RHD*01W.1 - RHD*weak D type 1
(ISBT table: Weak D and Del v5.0)
This entry is an RHD allele.
RHD(V270G), RHD*809G, RHD*809G (weak D type 1), RHD*809T>G, weak D type 1,
Molecular data
Phenotype
Main D phenotype: weak D (last update: Dec. 28, 2020)Reports by D phenotype
- D positive (apparently normal D or undetailed positive D)
- Mixed-field
- Undetailed ambiguous D phenotype
- Mixed-field
- Discrepant D phenotype (negative or positive depending on anti-D reagents and techniques)
- Mixed-field
- Weak D phenotype
- Mixed-field
- Very weak D phenotype
- Mixed-field
- DEL
- Mixed-field
- D negative
- Mixed-field
Other RH phenotypes: RH:-2, -3, -4,
Serology with monoclonal anti-D
- 1 monoclonal IgG anti-D non-reactive with variant, out of 60 monoclonal IgG anti 22 IgM anti-D tested
- 0 monoclonal IgG anti-D non-reactive with variant, tested with Diagast Dscreen kit
- only a few anti-D tested
- results are not detailed per Ab or per variant
- 6 anti-D non reactive with variant, out of 63 monoclonal IgG and 19 IgM tested,
- 0 monoclonal IgG anti-D non-reactive with variant, out of 22 monoclonal IgG tested (Table 2)
- tested with Diagast Dscreen kit and ID-Partial Rh D-Typing Set, results not detailed
- tested with Diagast Dscreen kit, one sample heterozygous with RHef00061
- 0 monoclonal IgG anti-D non-reactive with variant, 1 sample tested with 2 panels of monoclonal anti-D (17 IgG, 4 IgM) (Table 3)
- weak reactions (+ to ++), with a panel of 10 monoclonal anti-D
- Sample heterozygous with RHef00781; ALBAclone advanced partial RhD typing kit: "reactions consistent with weak D type 1 with the partial RhD kit."
Antigen Density (Ag/RBC)
- range: 533 - 1283, median: 759 Ag/RBC, with 6 IgG anti-D; 25 RH:1,2,-3,4,5 samples tested (table 3)
- 1285 Ag/RBC, derived from the results obtained with 59 of the 59 monoclonal IgG anti-D tested
- 144 Ag/RBC, 1 sample, heterozygous for RHef00061 and RHef00238
- range: 937 - 1059, median 1031 Ag/RBC, 4 R1r samples
- mean: 1278 Ag/RBC, 41 samples
- 814 Ag/RBC, 1 sample, 2 monoclonal anti-D
- 916 Ag/RBC, 1 sample, 2 monoclonal anti-D
- range: 889 - 1197, median: 978 Ag/RBC, 3 samples, median (range) with 11 IgG anti-D
- range: 367 - 386, median 376 Ag/RBC, 2 R1R1 samples
- 632 Ag/RBC, 1 sample used as control
- 791 Ag/RBC, 1 sample used as control
- 992 Ag/RBC, 1 sample used as control
- 751 Ag/RBC
- 815 Ag/RBC, sample used as control
- mean: 1128 Ag/RBC, 2 samples; Ag density estimated from a measure with a single monoclonal IgG anti-D, compared to a RH:1,2,3,4,5 control sample with an antigen density assumed to be about 27.500 Ag/RBC
More phenotype data
Haplotype
Main CcEe phenotype association: Ce is the most frequent association, ce is a rare association (last update: Jan. 8, 2021)ce | Ce | cE | CE | |
---|---|---|---|---|
ce | 27 | 253 | 1 | 0 |
Ce | 342 | 6 | 0 | |
cE | 0 | 0 | ||
CE | 0 |
Reports by CcEe phenotype
- with CcEe 3 samples
- with Ccee 1 sample (1 sample? used as control) (one sample, heterozygous with RHef00061)
- with Ce 95 samples (haplotype given, not complete phenotype)
- with ce 1 sample
- with ccEe 1 sample
1 sample
2 samples
3 samples (3 samples used as controls, may have been included in other studies)
23 samples
35 samples
28 samples
17 samples
38 samples
8 samples
54 samples
2 samples
15 samples
25 samples
4 samples (4 heterozygous samples, probably with RHef00442)
2 samples (haplotype given, not complete phenotype)
1 sample (haplotype given, not complete phenotype)
5 samples
19 samples (haplotype given, not complete phenotype)
60 samples (haplotype given, not complete phenotype)
9 samples (haplotype given, not complete phenotype)
13 samples (1 sample heterozygous with RHef00301)
138 samples (haplotype given, not complete phenotype)
0 samples (haplotype listed, not complete phenotype; presented as a general association) (no sample count, listed as a general association)
15 samples (haplotype given, not complete phenotype)
6 samples
3 samples
2 samples
Reports by allele association
Alloimmunization
Antibodies in carriers
Antibody specificity: D (RH1)
