2011Archives of NeurologyOpen access

Lack of Response to Monoclonal Antibody Therapy in Neuromyelitis Optica

Peiqing Qian, Anne H. Cross, Robert T. Naismith

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Abstract

T he article by Matiello et al 1 regarding a relapse of neuromyelitis optica (NMO) after autologous hematopoietic stem cell transplantation highlights the need to further understand the role of the immune system in this disease.Immunosuppressive therapeutics targeting B and T cells are used to prevent disabling relapses in NMO. 2 Rituximab is a monoclonal anti-CD20 antibody that is reported to be effective in NMO. 3 Alemtuzumab is a monoclonal anti-CD52 antibody with preliminary phase II data in multiple sclerosis, but not in NMO. 4 Here we describe a patient with 20 relapses in 5 years despite sequential treatment with 4 immunomodulatory therapeutics in combination with corticosteroids and plasma exchange for relapses.She appeared to paradoxically worsen, with profound weakness, after B cell depletion with rituximab and developed tumefactive cerebral lesions after alemtuzumab.Report of a Case.A 40-year-old African American woman presented with optic neuritis 5 years prior, with recovery of visual acuity to 20/20 after intravenous methylprednisolone (IVMP) (Figure).Three months later, dys-10.08.0 9.0 7.0

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T he article by Matiello et al 1 regarding a relapse of neuromyelitis optica (NMO) after autologous hematopoietic stem cell transplantation highlights the need to further understand the role of the immune system in this disease.Immunosuppressive therapeutics targeting B and T cells are used to prevent disabling relapses in NMO. 2 Rituximab is a monoclonal anti-CD20 antibody that is reported to be effective in NMO. 3 Alemtuzumab is a monoclonal anti-CD52 antibody with preliminary phase II data in multiple sclerosis, but not in NMO. 4 Here we describe a patient with 20 relapses in 5 years despite sequential treatment with 4 immunomodulatory therapeutics in combination with corticosteroids and plasma exchange for relapses.She appeared to paradoxically worsen, with profound weakness, after B cell depletion with rituximab and developed tumefactive cerebral lesions after alemtuzumab.Report of a Case.A 40-year-old African American woman presented with optic neuritis 5 years prior, with recovery of visual acuity to 20/20 after intravenous methylprednisolone (IVMP) (Figure).Three months later, dys-10.08.0 9.0 7.0

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Available abstract

T he article by Matiello et al 1 regarding a relapse of neuromyelitis optica (NMO) after autologous hematopoietic stem cell transplantation highlights the need to further understand the role of the immune system in this disease.Immunosuppressive therapeutics targeting B and T cells are used to prevent disabling relapses in NMO. 2 Rituximab is a monoclonal anti-CD20 antibody that is reported to be effective in NMO. 3 Alemtuzumab is a monoclonal anti-CD52 antibody with preliminary phase II data in multiple sclerosis, but not in NMO. 4 Here we describe a patient with 20 relapses in 5 years despite sequential treatment with 4 immunomodulatory therapeutics in combination with corticosteroids and plasma exchange for relapses.She appeared to paradoxically worsen, with profound weakness, after B cell depletion with rituximab and developed tumefactive cerebral lesions after alemtuzumab.Report of a Case.A 40-year-old African American woman presented with optic neuritis 5 years prior, with recovery of visual acuity to 20/20 after intravenous methylprednisolone (IVMP) (Figure).Three months later, dys-10.08.0 9.0 7.0

Key concepts: Alemtuzumab, CD52, Rituximab, Neuromyelitis optica, Medicine, Monoclonal antibody therapy, Monoclonal antibody, Multiple sclerosis

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