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  • Immunohematology


Article | 31-March-2021

Transfusion support during childbirth for a woman with anti-U and the RHD*weak D type 4.0 allele

Hemolytic disease of the fetus and newborn is reliably prevented by proper management, based on antenatal D typing and screening for red blood cell (RBC) antibodies. Many hospital laboratories do not determine the RHD genotype of pregnant women with a serologic weak D phenotype, because these women are often managed as D–.1 However, Rh immune globulin (RhIG) and provision of D– RBC units are unnecessary if D+ RBCs can safely be transfused. An Interorganizational Work Group on RHD Genotyping

Q. Yin, K. Srivastava, D.G. Brust, W.A. Flegel

Immunohematology, Volume 37 , ISSUE 1, 1–4

Article | 14-October-2020

Blood group antigen profile predicted by molecular biology— use of real-time polymerase chain reaction to genotype important KEL,JK, RHD, and RHCE alleles

The most clinically important blood group systems in transfusion medicine, excluding the ABO system, are the RH, Kell, and Kidd systems. Alloantibodies to antigens of these systems may be produced following blood transfusion or during pregnancy and can result in serious hemolytic transfusion reactions and hemolytic disease of the newborn.We developed rapid and robust techniques for RHD, RHCE, KEL, and JK genotyping with the use of a real-time polymerase chain reaction instrument. Two

Fernando Manuel Ferreira Araújo, Christiana Pereira, Fátima Monteiro, Isabel Henriques, Elsa Meireles, Pedro Lacerda, Ana Aleixo, Regina Celeste, Luis M. Cunha-Ribeiro, Maria J. Rodrigues

Immunohematology, Volume 18 , ISSUE 3, 59–64

Report | 01-December-2019

Prevalence of RHD*DOL and RHCE*ce(818T)  in two populations

The alleles RHCE*ceBI (RHCE*ce 48C, 712G, 818T, 1132G) and RHCE*ceSM (RHCE*ce 48C, 712G, 818T) encode the lowprevalence Rh antigen STEM. These alleles frequently travel in cis with RHD*DOL. To estimate the frequency of these alleles, we tested a total of more than 700 samples in two populations. Blood samples were obtained from patients with sickle cell disease and from blood donors of African descent. DNA extractions and analyses were performed by standard methods. In the United States, none

Christine Halter Hipsky, Daiane Cobianchi da Costa, Ricardo Omoto, Angela Zanette, Lilian Castilho, Marion E. Reid

Immunohematology, Volume 27 , ISSUE 2, 66–67

Report | 01-December-2019

Alloimmunization of patients by blood units harboring distinct DEL variants

The alloimmunization potential of many RHD variants is unknown, and it can be explored by lookback and traceback studies. Héma-Québec (HQ) investigated the RHD status of 3980 D– repeat blood donors. Thirteen were found to be RHD positive: 4 RHD*ψ, and 1 RHD*487delACAG, which show a D– phenotype; and 1 RHD*885T and 7 RHD*(93–94insT) causing a DEL phenotype when C antigen is present. Lookback studies were done to verify the alloimmunization potential of these

Maryse St-Louis, André Lebrun, Mindy Goldman, Marianne Lavoie

Immunohematology, Volume 29 , ISSUE 4, 136–140

Case report | 25-March-2020

RHD deletion in a patient with chronic myeloid leukemia

August 2006 typed D– by both direct hemagglutination and the IAT.  The D– typing persisted until the patient’s death in September 2006.  To study the underlying cause of the change in D type, PCR-based assays were performed on DNA extracted from peripheral WBCs from the patient’s sample collected in August 2006.  No amplification was obtained using primers designed to amplify RHD exons 5, 8, or 10, and intron 4.  Very weak amplification was obtained using

Ann Murdock, Deborah Assip, Kim Hue-Roye, Christine Lomas-Francis, Zong Hu, Sunitha Vege, Connie M. Westhoff, Marion E. Reid

Immunohematology, Volume 24 , ISSUE 4, 160–164

Article | 17-February-2021

Identifying obstetrics patients in whom RHD genotyping can be used to assess risk of D alloimmunization

The D antigen is different from many other blood group antigens in that the antigen is not derived from one or a few amino acids, but rather from the presence of the entire protein; thus it contains many epitopes. Genetic variation within the RHD gene can alter expression of the antigen both qualitatively and quantitatively. A D protein that lacks one or more of the epitopes is referred to as a partial D antigen, and loss of epitopes is associated with risk of alloimmunization from exposure to