Summary: not considered at risk for allo-anti-D despite exceptional anti-D descriptions (last update: Dec. 28, 2020)Detailed information
-
Yazer MH et al. Transfusion (2016)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 1
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment: "potentially alloimmunized patient"
-
Denomme GA et al. Transfusion (2005)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 0
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment: lists exposures to standard D antigen and patient blood management for several carriers
-
Pham BN et al. Immunohematology (2013)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-: 7
- Number of carriers of the allele assessed: 138
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: ND
- Pregnancy history:
- Anti-D Ig history: ND
- Context: ND
- Hemolytic consequences: ND
- Comment: 7 anti-D in 138 individuals with this allele; anti-D in carriers of this allele are considered auto-anti-D by authors (see 21658048)
-
St-Louis M et al. Immunohematology (2011)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-: 1
- Number of carriers of the allele assessed: 5
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
-
Yazer MH et al. Transfusion (2016)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-: 1
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
-
Wagner FF et al. Blood (2000)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-: 1
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution: positive: anti-D
- Autoadsorption:
- Titer: 1
- Was anti-LW excluded?:
- Other antibodies detected: anti-E
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
Wagner FF et al. Transfus Med Hemother (2014) (RIR n°6)
-
J S. Woo et al. Transfusion (2018)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-: 1
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT: negative
- Autologuous control:
- Elution: positive: anti-D (4 weeks after transfusion)
- Autoadsorption: not autoadsorbable
- Titer:
- Was anti-LW excluded?: ruled out, Ab to carboplatin or paclitaxel that the patient was receiving were ruled out
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types): anti-D reacted with D variant RBCs (DIII, DIV, DV, DVI, DVII, R0Har) but not with RHef00238 RBCs
- Transfusion history: received 7 D+ RBC units
- Pregnancy history:
- Anti-D Ig history:
- Context: cancer patient
- Hemolytic consequences: worsening anemia and slight increase in bilirubin 4 weeks after her last transfusion
- Comment: anti-D was detected 2 months later, anti-D + anti-K 8 months later, anti-D reactivity started weakening 9 months and 1/2 after the last D+ transfusion
-
Flegel WA et al. Curr Opin Hematol (2006)
(some samples overlap with other reports)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-: 0
- Number listed as auto-: 15
- Number of carriers of the allele assessed: 15
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: ND
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: ND
- Hemolytic consequences: ND
- Comment: "reports of the Rhesus Immunization Registery as of June 2006"
Wagner FF et al. Transfus Med Hemother (2014)
-
Pham BN et al. Transfusion (2011)
- Ab specificity: D (RH1)
- Number (auto- or allo-):
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed:
- DAT:
- Autologuous control:
- Elution:
- Autoadsorption:
- Titer:
- Was anti-LW excluded?:
- Other antibodies detected:
- Cross matches (with Ab and RBCs from different partial types):
- Transfusion history:
- Pregnancy history:
- Anti-D Ig history:
- Context:
- Hemolytic consequences:
- Comment:
-
Daniels G et al. Br J Haematol (2013)
(review)
- Ab specificity: D (RH1)
- Number (auto- or allo-): no new case detailed
- Number listed as allo-:
- Number listed as auto-: ND
- Number of carriers of the allele assessed: ND
- DAT: ND
- Autologuous control: ND
- Elution: ND
- Autoadsorption: ND
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: ND
- Pregnancy history:
- Anti-D Ig history: ND
- Context: ND
- Hemolytic consequences: ND
- Comment: "individuals with RHef00238, RHef00288, and RHef00301 make alloanti-D only extremely rarely, if at all"
