Case Report: Severe Pneumocystis jirovecii pneumonia following zuberitamab treatment in autoimmune hemolytic anemia

Abstract

The pathogenesis of autoimmune hemolytic anemia (AIHA) remains incompletely understood, typically associated with immune dysfunction and the production of autoantibodies. Zuberitamab, a novel anti-CD20 monoclonal antibody, represents an important therapeutic strategy for managing autoimmune diseases. Here, we present the first case of a patient diagnosed with AIHA who developed severe immunosuppression, lymphopenia, and B-cell depletion following zuberitamab treatment, ultimately resulting in severe Pneumocystis jirovecii pneumonia(PJP). This case highlights the complexities of B-cell-targeted immunotherapy and underscores the necessity of close monitoring of immune status in patients receiving zuberitamab or other targeted immunotherapies to mitigate the risk of severe immune-related adverse events.

Keywords: B-cell depletion; autoimmune diseases; autoimmune hemolytic anemia; case report; severe Pneumocystis jirovecii pneumonia; zuberitamab.

Figure 1

Chest CT on May 24, 2024, showed no signs of infection (A). Chest CT scans from August 4 to September 2, 2024, revealed a gradually expanding infectious focus in the lungs, progressively increasing lung parenchymal density, and bronchiectasis with traction signs (B-G).

Figure 2

The timeline of antimicrobial medication. VOR,Voriconazole;MEM,Meropenem;IPM,Imipenem;TZP,Piperacillin/Tazobactam;GCV,Ganciclovir;mNGS,metagenomic next-generation sequencing;TMP-SMZ,trimethoprim-sulfamethoxazole;CAS,Caspofungin;VAN,Vancomycin;AMK,Amikacin; CMV, Cytomegalovirus.

Figure 3

Pathological examination revealed lung parenchyma with alveolar collapse, widened alveolar septa accompanied by scattered lymphoplasmacytic infiltration, fibrous tissue hyperplasia, and focal foam-like cellular deposits within alveolar spaces.