Hypereosinophilic Syndrome a Rare Cause of Multifocal Cerebral Infarcts: A Case Report
Hamza Khan1, Seajin H. Yi2, Hassan Khalid3, Ameerdad Khan4, Abdullah Zaki5, Saqib Chaudhry1, Mohammad Rauf Chaudhry6
1Neuroscience, 2Neurology, Inova Fairfax Medical Campus, 3Biochemistry, Liaquat National Hospital and Medical College, 4Cardiology, Shifa International Hospital, 5Neurology, DHQ teaching hospital Gujranwala, 6Neurology, Inova Loudoun Hospital
Objective:
To report a rare case of multifocal cerebral infarctions associated with hypereosinophilic syndrome (HES).
Background:
Hypereosinophilia (HE) is characterized by persistent elevation in the absolute eosinophil counts. HE is associated with eosinophil-mediated organ damage is categorized as HES, which can manifest with various organ system involvements, including the skin, lungs, heart, brain, and peripheral nervous system. Neurological manifestations include encephalopathy, peripheral neuropathy, and stroke.
Results:
A 41-year-old man with a history of dyslipidemia presented with a worsening skin rash that began near both ankles and legs, escalating over several months despite topical cream use. Initially, fungal infection was suspected; however, investigations revealed a white blood cell count of 178.57 with an absolute eosinophil count of 163.16. The patient also experienced intermittent blurry vision and transient right monocular partial vision loss, describing a "dark spot" in the left upper corner. Brain MRI showed extensive multifocal small signal abnormalities across cerebral and cerebellar hemispheres. Imaging of orbit, angiography, and transesophageal echocardiography yielded no significant findings. Extensive investigations for eosinophilia causation, including various tests and a bone marrow biopsy, proved inconclusive. Treatment with prednisone, imatinib, hydroxyurea, and leukapheresis did not significantly improve eosinophil counts. A subsequent treatment with cytarabine led to a reduction in eosinophil count, and the patient was discharged for outpatient follow-up with hematology. Despite efforts, no definite cause for the eosinophilia has been identified.
Conclusions:
Eosinophilia-related strokes have been reported previously with cardiac embolism and direct eosinophil toxicity are the likely causes. Eosinophilia can damage the endocardium and myocardium, rendering the heart a potential source of emboli. Response to use to anticoagulant or antiplatelets is variable but likely rapid lowering of eosinophils can result in better outcomes.