Low-dose rituximab in AChR antibody-positive ocular myasthenia gravis: Efficacy and safety—A preliminary study

This study evaluates the efficacy and safety of low-dose rituximab (RTX) in patients with acetylcholine receptor antibody (AChR-Ab)-positive ocular myasthenia gravis (OMG). This was a single-center retrospective observational study that included 9 patients with AChR-Ab-positive OMG who received low-dose RTX treatment (200 mg, once every 6 months to 1 year) between January 2023 and January 2024. Evaluation indicators included MGFA-PIS status, MG-ARS score, Quantitative Myasthenia Gravis Score, peripheral blood B-cell levels (CD19+), corticosteroid usage, and adverse events at 1, 3, 6, and 12 months before and after treatment. The Wilcoxon signed-rank test was used for statistical analysis, with Z-values and effect size r calculated. A P-value < .05 was considered statistically significant. All patients showed varying degrees of clinical improvement within the 12-month follow-up period. MGFA-PIS indicated complete remission in 5 cases (55.6%), pharmacologic remission in 3 cases (33.3%), and improvement in 1 case (11.1%). The median MG-ARS score decreased significantly from 10 at baseline to 0 at 12 months (Z = 2.71, P < .001); the median Quantitative Myasthenia Gravis Score decreased from 4 to 0 (Z = 1.36, P < .001). Eight patients reduced corticosteroid use by 100%, and one patient by 83.3%. The percentage of peripheral B cells significantly decreased from 0.1543% at baseline to 0.0103% (Z = -2.52, P = .0078); absolute B-cell count decreased from 303.0/μL to 16.5/μL (Z = -2.49, P = .0078). Ptosis resolved within 2 to 8 weeks in 66.7% of patients; diplopia was less common and took longer to resolve. No serious adverse reactions were observed, and treatment was well tolerated. Low-dose rituximab demonstrates good clinical efficacy and safety in AChR antibody-positive OMG patients, effectively alleviating symptoms, reducing corticosteroid dependence, and sustainably suppressing B-cell activity through targeted depletion and functional exhaustion of B cells, thereby interrupting the antibody-mediated autoimmune response. This treatment offers a feasible and well-tolerated immunotherapeutic option for OMG patients and warrants further prospective validation with larger sample sizes.