Abstract
Myelodysplastic syndromes (MDS) are characterized by progressive refractory cytopenias with cellular dysfunction and defective myeloid maturation involving at least two and generally three hematopoietic cell lineages. According to the definition of the French-American-British Group, patients with less than 5% blast cells in the bone marrow are classified as refractory anemia (RA) or RA with ring sideroblasts (RARS), patients with 5%–20% blast cells in the marrow as RA with excess of blasts (RAEB), and patients with 20%–30% bone marrow blasts as RAEB in transformation (RAEB-T) [1]. Patients with chronic myelomonocytic leukemia (CMML) have a significant proportion of monocytes in the circulation (>1000/μ1) and up to 20% blast cells in the bone marrow. Depending on the initial blast cell load, 10%–40% of these patients proceed to acute myeloid leukemia. Infections due to neutropenia and thrombocytopenic bleeding are the most frequent causes of death in patients with MDS [2].
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