Eosinophilia in asthma or rhinitis is usually considered to be reactive to the allergic diseases. We report a 33-year-old man with asthma and rhinitis, and progressive hypereosinophilia. Fluorescence in situ hybridization analysis detected interstitial chromosomal deletion at 4q12 in cells of the bone marrow. The patient was diagnosed as myeloproliferative neoplasm with a FIP1L1-PDGFRA fusion gene, and successfully treated with the tyrosine kinase inhibitor, imatinib. Clonal expansion of eosinophils due to the FIP1L1-PDGFRA fusion gene could underlie refractory mechanisms in patients with bronchial asthma or allergic rhinitis.
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Contributors MS, RK, RJ and IT were involved in acquisition, analysis and interpretation of clinical information and data. MS and IT prepared the manuscript.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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