Abstract Background Eosinophilic pulmonary diseases may coexist, with 15 cases described worldwide of Allergic bronchopulmonary fungal disease (ABPFD), with its prototypical form allergic bronchopulmonary aspergillosis (ABPA), and Eosinophilic granulomatosis with polyangiitis (EGPA). The Distinguishing coexistence may be clinically challenging, and many times undiagnosed. This case has the purpose of increased awareness of correlation of beforementioned diseases, leading to prompt appropriate therapy. Case Presentation A 58-year-old woman with a 5-year history of allergic rhinitis, nasal polyps, eosinophilic bronchiectasis and bronchioalveolar lavage (BAL) culture positive for Aspergillus terreus presented with sudden bilateral upper arm and shoulder pain unresponsive to analgesics. Laboratory studies revealed leukocytosis (35.4 k/µL) with marked eosinophilia (21.6 k/µL), elevated CRP (3.2 mg/dL) and ESR (55 mm/hr). Chest CT demonstrated worsening bronchiectasis, mucus plugging, and a new left lower lobe ground-glass opacity. BAL and serum Aspergillus antigens and galactomannan were repeatedly negative.Further testing showed positive c-ANCA (1:640), MPO antibodies (226 AU/mL), elevated IgG4 (424 mg/dL), and high complement activity (CH50 95 U/mL). Eosinophil counts normalized after corticosteroid therapy with improvement in respiratory symptoms. Video-assisted thoracoscopic (VATS) lung biopsy revealed lymphocytic bronchiolitis with airway-centered eosinophilic inflammation, Charcot–Leyden crystals, and goblet cell metaplasia, without fungal forms or granulomas, consistent with severe chronic small airway disease and features of ABPFD, but no histologic evidence of vasculitis. Symptoms recurred every time steroids were tapered off. Discussion ABPFD and EGPA share clinical findings such as severe allergic rhinitis, adult-onset asthma, eosinophilia, bronchiectasis and resolution of symptoms with steroids. Pathology may be helpful to distinguish both based on location of eosinophils. However, it is obscured in many cases due to use of high dose steroids before biopsy. This case underscores the limitations of diagnostic modalities like BAL cultures and galactomannan testing and tissue biopsy in achieving diagnostic clarity. EGPA remains a clinical diagnosis per 2022 ACR/EULAR criteria; and ABPFD, particularly ABPA, similarly relies on integrated clinical, radiologic, and immunologic assessment.The coexistence of ABPFD and EGPA likely reflects shared Th2-driven immunopathogenesis. Recognition of this overlap is crucial for accurate diagnosis and individualized management. The patient’s relapse after steroid taper emphasizes the need for long-term therapy and consideration of emerging biologic agents targeting IL-5 and CD20 pathways. Conclusion This case illustrates the overlapping features and shared immunologic mechanisms of ABPFD and EGPA. Recognition of their coexistence is essential for accurate diagnosis and individualized, long-term management. This abstract is funded by: None
Najera et al. (Fri,) studied this question.