Abstract
Myasthenia gravis (MG) is an autoimmune neuromuscular disorder which is characterized by presence of antibodies against acetylcholine receptors (AChRs) or other proteins of the postsynaptic membrane resulting in damage to postsynaptic membrane, decreased number of AChRs or blocking of the receptors by autoantibodies. A number of drugs such as immune checkpoint inhibitors, penicillamine, tyrosine kinase inhibitors and interferons may induce de novo MG by altering the immune homeostasis mechanisms which prevent emergence of autoimmune diseases such as MG. Other drugs, especially certain antibiotics, antiarrhythmics, anesthetics and neuromuscular blockers, have deleterious effects on neuromuscular transmission, resulting in increased weakness in MG or MG-like symptoms in patients who do not have MG, with the latter usually being under medical circumstances such as kidney failure. This review summarizes the drugs which can cause de novo MG, MG exacerbation or MG-like symptoms in nonmyasthenic patients.
Highlights
Myasthenia gravis (MG) is the most common type of neuromuscular transmission disease and is caused by autoantibodies against acetylcholine receptors (AChRs) in the neuromuscular junction or their adjacent proteins
Emergence of symptoms consistent with ocular myasthenia gravis
Antipsychotics: Chlorpromazine was the first typical antipsychotic reported to be associated with MG exacerbation [142]; it was subsequently shown to impair neuromuscular transmission both at the postsynaptic membrane and to inhibit of ACh release from the presynaptic membrane
Summary
Myasthenia gravis (MG) is the most common type of neuromuscular transmission disease and is caused by autoantibodies against acetylcholine receptors (AChRs) in the neuromuscular junction or their adjacent proteins. The weakness is generally symmetric (except for symptoms related to the eyes which is often asymmetric) and has more proximal than distal muscle involvement [4]. A number of medications precipitate autoimmunity and symptomatic MG; many more drugs adversely affect the neuromuscular junction transmission and have been implicated in worsening of MG symptomatology, including precipitation of MG crisis, or unmasking of a previously undiagnosed MG. There are two general mechanisms for a drug to cause MG or MG-like symptoms: 1. Drugs which impair neuromuscular transmission can block the nerve action potential or impair release of ACh from the presynaptic membrane, such as by inhibiting the presynaptic calcium channels (1 and 2). *: may affect neuromuscular transmission; ADR: adverse drug reaction. Impair neuromuscular transmission at presynaptic and postsynaptic levels Presynaptic: reduction in ACh synthesis and release; postsynaptic: reduction in number of AChRs. IVIG or plasmapheresis Avoid if possible, may be offered with caution and slow dose titration to patients with mild/stable MG who have blepharospasm or cervical dystonia
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