Analysis of RHD genes in Taiwanese RhD-negative donors by the multiplex PCR method

• Published in: Journal of clinical laboratory analysis Vol. 17; no. 3; pp. 80 - 84
• Main Authors: Lee, Y.-L., Chiou, H.-L., Hu, S.-N., Wang, L.
• Format: Journal Article
• Language: English
• Published: New York Wiley Subscription Services, Inc., A Wiley Company 2003
• Subjects: Blood Grouping and Crossmatching; Chinese; Del; DNA Primers; Exons; Genotype; Humans; Infant, Newborn; multiplex PCR; Oncogene Proteins, Fusion - analysis; Oncogene Proteins, Fusion - blood; Oncogene Proteins, Fusion - genetics; Original; partial D; Phenotype; Polymerase Chain Reaction - methods; Recombinant Fusion Proteins; Rh-Hr Blood-Group System - blood; Rh-Hr Blood-Group System - classification; RhD-negative; Sequence Analysis, DNA; Taiwan; Taiwan
• ISSN: 0887-8013; 1098-2825
• DOI: 10.1002/jcla.10073

The determination of the RhD phenotype is important in transfusion medicine. However, due to the complexity of D antigen expression, the routine serological method cannot differentiate all RhD variants. In addition, the induction of the anti‐D antibody is still the major cause of severe hemolytic disease of the newborn (HDN). Therefore, it is important to understand RHD gene profiles. To analyze the RHD gene profiles of Taiwanese RhD‐negative donors, the multiplex PCR method was applied to amplify RHD specific exons 3, 4, 5, 7, and 9. Based on the PCR results, the 156 RhD‐negative donors were divided into 12 groups according to the different expression patterns of the RHD gene. These 12 groups were further divided into three categories: type I=Rh Del (21.8%); type II = partial D, containing some exons (9.0%); and type III = true RhD‐negative (69.2%). The results indicated that 21.8% of RhD‐negative donors in Taiwan were RhDel, and 9% carried a part of the RHD gene. Six defined RhD variants were found in this study: four ROHar, one DVa, and two DIVb. However, no true RhD‐negative or RhDel donor with the CcdEe phenotype was found in this analysis. J. Clin. Lab. Anal. 17:80–84, 2003. © 2003 Wiley‐Liss, Inc.