100276 - Allergic Bronchopulmonary Aspergillosis Masked by Asthma and Recurrent Pneumonia

Background

Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to Aspergillus fumigatus, typically occurring in patients with asthma or cystic fibrosis. It is characterized by exaggerated immune response leading to airway inflammation. Clinically, ABPA commonly presents with worsening asthma control, recurrent pneumonia-like episodes, and bronchiectasis. Elevated total immunoglobulin E (IgE), peripheral eosinophilia, and central bronchiectasis or mucus plugging on chest computed tomography are key diagnostic features. Because it may mimic recurrent respiratory infections, diagnosis is frequently delayed. Failure to recognize and treat ABPA early can result in irreversible lung damage and progressive bronchiectasis.

Case Presentation

A 24-year-old male with a history of childhood-onset asthma had been followed for recurrent lower respiratory tract infections and pneumonia for several years. He was referred to our clinic because of frequent infections. Over the previous three years, he had experienced three radiologically confirmed pneumonia episodes requiring hospitalization. Evaluation for inborn errors of immunity was unremarkable, and he was placed under follow-up. Pulmonology follow-up continued due to persistent asthma and recurrent pneumonia. During follow-up, marked peripheral eosinophilia (absolute eosinophil count >1400/µL) and elevated total IgE (1440 IU/mL) were detected. Chest computed tomography demonstrated central bronchiectasis and mucus plugging. Based on clinical, laboratory, and radiologic findings, a diagnosis of allergic bronchopulmonary aspergillosis was established. Systemic corticosteroid (prednisolone) and voriconazole therapy were initiated, resulting in initial clinical and biochemical improvement (total IgE: 80.4 IU/mL). However, during steroid tapering, total IgE levels progressively increased within one year (114, 145, and 219 IU/mL), accompanied by recurrent exacerbations. Due to steroid dependence and inadequate disease control, the patient was reassessed for anti–interleukin-5 therapy. At that time, total IgE was 1510 IU/mL, absolute eosinophil count was 1000/µL, and Asthma Control Test score was 5. Given the severe eosinophilic phenotype, benralizumab was initiated. Following treatment, significant clinical improvement and regression of pulmonary infiltrates were observed.

Discussion

This case illustrates that ABPA may be overlooked in patients with longstanding asthma and recurrent pneumonia. The later emergence of marked eosinophilia, elevated total IgE, and central bronchiectasis led to the correct diagnosis, emphasizing the need to reconsider ABPA in patients with recurrent pulmonary infiltrates. Although initial corticosteroid and antifungal therapy achieved temporary control, relapse occurred during steroid tapering, resulting in steroid dependence. Initiation of anti–interleukin-5 therapy with benralizumab led to significant clinical and radiologic improvement, supporting the role of biologic agents in refractory ABPA.