Key result
PFO occlusion and glucocorticoids linked to zero recurrent cerebral infarctions in a hypereosinophilic syndrome case.
Case Report (n=1)
No
Highlights the importance of considering unusual etiologies like HES and PFO in young patients presenting with cerebral infarction.
Supports combined glucocorticoid and PFO closure therapy in HES-related stroke; hypothesis-generating for embolic source identification and requires prospective confirmation.
Hypereosinophilic syndrome (HES), characterized by an increased number of eosinophils in tissues and/or blood, presents with heterogeneous clinical manifestations. Studies have shown that HES can affect the nervous system and may be associated with cerebral infarction. Patent foramen ovale (PFO) is the most common congenital intracardiac defect that can cause right-to-left shunting and contribute to the paradoxical embolization of venous emboli, and even lead to stroke. We report the case of a young man who presented with cerebral infarction accompanied by both HES and PFO. The patient underwent thorough evaluation to determine the source of emboli and the potential pathogenesis. In this case, HES was confirmed and glucocorticoid treatment was conducted. Direct imaging using optical coherence tomography (OCT) confirmed that the embolus originated from the PFO. Therefore, we performed PFO occlusion. The patient recovered well, and no new cerebral infarction was observed at 6-month follow-up. Based on the results of our study, we conclude that it is important to consider unusual etiologies of cerebral infarction, particularly in younger patients.
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Liu et al. (2024) conducted a case report in Cerebral infarction with Hypereosinophilic syndrome and Patent foramen ovale (n=1). PFO occlusion and glucocorticoid treatment was evaluated on Recurrent cerebral infarction. In a 43-year-old man with cerebral infarction, hypereosinophilic syndrome, and patent foramen ovale, PFO occlusion and glucocorticoid treatment resulted in no new cerebral infarctions at 6-month follow-up.
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