Transfusion · 2011
Is current serologic RhD typing of blood donors sufficient for avoiding immunization of recipients?
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Krog Grethe Risum, Clausen Frederik Banch, Berkowicz Adela, Jørgensen Lone, Rieneck Klaus, Nielsen Leif Kofoed, Dziegiel Morten Hanefeld
Аннотация
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.
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.