Methods: A retrospective chart review was performed of a patient who received 2 doses of belimumab, for SLE poorly responsive to anti-malarial and corticosteroid treatment, which was discontinued due to development of acute pancreatitis. An immune evaluation 2 years after receiving the BLyS-specific inhibitor, fulfilled diagnostic criteria for CVID and immunoglobulin replacement was initiated.
Results: Two years after limited treatment with a humoral immunomodulator, an evaluation due to continued severe symptoms, without reported recurrent infections, revealed hypogammaglobulinemia, and sub-protective levels of pneumococcal and tetanus antibodies. Immune evaluation prior to therapy was not conducted, complicating the diagnosis of CVID as delayed diagnosis versus a secondary immunodeficiency.
Conclusions: Although a small extension of a phase II study of belimumab demonstrated modest decrease in memory B cells and plasma cells, the possibility of provoked B-cell dysfunction exists. A case series identifying 11 patients with secondary rituximab-induced immunodeficiency, long after discontinuation of the anti-CD20 antibody, supports this supposition. As the utilization of immunomodulatory therapy increases, it will be important to perform baseline serum immunoglobulin levels and B cell population analysis prior to starting B-cell specific biologic therapies.