Rituximab for myasthenia gravis

Stieglbauer, Karl; Topakian, Raffi; Schäffer, Viktoria; Aichner, F.

doi:10.1016/j.jns.2009.02.357

Cited by 55 publications

(8 citation statements)

References 16 publications

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“…We also observed a statistically significant reduction in AChR antibody titers in those patients, whose reports were available. Our study supports the established fact that rituximab is useful in management of refractory MG [ 39 ], [ 40 ], [ 41 ], [ 42 ], [ 43 ], [ 44 ], [ 45 ].…”

Section: Discussionsupporting

confidence: 88%

Refractory myasthenia gravis – clinical profile, comorbidities and response to rituximab

Sudulagunta

Sepehrar

Sodalagunta

et al. 2016

GMS German Medical Science; 14:Doc12

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Section: Discussionsupporting

confidence: 88%

Refractory myasthenia gravis – clinical profile, comorbidities and response to rituximab

Sudulagunta

Sepehrar

Sodalagunta

et al. 2016

GMS German Medical Science; 14:Doc12

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“…Rituximab provides promising expectations for the treatment of MG,67–70 although no RCTs have been conducted so far.…”

Section: New Treatment Optionsmentioning

confidence: 99%

Current and emerging therapies for the treatment of myasthenia gravis

Mantegazza

Bonanno²,

Camera³

et al. 2011

NDT

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Myasthenia gravis (MG) is an autoimmmune disease in which autoantibodies to different antigens of the neuromuscular junction cause the typical weakness and fatigability. Treatment includes anticholinesterase drugs, immunosuppression, immunomodulation, and thymectomy. The autoimmune response is maintained under control by corticosteroids frequently associated with immunosuppressive drugs, with improvement in the majority of patients. In case of acute exacerbations with bulbar symptoms or repeated relapses, modulation of autoantibody activity by plasmapheresis or intravenous immunoglobulins provides rapid improvement. Recently, techniques removing only circulating immunoglobulins have been developed for the chronic management of treatment-resistant patients. The rationale for thymectomy relies on the central role of the thymus. Despite the lack of controlled studies, thymectomy is recommended as an option to improve the clinical outcome or promote complete remission. New videothoracoscopic techniques have been developed to offer the maximal surgical approach with the minimal invasiveness and hence patient tolerability. The use of biological drugs such as anti-CD20 antibodies is still limited but promising. Studies performed in the animal model of MG demonstrated that several more selective or antigen-specific approaches, ranging from mucosal tolerization to inhibition of complement activity or cellular therapy, might be feasible. Investigation of the transfer of these therapeutic approaches to the human disease will be the challenge for the future.

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“…Therefore, natalizumab blocking VLA-4 interaction with VCAM-1 or fibronectin prevents infiltration of lymphocytes during inflammation (Rice et al 2005). Rituximab (Rituxan ® , IDEC Pharmaceuticals) is a chimeric mouse–human monoclonal antibody directed against CD20, which is expressed on B cells (Grillo-Lopez et al 2000) and is used for the treatment of non-Hodgkin lymphomas (Fanale and Younes 2007), rheumatoid arthritis (Schuna 2007), autoimmune hematological disorders including autoimmune hemolytic anemia, acquired hemophilia, thrombotic thrombocytopenic and purpura (Garvey 2008), SLE (Ramos-Casals et al 2009), myasthenia gravis (Stieglbauer et al 2009), and MS (Cree et al 2005; Wingerchuk and Weinshenker 2005; Bar-Or et al 2008; Hauser et al 2008; Linker et al 2008). Binding of rituximab to CD20 on B cells results in their lysis and subsequent depletion of the B cell population in peripheral blood and CSF (Maloney et al 1997; Monson et al 2005).…”

Section: New Concerns: Pml As a Results Of Monoclonal Antibody Therapymentioning

confidence: 99%

Molecular Regulation of JC Virus Tropism: Insights into Potential Therapeutic Targets for Progressive Multifocal Leukoencephalopathy

Marshall

Major

2010

J Neuroimmune Pharmacol

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Progressive multifocal leukoencephalopathy (PML) is a growing concern for patients undergoing immune modulatory therapies for treatment of autoimmune diseases such as multiple sclerosis. Currently, there are no drugs approved for the treatment of PML that have been demonstrated in the patient to effectively and reproducibly alter the course of disease progression. The human polyoma virus JC is the causative agent of PML. JC virus (JCV) dissemination is tightly controlled by regulation of viral gene expression from the promoter by cellular transcription factors expressed in cells permissive for infection. JCV infection likely occurs during childhood, and latent virus containing PML-associated promoter sequences is maintained in lymphoid cells within the bone marrow. Because development of PML is tightly linked to suppression and or modulation of the immune system as in development of hematological malignancies, AIDS, and monoclonal antibody treatments, further scrutiny of the course of JCV infection in immune cells will be essential to our understanding of development of PML and identification of new therapeutic targets.

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Rituximab for myasthenia gravis

Cited by 55 publications

References 16 publications

Refractory myasthenia gravis – clinical profile, comorbidities and response to rituximab

Refractory myasthenia gravis – clinical profile, comorbidities and response to rituximab

Current and emerging therapies for the treatment of myasthenia gravis

Molecular Regulation of JC Virus Tropism: Insights into Potential Therapeutic Targets for Progressive Multifocal Leukoencephalopathy

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