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Introduction: DEL is known to be one of the weakest D variants, which can be detected by the adsorption-elution technique or by molecular study. Currently, in Thailand, we do not routinely test for DEL variants serologically or genetically among serologic RhD-negative blood donors. Case Presentation: We reported 2 cases of alloimmunization after transfused with Rh DEL, RHD*DEL1 allele, in the Thai population. The first case was a 73-year-old male with anemia who presented with post-cardiac arrest and septic shock. The patient was group B, RhD-negative, and was transfused with RhD-negative red blood cells (RBCs). Antibody screening and identification found that the patient developed anti-D and anti-Mia during the admission course. The second case was a 38-year-old woman with pseudomyxoma peritonei who developed anti-D after receiving four units of RhD-negative RBCs during cytoreductive surgery with hyperthermic intraperitoneal chemotherapy. Both patients did not receive anti-D immunoglobulin and had no previous history of anti-D detection. We retrospectively investigated and found two units of RHD*DEL1 among the RBCs transfused to these patients. Discussion: Previous reports of several cases of anti-D alloimmunization in RhD-negative recipients transfused by RHD*DEL1, an Asian-type DEL, are limited only to East Asia. We first identified 2 patients with anti-D alloimmunization after receiving the RHD*DEL1 RBCs in the Thai population. This raises concern about Rh DEL screening among D-negative Thai blood donors and whether to remove DEL units from the D-negative inventory to improve patient safety. [ABSTRACT FROM AUTHOR]

Introduction: Exposure to normal or variably expressed RhD antigens in an antigen‐negative individual can elicit an immune response and lead to the formation of clinically significant anti‐D alloantibodies. We present the case of anti‐D alloimmunization by DEL variant missed in routine blood donor screening. Material and Methods: Blood donors were typed for D antigen using the direct serologic micromethod. Nonreactive samples were confirmed in the indirect antiglobulin method with an IgM/IgG anti‐D monoclonal reagent. Genomic DNA was extracted using a commercial QIAamp DNA Blood Mini kit on the QIAcube device (Qiaqen, Germany). RHD genotyping was performed using the PCR‐SSP genotyping kits‐ Ready Gene D weak, Ready Gene D weak screen, Ready Gene CDE, and Ready Gene D AddOn (Inno‐Train, Germany). Unidentified alleles were sent for DNA genome sequencing. Results: After identifying DEL positive blood units in RhD negative blood donor pool, a look‐back study was performed to determine if their previous donations caused alloimmunization in recipients. Out of 40 D negative recipients, one developed anti‐D alloantibody after 45 days. The patient did not receive other RhD positive blood products. Blood donor typed D negative in direct and indirect agglutination method. RHD screening was positive, but RHD genotyping and DNA sequencing showed no mutation indicating the normal genotype. Conclusion: Currently used methods in RHD genotyping are insufficient to identify many variant alleles, especially intronic variations. We suggest additional gene investigation including yet unexplored regions of regulation and intron regions to justify our serological finding. [ABSTRACT FROM AUTHOR]