A60-24 Allergic Bronchopulmonary Aspergillosis in a Pediatric Patient on Infliximab for Crohn’s Disease

Introduction Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity response to Aspergillus fumigatus that typically occurs in patients with asthma or cystic fibrosis. Heightened Th2 CD4+ cell activity against Aspergillus leads to cytokine release, eosinophilia, and elevated IgE which are hallmarks of the disorder. We present a unique case of ABPA in a pediatric patient with Crohn’s disease receiving infliximab therapy. Case Description A 14-year-old female with Crohn’s disease and allergic history was referred for evaluation of presumed asthma after one year of progressive cough, dyspnea, and chest pain, which improved with albuterol. Spirometry demonstrated a moderate obstructive defect without bronchodilator response. Chest radiographs revealed bilateral upper lobe infiltrates, prompting hospital admission for further evaluation and IV antibiotics. Non-contrast chest CT showed bilateral posterior upper lobe airspace consolidation and tree-in-bud nodularity, without cavitations or bronchiectasis. Bronchoscopy revealed tenacious green-yellow secretions in both upper lobes. Though a possible fistula-like lesion was seen in the right bronchus intermedius, it was not confirmed on CT review. Bronchoalveolar lavage showed eosinophilia (16.7%), and cultures identified Aspergillus species. Laboratory results revealed eosinophilia (2,580 cells/μL) and markedly elevated total IgE (3,107 kU/L). An ABPA panel was positive for Aspergillus-specific IgE and precipitating IgG antibodies. The patient, an avid horseback rider with frequent exposure to stable, was diagnosed with ABPA. Treatment included prednisone 0.5 mg/kg/day for one week, followed by every-other-day treatment for 8 weeks, followed by slow taper over 6 weeks. Alongside treated with voriconazole for 16 weeks given her immunocompromised status from infliximab. Symptoms and radiographic findings improved, though persistent mild airflow obstruction remained. Following these therapies, her repeat IGE following therapy reduced to 544 IU/mL. Following steroid wean, she had then relapse of ABPA along with elevated IgE to 2324 IU/mL, due to which she was restarted on prednisolone regimen with taper as above, voriconazole course for 16 weeks, and initiated Omalizumab as an adjunctive therapy. Discussion This case highlights ABPA developing in a pediatric patient treated with infliximab for Crohn’s disease. Although her atopic predisposition may have contributed, prior adult reports possibly link anti–TNF-alpha therapy to ABPA in autoimmune disease settings, including rheumatoid arthritis, sarcoidosis, and Crohn’s disease. It is hypothesized that TNF-alpha inhibition suppresses Th1 pathways, skewing immune balance toward Th2-mediated hypersensitivity and predisposing to ABPA. To our knowledge, this represents the first documented pediatric case of ABPA associated with infliximab therapy.