Hypereosinophilia, either clonal or reactive, has been described in association with multiple hematological malignancies. We describe a case of a patient presenting with hypereosinophilia that evolved into T-cell lymphoblastic lymphoma. Complete remission was achieved with chemotherapy; however, hypereosinophilia recurred 5 months later in association with myeloblastic bone marrow infiltration and without evidence of lymphoblastic lymphoma relapse. Cytogenetic analysis of the bone marrow showed a complex translocation involving chromosomes 7, 12, and 16. A rearrangement of ETV6 gene (12p13) was demonstrated by FISH studies, thus confirming the clonality of this population. The association of lymphoblastic lymphoma, eosinophilia, and myeloid hyperplasia has been described in disorders with FGFR1 rearrangements. We hypothesize that other clonal eosinophilic disorders lacking this rearrangement could behave in a similar fashion through different pathogenic mechanisms. 1. Background Hypereosinophilia (HE) can be associated with a wide range of both reactive and malignant disorders. In hematologic malignancies, HE may appear in disorders where the eosinophils are a part of the malignant clone, such as the myeloproliferative neoplasms, or result from stimulation by growth factors or cytokines produced by the malignant clone. These include lymphoproliferative neoplasms, particularly T-cell non-Hodgkin lymphoma, and Hodgkin lymphoma. Eosinophilia has also been described in association with acute lymphoblastic leukemia, more frequently of B-cell origin [1, 2]. Its appearance sometimes precedes the diagnosis of malignancy by several years [3], and thus, after the exclusion of reactive causes, the presence of eosinophilia should lead to the investigation of an underlying clonal disease. 2. Case Report We report the case of a 58-year-old female, with a known history of multiple sclerosis that was at the time asymptomatic and under no specific therapy. She was otherwise healthy, not taking any medication. Her family history was unremarkable. The patient was referred to the hematology department with the diagnosis of T-cell lymphoblastic lymphoma. She had been observed in her local hospital two months earlier, after the incidental discovery of leukocytosis with eosinophilia, bicytopenia, and elevated lactate dehydrogenase (LDH) (Table 1). At the time, a bone marrow aspirate was performed and revealed a hypercellular bone marrow (BM) with marked hypereosinophilia, no increase in the number of blasts, and no specific morphologic alterations. Immunophenotyping and
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