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Immunohematology and Genetic Testing (red cells, leukocytes and platelets)

(P-IG-9) Autoanti-H Can Behave Like Alloanti-H in Patients With Lymphoma

Sunday, October 20, 2024
12:00 PM - 1:00 PM  
Background/Case Studies: Auto vs Allo anti-H can occasionally be difficult to discern. Review of the literature suggests that this antibody can behave as both. Our patient was a 63 y.o. man with recurrent Hodgkin’s lymphoma with anemia following chemotherapy and no history of transfusion. Type and screen results performed 8 years prior were resulted as group AB, RhD positive with negative antibody screen. The current sample showed an ABO discrepancy with forward typing group AB and reverse typing group O. Antibody screen revealed anti-H.

Study

Design/Methods:

Phenotype for H was obtained using H lectin and human anti-sera. Resolution of the reverse grouping discrepancy was accomplished using Determination of Serum group Without Centrifugation. Underlying alloantibodies were excluded using alloadsorption. Eluate was prepared by acid elution. Further antibody characterization methods included plasma treatment with 0.01M DTT. Sequencing of FUT1 exon 4 was done by an external genomic laboratory.

Results/Findings:

The patient cells tested H-negative. Tube DAT was 3+ with C3. Antibody panel using tube- LISS and saline methods revealed a strong panagglutinin at the immediate spin (IS) phase with positive autocontrol. Variable weak reactivity was observed at 37 and AHG phase of testing; Oh cells were compatible at all phases. Reverse grouping performed at immediate spin against AsubB cells, A1 and B cells was strongly positive at immediate spin and weakly positive at saline-IAT. The antibody was still reactive in IS when using prewarm technique, and 0.01M DTT failed to abolish the activity.  Crossmatch compatible red cell units were obtained by prewarm technique with A1B red cells.  Transfusion through a blood warmer was uneventful. Weeks later, sequencing revealed FUT1*01/01, predictive of H expression on red cells.   Several months into his treatment course, a group O RBC was issued. The patient experienced signs of intravascular hemolysis within the first 30 minutes and the transfusion was discontinued. Vital signs remained stable. Hemolysis was evident and DAT was 3+ with C3.

Conclusions:

Sequencing suggests that the patient has an H-positive phenotype. There are 2 prior case reports of patients with lymphoma who had severe AIHA from autoanti-H. One of the 2 patients (also with a strong cold-reacting antibody) died from intravascular hemolysis following receipt of emergent group O red cells. Our group AB patient experienced hemolysis following the transfusion of group O RBCs. The combined findings suggests that autoanti-H in the setting of lymphoma can cause severe AIHA and can behave like alloanti-H.  Transfusion may be attempted by giving a test dose of ABO-specific cells  through a blood warmer. If intravascular hemolysis occurs, the options are no transfusion or Oh cells.