Due to the circumstances brought about by the COVID-19 pandemic, the 25th European Hematology Association (EHA) Annual Congress had to take place as a virtual edition, although this raised new possibilities such as a 10-day program.

Within the group of non-Hodgkin lymphoma, Waldenström’s macroglobulinemia (WM), an indolent B-cell lymphoplasmacytic lymphoma, accounts for approximately 2 % of cases. This disease is deemed incurable and typically involves infiltration of tissues such as bone marrow, lymph nodes and/or spleen with clonal lymphoplasmacytic cells, as well as serum monoclonal paraprotein production.

In both treatment-naïve and relapsed/refractory patients with chronic lymphocytic leukemia (CLL) and small lymphocytic leukemia (SLL), inhibition of Bruton’s tyrosine kinase (BTK) represents a treatment standard as it has improved clinical outcomes. Compared to the first-generation agent ibrutinib, the second-generation, highly selective BTK inhibitor acalabrutinib shows minimal off-target kinase inhibition, thus potentially offering an optimized safety profile.

Mantle cell lymphoma (MCL) is a rare, heterogenous and generally aggressive subtype of B-cell non-Hodgkin lymphoma that remains incurable in the majority of cases. Median survival in non-trial patients has been estimated at 3 to 5 years. First-line therapy usually consists of chemoimmunotherapy, while both immunochemotherapy and targeted agents are recommended in relapsed disease.

BTK inhibitors are active in many B-cell malignancies such as mantle cell lymphoma, CLL and Waldenström’s macro­globulinemia, but also in diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), and marginal zone lymphoma (MZL). Zanubrutinib is currently being assessed in pivotal phase II and III studies in all of these indications.

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, potentially life-threatening clonal hematopoietic stem cell disorder characterized by hemolytic anemia, bone marrow failure, thrombosis, and peripheral blood cytopenia. The disease results from an acquired loss-of-function mutation of the PIGA gene involved in the synthesis of the glycosylphosphatidylinositol-anchored complement inhibitors CD55 and CD59.

Cold agglutinin disease (CAD) is a rare type of autoimmune hemolytic anemia (AIHA) elicited by cold-sensitive antibodies including cold agglutinins. Ninety percent of cold agglutinins belong to the IgM kappa category and bind to red blood cell surface antigens at temperatures of ≤ 37 °C, thus inducing hemolysis.

A retrospective analysis hints at the wide range of cold agglutinin disease (CAD) clinical behavior. Koudouna et al. investigated the characteristics of 8 patients with CAD at the time of diagnosis [1]. Median age was 62 years, and 5 patients were women. Hematologic malignancies constituted 50 % of underlying medical conditions; in 37 %, hepatitis B/C was the associated disease, and in 13 %, autoimmune disorders.