Introduction Patients after allogeneic stem cell transplantation are at high risk for infection‐related complications, and vaccination efficacy might be impaired depending on the immune reconstitution. In this study, we evaluate their response to mRNA vaccines against SARS‐CoV‐2. Methods During routine follow‐up visits, patients were asked about their vaccination status and if they had a previous infection with SARS‐CoV‐2. In fully vaccinated patients, the antibody titer was measured using the Roche Elecsys Anti‐SARS‐CoV‐2 S test. A titer of <1 U/L was considered as negative, titers of ≥250 U/ml as a high antibody titer, and a titer of 50–249 U/ml as a low antibody titer. Patient characteristics were evaluated by chart review to identify risk factors for poor vaccination response. Results The majority of patients developed a high antibody titer (138 out 182 patients, 75.8%). Risk factors for a low antibody titer were immunosuppressive therapy, a lymphocyte count <0.9 G/L, ongoing treatment for the underlying malignancy, and active graft‐versus‐host disease (GvHD). Donor type, underlying disease, a previous SARS‐CoV‐2 infection, and sex did not significantly influence the response to the vaccination. Discussion While patients undergoing allogeneic stem cell transplantation have been excluded from the initial registration trials, our real‐world experience with a large patient cohort confirms the data of previous studies, showing that most patients do have a good response to mRNA vaccines against SARS‐CoV‐2. Nevertheless, a significant proportion of patients shows an inadequate vaccination, which can be improved after a third vaccination in most cases despite immunosuppressive therapy.

Cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS) are severe, potentially life-threatening side effects of chimeric antigen receptor T-cell (CAR T) therapy caused by the release of cytokines by proliferating and activated CAR T-cells. Current mainstay treatment includes interleukin-1 and interleukin-6 (IL-6) blockade and steroids. The use of steroids is still controversial, since they may have the potential to irreversibly damage CAR T-cells and thus increase the risk of relapse. Therefore, additional treatment options need to be explored. We report the successful treatment of a patient with a grade 3 CRS and grade 4 ICANS refractory to IL-6 blockade and steroids with the tyrosine kinase inhibitor dasatinib. The use of dasatinib for treatment of CAR T-cell therapy-related severe complications warrants further studies.

Introduction Patients undergoing allogeneic hematopoietic stem cell transplantation (HSCT) may require red blood cell (RBC) transfusions. AB0 blood group barrier is the clinically most important RBC group in transfusion medicine and HSCT and patients always receive AB0 compatible RBC transfusions. Some patients however develop allo-antibodies against minor RBC antigens. To date there is only limited information about the specificity, immuniser and risk factors for the development of RBC allo-antibodies. In this retrospective single centre study we aimed to identify specificities, risk factors and clinical significance of the development of RBC allo-antibodies in HSCT patients. Methods In this study, we examined the occurrence of RBC alloantibodies in all consecutive patients treated with allogeneic HSCT at the University Hospital Basel between 1996 and 2017 receiving RBC transfusions. RBC and PLT components were all leukocyte depleted. As of 2012, all PLT components were pathogen reduced using the Intercept Blood system. AB0 and extended RBC typing of donor/ recipient pairs, the total number of RBC transfusions and their blood group typing (AB0 and extended RBC antigen typing when available) and the detection of RBC allo-antibodies were analysed and related to clinical outcome parameters. Results 1314 donor/ recipient pairs were analysed. 110 (13%) of patients developed RBC allo-antibodies, 66 patients (5%) prior to HSCT, and 103 (8%) developed the first RBC allo-antibody after HSCT. 8 patients (0.6%) with an RBC allo-antibody before HSCT developed further RBC allo-antibodies after HSCT. Most patients developed only one RBC allo-antibody but in single patients up to 6 antibodies could be detected. The median time between HSCT and the detection of the antibody was 61 days, corresponding to the phase of the most intensive immunosuppressive treatment. In 60% of the patients developing RBC allo-antibodies after HSCT, the antibody was neither directed against the stem cell donor nor the recipient. In these cases, immunization occurred most likely by RBC transfusion. Anti-Rhesus-group antibodies are the most common antibodies (57%). >10 RBC transfusions and the development of GvHD were risk factors for the development of antibodies. There was no significant difference in the occurrence of RBC allo-antibodies between donor type (related vs. unrelated), age or sex of the recipient. Only few patients showed significant haemolysis in the period of the detection of the antibody. The direct antiglobulin test (DAT) was positive in 66% of the cases. Haemolysis defined as an increase of bilirubin, LDH or reticulocytes and a haemoglobin drop of more than 10 g/l could only be reported in 6% of the cases with antibodies detected. The development of RBC allo-antibodies per se has no effect on the survival of patients (1y-survival 70±3% (without antibody) versus 68 ± 9%). However, evidence of haemolysis (even without drop of haemoglobin) in the context of allo-antibodies, is associated with significantly worse survival (1y- survival 75 ± 10% versus 42 ± 20%). Conclusion Allo-Antibodies after HSCT significantly contribute to the difficulties in transfusion management of these patients. Formation of RBC allo-antibodies is not frequent, but patients showing haemolysis after the development of an RBC allo-antibody show decreased survival. Most RBC allo-antibodies appear to be induced by RBC transfusion rather than by minor blood group mismatching between donor/ recipient pairs. Disclosures Heim: Novartis: Research Funding.

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