Lymphocyte variant hypereosinophilic syndrome (LV-HES) is a rare cause of eosinophilia that is due to eosinophilipoietic cytokine production by an immunophenotypically abnormal T-cell clone. The molecular pathogenesis of this disorder is largely unknown and only 1 case of LV-HES with a pathogenic STAT3 mutation has been described thus far. Here we report 2 cases of LV-HES with STAT3 SH2 domain mutations. These cases further support the model that activation of STAT3 signaling through STAT3 SH2 domain mutations is a recurrent event in LV-HES.
Conflicts of Interest and Source of Funding: Y.H.K.’s effort on this work has been supported in part by funding from the Haas Family Foundation and the Spatz Family Foundation. The authors have disclosed that they have no significant relationships with, or financial interest in, any commercial companies pertaining to this article.
Correspondence: Sebastian Fernandez-Pol, MD, PhD, Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Room H2110, Stanford, CA 94305 (e-mail: sfernand@stanford.edu).
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