Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder

Background: Neurofilament light chain (NfL) and glial fibrilliary acidic protein (GFAP) have been suggested to be biomarkers of the pathophysiological process of neuromyelitis optica spectrum disorders (NMOSD), but the relationship between the plasma levels of these molecules with disease activity a...

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Autores principales:	Tian-Xiang Zhang, Jing-Shan Chen, Chen Du, Pei Zeng, Huiming Zhang, Xuejiao Wang, Ye Liu, Zhenning Huang, Meng Yuan, Yu-Lin Li, Dongmei Jia, Fu-Dong Shi, Chao Zhang
Formato:	article
Lenguaje:	EN
Publicado:	SAGE Publishing 2021
Materias:	Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/1551137cc52a4a8eac086cd78f034255
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spelling	oai:doaj.org-article:1551137cc52a4a8eac086cd78f0342552021-11-03T22:03:46ZLongitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder1756-286410.1177/17562864211054952https://doaj.org/article/1551137cc52a4a8eac086cd78f0342552021-11-01T00:00:00Zhttps://doi.org/10.1177/17562864211054952https://doaj.org/toc/1756-2864Background: Neurofilament light chain (NfL) and glial fibrilliary acidic protein (GFAP) have been suggested to be biomarkers of the pathophysiological process of neuromyelitis optica spectrum disorders (NMOSD), but the relationship between the plasma levels of these molecules with disease activity and treatment is incompletely understood. Objective: To investigate the treatment effects of disease-modifying drugs on plasma neurofilament light chain (pNfL) and plasma glial fibrillary acidic protein (pGFAP) and explore the predictive value of pNfL and pGFAP in the activity of NMOSD. Methods: pNfL and pGFAP levels were measured using single-molecule arrays in 72 patients with NMOSD and 38 healthy controls (HCs). Patients with NMOSD received tocilizumab ( n = 29), rituximab ( n = 23), oral prednisone ( n = 16), and oral azathioprine or mycophenolate mofetil ( n = 4). Results: NMOSD patients had significantly higher pNfL and pGFAP levels than HCs (pNfL, 18.3 (11.2–39.3) versus 11.5 (7.0–23.3) pg/mL; p = 0.001; pGFAP, 149.7 (88.6–406.5) versus 68.7 (59.4–80.8) pg/mL; p < 0.001). Multivariable regression analyses indicated that baseline pNfL concentration was associated with age ( p = 0.017), Expanded Disability Status Scale (EDSS) score ( p = 0.002), and recent relapses ( p < 0.001). Baseline pGFAP concentration was also associated with EDSS ( p < 0.001) and recent relapses ( p < 0.001). Compared with prednisone, tocilizumab and rituximab significantly reduced pNfL [tocilizumab, exp(β), 0.65; 95% confidence interval (CI), 0.56–0.75; p < 0.001; rituximab, exp(β), 0.79; 95% CI = 0.68–0.93; p = 0.005] and pGFAP levels [tocilizumab, exp(β), 0.64; 95% CI, 0.51–0.80; p < 0.001; rituximab, exp(β), 0.77; 95% CI, 0.61–0.98; p = 0.041] at the end of the study. The pNfL levels in the tocilizumab and rituximab groups were reduced to those of HCs [tocilizumab, 8.5 (7.06–17.90) pg/mL; p = 0.426; rituximab, 14.0 (9.94–21.80) pg/mL; p = 0.216]. However, the pGFAP levels did not decrease to those of HCs in NMOSD patients at the end of study [tocilizumab, 88.9 (63.4–131.8) pg/mL; p = 0.012; rituximab, 141.7 (90.8–192.7) pg/mL; p < 0.001]. Conclusion: pNfL and pGFAP may serve as biomarkers for NMOSD disease activity and treatment effects.Tian-Xiang ZhangJing-Shan ChenChen DuPei ZengHuiming ZhangXuejiao WangYe LiuZhenning HuangMeng YuanYu-Lin LiDongmei JiaFu-Dong ShiChao ZhangSAGE PublishingarticleNeurology. Diseases of the nervous systemRC346-429ENTherapeutic Advances in Neurological Disorders, Vol 14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neurology. Diseases of the nervous system RC346-429
