Possible Exacerbation of Myasthenia Gravis by Ciprofloxacin

Moore, Brian R.; Safani, Michael; Keesey, John

doi:10.1016/s0140-6736(88)91627-3

Cited by 38 publications

(6 citation statements)

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“…Fluoroquinolones: Worsening of MG has been reported after starting ciprofloxacin, norfloxacin and ofloxacin with a latency of 2 h to 5 days [ 54 , 55 , 56 , 57 , 58 ]. Wang et al reported nine patients that received fluoroquinolones (4 ciprofloxacin, 4 moxifloxacin and 1 levofloxacin) and developed MG exacerbation and an average increase of 10 points in quantitative MG score with a latency of 15 min to 4 days after starting the drug [ 59 ].…”

Section: Drugs That Worsen Mg or Cause Mg-like Symptoms Through DImentioning

confidence: 99%

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Sheikh

Alvi

Soliven

et al. 2021

JCM

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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.

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Section: Drugs That Worsen Mg or Cause Mg-like Symptoms Through DImentioning

confidence: 99%

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Sheikh

Alvi

Soliven

et al. 2021

JCM

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“…Myasthenia gravis (MG) is an autoimmune neuromuscular disorder. 1 Case reports have described worsening of MG symptoms after administration of antibiotics, including fluoroquinolones, [2][3][4][5][6][7] macrolides, 8,9 and aminoglycosides. [10][11][12] While aminoglycosides are known to cause competitive blockade of the neuromuscular junction, 13 the potential mechanisms by which other antibiotics may worsen MG symptoms are unknown.…”

Section: Introductionmentioning

confidence: 99%

Pharmacosafety of fluoroquinolone and macrolide antibiotics in the clinical care of patients with myasthenia gravis

et al. 2021

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Introduction/Aims Anecdotal case reports have suggested a potential association of fluoroquinolones and macrolides with myasthenia gravis (MG) exacerbation, prompting warnings against the use of these drugs in this population. However, large‐scale and reliable population‐based data that demonstrate this association are lacking. This study aims to examine the association between outpatient treatment with fluoroquinolones or macrolides and MG‐related hospitalization. Methods A retrospective cohort study consisting of adult MG patients was conducted using a large de‐identified healthcare claims database. Antibiotic prescription claims were identified, and MG‐related hospitalizations were assessed at 15, 30, and 90 days after the date of prescription. We used mixed effects survival regression with log‐logistic distribution and independent covariance matrix to estimate odds ratios (ORs) of hospitalization for each potentially exacerbating antibiotic using beta‐lactam as the reference and adjusting for covariates. Results Among 1556 MG patients receiving 894 fluoroquinolone prescriptions, 729 macrolide prescriptions, and 1608 beta‐lactam prescriptions during the study period, there was no difference in 15, 30, or 90‐day odds of MG‐related hospitalization between fluoroquinolone or macrolide users compared to prescribed beta‐lactams. However, estimates were higher for fluoroquinolones than macrolides, even after covariate adjustment (adjusted OR [aOR] 4.60, 95% confidence interval [CI] 0.55‐38.57 for fluoroquinolones and OR 0.56, 95% CI 0.32‐0.97 for macrolides, respectively, at 15 days). Discussion Fluoroquinolone and macrolide antibiotics are prescribed frequently to patients with MG. While statistical imprecision precludes a definitive conclusion, elevated ORs for fluoroquinolones raise the possibility of an underpowered association that merits further investigation.

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“…Magnesium competitively blocks the entry of calcium into the presynaptic nerve terminal -a process that is crucial for the release of ACh into the synaptic cleft. The Pittinger and Adamson, 1972;Singh et al, 1978a,b;Caputy et al, 1981;Kaeser, 1984 Fluoroquinolone antibiotics Moore et al, 1988;Mumford and Ginsberg, 1990;Azevedo et al, 1993;Roquer et al, 1996;De Sarro and De Sarro, 2001;Gunduz et al, 2006 Macrolide/ ketolide antibiotics (telithromycin)…”

Section: Electrolyte-related Neuromuscular Junction Effectsmentioning

confidence: 99%

“…There is a long list of anecdotal reports indicating (sometimes severe) symptom deterioration following the administration of fluoroquinolones, i.e., gyrase inhibitors, which led to a "black box" warning by the FDA, for their use in patients with MG (De Sarro and De Sarro, 2001). Notably, the fluoroquinolones, particularly levofloxacin, ofloxacin and ciprofloxacin, may cause acute and severe exacerbations of myasthenic symptoms (Moore et al, 1988;Mumford and Ginsberg, 1990;Azevedo et al, 1993;Roquer et al, 1996;Gunduz et al, 2006). From a biochemical perspective, these adverse effects may in part be explained by the structural similarities to quinine and chloroquine, which have been shown to cause a neuromuscular blockade (Sieb et al, 1996).…”

Section: Postsynaptic 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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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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Possible Exacerbation of Myasthenia Gravis by Ciprofloxacin

Cited by 38 publications

References 1 publication

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Drugs That Induce or Cause Deterioration of Myasthenia Gravis: An Update

Pharmacosafety of fluoroquinolone and macrolide antibiotics in the clinical care of patients with myasthenia gravis

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

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