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Prepublished online as a Blood First Edition Paper on December 27, 2002; DOI 10.1182/blood-2002-10-3103. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-10-3103v1 101/9/3391    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Pardanani, A. Articles by Tefferi, A. Search for Related Content PubMed PubMed Citation Articles by Pardanani, A. Articles by Tefferi, A. Related Collections Neoplasia Phagocytes Clinical Trials and Observations Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 May 2003, Vol. 101, No. 9, pp. 3391-3397 CLINICAL OBSERVATIONS, INTERVENTIONS, AND THERAPEUTIC TRIALS Imatinib therapy for hypereosinophilic syndrome and other eosinophilic disorders Animesh Pardanani, Terra Reeder, Luis F. Porrata, Chin-Yang Li, Henry D. Tazelaar, E. Joanna Baxter, Thomas E. Witzig, Nicholas C. P. Cross, and Ayalew Tefferi From the Divisions of Hematology and Internal Medicine, Hematopathology, and Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN; and Wessex Regional Genetics Laboratory, Salisbury District Hospital, Salisbury, United Kingdom. Imatinib mesylate (Gleevec), a small molecule inhibitor of abl, kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases, has been reported to be effective in the treatment of hypereosinophilic syndrome (HES) and a rare eosinophilia-associated chronic myeloid disorder (eos-CMD) characterized by the t(5;12)(q33;p13) cytogenetic abnormality. In the current study, we sought to confirm the preliminary observations in HES as well as evaluate the therapeutic value of imatinib in eos-CMD that is not associated with t(5;12)(q33;p13). Five patients with HES (all men, median age = 46 years) and 2 with eos-CMD (both men, aged 45 and 58 years) were treated with imatinib at a starting dose of 100 to 400 mg/day. Cytogenetic studies showed no evidence of either the bcr-abl translocation or t(5;12)(q33;p13) in any patient. Screening of exons encoding the intracellular catalytic domains and extracellular ligand binding domains of PDGFR (exons 2-23) and c-kit (exons 1-21) in 6 patients demonstrated mostly previously known polymorphisms. At a median follow-up of 17 weeks (range, 10-33 weeks), 2 patients with HES and 1 with eos-CMD have achieved complete clinical remission and 1 additional patient with HES has achieved a partial remission. In contrast to previous observations, all 4 responding patients had elevated serum interleukin-5 levels. Although the drug was well tolerated in most patients, a previously unrecognized treatment toxicity of acute left ventricular dysfunction occurred in a responding patient with HES within the first week of treatment. Myocardial biopsy revealed eosinophilic infiltration and degranulation, and the cardiogenic shock was reversed with the prompt institution of corticosteroid therapy. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Letter in Blood Online: Serum concentration of cardiac Troponin T in patients with hypereosinophilic syndrome treated with imatinib is predictive of adverse outcomes Vincenzo Pitini, Carmela Arrigo, Domenico Azzarello, Gaetana La Gattuta, Cinzia Amata, Maria Righi, Sebastiano Coglitore, Ayalew Tefferi, and Animesh Pardanani Blood 2003 102: 3456-3457. [Full Text] [PDF] This article has been cited by other articles: A. D. Klion How I treat hypereosinophilic syndromes Blood, October 29, 2009; 114(18): 3736 - 3741. [Abstract] [Full Text] [PDF] C. Louvet, G. L. Szot, J. Lang, M. R. Lee, N. Martinier, G. Bollag, S. Zhu, A. Weiss, and J. A. 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