Abstract
BackgroundRituximab is a B cell depleting anti-CD20 monoclonal antibody. CD20 is not expressed on mature plasma cells and accordingly rituximab does not have immediate effects on immunoglobulin levels. However, after rituximab some patients develop hypogammaglobulinaemia.MethodsWe performed a single centre retrospective review of 177 patients with multisystem autoimmune disease receiving rituximab between 2002 and 2010. The incidence, severity and complications of hypogammaglobulinaemia were investigated.ResultsMedian rituximab dose was 6 g (1–20.2) and total follow-up was 8012 patient-months. At first rituximab, the proportion of patients with IgG <6 g/L was 13% and remained stable at 17% at 24 months and 14% at 60 months. Following rituximab, 61/177 patients (34%) had IgG <6 g/L for at least three consecutive months, of whom 7/177 (4%) had IgG <3 g/L. Low immunoglobulin levels were associated with higher glucocorticoid doses during follow up and there was a trend for median IgG levels to fall after ≥ 6 g rituximab. 45/115 (39%) with IgG ≥6 g/L versus 26/62 (42%) with IgG <6 g/L experienced severe infections (p = 0.750). 6/177 patients (3%) received intravenous immunoglobulin replacement therapy, all with IgG <5 g/L and recurrent infection.ConclusionsIn multi-system autoimmune disease, prior cyclophosphamide exposure and glucocorticoid therapy but not cumulative rituximab dose was associated with an increased incidence of hypogammaglobulinaemia. Severe infections were common but were not associated with immunoglobulin levels. Repeat dose rituximab therapy appears safe with judicious monitoring.
Highlights
Rituximab is a B cell depleting anti-CD20 monoclonal antibody
Rituximab was licensed for the treatment of B cell lymphoma in 1997 [10], rheumatoid arthritis (RA) in 2006 [11,12,13] and ANCA associated vasculitis (AAV) in 2011
Hypogammaglobulinaemia has occurred in more than 50% of non-Hodgkin’s lymphoma (NHL) patients, especially in those receiving rituximab in combination with chemotherapy or bone marrow transplantation [15,16,17,18], and less so in RA patients treated with rituximab where 3.5% had IgG levels below the normal range [19]
Summary
Rituximab is a B cell depleting anti-CD20 monoclonal antibody. Rituximab is a chimeric murine/human monoclonal antibody that results in complete peripheral blood B cell strategies resulting in prolonged B cell depletion, preexisting humoral immunity maybe impaired. Hypogammaglobulinaemia has been reported in small cohorts with primary systemic vasculitis treated with rituximab [20,21,22,23], the impact of prior high immunosuppression exposure, and repeat rituximab dosing, as is widely used in clinical practice, are unclear. The potential development of secondary immunodeficiency due to immunosuppressive medication, including the impact of prolonged B cell depletion on IgG levels and infection risk, is not well studied in patients with autoimmune disease
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