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

Tallantyre, Emma ORCID: https://orcid.org/0000-0002-3760-6634, Whittam, D. H., Jolles, Stephen, Paling, D., Constantinescu, C., Robertson, Neil ORCID: https://orcid.org/0000-0002-5409-4909 and Jacob, A. 2018. Secondary antibody deficiency: a complication of anti-CD20 therapy for neuroinflammation. Journal of Neurology 265 (5) , pp. 1115-1122. 10.1007/s00415-018-8812-0

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Abstract

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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Publisher:	Springer Verlag (Germany)
ISSN:	0340-5354
Funders:	N/A
Date of First Compliant Deposit:	22 March 2018
Date of Acceptance:	24 February 2018
Last Modified:	11 Oct 2023 18:59
URI:	https://orca.cardiff.ac.uk/id/eprint/109712

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