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Six years' experience performing RHD genotyping to confirm D− red blood cell units in Germany for preventing anti-D immunizations

Authors

  • Willy A. Flegel,

    1. From the German Red Cross (DRK) Blood Donor Service Baden-Württemberg-Hessen, Institute Ulm, Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, and Institute of Transfusion Medicine, University Hospital Ulm, Ulm, Germany.
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  • Inge Von Zabern,

    1. From the German Red Cross (DRK) Blood Donor Service Baden-Württemberg-Hessen, Institute Ulm, Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, and Institute of Transfusion Medicine, University Hospital Ulm, Ulm, Germany.
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  • Franz F. Wagner

    1. From the German Red Cross (DRK) Blood Donor Service Baden-Württemberg-Hessen, Institute Ulm, Institute of Clinical Transfusion Medicine and Immunogenetics Ulm, and Institute of Transfusion Medicine, University Hospital Ulm, Ulm, Germany.
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  • This work was supported in part by intramural research grants from the DRK Blutspendedienst Baden-Württemberg-Hessen and the Deutsche Gesellschaft für Transfusionsmedizin und Immunhämatologie (Project DGTI/fle/2003-01).

  • Conflict-of-interest disclosure: The authors are current or former employees of the DRK Blutspendedienst Baden-Württemberg-Hessen. DRK and WAF hold patents or have patents pending on nucleotide sequences and their use in molecular genetics for weak D, DEL, and the Rhesus box.

  • WAF designed the study, collected and interpreted the data, and wrote the manuscript; IvZ collected, analyzed, and interpreted data and wrote the manuscript; and FFW analyzed the samples collected in 2002 and 2003.

Prof. Dr. med. Willy A. Flegel, Institut für Klinische Transfusionsmedizin und Immungenetik Ulm, Helmholtzstrasse 10, D-89081 Ulm, Germany; e-mail: willy.flegel@uni-ulm.de.

Abstract

BACKGROUND: Red blood cell (RBC) units of D+ donors are falsely labeled D− if regular serologic typing fails to detect low D antigen expression or chimerism. The limitations of serology can be overcome by molecular typing.

STUDY DESIGN AND METHODS: In January 2002, we introduced a polymerase chain reaction (PCR)-based assay for RHD as a routine test for first-time donors who typed D− by serologic methods including the indirect antiglobulin test. Samples were tested in pools of 20 for the RHD-specific polymorphism in Intron 4. RHD alleles were identified by PCR and nucleotide sequencing.

RESULTS: Within 6 years, 46,133 serologically D− first-time donors were screened for the RHD gene. The prevalence of RHD gene carriers detected by this method was 0.21 percent. Twenty-three RHD alleles were found of which 15 were new. Approximately one-half of the RHD gene carriers harbored alleles expressing a DEL phenotype resulting in a prevalence of 0.1 percent.

CONCLUSION: The integration of RHD genotyping into the routine screening program was practical. We report 6 years' experience of this donor testing policy, which is not performed in most transfusion services worldwide. RBC units of donors with DEL phenotype have been reported to anti-D immunize D− recipients. We transferred those donors to the D+ donor pool with the rationale of preventing anti-D immunizations, especially dreaded in pregnancies. For each population, it will be necessary to adapt the RHD genotyping strategy to the spectrum of prevalent alleles.

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