Anti-IL-5 and hypereosinophilic syndromes

Neglected tropical cardiomyopathies: II. Endomyocardial fibrosis

“…These syndromes have been classified as idiopathic, clonal and reactive. The similarity of mechanisms responsible for EMF and the hypereosinophilic syndromes could have exciting therapeutic implications 6. Eosinophils in patients with hypereosinophilia have unusual morphology, are metabolically and functionally more effective than normal, and show a preponderance of multilobed forms and evidence of degranulation.…”

“…EMF appears to have an initial stage of febrile illness and pancarditis,9 frequently associated with hypereosinophilia, facial and peri-orbital swelling, body itching, urticaria and neurological features 6. This febrile episode, triggered by one or more unknown factors, is followed by ventricular thrombosis affecting usually the apices and the subvalvar apparatus.…”

The FIP1L1-PDGFRA fusion gene cooperates with IL-5 to induce murine hypereosinophilic syndrome (HES)/chronic eosinophilic leukemia (CEL)–like disease

“…46 Indeed, anti-IL-5 therapy appears to be an effective therapy even in patients with undetectable or low levels of IL-5. 47,48 In addition to circulating IL-5, paracrine effects of IL-5 locally produced by T cells 18 and/or eosinophils 49 may have critical roles in HES.…”

Infliximab as a Therapy for Idiopathic Hypereosinophilic Syndrome

“…It carries a good prognosis, with prolonged survival, and may respond to glucocorticoid therapy or to treatment with human monoclonal antiinterleukin 5 antibody. 4,5 Cutaneous lesions are common in l-HES and vary from pruritic erythematous macules, papules, plaques, or nodules to urticaria and angioedema. 4 Myeloproliferative HES (m-IHES) is characterized by clonally derived eosinophils, carries a poor prognosis, and may respond to imatinib mesylate (a tyrosine kinase inhibitor) therapy, particularly in the presence of FIP1L1-PDGFRA gene fusion.…”