CXCL13 Is a Biomarker of Anti-Leucine-Rich Glioma-Inactivated Protein 1 Encephalitis Patients [Letter]
Authors Wei M, Duan Z
Received 30 October 2019
Accepted for publication 13 January 2020
Published 20 January 2020 Volume 2020:16 Pages 181—182
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Jun Chen
Mingyu Wei, 1 Zuowei Duan 2
1Medical College of Yangzhou University, Yangzhou 225000, Jiangsu, People’s Republic of China; 2Department of Neurology, The Affiliated Hospital of Yangzhou University, Yangzhou 225000, Jiangsu, People’s Republic of China
Correspondence: Zuowei Duan
We recently read the original report by Lin and colleagues with great interest. In this study, the authors concluded that both serum and cerebrospinal fluid (CSF) levels of CXCL13, a B cell chemotactic factor, were significantly higher in patients with anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis compared to non-inflammatory neurologic disorder control groups. 1 However, we have some concerns about the interpretation of their data.
A Response to Letter has been published for this article.
View the original paper by Lin and colleagues.
We recently read the original report by Lin and colleagues with great interest. In this study, the authors concluded that both serum and cerebrospinal fluid (CSF) levels of CXCL13, a B cell chemotactic factor, were significantly higher in patients with anti-leucine-rich glioma-inactivated protein 1 (anti-LGI1) encephalitis compared to non-inflammatory neurologic disorder control groups.1 However, we have some concerns about the interpretation of their data.
Previous research has shown that patients with anti-LGI1 encephalitis do not show significant cytokine and chemokine alterations in the CSF.2 However, the authors inferred an opposite conclusion that both serum and CSF levels of CXCL13 were significantly higher in patients with anti-LGI1 encephalitis versus non-inflammatory neurologic disorder control groups. Specifically, the dispersion around the mean serum level of CXCL13 (36.32 ± 34.71 pg/mL) was much larger in this study, compared to other cytokine and chemokine levels that remained unchanged between groups. We believe that the statistical significance of this major finding of the study may be over-estimated, as the authors did not use a Bonferroni correction or a multifactorial analysis of variance. Furthermore, the blood-brain barrier permeability as measured by albumin index (i.e., the albumin level ratio, CSF/serum)3 was not accounted for in this study. Therefore, it is unclear if serum or CSF CXCL13 plays a more important role in the pathogenesis of anti-LGI1 encephalitis. Additionally, increased circulating CXCL13 levels can also be found in other autoimmune diseases such as rheumatoid arthritis.4 Thus, the specificity of CXCL13 as a biomarker for anti-LGI1 encephalitis, may not be as high as the authors would predict, due to potential coexistence of anti-LGI1 encephalitis and other autoimmune diseases. We recommend that these potential confounders be noted by the editors to ensure that other researchers are similarly critical in their interpretation of these data.
The authors report no conflicts of interest in this communication.
1. Lin Y, Yang X, Lv J, Liu XW, Wang SJ. CXCL13 is a biomarker of anti-leucine-rich glioma-inactivated protein 1 encephalitis patients. Neuropsychiatr Dis Treat. 2019;15:2909–2915. doi:10.2147/NDT.S222258
2. Byun JI, Lee ST, Moon J, et al. Distinct intrathecal interleukin-17/interleukin-6 activation in anti-N-methyl-d-aspartate receptor encephalitis. J Neuroimmunol. 2016;297:141–147. doi:10.1016/j.jneuroim.2016.05.023
3. Wang Y, Zhu M, Liu C, et al. Blood brain barrier permeability could be a biomarker to predict severity of neuromyelitis optica spectrum disorders: a retrospective analysis. Front Neurol. 2018;9:648. doi:10.3389/fneur.2018.00648
4. Bao Y, Wang J, Dai Z, et al. Increased circulating CXCL13 levels in systemic lupus erythematosus and rheumatoid arthritis: a meta-analysis. Clin Rheumatol. 2019:1–10 doi:10.1007/s10067-019-04775-z
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