Therapeutic options for patients with clonal and idiopathic hypereosinophia

Alfonso Quintás-Cardama, Jorge Cortes

Research output: Contribution to journalReview article

Abstract

Background: The hypereosinophilic syndrome (HES) comprises a heterogeneous group of disorders characterized by chronic, unexplained hypereosinophilia with organ involvement. The discovery of novel molecular targets has changed the therapeutic paradigm in HES. Objective: This article reviews the current medical management of patients with clonal and idiopathic hypereosinophilia with a particular emphasis on emerging new targeted therapies. Methods: The information contain in this review was obtained from public sources such as Journals and scientific meeting abstracts. The opinions expressed in this review are solely those of the authors. Results/Conclusion: The development of Imatinib-resistant mutations in the FIP1L1-PDGFR-α kinase domain has spurred the development of an array of new tyrosine kinas inhibitors. Moreover, the elucidation of the role of interleukin-5 in the pathogenesis of the lymphocytic variant of HES and the fact that CD52 is expressed on the surface of eosinophils and T cells have led to the clinical use of monoclonal antibodies such as mepolizumab, reslizumumab, and alemtuzymab for the treatment of different forms of hypereosinophilia.

Original languageEnglish (US)
Pages (from-to)1039-1050
Number of pages12
JournalExpert Opinion on Investigational Drugs
Volume17
Issue number7
DOIs
StatePublished - Jul 1 2008
Externally publishedYes

Fingerprint

Hypereosinophilic Syndrome
Interleukin-5
Eosinophils
Tyrosine
Phosphotransferases
Therapeutics
Monoclonal Antibodies
T-Lymphocytes
Mutation

Keywords

  • Alemtuzumab
  • FIP1L1-PDGFR-α
  • HES
  • Imatinib
  • Mepolizumab

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)

Cite this

Therapeutic options for patients with clonal and idiopathic hypereosinophia. / Quintás-Cardama, Alfonso; Cortes, Jorge.

In: Expert Opinion on Investigational Drugs, Vol. 17, No. 7, 01.07.2008, p. 1039-1050.

Research output: Contribution to journalReview article

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