Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-12-21
pubmed:abstractText
Therapy principles of the last decade and recent advances in the research of polynuclear eosinophil have led to a new approach in the hypereosinophilic syndrome (HES), with important consequences on the development of new and effective therapies. HES is defined by persistent and marked eosinophilia and eosinophil-related organ damage in the absence of any evident cause of hypereosinophilia. Two variants of HES have been characterized, with different prognosis and possible associations with malignant diseases such as myeloid leukemia or T-cell lymphomas. The lymphocytic variant of HES (L-HES) is characterized by the presence of T cell clones, IL-5 expression and possible progression to T-cell lymphoma. Besides steroid therapy, the anti-IL-5 monoclonal antibody mepolizumab is considered as a target therapy for L-HES. The myeloproliferative variant of HES (M-HES) is associated with an increased risk of myeloid leukemia and good response to anti-tyrosine-kinase therapy. The imatinib target is a kinase resulting from an 800-kb deletion on chromosome 4. The fusion gene Fip1-like 1-platelet-derived growth factor receptor alpha (FIP1L1-PDGFRA) has been validated as a marker of response to anti-tyrosine-kinase therapy. Early identification of HES variants is crucial for the rapid introduction of early and appropriately adjusted therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:issn
1330-027X
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
323-30
pubmed:dateRevised
2011-9-13
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Hypereosinophilic syndrome and proliferative diseases.
pubmed:affiliation
Inserm U728, Paris, France.
pubmed:publicationType
Journal Article, Review