T.N. Horn, J. Keller, M.A. Keller, L. Klinger

Immunohematology, Volume 36 , ISSUE 4, 146–151

Report | 01-December-2019

Molecular background of RH in Bastiaan, the RH:–31,–34 index case, and two novel  RHD alleles

available reagents. We tested a cohort of African Americans to estimate the frequency of the RHCE*ce 48C, 733G, 1006T allele, and in addition found two novel RHD alleles. Hemagglutination tests and DNA analyses were performed by standard methods. Analyses revealed homozygosity for RHCE*ce 48C, 733G, 1006T in Bastiaan. RBCs from Bastiaan were strongly agglutinated by three commercial anti-e reagents. Testing RBCs from people homozygous for RHCE*ce 48C, 733G, 1006T showed that anti-e MS16, MS17, and MS63

Marion E Reid, Christine Halter Hipsky, Randall W. Velliquette, Christine Lomas-Francis, Kathleen Larimore, Coral Olsen

Immunohematology, Volume 28 , ISSUE 3, 97–103

Article | 17-February-2021

Weak D types 38 and 11: determination of frequencies in a Brazilian population and validation of an easy molecular assay for detection

D antigen is very important in transfusion practice because of its high immunogenicity and involvement with post-transfusion hemolytic reactions and hemolytic disease of the fetus and newborn.1 The RHD locus is complex, and diverse gene variations (point mutations, insertions, deletions, and gene conversions) can affect the RhD phenotype and lead to variant antigens.2–4 RhD variants may explain red blood cell (RBC) alloimmunization in the case of partial antigens or can result in

M.R. Dezan, V.B. Oliveira, M. Conrado, F. Luz, A. Gallucci, T.G.M. Oliveira, E.C. Sabino, V. Rocha, A. Mendrone, C.L. Dinardo

Immunohematology, Volume 36 , ISSUE 2, 47–53

Case report | 09-October-2019

Two cases of the variant RHD*DAU5 allele associated with maternal alloanti-D  

(HDFN) as D alloimmunization can occur with some D variants. Here, we describe two cases of the RHD*DAU5 allele associated with maternal alloanti-D in patients of African ancestry. Two obstetric patients were initially serologically classified as D+ with negative antibody detection tests on routine prenatal testing. Repeat testing at delivery identified anti-D in both patients with no history of RhIG administration or transfusion. DNA sequencing revealed that both patients possessed the RHD*DAU5

Jennifer A. Duncan, Susan Nahirniak, Rodrigo Onell, Gwen Clarke

Immunohematology, Volume 33 , ISSUE 2, 60–63

Case report

Weak D type 67 in four related Canadian blood donors

donors are investigated by other methods. We describe four weak D type 67 (RHD*01W.67) donors whose samples tested as D– by automated microplate and manual methods but were later determined to be D+ by automated solid-phase and RHD gene analysis. Solidphase serologic and molecular typing results of all four donors were identical. It was identified that the donors are of EnglishIrish descent; two are brothers and the others are cousins.  Transfusion of blood from one of these donors likely

Philip Berardi, Emma Bessette, Michiko Ng, Nancy Angus, Debra Lane, Lise Gariepy, Katerina Pavenski, Gorka Ochoa-Garay, Jacqueline Cote, Mindy Goldman

Immunohematology, Volume 31 , ISSUE 4, 159–162

Case report | 12-March-2020

Alloimmunization to the D antigen by a patient with weak D type 21

Antibodies of apparent D specificity may be found in D+ patients. We report a D+, multi-transfused Caucasian woman with myelodysplasia who exhibited several alloantibodies. One antibody was a moderately strong (2+) anti-D that persisted for 9 months, until the woman died. Molecular analysis of the patient’s RHD gene identified the rare weak D type 21 (938C>T) allele. D alloantibodies do not occur in patients with most weak D types, but some patients with a weak D phenotype, including

Heather McGann, Robert E. Wenk

Immunohematology, Volume 26 , ISSUE 1, 27–29

Report | 01-December-2019

Identifying D-positive donors using a second automated testing platform

Because of the variability of D expression, one method may be inadequate to correctly classify donors with variant RHD alleles. We evaluated the use of a solid-phase automated platform (ImmucorGamma Galileo) to confirm D– test results obtained on first-time donors on the Beckman Coulter PK7300 automated microplate test system. Samples with discordant results were analyzed by serologic tube methods, RHD genotyping using the BLOODchip platform (Progenika), and, if necessary, sequencing. We

Mindy Goldman, Ilona Resz, Jacqueline Cote, Gorka Ochoa, Nancy Angus

Immunohematology, Volume 29 , ISSUE 3, 97–100

Case report | 01-December-2019

Serologic and molecular characterization of D variants in Brazilians: impact for typing and transfusion strategy

