Myasthenia gravis associated with etanercept therapy

Fee, Dominic B.; Kasarskis, Edward J.

doi:10.1002/mus.21280

Cited by 52 publications

(31 citation statements)

References 45 publications

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“…It has been reported to cause neuromuscular complications, including autoimmune peripheral nerve disorders such as chronic inflammatory demyelinating polyradiculoneuropathy, Guillain-Barré syndrome, mononeuritis and MG 57. Further well-organized studies are thus required to determine the efficacy and adverse effects of this drug in MG.…”

Section: Immunomodulating Treatmentsmentioning

confidence: 99%

Treatment of Myasthenia Gravis Based on Its Immunopathogenesis

2011

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The prognosis of myasthenia gravis (MG) has improved dramatically due to advances in critical-care medicine and symptomatic treatments. Its immunopathogenesis is fundamentally a T-cell-dependent autoimmune process resulting from loss of tolerance toward self-antigens in the thymus. Thymectomy is based on this immunological background. For MG patients who are inadequately controlled with sufficient symptomatic treatment or fail to achieve remission after thymectomy, remission is usually achieved through the addition of other immunotherapies. These immunotherapies can be classified into two groups: rapid induction and long-term maintenance. Rapid induction therapy includes intravenous immunoglobulin (IVIg) and plasma exchange (PE). These produce improvement within a few days after initiation, and so are useful for acute exacerbation including myasthenic crisis or in the perioperative period. High-dose prednisone has been more universally preferred for remission induction, but it acts more slowly than IVIg and PE, commonly only after a delay of several weeks. Slow tapering of steroids after a high-dose pulse offers a method of maintaining the state of remission. However, because of significant side effects, other immunosuppressants (ISs) are frequently added as "steroid-sparing agents". The currently available ISs exert their immunosuppressive effects by three mechanisms: 1) blocking the synthesis of DNA and RNA, 2) inhibiting T-cell activation and 3) depleting the B-cell population. In addition, newer drugs including antisense molecule, tumor necrosis factor alpha receptor blocker and complement inhibitors are currently under investigation to confirm their effectiveness. Until now, the treatment of MG has been based primarily on experience rather than gold-standard evidence from randomized controlled trials. It is hoped that well-organized studies and newer experimental trials will lead to improved treatments.

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Section: Immunomodulating Treatmentsmentioning

confidence: 99%

Treatment of Myasthenia Gravis Based on Its Immunopathogenesis

2011

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“…Our patient's symptoms certainly seem to have been attributable to her infliximab treatment, and this possibility is supported by the fact that the following criteria previously published in the literature were met [3,6,13]: obvious chronological concordance (the signs developed 10 days after the second infusion), the lack of any other plausible explanations, the stabilisation and improvement in the symptoms observed when infliximab was stopped, the pharmacodynamic pattern, and previous reports of other cases of central dysimmune neurological disorders induced by TNF-alpha antagonist drugs [2][3][4].…”

Section: Discussionmentioning

confidence: 83%

“…However, approximately 400 cases have been reported to date where these molecules have caused dysimmune conditions [1], including central neurological disorders (the induction or aggravation of multiple sclerosis and retrobulbar optic neuritis), myasthenia gravis [2], and various forms of demyelinating neuropathy (amounting to less than 50 cases in the literature) [3][4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Acute motor and sensory axonal neuropathy and concomitant encephalopathy during tumor necrosis factor-alpha antagonist therapy

Faivre

Franques

Paula

et al. 2010

Journal of the Neurological Sciences

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“…The use of Tregs-based therapies could be inefficient if this environment is predominantly sustained in MG, and a therapy that targets these cytokines could enhance the function of immune regulation system. Etanercept (a soluble and a recombinant TNF receptor blocker) has also been shown to have steroid-sparing effects in studies on small groups of MG patients [109], but this therapy can have significant side effects [110]. On the other hand, treatment of myasthenic rats by neutralizing anti-IL-6 Abs enhanced Tregs and led to suppression of EAMG [63].…”

Section: Blockage Of Pro-inflammatory Cytokinesmentioning

confidence: 97%

The role of T regulatory cells in immunopathogenesis of myasthenia gravis: implications for therapeutics

Alahgholi-Hajibehzad

Kasapoğlu

Jafari

et al. 2015

Expert Review of Clinical Immunology

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T regulatory cells (Tregs) are crucial for the development of self-tolerance and are the major focus in many studies interpreting the pathogenesis of myasthenia gravis (MG), an autoimmune-based disease. In normal conditions, Tregs regulate the immune responses, while impaired regulatory function of these cells can lead to autoimmunity. Recent studies have confirmed that the thymic and peripheral blood CD4(+)CD25(+) Tregs of MG are defective in functions and/or in numbers, which are associated with disease severity; approaches to correct the defects of these Tregs may be promising in the treatment of MG. This review discusses recent studies on characteristics, quantitative and qualitative changes of Tregs and possible mechanisms that are involved in the impairment of these cells in MG pathogenesis. In addition, new approaches inducing Treg generation that are currently being investigated as therapies for MG, will be discussed as well as proposed approaches for future therapies.

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Myasthenia gravis associated with etanercept therapy

Cited by 52 publications

References 45 publications

Treatment of Myasthenia Gravis Based on Its Immunopathogenesis

Treatment of Myasthenia Gravis Based on Its Immunopathogenesis

Acute motor and sensory axonal neuropathy and concomitant encephalopathy during tumor necrosis factor-alpha antagonist therapy

The role of T regulatory cells in immunopathogenesis of myasthenia gravis: implications for therapeutics

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