Bonaventura et al question our suggestion that one mechanism for the amelioration in muscle strength that follows intravenously administered immunoglobulin is interference with the interaction between acetylcholine-receptor antibodies (anti-AChR antibodies) and acetylcholine receptor (AChR). As all of our patients were anti-AChR antibody positive, I would have to disagree and state that the generally accepted pathogenesis of antibody-positive myasthenia gravis hinges on anti-AChR antibody's ability to block and, more importantly, to increase turnover of AChR by cross-linking 2 AChRs via 2 antigen-binding fragment—portions of IgG accelerating internalization and degradation of AChR.1 Complement fixation and activation of the terminal phase of complement cascade would also increase AChR destruction.2 The patient that they present (provided a congenital myasthenic syndrome has been excluded from diagnosis) who was repeatedly anti-AChR negative falls into a distinct subset of patients with myasthenia gravis different from our patients3 and, therefore, not comparable. In patients such
Arsura E. High-Dose Intravenous Immunoglobulin in the Management of Myasthenia Gravis-Reply. Arch Intern Med. 1987;147(2):211. doi:10.1001/archinte.1987.00370020031020
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