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Autoimmune myasthenia gravis (MG) is a prototypical, antibody-mediated disorder involving fluctuating ocular and generalized skeletal muscle weakness. In over 90% of patients with generalized MG, serum antibodies develop against one of 3 endplate proteins (acetylcholine receptor [AChR], muscle-specific tyrosine kinase [MuSK], and lipoprotein receptor-related 4). Antibodies are pathogenic in their disruption of normal neuromuscular transmission and their presence is usually diagnostic.1 However, while antibody levels are a biomarker in MuSK MG,2,3 they do not correlate well with disease severity or treatment response in AChR antibody-positive MG; AChR antibody titers generally fall with immunosuppressive therapy whether or not the patient improves clinically.4
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