Advocate Aurora Health Milwaukee, Wisconsin, United States
Background/Case Studies: Acute hemolytic transfusion reactions (AHTR) following transfusion of ABO incompatible plasma are rare events, and when these occur, often involve transfusion of out-of-group platelets. AHTR from group O RBCs is even less common due to lower volume of incompatible plasma. Also, high donor ABO titer does not always predict risk of a hemolytic reaction. Other factors can play a role. We report a case of O negative double apheresis RBCs with high titer anti-A in which each component was transfused to a different group A patient, but only one experienced an AHTR. Patient #1 (BMI 24.2) presented with colon cancer and Hgb 7.0 g/dL. Pretransfusion, blood type was A positive and antibody detection test was negative. After infusion of 196mL of 1st component of a short-date, O negative, double apheresis RBC, patient developed sudden hypoxia, hypotension, rigors, and fever to 104F. The next day, patient #2 (BMI 28.8) was transfused with 2nd component of the double apheresis RBC. Eight days prior she received an allogeneic stem cell transplant for acute myeloid leukemia. Pretransfusion labs showed Hgb 6.1 g/dL, blood type A negative, and negative antibody detection test. This transfusion was uneventful and post transfusion Hgb increased to 7.6 g/dL.
Study
Design/Methods: Gel column testing was used for blood typing, IAT, polyspecific DAT, acid eluate testing, and ABO IgG titrations, while monospecific DATs were performed by tube testing. RBC H expression was determined by flow cytometry with H-specific monoclonal BRIC198.
Results/Findings: Posttransfusion workup of patient #1 showed DAT 2+ with IgG only and IgG anti-A in the eluate. There was no rise in post-transfusion Hgb and no visible hemolysis noted in patient’s serum. ABO titration requested on the donor’s plasma showed Anti-A 16,384 and Anti-B 2048. (Typical IgG anti-A titer 16-32; IgG anti-B 8). Due to difference in posttransfusion outcomes, we speculated that RBCs from patient #1 might express higher levels of A antigen than patient #2 RBCs and bind more donor anti-A causing destruction of autologous A RBCs and AHTR. To prevent interference by RBC agglutination in flow cytometry, RBC levels of H substance not converted to A were measured instead of direct measurement of RBC A antigen. Patient #1 RBCs had very high levels of A antigen (22% H compared to normal), and patient #2 RBCs expressed low levels of A (115% H compared to normal) and later was confirmed to be A2 by anti-A1 lectin (Fig 1). Conclusions: Group O RBCs stored in additive solution contain less than 20 mL of residual plasma so the risk of an AHTR is low if transfused to a group A or B adult recipient. However, our two cases uniquely demonstrate that AHTR can occur if O donor RBCs with high titer anti-A are transfused to a recipient with high expressing A RBCs, but the same donor RBCs can be safely transfused to a group A2 recipient with lower expression of A.
Importance of research: Group O donor units are commonly transfused to non-group O individuals. This is a rare case of a high titer anti-A in a group O donor apheresis red cell that caused acute hemolytic transfusion reaction in one patient, but not in another.
