Exploring the depths of hypogammaglobulinemia in lymphoid malignancies: Pathophysiology, clinical implications, management options, and future directions.

Abstract

The treatment of lymphoid malignancies is rapidly advancing with recognition of hypogammaglobulinemia (HG) and increased infection risk with the use of cellular-targeted therapies, such as chimeric antigen receptor (CAR) T cell and bispecific antibody (BsAb) therapy. Underlying adaptive immune dysfunction seen in malignancy, immunoparesis, and prior lines of B cell-targeting therapies also predispose patients to HG and infections prior to more advanced cellular therapies. Clinicians should become familiar with how to evaluate adaptive immunity and causes of HG. Various strategies exist to reduce infections in immunosuppressed patients, including risk-reducing practices, vaccination, prophylactic antibiotics, and IgG replacement therapy (IgG-RT). Future research should focus on identifying biomarkers to help with infectious risk-stratification and identify populations that would best benefit from IgG-RT.