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Hypereosinophilic syndrome terminating in acute myelogenous leukemia.

Tadashi Koike, MD, First Department of Internal Medicine, Niigata University School of Medicine, Asahimachidori, Niigata 951 Japan Hypereosinophilic syndrome (HES) is defined as a circulating eosinophil count greater than 1,500 cells/μl, of duration in excess of 6 months, and with no other identifiable cause of the eosinophilia [1]. In the majority of patients with HES the proliferation of eosinophils is thought to be due to a reaction to an unknown agent rather than to a clo-nal expansion, although this syndrome often results in marked morbidity and mortality due to eosinophilic infiltration into various organs, especially the heart. Only a few cases of HES have been reported to terminate in acute myeloid leukemia (AML) [2-7], although the diagnosis of acute lymphoid leukemia has recently been noted to be preceded or masked by HES in some patients [8]. In this paper we describe a patient with typical HES who suffered from cardiac symptoms due to hypereosinophilia and thromboembolic complications for nearly 5 years; the disease terminated in AML. A 55-year-old Japanese man was admitted in July 1984 for the further examination of malaise. On physical examination there was no hepatosplenomegaly or lymphadeno-pathy. The white blood cell (WBC) count was 39,500/μl with 68% eosinophils, 14% neutrophils, 11% lymphocytes and 1% basophils. Hemoglobin was 14.8 g/dl; platelets were 189,000/μl. Blood chemistries were normal. Neutro-phil alkaline phosphatase score was within normal limits; serum B12 was 1,533 pg/ml. Antinuclear antibodies were not detected and IgE was 219 U/ml. Coprology showed no parasite ova. No antibodies to several worms were detected by the Ouchterlony technique. Bone marrow aspiration showed normocellular marrow with 50% eosinophils at various stages of maturation. Cytogenetic study revealed a normal karyotype. Basophilia, myelodysplasia, and myelofibrosis were not seen. He was diagnosed with idiopathic HES. Hypereosinophilia was treated with prednisolone on an outpatient basis. However, he had been suffering from cardiac failure since October 1984. The cardiac echogram revealed mural thrombi on the myocardial wall and valvular insufficiency. Since a fall in 1988, he also suffered from an ulcer in his right toe. He was readmitted for the control of cardiac failure and the ulcer in January 1989. The ulcer progressed to necrosis and the right lower leg was amputated in March 1989. For the control of