Hypereosinophilic syndrome is a disease characterized by a persistently elevated eosinophil count (≥ 1500 eosinophils/mm³) in the blood for at least six months without any recognizable cause, with involvement of either the heart, nervous system, or bone marrow.

[5] Hypereosinophilic syndrome can manifest in many different ways from nonspecific symptoms and fatigue to neurological impairment and endomyocardial fibrosis, which may be fatal.

[16] Patients can develop a range of nonspecific symptoms, including fever, diarrhea, rash, angioedema, weakness, exhaustion, coughing, and dyspnea.

[17] The common and non-specific cutaneous manifestations are either erythematous, itchy papules and nodules that resemble eczema, or urticarial and angioedematous lesions.

A thrombotic stage ensues after this one, during which thrombi form in the cardiac chambers along the injured endocardium and may separate, resulting in peripheral emboli.

[13] When there are no radiological abnormalities, lung involvement can vary from a persistent dry cough and/or bronchial hyperreactivity to restrictive disease with pulmonary infiltrates.

[17] Despite the lack of knowledge regarding the precise mechanism underlying eosinophil-induced tissue damage, eosinophil accumulation seems to have pathological outcomes.

[17] Eosinophils cause direct cytotoxicity by releasing harmful substances locally, such as enzymes, pro-inflammatory cytokines, reactive oxygen species, cationic proteins, and factors derived from arachidonic acid.

[11] Secondly, various imaging and diagnostic technological methods are utilised to detect defects to the heart and other organs, such as valvular dysfunction and arrhythmias by means of echocardiography.

Chest radiographs may indicate pleural effusions and/or fibrosis,[11] and neurological tests such as CT scans can show strokes and increased cerebrospinal fluid pressure.

[11] A proportion of patients have a mutation involving the PDGFRA and FIP1L1 genes on the fourth chromosome, leading to a tyrosine kinase fusion protein.

[26] It has been demonstrated that immunomodulatory drugs, such as interferon-alpha, cyclosporine, and intravenous immunoglobulin, that influence Th2 cytokine production and T cell proliferation can be therapeutically effective in HES.

[27] The U.S. Food and Drug Administration (FDA) has approved imatinib mesylate, a tyrosine kinase inhibitor, as the first treatment for HES.