OA2‐AM23‐TU‐12 | RHD Genotyping for Transfusion of D+ RHD Genotype‐Matched Units to D+ Patients with History of Anti‐D

Sherry Hsiang‐Yi Chou, J. Mewha,David F. Friedman, J. Mlkvy,Kim Hue‐Roye,Sunitha Vege,Connie M. Westhoff

Transfusion(2023)

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摘要
RH diversity among Black patients and donors contributes to Rh immunization in the sickle cell disease (SCD) population. Anti-D can occur in D+ patients with RHD variants that encode partial D antigens. Anti-D has also been reported in patients with conventional RHD transfused primarily with units from Black donors who frequently have variant RHD. Finally, it can be difficult to discern an autoantibody in those recently or chronically transfused. Once anti-D is identified, patients are typically transfused with D- units, which can strain the local D- blood supply. RH genotyping of D+ donor units may allow safe transfusion of D+ RHD genotype-matched units to these patients in lieu of D- red cells. We performed a limited IRB-approved study to transfuse 3 D+ patients with SCD and conventional RHD alleles who had previously demonstrated anti-D, to D+ RHD genotype-matched units from Black donors. All three patients were on a chronic red cell exchange (RCE) and no longer demonstrated anti-D. Black donor units at the blood center were genotyped by the Human Erythrocyte Antigen array and in-house RH assays and those without variants had comprehensive RH genotyping. Each subject received 1 D+ genotype-matched unit for two consecutive RCEs (remaining units were D-), and then increased by 1 D+ unit at each subsequent visit, until all units required for RCE were D+ (Figure 1). Study subjects returned 5–12 days post-RCE for a complete blood count (CBC), hemoglobin (Hb) quantification, antibody test, and comprehensive metabolic panel. A CBC, Hb quantification, and antibody test were also performed within 3 days prior to each RCE visit. Three patients with SCD who were homozygous for conventional RHD completed all study visits reaching a maximum of 4 to 5 D+ units transfused with no new anti-D identified. Patients 1, 2, and 3 received 11, 16, and 14 D+ RHD genotype-matched units during the study period, respectively, and all reached the goal of receiving all D+ units for their final RCE study visit. Among the transfused D+ units from Black donors, 37 had only conventional RHD alleles and 4 had a RHD*DAU0 which has not been shown to be lack epitopes or result in new antigens. The average pre-transfusion Hb and HbS for the six RCEs prior to study and on study were not statistically different (p > .05, paired two-tailed t-test). The mean Hb for patients 1, 2, and 3 was 11.1, 10.1, and 9.5 g/dL pre-study and 10.8, 10.2, and 9.2 g/dL on study. The mean HbS was 47.9%, 29.6%, and 37.4% pre-study and 51.2%, 31.7%, and 34.2% on study. FIGURE 1. Example transfusion protocol for D+ patient with history of anti-D that is not currently detectable and requires six units per RBC exchange every 3 weeks.
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