Hypereosinophilic syndrome (HES) is a disorder characterized by elevated levels of eosinophils, which may be associated with multi-organ involvement depending on severity. The recent diagnostic criteria for idiopathic HES require an elevated absolute eosinophil count (AEC) above 1500 cells/mcL with evidence of tissue damage. We present a case of a 37-year-old male firefighter with a purported history of eosinophilic bronchitis who was referred to the hospital with syncopal episodes and a persistent productive cough. The patient showed an AEC of 4500 cells/mcL on admission associated with high inflammatory markers. Cardiac imaging demonstrated acute myocarditis with heart failure and a reduced ejection fraction. Chest imaging was initially suggestive of community-acquired pneumonia. Workup was negative for a malignant etiology; infectious causes similarly were excluded. After a multidisciplinary evaluation, a diagnosis of idiopathic HES was made and steroids were instituted with rapid resolution of symptoms. Our case illustrates the importance of considering hypereosinophilia as a precipitating factor for acute heart failure in an otherwise healthy adult. An expeditious diagnosis can lead to early initiation of steroids to avoid progression toward multi-organ failure.

Hypereosinophilia is a rare condition, defined as a persistent elevation of absolute eosinophil count greater than 1.5x109/L and/or tissue eosinophilia. This condition can be caused by numerous different etiologies, both hematological (clonal) and non-hematological (reactive). Reactive hypereosinophilia encompasses all disorders, including infections. Patients with hypereosinophilia may experience a spectrum of clinical consequences due to multiple organ damage, including neurologic and thrombotic complications, associated with organ dysfunction and potentially life-threatening sequelae. Cerebral venous thrombosis (CVT) is the term used to describe thrombotic occlusion of veins and/or venous sinuses in the brain. This condition can occur at all ages and CVT related to hypereosinophilia is a rare disease. Diagnosis of the disease must be done quickly because thrombosis causes blockage of cerebral drainage, venous congestion, disruption of cerebrospinal fluid reabsorption, ischemic neuronal damage, cerebral edema, and hemorrhage, leading to severe neurological complications. Management of intracranial hemorrhage from CVT due to hypereosinophilia is a challenging task for clinicians, based on anticoagulation therapy, systemic corticosteroid, management of elevated intracranial pressure, and potentially progressive hemorrhage due to anticoagulant. The outcome of the patient generally relies on early detection, prompt, and appropriate treatment. In this case report, we discuss a rare case of CVT with hypereosinophilia and positive dengue serology in a child, in the context of intracranial hemorrhage, enlightening the importance of considering a personalized strategy in the management of this complex scenario.

Left ventricular thrombus (LVT) has historically been reported as a complication of acute left ventricular (LV) myocardial infarction. It is most commonly observed in cases of LV systolic dysfunction attributed to ischemic or nonischemic etiologies. Conversely, the occurrence of LVT in normal LV systolic function is an exceptionally rare presentation and is predominantly associated with conditions such as hypereosinophilic syndrome (HES), cardiac amyloidosis, left ventricular noncompaction, hypertrophic cardiomyopathy (HCM), hypercoagulability states, immune-mediated disorders, and malignancies. Notably, hypereosinophilia (HE) has been linked with thrombotic events. Intracardiac thrombus is a well-known complication of eosinophilic myocarditis (EM) or Loeffler endomyocarditis, both of which are considered clinical manifestations of HES. We present a case of a 63-year-old male with normal LV systolic function, HE, and noncontributory hypercoagulability workup, who presented with thromboembolic complications arising from LVT. Interestingly, the diagnostic evaluation for EM and Loeffler endocarditis was nonconfirmatory. Additionally, we performed a literature review to delineate all similar cases. This article also outlines the pathophysiology, diagnosis, and treatment approaches for hypereosinophilic cardiac involvement with a specific focus on LVT.

Hypereosinophilia is a rare presentation in all age groups, particularly when it is severe, persistent, and progressive. We describe the clinical characteristics and course of severe hypereosinophilia in a full-term Saudi female neonate. A febrile respiratory illness evolved with a progressive increase in peripheral blood leukocyte and eosinophil counts, reaching 44.9% of leukocytes and an absolute value of 57,000 cells/µl. Different etiological examinations (for viral, bacterial, immunodeficiency, hyper IgE syndrome, gene mutations) revealed extremely high CMV antigenemia and a homozygous mutation in the STAT1 gene. Anhelation was relieved by oxygen and anti-viral treatment. Steroids brought a dramatic response in peripheral blood counts within 24 h. After a 6-week course of antiviral and steroid treatment at home, she had an excellent general condition. Conclusion: Although a rare pathology, it is important to consider genetic disorders when there is an atypical immune response to viral infections.

