Contributions
Abstract: P1173
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background and goals: Serum and cerebrospinal fluid (CSF) neurofilament light chain (NfL) levels reflect axonal damage in different inflammatory and degenerative neurological disorders. In particular, NfL levels were shown to correlate with disease severity and to predict clinical and radiological outcomes in patients with multiple sclerosis. Aim of our study was to assess the potential usefulness of serum and CSF NfL levels in monitoring disease activity and predicting long-term outcome in subjects with myelin oligodendrocyte glycoprotein antibodies (MOG-Ab)-related disorders.
Methods: We analysed clinical, radiological, and laboratory data of consecutive patients resulted positive for serum myelin oligodendrocyte glycoprotein antibodies (MOG-Ab), tested with a live-cell immunofluorescence assay between March 2014 and April 2018. Serum and, when available, CSF and follow-up samples were analysed for NfL using a high sensitive technology (Simoa, Quanterix) at the Neuropathology laboratory, University of Verona, Italy. A group of age-matched unaffected controls was also included.
Results: 76 subjects were included (38 MOG-Ab positive and 38 controls). There was a significant correlation between serum NfL concentration and age at sampling. Serum NfL levels were higher in MOG-Ab positive patients (median 10.7 pg/ml, range 2.1-101.5) than in controls (median 5.9, range 1.3-13.8); p=0.005. In the MOG-Ab positive group, females had significantly higher serum NfL concentration compared to males (11.8 [4.0-101.5] vs. 7.3 [2.1-42.9], p=0.016), and serum NfL levels strongly correlated to that in CSF (r=0.72, p=0.006, N=13). Moreover, NfL concentration was higher (median 15.3 pg/ml, range 4-101.5) in subjects with a severe attack (severe motor impairment/severe encephalopathy/severe visual impairment with visual acuity < 2/10) compared to those with a mild-to-moderate event (median 7.3, range 2.1-23.0); p=0.002. Finally, we observed a correlation between NfL levels and EDSS score at sampling (r=0.47, p=0.003) and - to a lesser extent - with EDSS score at last follow-up (r=0.29, p=0.07). Median follow-up duration was 20 months (2-266).
Conclusions. Our data provide further evidence of axonal damage in MOG-Ab associated disorders and support the role of NfL as a possible biomarker in these disorders.
Disclosure: Sara Mariotto: nothing to disclose.
Sergio Ferrari: was sponsored by Shire for attending a neurological meeting in Italy.
Matteo Gastaldi, Diego Franciotta, Elia Sechi, Chiara Mancinelli, Kathrin Schanda, Daniela Alberti, Roberto Bombardi, Luigi Zuliani, Marco Zoccarato, Maria Donata Benedetti, Raffaella Tanel, Francesca Calabria, Alberto Polo, Francesca Rossi, Antonino Pavone, Luisa Grazian, GianPietro Sechi, Lucia Batzu, Noemi Murdeu, Francesco Janes, Vincenza Fetoni, Daniela Fulitano, Gianola Stenta, Lisa Federle, Gaetano Cantalupo: nothing to disclose.
Ruggero Capra: received lecture fees and/or travel grants from Novartis, Biogen, Celgene, Novartis, TEVA, Genzyme and Sanofi-Aventis.
Markus Reindl: the clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Markus Reindl was supported by a research grant from the Austrian Science Promotion Agency (FFG). The University Hospital and Medical University of Innsbruck (Austria; M.R.) receives payments for antibody assays (MOG, AQP4, and other autoantibodies) and for MOG and AQP4 antibody validation experiments organized by Euroimmun (Lübeck, Germany).
Salvatore Monaco: received honoraria from Biogen.
Alberto Gajofatto: received research support funding from Merck.
Abstract: P1173
Type: Poster Sessions
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Background and goals: Serum and cerebrospinal fluid (CSF) neurofilament light chain (NfL) levels reflect axonal damage in different inflammatory and degenerative neurological disorders. In particular, NfL levels were shown to correlate with disease severity and to predict clinical and radiological outcomes in patients with multiple sclerosis. Aim of our study was to assess the potential usefulness of serum and CSF NfL levels in monitoring disease activity and predicting long-term outcome in subjects with myelin oligodendrocyte glycoprotein antibodies (MOG-Ab)-related disorders.
Methods: We analysed clinical, radiological, and laboratory data of consecutive patients resulted positive for serum myelin oligodendrocyte glycoprotein antibodies (MOG-Ab), tested with a live-cell immunofluorescence assay between March 2014 and April 2018. Serum and, when available, CSF and follow-up samples were analysed for NfL using a high sensitive technology (Simoa, Quanterix) at the Neuropathology laboratory, University of Verona, Italy. A group of age-matched unaffected controls was also included.
Results: 76 subjects were included (38 MOG-Ab positive and 38 controls). There was a significant correlation between serum NfL concentration and age at sampling. Serum NfL levels were higher in MOG-Ab positive patients (median 10.7 pg/ml, range 2.1-101.5) than in controls (median 5.9, range 1.3-13.8); p=0.005. In the MOG-Ab positive group, females had significantly higher serum NfL concentration compared to males (11.8 [4.0-101.5] vs. 7.3 [2.1-42.9], p=0.016), and serum NfL levels strongly correlated to that in CSF (r=0.72, p=0.006, N=13). Moreover, NfL concentration was higher (median 15.3 pg/ml, range 4-101.5) in subjects with a severe attack (severe motor impairment/severe encephalopathy/severe visual impairment with visual acuity < 2/10) compared to those with a mild-to-moderate event (median 7.3, range 2.1-23.0); p=0.002. Finally, we observed a correlation between NfL levels and EDSS score at sampling (r=0.47, p=0.003) and - to a lesser extent - with EDSS score at last follow-up (r=0.29, p=0.07). Median follow-up duration was 20 months (2-266).
Conclusions. Our data provide further evidence of axonal damage in MOG-Ab associated disorders and support the role of NfL as a possible biomarker in these disorders.
Disclosure: Sara Mariotto: nothing to disclose.
Sergio Ferrari: was sponsored by Shire for attending a neurological meeting in Italy.
Matteo Gastaldi, Diego Franciotta, Elia Sechi, Chiara Mancinelli, Kathrin Schanda, Daniela Alberti, Roberto Bombardi, Luigi Zuliani, Marco Zoccarato, Maria Donata Benedetti, Raffaella Tanel, Francesca Calabria, Alberto Polo, Francesca Rossi, Antonino Pavone, Luisa Grazian, GianPietro Sechi, Lucia Batzu, Noemi Murdeu, Francesco Janes, Vincenza Fetoni, Daniela Fulitano, Gianola Stenta, Lisa Federle, Gaetano Cantalupo: nothing to disclose.
Ruggero Capra: received lecture fees and/or travel grants from Novartis, Biogen, Celgene, Novartis, TEVA, Genzyme and Sanofi-Aventis.
Markus Reindl: the clinical Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria. Markus Reindl was supported by a research grant from the Austrian Science Promotion Agency (FFG). The University Hospital and Medical University of Innsbruck (Austria; M.R.) receives payments for antibody assays (MOG, AQP4, and other autoantibodies) and for MOG and AQP4 antibody validation experiments organized by Euroimmun (Lübeck, Germany).
Salvatore Monaco: received honoraria from Biogen.
Alberto Gajofatto: received research support funding from Merck.