Comparison of the Response to Rituximab between Myelin Oligodendrocyte Glycoprotein and Aquaporin‐4 Antibody Diseases. Issue 2 (27th November 2019)

• Record Type: Journal Article
• Authors: Durozard, Pierre; Rico, Audrey; Boutiere, Clémence; Maarouf, Adil; Lacroix, Romaric; Cointe, Sylvie; Fritz, Shirley; Brunet, Corinne; Pelletier, Jean; Marignier, Romain; Audoin, Bertrand
• Is Part Of: Annals of neurology. Volume 87:Issue 2(2020)
• Page Start: 256
• Page End: 266
• Publication Date: 2019-11-27
• Subjects: Neurology -- Periodicals; Pediatric neurology -- Periodicals; Nervous system -- Surgery -- Periodicals; 616.8
• DOI: 10.1002/ana.25648
• Languages: English
• ISSNs: 0364-5134

Abstract

Abstract : Objective: To compare response to rituximab (RTX) between adult patients positive for myelin oligodendrocyte glycoprotein (MOG) and aquaporin‐4 (AQP4) antibodies. Methods: We prospectively studied adult patients with MOG or AQP4 antibodies who received RTX under an individualized dosing schedule adapted to the biological effect of RTX monitored by memory B‐cell measurement. Memory B cells were counted monthly and when relapse occurred. The biological effect of RTX was considered significant with <0.05% memory B cells in peripheral blood lymphocytes. Results: In 16 patients with MOG antibodies and 29 with AQP4 antibodies, mean follow‐up was 19 (range = 9–38) and 38 (13–79) months. Under RTX, 10 relapses occurred in 6 of 16 (37.5%) patients with MOG antibodies, and 13 occurred in 7 of 29 (24%) with AQP4 antibodies. The median time of relapse after the most recent infusion was 2.6 (0.6–5.8) and 7 (0.8–13) months, respectively ( p < 0.001). Memory B cells had reemerged in 2 of 10 (20%) relapses in patients with MOG antibodies and 12 of 13 (92.5%) with AQP4 antibodies ( p < 0.001). Interpretation: In AQP4 antibody–associated disorder, relapse mostly occurs when the biological effect of RTX decreases, which argues for treatment efficacy. In MOG antibody–associated disorder, the efficacy of RTX is not constant, because one‐third of patients showed relapse despite an effective biological effect of RTX. In this subpopulation, memory B‐cell depletion was unable to prevent relapse, which was probably caused by different immunological mechanisms. These findings should be used to improve treatment strategies for MOG antibody–associated disorder. ANN NEUROL 2020;87:256–266