Allergic Bronchopulmonary Aspergillosis (ABPA) is an immune-mediated airway disease caused by hypersensitivity to Aspergillus fumigatus in genetically and immunologically susceptible people, most often those with asthma or Cystic Fibrosis (CF). Persistent luminal fungus, impaired mucociliary clearance, and exaggerated type 2 immunity interact to produce mucus plugging, eosinophilic inflammation, bronchiectasis, and, in advanced disease, respiratory failure. The 2024 International Society for Human and Animal Mycology (ISHAM) criteria require A. fumigatus sensitization and total immunoglobulin E (IgE) ≥500 IU/mL, together with supportive immunologic or imaging evidence. Sensitization without active ABPA is a related but distinct state and is not routinely treated. This narrative review integrates evidence on epidemiology, immunopathogenesis, diagnosis, clinical classification, radiology, differential diagnosis, complications, and treatment. Prednisolone or itraconazole monotherapy is appropriate for most acute disease; combined therapy is generally reserved for recurrent exacerbations. Therapeutic Drug Monitoring (TDM) is important during azole treatment. Biologics directed against IgE, interleukin (IL)-5/IL-5 receptor α, or IL-4 receptor α are increasingly used for treatment-dependent disease, but the evidence is mainly observational. Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) modulators may reduce airway fungal burden but create clinically important cytochrome P450 3A4 (CYP3A4) interactions with azoles. Response and relapse should be judged against a patient-specific stable IgE baseline together with symptoms and imaging.
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Turki M. Almalki (2026) studied this question.
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