Acute megakaryoblastic blast crisis as a presentation manifestation of chronic myelogenous leukemia

s) 2008;112(Suppl);abst 2694. 11. Jensen PD, Heickendorff L, Pedersen B, et al. The effect of iron chelation on haemopoiesis in MDS patients with transfusional iron overload. Br J Haematol 1996;94:288-99. 12. Glickstein H, Nick H, Cabantchik ZI. Susceptibility of endocrine, cardiac, and macrophage cell lines to iron-mediated oxidative damage and the cytoprotective effect of the orally active chelator deferasirox (ExjadeR, ICL670). Blood (ASH Annual Meeting Abstracts) 2007;110(Suppl):abst 3825.s) 2007;110(Suppl):abst 3825. Acute megakaryoblastic blast crisis as a presentation manifestation of chronic myelogenous leukemia TO THE EDITOR: Blast crisis may be encountered during the course of chronic myelogenous leukemia, commonly myeloid and less frequently lymphoid or megakaryoblastic. Why or how a patient will progress to myeloid, lymphoid, or megakaryoblastic crisis is still unknown. However, this transition has been attributed to the accumulation of various mutations. The prognosis in such cases varies depending on the type of blast crisis and the molecular signature of the patient. We present a case of CML presenting initially in the chronic phase and progressing to megakaryoblastic crisis in a short period despite receiving treatment. Chronic myelogenous leukemia (CML) is a clonal disorder of pluripotent hematopoietic stem cells characterized by a balanced, reciprocal translocation involving chromosomes 9 and 22. Most cases present in the chronic phase (CP) of the disease. The progression from CP to the accelerated phase (AP) or blast crisis (BC) may be seen in patients on maintenance therapy due to the accumulation of various mutations. The most common BC type is myeloid, followed by lymphoid, and rarely megakaryoblastic. We report a case of megakaryoblastic crisis in CML, which is extremely rare and has been documented in very few cases to date. Case A 42-year-old man presented with complaints of abdominal distension accompanied by fatigue, weakness, and weight loss for the past three months. His medical history did not include any preexisting hematological or medical disorders. Upon examination, he had mild pallor, and a local abdominal examination revealed massive splenomegaly (6 cm below the costal margin). Complete blood counts showed leukocytosis (White blood cells (WBC), 35×10/L), severe thrombocytosis (platelet count, 10×10/L), and mild anemia (hemoglobin (Hb), 9.5 g/dL). A peripheral blood smear revealed a normocytic red blood cells along with the presence of immature myeloid precursors (differential count: 5% blasts, 17% promyelocytes, 15% myelocytes, 10% metamyelocytes, 2% basophils, 1% eosinophil, and 50% segmented neutrophils). Based on the above findings, a diagnosis of CML was suggested, which was confirmed by PCR for the bcr-abl transcript (Fig. 1A). The patient was orally administered 400 mg of imatinib (Gleevac) and 20 mg/kg of hydroxyurea once daily and was followed up regularly. Upon re-examination after three months of therapy, the patient showed no response to therapy as his cell counts remained unaltered, so he was switched to oral administration of 100 mg of dasatinib once daily. After this, the patient was lost to follow-up and presented after one year with rashes, pain in the upper abdomen and limbs, and general ill health. His counts revealed extreme leukocytosis (WBC: 90×10/L) with anemia and marked thrombocytosis (Hb: 8 g/dL, platelet count: 19.10×10/L). A peripheral blood smear examination revealed large blasts constituting 65% of total leucocytes along with platelet aggregates, marked platelet anisocytosis, and giant platelets. Bone marrow aspirate was markedly hypercellular with the presence of 80% of blasts having a round nucleus, open-structured nuclear chromatin, prominent nucleoli, and an abundant granular cytoplasm (Fig. 2A). A flow cytometric evaluation was performed on peripheral blood, which identified two populations of blasts. One population (constituting around 40%) was negative for CD45, all B-cell (CD19, CD10, CD20), T-cell (CD4, CD8, CD3, CD7), and myeloid markers (CD13, CD14, CD33, CD117, CD64), as well as CD34, HLA-DR, CD56. The other population of blasts (constituting around