marker. However CXCL13 is also expressed in other inflammatory diseases driven by lymphoid organization, for example Sjogren’s syndrome, where levels correlate with the extent of salivary gland inflammation and subsequent lymphoma development [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

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A systematic review of CXCL13 as a biomarker of disease and treatment response in rheumatoid arthritis

et al. 2020

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Background 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. Methods 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. Results 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. Conclusion 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.

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