Serum neurofilament light chain levels correlate with peripapillary retinal nerve fibre layerthinning as measured by optical coherence tomography in multiple sclerosis
ECTRIMS Online Library. Bsteh G. 09/13/19; 279547; 285
Gabriel Bsteh
Gabriel Bsteh
Contributions
Abstract

Abstract: 285

Type: Scientific Session

Abstract Category: Pathology and pathogenesis of MS - OCT

G. Bsteh1,2, K. Berek2, H. Hegen2, B. Teuchner3, M. Auer2, S. Wurth2, A. Zinganell2, F. Di Pauli2, F. Deisenhammer2, M. Khalil4, T. Berger1

1Neurology, Medical University of Vienna, Vienna, 2Neurology, 3Ophtalmology, Medical University of Innsbruck, Innsbruck, 4Neurology, Medical University of Graz, Graz, Austria

Background: Serum neurofilament light chain levels (sNfL) and peripapillary retinal nerve fiber layer (pRNFL) thinning are both emerging biomarkers of neuro-axonal damage in MS. However, data on the relation between sNfL and pRNFL are lacking.
Objectives: We aimed to determine the relation of sNfL levels and pRNFL thinning in a large cohort of relapsing-remitting (RR)-MS patients.
Methods: We identified 80 patients from a prospective, 3-year observational study on retinal changes in RRMS with annual blood samples available. sNfL was measured using a single molecule array (SIMOA) assay. Annualized pRNFLthinning rates (aLpRNFL) were determined by individual linear regression models.Correlations between single and averaged sNfL levels and aLpRNFL were analyzed using univariate and multivariate linear regression models.
Results: We found a significant association after correction for sex, age and disease duration between aLpRNFL and sNfL levels at years 1 and 2 with an increase of 10pg/ml transferring to an additional aLpRNFLof 0.9mm (95%CI: 0.4 - 1.5; p=0.002) and 0.7mm (95%CI: -1.4 - -0.1; p=0.042), respectively. About 15-20% of the aLpRNFL variance could be predicted from sNfL levels.
Conclusions: sNfL contributes to the prediction of retinal thinning in patients with RRMS strengthening its value as biomarker of neuro-axonal damage.
Disclosure: Gabriel Bsteh: hasparticipated in meetings sponsored by, received speaker honoraria or travel funding fromBiogen, Merck,Novartis, Sanofi-Genzymeand Teva, and received honoraria for consulting Biogen, Roche and Teva.
Klaus Berek: declares no conflicts of interest.
Harald Hegen: has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Merck, Novartis and Sanofi-Genzyme, and received honoraria for consulting Teva.
Barbara Teuchner: declares no conflicts of interest.
Michael Auer: received speaker honoraria and/or travel grants from Merck, Novartis and Biogen.
Sebastian Wurth: has participated in meetings sponsored by, received honoraria or travel funding from Biogen, Merck,Novartis, Sanofi Genzyme, Teva, Allergan, Ipsen Pharma and Roche.
Anne Zinganell: declares no conflicts of interest.
Franziska Di Pauli: has received speaking honoraria from Biogen and Sanofi-Genzyme.
Florian Deisenhammer: has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Bayer, Biogen, Sanofi-Genzyme, Merck, Novartis, and Roche.
Michael Khalil: declares no conflicts of interest.
Thomas Berger: has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for MS: Allergan, Bayer, Biogen, Bionorica, Celgene, MedDay, Merck, Novartis, Octapharma, Roche, Sanofi-Genzyme, Teva. His institution has received financial support in the past 12 months by unrestricted research grants (Biogen, Bayer, Merck, Novartis, Sanofi Aventis, Teva and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Octapharma, Roche, Sanofi-Genzyme, Teva.

Abstract: 285

Type: Scientific Session

Abstract Category: Pathology and pathogenesis of MS - OCT

G. Bsteh1,2, K. Berek2, H. Hegen2, B. Teuchner3, M. Auer2, S. Wurth2, A. Zinganell2, F. Di Pauli2, F. Deisenhammer2, M. Khalil4, T. Berger1

1Neurology, Medical University of Vienna, Vienna, 2Neurology, 3Ophtalmology, Medical University of Innsbruck, Innsbruck, 4Neurology, Medical University of Graz, Graz, Austria

Background: Serum neurofilament light chain levels (sNfL) and peripapillary retinal nerve fiber layer (pRNFL) thinning are both emerging biomarkers of neuro-axonal damage in MS. However, data on the relation between sNfL and pRNFL are lacking.
Objectives: We aimed to determine the relation of sNfL levels and pRNFL thinning in a large cohort of relapsing-remitting (RR)-MS patients.
Methods: We identified 80 patients from a prospective, 3-year observational study on retinal changes in RRMS with annual blood samples available. sNfL was measured using a single molecule array (SIMOA) assay. Annualized pRNFLthinning rates (aLpRNFL) were determined by individual linear regression models.Correlations between single and averaged sNfL levels and aLpRNFL were analyzed using univariate and multivariate linear regression models.
Results: We found a significant association after correction for sex, age and disease duration between aLpRNFL and sNfL levels at years 1 and 2 with an increase of 10pg/ml transferring to an additional aLpRNFLof 0.9mm (95%CI: 0.4 - 1.5; p=0.002) and 0.7mm (95%CI: -1.4 - -0.1; p=0.042), respectively. About 15-20% of the aLpRNFL variance could be predicted from sNfL levels.
Conclusions: sNfL contributes to the prediction of retinal thinning in patients with RRMS strengthening its value as biomarker of neuro-axonal damage.
Disclosure: Gabriel Bsteh: hasparticipated in meetings sponsored by, received speaker honoraria or travel funding fromBiogen, Merck,Novartis, Sanofi-Genzymeand Teva, and received honoraria for consulting Biogen, Roche and Teva.
Klaus Berek: declares no conflicts of interest.
Harald Hegen: has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Merck, Novartis and Sanofi-Genzyme, and received honoraria for consulting Teva.
Barbara Teuchner: declares no conflicts of interest.
Michael Auer: received speaker honoraria and/or travel grants from Merck, Novartis and Biogen.
Sebastian Wurth: has participated in meetings sponsored by, received honoraria or travel funding from Biogen, Merck,Novartis, Sanofi Genzyme, Teva, Allergan, Ipsen Pharma and Roche.
Anne Zinganell: declares no conflicts of interest.
Franziska Di Pauli: has received speaking honoraria from Biogen and Sanofi-Genzyme.
Florian Deisenhammer: has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Bayer, Biogen, Sanofi-Genzyme, Merck, Novartis, and Roche.
Michael Khalil: declares no conflicts of interest.
Thomas Berger: has participated in meetings sponsored by and received honoraria (lectures, advisory boards, consultations) from pharmaceutical companies marketing treatments for MS: Allergan, Bayer, Biogen, Bionorica, Celgene, MedDay, Merck, Novartis, Octapharma, Roche, Sanofi-Genzyme, Teva. His institution has received financial support in the past 12 months by unrestricted research grants (Biogen, Bayer, Merck, Novartis, Sanofi Aventis, Teva and for participation in clinical trials in multiple sclerosis sponsored by Alexion, Bayer, Biogen, Merck, Novartis, Octapharma, Roche, Sanofi-Genzyme, Teva.

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