Patients undergoing treatment of acute lymphoblastic leukemia (ALL) are at risk for thrombosis, caused in part by the use of l-asparaginase (L-ASP). Antithrombin (AT) replacement has been suggested to prevent venous thromboembolism (VTE) and thus may increase exposure to ASP. We report herein the results of the prophylactic replacement strategy in the pediatrics-inspired prospective GRAALL-2005 study.
View Article and Find Full Text PDFB-cell acute lymphoblastic leukemia associated with t(5;14)(q31;q32); is an exceptional cause of eosinophilia. The enhancer on 14q32 is juxtaposed to the gene on 5q31, leading to interleukin-3 overproduction and release of mature eosinophils in the blood. Clinical, biological and outcome data are extremely scarce in the literature.
View Article and Find Full Text PDFPurpose: Carfilzomib is a novel generation proteasome inhibitor. The Carmysap trial demonstrated that twice-weekly KMP (carfilzomib, melphalan, prednisone) might challenge the MPV (melphalan, prednisone, bortezomib) standard. We sought to study KMP weekly, allowing to increase carfilzomib's dose with maintained efficacy and improved safety profile.
View Article and Find Full Text PDFCentral nervous system (CNS) thrombotic events are a well-known complication of acute lymphoblastic leukemia (ALL) induction therapy, especially with treatments including l-asparaginase (l-ASP). Data on risk factors and clinical evolution is still lacking in adult patients. We report on the clinical evolution of 22 CNS venous thrombosis cases occurring in 708 adults treated for ALL or lymphoblastic lymphoma (LL) with the Group for Research on Adult Acute Lymphoblastic Leukemia (GRAALL)-induction protocol, which included eight L-ASP (6,000 IU/m(2) ) infusions.
View Article and Find Full Text PDFWe reported here a case of acute myeloid leukaemia (AML) in a 28-year-old male patient, which diagnosis is discussed according to the different classifications. This case focused on some new criteria and changes in the new WHO classification (2008) of AML, especially when erythroid precursors represent over 50% of bone marrow nucleated cells. It also pointed on some gene mutations (NPM1, CEPBA, FLT3, WT1…) and their prognostic features in AML with a normal karyotype, leading to individualize two new provisional entities in the WHO classification of tumours of hematopoietic and lymphoid tissues 2008.
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