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Intravenous Immunoglobulin for the Treatment of Acquired Myasthenia Gravis

From the Department of Neurology and the Laboratory for Myasthenia Gravis Research, University of North Carolina at Chapel Hill, Chapel Hill, NC.

Address correspondence and reprint requests to Dr. James F. Howard, Jr., Department of Neurology, 751 Clinical Sciences Bldg., CB #7025, University of North Carolina, Chapel Hill, NC 27599-7025.

Abstract.

Acquired myasthenia gravis (MG) is an autoimmune disorder characterized by exertional fatigue and weakness that is made worse with activity and improved with rest, only to recur with the resumption of activity. The pathology results from an antibody-mediated attack to several different epitopes of the acetylcholine receptor (AChR) complex. The consensus of an expert panel is that intravenous immunoglobulin (IVIg) is effective in reversing myasthenic weakness. Although the mechanism of action is not known, it is likely that there is a downregulation of antibody production. IVIg appears to have a role as an acute treatment intervention in rapidly progressive weakness or as a chronic maintenance therapy when all other treatment modalities have failed. Its response is similar to but slower than the response of plasma exchange (PE), but it offers advantages when therapeutic apheresis is not available or when vascular access is problematic.