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Cited by 230Multiple Sclerosis Research StudiesPeripheral Neuropathies and DisordersAutoimmune Neurological Disorders and Treatments

Myelin oligodendrocyte glycoprotein antibodies are associated with a non-MS course in children

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Hacohen, Yael, Absoud, Michael, Deiva, Kumaran, Hemingway, Cheryl, Nytrova, Petra, Woodhall, Mark, Palace, Jacqueline, Wassmer, Evangeline +4 more·2015·Neurology Neuroimmunology & Neuroinflammation
DOI 10.1212/nxi.0000000000000081PMC PMC4360800
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Abstract

OBJECTIVE: To determine whether myelin oligodendrocyte glycoprotein antibodies (MOG-Abs) were predictive of a demyelination phenotype in children presenting with acquired demyelinating syndrome (ADS). METHOD: Sixty-five children with a first episode of ADS (12 acute disseminated encephalomyelitis, 24 optic neuritis, 18 transverse myelitis, 11 other clinically isolated syndrome) were identified from 2 national demyelination programs in the United Kingdom and France. Acute serum samples were tested for MOG-Abs by cell-based assay. Antibodies were used to predict diagnosis of multiple sclerosis (MS) at 1 year. RESULTS: Twenty-three of 65 (35%) children had MOG-Abs. Antibody-positive and antibody-negative patients were not clinically different at presentation, but identification of MOG-Abs predicted a non-MS course at 1-year follow-up: only 2/23 (9%) MOG-Ab-positive patients were diagnosed with MS compared to 16/42 (38%) MOG-Ab-negative patients (p = 0.019, Fisher exact test). Antibody positivity at outset was a useful predictor for a non-MS disease course, with a positive predictive value of 91% (95% confidence interval [CI] 72-99), negative predictive value of 38% (95% CI 24-54), positive likelihood ratio of 4.02 (CI 1.0-15.4), and odds ratio of 6.5 (CI 1.3-31.3). CONCLUSIONS: MOG-Abs are found at presentation in 35% of patients with childhood ADS, across a range of demyelinating disorders. Antibody positivity can be useful in predicting a non-MS disease course at onset.

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  • Diagnosis of NMOSD has been facilitated by the development and use of serologic testing for antibodies reactive with the AQP4 water channel and validation of the antibodies not only as a marker of NMOSD but also as a pathogenic factor.

    “Diagnosis of NMOSD has been facilitated by the development and use of serologic testing for antibodies reactive with the AQP4 water channel and validation of the antibodies not only as a marker of NMOSD but also as a pathogenic factor. 45,46”

    From Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria (2018) · cites this paper as [45]

    The Discussion (page unavailable) describes NMOSD as a diagnosis unified by detection of AQP4 antibodies, supporting their diagnostic relevance. It does not say that serologic testing facilitated diagnosis or that the antibodies were validated as a pathogenic factor; the study focuses on MOG antibodies. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • MOG-IgG is also found in some patients with ADEM (particularly in children), and in ADEM followed by optic neuritis, and isolated or recurrent optic neuritis.

    “MOG-IgG is also found in some patients with ADEM (particularly in children), and in ADEM followed by optic neuritis, and isolated or recurrent optic neuritis.58,59”

    From Diagnosis of multiple sclerosis: progress and challenges (2017) · cites this paper as [59]

    The Results (page unavailable) report MOG antibodies in 4/12 children presenting with ADEM and 12/24 presenting with optic neuritis. The Discussion mentions recurrent optic neuritis as a possible MOG-positive phenotype, but our copy does not document ADEM followed by optic neuritis or establish recurrent optic neuritis among this cohort’s antibody-positive cases. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • AQP4 serologic testing generally differentiates NMOSD from MS.

