Abstract

<h3>Introduction</h3> Eosinophilic inflammation in lung transplant (LTX) is challenging. Eosinophils may be found in transplant grafts during rejection episodes; however, it is unclear if they are bystanders or pathogenic. We did not find any prior use of biologics to disrupt the interleukin-5 (IL-5) pathway in the transplant literature. We discuss the novel use of benralizumab, a monoclonal antibody that targets IL-5 receptor. <h3>Case Report</h3> 19 year-old female with cystic fibrosis presented 18 months post-LTX with cough and chest pain and was treated with amoxicillin-clavulanate for community acquired pneumonia. She had mild leukocytosis and elevated absolute eosinophil count. She worsened and developed respiratory distress and fever, requiring bilevel positive airway pressure (BiPAP). Computed tomography showed total opacification of right lung. Bronchoscopy identified mild acute cellular rejection, low-grade small airway inflammation, chronic airway rejection, and marked eosinophilic inflammation in tissue and bronchoalveolar lavage (18%). Broad infectious work up was unrevealing. Peripheral eosinophils decreased to undetectable after methylprednisolone pulse, but rebounded one week later. She remained in intensive care unit on BiPAP. Due to favorable side effect profile and deteriorating clinical picture, we initiated benralizumab. Peripheral eosinophilia resolved, and she was weaned off respiratory support. Her two-year post-LTX surveillance bronchoscopy demonstrated resolution of eosinophilic inflammation. <h3>Summary</h3> Eosinophilic inflammation with acute respiratory failure justified the use of benralizumab, which successfully treated eosinophilic associated rejection. We selected benralizumab over other IL-5 disrupters because it theoretically targets IL-5 receptors in the tissue, thereby impacting tissue resident eosinophils. Further study of the role of eosinophils in LTX and the efficacy of IL-5 blockade should be considered.

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