spellingShingle	Neurology. Diseases of the nervous system RC346-429 Tian-Xiang Zhang Jing-Shan Chen Chen Du Pei Zeng Huiming Zhang Xuejiao Wang Ye Liu Zhenning Huang Meng Yuan Yu-Lin Li Dongmei Jia Fu-Dong Shi Chao Zhang Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
description	Background: Neurofilament light chain (NfL) and glial fibrilliary acidic protein (GFAP) have been suggested to be biomarkers of the pathophysiological process of neuromyelitis optica spectrum disorders (NMOSD), but the relationship between the plasma levels of these molecules with disease activity and treatment is incompletely understood. Objective: To investigate the treatment effects of disease-modifying drugs on plasma neurofilament light chain (pNfL) and plasma glial fibrillary acidic protein (pGFAP) and explore the predictive value of pNfL and pGFAP in the activity of NMOSD. Methods: pNfL and pGFAP levels were measured using single-molecule arrays in 72 patients with NMOSD and 38 healthy controls (HCs). Patients with NMOSD received tocilizumab ( n = 29), rituximab ( n = 23), oral prednisone ( n = 16), and oral azathioprine or mycophenolate mofetil ( n = 4). Results: NMOSD patients had significantly higher pNfL and pGFAP levels than HCs (pNfL, 18.3 (11.2–39.3) versus 11.5 (7.0–23.3) pg/mL; p = 0.001; pGFAP, 149.7 (88.6–406.5) versus 68.7 (59.4–80.8) pg/mL; p < 0.001). Multivariable regression analyses indicated that baseline pNfL concentration was associated with age ( p = 0.017), Expanded Disability Status Scale (EDSS) score ( p = 0.002), and recent relapses ( p < 0.001). Baseline pGFAP concentration was also associated with EDSS ( p < 0.001) and recent relapses ( p < 0.001). Compared with prednisone, tocilizumab and rituximab significantly reduced pNfL [tocilizumab, exp(β), 0.65; 95% confidence interval (CI), 0.56–0.75; p < 0.001; rituximab, exp(β), 0.79; 95% CI = 0.68–0.93; p = 0.005] and pGFAP levels [tocilizumab, exp(β), 0.64; 95% CI, 0.51–0.80; p < 0.001; rituximab, exp(β), 0.77; 95% CI, 0.61–0.98; p = 0.041] at the end of the study. The pNfL levels in the tocilizumab and rituximab groups were reduced to those of HCs [tocilizumab, 8.5 (7.06–17.90) pg/mL; p = 0.426; rituximab, 14.0 (9.94–21.80) pg/mL; p = 0.216]. However, the pGFAP levels did not decrease to those of HCs in NMOSD patients at the end of study [tocilizumab, 88.9 (63.4–131.8) pg/mL; p = 0.012; rituximab, 141.7 (90.8–192.7) pg/mL; p < 0.001]. Conclusion: pNfL and pGFAP may serve as biomarkers for NMOSD disease activity and treatment effects.
format	article
author	Tian-Xiang Zhang Jing-Shan Chen Chen Du Pei Zeng Huiming Zhang Xuejiao Wang Ye Liu Zhenning Huang Meng Yuan Yu-Lin Li Dongmei Jia Fu-Dong Shi Chao Zhang
author_facet	Tian-Xiang Zhang Jing-Shan Chen Chen Du Pei Zeng Huiming Zhang Xuejiao Wang Ye Liu Zhenning Huang Meng Yuan Yu-Lin Li Dongmei Jia Fu-Dong Shi Chao Zhang
author_sort	Tian-Xiang Zhang
title	Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
title_short	Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
title_full	Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
title_fullStr	Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
title_full_unstemmed	Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
title_sort	longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder
publisher	SAGE Publishing
publishDate	2021
url	https://doaj.org/article/1551137cc52a4a8eac086cd78f034255
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Longitudinal treatment responsiveness on plasma neurofilament light chain and glial fibrillary acidic protein levels in neuromyelitis optica spectrum disorder

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