Yann Fichou1, Cédric Le Maréchal2, Virginie Scotet1, Déborah Jamet3, Claude Férec2. 1. French Blood Institute (EFS-Bretagne), Brest, France; National Institute of Health and Medical Research (Inserm, UMR1078), Brest, France. 2. French Blood Institute (EFS-Bretagne), Brest, France; National Institute of Health and Medical Research (Inserm, UMR1078), Brest, France; Faculty of Medicine and Health Sciences, University of Western Brittany, Brest, France; Molecular Genetics and Histocompatibility Laboratory, Regional University Hospital (CHRU), Morvan Hospital, Brest, France. 3. French Blood Institute (EFS-Bretagne), Brest, France.
Abstract
BACKGROUND: Although systematic blood group genotyping of patients/donors is virtually possible, serological studies remain the gold standard to identify samples of clinical interest that may be further genotyped. In this context, we sought to identify variant D alleles that are likely to be clinically relevant in terms of other Rh antigens in a subset of population genotyped in Western France. METHODS: Samples presenting with the RHD*weak D type 4.2.2 allele (n = 47) were selected for the study. RHCE exons 1-7 were directly sequenced, and expression of Rh antigens was predicted on the basis of the molecular data. RESULTS: Of the 47 samples tested, 19 (40.4%) were predicted to be of potential clinical interest. Moreover, we could show that selecting the samples to be genotyped by the nature of their variant D allele (i.e., RHD*weak D type 4.2.2 allele) rather than by their Duffy-null status appears to increase significantly the likelihood of identifying clinically relevant individuals for Rh status. CONCLUSION: On the basis of our findings we suggest that all individuals genotyped as weak D type 4.2.2 should be systematically screened for RHCE variants by molecular analysis on a routine basis.
BACKGROUND: Although systematic blood group genotyping of patients/donors is virtually possible, serological studies remain the gold standard to identify samples of clinical interest that may be further genotyped. In this context, we sought to identify variant D alleles that are likely to be clinically relevant in terms of other Rh antigens in a subset of population genotyped in Western France. METHODS: Samples presenting with the RHD*weak D type 4.2.2 allele (n = 47) were selected for the study. RHCE exons 1-7 were directly sequenced, and expression of Rh antigens was predicted on the basis of the molecular data. RESULTS: Of the 47 samples tested, 19 (40.4%) were predicted to be of potential clinical interest. Moreover, we could show that selecting the samples to be genotyped by the nature of their variant D allele (i.e., RHD*weak D type 4.2.2 allele) rather than by their Duffy-null status appears to increase significantly the likelihood of identifying clinically relevant individuals for Rh status. CONCLUSION: On the basis of our findings we suggest that all individuals genotyped as weak D type 4.2.2 should be systematically screened for RHCE variants by molecular analysis on a routine basis.
Authors: G L Daniels; B H Faas; C A Green; E Smart; P A Maaskant-van Wijk; N D Avent; H A Zondervan; A E von dem Borne; C E van der Schoot Journal: Transfusion Date: 1998-10 Impact factor: 3.157
Authors: Kshitij Srivastava; Helene Polin; Sherry Lynne Sheldon; Franz Friedrich Wagner; Christoph Grabmer; Christian Gabriel; Gregory Andrew Denomme; Willy Albert Flegel Journal: Transfusion Date: 2016-08-02 Impact factor: 3.157