BACKGROUND: Avoiding immunization with clinically important antibodies is a primary objective in transfusion medicine. Therefore, it is central to identify the extent of D antigens that escape routine RhD typing of blood donors and to improve methodology if necessary. STUDY DESIGN AND METHODS: We screened 5058 D- donors for the presence of the RHD gene, targeting Exons 5, 7, and 10 with real-time polymerase chain reaction. Samples that were positive in the screen test were investigated further by adsorption-elution, antibody consumption, flow cytometry, and sequencing of all RHD exons with intron-specific primers. Lookback was performed on all recipients of RBCs from RHD+ donors. RESULTS: We found 13 RHD+ samples (0.26%). No variants or chimeras were found. Characterization of DNA revealed a novel DEL type (IVS2-2 A>G). In the lookback of the 136 transfusions with subsequent antibody follow-up, of which 13 were from DEL donors, one recipient developed anti-D. However, in this case, a competing and more likely cause of immunization was the concurrent transfusion of D+ platelets. Eleven recipients were immunized with 13 antibodies different from anti-D, of which five were anti-K. CONCLUSION: In our laboratory, serologic RhD typing was safe. We detected all D variants and only missed DEL types. In assessing the immunization risk we included a DEL donor, found previous to this study, that did immunize a recipient with anti-D. We conclude that inadvertent immunization with D antigens in our setting was rare and in the order of 1.4 in 100,000 D- transfusions.
BACKGROUND: Avoiding immunization with clinically important antibodies is a primary objective in transfusion medicine. Therefore, it is central to identify the extent of D antigens that escape routine RhD typing of blood donors and to improve methodology if necessary. STUDY DESIGN AND METHODS: We screened 5058 D- donors for the presence of the RHD gene, targeting Exons 5, 7, and 10 with real-time polymerase chain reaction. Samples that were positive in the screen test were investigated further by adsorption-elution, antibody consumption, flow cytometry, and sequencing of all RHD exons with intron-specific primers. Lookback was performed on all recipients of RBCs from RHD+ donors. RESULTS: We found 13 RHD+ samples (0.26%). No variants or chimeras were found. Characterization of DNA revealed a novel DEL type (IVS2-2 A>G). In the lookback of the 136 transfusions with subsequent antibody follow-up, of which 13 were from DEL donors, one recipient developed anti-D. However, in this case, a competing and more likely cause of immunization was the concurrent transfusion of D+ platelets. Eleven recipients were immunized with 13 antibodies different from anti-D, of which five were anti-K. CONCLUSION: In our laboratory, serologic RhD typing was safe. We detected all D variants and only missed DEL types. In assessing the immunization risk we included a DEL donor, found previous to this study, that did immunize a recipient with anti-D. We conclude that inadvertent immunization with D antigens in our setting was rare and in the order of 1.4 in 100,000 D- transfusions.
Authors: S Gerald Sandler; Willy A Flegel; Connie M Westhoff; Gregory A Denomme; Meghan Delaney; Margaret A Keller; Susan T Johnson; Louis Katz; John T Queenan; Ralph R Vassallo; Clayton D Simon Journal: Transfusion Date: 2014-12-01 Impact factor: 3.157
Authors: Tae Yeul Kim; Yun Ji Hong; Mi Jung Kim; Hyungsuk Kim; Taek Soo Kim; Jeong Su Park; Kyoung Un Park; Kyou-Sup Han Journal: Transfus Med Hemother Date: 2019-05-17 Impact factor: 3.747