Evidence map›Paper›PMID 41536447›Full record

ArticleEuropean journal of case reports in internal medicine2025

Fulminant Idiopathic Hypereosinophilic Syndrome Presenting with Cardiac, Neurologic and Haematologic Involvement.

Nawras Ibrahim, Abboud Batri, Robert Rueda Rivera, Amer Zwein

Abstract read
In one paragraph

Article in European journal of case reports in internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Nawras IbrahimHCA Houston Healthcare Clear Lake/University of Houston College of Medicine, Houston, USA.
Abboud BatriHCA Houston Healthcare Clear Lake/University of Houston College of Medicine, Houston, USA.
Robert Rueda RiveraHCA Houston Healthcare Clear Lake/University of Houston College of Medicine, Houston, USA.
Amer ZweinHCA Houston Healthcare Clear Lake/University of Houston College of Medicine, Houston, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Hypereosinophilic syndrome (HES) is a rare condition characterised by persistent peripheral eosinophilia and associated with multi-organ damage. The most common sources of both morbidity and mortality in HES patients relate to cardiac or neurologic complications, necessitating early recognition and intervention. Case description: A 44-year-old male was admitted with acute chest pain followed by progressive encephalopathy which worsened, indicating the need for intubation. Laboratory studies were significant for marked hypereosinophilia, massive troponin elevation and profound thrombocytopenia. Brain magnetic resonance imaging (MRI) revealed bilateral watershed infarcts. Despite normal ventricular function and mobility on echocardiography, the onset of peak troponin levels concurrently with eosinophilia, resolving promptly after treatment, led us to consider probable acute eosinophilic myocarditis (EM). Thorough workup excluded secondary (parasitic, autoimmune) clonal causes, thus fulfilling consensus-defined criteria for idiopathic HES. High-dose intravenous corticosteroids (methylprednisolone 1 g/day × 3 days) resulted in rapid, synchronous normalisation of eosinophilia, troponin levels and platelet counts, confirming a steroid-responsive, eosinophil-driven pathology. The patient was left with persistent severe neurologic deficits. Conclusion: This case highlights the destructive potential of acute eosinophil degranulation across multiple organs. The rapid improvement with corticosteroids underscores the importance of early recognition and immediate immunosuppressive therapy to limit organ damage. Clinicians should maintain high suspicion for HES in adults with unexplained eosinophilia and multi-organ involvement. LEARNING POINTS: Maintain suspicion for HES in unexplained eosinophilia with multi-organ dysfunction.Eosinophilic myocarditis may present with high troponin despite normal echocardiogram.Bilateral watershed infarcts reflect microvascular hypoperfusion due to eosinophilic endothelial injury.Thrombocytopenia often resolves rapidly with corticosteroids.Early immunosuppression prevents irreversible organ damage.

Indexed as

corticosteroidseosinophilic myocarditisHypereosinophilic syndromethrombocytopeniawatershed stroke

Identifiers

PMID41536447
PMCPMC12799074

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