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- W2036617963 abstract "Of all neurological diseases, the one that virtually all third year medical students get right on final exams is myasthenia gravis (MG). MG is an autoimmune disorder that causes weakness and fatigue of skeletal muscles due to an antibody-mediated attack directed against AChRs at neuromuscular junctions (1). It is easy to learn and remember the pathogenesis, immunology, and treatment of MG because the pieces of the puzzle fit together nearly perfectly. In this issue of the JCI, Lennon et al. now provide intriguing evidence of another putative autoimmune disease of AChRs — autoimmune autonomic neuropathy (AAN) (2). They have shown that immunization of rabbits with a fragment of ganglionic AChR induces a condition that mimics the human disease. AAN is very rare but can be life threatening. It is manifested by autonomic disturbances affecting the sympathetic and parasympathetic nervous systems: abnormal gastrointestinal motility with stalled traffic in the intestines, impaired contraction and striking dilatation of the bladder, and disturbances of blood pressure, sweating, salivation, pupillary reactions, and sexual function (3). Based on these experiments and other evidence (4), Lennon et al. suggest that: (a) an antibody-mediated attack directed against neuronal AChRs of autonomic ganglia may be implicated in at least some cases of AAN; and (b) the autoimmune response in some of these patients may be triggered by a remote neoplasm that incidentally expresses the autoantigen. These new findings provide interesting insights into the concepts of autoimmune and paraneoplastic diseases of the nervous system, and information that may be useful for practical treatment of AAN." @default.
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- W2036617963 date "2003-03-15" @default.
- W2036617963 modified "2023-09-27" @default.
- W2036617963 title "Autonomic “myasthenia”: the case for an autoimmune pathogenesis" @default.
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- W2036617963 doi "https://doi.org/10.1172/jci18180" @default.
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