Hypereosinophilic syndromes

Groh, Matthieu; Lefevre, Guillaume; Ackermann, Felix; Etienne, Nicolas; Kahn, Jean-Emmannuel

Type de document :

Article dans une revue scientifique: Article original

PMID :

32233322

URL permanente :

http://hdl.handle.net/20.500.12210/104780

Titre :

Hypereosinophilic syndromes

Auteur(s) :

Groh, Matthieu [Auteur]
Lefevre, Guillaume [Auteur]

Ackermann, Felix [Auteur]
Etienne, Nicolas [Auteur]
Kahn, Jean-Emmannuel [Auteur]

Titre de la revue :

La Revue Du Praticien

Nom court de la revue :

Rev Prat

Numéro :

Pagination :

767-773

Date de publication :

2019-09-01

ISSN :

2101-017X

Discipline(s) HAL :

Sciences du Vivant [q-bio]

Résumé en anglais : [en]

Hypereosinophilic syndromes. Hypereosinophilic syndromes (HES) is a protean condition defined by chronic blood eosinophilia ≥ 1.5 G/L (> 1 month) leading to eosinophilic-related organ damage. HES subtypes includes neoplastic ...
Lire la suite >Hypereosinophilic syndromes. Hypereosinophilic syndromes (HES) is a protean condition defined by chronic blood eosinophilia ≥ 1.5 G/L (> 1 month) leading to eosinophilic-related organ damage. HES subtypes includes neoplastic (clonal) disorders (HESN, that comprises FIP1L1-PDGFRA- related chronic eosinophilic leukemia and myeloproliferative and myelodysplastic syndromes associated with eosinophilia) and reactive HES (HESR, that aggregates all conditions e.g. parasitic infections, adverse drug reactions, inflammatory or neoplastic diseases that lead to the production of Th2-related cytokines and thereby to non-clonal hypereosinophilia). HESR also includes the lymphoid variant of HES (HESL), a chronic clonal indolent T-cell lymphoproliferative disorder in which mature peripheral T cells secrete high amounts of IL-5, leading to the polyclonal expansion of eosinophils. Despite an extensive etiological workup, approximately 50% of HES remain of undetermined cause. HES-related clinical manifestations are highly diverse, but dermatological, respiratory and gastro-intestinal symptoms are the most frequent. The long-term prognosis is driven by cardiac involvement and, for patients with HESN and HESL, by the risk of acute transformation into high-grade hematological malignancies. Treatment of HESN relies on tyrosine kinase inhibitors (e.g. imatinib mesylate), while oral glucocorticoids are the usual the fist-line therapy for HESR (including SHEL). In this setting, second-line treatments include hydroxyurea and Peg-interferon alfa-2a. IL-5-targeted therapies are very promising (except for HESN). Yet, to date, their use is restricted to clinical trials and to a compassionate use program dedicated to severe and refractory patients.Lire moins >

Langue :

Anglais

Audience :

Internationale

Vulgarisation :

Non

Établissement(s) :

CHU Lille
Inserm
Université de Lille

Collections :

Institut de Recherche Translationnelle sur l'Inflammation (INFINITE) - U1286

Date de dépôt :

2024-01-30T10:26:28Z

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