Myasthenia gravis (MG), an autoimmune disease, is characterized by physical exhaustion and weakness caused by autoantibody-induced dysfunction of the neuromuscular junction. MG is frequently accompanied with thymoma, and approximately 25%… Click to show full abstract
Myasthenia gravis (MG), an autoimmune disease, is characterized by physical exhaustion and weakness caused by autoantibody-induced dysfunction of the neuromuscular junction. MG is frequently accompanied with thymoma, and approximately 25% of patients with thymoma-associated MG exhibit at least one non-motor symptom (taste disorder, myocarditis, neuromyotonia, limbic encephalitis, pure red cell aplasia, immunodeficiency, or alopecia areata) [1]. Further, approximately 74%–88% of patients with MG have anti-acetylcholine receptor (AChR) antibodies that bind to postsynaptic membrane and induce complement-mediated injury [2]. Moreover, anti-striational antibodies are often detected in patients with thymoma-associated refractory MG [3, 4], which putatively induce complement activation [5]. Herein, we report the case of refractory thymoma-associated generalized MG with anti-AChR and anti-striational antibodies. The motor symptoms remarkably improved by the administration of eculizumab, a humanized monoclonal antibody that targets the terminal complement protein C5 [6]. Moreover, taste disorder was alleviated, suggesting the involvement of complement activation in the onset of taste disorder in patients with MG.
               
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