Publications by authors named "Daniela Ostroveanu"

The use of imatinib mesylate (IM) (Gleevec, Novartis) in chronic myeloid leukemia (CML) and other neoplastic disorders is in a dramatic increase, inducing long-standing survival. Therefore, the interest in the associated events with this treatment is more and more manifest. We describe a case of CML in which, at the usual antileukemic dose, IM induced a rapid and persistent normalization of the levels of serum cholesterol, triglycerides, low- and high-density lipoproteins and glucose.

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A 20 years old male patient was diagnosed as hypoplastic myelodysplastic syndrome (hMDS) - refractory cytopenia with multilineage dysplasia in November 2002. He received packed blood cells, methylprednisolon and dexamethason but no persistent improvement and even worsening of the thrombocytopenia and the appearance of neutropenia were registered. Laparoscopic splenectomy has been performed in January 2003, when the platelets were approximately 15000/mm3, without intraoperative incidents.

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Chronic myelomonocytic leukemia (CMML) has long been recognized as a disorder with both myelodysplastic and myeloproliferative characteristics, some patients showing clinical and morphological features resembling myelodysplastic syndrome (MDS) especially refractory anemia with excess of blasts (RAEB) with monocytosis, and others leukocytosis with neutrophilia, monocytosis and splenomegaly resembling myeloproliferative syndrome (MPS). The intrinsec differences determined at first the separation of CMML in two forms, one named "dysplastic", more similar with RAEB, and the other "proliferative", closer to chronic myeloid leukemia and then included by the recent WHO classification into a separate new created group--myelodysplastic diseases (MDD)/chronic myeloproliferative diseases (CMPD). The aim of this study was the analysis of some features of 20 cases of CMML, with emphasis on the differences between the two forms.

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The apparent contradiction between clonal expansion and marrow failure encountered in myelodysplastic syndromes (MDS) is more evident in hypocellular forms at presentation. Hypoplastic MDS (hMDS) appears to be a distinct clinicopathologic entity, accounting for about 15% from all MDS. The pathogeny is supposed to result from immunosupressive mechanisms and some observations on successful treatment with Cyclosporine A (CsA) are reported.

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