Induction of lymphocyte depletion is becoming more popular as a treatment for central and peripheral neuroinflammatory disorders. However, there is rising awareness of secondary antibody deficit as a treatment-related consequence (SAD). Although hypogammaglobulinemia is a documented condition during immunomodulation, convincing data on the confluence of compromised immune responses with severe and/or unusual infections is lacking. The study examines the research regarding SAD in anti-CD20 treatment. Several risk factors for SAD have since been discovered, including low immunoglobulin levels before to beginning B-cell ablation therapy, length of maintenance therapy, and concurrent or prior use of other immunosuppressive drugs such as cyclophosphamide and steroids. Measuring disease-specific antibodies and vaccination response are expected to be useful supplements to measuring serum immunoglobulin levels after B-cell depleting treatment. Modifying the treatment plan to reduce the cumulative dosage may be considered supportive therapy.
In neurology, B-cell depleting medications provide significant therapeutic effects. We suggest changes to existing management, such as risk stratification and early detection of SAD, with the goal of reducing morbidity and death associated with this unappreciated disease.
