A 69-year-old man was admitted to our hospital with right pleural effusion, ascites, and hypereosinophilia. Ten days later, he developed impaired consciousness and involuntary movement in the right upper limb was noted. A neurological examination revealed muscle weakness in all extremities and negative pyramidal tract signs. Cranial diffusion-weighted images showed multiple hyperintensity lesions in the watershed area of white matter and the cortex, suggesting acute brain infarctions. Cerebrospinal fluid (CSF) analysis revealed pleocytosis and extremely elevated protein level (4,504 mg/dl), while cytology of the CSF showed atypical lymphocytes, leading us to suspect T-cell lymphoma. Cytology of pleural effusion and ascites specimens revealed no apparent malignant cells, though Southern blotting of a pleural effusion sample showed clonal rearrangement of the T-cell receptor Cβ1 gene. The cerebral borderzone infarctions were speculated to have been caused by hypereosinophilia secondary to IL-5 over-production by a T-cell lymphoma. Methyl prednisolone pulse therapy was administered to reduce eosinophils. The patient was diagnosed with progressive disease after one cycle of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone). Unfortunately, he died of multiple organ failure 58 days after admission. A postmortem examination revealed widespread infiltration of lymphoma cells in various organs including the gastrointestinal tract and brain, though no eosinophils were found in examined brain or heart tissues. Hypereosinophilic syndrome should be considered as a differential diagnosis in patients with multiple borderzone infarctions.
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