rituximab can cause hypogammaglobulinemia
- related: Pulmonology
- tags: #literature #pulmonary
Links to this note
- targets CD20 and depletes peripheral B cells
- monitor Ig levels at baseline and periodically
- vaccinate prior to rituximab: particularly polysaccharides
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Baseline and periodic monitoring of serum immunoglobulin levels (IgG, IgA, and IgM) and peripheral B cells prior to initiation of rituximab is recommended to identify those at risk of developing hypogammaglobulinemia during treatment, as occurred in the current case (choice D is correct) (Figure 4), and those who might potentially benefit from replacement therapy.
Rituximab is a chimeric immunoglobulin (Ig) G1 directed against CD20, targeting B-cell lineages from the pre-B cell through preplasma cells, inducing antibody-dependent, cell-mediated lysis. Rituximab is used for the treatment of B-cell malignancies and other autoimmune disorders such as a rheumatoid arthritis, Sjogren’s syndrome, autoimmune cytopenias, pemphigus, and pemphigoid autoimmune vasculitis.
Secondary immunodeficiency may be induced by rituximab by several different mechanisms. While rituximab depletes peripheral blood B cells following therapy, recovery or normalization of the peripheral B-cell population typically occurs in approximately 9 months following the infusion. With repeated doses of rituximab, persistent hypogammaglobulinemia with an increased risk of infection may occur in a subset of patients and be clinically significant, requiring immune globulin replacement therapy. Additionally, with repeated doses of rituximab, altered T-cell immunity, but not T-cell lymphopenia, have been observed with an increased risk of viral and fungal infections (choice A is incorrect).
An impaired or submaximal response to vaccination following treatment with rituximab has been identified, particularly in polysaccharide vaccines (choice B is incorrect). This may be further complicated by quantitative and qualitative abnormalities accompanying the underlying autoimmune or lymphoproliferative disease for which rituximab is being utilized. Therefore, appropriate vaccination and immunization should be considered prior to treatment with rituximab. While neutropenia may occur following the use of rituximab, it is rare and is not the most likely contributor to the development of nontuberculous mycobacteria noted in this patient (choice C is incorrect).
The HRCT imaging from 2011 to 2018 revealed a background mosaic attenuation pattern with expiratory imaging showing marked multifocal air trapping with moderate diffuse airway wall thickening and mildly extensive foci of cylindrical bronchiectasis. Predominant foci of cylindrical bronchiectasis are present. There is a moderately extensive component of nodularity, ground glass, and foci of bronchovascular consolidation. Overall, the pattern is one of progressive multifocal nodularity, mucous plugging, and consolidation concerning for infection or aspiration. Nontuberculous mycobacterial infection should be considered.1