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Acetylcholinesterase inhibitors in MG: To be or not to be?
Author(s) -
Punga Anna Rostedt,
Stålberg Erik
Publication year - 2009
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21319
Subject(s) - myasthenia gravis , acetylcholinesterase , neuromuscular transmission , neuromuscular junction , acetylcholine receptor , medicine , muscle weakness , pharmacology , weakness , antibody , acetylcholine , tyrosine kinase , endocrinology , chemistry , immunology , receptor , enzyme , psychology , neuroscience , biochemistry , surgery
Myasthenia gravis (MG) is an autoimmune disorder usually caused by antibodies against either the acetylcholine receptor (AChR) or muscle‐specific tyrosine kinase (MuSK) at the neuromuscular junction. Neuromuscular transmission failure results in muscle fatigue and weakness that can be treated symptomatically with acetylcholinesterase inhibitors (AChEIs). Long‐term treatment with nonselective AChEIs may have considerable drawbacks; thus, this medication is ideally tapered when strength improves. Patients with AChR antibodies respond beneficially to treatment, whereas patients with MuSK antibodies generally do not. Recently, the selective AChEI EN101, which specifically targets the isoform of “read‐through” AChE (AChE‐R), has been developed and may be of importance for symptomatic relief in AChR‐antibody seropositive MG. This article is a review of the mechanisms, therapeutic effects, and drawbacks, with both old and new AChEIs in MG. Muscle Nerve, 2009