Five-year follow-up with low-dose tacrolimus in patients with myasthenia gravis

Minami, Naoya; Fujiki, Naoto; Doi, Shizuki; Shima, Koji; Niino, Masaaki; Kikuchi, Seiji; Sasaki, Hidenao

doi:10.1016/j.jns.2010.09.033

Cited by 29 publications

(10 citation statements)

References 16 publications

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“…The drug inhibits the proliferation of activated T lymphocytes, but also acts on ryanodine receptor-mediated calcium release from sarcoplasmic reticulum in muscle cells. The drug has shown a beneficial effect in MG, and it represents an alternative second-choice drug for moderate to severe MG [3, 14–18], perhaps especially for MG patients with ryanodine receptor autoantibodies [23]. …”

Section: Drug Treatmentmentioning

confidence: 99%

Myasthenia Gravis: A Review of Available Treatment Approaches

Gilhus

Owe

Hoff

et al. 2011

Autoimmune Diseases

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Patients with autoimmune myasthenia gravis (MG) should be further classified before initiating therapy, as treatment response varies for ocular versus generalised, early onset versus late onset, and acetylcholine receptor antibody positive versus MuSK antibody positive disease. Most patients need immunosuppression in addition to symptomatic therapy. Prednisolone and azathioprine represent first choice drugs, whereas several second choice options are recommended and should be considered. Thymectomy should be undertaken in MG with thymoma and in generalised, early-onset MG. For MG crises and other acute exacerbations, intravenous immunoglobulin (IvIg) and plasma exchange are equally effective and safe treatments. Children and females in child bearing age need special attention regarding potential side effects of immunosuppressive therapy. MG pathogenesis is known in detail, but the immune therapy is still surprisingly unspecific, without a pin-pointed attack on the defined disease-inducing antigen-antibody reaction being available.

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Section: Drug Treatmentmentioning

confidence: 99%

Myasthenia Gravis: A Review of Available Treatment Approaches

Gilhus

Owe

Hoff

et al. 2011

Autoimmune Diseases

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“…Tacrolimus suppresses the induction of experimental autoimmune myasthenianin rats . In several small case–series tacrolimus lowered steroid requirements and induced stable remissions in MG . Recently, a double‐blind, placebo‐controlled, parallel group study focused on the ability of tacrolimus to reduce the corticosteroid dose in patients with stable myasthenic symptoms on prednisolone at doses equivalent to 10–20 mg/day .…”

Section: Introductionmentioning

confidence: 99%

Myasthenia gravis: an update for the clinician

Sieb

2014

Clinical and Experimental Immunology

227

151

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OTHER ARTICLES PUBLISHED IN THIS SERIESParaneoplastic neurological syndromes. Clinical and Experimental Immunology 2014, 175: 336-48. Diagnosis, pathogenesis and treatment of myositis: recent advances. Clinical and Experimental Immunology 2014, 175: 349-58. Disease-modifying therapy in multiple sclerosis and chronic inflammatory demyelinating polyradiculoneuropathy: common and divergent current and future strategies. Clinical and Experimental Immunology 2014, 175: 359-72 SummaryThis paper provides a thorough overview of the current advances in diagnosis and therapy of myasthenia gravis (MG). Nowadays the term 'myasthenia gravis' includes heterogeneous autoimmune diseases, with a postsynaptic defect of neuromuscular transmission as the common feature. Myasthenia gravis should be classified according to the antibody specificity [acetylcholine, muscle-specific receptor tyrosine kinase (MuSK), low-density lipoprotein receptor-related protein 4 (LRP4), seronegative], thymus histology (thymitis, thymoma, atrophy), age at onset (in children; aged less than or more than 50 years) and type of course (ocular or generalized). With optimal treatment, the prognosis is good in terms of daily functions, quality of life and survival. Symptomatic treatment with acetylcholine esterase inhibition is usually combined with immunosuppression. Azathioprine still remains the first choice for long-term immunosuppressive therapy. Alternative immunosuppressive options to azathioprine include cyclosporin, cyclophosphamide, methotrexate, mycophenolate mofetil and tacrolimus. Rituximab is a promising new drug for severe generalized MG. Emerging therapy options include belimumab, eculizumab and the granulocyte-macrophage colonystimulating factor. One pilot study on etanercept has given disappointing results. For decades, thymectomy has been performed in younger adults to improve non-paraneoplastic MG. However, controlled prospective studies on the suspected benefit of this surgical procedure are still lacking. In acute exacerbations, including myasthenic crisis, intravenous immunoglobulin, plasmapheresis and immunoadsorption are similarly effective.

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“…Recently Minami et al . reported data from 9 patients with steroid-dependent generalized MG treated with low-dose tacrolimus (2–3 mg/day) for 5 years [28]. Following treatment with tacrolimus, the mean MG activities of daily living score improved and mean dose of prednisolone could also be reduced.…”

Section: Discussionmentioning

confidence: 99%

FK506 attenuates thymic output in patients with myasthenia gravis

Mitsui¹,

Kuroda²,

Ueno³

et al. 2013

aoms

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IntroductionMyasthenia gravis (MG) is an antibody-mediated, T-cell-dependent autoimmune disease. The symptoms are caused by high-affinity IgG against the muscle acetylcholine receptor (AChR) at the neuromuscular junction. The production of these antibodies in B-cells depends on AChR-specific CD4+ T-cells and the thymus gland seems to play a significant role in the pathogenesis of MG. Altered thymic T-cell export seems to be associated with a pathological mechanism in myasthenia gravis. Tacrolimus (FK506) has recently been used to treat MG.Material and methodsWe examined the effects of tacrolimus on thymic T-cell export in patients with MG. Sixteen patients with nonthymomatous and/or thymectomized MG were treated with oral administrations of tacrolimus. To assess the effect of tacrolimus on the thymic output, we assayed the levels of T-cell receptor excision circle (TREC), a molecular marker of thymus emigrants.ResultsT-cell receptor excision circle was not significantly different from those in age-matched controls before tacrolimus therapy, but they were partially decreased 4 months after tacrolimus therapy. T-cell receptor excision circle levels were significantly decreased in the thymomatous group (p < 0.05), but not in the nonthymomatous group. Tacrolimus treatment significantly attenuated TREC levels in cultured CD4–CD8+ cells (p < 0.05), but total cell counts were not significantly changed.ConclusionsThese results indicate that TREC levels may become a marker of the curative effect of tacrolimus therapy for thymomatous MG, and that tacrolimus suppresses not only activating T-lymphocytes, but also naïve T-cells.

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Five-year follow-up with low-dose tacrolimus in patients with myasthenia gravis

Cited by 29 publications

References 16 publications

Myasthenia Gravis: A Review of Available Treatment Approaches

Myasthenia Gravis: A Review of Available Treatment Approaches

Myasthenia gravis: an update for the clinician

FK506 attenuates thymic output in patients with myasthenia gravis

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