Myasthenia gravis (MG) is the prototypic autoimmune neurologic disease caused by an antibody to the nicotinic acetylcholine receptor (AChR) in most patients. Less often, an antibody to muscle-specific tyrosine kinase (MuSK) and a growing number of other postsynaptic proteins are believed to be responsible. Although MG is usually treated effectively with acetylcholinesterase inhibitors, corticosteroids, or so-called corticosteroid-sparing agents, such as azathioprine and mycophenolate mofetil, 10% to 15% of patients have difficult-to-control disease, commonly referred to as treatment-refractory MG.1 Maintenance treatment options in refractory MG are somewhat limited but may include long-term use of high-dose corticosteroids, intravenous immunoglobulin (IVIg), or plasma exchange (PE). In the past decade, rituximab, a chimeric murine-human monoclonal antibody against CD20+ B cells, has been the centerpiece of an increasing number of reports claiming success in managing refractory MG.
Silvestri NJ, Wolfe GI. Rituximab in Treatment-Refractory Myasthenia Gravis. JAMA Neurol. 2017;74(1):21–23. doi:10.1001/jamaneurol.2016.4367
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