BJH - volume 7, issue 4, september 2016
K. Beel MD, PhD
(BELG J HEMATOL 2016;7(4):166–9)
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T. Feys MBA, MSc
Defects in the platelet haemostasis can lead to the development of thrombocytopaenia and thrombosis. During the 2016 annual meeting of the European Hematology Association (EHA) several presentations focussed on prognostic, clinical and biochemical aspects of these conditions. In addition to this, several new therapeutic options were discussed together with a study looking into cancer-associated thrombosis.
(BELG J HEMATOL 2016;7(4):170–3)
Read moreBJH - volume 7, issue 4, september 2016
T. Feys MBA, MSc
Haemophilia B is a genetic condition that is caused by a shortage in clotting factor IX (FIX). The severity of the haemophilia is determined by the clotting activity of FIX in the blood. The standard of care for patients with haemophilia B consists of substitution therapy with FIX. In this procedure, FIX, either prepared from human plasma or a recombinant form, is administered through an intravenous (IV) infusion with a frequency that depends on the severity of the haemophilia. These infusions are given once or twice a week and lay a heavy burden on patients. In addition to this, the presence of inhibitory antibodies in haemophilia patients can hamper the treatment. In these cases, FIX is no longer active, or is sometimes even eradicated. More recently, important advances have been made in the development of gene therapy for haemophilia B patients. With this technique, a non-mutated FIX gene is introduced into the DNA of patients using a viral vector that targets the hepatocytes of patients. As such, the missing clotting factor is reintroduced in patients allowing them to produce sufficient amounts of the clotting factor. During the 2016 annual EHA meeting, several haemophilia studies addressed this technique.
(BELG J HEMATOL 2016;7(4):174–5)
Read moreBJH - volume 7, issue 2, april 2016
A. Bosly MD, PhD
Overview of the ASH 2015 plenary scientific session held on Sunday, December 6th, 2015.
(BELG J HEMATOL 2016;7(2):90–2)
Read moreBJH - volume 7, issue 1, february 2016
A. Janssens MD, PhD
As new data on indolent non-hodgkin lymphoma (iNHL) were not that compelling, only highlights on chronic lymphocytic leukemia (CLL) will be presented in the following summary. The recently published “updated BHS guidelines for the treatment of CLL, anno 2016”, incorporated obinutuzumab, ibrutinib and idelalisib. Results of multiple plase 3 trials were presented at ASH 2015 and will probably challenge the proposed guidelines in the near future.1
(BELG J HEMATOL 2016; 7(1):3–8)
Read moreBJH - volume 7, issue 1, february 2016
T. Feys MBA, MSc
Major therapeutic progress has been accomplished in chronic myeloid leukemia (CML) and myeloproliferative neoplasms (MPN) over the past 40 years. Therapeutic progress happened through better understanding of disease pathophysiologiy and rational development of targeted agents, like imatinib mesylate in CML. This report will discuss the key studies related to CML or MDS, presented during the 2015 annual ASH meeting of the American Society of Hematology (ASH).
(BELG J HEMATOL 2016; 7(1):9–13)
Read moreBJH - volume 7, issue 1, february 2016
M-C. Vekemans MD
Myelodysplastic syndromes (MDS) represent a heterogeneous group of clonal hematopoietic malignancies characterized by peripheral blood cytopenias, due to ineffective erythropoiesis and a risk for progression to acute myeloid leukemia (AML). Progress in this field aims to decrease the transfusion burden, delay progression to AML, improve the quality-of-life of patients and extend survival.
(BELG J HEMATOL 2016; 7(1): 20–4)
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