-
G Shakarian et al. Transfusion (2014)
- Ab specificity: D (RH1)
- Number (auto- or allo-): 1 (htz with RHef00781)
- Number listed as allo-:
- Number listed as auto-:
- Number of carriers of the allele assessed: 1
- DAT: very weak positive
- Autologuous control: ND
- Elution: anti-D (but recent transfusion)
- Autoadsorption: ND (recent transfusion)
- Titer: ND
- Was anti-LW excluded?: ND
- Other antibodies detected: ND
- Cross matches (with Ab and RBCs from different partial types): ND
- Transfusion history: 2 D positive RBCs 2 months earlier
- Pregnancy history:
- Anti-D Ig history: ND, probably none
- Context: ND
- Hemolytic consequences: ND
- Comment:
Reports
Summary: common allele, mainly in individuals of Western Europen (Caucasian) descent, or compatible with such descent (last update: Dec. 28, 2020)Detailed reports
- 95/161 random donors with weak D phenotype; DVI samples were excluded by serologic testing in the German population (Southwestern Germany), White (Table 5)
- 38/99 donors with weak D phenotype Australian
- 169/270 donors with weak D phenotype White, in the German (Northern Germany) population
- 43/146 (+ 1 heterozygous with RHef00301) donors with weak D phenotype White, in the Austrian (Tyrol) population
- 30/168 among 168 samples referred for weak D phenotype and/or allo anti-D in D positive individuals, 137 were characterized in the study (70 by serology, 67 by molecular analysis, 31 could not be typed because serologic typing was inconclusive and molecular typing could not be performed) in the French population (Caucasian)
- 0/738 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Austrian (state of Tyrol) population
- 0/104 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Swiss (Bern and the canton of Bern) population
- 0/400 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the German (states of Lower Saxony, Saxony- Anhalt, Thuringia, Oldenburg, and Bremen) population
- 0/71 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Russian (Kirov Oblast) population
- 1/333 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the Slovenian population
- 0/54 samples with D negative, but C and/or E positive phenotype, screened for RHD specific sequences (in the 5'UTR region, exon 3 and exon 10) in the German (city of Braunschweig and eastern parts of Lower Saxony) population
- 0/250 250 donors with RH:1,2,–3,4,5 phenotype among 1000 donors screened for RHD molecular variants by several PCR-SSP and exon 5 sequencing of all samples (500 R0r, 250 R1R, 250 R2r) in the German population (southwestern Germany)
- 16/55 55 discrepant or weak D phenotypes among 33864 multiethnic patients (of African, Asian, Indoasian and European extraction) in the Canadian (Toronto) population
- 6/23 121022 donors tested: 201 had weak D phenotype and, among those, 23 very weak D phenotype German
- 16/99 weak D phenotype Portuguese
- 2/8 530 RH:1,2,-3,4,5 random donor samples were tested for D antigen density, 8 were in the lower range of antigen density and were genotyped German
- 93/289 289 samples with ambiguous D phenotype (333 consecutive samples with ambiguous D phenotype studied but 44 were hybrid alleles, excluded from the study) in the French (Western France) population
- 72/191 (47 donors and 25 patients) among 191 samples with weak D expression or unclear D phenotype within 44,743 donors and 8,604 patients tested in the Austrian population, Upper Austria
- 23/55162 among samples C or E positive and positive for "Du test" (55162 samples were typed; 314 were ddCcee, with 63 positive for "Du test" and 154 were ddccEe, with 30 positive for "Du test"; of the 93 "Du positive", 60 underwent molecular analysis) in the French population
- 60/101 donors with weak D phenotype Danish
- 1/1113 pregnant D negative women tested for fetal non invasive genotyping, RHD exons 5 and 7 in the German population
- 1/23330 donor samples with D negative phenotype tested for RHD exons 4, 7 and 10 (94 were PCR positive, 74 weak D or DEL in subsequent serologic analysis) in the Austrian population, Upper Austria
