Secondary antibody deficiency in neurology

Induction of lymphocyte depletion is increasingly used as a therapeutic strategy for central and peripheral neuroinflammatory disease. However, there is also a growing recognition of the treatment-related complication of secondary antibody deficiency (SAD). Although the occurrence of hypogammaglobulinaemia is a recognized phenomenon during immunomodulation, robust data on the coexistence of impaired responses to immunization, and significant and/or atypical infections is scarce. Here we review the literature on SAD in anti-CD20 therapy.

Several factors that may increase the incidence of SAD have now been identified, including low levels of immunoglobulins prior to the commencement of B-cell ablation therapy, duration of maintenance therapy, and concurrent or prior use of other immunosuppressing agents such as cyclophosphamide and steroids. Measurement of disease-specific antibodies and vaccine response are likely to be helpful adjuncts to measurement of serum immunoglobulin levels during B-cell depleting therapy. Supportive treatment may include amending the treatment schedule to limit cumulative dose.

B-cell depleting agents offer considerable therapeutic benefit in neurology. We propose modifications in current practice that include risk stratification and early identification of SAD, with the aim of minimising morbidity and mortality related to this underappreciated condition.