UNASSIGNED: Hypereosinophilic Syndrome (HES) is a rare disorder characterized by persistent elevation of eosinophils, leading to multi-organ infiltration and damage. Eosinophilic Myocarditis (EM) is one of its severe complications contributing significantly to morbidity and mortality. Herein, we describe the diagnostic and therapeutic challenges of EM, emphasizing the significance of early recognition and multidisciplinary management.
UNASSIGNED: A 51-year-old female with a history of EM, heart failure, and peripheral eosinophilia presented with NYHA class 3b symptoms. Laboratory findings revealed elevated peripheral eosinophil count, NT-Pro BNP, and characteristic electrocardiogram abnormalities. Imaging studies confirmed biventricular thrombi and myocardial abnormalities consistent with EM. Treatment involved Solu-Medrol for HES and heparin for ventricular thrombi, leading to initial clinical improvement. However, refractory heart failure necessitated urgent heart transplantation.
UNASSIGNED: EM, an under-recognized complication of HES, poses diagnostic and management challenges. Management includes standard heart failure treatments, steroids, and emerging therapies like Mepolizumab. Early diagnosis and aggressive management are pivotal for improving outcomes in this rare and potentially fatal condition.
UNASSIGNED: Advancements in the detection of complications, surgical management, and therapeutic options have improved outcomes in HES. Ongoing research is essential to further understand and address the diagnostic and therapeutic challenges of HES and EM.

Type 2 inflammation is a heterogeneous condition due to the complex activation of different immunological pathways. Rapid progress in research to evaluate the efficacy of biologics for chronic rhinosinusitis with nasal polyps and asthma has led to the availability of effective therapeutic options. These drugs are safe, but temporary iatrogenic hypereosinophilia may sometimes be associated with clinical symptoms or organ damage. Here, we describe a case of severe hypereosinophilia in a patient with chronic rhinosinusitis with nasal polyps and asthma treated with dupilumab and a subsequent therapeutic shift to mepolizumab that led to maintenance of symptom control and concomitant normalization of blood eosinophil count.

Understand the importance of considering alternative diagnosis in patients presenting with atypical features. Understand the importance of considering common presentations of rare cases. Underscoring the critical importance of timely recognition and appropriate management of potentially life-threatening condition.

Eosinophilia is known to be associated with a multitude of co-morbidities. However, unexplained eosinophilia poses a diagnostic challenge, and the methods used to investigate unexplained eosinophilia vary from region to region. In this case report, we describe a unique case of a young female presenting with marked eosinophilia to a tertiary hospital in the northeastern United States. Our patient presented with a few weeks of lower extremity rash, gait instability, and new onset marked eosinophilia. We further report the investigations undertaken during the hospitalization to highlight the broad differential diagnoses. Later, we provide a consolidated diagnosis of eosinophilic granulomatosis with polyangiitis (EPGA) based on the clinical context. Our patient was eventually started on a high-dose steroid taper. In the following weeks, while we noted gait improvement, we observed biomarker (eosinophilia) relapse after steroid taper. Depending on symptom progression, we planned for future remission induction with immunomodulatory agents. The report further discusses the pleomorphic presentation of EPGA cases, the natural course of disease, and currently available prognostic indices.

Existence of poorly differentiated tumour cells or paraneoplastic hypereosinophilia indicates extensive disease progression and poor prognosis in patients with malignancy. When these conditions are present, it is necessary to consider the possibility of intracardiac metastasis even in cases of lung adenocarcinoma.

In recent years, there has been growing recognition of the association between lice infestation and iron deficiency anemia (IDA). The head lice, known as Pediculosis humanus capitis, and the body lice, known as Pediculosis humanus corporis, are responsible for causing these infestations. This case report focuses on the clinical findings of a 63-year-old woman who sought medical attention in the emergency department because of severe pruritus and generalized pain. Upon initial physical examination, the patient was found to have a severe lice infestation, and laboratory findings revealed IDA (Hb: 6.8 g/dL, MCV: 70 fL, iron: 21 mcg/dL) and hypereosinophilia (3,500/μL). Treatment involved the administration of Permethrin 1% lotion, Ivermectin, and intravenous iron sucrose supplementation. On the fifth day of presentation, the patient\'s hemoglobin level improved to 8.6 g/dL, and the eosinophil count decreased to 2,000/μL. Despite extensive investigation of the patient\'s IDA and hypereosinophilia, no clear etiology of IDA was identified. Consequently, the patient was diagnosed with hypereosinophilia and IDA, secondary to severe chronic pediculosis. This case report aims to raise awareness of the possibility of severe pediculosis as a risk factor for iron deficiency and hypereosinophilia.