- 1/25 donors with "weak D or questionnable D status" explored by NGS to compare with Sanger sequencing in the Austrian population, Upper Austria
- 63/167 discrepant D testing results (donors?) Croatian
- 11/45 (prevalence among weak D phenotype) or 11/12672 (phenotypic prevalence in population) 45 patients with weak D phenotype were genotyped in a cohort of 12672 patients from a public hospital Argentinean
- 10/43 (prevalence among weak D) or 10/5707 (phenotypic prevalence in population) 43 patients with weak D phenotype were genotyped in a cohort of 5707 patients from a private laboratory Argentinean
- 2/16 among 2007 unrelated donors, 16 had weak D phenotype in the Brazilian population (Sao Paulo, mainly racially mixed non-white skin color individuals)
- 19 samples, including 5/26 among 26 French Canadian with weak D phenotype or D positive phenotype and anti-D Caucasian, French Canadian
- 1/101 among 2450 donors with D negative phenotype tested for RHD specific polymorphisms (101 were positive for the polymorphisms) Caucasian descent in Brazilian (Southeast and Northeast Brazil)
- 2/50 (both patients) 50 samples (33 donors and 17 patients) with discrepant or weak D phenotyping in the Egyptian population
- 1 sample (htz with RHef00567) reported by a French lab from Brest, Brittany
- 138/748 among 748 individuals with D anomaly (weak or discrepant D phenotype or anti-D in individuals with D positive phenotype), 459 had D variants "that could be named weak D" (including alleles RHef00313, RHef00317 and RHef00318, as well as RHef00197 and RHef00283), 138 had partial D, 65 had no variant, 86 were not persued further (two variant alleles or incomplete or pending analysis) in the French population
- 1/520 (heterozygous with RHef00061) among 520 donors with D negative phenotype, C and/or E positive in the Brazilian population (Sao Paulo)
- 19/360 donors with atypical D phenotype (discrepancies or reactivity weaker than 3+) Brazilian
- 38/58 (one heterozygous with RHef00301) within a donor population of 38836, 4272 initially typed D negative and 58 of these were found to be weak D with different reagents Albanian
- 265/627 weak D typing (95% from patients, 5% from donors; 21,2% were identified as RHef00442 or RHef00446 by authors, "mostly (…) inconclusive serology consequent to recent transfusion") in the Belgian (Flanders) population
- 3/37782 270 women with variant alleles among 37782 women with D negative phenotype, tested by quantitative fetal RHD genotyping designed to detect RHD exons 5 and 7 in the Dutch population
- 15/400 among random blood and bone marrow donors genotyped for RHD in the Brazilian population (Parana state, Southern Brazil)
- 119/351 (+5 heterozygous: 3 for RHef00238 and RHef00301, 1 for RHef00238 and RHef00288, 1 for RHef00602 and RHef00238) out of 351 prenatal patients with discrepant D phenotyping results (population tested 608486 patients) Canadian
- 42/100 (+2 heterozygous with RHef00238 and RHef00107) donors with weak D phenotype Australian
- 9/104 (prevalence among weak D) or 9/21353 (phenotypic prevalence in population) 104 with weak D phenotype were genotyped in a cohort of 21353 pregnant women admixed Brazilian
- 1/662 among 662 pregnant patients with apparent D negative phenotype, enroled for fetal genotyping in the Australian population
- 255/256 samples with RHD c.809T>G mutation (typical of RHef00238) in the French population (Western France)
- 0/223 donors with D negative phenotype initially, found to have D positive phenotype (67 of the 223 samples of the cohort) or samples referred with discrepant or weak D typing, or discrepancies with previous typings, or anti-D in D positive individuals (156 of the 223 samples of the cohort) in the Indian population
- 13/26 26 samples with weak D phenotype, analyzed by NGS Caucasian, in the UK (Bristol) population
- 1/23 donors with weak D phenotype (among 4458 random donors, 4028 types D positive including 19 weak D phenotype, 420 typed D negative including 4 showed to be weak D by further serological testing; in total 23 donors had weak D phenotype) in the Maroccan population
