Abstract Pulmonary eosinophilia is the infiltration of the lungs with eosinophils. Few conditions present with new-onset asthma and pulmonary eosinophilia, prompting extensive workup. We present the case of a 64 year old male with a history of allergic rhinitis, chronic sinusitis, hypertension and hyperlipidemia who initially developed recurrent idiopathic urticaria, followed by an episode of anaphylaxis of unknown source. He began experiencing progressive shortness of breath, productive cough, nasal congestion, and sleep disturbances with memory impairment. Spirometry demonstrated obstruction with bronchodilator response, and he was diagnosed with adult-onset allergic asthma. Imaging of the sinuses revealed severe paranasal sinus disease. Multiple respiratory flares resulted in maintenance prednisone use. The patient underwent further workup, revealing peripheral eosinophilia and significantly elevated immunoglobulin E. Computed tomography of the chest revealed scattered ground glass opacities and extensive mediastinal and hilar adenopathy. Bronchoscopy with lymph node biopsy was performed, and bronchoalveolar lavage demonstrated marked pulmonary eosinophilia. Repeat chest imaging showed progression of ground glass opacities with mucus plugging and bronchial wall thickening. He was resumed on high dose prednisone with taper and initiated on mepolizumab. His symptoms improved on biologic therapy as he continued prolonged steroid taper. Repeat chest imaging demonstrated resolving pulmonary infiltrates. Although the patient had elements of both eosinophilic granulomatosis with polyangiitis and chronic eosinophilic pneumonia, lack of definitive findings of vasculitis ultimately lead to a diagnosis of chronic eosinophilic pneumonia. The case presented highlights the difficulties in diagnosing and managing eosinophilic lung disease. There are a handful of known causes of pulmonary eosinophilia, requiring careful investigation of medications, travel, exposures and extra-pulmonary manifestations. Cases with new-onset or worsening asthma are often the result of allergic bronchopulmonary aspergillosis/mycosis, eosinophilic granulomatosis with polyangiitis or chronic eosinophilic pneumonia. These conditions have significant clinical overlap, making it difficult to distinguish the underlying etiology. Corticosteroids have historically been first line agents for eosinophilic lung disease, however, the advent of biologic therapies are changing the scope of management. Through eosinophilic depletion, anti-interleukin-5 agents have the potential to reduce steroid burden and improve disease control. This abstract is funded by: none
Swartzman et al. (Fri,) studied this question.