ArticleTransfusion2022
RHD genotyping to resolve weak and discrepant RhD patient phenotypes.
Article in Transfusion, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Prevalence of Serologic Weak D Phenotype in Iranian Blood Donors: A Nationwide Retrospective Cross-Sectional Study.Health science reports · 2026Article
- On the Differentiation of Auto- and Allo-Anti-D: The Significance of DAT and Autocontrol.Iranian journal of pathology · 2026Article
- An RHD gene variant, common in southern Chinese Han, involves a short 688 bp deletion and a long 21.8 kb insertion in the RHD exon 10 non-coding region, affecting the accuracy of red cell genotyping.Journal of translational medicine · 2026Article
- Functional investigation of the RHD gene promoter: Molecular changes are rarely responsible for variant D phenotype in Thai donors.Transfusion · 2026Article
- A novel RHD allele combining partial D (c.455A>C) and weak D (c.1154G>C) variants.Transfusion · 2025Article
- Weak D phenotype in transfusion medicine and obstetrics: Challenges and opportunities.World journal of experimental medicine · 2025Review
- IntegratingMedicina (Kaunas, Lithuania) · 2025Article
- RHD genotyping to resolve weak and discrepant RhD patient phenotypes.Transfusion · 2022Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe instituted RHD genotyping in our transfusion service for obstetrical patients and transfusion candidates. We sought to examine how RHD genotyping resolved weak or discrepant automated microplate direct agglutination (MDA) RhD phenotypings and impacted needs for Rh Immune Globulin (RhIG) and D-negative RBCs. STUDY DESIGN AND
methodsWe investigated RhD phenotypes with equivocal or reagent-discrepant automated MDA (Immucor, Norcross, GA), weak-2+ immediate-spin tube typings, historically discrepant RhD typings, or D+ typings with anti-D. We performed microarray RHD genotyping (RHD BeadChip, Immucor BioArray Solutions, Warren, NJ). Patients were managed as D+ with weak-D types 1, 2, and 3, and as D-negative with all other results.
resultsOur weak-D prevalence was 0.14%. Among 138 patients (73 obstetrics, 65 transfusion candidates), 38% had weak-D types 1, 2 or 3, 25% weak partial type 4.0, 21% other partial-D variant alleles, and 15% no variant detected. One novel allele with weak partial type 4.0 variants plus c.150T>C (Val50Val) was discovered. Weak D types 1, 2 or 3 were identified in 66% (48/73) of Whites versus 3% (2/62) of diverse ethnic patients (p < .0001). RHD genotyping changed RhD management in 60 patients (43%) (49 to D+, 11 to D-negative), resulting in net conservation of D-negative RBCs (98 avoided, 14 given) and RhIG (8 avoided, 3 given).
conclusionIn our patient population, equivocal or reagent-discrepant MDA RhD phenotypes were highly specific for weak-D or partial-D RHD genotypes. Resolution of RHD genotype status reduced our use of D-negative RBCs and RhIG.
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