A-150 Abo Subgroup Incompatibility Leading to Red Cell Engraftment Failure and Fatal Outcome: A Rare But Preventable Complication in Related Allogeneic HSCT

Abstract

Abstract Background Pre-allogeneic hematopoietic stem cell transplant (HCST) testing includes, among others, ABO and HLA typing and testing for anti-HLA antibodies. ABO subgroup typing is not routinely performed, as A2 subgroup representes 1% of the total group A population and only 0.4% of A2 individuals have anti-A1 in their serum. ABO antigens are also found on the platelet surface. We describe a case of alloHSCT performed between siblings, the donor A1 and the recipient A2, with a fatal outcome caused by red cell and platelet engraftment failure due to anti-A1 antibodies, and emphasize the need to routinely investigate subgroup incompatibility in the pre-alloHSCT workup. Methods Patient data was collected from hospital and laboratory electronic records. Blood typing and immunohematological investigation was performed at the hospital blood bank using gel cards for ABO typing, DAT and antibody screening panels (Grifols, Barcelona). Tube method was used for A subgroup typing (Fresenius, Germany). Bone marrow analysis and other blood tests were performed at local hospital laboratory. HLA typing and antibody screening (Luminex, USA) were sent to a specialized laboratory. Results A 51 year-old male with Non-Hodgkin lymphoma underwent a full-match ABO compatible allogeneic HSCT, both brother/donor and recipient group A. Pre-transplant anti-HLA or ABO antibodies were negative. WBC recovery was achieved on D + 22. The patient had a catheter infection on D + 15 (Permcath removed), CMV infection on D + 24 (treated with gancyclovir) and received several blood transfusions. On D + 22, he had a hemolytic transfusion reaction with fever (38.5°C), chills and a decline in hemoglobin (7.3 g/dL to 6.6 g/dL in the following day), low haptoglobin and increased indirect bilirrubin levels. Immunohematological investigation revealed a positive DAT with an anti-A antibody in the eluate. Subgroup incompatibility was suspected and the patient was found to be subgroup A2, whereas the donor typed A1. Three days later the DAT became negative and anti-A1 was no longer detected. Other RBC antibodies were also excluded. Only group O RBCs and A / AB platelets were transfused thereafter to prevent further hemolysis. On D + 35 the patient was diagnosed with GI-GVHD, which responded to corticosteroids. He never achieved transfusion independence and received RBC and platelet transfusions on a regular basis. Failure of RBC and platelet engraftment was confirmed by a bone marrow aspirate on D + 45, showing only 20% erythroid lineage and absence of megakaryocytes. Marrow chimerism revealed 83% of donor origin. Sepsis by S. aureus ensued on D + 57 and three days later he had fever (38.2°C) and dyspnea after a platelet transfusion. Despite entubation and mechanical ventilation, he evolved to RCP and died on D + 60. Conclusion ABO subgroup typing is a simple and low-cost technique routinely available in the blood bank. Detection of A subgroup incompatibility impacts on key decisions, such as donor choice (if more than one candidate) and the need for erythrocyte depletion of donor stem cells and recipient plasmapheresis if the anti-A1 titer is high. Since graft failure due to ABO subgroup incompatibility can be hazardous, we recommend routinely ABO subgroup typing in the pre-alloHSCT workup to increase donor safety.