We retrospectively analyzed recurrent SVT related to HES in 3 patients. All of the patients satisfied the criteria of Chusid et al.8 Superficial venous thrombophlebitis was confirmed by Doppler ultrasonography or biopsy findings in all patients. We found no evidence of acquired or inherited thrombophilia (ie, anticardiolipin antibodies and lupus anticoagulant, hyperhomocysteinemia, factor V Leiden, the prothrombin 20210A mutation, elevated factor VIII level, or antithrombin or protein C and S deficiencies). We excluded Behçet disease, neoplasia, and Buerger disease through medical history and follow-up, and there was no detectable glycosylphosphatidylinositol-deficient hematopoietic clone (for the diagnosis of paroxysmal nocturnal hemoglobinuria). The diagnosis of HES was considered in all 3 patients after exclusion of other known causes of eosinophilia, especially parasitic disease. In all patients, results of renal function and hepatic tests were within reference limits, and results of serum electrophoresis, chest radiography, echocardiography, eyeground examination, bacterial cultures, tests for rheumatoid factor, antinuclear antibodies, antineutrophil cytoplasmic antibodies, cryoglobulinemia, and parasitic feces, appropriate parasitic and viral (hepatitis C virus and human immunodeficiency virus) serologic tests, and bone marrow biopsy were negative. We evaluated for the presence of hypodense eosinophils by means of blood smear examination. The patients underwent screening for the FIP1L1-PDGFRA fusion gene by fluorescence in situ hybridization, analysis of the T-cell receptor gene to detect clonal rearrangement, and peripheral T-cell phenotyping. We noted clinical and biological features, outcome, and response to therapy. The patients were monitored for endomyocardial disease by electrocardiography and echocardiography, and for embolic phenomena by physical examination and Doppler ultrasonography. The mean duration of follow-up was 38 months (25, 59, and 30 months).