The Journal of Allergy and Clinical Immunology
Volume 117, Issue 6 , Pages 1292-1302 , June 2006

Approaches to the treatment of hypereosinophilic syndromes: A workshop summary report

  • Amy D. Klion, MD

      Affiliations

    • From the Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda
    • Corresponding Author InformationReprint requests: Amy D. Klion, MD, Bldg 4, Rm 126, National Institutes of Health, 4 Center Dr, Bethesda, MD 20892.
    • ,
  • Bruce S. Bochner, MD

      Affiliations

    • Johns Hopkins Asthma and Allergy Center, Baltimore
    • ,
  • Gerald J. Gleich, MD

      Affiliations

    • Departments of Dermatology and Medicine, University of Utah, Salt Lake City
    • ,
  • Thomas B. Nutman, MD

      Affiliations

    • From the Laboratory of Parasitic Diseases, National Institutes of Health, Bethesda
    • ,
  • Marc E. Rothenberg, MD, PhD

      Affiliations

    • Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati
    • ,
  • Hans-Uwe Simon, MD, PhD

      Affiliations

    • Department of Pharmacology, University of Bern
    • ,
  • Michael E. Wechsler, MD

      Affiliations

    • Harvard Medical School, Pulmonary and Critical Care Division, Brigham and Women's Hospital, Boston
    • ,
  • Peter F. Weller, MD

      Affiliations

    • Harvard Medical School, Department of Medicine, Beth Israel Deaconess Medical Center, Boston
    • ,
  • the Hypereosinophilic Syndromes Working Group

      Affiliations

    • The members of the Hypereosinophilic Syndromes Working Group are shown in the Acknowledgments.

Received 19 September 2005 ,Revised 22 February 2006 ,Accepted 24 February 2006.

  • Image Result

    Classification of HESs. Specific syndromes discussed at the workshop are indicated in bold. ∗Incomplete criteria, apparent restriction to specific tissues-organs. ∗∗Peripheral eosinophilia ≥1500/mm3 i

    Classification of HESs. Specific syndromes discussed at the workshop are indicated in bold. ∗Incomplete criteria, apparent restriction to specific tissues-organs. ∗∗Peripheral eosinophilia ≥1500/mm3 in association with a defined diagnosis. †Presence of the FIP1L1/PDGFRA mutation. ∗∗∗Clonality analysis based on the digestion of genomic DNA with methylation-sensitive restriction enzymes followed by PCR amplification of the CAG repeat at the human androgen receptor gene (HUMARA) locus at the X chromosome. FISH, Fluorescence in situ hybridization.

 The workshop was funded by Office of Rare Diseases Research of the National Institutes of Health, GlaxoSmithKline (GSK), and the American Partnership for Eosinophilic Disorders.Disclosure of potential conflict of interest: B. Bochner has consultant arrangements with GlaxoSmithKline. G. Gleich has consultant arrangements with GlaxoSmithKline, Ception Therapeutics, Eosynos, and Novartis Genentech; owns stock in Ception Therapeutics; is founder of Eosynos; has received grants from GlaxoSmithKline and Novartis Genentech; and is on the speakers' bureau for Novartis Genentech. M. Rothenberg has consultant arrangements with GlaxoSmithKline, Ception Therapeutics, and Cambridge Antibody Technology; owns stock in Ception Therapeutics; has received grants from Cambridge Antibody Technology; is on the speakers' bureau for Merck; and is an Honorarium from Tanox. H. Simon has consultant arrangements with GlaxoSmithKline, Greenford, United Kingdom, and has received grants from the Swiss National Science Foundation. M. Wechsler has consultant arrangements with Novartis Genentech; has received grants from Merck; and is on the speakers' bureau for Novartis Genentech and Merck. The rest of the authors have declared that they have no conflict of interest.

PII: S0091-6749(06)00520-3

doi: 10.1016/j.jaci.2006.02.042

The Journal of Allergy and Clinical Immunology
Volume 117, Issue 6 , Pages 1292-1302 , June 2006

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