Two-year regional grey and white matter volume changes with natalizumab and fingolimod.
Adult
Atrophy
Brain
/ diagnostic imaging
Disease Progression
Female
Fingolimod Hydrochloride
/ therapeutic use
Gray Matter
/ diagnostic imaging
Humans
Immunologic Factors
/ therapeutic use
Longitudinal Studies
Magnetic Resonance Imaging
Male
Multiple Sclerosis, Relapsing-Remitting
/ diagnostic imaging
Natalizumab
/ therapeutic use
Neuroimaging
Prospective Studies
White Matter
/ diagnostic imaging
Journal
Journal of neurology, neurosurgery, and psychiatry
ISSN: 1468-330X
Titre abrégé: J Neurol Neurosurg Psychiatry
Pays: England
ID NLM: 2985191R
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
13
11
2019
revised:
03
02
2020
accepted:
04
02
2020
pubmed:
1
3
2020
medline:
13
11
2020
entrez:
1
3
2020
Statut:
ppublish
Résumé
To compare the efficacy of fingolimod and natalizumab in preventing regional grey matter (GM) and white matter (WM) atrophy in relapsing-remitting multiple sclerosis (RRMS) over 2 years. Patients with RRMS starting fingolimod (n=25) or natalizumab (n=30) underwent clinical examination and 3T MRI scans at baseline (month (M) 0), M6, M12 and M24. Seventeen healthy controls were also scanned at M0 and M24. Tensor-based morphometry and SPM12 were used to assess the longitudinal regional GM/WM volume changes. At M0, no clinical or GM/WM volume differences were found between treatment groups. At M24, both drugs reduced relapse rate (p<0.001 for both) and stabilised disability. At M6 vs M0, both groups experienced significant atrophy of several areas in the cortex, deep GM nuclei and supratentorial WM. Significant bilateral cerebellar GM and WM atrophy occurred in fingolimod patients only. At M12 vs M6 and M24 vs M12, further supratentorial GM and WM atrophy occurred in both groups. Bilateral GM/WM cerebellar atrophy continued to progress in fingolimod patients only. Compared with natalizumab, fingolimod-treated patients showed a significant cerebellar GM/WM atrophy, mainly at M6 vs M0, but still occurring up to M24. Compared with fingolimod, natalizumab-treated patients had a small number of areas of GM atrophy in temporo-occipital regions at the different time-points. Natalizumab and fingolimod are associated with heterogeneous temporal and regional patterns of GM and WM atrophy progression. Compared with natalizumab, fingolimod-treated patients experience accelerated GM and WM atrophy in the cerebellum, while both drugs show minimal regional volumetric differences in supratentorial regions.
Identifiants
pubmed: 32111638
pii: jnnp-2019-322439
doi: 10.1136/jnnp-2019-322439
doi:
Substances chimiques
Immunologic Factors
0
Natalizumab
0
Fingolimod Hydrochloride
G926EC510T
Types de publication
Clinical Trial
Comparative Study
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
493-502Informations de copyright
© Author(s) (or their employer(s)) 2020. No commercial re-use. See rights and permissions. Published by BMJ.
Déclaration de conflit d'intérêts
Competing interests: Potential conflicts of interest outside the submitted work are as follows. PP received speakers honoraria from Biogen Idec, Novartis, Merck Serono and ExceMED. MAR received speakers honoraria from Biogen Idec, Novartis, Genzyme, Teva, Merck Serono, Roche, Celgene and Bayer and receives research support from the Italian Ministry of Health, MS Society of Canada and Fondazione Italiana Sclerosi Multipla. LM has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Sanofi-Genzyme, Novartis, Teva, Merck-Serono, Biogen, Roche, Excemed. MF Editor-in-Chief of the Journal of Neurology; received compensation for consulting services and/or speaking activities from Bayer, Biogen Idec, Merck-Serono, Novartis, Roche, Sanofi Genzyme, Takeda and Teva Pharmaceutical Industries and receives research support from Biogen Idec, Merck-Serono, Novartis, Roche, Teva Pharmaceutical Industries, Italian Ministry of Health, Fondazione Italiana Sclerosi Multipla and ARiSLA (Fondazione Italiana di Ricerca per la SLA).