(P-IG-7) Anti-Vel Mimicking Anti-I Specificity Removed By Rabbit Erythrocyte Stroma

A Caucasian male diagnosed with metastatic adenocarcinoma was referred to our laboratory for serologic evaluation before undergoing invasive endoscopy. He presented with mild anemia (Hgb 7.3 g/dL) with suspicion of gastrointestinal bleeding. Initial antibody identification demonstrated a cold reacting antibody with anti-I specificity and a panagglutinin. Further serologic investigation revealed an anti-Vel.

Study

Design/Methods:

ABO/Rh grouping, antibody detection and identification using standard tube hemagglutination techniques were performed. Monoclonal anti-A, -B, -A,B, -D and Rh control reagents were used for the forward ABO/Rh grouping and A1, A2, and B cells for the reverse grouping at immediate spin (IS). Low ionic strength solution (LISS) and polyethylene glycol (PeG) potentiators were utilized for antibody identification. A direct antiglobulin test (DAT) was conducted with polyspecific antihuman globulin (PS), monospecific anti-IgG, and monospecific anti-C3b,d reagents tested at IS and room temperature (RT) incubation. Rabbit erythrocyte stroma (RESt) was used to remove cold antibody reactivity. Reagent red cells were treated with ficin and dithiothreitol (DTT).

Results/Findings:

The initial serologic evaluation determined that the patient was group B Rh positive with a positive antibody detection test and positive DAT with complement only. Initial antibody identification demonstrated a cold reacting antibody with anti-I specificity at IS, RT and 4°C and a panagglutinin at LISS and PeG indirect antiglobulin test (IAT) phases with a negative autologous control. The sample provided was not sufficient to fully characterize the panagglutinin. Subsequent sample drawn continued to demonstrate anti-I specificity. The plasma was incubated with RESt and reactivity was removed at LISS and PeG IAT. Autologous adsorptions at 4°C were attempted but proved ineffective in removing reactivity. This prompted suspicion that the plasma contained an antibody to high prevalence antigen, leading to further serologic investigation. The plasma reacted with ficin treated cells but did not react with ficin treated autologous cells, and reactivity was diminished with DTT-treated cells. The plasma was then tested with rare red cells lacking high prevalence antigens and was found to be nonreactive with two Vel- cells.

Conclusions:

Potentially clinically significant antibodies can mimic cold reacting antibodies that are generally thought of as nuisance. Cold reacting antibodies should be well characterized before transfusion. Anti-Vel mimicking anti-I specificity removed by RESt was identified in the patient’s plasma. Due to the need for transfusion, a search for rare donors was initiated through the American Rare Donor Program. Two units of Vel- blood were transfused without incident.