27660 Parasite infection in a patient with a CD30 clonal T-cell lymphocytic variant of hypereosinophilic syndrome: Cause or coincidence

Abstract

Hypereosinophilic syndromes (HES) are defined by the presence of blood and/or tissue hypereosinophilia producing organ damage. HES can arise from a primary (neoplastic) growth of eosinophils or a reactive proliferation of eosinophils secondary to parasitic infestations, inflammatory diseases or neoplasms. A lymphocytic variant (L-HES) has been recently described in which a clonal T-cell population releasing Th2-related cytokines induce eosinophil proliferation. Cutaneous lesions in HES are frequent and nonspecific. A 65-year-old Dominican male presented with a progressive generalized rash and dyspnea for 2 years. A skin biopsy was performed, showing an unspecific spongiotic dermatitis. Blood tests revealed eosinophilia (6.4ˆ3/uL) and IgE 1.050 UI/mL. Strongyloides stercolaris, Schistosoma mansoni, and Hymenolepsis nana were detected in the stool. Antiparasitic treatment was carried out and stool parasites were no longer detectable. However, both the dyspnea and the skin rash progressed. Hyperesosinophilia persisted. A CT scan and a lung biopsy confirmed an eosinophilic pneumonia. A new cutaneous specimen showed a perivascular and interstistitial infiltrated composed of eosinophils and atypical CD30+ T cells. Bone marrow biopsy was normal. Clonality of T-cell receptor was detected in peripheral blood. Brentuximab and meplizumab were introduced with rash and dyspnea improvement. Herein, we present a case of HES in which a parasite infestation was first diagnosed and correctly treated, yet without resolution of the symptoms. The subsequent hematologic investigations and skin biopsy revealed the presence of a clonal, atypical T cell proliferation consistent with the diagnosis of a L-HES. To our knowledge, this coincidence has not previously described.