Submitted by: Niranjan Singh, MD
Edited by: Rebecca O’Bryan, MD
Hänggi P, Aliu B, Martin K, Herrendorff R, Steck AJ. Decrease in serum anti-MAG autoantibodies is associated with therapy response in patients with anti-MAG neuropathy: Retrospective study. Neurol Neuroimmunol Neuroinflamm
. 2021;9(1):e1109. Published 2021 Nov 10. doi:10.1212/NXI.0000000000001109
This retrospective analysis tested the hypothesis that changes in serum anti-myelin-associated glycoprotein (MAG) autoantibodies are associated with clinical response to immunotherapy in patients with anti-MAG neuropathy. The study evaluated relative change in anti-MAG immunoglobulin M (IgM) titers, paraprotein level, or total IgM, before, during or post treatment. Patients were assigned to either the "responders", "nonresponders", or "acute deteriorating" category. Various treatments included steroids, intravenous immunoglobulin, rituximab, plasma exchange, and other immunosuppressants.
The study included 410 patients with anti-MAG neuropathy. 303 patients supported the hypothesis that responder patients had a relative reduction of anti-MAG antibody titers, while the non-responder patients exhibited no significant change in anti-MAG IgM autoantibodies.
The study concluded that a relative reduction in serum anti-MAG IgM antibodies was associated with a clinical response to immunotherapies. Sustained reduction of 50% or more with pretreatment titers could be valuable indicator for therapeutic response.
The significance of anti-MAG antibody titers or levels as predictive of response to therapy is controversial. Although there is considerable evidence of pathogenicity of autoantibodies, association of reduced serum level is less clear. There are conflicting studies that do not support the hypothesis that reduced serum level associates with clinical response to immunotherapy. The variety of clinical outcome measures including disability score makes a direct comparison between clinical studies difficult. A correlation coefficient was not calculated for reduction of autoantibodies and clinical improvement.
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