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The following is a summary of “Relapses during treatment with monoclonal antibodies targeting B-cells in NMOSD,” published in the May 2025 issue of Journal of Neurology by Cao et al.
Sustained B-cell depletion helps maintain relapse-free status in patients with neuromyelitis optica spectrum disorder (NMOSD). However, B-cell therapies are not effective for all cases.
Researchers conducted a retrospective study to identify risk factors for relapses during B-cell-targeting monoclonal antibody (mAb) treatment in patients with NMOSD.
They retrospectively analyzed baseline clinical data, B-cell test results, and relapse records from patients with NMOSD treated with B-cell-targeting mAbs at 4 centers between July 2014 and September 2024. They compared annualized relapse rates (ARR) before and after treatment and used a Cox proportional hazard model to evaluate relapse risk factors during mAb therapy.
The results showed that the study included 101 patients with NMOSD, 14 treated by inebilizumab and 87 by rituximab. The mean age at mAb initiation was 49 years (range 10–74), and the median follow-up was 21.5 months (9.4, 37.6). About 2 patients were lost to follow-up, 1 died, and 17 relapsed, with a relapse-free rate of 83.2%. The annualized relapse rate decreased significantly from 0.3 (0, 0.9) before treatment to 0 (0, 0) after treatment (P = 0.002). Kaplan–Meier analysis showed higher relapse risk in patients with clustered attacks (P < 0.001) and those with EDSS scores ≥ 6 (P = 0.006) before treatment. Cox models identified total attacks, disease duration, ARR, and EDSS ≥ 6 as significant relapse risk factors. Patients relapsing with CD19+ B-cell levels < 1% had more attacks one year before treatment (P = 0.015) and more clustered attacks (P = 0.035) than those with CD19+ levels ≥ 1%.
Investigators found that attack frequency and cumulative disability before mAb initiation predicted relapses during targeted B-cell mAb treatment for neuromyelitis optica spectrum disorder. They concluded that preventing clustered attacks could reduce mAb treatment failure.
Source: link.springer.com/article/10.1007/s00415-025-13118-9
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