    “While AQP4 serologic testing generally differentiates NMOSD from MS, 45 less is known about the performance of testing for MOG antibodies. 41,47-49”

    From Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria (2018) · cites this paper as [45]

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Research works printed but not linked: 25

  1. [1]Hemmer B Archelos JJ Hartung HP New concepts in the immunopathogenesis of multiple sclerosis. Nat Rev Neurosci 2002; 3: 291– 301. 11967559
  2. [2]Elliott C Lindner M Arthur A Functional identification of pathogenic autoantibody responses in patients with multiple sclerosis. Brain 2012; 135: 1819– 1833. 22561643 PMC3359756
  3. [3]Reindl M Di Pauli F Rostasy K Berger T The spectrum of MOG autoantibody-associated demyelinating diseases. Nat Rev Neurol 2013; 9: 455– 461. 23797245
  4. [4]O'Connor KC McLaughlin KA De Jager PL Self-antigen tetramers discriminate between myelin autoantibodies to native or denatured protein. Nat Med 2007; 13: 211– 217. 17237795 PMC3429369
  5. [5]Rostasy K Reindl M Role of autoantibodies in acquired inflammatory demyelinating diseases of the central nervous system in children. Neuropediatrics 2013; 44: 297– 301. 24166146
  6. [6]Kitley J Woodhall M Waters P Myelin-oligodendrocyte glycoprotein antibodies in adults with a neuromyelitis optica phenotype. Neurology 2012; 79: 1273– 1277. 22914827
  7. [7]Absoud M Lim MJ Chong WK Paediatric acquired demyelinating syndromes: incidence, clinical and magnetic resonance imaging features. Mult Scler 2013; 19: 76– 86. 22516794 PMC3409874
  8. [8]Mikaeloff Y Suissa S Vallee L First episode of acute CNS inflammatory demyelination in childhood: prognostic factors for multiple sclerosis and disability. J Pediatr 2004; 144: 246– 252. 14760270
  9. [9]Verhey LH Branson HM Shroff MM MRI parameters for prediction of multiple sclerosis diagnosis in children with acute CNS demyelination: a prospective national cohort study. Lancet Neurol 2011; 10: 1065– 1073. 22067635
  10. [11]Rostasy K Mader S Schanda K Anti-myelin oligodendrocyte glycoprotein antibodies in pediatric patients with optic neuritis. Arch Neurol 2012; 69: 752– 756. 22371853
  11. [12]Hacohen Y Absoud M Woodhall M Autoantibody biomarkers in childhood-acquired demyelinating syndromes: results from a national surveillance cohort. J Neurol Neurosurg Psychiatry 2014; 85: 456– 461. 24133290
  12. [13]Banwell B Bar-Or A Arnold DL Clinical, environmental, and genetic determinants of multiple sclerosis in children with acute demyelination: a prospective national cohort study. Lancet Neurol 2011; 10: 436– 445. 21459044
  13. [14]Baumann M Sahin K Lechner C Clinical and neuroradiological differences of paediatric acute disseminating encephalomyelitis with and without antibodies to the myelin oligodendrocyte glycoprotein. J Neurol Neurosurg Psychiatry Epub 2014 Aug 13; doi: 10.1136/jnnp-2014-308346. 25121570 · DOI
  14. [15]Banwell B Tenembaum S Lennon VA Neuromyelitis optica-IgG in childhood inflammatory demyelinating CNS disorders. Neurology 2008; 70: 344– 352. 18094334
  15. [16]Huppke P Rostasy K Karenfort M Acute disseminated encephalomyelitis followed by recurrent or monophasic optic neuritis in pediatric patients. Mult Scler 2013; 19: 941– 946. 23128668
  16. [17]Rostasy K Mader S Hennes EM Persisting myelin oligodendrocyte glycoprotein antibodies in aquaporin-4 antibody negative pediatric neuromyelitis optica. Mult Scler 2013; 19: 1052– 1059. 23257621
  17. [18]Probstel AK Dornmair K Bittner R Antibodies to MOG are transient in childhood acute disseminated encephalomyelitis. Neurology 2011; 77: 580– 588. 21795651
  18. [19]Wingerchuk DM Lennon VA Pittock SJ Lucchinetti CF Weinshenker BG Revised diagnostic criteria for neuromyelitis optica. Neurology 2006; 66: 1485– 1489. 16717206
  19. [20]Jacob A McKeon A Nakashima I Current concept of neuromyelitis optica (NMO) and NMO spectrum disorders. J Neurol Neurosurg Psychiatry 2013; 84: 922– 930. 23142960
  20. [21]Palace J Leite MI Nairne A Vincent A Interferon Beta treatment in neuromyelitis optica: increase in relapses and aquaporin 4 antibody titers. Arch Neurol 2010; 67: 1016– 1017. 20697055
  21. [22]Kitley J Evangelou N Kuker W Jacob A Leite MI Palace J Catastrophic brain relapse in seronegative NMO after a single dose of natalizumab. J Neurol Sci 2014; 339: 223– 225. 24576801
  22. [23]Banwell B Bar-Or A Giovannoni G Dale RC Tardieu M Therapies for multiple sclerosis: considerations in the pediatric patient. Nat Rev Neurol 2011; 7: 109– 122. 21224883
  23. [24]Di Pauli F Mader S Rostasy K Temporal dynamics of anti-MOG antibodies in CNS demyelinating diseases. Clin Immunol 2011; 138: 247– 254. 21169067
  24. [25]Höftberger R Sepulveda M Armangue T Antibodies to MOG and AQP4 in adults with neuromyelitis optica and suspected limited forms of the disease. Mult Scler Epub 2014 Oct 24; pii: 1352458514555785. PMC4824843 25344373
  25. [26]Waters P Woodhall MR O'Connor KC MOG cell-based assay detects non-MS patients with inflammatory neurologic disease. Neurol Neuroimmunol Neuroinflamm 2015; 2: e89 doi: 10.1212/NXI.0000000000000089 (in press). PMC4370386 25821844 · DOI

