Acquired myasthenia gravis (MG) is a chronic autoimmune disorder of the neuromuscular junction, characterized by muscle weakness and fatigability on exertion. MG is caused by autoantibodies against acetylcholine receptors in the postsynaptic membrane.1 The path-ogenesis involved in acetylcholine receptor impairment includes: accelerated endocytosis and degradation of acetylcholine receptors, functional blockade of the acetylcholine binding site, and complement-mediated damage of the postsynaptic membrane. The initiating event of MG is unknown, but speculations have been made about viral infections as a possible trigger.
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