Lack of response to monoclonal antibody therapy in neuromyelitis optica.

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. Rituximab is a monoclonal antiCD20 antibody that is reported to be effective in NMO. Alemtuzumab is a monoclonal anti-CD52 antibody with preliminary phase II data in multiple sclerosis, but not in NMO. 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.