Objectives A treatment regimen consisting of bendamustine and brentuximab vedotin (BV) has been described as a highly potent salvage therapy and as an effective induction therapy leading to high response rates before autologous stem cell transplantation (ASCT) in patients with classical Hodgkin lymphoma (cHL). In this retrospective analysis, we aimed to assess this therapy's efficacy in unselected patients with cHL and CD30+ peripheral T‐cell lymphoma (PTCL). Patients and methods Data of 28 patients with cHL and five patients with PTCL treated with a combination of bendamustine and BV at three Austrian tertiary cancer centers were analyzed. Results In patients with cHL, the ORR was 100% (78.6% CR, 21.4% PR). After 17 months median follow‐up, median survival times were not reached; 1‐year PFS was 81.9%, and 1‐year OS was 95.7%. Thirteen eligible patients (46.4%) successfully underwent planned ASCT after salvage therapy with bendamustine and BV and subsequent high‐dose chemotherapy. Three of the five PTCL patients achieved CR, while two did not respond and died during or shortly after therapy. Conclusion A combination of bendamustine and BV is an effective salvage and induction therapy before ASCT in patients with relapsed/refractory cHL. Further research is warranted to evaluate the use in patients with PTCL.

Background: The extent of expression of the blood group A on platelets is controversial. Further, the relation between platelets' blood group A expression and the titers of isoagglutinins has not been thoroughly investigated, so far. Methods: We evaluated the relation between the genotype with platelets' blood group A and H expression estimated by flow cytometry and the titers of isoagglutinins. Results: The A expression varied between genotypes and within genotypes. However, the expression in A₁ was stronger than in all other genotypes (p < 0.0001). An overlap of expression levels was apparent between homozygous A₁A₁ and heterozygous A₁ individuals. Still, The A₁A₁ genotype is associated with a particularly high antigen expression (p = 0.009). Platelets' A expression in A₂ versus blood group O donors was also significant (p = 0.007), but there was again an overlap of expression. The secretor status had only little influence on the expression (p = 0.18). Also, isoagglutinin titers were not associated with genotypes. Conclusion: To distinguish between A₁ and A₂ donors may reduce incompatible platelet transfusions and therefore be favorable on platelet transfusion increment. Clinical data are needed to support this notion.

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