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Authors
Hacohen, Y., Absoud, M., Deiva, K., Hemingway, C., Nytrova, P., Woodhall, M., Palace, J., Wassmer, E., Tardieu, M., Vincent, A., Lim, M., & Waters, P.
Affiliations
  • Guy's and St Thomas' NHS Foundation Trust (GB)
  • From the Nuffield Department of Clinical Neurosciences (Y.H., M.W., J.P., A.V., M.L., P.W.), John Radcliffe Hospital, University of Oxford, UK; Children's Neurosciences (M.A., M.L.), Evelina Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, King's Health Partners Academic Health Science Centre, London, UK; Assistance Publique Hôpitaux de Paris (K.D., M.T.), Hopitaux Universitaires Paris Sud, France; Pediatric Neurology Department and National Referral Center for Neuroinflammatory...
Corresponding author
Lim, Ming
ORCID
Venue
Neurology Neuroimmunology & Neuroinflammation
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2015-04
Volume
2
Issue
2
Pages
e81-e81
ISSN
2332-7812 (ISSN-L)
DOI
10.1212/nxi.0000000000000081
PMC
PMC4360800
OpenAlex
W2116294933
Cited by
230
References
1
Citations by year
2026: 9 · 2025: 7 · 2024: 12 · 2023: 13 · 2022: 21 · 2021: 22 · 2020: 24 · 2019: 30 · 2018: 30 · 2017: 31 · 2016: 24 · 2015: 7
FWCI
24.36
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Neurology Neuroimmunology & Neuroinflammation (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Research Portal (King's College London) (submittedVersion, cc-by-nc-nd)
Funders
  • Action Medical Research
  • National Institute for Health and Care Research
  • University of Oxford
  • Oxford University Clinical Academic Graduate School
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Health Sciences › Medicine › Neurology › Peripheral Neuropathies and Disorders
  • Health Sciences › Medicine › Neurology › Autoimmune Neurological Disorders and Treatments
Keywords
myelin oligodendrocyte glycoprotein antibodies, acquired demyelinating syndromes, acute disseminated encephalomyelitis, optic neuritis, transverse myelitis, clinically isolated syndrome

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