ArticleJournal of neurology2025
Fluctuations in serum aquaporin-4 antibody titers: the clinical significance in neuromyelitis optica spectrum disorder.
Article in Journal of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- AQP4-IgG Dynamics and Exploratory Assessment of SERA-3 in Neuromyelitis Optica Spectrum Disorder Treated with Satralizumab.Neurology and therapy · 2026Article
- Use of Fluid Biomarkers in NMOSD and MOGAD: Clinical and Research Applications.Neurology(R) neuroimmunology & neuroinflammation · 2026Review
- Obinutuzumab β for aquaporin-4-positive neuromyelitis optica spectrum disorder: a phase 3 randomized controlled trial.Nature medicine · 2026Article
- Consistent Detection of Aquaporin-4 Antibodies: A Comparative Analysis Between Fixed and Live Cell-Based Assays.Journal of clinical neurology (Seoul, Korea) · 2026Article
- Biomarkers for satralizumab treatment in neuromyelitis optica spectrum disorders: a prospective case series.BMC neurology · 2026Article
- Outcomes and predictors of relapse and severe pneumonia in Chinese patients with AQP4-IgG-positive neuromyelitis optica spectrum disorder receiving inebilizumab: a prospective cohort study.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
objectivesTo evaluate the relationship between aquaporin-4 immunoglobulin G (AQP4-IgG) titer dynamics and relapse in neuromyelitis optica spectrum disorder (NMOSD), compare AQP4-IgG dynamics across different maintenance therapy strategies, and identify factors associated with AQP4-IgG titer seroreversion to negativity.
methodsAltogether 171 patients with ≥ 2 serum AQP4-IgG tests by fixed cell-based assay 30 days apart and at least once positive were included. Their clinical and treatment data were reviewed.
resultsAmong the 171 NMOSD patients with a median disease duration of 81.3 months, 44 (25.7%) became AQP4-IgG seronegative, accompanied by a reduction in annualized relapse rate (0.16 vs. 0.00, P < 0.001). Decline in serum AQP4-IgG titers emerged as the protective factor against relapse (HR 0.53, 95% CI 0.36-0.79, P = 0.002). Patients receiving monoclonal antibodies (mostly B cell-depleting therapies) as their initial and sole therapy throughout disease demonstrated higher likelihood of AQP4-IgG seroreversion compared to those treated with non-specific immunosuppressants (HR 3.01, 95% CI 1.23-7.34, P = 0.016) or those started with immunosuppressants and later switched to monoclonal antibodies (HR 6.17, 95% CI 2.13-17.54, P < 0.001). Male (OR 3.95, 95% CI 1.35-11.63, P = 0.012), baseline AQP4-IgG titer (OR 0.71, 95% CI 0.55-0.92, P = 0.008) and monoclonal antibody treatment throughout disease (OR 4.07, 95% CI 1.45-11.40, P = 0.008) were independently associated with AQP4-IgG seroreversion.
interpretationSerum AQP4-IgG titer is related with relapse risk. Early initiation of monoclonal antibodies shows a superior suppressive effect on AQP4 autoimmunity.
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