Hypereosinophilia (HE), defined as an absolute eosinophil count (AEC) exceeding 1,500/µL, is an uncommon finding with heterogeneous etiologies, including neoplastic causes. When associated with organ damage, it is defined as hypereosinophilic syndrome. Although hematological malignancies more frequently drive hypereosinophilia, it can rarely occur as a paraneoplastic phenomenon in solid tumors. Crucially, peripheral eosinophil counts do not reliably correlate with the severity of tissue injury, and significant organ dysfunction may arise even with mild-to-moderate eosinophilia. We report the case of a 66-year-old man, an active smoker, who presented with retrosternal chest pain, elevated high-sensitivity troponin, and markedly increased D-dimer levels. Initial chest computed tomography (CT) angiography revealed a solid pulmonary nodule. The patient was admitted under a diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI). During hospitalization, peripheral AEC peaked at 2,900 cells/μL. A paraneoplastic aetiology was established after ruling out secondary and clonal causes. Clinical course was marked by rapidly progressive multiorgan complications, including cerebral ischemia, splenic and renal infarctions, cutaneous embolic phenomena, and severe eosinophilic endomyocarditis. Although diagnosis of metastatic lung adenocarcinoma was confirmed by cervical lymph node biopsy, the patient suffered rapid deterioration and died before tumour-directed therapy could be initiated. Paraneoplastic hypereosinophilia in lung adenocarcinoma is an exceptionally rare manifestation associated with an aggressive tumor biology and poor prognosis. This case highlights its potential for devastating multiorgan involvement despite non-extreme peripheral eosinophilia, underscoring the vital need for early etiological recognition to prevent irreversible clinical deterioration.
Bravo et al. (Tue,) studied this question.
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