Hypereosinophilic Syndrome View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2007

AUTHORS

Elizabeth H. Stover , Jason Gotlib , Jan Cools , D. Gary Gilliland

ABSTRACT

Hypereosinophilic syndrome (HES) is characterized by persistent overproduction of eosinophils, and the exclusion of other known causes of eosinophilia. Clinical manifestations of HES are related to eosinophilic infiltration of end organs that may include the skin, heart, lung, central nervous system, and gastrointestinal tract. Treatment has been largely empirically derived, and may include steroids, cytotoxic agents, and immunomodulatory agents. It was recently observed that a subset of patients diagnosed with HES demonstrated remarkable clinical responses to empiric treatment with the small molecule tyrosine kinase inhibitor imatinib. These responses suggested that an imatinib-sensitive tyrosine kinase contributed to pathogenesis of HES in these cases, and led to the cloning of FIP1L1-PDGFRA. FIP1L1-PPDGFRA is a constitutively activated tyrosine kinase that is imatinib sensitive, and is expressed as a consequence of an interstitial chromosomal deletion on chromosome 4. In addition to imatinib, other targeted therapies have evolved for treatment of HES, including monoclonal antibody therapy directed against IL-5. Thus, significant progress has been made in our understanding of the pathogenesis and therapy of HES in recent years, and has had an impact on approach to classification and clinical management. More... »

PAGES

235-251

References to SciGraph publications

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  • Book

    TITLE

    Myeloproliferative Disorders

    ISBN

    978-3-540-34505-3

    Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1007/978-3-540-34506-0_14

    DOI

    http://dx.doi.org/10.1007/978-3-540-34506-0_14

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1023903881


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