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Previous Volume 349:2334-2339 December 11, 2003 Number 24 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The hypereosinophilic syndrome comprises a heterogeneous group of conditions characterized by hypereosinophilia and organ dysfunction caused by eosinophil-mediated tissue damage.^1,2 The highly variable response to treatment reflects the heterogeneity of the syndrome. Current therapies include corticosteroids, hydroxyurea, interferon alfa, and imatinib mesylate. Imatinib can be effective in patients with the syndrome who have normal³ or increased⁴ serum concentrations of interleukin-5. Recently, patients with hypereosinophilia and fusion of the Fip1-like 1 gene (FIP1L1) and the gene that encodes platelet-derived growth factor receptor (PDGFRA) were found to have a response to imatinib mesylate.⁵ Such patients probably have a . . . [Full Text of this Article]

Case Reports

Patient 1

Patient 2

Patient 3

Methods

Clinical Features

Treatment

Laboratory Assessments

Results

Discussion

Source Information

From the Division of Environmental Dermatology and Allergy GSF/TUM, the Center for Allergy and Environment (S.-G.P., H.B.), and the Department of Dermatology and Allergy (U.D., R.H., J.R.), Technical University, Munich, Germany; the Departments of Pharmacology (H.-U.S., E.V., S.Y.) and Dermatology (D.S.), University of Bern, Bern, Switzerland; and GlaxoSmithKline, Essex, United Kingdom (T.S.).

Drs. Plötz and Simon contributed equally to the article.

Address reprint requests to Dr. Simon at the Department of Pharmacology, University of Bern, Friedbühlstrasse 49, CH-3010 Bern, Switzerland, or at hus@pki.unibe.ch.

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