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Secondary antibody deficiency: a complication of anti-CD20 therapy for neuroinflammation.

J Neurol. 2018 Mar 6. doi: 10.1007/s00415-018-8812-0. [Epub ahead of print]

Tallantyre EC1,2, Whittam DH3,4, Jolles S1,2, Paling D5,6, Constantinesecu C7, Robertson NP1,2, Jacob A8,9.

B-cell depleting anti-CD20 monoclonal antibody therapies are being increasingly used as long-term maintenance therapy for neuroinflammatory disease compared to many non-neurological diseases where they are used as remission-inducing agents. While hypogammaglobulinaemia is known to occur in over half of patients treated with medium to long-term B-cell-depleting therapy (in our cohort IgG 38, IgM 56 and IgA 18%), the risk of infections it poses seems to be under-recognised. Here, we report five cases of serious infections associated with hypogammaglobulinaemia occurring in patients receiving rituximab for neuromyelitis optica spectrum disorders. Sixty-four per cent of the whole cohort of patients studied had hypogammaglobulinemia. We discuss the implications of these cases to the wider use of anti-CD20 therapy in neuroinflammatory disease.

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