- 30/85 donors with weak D phenotype Bosnia Herzegovinian
- 26/61 donors with weak D phenotype Serbian
- 2/92 donors with apparent D negative phenotype, C and/or E positive Bosnia Herzegovinian
- 37/64 among 175000 donors, 64 had weak D phenotype and underwent molecular identification in the Greek population
- 37/231 231 donors with weak D phenotype in the Argentinean population (Northwestern Argentina)
- 12/273 donors with weak D phenotype in the Brazilian population
- 45/57 samples with ambiguous D phenotype among about 15,800 samples tested (22/5,800 donors and 35/10,000 patients had ambiguous D phenotype) presumed Caucasian, in the Danish population (91,4% Caucasian)
- 13/18537 18537 donors with D negative phenotype were tested for the presence of RHD DNA sequences, 154 samples were positive for one or several RHD exons in the Swiss population
- 1 sample (heterozygous with RHef00781) African American
- 15/185 RH:–1,–4 or RH:–1,–5 recipients reported by a French lab
- 1 sample Caucasian, in the American population
- 4/94 donors with discreapancies in D typing Southeast Brazilian
- 4/45 45 samples referred for D typing discrepancies in the USA population (Table 2)
- 24/163 (including 1 heterozygous with RHef0452 and 1 with RHef00107) selected variants included for the development of a genotyping assay mainly in the Dutch population (samples may have been included in other studies)
- 112/430 (2 heterozygous) among samples with ambigous D phenotype in the French population (Table S1)
-
4/2000 all heterozygous samples among 2000 random donors (1777 typed D positive), all donors were genotyped for 809G in the Tunisian population
(study may overlap with
24014941 ) -
0/45 among 763408 donors, after ruling out partial D phenotypes by using 5 monoclonal anti-D, 75 were considered weak D phenotype and 45 were genotyped Japanese
(some samples in common with
27183894 ) -
0/226 226 donors considered weak D phenotype, after ruling out partial D phenotypes by using 5 monoclonal anti-D Japanese
(1 sample in common with
26340140 ) - 88/353 samples referred for discrepant or weak D typing mainly Whites, in the USA population
- 1 hemizygote among 278 samples selected for the development of nonspecific quantitative next-generation sequencing. (non-random samples, may have been reported in other studies)
Allele or phenotype frequency
- 1/277 estimated allele frequency in the German population (Southwestern Germany), White
- 0.002964 estimated prevalence in the German population
- 1/23330 (CI: 1/4926 - 1/500000) estimated allele frequency in individuals with D negative phenotype in the Austrian population, Upper Austria
- 1/2044 (CI: 1/2890 - 1/1490) estimated allele frequency Albanian
- 0.052 allele frequency in 58 patients with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)
- 0.038 allele frequency in 106 donors with weak D phenotype Brazilian (mixed origin, mainly between African and European descent)
Structure mapping
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References
- International Society of Blood Transfusion et al. International Society of Blood Transfusion (ISBT) allele table Online ressource, 1935. — Online ressource — [RHeference]
- Wagner FF et al. Molecular basis of weak D phenotypes. Blood, 1999. [Citation] [RHeference]
- Wagner FF et al. Weak D alleles express distinct phenotypes. Blood, 2000. [Citation] [RHeference]
- Cowley NM et al. RHD gene mutations and the weak D phenotype: an Australian blood donor study. Vox Sang, 2000. [Citation] [RHeference]
- Kamesaki T et al. Molecular characterization of weak D phenotypes by site-directed mutagenesis and expression of mutant Rh-green fluorescence protein fusions in K562 cells. Vox Sang, 2001. [Citation] [RHeference]
- Müller TH et al. PCR screening for common weak D types shows different distributions in three Central European populations. Transfusion, 2001. [Citation] [RHeference]
- Wagner FF et al. The DAU allele cluster of the RHD gene. Blood, 2002. [Citation] [RHeference]
