Abstract Introduction Pulmonary eosinophilia can result from a variety of causes, including allergic, infectious, vasculitic, malignant, and drug-induced processes. Paraneoplastic eosinophilia, though rare, can mimic pulmonary eosinophilia and confound an early diagnosis. We present an interesting case of a patient with marked eosinophilia and pulmonary infiltrates suggestive of eosinophilic pneumonia who was ultimately found to have metastatic lung adenocarcinoma. Case Presentation A 55-year-old man with well-controlled HIV, 60 pack-year smoking history, and intermittent crack cocaine use, presented with progressive dyspnea and hypoxic respiratory failure following outpatient treatment for suspected pneumonia. CT chest revealed multifocal opacities consistent with multifocal pneumonia. Laboratory results showed leukocytosis (WBC 17) with marked eosinophilia (19% eosinophils). Peripheral smear confirmed mature eosinophilia. Initial differential included acute eosinophilic pneumonia, hypereosinophilic syndrome, infection, and malignancy. Hematology workup for myeloproliferative neoplasm (BCR-ABL, JAK2, CALR) was negative. Solumedrol was given for presumed eosinophilic pneumonia, with improvement in eosinophilia; however, repeat imaging showed persistent consolidations, and eosinophilia recurred during a steroid taper. Hospital course was complicated by multifocal embolic infarcts related to a probable patent foramen ovale seen on TEE. Infectious, autoimmune, and hematologic workup were unrevealing. A bronchoscopy was eventually performed, with cytology revealing poorly differentiated adenocarcinoma. Additional imaging later showed lymphangitic carcinomatosis, necrotizing pneumonia, osteolytic lesions, and adrenal metastases - consistent with stage IV lung adenocarcinoma. Discussion Malignancy-associated eosinophilia is a rare but recognized paraneoplastic manifestation most often seen with solid tumors. Tumor-derived cytokines such as IL-5, IL-3, and GM-CSF drive eosinophil proliferation and tissue infiltration. In the lungs, this process can mimic the presentation of eosinophilic pneumonia or vasculitis. Diagnostic complexity was heightened in this case as eosinophilia can also reflect drug reactions, parasitic infections, or inflammatory pneumonitis. The patient’s HIV status, polysubstance use (including cocaine), and initial steroid responsiveness further confounded the clinical picture and delayed recognition of an underlying malignant process despite appropriate initial management. Persistent pulmonary opacities despite eosinophil resolution should prompt tissue diagnosis, as radiographic improvement in eosinophilic pneumonia typically occurs within days of corticosteroid initiation. Reported cases of adenocarcinoma presenting as eosinophilic pneumonia are rare but clinically significant, as early recognition can alter management and prognosis. This case underscores the importance of maintaining a broad differential and integrating serial imaging, laboratory data, and tissue sampling when findings are refractory to standard therapy. This abstract is funded by: None
Samuel et al. (Fri,) studied this question.