Hematology

C’est l’histoire d’un garçon de 5 ans qui présente de nombreuses hémorragies survenant le plus souvent quand il joue. Le petit patient a été transfusé à de nombreuses reprises, chaque transfusion entrainant l’arrêt du saignement. Son cas a été publié le 27 décembre 1952 dans le numéro de Noël du British Medical Journal (BMJ). Il …

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Follicular lymphoma (FL) is an indolent yet incurable germinal center B-cell lymphoma retaining a characteristic follicular architecture. FL tumor B cells are h

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The ability to eliminate specific pathologic cells is creating more options for multiple myeloma patients. Several targeting approaches are in development.

Tissue inflammation is a hallmark of tumour microenvironments. In the bone marrow, tumour-associated inflammation impacts normal niches for haematopoietic progenitor cells and mature immune cells and supports the outgrowth and survival of malignant cells residing in these niche compartments. This Review provides an overview of our current understanding of inflammatory changes in the bone marrow microenvironment of myeloid and lymphoid malignancies, using acute myeloid leukaemia and multiple myeloma as examples and highlights unique and shared features of inflammation in niches for progenitor cells and plasma cells. Importantly, inflammation exerts profoundly different effects on normal bone marrow niches in these malignancies, and we provide context for possible drivers of these divergent effects. We explore the role of tumour cells in inflammatory changes, as well as the role of cellular constituents of normal bone marrow niches, including myeloid cells and stromal cells. Integrating knowledge of disease-specific dynamics of malignancy-associated bone marrow inflammation will provide a necessary framework for future targeting of these processes to improve patient outcome. Haematological malignancies are associated with inflammation in the bone marrow. In this Review, the authors discuss how tumour-associated inflammation affects the normal functions of the bone marrow and supports the outgrowth and survival of malignant cells. Moreover, they describe how the inflammatory changes in the bone marrow differ in myeloid and lymphoid malignancies.

A anemia no idoso tem uma elevada prevalência sendo de 26% em indivíduos com +75 anos, onde neste grupo etário a prevalência da deficiência de ferro é de 37%.
No idoso 1/3 dos casos de anemia são devidos a uma alimentação
deficiente em elementos nutricionais essenciais e 1/3 a doença crónica, nomeadamente gastrointestinal, cardíaca ou renal.

The FDA has approved the world’s first medicine based on CRISPR gene-editing technology, a groundbreaking treatment for sickle cell disease.

MECOM deficiency is a recently identified inborn error of immunity and inherited bone marrow failure syndrome caused by haploinsufficiency of the hematopoietic transcription factor MECOM. It is unique among inherited bone marrow failure syndromes, many of which present during later childhood or adol …

Multiple Myeloma (MM) remains a difficult to treat disease mainly due to its biological heterogeneity, of which we are more and more knowledgeable thanks to the development of increasingly sensitive molecular methods that allow us to build better prognostication models.

Immune thrombocytopenia (ITP) is a rare autoimmune disorder caused by peripheral platelet destruction and inappropriate bone marrow production. The management of ITP is based on the utilization of steroids, intravenous immunoglobulins, rituximab, thrombopoietin receptor agonists (TPO-RAs), immunosuppressants and splenectomy. Recent advances in the understanding of its pathogenesis have opened new fields of therapeutic interventions. The phagocytosis of platelets by splenic macrophages could be inhibited by spleen tyrosine kinase (Syk) or Bruton tyrosine kinase (BTK) inhibitors. The clearance of antiplatelet antibodies could be accelerated by blocking the neonatal Fc receptor (FcRn), while new strategies targeting B cells and/or plasma cells could improve the reduction of pathogenic autoantibodies. The inhibition of the classical complement pathway that participates in platelet destruction also represents a new target. Platelet desialylation has emerged as a new mechanism of platelet destruction in ITP, and the inhibition of neuraminidase could dampen this phenomenon. T cells that support the autoimmune B cell response also represent an interesting target. Beyond the inhibition of the autoimmune response, new TPO-RAs that stimulate platelet production have been developed. The upcoming challenges will be the determination of predictive factors of response to treatments at a patient scale to optimize their management.

HemaSphere, a premier hematology information resource, publishes results of highly relevant basic, translational and clinical research in hematology.