The risk of worsening of myasthenia by cardiovascular medication as reflected by reporting frequency.
Ca antagonists
adverse drug reaction
alpha-blocker
beta-blocker
hypertension
myasthenia
Journal
European journal of neurology
ISSN: 1468-1331
Titre abrégé: Eur J Neurol
Pays: England
ID NLM: 9506311
Informations de publication
Date de publication:
09 2021
09 2021
Historique:
revised:
31
05
2021
received:
21
04
2021
accepted:
24
06
2021
pubmed:
30
6
2021
medline:
21
10
2021
entrez:
29
6
2021
Statut:
ppublish
Résumé
Some groups of cardiovascular drugs (beta-blocking drugs, Ca antagonists, antiarrhythmics) are listed as potentially worsening myasthenia. An empirical basis for alternative recommendations for antihypertensive and antiarrhythmic therapy in myasthenia patients has not yet been provided. From the World Health Organization pharmacovigilance database, we retrieved total and myasthenia-related counts of adverse drug reactions for various groups of drugs used in cardiovascular disease and drugs with related mechanism of action used in other indications. We calculated the reporting odds ratio as a measure of a disproportional fraction of myasthenia-related events among all events. A 95% confidence interval of reporting odds ratio (ROR) >1 was taken as an indication for a higher risk. Because our approach involves a considerable number of tests, this situation is referred to as a signal that requires additional confirmation. A signal for an increased risk was noted for tizanidine, for alpha-blocking drugs, for beta-blocking drugs, and for Ca antagonists. ROR indicated a lower-than-average risk for salbutamol, angiotensin receptor antagonists, oral anticoagulants, thrombocytic function inhibitors, and heparins. Angiotensin receptor antagonists, angiotensin-converting enzyme inhibitors, and diuretics seem to be safe in antihypertensive therapy. Surprisingly, and yet requiring confirmation by case reports, alpha receptor-blocking drugs seem to carry a risk of myasthenia worsening. Amiodarone seems to be a safe alternative in antiarrhythmic therapy in patients with myasthenia.
Sections du résumé
BACKGROUND AND PURPOSE
Some groups of cardiovascular drugs (beta-blocking drugs, Ca antagonists, antiarrhythmics) are listed as potentially worsening myasthenia. An empirical basis for alternative recommendations for antihypertensive and antiarrhythmic therapy in myasthenia patients has not yet been provided.
METHODS
From the World Health Organization pharmacovigilance database, we retrieved total and myasthenia-related counts of adverse drug reactions for various groups of drugs used in cardiovascular disease and drugs with related mechanism of action used in other indications. We calculated the reporting odds ratio as a measure of a disproportional fraction of myasthenia-related events among all events. A 95% confidence interval of reporting odds ratio (ROR) >1 was taken as an indication for a higher risk. Because our approach involves a considerable number of tests, this situation is referred to as a signal that requires additional confirmation.
RESULTS
A signal for an increased risk was noted for tizanidine, for alpha-blocking drugs, for beta-blocking drugs, and for Ca antagonists. ROR indicated a lower-than-average risk for salbutamol, angiotensin receptor antagonists, oral anticoagulants, thrombocytic function inhibitors, and heparins.
CONCLUSIONS
Angiotensin receptor antagonists, angiotensin-converting enzyme inhibitors, and diuretics seem to be safe in antihypertensive therapy. Surprisingly, and yet requiring confirmation by case reports, alpha receptor-blocking drugs seem to carry a risk of myasthenia worsening. Amiodarone seems to be a safe alternative in antiarrhythmic therapy in patients with myasthenia.
Substances chimiques
Angiotensin Receptor Antagonists
0
Angiotensin-Converting Enzyme Inhibitors
0
Antihypertensive Agents
0
Diuretics
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
2965-2970Informations de copyright
© 2021 The Authors. European Journal of Neurology published by John Wiley & Sons Ltd on behalf of European Academy of Neurology.
Références
Krenn M, Grisold A, Wohlfarth P, et al. Pathomechanisms and clinical implications of myasthenic syndromes exacerbated and induced by medical treatments. Front Mol Neurosci. 2020;13:156.
Gummi RR, Kukulka NA, Deroche CB, Govindarajan R. Factors associated with acute exacerbations of myasthenia gravis. Muscle Nerve. 2019;60:693-699.
Lindquist M. VigiBase, the WHO Global ICSR database system: basic facts. Drug Inf J. 2008;42:409-419.
Faillie JL. Case-non-case studies: principle, methods, bias and interpretation. Therapie. 2019;74:225-232.
Rothman KJ, Lanes S, Sacks ST. The reporting odds ratio and its advantages over the proportional reporting ratio. Pharmacoepidemiol Drug Saf. 2004;13:519-523.
Gras-Champel V, Batteux B, Masmoudi K, Liabeuf S. Statin-induced myasthenia: a disproportionality analysis of the WHO's VigiBase pharmacovigilance database. Muscle Nerve. 2019;60:382-386.
