Secondary Antibody Deficiency and infection following B-cell depletion for CNS neuroinflammation
ECTRIMS Online Library. Tallantyre E. 10/25/17; 199742; EP1722
Emma C. Tallantyre
Emma C. Tallantyre
Contributions
Abstract

Abstract: EP1722

Type: ePoster

Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments

B-cell depleting anti-CD20 monoclonal antibody therapies have demonstrated promising clinical efficacy in suppressing relapses in individuals with neuromyelitis optica (NMO) and multiple sclerosis (MS). However, uncertainties remain about the optimum treatment schedule. In rheumatological disease, anti-CD20 agents are most often employed for short-term induction therapy and are subsequently replaced by longer-term maintenance therapy. In contrast, repeated cycles of anti-CD20 monoclonal antibody therapy are proposed as maintenance therapy for CNS neuro-inflammatory disorders. Post-marketing surveillance will be essential to fully uncover the long-term safety profile of repeated B-cell depletion. Hypogammaglobulinaemia is a recognised consequence in a proportion of patients treated with medium- to long-term B-cell therapy and may play a role in the increased incidence of infection observed in the anti-CD20 arms of treatment trials. We report 5 cases of serious infection associated with hypogammaglobulinaemia occurring in patients receiving rituximab for NMO. The cases were all female, all had low IgG with variable reductions in IgM and IgA. The cases had a mean treatment duration of 3.1 years, but not all cases had had extensive exposure (treatment duration range 0.5 - 6.2y). We review the evidence relating to hypogammaglobulinaemia following anti-CD20 treatment for neuroinflammatory disorders and propose an algorithm for monitoring and treatment of this recognised complication.
Disclosure:
E C Tallantyre: has received research support from Biogen Idec.
D Whittam: nothing to disclose.
N P Robertson: has served on the scientific advisory board for Genzyme, Roche, Novartis, and Biogen, received travel funding and/or speaker honoraria from Biogen and Genzyme and received research support from Genzyme, Novartis, National Institute of Health Wales, Multiple Sclerosis Society of Great Britain, and Northern Ireland Welcome Trust.
A Jacob: has received research grants from Biogen Idec, Alexion Pharmaceuticals and speakers fees from Biogen, Chugai, Sanofi-Genzyme and Terumo-BCT.

Abstract: EP1722

Type: ePoster

Abstract Category: Therapy - disease modifying - 29 Risk management for disease modifying treatments

B-cell depleting anti-CD20 monoclonal antibody therapies have demonstrated promising clinical efficacy in suppressing relapses in individuals with neuromyelitis optica (NMO) and multiple sclerosis (MS). However, uncertainties remain about the optimum treatment schedule. In rheumatological disease, anti-CD20 agents are most often employed for short-term induction therapy and are subsequently replaced by longer-term maintenance therapy. In contrast, repeated cycles of anti-CD20 monoclonal antibody therapy are proposed as maintenance therapy for CNS neuro-inflammatory disorders. Post-marketing surveillance will be essential to fully uncover the long-term safety profile of repeated B-cell depletion. Hypogammaglobulinaemia is a recognised consequence in a proportion of patients treated with medium- to long-term B-cell therapy and may play a role in the increased incidence of infection observed in the anti-CD20 arms of treatment trials. We report 5 cases of serious infection associated with hypogammaglobulinaemia occurring in patients receiving rituximab for NMO. The cases were all female, all had low IgG with variable reductions in IgM and IgA. The cases had a mean treatment duration of 3.1 years, but not all cases had had extensive exposure (treatment duration range 0.5 - 6.2y). We review the evidence relating to hypogammaglobulinaemia following anti-CD20 treatment for neuroinflammatory disorders and propose an algorithm for monitoring and treatment of this recognised complication.
Disclosure:
E C Tallantyre: has received research support from Biogen Idec.
D Whittam: nothing to disclose.
N P Robertson: has served on the scientific advisory board for Genzyme, Roche, Novartis, and Biogen, received travel funding and/or speaker honoraria from Biogen and Genzyme and received research support from Genzyme, Novartis, National Institute of Health Wales, Multiple Sclerosis Society of Great Britain, and Northern Ireland Welcome Trust.
A Jacob: has received research grants from Biogen Idec, Alexion Pharmaceuticals and speakers fees from Biogen, Chugai, Sanofi-Genzyme and Terumo-BCT.

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