Several investigators have now shown that a fall in the level of anti-AChR antibody is not necessary for clinical or electrophysiological improvement after thymectomy or plasma exchange in MG.1,2 Possible explanations for this poor correlation are as follows: (1) Serum antibody levels may not reflect the amount of immune complex bound to AChR. (2) A subpopulation of anti-AChR antibodies could exist that is not measured by current assays. (3) If the number of unblocked AChRs were just below the safety margin for normal neuromuscular transmission, even a small increase in the number of "free" receptors could restore full neuromuscular transmission without a measurable fall in antibody level.Some investigators have not found these or other explanations attractive enough to remain on the anti-AChR antibody "bandwagon," despite the fact that substantial titers of these antibodies are found in approximately 90% of patients with MG, and no anti-AChR antibodies
Hochman MS. Antiacetylcholine Receptor Antibodies and Myasthenia Gravis-Reply. JAMA. 1982;247(22):3082–3083. doi:10.1001/jama.1982.03320470030023
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