Acute effects of intravenous injection of beta‐adrenoreceptor‐ and calcium‐channel antagonists and agonists in myasthenia gravis

Jonkers, I.J.A.M.; Swerup, C.; Pirskanen, Ritva; Bjelak, Sapko; Matell, G.

doi:10.1002/(sici)1097-4598(199608)19:8<959::aid-mus4>3.3.co;2-i

Cited by 4 publications

(8 citation statements)

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“…One hundred and thirty‐five patients were treated with cholinesterase inhibitors. Nineteen patients were treated with the β 2 ‐AR‐stimulating drug terbutaline sulphate which temporarily improves skeletal muscle function [17]. The evaluation of clinical stages and evidence for cardiovascular diseases was done by one of us (R.P.…”

Section: Methodsmentioning

confidence: 99%

β2-adrenergic receptor gene polymorphisms in myasthenia gravis (MG)

Huang²,

Pirskanen

et al. 2000

Clinical and Experimental Immunology

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SUMMARYThe b 2 -adrenergic receptor (b 2 -AR) belongs to the group of G-protein coupled receptors and is present mainly on skeletal and cardiac muscle cells and lymphocytes. The gene encoding b 2 -AR (ADRB2) displays a moderate degree of heterogeneity in the human population. The distribution of polymorphisms at amino acid positions 16, 27 and 164 is changed in asthma, hypertension and obesity. We have earlier reported a decreased density of the b 2 -AR on peripheral blood mononuclear cells and the presence of b 2 -AR antibodies in patients with MG. Since certain polymorphisms affect the function of the b 2 -AR, it was of interest to analyse these in MG. Using allele-specific polymerase chain reaction amplification, we revealed an over-representation of homozygosity for Arg16 and a lower prevalence of homozygosity for Gly16 in MG patients compared with healthy individuals. The increased frequency of homozygosity for Arg16 was due to a contribution from patients with generalized MG but not from patients with only ocular disease. Homozygosity for Glu27 was negatively associated with both the presence of b 2 -AR antibodies and severity of disease. Moreover, acetylcholine receptor (AChR) antibodies were more often present in patients being homozygous for Gln27. Our results imply that homozygosity for Arg16 confers susceptibility to generalized MG, and that certain polymorphisms at amino acid position 27 are associated with subgroups of patients.Keywords myasthenia gravis b-adrenergic receptor gene polymorphisms b-adrenergic receptor antibody acetylcholine receptor antibody

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Section: Methodsmentioning

confidence: 99%

β2-adrenergic receptor gene polymorphisms in myasthenia gravis (MG)

Huang²,

Pirskanen

et al. 2000

Clinical and Experimental Immunology

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“…The effect of verapamil on neuromuscular transmission was addressed by Jonkers et al, who studied the influence of intravenous verapamil on repetitive nerve stimulation and clinical function in 10 patients with MG. However, no reproducible effects on neuromuscular transmission were found in this study, that was mainly limited by its small sample size (Jonkers et al, 1996).…”

Section: Calcium-dependent Presynaptic Effectsmentioning

confidence: 63%

“…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%

“…A retrospective chart review study showed that the odds of developing a transient aggravation of MG is increased 2.7-fold under beta-adrenergic antagonists in general, which represents a statistically significant signal (Gummi et al, 2019). A small-scale systematic trial studying the neuromuscular effects of an intravenously applied beta blocker (propranolol) in 10 patients could not prove an acute and significant deterioration of neuromuscular transmission in MG using repetitive nerve stimulation and clinical tests, but the work was clearly limited by the small number of participants (Jonkers et al, 1996). Several case reports indicated that latent myasthenia may be unmasked by beta blocker treatment (Leys et al, 1987;Confavreux et al, 1990).…”

Section: Effects Of Beta-adrenergic Blockadementioning

confidence: 99%

See 1 more Smart Citation

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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“…3–5 These drugs may be lifesaving in common cardiovascular diseases. Some case reports concerning these drugs in MG have been published, 6–10 but our studies 11 are to our knowledge the first controlled systematic ones on human MG. We aimed at (i) determining the effects of intravenous (iv) 11 as well as oral β‐ and calcium channel‐blocker drugs on MG both clinically and neurophysiologically and (ii) developing methods for the prediction of the individual responses of these drugs. In this short paper, we summarize the results of two studies.…”

Section: Introduction and Aimmentioning

confidence: 90%