Background Neuromyelitis optica spectrum disorder (NMOSD) causes relapsing inflammatory attacks in the central nervous system, leading to disability. As rituximab, a B-lymphocyte-depleting monoclonal antibody, is an effective in preventing NMOSD relapses, we hypothesised that earlier initiation of rituximab can also reduce long-term disability of patients with NMOSD.
Methods This multicentre retrospective study involving 19 South Korean referral centres included patients with NMOSD with aquaporin-4 antibodies receiving rituximab treatment. Factors associated with the long-term Expanded Disability Status Scale (EDSS) were assessed using multivariable regression analysis.
Results In total, 145 patients with rituximab treatment (mean age of onset, 39.5 years; 88.3% female; 98.6% on immunosuppressants/oral steroids before rituximab treatment; mean disease duration of 121 months) were included. Multivariable analysis revealed that the EDSS at the last follow-up was associated with time to rituximab initiation (interval from first symptom onset to initiation of rituximab treatment). EDSS at the last follow-up was also associated with maximum EDSS before rituximab treatment. In subgroup analysis, the time to initiation of rituximab was associated with EDSS at last follow-up in patients aged less than 50 years, female and those with a maximum EDSS score ≥6 before rituximab treatment.
Conclusions Earlier initiation of rituximab treatment may prevent long-term disability worsening in patients with NMOSD, especially among those with early to middle-age onset, female sex and severe attacks.
Data availability statement
No data are available.
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BJK and S-MK contributed equally.
Contributors Conception and design of the study: S-MK and BJK. Data collection and manuscript editing: YNK, SK, SHK, JKK, J-SK, T-SN, KSP, J-SP, JMS, ES, KJS, J-HS, HYS, S-IO, JYO, B-AY, SGL, J-ML, HLL, KC, S-YH, J-HM and J-JS. Data analysis and interpretation: YGM, M-JJ, SYP and S-MK Drafting the article: SYP. Critical revision of the article: SYP, M-JJ and S-MK. Final approval of the version to be published: all authors.
Funding This work was supported by the Korea Health Industry Development Institute, Ministry of Health and Welfare, Republic of Korea (HI21C0539) and by Korea Disease Control and Prevention Agency (2020-ER6901-02). Some of the biospecimens for AQP4-IgG assay were provided by the Seoul National University Hospital Human Biobank, a member of the Korea Biobank Network, which is supported by the Ministry of Health and Welfare. All samples derived from the National Biobank of Korea were obtained with informed consent under institutional review board-approved protocols.
Disclaimer The funders had no role in the study design, data collection and analysis, decision to publish, or manuscript preparation.
Competing interests S-MK has lectured, consulted and received honoraria from Bayer Schering Pharma, Genzyme, Merck Serono and UCB; received a grant from the National Research Foundation of Korea and the Korea Health Industry Development Institute Research. S-MK and KSP are associate editors of the Journal of Clinical Neurology. S-MK, KSP, Seoul National University and Seoul National University Hospital have transferred the technology of the flow cytometric autoantibody assay to the EONE Laboratory, Korea. Byoung Joon Kim; honoraria/consulting fees (Biogen, Genzyme, Merck, Sanofi, Astellas, Merk); member of advisory boards (Astellas, Korean FDA).
Provenance and peer review Not commissioned; externally peer reviewed.
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