BJH - volume 9, issue 3, june 2018
Y. Serroukh MD, PhD, H. Claerhout MD, A. Janssens MD, PhD, T. Tousseyn MD, PhD, N. Boeckx MD, PhD, J. Maertens MD, PhD, T. Devos MD, PhD
Aplastic anaemia is a rare condition characterised by pancytopenia and bone marrow hypocellularity and caused by the immune-mediated destruction of the haematopoietic precursors. The early complications are related to cytopaenias with infections being the major cause of morbi-mortality. The main long-term issue is clonal evolution to myelodysplastic syndrome or acute leukaemia. The diagnosis relies on exclusion of other causes of pancytopenia and characteristic pathologic findings. Severity is stratified according to peripheral blood counts. Nowadays, the survival of treated patients reaches 80–90%. The treatment of the severe form of aplastic anaemia consists on haematopoietic stem cell transplantation in eligible patients and immunosuppressive therapy in non-transplant candidates. Supportive therapy is an option in frail and/or elderly patients. Here, we define and briefly review the pathogenesis of aplastic anaemia. We propose a diagnostic and therapeutic strategy based on existing literature and experts’ recommendations. We finally report three cases illustrating particular clinical associations with pregnancy, hepatitis and paroxysmal nocturnal haemoglobinuria.
(BELG J HEMATOL 2018;9(3):76–85)
Read moreBJH - 2018, issue Abstract Book BHS, february 2018
T. Demuynck , P. Vandenberghe MD, PhD, G. Verhoef MD, PhD, T. Devos MD, PhD
BJH - 2018, issue Abstract Book BHS, february 2018
L. De Roeck , L. Michaux MD, PhD, K. Debackere MD, E. Lierman PhD, P. Vandenberghe MD, PhD, T. Devos MD, PhD
BJH - 2018, issue Abstract Book BHS, february 2018
Ir J. Van Ham , M. Delforge MD, PhD, A. Janssens MD, PhD, J. Raddoux , M. Beckers MD, PhD, T. Devos MD, PhD, D. Dierickx MD, PhD, V. Vergote MD, J. Maertens MD, PhD, H. Schoemans MD, PhD, P. Vandenberghe MD, PhD
BJH - volume 8, issue 1, february 2017
T. Devos MD, PhD
The presentations on myeloproliferative neoplasms at this year’s ASH congress were inspiring and innovative. As expected, the main topic in chronic myeloid leukemia (CML) was treatment-free remission (TFR). About 30 oral or poster abstracts on this topic were presented during ASH 2016. An update of the important EURO-SKI trial and new results were presented: TFR-studies after treatment with 1st and 2nd generation tyrosine kinase inhibitors (TKI), as well as TFR-studies after both first and second attempts of TKI-discontinuation. While stopping TKI-treatment is considered in CML, starting new treatments and when to start was the main topic regarding the BCR-ABL negative MPNs polycythemia vera (PV), essential thrombocythemia (ET) and myelofibrosis (MF). A wide panoply of MPN-related topics has been presented at San Diego: late-breaking results of the second-generation JAK-inhibitor pacritinib in MF, interferon-trials in PV and ET, long-term treatment data of the JAK-TKI momelotinib and ruxolitinib, new molecules and novel molecular data, and finally, a special focus on quality of life (QOL). QOL has been a major topic in CML/MPN since several years. In this paper, some key abstracts on CML and MPN, presented at ASH 2016, are selected and commented. I’m aware that this selection excludes many other abstracts, not reducing their intrinsic value. The aim is to present a broad and representative spectrum of studies on each topic. At the end of the article, some ‘take-home messages’ will be given.
(BELG J HEMATOL 2017;8(1):16–22)
Read moreBJH - volume 7, issue 6, december 2016
M. Beckers MD, PhD, D. Dierickx MD, PhD, T. Devos MD, PhD, S. Fevery MD, PhD, B. Sprangers MD, PhD
One of the hallmarks of failure of elimination of malignant cells by activated T-cells is the immunosuppressive environment of the tumour. Myeloid-derived suppressor cells contribute to this immunosuppressive environment by inhibition of the adaptive and innate immune system. In this article we describe the current knowledge of the role of myeloid-derived suppressor cells in the progression of haematological malignancies.
(BELG J HEMATOL 2016;7(6):213–6)
Read moreBJH - volume 7, issue 5, october 2016
P. Mineur MD, C. Doyen MD, N. Straetmans MD, PhD, K. Van Eygen MD, D. Pranger MD, A. Bosly MD, PhD, M. André MD, PhD, T. Devos MD, PhD, L. Knoops MD, PhD, On behalf of the MPN Belgian Hematological Society subcommittee
This article describes the Belgian register of chronic myeloid leukaemia patients who have stopped their treatment with imatinib in conditions comparable to the French STIM trial results: 44% remained in major molecular response off therapy; relapses appear rapidly after stopping imatinib and are responsive when the treatment is resumed.
(BELG J HEMATOL 2016;7(5):184–6)
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