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Sideroblastic anemia following treatment of chronic myeloid leukemia with busulfan

Leukemia volume 14, pages 214–215 (2000)Cite this article

An increasing proportion of patients with myelodysplastic syndromes (MDS) have had previous exposure to chemotherapeutic agents, classically alkylating drugs, but recently also purine analogues, anthracyclines and epipodophyllotoxins.1234 Most cases follow treatment after a median interval of 4–5 years and are associated with prominent dysplasia, mild to marked reticular fibrosis and cytogenetic abnormalities in chromosomes 5 and 7. Busulfan, as an alkylating agent, has a known leukemogenic potential. Evidence is suggestive that the increasing duration of chemotherapy and the cumulative dose of the drug influence the development of secondary MDS (s-MDS) and increase the risk of leukemogenesis.13 We report a patient with chronic myeloid leukemia (CML) who had received busulfan over a 2-month period and developed dysplastic features including sideroblastic erythropoiesis shortly after the drug was discontinued.

In the present case, the diagnosis of typical CML was based on clinical and hematological features and later confirmed by cytogenetic and molecular analysis.56 In spite of a marked erythroid hypoplasia no ringed sideroblasts were seen at diagnosis.7 After discontinuation of short-term therapy with busulfan, a long-lasting pancytopenia was observed. A bone marrow examination performed 4 months later showed normal cellularity with no reticular fibrosis but with dysplastic features and ringed sideroblasts. Neutropenia remitted spontaneously 18 months later. Bone marrow analysis showed persistent cell atypias and reversal of sideroblastic erythropoiesis. To our knowledge, this is the fourth case in the literature reporting sideroblastic changes related to busulfan exposure.8 In at least one of these patients the abnormality was reversible, as was observed in our case. Although cytogenetic and molecular studies performed 18 months after therapy discontinuance showed no alterations other than that usually seen in CML,56 the persistent dysplastic hemopoiesis probably indicates permanent damage. There is still no evidence of an accelerated phase, blast crisis or a more aggressive disease over a 21-month follow-up, but these events cannot be ruled out.

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Acknowledgements

We are grateful to the Molecular Biology Laboratory of the State University of Campinas and CAC – Central de Análises Clínicas (Fortaleza – Ceará) for kind collaboration.

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  1. HEMOCE/Federal University of Ceará, Brazil

    SMM Magalhães, FB Duarte, SCC Ribeiro & CL Borovik

  2. UNICAMP/State University of Campinas, Brazil

    I Lorand-Metze

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Magalhães, S., Duarte, F., Ribeiro, S. et al. Sideroblastic anemia following treatment of chronic myeloid leukemia with busulfan. Leukemia 14, 214–215 (2000). https://doi.org/10.1038/sj.leu.2401613

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