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Abstract
Henter and colleagues present the case of a patient with familial hemophagocytic (or erythrophagocytic) lymphohistiocytosis (FEL), who developed a myelodysplastic syndrome after an accumulated 42 weeks of treatment with teniposide or etoposide, with steroids. They suggest that either there is some predisposition toward myeloproliferative disorders in patients with FEL, which has remained hidden because of the dismal prognosis associated with this disease, or that the epipodophyllotoxins produced the myelodysplasia. Presumably the bone marrow transplant that cured the patient's FEL also saved him from the acute myeloid leukemia which otherwise would have arisen from his RAEBiT.