Demichelis C, Balestra A, Lapucci C, et al. Neuromuscular complications following targeted therapy in cancer patients: beyond the immune checkpoint inhibitors. Case reports and review of the literature. Neurol Sci. 2021;42(4):1405-1409.
Trillenberg P, Thern J. Antibiotic-induced myasthenia worsening-an estimation of risk based on reporting frequency. J Antimicrob Chemother. 2020;75:3408-3410.
Trillenberg P, Katalinic A, Junghanns K, Thern J. Worsening of myasthenia due to antiepileptic, antipsychotic, antidepressant and sedative medication an estimation of risk based on reporting frequency. Eur J Neurol. 2021;28(7):2349-2356.
Confavreux C, Charles N, Aimard G. Fulminant myasthenia gravis soon after initiation of acebutolol therapy. Eur Neurol. 1990;30:279-281.
Coppeto JR. Timolol-associated myasthenia gravis. Am J Ophthalmol. 1984;98:244-245.
Leys D, Pasquier F, Vermersch P, et al. Possible revelation of latent myasthenia gravis by labetalol chlorhydrate. Acta Clin Belg. 1987;42:475-476.
Shaivitz SA. Timolol and myasthenia gravis. JAMA. 1979;242:1611-1612.
Verkijk A. Worsening of myasthenia gravis with timolol maleate eyedrops. Ann Neurol. 1985;17:211-212.
Argov Z, Mastaglia FL. Drug therapy: Disorders of neuromuscular transmission caused by drugs. N Engl J Med. 1979;301:409-413.
Barrons RW. Drug-induced neuromuscular blockade and myasthenia gravis. Pharmacotherapy. 1997;17:1220-1232.
Bedlack RS, Sanders DB. How to handle myasthenic crisis. Essential steps in patient care. Postgrad Med. 2000;107:211-214, 220-222.
Howard JF Jr. Adverse drug effects on neuromuscular transmission. Semin Neurol. 1990;10:89-102.
Jones SC, Sorbello A, Boucher RM. Fluoroquinolone-associated myasthenia gravis exacerbation: evaluation of postmarketing reports from the US FDA adverse event reporting system and a literature review. Drug Saf. 2011;34:839-847.
Narayanaswami P, Sanders DB, Wolfe G, et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology. 2021;96:114-122.
Raschi E, Poluzzi E, Salvo F, et al. Pharmacovigilance of sodium-glucose co-transporter-2 inhibitors: what a clinician should know on disproportionality analysis of spontaneous reporting systems. Nutr Metab Cardiovasc Dis. 2018;28:533-542.
Khan MM, Lustrino D, Silveira WA, et al. Sympathetic innervation controls homeostasis of neuromuscular junctions in health and disease. Proc Natl Acad Sci USA. 2016;113:746-750.
Tsentsevitsky A, Nurullin L, Tyapkina O, Bukharaeva E. Sympathomimetics regulate quantal acetylcholine release at neuromuscular junctions through various types of adrenoreceptors. Mol Cell Neurosci. 2020;108:103550.
Rodrigues AZC, Wang ZM, Messi ML, Delbono O. Sympathomimetics regulate neuromuscular junction transmission through TRPV1, P/Q- and N-type Ca(2+) channels. Mol Cell Neurosci. 2019;95:59-70.
Tsentsevitsky AN, Kovyazina IV, Bukharaeva EA. Diverse effects of noradrenaline and adrenaline on the quantal secretion of acetylcholine at the mouse neuromuscular junction. Neuroscience. 2019;423:162-171.
Lipka AF, Vrinten C, van Zwet EW, et al. Ephedrine treatment for autoimmune myasthenia gravis. Neuromuscul Disord. 2017;27:259-265.
Soliven B, Rezania K, Gundogdu B, Harding-Clay B, Oger J, Arnason BG. Terbutaline in myasthenia gravis: a pilot study. J Neurol Sci. 2009;277:150-154.
Jonkers I, Swerup C, Pirskanen R, Bjelak S, Matell G. Acute effects of intravenous injection of beta-adrenoreceptor- and calcium channel at antagonists and agonists in myasthenia gravis. Muscle Nerve. 1996;19:959-965.
Rank MM, Murray KC, Stephens MJ, D'Amico J, Gorassini MA, Bennett DJ. Adrenergic receptors modulate motoneuron excitability, sensory synaptic transmission and muscle spasms after chronic spinal cord injury. J Neurophysiol. 2011;105:410-422.
Akinaga J, Garcia-Sainz JA, Pupo AS. Updates in the function and regulation of alpha1 -adrenoceptors. Br J Pharmacol. 2019;176:2343-2357.
Diochot S, Richard S, Baldy-Moulinier M, Nargeot J, Valmier J. Dihydropyridines, phenylalkylamines and benzothiazepines block N-, P/Q- and R-type calcium currents. Pflugers Arch. 1995;431:10-19.
Wirguin I, Brenner T, Sicsic C, Argov Z. Variable effect of calcium channel blockers on the decremental response in experimental autoimmune myasthenia gravis. Muscle Nerve. 1994;17:523-527.