Abstract

Myasthenia gravis (MG) is an autoimmune disorder involving the neuromuscular junction characterized by fatigable weakness of the striated muscles [1]. It is primarily mediated by autoantibodies against the acetylcholine receptors (AChR) on post-synaptic membrane of the motor end plate and are present in the serum of 85% of MG patients [1]. Recently, antibodies recognizing other skeletal muscle components have been detected which have provide additional diagnostic and prognostic information [2]. Anti-titin antibodies fall under this category and are found in 20–40% of anti-AChR antibody positive patients.

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