Abstract
Much of the improvement in the treatment of myasthenia gravis (MG) over the past 125 years can be attributed to the effectiveness of general medical measures such as advances in respiratory care and the discovery of antibiotics. Although MG became the model of an antibody-mediated autoimmune disease in the 1970s (the most documented antigen being the muscle acetylcholine receptor at the neuromuscular junction), the pathogenesis of MG has not been the rationale for most treatments found to be useful for this disease. The serendipitous benefit of anticholinesterases for MG in the 1930s subsequently focused attention on the neuromuscular junction. The beginnings of the controversy over thymectomy for MG in the 1940s and 1950s preceded the discovery in 1960 of the function of the thymus. Before the autoimmune pathogenesis of MG was known, adrenocorticotropic hormone (ACTH) and steroids for MG were tried for reasons that turned out to be incorrect. Further immunosuppressive treatments for MG were largely empirical, following their use in organ transplantation and other autoimmune diseases. More specific treatments, based on our knowledge of pathogenesis, are still experimental but hopefully will be the history of the future.
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