ECTRIMS eLearning

Serum neurofilament light chain predicts disease activity in relapsing remitting multiple sclerosis
ECTRIMS Learn. Varhaug K. 10/27/17; 200783; P1128
Kristin Varhaug
Kristin Varhaug
Contributions
Abstract

Abstract: P1128

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers

Objective: To investigate if serum neurofilament-light chain (NF-L) and chitinase 3-like 1 (CHI3L1) predict disease activity in relapsing-remitting multiple sclerosis.
Methods: A cohort of 85 patients with relapsing-remitting multiple sclerosis was followed for two years (six months without any disease modifying treatment and 18 months with interferon-beta 1a). Disability was scored (Expanded Disability Status Scale) at baseline and every six months thereafter. Magnetic resonance imaging (MRI) was performed at baseline and monthly for 9 months and then at months 12 and 24. Serum samples collected at baseline, months 3, 6, 12 and 24 were included in the analyses. We analyzed serum levels of NF-L using a single-molecule array assay and CHI3L1 by enzyme-linked immunosorbent assay. We estimated the association with clinical and MRI disease activity using mixed-effects models.
Results: We found significant associations between serum NF-L levels and new T1 gadolinium-enhanced lesions (p< 0.001) and new T2 lesions (p< 0.001). Further, NF-L levels were significantly associated with the presence of T1 gadolinium-enhanced lesions up to two months before (p< 0.001) and one month after (p=0.009) the time of biomarker measurement. NF-L levels fell significantly after initiation of interferon-beta 1a treatment (p< 0.001). Changes in CHI3L1 were not associated with clinical or MRI disease activity, or interferon-beta 1a treatment.
Conclusion: Serum NF-L appears to be a promising biomarker for MS disease activity and displays potential as a biomarker for treatment response. In clinical stable patients, serum NF-L measurements may offer an alternative to MRI monitoring for subclinical disease activity.
Disclosure:
Kristin N. Varhaug reports no disclosures
Christian Barro has received travel support from Teva and Novartis.
Kjetil Bjørnevik reports no disclosures
Kjell-Morten Myhr reports unrestricted grants and/or scientific advisory board or speaker honoraria from Almirall, Biogen, Genzyme, Merck, Novartis, and Roche outside the submitted work.
Øivind Torkildsen reports no disclosures
Stig Wergeland reports no disclosures
Laurence A. Bindoff reports no disclosures
Jens Kuhle reports Dr Kuhle's institution (University Hospital Basel) received and used exclusively for research support: consulting fees from Novartis, Protagen AG, Roche, Teva; speaker fees from the Swiss MS Society, Biogen, Novartis, Roche, Genzyme; travel expenses from Merck Serono, Novartis, Roche; grants from ECTRIMS Research Fellowship Programme, University of Basel, Swiss MS Society, Swiss National Research Foundation, Bayer AG, Biogen, Genzyme, Merck, Novartis, Roche.
Christian Vedeler reports no disclosures.

Abstract: P1128

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 25 Biomarkers

Objective: To investigate if serum neurofilament-light chain (NF-L) and chitinase 3-like 1 (CHI3L1) predict disease activity in relapsing-remitting multiple sclerosis.
Methods: A cohort of 85 patients with relapsing-remitting multiple sclerosis was followed for two years (six months without any disease modifying treatment and 18 months with interferon-beta 1a). Disability was scored (Expanded Disability Status Scale) at baseline and every six months thereafter. Magnetic resonance imaging (MRI) was performed at baseline and monthly for 9 months and then at months 12 and 24. Serum samples collected at baseline, months 3, 6, 12 and 24 were included in the analyses. We analyzed serum levels of NF-L using a single-molecule array assay and CHI3L1 by enzyme-linked immunosorbent assay. We estimated the association with clinical and MRI disease activity using mixed-effects models.
Results: We found significant associations between serum NF-L levels and new T1 gadolinium-enhanced lesions (p< 0.001) and new T2 lesions (p< 0.001). Further, NF-L levels were significantly associated with the presence of T1 gadolinium-enhanced lesions up to two months before (p< 0.001) and one month after (p=0.009) the time of biomarker measurement. NF-L levels fell significantly after initiation of interferon-beta 1a treatment (p< 0.001). Changes in CHI3L1 were not associated with clinical or MRI disease activity, or interferon-beta 1a treatment.
Conclusion: Serum NF-L appears to be a promising biomarker for MS disease activity and displays potential as a biomarker for treatment response. In clinical stable patients, serum NF-L measurements may offer an alternative to MRI monitoring for subclinical disease activity.
Disclosure:
Kristin N. Varhaug reports no disclosures
Christian Barro has received travel support from Teva and Novartis.
Kjetil Bjørnevik reports no disclosures
Kjell-Morten Myhr reports unrestricted grants and/or scientific advisory board or speaker honoraria from Almirall, Biogen, Genzyme, Merck, Novartis, and Roche outside the submitted work.
Øivind Torkildsen reports no disclosures
Stig Wergeland reports no disclosures
Laurence A. Bindoff reports no disclosures
Jens Kuhle reports Dr Kuhle's institution (University Hospital Basel) received and used exclusively for research support: consulting fees from Novartis, Protagen AG, Roche, Teva; speaker fees from the Swiss MS Society, Biogen, Novartis, Roche, Genzyme; travel expenses from Merck Serono, Novartis, Roche; grants from ECTRIMS Research Fellowship Programme, University of Basel, Swiss MS Society, Swiss National Research Foundation, Bayer AG, Biogen, Genzyme, Merck, Novartis, Roche.
Christian Vedeler reports no disclosures.

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