The clinical course, therapeutic responses, and outcomes in relapsing MOG antibody-associated demyelination
ECTRIMS Online Library. Ramanathan S. Oct 25, 2017; 202395; 52
Sudarshini Ramanathan
Sudarshini Ramanathan

Abstract: 52

Type: Oral

Abstract Category: Therapy - disease modifying - 26 Immunomodulation/Immunosuppression

Background: There is increasing recognition of patients with demyelination who have antibodies targeting myelin oligodendrocyte glycoprotein (MOG) antibodies and exhibit a relapsing clinical course. Data regarding the efficacy of immunosuppressive agents in patients with MOG antibodies is limited.
Objective: We characterised the clinical course, treatment, and outcomes in 59 patients with relapsing MOG antibody-associated demyelination.
Methods: We evaluated clinical phenotypes, annualised relapse rates (ARR) prior to and on immunotherapy, and expanded disability status scales (EDSS), in 216 demyelinating episodes from 33 paediatric and 26 adult patients, with an average follow-up of five years.
Results: The most common initial presentation was optic neuritis (ON) in 54% [bilateral (BON) 32%, unilateral (UON) 22%], followed by acute disseminated encephalomyelitis (20%) which occurred exclusively in children. ON was the dominant phenotype (UON 34% BON 19%) of all 216 clinical episodes. Only 25% of the total cohort fulfilled 2015 revised criteria for neuromyelitis optica spectrum disorders. 107/224 (48%) MRIs had no brain lesions. Patients were steroid responsive but 70% of episodes treated with oral prednisone relapsed, especially at doses < 10 mg daily, within two months of cessation, and in patients with a taper duration of less than six weeks. Immunotherapy, including maintenance prednisone (P=0.0004), intravenous immunoglobulin (IVIg), rituximab, and mycophenolate, all reduced median ARRs on-treatment. Treatment failure rates were lowest with maintenance prednisone (6%). Switching therapy in those who failed the first immunosuppressive agent reduced on-treatment ARR (P=0.03). 59% of patients experienced residual disability (average follow-up 60 months, visual loss in 25%). Patients with ≥ 3 demyelinating episodes were more likely to have a follow-up EDSS of ≥2
(OR 4.0, 95% CI 1.22-13.13, P=0.019).
Conclusion: Relapsing MOG antibody-associated demyelination is strongly associated with ON, is steroid responsive but vulnerable to relapse on withdrawal, and responsive to maintenance corticosteroids, IVIg, or immunosuppression. A subgroup of patients with MOG antibodies can have poor outcomes. Increasing relapses lead to sustained disability.
Dr Sudarshini Ramanathan has received a scholarship from the National Health and Medical Research Council (Australia) and a research stipend from the Petre Foundation (Australia)
Dr Shekeeb Mohammad has received a scholarship from the National Health and Medical Research Council (Australia) and funding from the National Blood Authority IVIG Grant
Dr Esther M Tantsis: nothing to disclose
Ms Tina K Nguyen: nothing to disclose
Ms Vera Merheb: nothing to disclose
Associate Professor Victor SC Fung: nothing to disclose
Associate Professor Owen B White: nothing to disclose
Professor Simon A Broadley has received honoraria for attendance at advisory boards and travel sponsorship from Bayer-Scherring, Biogen-Idec, Merck-Serono, Novartis, and Sanofi-Genzyme, has received speakers honoraria from Biogen-Idec and Genzyme, is an investigator in clinical trials sponsored by Biogen Idec, Novartis and Genzyme, and was the recipient of an unencumbered research grant from Biogen-Idec.
Associate Professor Jeanette Lechner-Scott has accepted travel compensation from Novartis, Biogen and Merck Serono; and her institution receives the honoraria for talks and advisory board commitment as well as research grants from Bayer Health Care, Biogen, Genzyme Sanofi, Merck, Novartis and TEVA
Professor Steve Vucic: nothing to disclose
Dr Andrew Henderson: nothing to disclose
Associate Professor Michael Barnett: nothing to disclose
Associate Professor Stephen Reddel reports grants and personal fees from Genzyme Sanofi, personal fees and departmental support from the Government of Australia, Baxter, Biogen, CSL, and Merck; and departmental support from Novartis, outside the subject of the submitted work.
Associate Professor Fabienne Brilot has received research funding from the Star Scientific Foundation, The Trish Multiple Sclerosis Research Foundation, Multiple Sclerosis Research Australia, and the National Health Medical Research Council (Australia).
Professor Russell Dale has received research funding from the Star Scientific Foundation, The Trish Multiple Sclerosis Research Foundation, Multiple Sclerosis Research Australia, the Petre Foundation, and the National Health Medical Research Council (Australia), as well as honoraria from Biogen Idec as an invited speaker.
Funding acknowledgements: This work was supported by the National Health and Medical Research Council (NHMRC) (Australia), the Petre Foundation (Australia), Multiple Sclerosis Research Australia (MSRA) (Australia), the National Blood Authority IVIg grant (Australia), and the Sydney Research Excellence Initiative 2020 Neuroimmunology Group (University of Sydney, Australia).

By clicking “Accept Terms & all Cookies” or by continuing to browse, you agree to the storing of third-party cookies on your device to enhance your user experience and agree to the user terms and conditions of this learning management system (LMS).

Cookie Settings
Accept Terms & all Cookies