Antineoplastics Reactions 1680, p41 - 2 Dec 2017 Myelodysplastic syndrome progressed to acute myeloid leukaemia: case report A female child [exact age at the time of reaction onset not stated] who developed myelodysplastic syndrome (MDS), which progressed to acute myeloid leukaemia (AML) following treatment with carboplatin, cisplatin, cyclophosphamide, etoposide, ifosfamide and melphalan [not all routes and dosages stated; time to reactions onset and outcomes not stated]. The girl was diagnosed with stage 4 MYCN neuroblastoma (NB) at the age of 3 years. She was started on induction chemotherapy with cisplatin 600 mg/m , etoposide 2 2 1050 mg/m , cyclophosphamide 8000 mg/m and doxorubicin 150 mg/m . She also received ifosfamide. Following the induction chemotherapy, she achieved full remission. Subsequently, she was started on myeloablative chemotherapy with carboplatin 1700 mg/m , melphalan 2 2 210 mg/m and etoposide 1352 mg/m along with autologous stem cell transplant. She was started on maintenance therapy with cis-retinoic acid, which she was not able to tolerate. Hence, she was then started on maintenance therapy with oral cyclophosphamide. Her chemotherapy treatment was discontinued. Later, she developed macrocytic anaemia with mean corpuscular volume 106.6fL. During her subsequent follow-up visits, macrocytic anaemia persisted with hemoglobin levels ranged 9–10 g/dL. She was disease free and off of therapy for 30 months. During routine complete blood count analysis, she was found to have macrocytic anaemia and peripheral blasts. Bone marrow findings showed trilineage dysplasia, which was consistent with MDS. Cytogenetic analysis showed an unbalanced translocation between chromosome 1p25 and 6p23. Six weeks later, she was diagnosed with pancytopenia aggravation. A repeat bone marrow biopsy and aspiration showed 33% blasts by flow cytometry. An immunophenotype analysis showed that, the blasts were positive for CD117, CD13, CD64, cytoplasmic myeloperoxidase, CD19, CD22, cytoplasmic CD79a and nuclear TdT, which indicated a therapy-related mixed phenotype AML. It was considered that, the MDS rapidly progressed to AML. The girl was treated with 2 cycles of high-dose mitoxantrone and cytarabine. However, she developed bilateral invasive pulmonary Aspergillus niger infection, which was confirmed by biopsy. Bone marrow analysis showed 2% B-lymphoblastic linear blasts. The bone marrow transplantation was planned. However, she was considered to be not suitable for bone marrow transplant or further chemotherapy due to progressive invasive aspergillosis and residual leukaemia. Therefore, she was shifted to the palliative care. Nine months after the diagnosis of AML, she died [exact cause of death not stated]. Author comment: "Here we present a case of a patient . . . remained free of disease for 30 months before developing a therapy-related MDS, which rapidly progressed to AML with mixed phenotype." "The patient described above had exposure to multiple agents associated with secondary AML including ionizing radiation, several alkylating agents, (cisplatin, carboplatin, ifosfamide, cyclophosphamide and melphalan) as well as etoposide, a topoisomerase II inhibitor." Whittle SB, et al. Therapy-related Acute Leukemia With Mixed Phenotype and Novel t(1: 6)(q25;p23) After Treatment for High-risk Neuroblastoma. Journal of Pediatric Hematology/Oncology 39: e486-e488, No. 8, Nov 2017. Available from: URL: - USA 803285136 0114-9954/17/1680-0001/$14.95 Adis © 2017 Springer International Publishing AG. All rights reserved Reactions 2 Dec 2017 No. 1680 Reactions Weekly Springer Journals


Reactions Weekly , Volume 1680 (1) – Dec 2, 2017
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Springer International Publishing
Copyright © 2017 by Springer International Publishing AG, part of Springer Nature
Medicine & Public Health; Drug Safety and Pharmacovigilance; Pharmacology/Toxicology
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