Comparative study of AQP4-NMOSD, MOGAD and seronegative NMOSD: a single-center Belgian cohort.


Journal

Acta neurologica Belgica
ISSN: 2240-2993
Titre abrégé: Acta Neurol Belg
Pays: Italy
ID NLM: 0247035

Informations de publication

Date de publication:
Feb 2022
Historique:
received: 31 12 2020
accepted: 13 05 2021
pubmed: 8 6 2021
medline: 22 3 2022
entrez: 7 6 2021
Statut: ppublish

Résumé

To emphasize physio-pathological, clinical and prognosis differences between conditions causing serious and sometimes very similar clinical manifestations: anti-aquaporin-4 (AQP4) and anti-myelin oligodendrocyte glycoprotein (MOG) antibodies related diseases, and seronegative NMOSD (neuromyelitis optica spectrum disorders). Based on Wingerchuk et al. (Neurology 85:177-189, 2015) criteria for NMOSD and on those more recently proposed by Jarius et al. (J Neuroinflammation 15:134, 2018) for MOGAD (MOG associated disorders), we retrospectively surveyed 10 AQP4-NMOSD, 8 MOGAD and 2 seronegative NMOSD, followed at the specialized neuroimmunology unit of the CHU Liège. Female predominance was only observed in AQP4 group. Age at onset was 37.8 and 27.7 years old for AQP4-NMOSD and MOGAD respectively. In both groups, the first clinical event most often consisted of optic neuritis (ON), followed by isolated myelitis. Fifteen of our 20 patients encountered a relapsing course with 90% relapses in AQP4-NMOSD, 62.5% in MOGAD and 50% in seronegative group, and a mean period between first and second clinical event of 7.1 and 4.8 months for AQP4-NMOSD and MOGAD, respectively. In total we counted 54 ON, with more ON per patient in MOGAD. MOG-associated ON mainly affected the anterior part of the optic nerve with a papilledema in 79.2% of cases. Despite a fairly good visual outcome after MOG-associated ON, retinal nerve fibre layer (RNFL) thickness decreased, suggesting a fragility of the optic nerve toward further attacks. As observed in larger cohorts, our MOGAD and AQP4-NMOSD cases differ by clinical and prognostic features. A better understanding of these diseases should encourage prompt biological screening and hasten proper diagnosis and treatment.

Identifiants

pubmed: 34097296
doi: 10.1007/s13760-021-01712-3
pii: 10.1007/s13760-021-01712-3
pmc: PMC8894224
doi:

Substances chimiques

Aquaporin 4 0
Autoantibodies 0
Immunoglobulin G 0
MAG protein, human 0
Myelin-Associated Glycoprotein 0
Myelin-Oligodendrocyte Glycoprotein 0

Types de publication

Comparative Study Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

135-144

Informations de copyright

© 2021. The Author(s).

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Auteurs

Solène Dauby (S)

Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium. solene.dauby@chuliege.be.
GIGA-CRC in Vivo Imaging, University of Liège, Liège, Belgium. solene.dauby@chuliege.be.

Dominique Dive (D)

Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium.

Laurence Lutteri (L)

Clinical Chemistry Department, University Hospital of Liège, Liège, Belgium.

Cécile Andris (C)

Clinical Ophthalmological Unit, Ophthalmology Department, University Hospital of Liège, Liège, Belgium.

Isabelle Hansen (I)

Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium.

Pierre Maquet (P)

Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium.
GIGA-CRC in Vivo Imaging, University of Liège, Liège, Belgium.

Emilie Lommers (E)

Clinical Neuroimmunology Unit, Department of Neurology, CHU Liège, University Hospital of Liège, Liège, Belgium.
GIGA-CRC in Vivo Imaging, University of Liège, Liège, Belgium.

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