The risk of hemolytic transfusion reactions (HTRs) is approximately 1:70,000 per unit. Acute HTRs occurring during or within 24 h after administration of a blood product are usually caused by transfusion of incompatible red blood cells (RBCs), and, more rarely, of a large volume of incompatible plasma. Delayed HTRs are caused by a secondary immune response to an antigen on the donor’s RBCs. In some patients with delayed HTRs, an additional bystander hemolysis of the patient’s RBCs can be assumed. Different mechanisms lead to intra- and extravascular hemolysis, such as complete complement activation, phagocytosis of RBCs covered with C3b by macrophages after incomplete complement activation, or destruction of RBCs covered only with IgG by direct cell-cell contact with K cells. The clinical consequences of HTRs are triggered via several pathophysiological pathways like formation of anaphylatoxins, release of cytokines causing a systemic inflammatory response syndrome, activation of the kinin system, the intrinsic clotting cascade and fibrinolysis resulting in hypotension, disseminated intravascular coagulation, diffuse bleeding, and disruption of microcirculation leading to renal failure and shock. In the following, the symptoms of HTR are introduced, laboratory investigations and treatment are described, and some recommendations for prevention are given.

Summary In contrast to earlier reports, this study examined the relationship between plasma levels of factor VIII (FVIII) and von Willebrand factor (VWF) and ABO blood group and secretor status at the genetic level in 355 patients with venous thrombosis as well as in 236 controls. ABO glycosyl transferase alleles A1 and B were more frequent in the thrombosis collective and alleles O1, O2 and A2 were more frequent in the controls. A low‐risk group for venous thrombosis of individuals with genotypes O1O1, O1O2 and O1A2 (H‐antigen rich) could be distinguished from a high‐risk group with genotypes A1A1, A1B, O1A1 and O1B (H‐antigen poor). In both the thrombosis and control groups, the H‐antigen rich group showed significantly lower levels of FVIII coagulant activity (FVIII:C) and VWF antigen (VWF:Ag) than the H‐antigen poor group. The frequency of the different secretor genotypes in the thrombosis group was not different from that in the control group. No significant differences of FVIII:C and VWF:Ag levels were seen between SeSe, Sese and sese individuals in the thrombosis and in the control group. Thus the risk of venous thrombosis is associated with the ABO blood group genotype but not with secretor status.

A 13-year-old patient developed severe shock due to administration of a Yersinia enterocolitica-contaminated red blood cell concentrate. Y. enterocolitica (serotype O:9, biotype II) was cultivated from the residual blood in the blood bag and from a stool sample of the blood donor. In the donor's plasma immunoglobulin M (IgM), IgA, and IgG antibodies against Yersinia outer proteins (YopM, -H, -D, and -E) were found. Since the donor remembered a short-lasting, mild diarrhea 14 days prior to blood donation, a transient attack of Yersinia enteritis may be associated with a longer than expected period of asymptomatic bacteremia that causes contamination of donor blood. Serological screening for IgM antibodies against Yersinia outer proteins might offer a way to reduce the risk of transfusion-associated Y. enterocolitica sepsis.

The single-point mutation T500A in exon 4 of the RHCE gene is a molecular basis of the rare Rhesus antigen Ew.