title: Pathogenesis and classification of eosinophil disorders: a review of recent developments in the field.
abstract: Eosinophils and their products play an essential role in the pathogenesis of various reactive and neoplastic disorders. Depending on the underlying disease, molecular defect and involved cytokines, hypereosinophilia may develop and may lead to organ damage. In other patients, persistent eosinophilia is accompanied by typical clinical findings, but the causative role and impact of eosinophilia remain uncertain. For patients with eosinophil-mediated organ pathology, early therapeutic intervention with agents reducing eosinophil counts can be effective in limiting or preventing irreversible organ damage. Therefore, it is important to approach eosinophil disorders and related syndromes early by using established criteria, to perform all appropriate staging investigations, and to search for molecular targets of therapy. In this article, we review current concepts in the pathogenesis and evolution of eosinophilia and eosinophil-related organ damage in neoplastic and non-neoplastic conditions. In addition, we discuss classifications of eosinophil disorders and related syndromes as well as diagnostic algorithms and standard treatment for various eosinophil-related disorders.
authors.affiliation: Department of Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Vienna, Austria. peter.valent@meduniwien.ac.at
authors.forename: Peter
authors.initials: P
authors.lastname: Valent
authors.forename: Gerald J
authors.initials: GJ
authors.lastname: Gleich
authors.forename: Andreas
authors.initials: A
authors.lastname: Reiter
authors.forename: Florence
authors.initials: F
authors.lastname: Roufosse
authors.forename: Peter F
authors.initials: PF
authors.lastname: Weller
authors.forename: Andrzej
authors.initials: A
authors.lastname: Hellmann
authors.forename: Georgia
authors.initials: G
authors.lastname: Metzgeroth
authors.forename: Kristin M
authors.initials: KM
authors.lastname: Leiferman
authors.forename: Michel
authors.initials: M
authors.lastname: Arock
authors.forename: Karl
authors.initials: K
authors.lastname: Sotlar
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Butterfield
authors.forename: Sabine
authors.initials: S
authors.lastname: Cerny-Reiterer
authors.forename: Matthias
authors.initials: M
authors.lastname: Mayerhofer
authors.forename: Peter
authors.initials: P
authors.lastname: Vandenberghe
authors.forename: Torsten
authors.initials: T
authors.lastname: Haferlach
authors.forename: Bruce S
authors.initials: BS
authors.lastname: Bochner
authors.forename: Jason
authors.initials: J
authors.lastname: Gotlib
authors.forename: Hans-Peter
authors.initials: HP
authors.lastname: Horny
authors.forename: Hans-Uwe
authors.initials: HU
authors.lastname: Simon
authors.forename: Amy D
authors.initials: AD
authors.lastname: Klion
mesh_terms: D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002869:Chromosome Aberrations; D016207:Cytokines / Q000502:physiology; D004802:Eosinophilia / Q000175:diagnosis* / Q000473:pathology / Q000628:therapy; D004804:Eosinophils / Q000276:immunology / Q000378:metabolism*; D005938:Glucocorticoids / Q000627:therapeutic use; D006801:Humans; D015514:Oncogene Proteins, Fusion / Q000235:genetics; D010455:Peptides / Q000502:physiology; D051496:Receptor, Fibroblast Growth Factor, Type 1 / Q000235:genetics; D020796:Receptor, Platelet-Derived Growth Factor alpha / Q000235:genetics; D039221:mRNA Cleavage and Polyadenylation Factors / Q000235:genetics
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; D016207:Cytokines; D005938:Glucocorticoids; D015514:Oncogene Proteins, Fusion; D010455:Peptides; D039221:mRNA Cleavage and Polyadenylation Factors; C479819:FIP1L1-PDGFRA fusion protein, human; D051496:Receptor, Fibroblast Growth Factor, Type 1; D020796:Receptor, Platelet-Derived Growth Factor alpha