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    • "Certain genetic abnormalities, such as inactivation of the p53 tumor suppressor gene, are associated with MDS (Greenberg et al., 2006; Aul et al., 2002). The term myelodysplastic syndrome (MDS) is used, indeed, to describe a heterogeneous group of disorders that are characterized by clonal and ineffective hematopoiesis, morphological dysplasia, peripheral blood cytopenia and progressive bone marrow failure (Greenberg et al., 2006; Benetatos and Bourantas, 2005). MDS transforms to acute myeloid leukemia (AML) in approximately 30% of cases (Aul et al., 2002). "
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    ABSTRACT: The purpose of this study was to identify the sub-acute toxic effects of Khat (Catha edulis) on hemopoiesis and hematological indices of white albino rats. Two groups, each of 10 rats, were used. In the experimental group, a hydro-ethanol extract of C. edulis was administered orally to rats, daily, in single doses of 500 mg/kg body weight, for for weeks. The control group received equivalent amounts of normal saline. Our results show, for the first time, that oral administration of C. edulis hydro-ethanol extract caused significant derangement in hemopoiesis and in gross hematological indices in rats, characterized by macrocytic anemia and leucopenia. Our data show statistically significant decreases in total leukocytes count (TLC) in which, hemoglobin concentration (Hb. conc.), packed cell volume (PCV), and red cell count (RCC), accompanied by significant increases in mean cell volume (MCV), red blood cell distribution width (RDW) and platelets count with no change in mean hemoglobin concentration (MHC). In peripheral blood smears (PBS) of treated rats, there were evidences of dyserythropoiesis- impaired hemoglobinization, macrocytosis, poikilocytosis and anisocytosis, and dysgranulopoiesis- giant forms, hypersegmented neutrophils and bizarre nuclear shapes. In conclusion, our results indicate that oral administration of a hydro-ethanol extract of C. edulis adversely affected blood cell formation and induced macrocytic anemia and leukopenia in rats. However, the exact mechanisms of these hematological changes produced by Khat are still in need for further studies.
    AFRICAN JOURNAL OF BIOTECHNOLOGY 01/2014; 13(2):349. DOI:10.5897/AJB2013.13373 · 0.57 Impact Factor
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    ABSTRACT: The clinical and biological heterogeneity of the myelodysplastic syndromes (MDS) has engendered new expectations that therapy must be individualized. As a consequence, anemia management strategies for patients with MDS have evolved from a long-standing reliance upon supportive measures to active treatment guided by the risks posed by the disease. Median survival for a patient with MDS ranges from several months to ≥5 years with differing treatment goals, such as the promotion of hematopoiesis with recombinant cytokines to reducing the risk of leukemic transformation or death with agents such as azacitidine. As further insight into the molecular pathogenesis of these disorders has emerged, significant progress has been made in identifying new drug targets. Among these promising new agents are the farnesyl transferase inhibitors, immunosuppressive therapy, small-molecule tyrosine kinase inhibitors, and angiogenesis inhibitors. Phase I and II trials have shown encouraging activity with these agents and larger randomized trials are expected to define their place in the management of MDS.
    American Journal of Cancer 12/2005; 5(2):71-80. DOI:10.2165/00024669-200605020-00001
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    ABSTRACT: Although myocardial infiltration with leukemic blasts is a known finding in patients with acute leukemia, this phenomenon in myelodysplasia is not reported in the literature. Cardiac symptoms in patients with myelodysplasia are often due to anemia and may be due to iron overload and side effects of therapy. Herein we report the first case of neoplastic infiltration of the heart with associated myocardial necrosis in a patient with myelodysplasia. It was associated with unicellular and multifocal geographic areas of necrosis in the left ventricle and the interventricular septum. It is likely that cardiac compromise in our patient was due to a combination of restrictive cardiomyopathy due to leukemic infiltration, concomitant anemia, cardiac dilatation, conduction blocks and myocardial necrosis. Myocardial necrosis was most likely due to a combination of ischemic damage secondary to anemia and prolonged hypotension and extensive leukemic infiltration. Markedly rapid decrease in ejection fraction from 66% to 33% also suggests the role of ischemia, since leukemic infiltration is not expected to cause this degree of systolic dysfunction over a 24-hour period. The diagnosis was not suspected during life due to concomitant signs and symptoms of anemia, pulmonary infections, and pericardial and pleural effusions. The patient succumbed to cardiac failure. Hemopoietic cell infiltration was not considered in the differential diagnosis and contributed to this patient's morbidity and mortality. This case highlights the clinical importance of considering myocardial infiltration in patients with myelodysplasia and cardiac symptoms.
    BMC Blood Disorders 02/2006; 6:4. DOI:10.1186/1471-2326-6-4
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