Retinal layer thinning is reflecting disability progression independent of relapse activity in multiple sclerosis.

biomarker multiple sclerosis optical coherence tomography progression progression independent of relapse activity retinal thinning

Journal

Multiple sclerosis journal - experimental, translational and clinical
ISSN: 2055-2173
Titre abrégé: Mult Scler J Exp Transl Clin
Pays: United States
ID NLM: 101668877

Informations de publication

Date de publication:
Historique:
received: 06 07 2020
accepted: 04 09 2020
entrez: 16 11 2020
pubmed: 17 11 2020
medline: 17 11 2020
Statut: epublish

Résumé

PIRA (progression independent of relapse) has emerged as a term to quantify the proportion of disability worsening due to non-inflammatory neurodegenerative processes in multiple sclerosis (MS). To determine the impact of PIRA on retinal thinning, a biomarker of neuroaxonal degeneration in MS, in comparison to traditional disability worsening and relapse. In a 4-year, prospective observational study including 171 relapsing MS (RMS) patients, retinal thinning was determined by annual spectral-domain optical coherence tomography measuring macular ganglion-cell-and-inner-plexiform-layer (GCIPL) and peripapillary-retinal-nerve-fibre-layer (pRNFL). PIRA was defined as an expanded disability status scale (EDSS) or symbol digit modalities test (SDMT) worsening confirmed after 24 weeks with no relapse in the 30 days before or after the disability worsening. Each PIRA event was associated with a mean additional loss of GCIPL (1.8 µm) and pRNFL (1.9 µm), similar to the impact of EDSS and SDMT worsening. Overall relapse and relapse without subsequent EDSS worsening did not influence retinal thinning, while a relapse with EDSS worsening was associated with an additional loss of GCIPL (1.3 µm) and pRNFL (1.4 µm). PIRA is associated with retinal thinning, likely reflecting neurodegenerative processes, not directly associated with focal inflammation. It might be a clinical measure to identify MS patients with ongoing MS-associated neurodegeneration.

Sections du résumé

BACKGROUND BACKGROUND
PIRA (progression independent of relapse) has emerged as a term to quantify the proportion of disability worsening due to non-inflammatory neurodegenerative processes in multiple sclerosis (MS).
OBJECTIVE OBJECTIVE
To determine the impact of PIRA on retinal thinning, a biomarker of neuroaxonal degeneration in MS, in comparison to traditional disability worsening and relapse.
METHODS METHODS
In a 4-year, prospective observational study including 171 relapsing MS (RMS) patients, retinal thinning was determined by annual spectral-domain optical coherence tomography measuring macular ganglion-cell-and-inner-plexiform-layer (GCIPL) and peripapillary-retinal-nerve-fibre-layer (pRNFL). PIRA was defined as an expanded disability status scale (EDSS) or symbol digit modalities test (SDMT) worsening confirmed after 24 weeks with no relapse in the 30 days before or after the disability worsening.
RESULTS RESULTS
Each PIRA event was associated with a mean additional loss of GCIPL (1.8 µm) and pRNFL (1.9 µm), similar to the impact of EDSS and SDMT worsening. Overall relapse and relapse without subsequent EDSS worsening did not influence retinal thinning, while a relapse with EDSS worsening was associated with an additional loss of GCIPL (1.3 µm) and pRNFL (1.4 µm).
CONCLUSIONS CONCLUSIONS
PIRA is associated with retinal thinning, likely reflecting neurodegenerative processes, not directly associated with focal inflammation. It might be a clinical measure to identify MS patients with ongoing MS-associated neurodegeneration.

Identifiants

pubmed: 33194221
doi: 10.1177/2055217320966344
pii: 10.1177_2055217320966344
pmc: PMC7604994
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2055217320966344

Informations de copyright

© The Author(s) 2020.

Déclaration de conflit d'intérêts

Conflict of Interests: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: Gabriel Bsteh: has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Celgene, Merck, Novartis, Sanofi-Genzyme and Teva, and received honoraria for consulting Biogen, Roche and Teva. Harald Hegen: has participated in meetings sponsored by, received speaker honoraria or travel funding from Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Siemens and Teva, and received honoraria for consulting Biogen and Teva. Patrick Altmann: has participated in meetings sponsored by, received speaker honoraria or travel funding from Biogen, Merck, Roche, Sanofi-Genzyme and Teva, and received honoraria for consulting from Biogen. He received a research grant from Quanterix International and was awarded a combined sponsorship from Biogen, Merck, Sanofi-Genzyme, Roche, and Teva for a clinical study. Michael Auer: received speaker honoraria and/or travel grants from Biogen, Merck, Novartis and Sanofi Genzyme. Klaus Berek: has participated in meetings sponsored by and received travel funding from Roche. Franziska Di Pauli has participated in meetings sponsored by, received honoraria (lectures, advisory boards, consultations) or travel funding from Bayer, Biogen, Merck, Novartis, Sanofi-Genzyme, Teva, Celgene and Roche. Sebastian Wurth: has participated in meetings sponsored by, received honoraria or travel funding from Allergan, Biogen, Ipsen Pharma, Merck, Novartis, Roche, Sanofi Genzyme and Teva. Anne Zinganell: has participated in meetings sponsored by, received speaking honoraria or travel funding from Biogen, Merck, Sanofi-Genzyme and Teva. Paulus Rommer: has received honoraria for consultancy/speaking from AbbVie, Allmiral, Alexion, Biogen, Merck, Novartis, Roche, Sandoz, Sanofi Genzyme, has received research grants from Amicus, Biogen, Merck, Roche. Florian Deisenhammer: has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Alexion, Almirall, Biogen, Celgene, Merck, Novartis, Roche and Sanofi-Genzyme. His institution received scientific grants from Biogen and Sanofi-Genzyme. Fritz Leutmezer: has participated in meetings sponsored by or received honoraria for acting as an advisor/speaker for Bayer, Biogen, Celgene, MedDay, Merck, Novartis, Roche, Teva and Sanofi-Genzyme. 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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Auteurs

Gabriel Bsteh (G)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Harald Hegen (H)

Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Patrick Altmann (P)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Michael Auer (M)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Klaus Berek (K)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Franziska Di Pauli (FD)

Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Sebastian Wurth (S)

Department of Neurology, Medical University of Graz, Graz, Austria.

Anne Zinganell (A)

Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Paulus Rommer (P)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Florian Deisenhammer (F)

Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.

Fritz Leutmezer (F)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Thomas Berger (T)

Department of Neurology, Medical University of Vienna, Vienna, Austria.

Classifications MeSH