- Flegel WA et al. Section 1B: Rh flow cytometry. Coordinator's report. Rhesus index and antigen density: an analysis of the reproducibility of flow cytometric determination. Transfus Clin Biol, 2002. [Citation] [RHeference]
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- Körmöczi GF et al. A comprehensive analysis of DEL types: partial DEL individuals are prone to anti-D alloimmunization. Transfusion, 2005. [Citation] [RHeference]
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- Körmöczi GF et al. Novel weak D types 31 and 32: adsorption-elution-supported D antigen analysis and comparison to prevalent weak D types. Transfusion, 2005. [Citation] [RHeference]
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- Doescher A et al. Weak D type 1.1 exemplifies another complexity in weak D genotyping. Transfusion, 2005. [Citation] [RHeference]
- Denomme GA et al. Partial D, weak D types, and novel RHD alleles among 33,864 multiethnic patients: implications for anti-D alloimmunization and prevention. Transfusion, 2005. [Citation] [RHeference]
- Mota M et al. Anti-D alloimmunization by weak D type 1 red blood cells with a very low antigen density. Vox Sang, 2005. [Citation] [RHeference]
- Araújo F et al. Weak D type 2 is the most prevalent weak D type in Portugal. Transfus Med, 2006. [Citation] [RHeference]
- Esteban R et al. The D category VI type 4 allele is prevalent in the Spanish population. Transfusion, 2006. [Citation] [RHeference]
- Flegel WA et al. How I manage donors and patients with a weak D phenotype. Curr Opin Hematol, 2006. [Citation] [RHeference]
- Yu X et al. Outliers in RhD membrane integration are explained by variant RH haplotypes. Transfusion, 2006. [Citation] [RHeference]
- Westhoff CM et al. Rh complexities: serology and DNA genotyping. Transfusion, 2007. [Citation] [RHeference]
- Polin H et al. Effective molecular RHD typing strategy for blood donations. Transfusion, 2007. [Citation] [RHeference]
- Noizat-Pirenne F et al. Weak D phenotypes and transfusion safety: where do we stand in daily practice? Transfusion, 2007. [Citation] [RHeference]
- Le Maréchal C et al. Identification of 12 novel RHD alleles in western France by denaturing high-performance liquid chromatography analysis. Transfusion, 2007. [Citation] [RHeference]
- Christiansen M et al. Correlation between serology and genetics of weak D types in Denmark. Transfusion, 2008. [Citation] [RHeference]
- Müller SP et al. The determination of the fetal D status from maternal plasma for decision making on Rh prophylaxis is feasible. Transfusion, 2008. [Citation] [RHeference]
- Polin H et al. Identification of RHD alleles with the potential of anti-D immunization among seemingly D- blood donors in Upper Austria. Transfusion, 2009. [Citation] [RHeference]
- Pham BN et al. Anti-D investigations in individuals expressing weak D Type 1 or weak D Type 2: allo- or autoantibodies? Transfusion, 2011. [Citation] [RHeference]
- Dogic V et al. Distribution of weak D types in the Croatian population. Transfus Med, 2011. [Citation] [RHeference]
- Stabentheiner S et al. Overcoming methodical limits of standard RHD genotyping by next-generation sequencing. Vox Sang, 2011. [Citation] [RHeference]
- St-Louis M et al. Weak D type 42 cases found in individuals of European descent. Immunohematology, 2011. [Citation] [RHeference]
- Cruz BR et al. RHD alleles in Brazilian blood donors with weak D or D-negative phenotypes. Transfus Med, 2012. [Citation] [RHeference]
- Yazer MH et al. Anti-D alloimmunization propensity cannot be determined without information on D antigen exposure. Transfusion, 2012. [Citation] [RHeference]
- Flegel WA et al. Allo- and autoanti-D in weak D types and in partial D. Transfusion, 2012. [Citation] [RHeference]
- Brajovich ME et al. Comprehensive analysis of RHD alleles in Argentineans with variant D phenotypes. Transfusion, 2012. [Citation] [RHeference]
- Mota M et al. RHD allelic identification among D-Brazilian blood donors as a routine test using pools of DNA. J Clin Lab Anal, 2012. [Citation] [RHeference]
