Probable allergic bronchopulmonary aspergillosis with atypical serologic findings during eosinophil depletion and hypogammaglobulinemia: a case report

Allergic bronchopulmonary aspergillosis (ABPA) is typically diagnosed using eosinophilic and immunologic biomarkers combined with characteristic imaging. These biomarkers may be challenging to interpret during eosinophil-depleting therapy and profound humoral immunodeficiency. Here, we report a case of probable ABPA in a patient receiving both benralizumab and the B-cell maturation antigen-directed bispecific antibody elranatamab. A woman in her 50 s with asthma and heavily pretreated multiple myeloma presented with exertional dyspnea, productive cough, and progressive pulmonary opacities 30 days after benralizumab initiation. Computed tomography (CT) obtained during an asthma attack before benralizumab had shown neither bronchiectasis nor mucus plugging. At the index admission, CT and bronchoscopy showed tenacious mucus plugs, high-attenuation mucus (HAM) in the right upper-lobe and right middle lobe, and central bronchiectasis in the right upper-lobe B1 and B2 bronchi. Peripheral eosinophils were completely depleted, while total immunoglobulin E (IgE) and Aspergillus -specific IgE and IgG were low or negative. Cytologic examination of bronchial washing fluid showed septate, acute-angle-branching hyphae, while quantitative real-time polymerase chain reaction for Aspergillus DNA was positive (9 × 10 4 copies/mL). Five Japanese diagnostic criteria were unequivocally fulfilled; a sixth component, microscopic detection of fungal hyphae in bronchial mucus plugs, was supportive but uncertain because the specimen was washing fluid rather than an intact mucus plug. Probable ABPA was diagnosed based on the overall clinical and radiologic patterns, particularly HAM, while invasive pulmonary or tracheobronchial Aspergillus disease could not be completely excluded. Clinical, bronchoscopic, and radiologic improvement followed nearly simultaneous corticosteroid, antifungal, and bronchoscopic interventions, precluding attribution to any single treatment. In patients whose eosinophil counts and serologic markers may be pharmacologically suppressed, persistent or recurrent pulmonary opacities should prompt careful reassessment for mucus plugging, HAM, and central bronchiectasis. These imaging findings provide important clues to probable ABPA, while reinforcing that invasive Aspergillus disease should be evaluated separately in immunocompromised patients.