Use of an Anti–Interleukin-5 Antibody in the Hypereosinophilic Syndrome with Eosinophilic Dermatitis

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Abstract
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 α (PDGFRA) were found to have a response to imatinib mesylate.5 Such patients probably have a myeloproliferative disease or a clonal disorder that is largely independent of interleukin-5, a cytokine required for the differentiation, activation, and survival of eosinophils.5 However, in other patients with the syndrome — namely, those who have clonal T cells and polymorphous skin lesions — interleukin-5 does seem to have a critical role.6-9 Here we report the effect of mepolizumab, a neutralizing anti–interleukin-5 antibody,10,11 in three patients with a hypereosinophilic syndrome and dermatologic manifestations.12,13