Procainamide-Induced Myasthenia-Like Weakness and Dysphagia

Cd, Miller; Ma, Oleshansky; Gibson, Kevin J.; Lr, Cantilena

doi:10.1097/00007691-199306000-00013

Cited by 17 publications

(4 citation statements)

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“…Clinically, procainamide may lead to a rapid and severe deterioration of weakness in MG patients (Godley et al, 1990). Moreover, also the primary induction of myasthenic symptoms including bulbar features has been reported occasionally in the literature (Oh et al, 1986;Miller et al, 1993). Though immunological properties have been ascribed to this drug, the rapid clinical manifestation of neuromuscular symptoms rather supports a directly NMJrelated mechanism.…”

Section: Postsynaptic Neuromuscular Junction Effectsmentioning

confidence: 99%

“…Interference with protein synthesis via ribosomal 50S subunit Telithromycin withdrawn from market May and Calvert, 1990;Cadisch et al, 1996;Nieman et al, 2003;Jennett et al, 2006;Perrot et al, 2006;Liu and Somps, 2010 Class Quinidine used as a treatment in (slow channel) CMS Lee et al, 1983;Oh et al, 1986;Godley et al, 1990;Yeh et al, 1992;Miller et al, 1993 Class Krendel and Hopkins, 1986;Ribera and Nastuk, 1989;Swash and Ingram, 1992;Jonkers et al, 1996;Protti et al, 1996 Betaadrenergic blockers Harry et al, 1974;Verkijk, 1985;Leys et al, 1987;Confavreux et al, 1990;Clausen et al, 2018;Gummi et al, 2019 Botulinum toxin A Seybold and Drachman, 1974;Wilson et al, 1974;Abramsky et al, 1975;Dengler et al, 1979;Kim et al, 1979;Pascuzzi et al, 1984;Kanai et al, Lipsitz, 1971;Gutmann and Takamori, 1973;Cohen et al, 1976;Swift, 1979;Pritchard, 1979;Krendel, 1990;Singh et al, 2015 (Continued) Frontiers in Molecular Neuroscience | www.frontiersin.org Clinically used as a mood stabilizer…”

Section: Electrolyte-related Neuromuscular Junction Effectsmentioning

confidence: 99%

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Pathomechanisms and Clinical Implications of Myasthenic Syndromes Exacerbated and Induced by Medical Treatments

Krenn

Grisold

Wohlfarth

et al. 2020

Front. Mol. Neurosci.

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Myasthenic syndromes are typically characterized by muscle weakness and increased fatigability due to an impaired transmission at the neuromuscular junction (NMJ). Most cases are caused by acquired autoimmune conditions such as myasthenia gravis (MG), typically with antibodies against the acetylcholine receptor (AChR). Different drugs are among the major factors that may complicate pre-existing autoimmune myasthenic conditions by further impairing transmission at the NMJ. Some clinical observations are substantiated by experimental data, indicating that presynaptic, postsynaptic or more complex pathomechanisms at the NMJ may be involved, depending on the individual compound. Most robust data exist for the risks associated with some antibiotics (e.g., aminoglycosides, ketolides, fluoroquinolones) and cardiovascular medications (e.g., class Ia antiarrhythmics, beta blockers). Apart from primarily autoimmune-mediated disorders of the NMJ, de novo myasthenic manifestations may also be triggered by medical treatments that induce an autoimmune reaction. Most notably, there is growing evidence that the immune checkpoint inhibitors (ICI), a modern class of drugs to treat various malignancies, represent a relevant risk factor to develop severe and progressive medication-induced myasthenia via an immune-mediated mechanism. From a clinical perspective, it is of utmost importance for the treating physicians to be aware of such adverse treatment effects and their consequences. In this article, we aim to summarize existing evidence regarding the key molecular and immunological mechanisms as well as the clinical implications of medication-aggravated and medication-induced myasthenic syndromes.

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Section: Postsynaptic Neuromuscular Junction Effectsmentioning

confidence: 99%

Section: Electrolyte-related Neuromuscular Junction Effectsmentioning

confidence: 99%

Pathomechanisms and Clinical Implications of Myasthenic Syndromes Exacerbated and Induced by Medical Treatments

Krenn

Grisold

Wohlfarth

et al. 2020

Front. Mol. Neurosci.

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show abstract

“…The creatine phosphokinase (CPK) levels in procainamide-induced myopathy can be normal or greater than 10 000 IU per liter (Meschia and Biller, 1998). Lastly, procainamide can aggravate myasthenic symptoms in myasthenia gravis patients (Drachman and Skom, 1965;Godley et al, 1990;Meschia and Biller, 1998) and even cause myasthenic-like symptoms such as severe bulbar, limb, and respiratory weakness in nonmyasthenic patients in high doses (Niakan et al, 1981;Oh et al, 1986;Miller et al, 1993;Meschia and Biller, 1998).…”

Section: Antiarrhythmicsmentioning

confidence: 99%

Neurologic complications of arrhythmia treatment

Leary

Veluz

Caplan

2014

Handbook of Clinical Neurology

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“…However, the postsynaptic effects appear to be more significant. 2 In addition, short-term administration of procainamide has also been associated with the development of an acute myopathy that may mimic MG 3 and that in some cases has been necrotizing. We present a patient with chronic procainamide-associated myopathy (CPAM) and serologic evidence of procainamide-induced lupus and propose an autoimmune mechanism for development of the chronic myopathy.…”

Section: Introductionmentioning

confidence: 99%