The New England Journal of Medicine
e-mail icon  FREE NEJM E-TOC    HOME   |   SUBSCRIBE   |   CURRENT ISSUE   |   PAST ISSUES   |   COLLECTIONS   |    Advanced Search
Sign in | Get NEJM's E-Mail Table of Contents — Free | Subscribe
 
Correspondence
PreviousPrevious
Volume 348:2687 June 26, 2003 Number 26
NextNext

Hypereosinophilic Syndrome

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

 Sign up for free e-toc
 

This Article
-Full Text
- PDF
-PDA Full Text
-Purchase this article

Tools and Services
-Add to Personal Archive
-Add to Citation Manager
-Notify a Friend
-E-mail When Cited
-E-mail When Letters Appear

More Information
-Related Article
 by Cools, J.
-PubMed Citation
To the Editor: In some patients with idiopathic hypereosinophilic syndrome, Cools et al. (March 27 issue)1 detected a FIP1L1-PDGFRA fusion gene that was associated with a dramatic response to imatinib mesylate. Along with the recent description of the "lymphocytic variant" of the hypereosinophilic syndrome,2 their observation will provide clinicians with cornerstones for tailoring the management of this heterogeneous disease according to the underlying pathogenic mechanisms.

In their discussion, Cools et al. state that the hypereosinophilic syndrome is a myeloproliferative syndrome, thereby ignoring the involvement of interleukin-5–producing T cells in the pathogenesis of hypereosinophilia in approximately one fourth of patients with . . . [Full Text of this Article]




HOME  |  SUBSCRIBE  |  SEARCH  |  CURRENT ISSUE  |  PAST ISSUES  |  COLLECTIONS  |  PRIVACY  |  HELP  |  beta.nejm.org

Comments and questions? Please contact us.

The New England Journal of Medicine is owned, published, and copyrighted © 2008 Massachusetts Medical Society. All rights reserved.