Repeated Treatment With Rituximab Based on the Assessment of Peripheral Circulating Memory B Cells in Patients With Relapsing Neuromyelitis Optica Over 2 Years

Kim, Suhyun

doi:10.1001/archneurol.2011.154

Cited by 274 publications

(232 citation statements)

References 38 publications

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“…The current results, together with previous ones, demonstrate rituximab as a promising medication for NMO. [2][3][4][5][6] To further confirm the efficacy of …”

Section: Kinetics Of the B-cell Population In Patientsmentioning

confidence: 99%

“…Among the very few disease-modifying medications that have been tested in patients with NMO, rituximab therapy has achieved a 70% or greater response rate by depleting B cells. [2][3][4][5][6] However, most studies were performed in Caucasians, the dose of rituximab was adopted from those targeting B-cell malignancies, and the potential long-term side effects of rituximab are not known. 1 The dosage of rituximab given to patients with NMO is expected to be different than that given to B-cell lymphoma patients considering the different targeted treatments of these 2 diseases.…”

mentioning

confidence: 99%

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Responsiveness to reduced dosage of rituximab in Chinese patients with neuromyelitis optica

Yang

et al. 2013

Neurology

113

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Responsiveness to reduced dosage of rituximab in Chinese patients with neuromyelitis optica ABSTRACT Objective: To determine the effect of a lower dose of rituximab in depleting B lymphocytes, maintaining low B-cell counts, and relapse in patients with neuromyelitis optica (NMO) and NMO spectrum disorders. Methods:We treated 5 Chinese patients with deteriorating NMO and NMO spectrum disorders with a 100-mg IV infusion of rituximab once a week for 3 consecutive weeks, followed by additional infusion of the same dosage depending on circulating B-cell repopulation.Results: This reduced dosage of rituximab was sufficient to deplete B cells and maintain low B-cell counts. None of the treated patients experienced relapse, and all patients exhibited stabilized or improved neurologic function during the 1-year follow-up period. MRI revealed the absence of new lesions, no enhancement in spinal cord and brain, a significant shrinkage of spinal cord segments, and a reduction/disappearance of previous brain lesions. Conclusion:

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“…The current results, together with previous ones, demonstrate rituximab as a promising medication for NMO. [2][3][4][5][6] To further confirm the efficacy of …”

Section: Kinetics Of the B-cell Population In Patientsmentioning

confidence: 99%

mentioning

confidence: 99%

Responsiveness to reduced dosage of rituximab in Chinese patients with neuromyelitis optica

Yang

et al. 2013

Neurology

113

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“…The pivotal open-label study from Cree et al [21] established B-cell depletion as a therapeutic principle for NMOSD; 6/8 patients were relapse-free after 1 year of treatment. Several clinical case series and retrospective analyses (including 10-55 patients each, treatment up to 8 years) have confirmed these findings and reported a reduction of ARR in 87-96 %, freedom from relapses in 44-72 %, and an improvement of disability in 80-100 % of patients [79,81,97,[99][100][101][102]. Most patients in these studies were AQP4-IgG-positive, but response rates in patients with AQP4-IgG-negative NMOSD seem to be similar [97,102].…”

Section: Rituximab and Other B-cell-depleting Therapiesmentioning

confidence: 71%

“…More than 80 % of patients remain B-cell depleted 6 months after rituximab treatment [103], and re-dosing is often done at regular 6-month intervals [79], which however runs the risk that B cells in some patients are already repopulating. Another approach is to monitor B-cell counts closely and to re-dose rituximab before recurrence of circulating B cells (CD19 + or CD20 + B cells >0.1 % of total lymphocytes, CD27 + memory B cells >0.05 % of peripheral blood mononuclear cells) [99]. A genetic polymorphism in the fragment c gamma receptor 3A (FCGR3A) allele has been shown to be associated with insufficient memory B-cell depletion and an elevated risk of attacks during rituximab treatment [104].…”

Section: Rituximab and Other B-cell-depleting Therapiesmentioning

confidence: 99%

Present and Future Therapies in Neuromyelitis Optica Spectrum Disorders

Kleiter

Gold

2016

Neurotherapeutics

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Neuromyelitis optica spectrum disorders (NMOSD) are important evolving entities, which have reached much attention in the recent years. NMOSD are characterized by inflammatory lesions in the optic nerves, spinal cord, and central parts of the brain, as well as an autoimmune process directed against aquaporin-4. As disability in NMOSD accumulates by inflammatory damage from attacks, both the treatment and prevention of attacks are decisive for the long-term outcome. NMOSD attacks are treated with highdose intravenous corticosteroids and apheresis therapies, in particular therapeutic plasma exchange. In cases of incomplete remission, escalation of attack treatment is recommended. Preventive therapy is immunosuppressive and should by commenced as early as possible. Apart from classical immunosuppressants such as azathioprine and mycophenolate mofetil, repurposed biologicals are increasingly used. B-cell depletion with rituximab and other agents, inhibition of the interleukin-6 receptor with tocilizumab, and blockade of complement-mediated damage by eculizumab all are promising therapeutic strategies evaluated in randomized controlled trials. In this review, we will discuss present and future immunotherapies for NMOSD and also consider combination of treatments, plasma, cellular and other therapies. Current advances in immunopathological knowledge are translated into innovative concepts and begin a new era of NMOSD therapy.

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“…In NMO, a recent string of studies show that the repopulation of peripheral blood by B cells, especially memory B cells, coincides with clinical relapses [51,[61][62][63]. Compared with healthy controls, patients with NMO have higher serum BAFF levels, which further increases after rituximab treatment [62].…”

Section: Ms and Nmomentioning

confidence: 99%

Anti-B-Cell Therapies in Autoimmune Neurological Diseases: Rationale and Efficacy Trials

2016

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B cells have an ever-increasing role in the etiopathology of a number of autoimmune neurological disorders, acting as antibody-producing cells and, most importantly, as sensors, coordinators, and regulators of the immune response. B cells, among other functions, regulate the T-cell activation process through their participation in antigen presentation and production of cytokines. The availability of monoclonal antibodies or fusion proteins against B-cell surface molecules or Bcell trophic factors bestows a rational approach for treating autoimmune neurological disorders, even when T cells are the main effector cells. This review summarizes basic aspects of B-cell biology, discusses the role(s) of B cells in neurological autoimmunity, and presents anti-B-cell drugs that are either currently on the market or are expected to be available in the near future for treating neurological autoimmune disorders.

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Repeated Treatment With Rituximab Based on the Assessment of Peripheral Circulating Memory B Cells in Patients With Relapsing Neuromyelitis Optica Over 2 Years

Abstract: To evaluate the efficacy and safety of repeated rituximab treatment based on the assessment of peripheral circulating memory B cells over 24 months in patients with relapsing neuromyelitis optica (NMO).

Cited by 274 publications

References 38 publications

Responsiveness to reduced dosage of rituximab in Chinese patients with neuromyelitis optica

Responsiveness to reduced dosage of rituximab in Chinese patients with neuromyelitis optica

Present and Future Therapies in Neuromyelitis Optica Spectrum Disorders

Anti-B-Cell Therapies in Autoimmune Neurological Diseases: Rationale and Efficacy Trials

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