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

被引:19
作者
Lee, YL
Chiou, HL
Hu, SN
Wang, L
机构
[1] Chung Shan Med Univ, Sch Med Technol, Taichung 402, Taiwan
[2] Chung Shan Med Univ Hosp, Dept Lab Technol, Taichung, Taiwan
关键词
RhD-negative; del; partial D; multiplex PCR; chinese;
D O I
10.1002/jcla.10073
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
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 = RhDel (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 R-O(Har), one D-Va, and two D-IVb. However, no true RhD-negative or RhDel donor with the CcdEe phenotype was found in this analysis. (C) 2003 Wiiey-Liss, Inc.
引用
收藏
页码:80 / 84
页数:5
相关论文
共 28 条
[1]   Specificity and sensitivity of RHD genotyping methods by PCR-based DNA amplification [J].
Aubin, JT ;
Kim, CL ;
Mouro, I ;
Colin, Y ;
Bignozzi, C ;
Brossard, Y ;
Cartron, JP .
BRITISH JOURNAL OF HAEMATOLOGY, 1997, 98 (02) :356-364
[2]   Evidence of genetic diversity underlying Rh D-, weak D (D-u), and partial D phenotypes as determined by multiplex polymerase chain reaction analysis of the RHD gene [J].
Avent, ND ;
Martin, PG ;
ArmstrongFisher, SS ;
Liu, W ;
Finning, KM ;
Maddocks, D ;
Urbaniak, SJ .
BLOOD, 1997, 89 (07) :2568-2577
[3]  
AVENT ND, 1997, BRIT J BIOMED SCI, V54, P6
[4]   A STUDY OF THE PREVALENCE AND PATTERNS OF INHERITANCE OF PARTIAL-D ANTIGEN CATEGORY-VI IN A WHITE DONOR POPULATION [J].
BECKERS, EAM ;
THIJSSEN, PMHJ ;
GERAEDTS, JPM ;
VANRHENEN, DJ .
TRANSFUSION, 1994, 34 (05) :455-455
[5]   PRENATAL DETERMINATION OF FETAL RHD TYPE BY DNA AMPLIFICATION [J].
BENNETT, PR ;
KIM, CL ;
COLIN, Y ;
WARWICK, RM ;
CHERIFZAHAR, B ;
FISK, NM ;
CARTRON, JP .
NEW ENGLAND JOURNAL OF MEDICINE, 1993, 329 (09) :607-610
[6]   Prenatal RHD gene determination and dosage analysis by PCR: clinical evaluation [J].
Chan, FY ;
Cowley, NM ;
Wolter, L ;
Stone, M ;
Carmody, F ;
Saul, A ;
Hyland, CA .
PRENATAL DIAGNOSIS, 2001, 21 (04) :321-326
[7]   Human RhDel IS caused by a deletion of 1,013 bp between introns 8 and 9 including exon 9 of RHD gene [J].
Chang, JG ;
Wang, JC ;
Yang, TY ;
Tsan, KW ;
Shih, MC .
BLOOD, 1998, 92 (07) :2602-2604
[8]  
CHU ML, 1984, J FORMOS MED ASSOC, V83, P796
[9]   Differences between RhD-negative Africans and RhD-negative Europeans [J].
Daniels, G ;
Green, C ;
Smart, E .
LANCET, 1997, 350 (9081) :862-863
[10]  
Flegel WA, 1998, TRANSFUSION MED, V8, P281