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© 2003 American Society for Clinical Oncology
Fludarabine-Related Myeloid LeukemiaSt Vincent’s Catholic Medical Center Manhattan, New York, NY To the Editor: Morrison et al1 recently reported their experience with therapy-related myeloid leukemia in patients with chronic lymphocytic leukemia after treatment with fludarabine and chlorambucil. Only one of 188 patients treated with single-agent fludarabine developed a secondary leukemia, and that patient had been treated with single-agent chlorambucil before the development of a therapy-related myelodysplastic disorder. I report here the case of a patient with a low-grade non-Hodgkin’s lymphoma who developed acute myeloid leukemia (AML) within 1 year of completing a course of fludarabine followed by rituximab, with no other therapy having been given. The patient was a 62-year-old man with a nodular mixed lymphoma in a large abdominal and retroperitoneal mass. His bone marrow biopsy specimen was hypocellular with peritrabecular lymphoid aggregates, suggestive of marrow involvement with lymphoma. Flow cytometry on the bone marrow aspirate suggested the possibility of minimal lymphoma involvement. He elected to defer treatment initially, and then chose to be treated with single-agent fludarabine when he developed acute abdominal pain. He received six cycles of fludarabine at 25 mg/m2 on days 1 to 5, and repeated every 28 days. He had an excellent partial response to treatment, with near-complete resolution of the abdominal mass and normalization of bone marrow histology and flow cytometry. When regrowth of the abdominal mass was documented 4 months after completing treatment, he was given four weekly doses of rituximab at 375 mg/m2/wk. He had a minor response to this, but was asymptomatic and elected follow-up without additional antilymphoma treatment. After completion of rituximab, he had persistent neutropenia for which he received intermittent courses of granulocyte colony-stimulating factor. A bone marrow biopsy performed 3 months after completing rituximab was mildly hypocellular, with no evidence of lymphoma and a normal M:E ratio. Flow cytometry showed no evidence of a hematoproliferative disorder. Three months later (12 months after completing fludarabine treatment), he developed thrombocytopenia. The bone marrow aspirate was repeated and showed AML with M5b morphology. Flow cytometry was consistent with AML. Cytogenetic analysis showed monosomy 7. The patient refused treatment other than transfusion support. He died at home 3 months after the diagnosis of AML. Fludarabine therapy has not previously been associated with the development of subsequent AML,2 aside from anecdotal case reports.3 Rituximab has not been linked to the subsequent development of AML. While it is possible that the development of AML in this patient was coincidental, continued monitoring of fludarabine-treated patients for this complication is warranted. AUTHOR’S DISCLOSURES OF POTENTIAL CONFLICTS OF INTEREST The author indicated no potential conflicts of interest. REFERENCES
1. Morrison VA, Rai KR, Bercedis LP, et al: Therapy-related myeloid leukemias are observed in patients with chronic lymphocytic leukemia after treatment with fludarabine and chlorambucil: Results of an intergroup study, Cancer and Leukemia Group B 9011. J Clin Oncol 20:3878–3884, 2002
2. Keating MJ, O’Brien S, Lerner S, et al: Long-term follow-up of patients with chronic lymphocytic leukemia (CLL) receiving fludarabine regimens as initial therapy. Blood 92:1165–1171, 1998
3. Coso D, Costello R, Cohen-Valensi R, et al: Acute myeloid leukemia and myelodysplasia in patients with chronic lymphocytic leukemia receiving fludarabine as initial therapy. Ann Oncol 10:362–363, 1999
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Copyright © 2003 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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