A35-09 The Unexpected Hemorrhage: Acute Diffuse Alveolar Hemorrhage Leading to Diagnosis of Eosinophilic Granulomatosis With Polyangiitis Diagnosis

Abstract Introduction Eosinophilic granulomatosis with polyangiitis (EGPA) is a rare vasculitis affecting small- to medium-sized vessels, mainly in adults with asthma, chronic rhinosinusitis (often with nasal polyps), and peripheral eosinophilia. Incidence is ∼2 per million person-years and prevalence 30-35 per million, complicating diagnosis. Patients develop worsening asthma, sinonasal disease, and migratory pulmonary infiltrates; one-third are myeloperoxidase (MPO)-antineutrophil cytoplasmic antibody (ANCA)-positive. Serious complications include neuropathy, cardiac issues, and diffuse alveolar hemorrhage (DAH), which pose significant morbidity. We report a case of EGPA presenting with bronchoscopically confirmed DAH in a young woman, whose persistent asthma and sinonasal polyposis initially masked the vasculitis. Case A 29-year-old woman with severe persistent asthma and nasal polyps presented for elective bronchoscopy for cough and scant hemoptysis. For nine months, she developed worsening dyspnea and recurrent asthma/sinusitis exacerbations despite escalating inhaled therapy and repeated antibiotics and steroids. On admission, vitals were stable, and labs showed leukocytosis (14.32 × 10³/µL) with a normal eosinophil count—likely suppressed by prednisone 60mg started the day prior. Of note, outpatient lab showed peripheral eosinophilia (2,610/µL; 20%). Bronchoscopy showed progressively bloodier bronchoalveolar lavage fluid, consistent with DAH. The differential contained 70% eosinophils. Biopsy revealed chronic inflammation with increased eosinophils and focal granulation tissue. Serology was positive for p-ANCA with MPO specificity; IgE was elevated. Prior outpatient data supported vasculitic, type-2-driven airway disease: CT chest with peribronchovascular ground-glass nodules Figure 1; severe obstructive physiology with air trapping, diffuse sinonasal polyposis; and peripheral eosinophilia. The patient was started on pulse-dose intravenous glucocorticoids followed by taper and initiation of mepolizumab, then underwent sinus surgery with improvement. Follow-up with otolaryngology, rheumatology, and pulmonology was arranged. Discussion Our patient presented with hemoptysis alongside severe persistent asthma and chronic rhinosinusitis of unclear cause. EGPA involves two immune processes: a type-2, interleukin-5-driven eosinophilic pathway, and an ANCA-mediated vasculitis. She exemplifies this: refractory asthma with nasal polyps reflects the eosinophil/Th2 axis, while hemoptysis with DAH indicates vasculitic injury. Careful review of her history and testing led her pulmonologist to suspect EGPA and pursue bronchoscopy, which confirmed DAH with eosinophil predominance. Since EGPA often mimics difficult asthma and sinus disease, high clinical suspicion enabled timely glucocorticoids and IL-5-pathway biologic therapy, per guidelines. A coordinated multidisciplinary approach moved care beyond inhaler escalation to vasculitis-directed treatment, underscoring the need for vigilant reassessment when asthma therapies fail and continued work to refine EGPA diagnostic pathways for earlier, targeted management. This abstract is funded by: None