- Silvy M et al. Characterization of novel RHD alleles: relationship between phenotype, genotype, and trimeric architecture. Transfusion, 2012. [Citation] [RHeference]
- Rizzo C et al. Weak D and partial D: our experience in daily activity. Blood Transfus, 2012. [Citation] [RHeference]
- Abdelrazik AM et al. Combining serology and molecular typing of weak D role in improving D typing strategy in Egypt. Transfusion, 2013. [Citation] [RHeference]
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- Ye SH et al. A comprehensive investigation of RHD polymorphisms in the Chinese Han population in Xi'an. Blood Transfus, 2014. [Citation] [RHeference]
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- G Shakarian et al. Three New, Clinically Relevant RHD genes Transfusion, 2014. — Abstract — [RHeference]
- Xhetani M et al. Distribution of Rhesus blood group antigens and weak D alleles in the population of Albania. Blood Transfus, 2014. [Citation] [RHeference]
- A C Gaspardi et al. RHD variants in blood donors from Southeast Brazil. Transfusion, 2015. — Abstract — [RHeference]
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- Stegmann TC et al. Frequency and characterization of known and novel RHD variant alleles in 37 782 Dutch D-negative pregnant women. Br J Haematol, 2016. [Citation] [RHeference]
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- C Henny et al. Impact of the mandatory donor RHD screening in Switzerland Vox Sanguinis, 2016. — Abstract — [RHeference]
- Ogasawara K et al. Weak D alleles in Japanese: a c.960G>A silent mutation in exon 7 of the RHD gene that affects D expression. Vox Sang, 2016. [Citation] [RHeference]
- Zacarias JM et al. Frequency of RHD variants in Brazilian blood donors from Parana State, Southern Brazil. Transfus Apher Sci, 2016. [Citation] [RHeference]
- McGowan EC et al. Diverse and novel RHD variants in Australian blood donors with a weak D phenotype: implication for transfusion management. Vox Sang, 2017. [Citation] [RHeference]
- Hyland CA et al. Non-invasive fetal RHD genotyping for RhD negative women stratified into RHD gene deletion or variant groups: comparative accuracy using two blood collection tube types. Pathology, 2017. [Citation] [RHeference]
- S Vege et al. RHD Genotyping of Discrepant or Weak D Samples: Over a Year’s Experience. Transfusion, 2017. — Abstract — [RHeference]
- Fichou Y et al. Molecular basis of weak D expression in the Indian population and report of a novel, predominant variant RHD allele. Transfusion, 2018. [Citation] [RHeference]
- Jérôme Babinet et al. Erratum à l’article : « Résumés des Posters » [Transfus. Clin. Biol. 24 (2017) 3S] Transfusion Clinique et Biologique, 2018. — Abstract — [RHeference]
- Bub CB et al. RHD alleles among pregnant women with serologic discrepant weak D phenotypes from a multiethnic population and risk of alloimmunization. J Clin Lab Anal, 2018. [Citation] [RHeference]
- J S. Woo et al. Robust Allo-Anti-D with Subsequent Anti-K Production after Transfusion of D-Positive RBCs to a Patient with Weak D Type 1 Transfusion, 2018. — Abstract — [RHeference]
- Dezan MR et al. High frequency of variant RHD genotypes among donors and patients of mixed origin with serologic weak-D phenotype. J Clin Lab Anal, 2018. [Citation] [RHeference]
- Tounsi WA et al. Complete RHD next-generation sequencing: establishment of reference RHD alleles. Blood Adv, 2018. [Citation] [RHeference]
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- Arnoni CP et al. Correlation among automated scores of agglutination, antigen density by flow cytometry and genetics of D variants. Transfus Apher Sci, 2019. [Citation] [RHeference]
- Koutsouri T et al. Frequency distribution of RHD alleles among Greek donors with weak D phenotypes demonstrates a distinct pattern in central European countries. Transfus Med, 2019. [Citation] [RHeference]
- Trucco Boggione C et al. Characterization of RHD locus polymorphism in D negative and D variant donors from Northwestern Argentina. Transfusion, 2019. [Citation] [RHeference]
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Last update: Jan. 8, 2021