MOG-IgG1 and co-existence of neuronal autoantibodies.
MOG-IgG1
NMDA-R-IgG
autoimmune encephalitis
biomarkers
demyelination
neuronal antibodies
Journal
Multiple sclerosis (Houndmills, Basingstoke, England)
ISSN: 1477-0970
Titre abrégé: Mult Scler
Pays: England
ID NLM: 9509185
Informations de publication
Date de publication:
07 2021
07 2021
Historique:
pubmed:
11
9
2020
medline:
24
9
2021
entrez:
10
9
2020
Statut:
ppublish
Résumé
The presence of co-existent neuronal antibodies (neuronal-IgG) in patients with myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG1) is not yet well understood. The aim of this study was to investigate the co-existence of a broad range of neuronal-IgG in MOG-IgG1+ patients. MOG-IgG1+ patients were tested for 17 neuronal-IgGs in cerebrospinal fluid (CSF) and serum including NMDA-R-IgG, AMPA-R-IgG, GABAB-R-IgG, LGI1-IgG, CASPR2-IgG, GABAA-R-IgG, GAD65-IgG, mGLUR1-IgG, DPPX-IgG, CRMP5-IgG, amphiphysin-IgG, PCA1,2,Tr, and ANNA1,2,3. Clinical and radiological features of MOG-IgG1+ with NMDA-R-IgG in CSF were compared to a control cohort of MOG-IgG1+ patients without NMDA-R-IgG. A total of 376 MOG-IgG1+ patients underwent testing for neuronal-IgGs. Serum testing for neuronal-IgGs (113 adults, 142 children) identified one child with NMDA-R-IgG (0.7%), one child with CASPR2-IgG (0.7%), one adult with LGI1-IgG (0.9%) and one adult with GABAA-R-IgG (0.9%). CSF testing for neuronal-IgGs (97 adults, 169 children) identified seven children (4%) and seven adults (7%) with NMDA-R-IgG, and one adult with GABAA-R-IgG (1%). The MOG-IgG1+/NMDA-R-IgG+ patients had a median age of 17 (range: 2-39) years. Features associated with MOG-IgG1+/NMDA-R-IgG+ included encephalopathy ( NMDA-R-IgG was the most frequently detected neuronal-IgG to co-exist with MOG-IgG1. MOG-IgG1+/NMDA-R-IgG+ patients most often presented with encephalopathy and seizures. Testing for MOG-IgG1 and NMDA-R-IgG may be warranted in patients with encephalopathy and inflammatory demyelinating syndromes.
Sections du résumé
BACKGROUND
The presence of co-existent neuronal antibodies (neuronal-IgG) in patients with myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG1) is not yet well understood.
OBJECTIVES
The aim of this study was to investigate the co-existence of a broad range of neuronal-IgG in MOG-IgG1+ patients.
METHODS
MOG-IgG1+ patients were tested for 17 neuronal-IgGs in cerebrospinal fluid (CSF) and serum including NMDA-R-IgG, AMPA-R-IgG, GABAB-R-IgG, LGI1-IgG, CASPR2-IgG, GABAA-R-IgG, GAD65-IgG, mGLUR1-IgG, DPPX-IgG, CRMP5-IgG, amphiphysin-IgG, PCA1,2,Tr, and ANNA1,2,3. Clinical and radiological features of MOG-IgG1+ with NMDA-R-IgG in CSF were compared to a control cohort of MOG-IgG1+ patients without NMDA-R-IgG.
RESULTS
A total of 376 MOG-IgG1+ patients underwent testing for neuronal-IgGs. Serum testing for neuronal-IgGs (113 adults, 142 children) identified one child with NMDA-R-IgG (0.7%), one child with CASPR2-IgG (0.7%), one adult with LGI1-IgG (0.9%) and one adult with GABAA-R-IgG (0.9%). CSF testing for neuronal-IgGs (97 adults, 169 children) identified seven children (4%) and seven adults (7%) with NMDA-R-IgG, and one adult with GABAA-R-IgG (1%). The MOG-IgG1+/NMDA-R-IgG+ patients had a median age of 17 (range: 2-39) years. Features associated with MOG-IgG1+/NMDA-R-IgG+ included encephalopathy (
CONCLUSION
NMDA-R-IgG was the most frequently detected neuronal-IgG to co-exist with MOG-IgG1. MOG-IgG1+/NMDA-R-IgG+ patients most often presented with encephalopathy and seizures. Testing for MOG-IgG1 and NMDA-R-IgG may be warranted in patients with encephalopathy and inflammatory demyelinating syndromes.
Identifiants
pubmed: 32907470
doi: 10.1177/1352458520951046
pmc: PMC8454216
mid: NIHMS1616375
doi:
Substances chimiques
Autoantibodies
0
Immunoglobulin G
0
Myelin-Oligodendrocyte Glycoprotein
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1175-1186Subventions
Organisme : NINDS NIH HHS
ID : R01 NS113828
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001863
Pays : United States
Références
Ann Neurol. 2017 Feb;81(2):298-309
pubmed: 28120349
Lancet Neurol. 2020 Mar;19(3):234-246
pubmed: 32057303
Neurology. 2015 Jul 14;85(2):177-89
pubmed: 26092914
JAMA Neurol. 2020 May 1;77(5):648-649
pubmed: 32119057
J Neurol Neurosurg Psychiatry. 2012 Feb;83(2):195-8
pubmed: 21933952
Ann Neurol. 2014 Mar;75(3):411-28
pubmed: 24700511
Nat Rev Neurol. 2013 Aug;9(8):455-61
pubmed: 23797245
J Epilepsy Res. 2015 Jun 30;5(1):17-9
pubmed: 26157669
Ann Neurol. 2012 Aug;72(2):241-55
pubmed: 22473710
Lancet Neurol. 2013 Feb;12(2):157-65
pubmed: 23290630
Neurology. 2013 Sep 3;81(10):882-7
pubmed: 23925760
Neurology. 2015 Nov 17;85(20):1736-43
pubmed: 26491084
Brain. 2017 Dec 1;140(12):3128-3138
pubmed: 29136091
J Neuroimmunol. 2019 Mar 15;328:86-88
pubmed: 30599296
Am J Ophthalmol. 2018 Nov;195:8-15
pubmed: 30055153
Neurology. 2020 Jun 2;94(22):e2302-e2310
pubmed: 32161029
Ann Neurol. 2009 Dec;66(6):833-42
pubmed: 20033986
Neurology. 2019 Mar 12;92(11):e1250-e1255
pubmed: 30728305
JAMA Neurol. 2020 Feb 1;77(2):257-259
pubmed: 31657826
PLoS One. 2020 Mar 25;15(3):e0230436
pubmed: 32210460
Neurol Neuroimmunol Neuroinflamm. 2017 Jan 16;4(2):e322
pubmed: 28105459
Neurol Neuroimmunol Neuroinflamm. 2019 Apr 04;6(3):e552
pubmed: 31119187
JAMA Neurol. 2020 Jan 1;77(1):82-93
pubmed: 31545352
Mult Scler Relat Disord. 2017 Nov;18:90-92
pubmed: 29141829
Lancet Neurol. 2016 Apr;15(4):391-404
pubmed: 26906964
Epilepsy Behav Rep. 2019 Oct 25;12:100338
pubmed: 31737864
Mult Scler. 2013 Sep;19(10):1261-7
pubmed: 23572237
Neurology. 2015 Jun 16;84(24):2403-12
pubmed: 25979696
Mayo Clin Proc. 2006 Sep;81(9):1207-14
pubmed: 16970217