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J Neurol. 2018 May;265(5):1115-1122. doi: 10.1007/s00415-018-8812-0. Epub 2018 Mar 6.

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

Author information

1
University Hospital of Wales, Cardiff, UK.
2
Cardiff University School of Medicine, Cardiff, UK.
3
The Walton Centre NHS Trust, Liverpool, L97LJ, UK.
4
University of Liverpool, Liverpool, UK.
5
NIHR Sheffield Biomedical Research Centre (Translational Neuroscience), Sheffield, UK.
6
Royal Hallamshire Hospital, Sheffield, UK.
7
University of Nottingham, Nottingham, UK.
8
The Walton Centre NHS Trust, Liverpool, L97LJ, UK. Anu.Jacob@thewaltoncentre.nhs.uk.
9
University of Liverpool, Liverpool, UK. Anu.Jacob@thewaltoncentre.nhs.uk.

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.

KEYWORDS:

Anti-CD20; Complication; Infection; Rituximab; Secondary antibody deficiency

PMID:
29511864
PMCID:
PMC5937879
DOI:
10.1007/s00415-018-8812-0
[Indexed for MEDLINE]
Free PMC Article

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