Background/Case Studies: The ABO blood group is the most clinically significant and immunogenic of all blood groups and ABO incompatibility in transfusion can lead to acute hemolytic reactions and death. ABO typing is routinely performed via serologic testing and discrepancies are a common occurrence, especially for patients with A2 subgroups. Despite the conventional classification of ABO blood groups into A, B, AB, and O, there are over 300 ABO alleles in a spectrum of diverse antigen and antibody profiles. As blood supply limitations prevent the repeated use of group O RBC’s or group AB plasma, extended measures including molecular genotyping are needed to resolve the discrepancies. We aim to identify and correlate genotypes with concurrent serologic testing in patients across multiple institutions in the Midwestern US to uncover inconsistent patterns of reactivity and support the clinical value of ABO genotyping.
Study
Design/Methods: A retrospective observational study was performed using blood bank records of patients with ABO serologic typing discrepancies and concomitant ABO molecular genotyping performed in the last 7 years (1/1/2018-2/5/25) at two midwestern academic medical centers. Patients with only serologic or genotyping results were excluded. Forward and reverse typing results, anti-A1 lectin testing, additional serologic testing, ABO genotype alleles, and patient history were recorded.
Results/Findings: In total fifty-seven patients with discrepant ABO serologic results and concomitant molecular genotyping were identified, including twenty-two patients (39%) with a predicted phenotype of A2 or A2B based on molecular genotyping. Of the twenty-two patients with a predicted A2 or A2B phenotype, testing with anti-A showed: four cases (18%) with mixed field (MF) reactivity, two cases (9%) with 1+ reactivity and the remaining sixteen were strongly 4+ reactive (Table 1). Only five cases (23%) showed reactivity with A1 cells on the reverse type with reactivity ranging from 1+ to 4+. Seventeen of the patients (77%) with predicted A2 or A2B phenotype were weakly reactive with anti-A1 lectin while the remaining 5 (23%) were negative. Conclusions: Our investigation found that serologic results vary between A2 subgroup patients with identical genotype or predicted phenotype. In group A2 or A2B patients, neither the anti-A reactivity on forward type nor reactivity to A1 cells on reverse type correlated with the known feature of A2 subgroup. This demonstrates the importance of ABO genotyping as blood type cannot be consistently identified via traditional serologic and lectin testing patterns. Due to variability in serologic testing, one institution updated its workflow to reflexively send any patient with anti-A1 lectin reactivity ≤2+ for ABO genotyping, while the other opted for case-by-case molecular testing.