Rh discrepancies are a problem during routine testing because of partial D or weak D phenotypes. Panels of monoclonal antibodies (MoAb) are being developed to identify D variants such as partial D and weak D when there are anomalous D typing results; however, molecular characterization offers a more specific classification of weak and partial D. The weak D and partial D phenotypes are caused by many different RHD alleles encoding aberrant D proteins, resulting in distinct serologic phenotypes

Débora Castilho Credidio, Jordão Pellegrino Jr., Lilian Castilho

Immunohematology, Volume 27 , ISSUE 1, 6–11


Multiplex ligation-dependent probe amplification assay for blood group genotyping, copy number quantification, and analysis of  RH variants

, and software for analysis of the MLPA results is available free of charge. In addition to the analysis of genetic variation in blood group genes, a major advantage of the test is the ability to detect aberrations in gene copy numbers, which is especially useful for the determination of homo- or hemizygous status of RHD or other blood group genes and for detection of blood chimerism. A relatively large number of RH wild-type and mutation-specific probes are included in the assay, allowing an

Barbera Veldhuisen, C. Ellen van der Schoot, Masja de Haas

Immunohematology, Volume 31 , ISSUE 2, 58–61

Review | 09-October-2019

DEL phenotype

are associated with the RHD*DEL1 or RHD*01EL.01 allele. The prevalence of DEL phenotypes has been reported among D– Han Chinese (30%), Japanese (28%), and Korean (17%) populations. The prevalence of DEL phenotypes is significantly lower among D– Caucasian populations (0.1%). Among the 3–5 percent of African individuals who are D–, there are no reports of the DEL phenotype. Case reports from East Asia indicate that transfusion of DEL RBCs to D– recipients has been

Dong Hyang Kwon, S. Gerald Sandler, Willy Albert Flegel

Immunohematology, Volume 33 , ISSUE 3, 125–132

Case report | 01-December-2019

Molecular analysis of patients with weak D and serologic analysis of those with anti-D (excluding type 1 and type 2)

included autologous controls, direct antiglobulin test, elution, and titration of anti-D before and after adsorption of serum onto autologous RBCs. From molecular analyses, 459 individuals exhibited a weak D type. We described seven novel RHD variant alleles. The most frequent types of weak D were type 1 (30.1%), type 2 (23.7%), type 4.0 (10.2%), type 4.2.2 (20.3%), type 11 (3.9%), and type 15 (3.7%). Anti-D was identified in the sera of 9 of 47 individuals with weak D type 4.0, in 14 of 93 with weak D

Bach-Nga Pham, Michèle Roussel, Dominique Gien, Maryline Ripaux, Carine Auxerre, Pierre-Yves Le Pennec, Christine Andre-Botte

Immunohematology, Volume 29 , ISSUE 2, 55–62

Case report | 01-December-2019

Molecular RH blood group typing of serologically D–/CE+ donors: the use of a polymerase chain reaction–sequence-specific primer test kit with pooled samples

The known presence of RHD blood group alleles in apparently D– individuals who are positive for C or E antigens leads to an appropriate investigation for the RHD gene on the red blood cells (RBCs) of D– blood donors, thus preventing their RBCs from immunizing D– recipients. Ready-to-use polymerase chain reaction–sequence-specific primer (PCR-SSP) typing kits are available and allow single-sample results. The need to perform this testing on a large number of donors

Donatella Londero, Mauro Fiorino, Valeria Miotti, Vincenzo de Angelis

Immunohematology, Volume 27 , ISSUE 1, 25–28

Case report | 01-December-2019

Weak D type 42 cases found in individuals of European descent

Patient samples were referred to our immunohematology reference laboratory to investigate the presence of a weak D antigen. In the last 3 years, 26 samples were received. Serology and molecular analyses were performed to identify the weak D variant. RHD mRNA from all patients was reverse transcribed, and cDNA was sequenced. The results were compared with a normal RHD sequence to identify the polymorphisms causing the weak D phenotype. Five different already known RHD variants were observed

Maryse St-Louis, Martine Richard, Marie Côté, Carole Éthier, Anne Long

Immunohematology, Volume 27 , ISSUE 1, 20–24

Report | 12-March-2020

RHCE*ceAR encodes a partial c (RH4) antigen

procedures. RBCs from the patient typed C+c+ but his plasma contained alloanti-c. DNA analyses showed the presence of RHCE*Ce in trans to RHCE*ceAR with RHD*D and RHD*Weak D Type 4.2.2. The amino acid changes on RhceAR are such that a C+c+ patient made alloanti-c. This case shows that RhceAR carries a partial c antigen and illustrates the value of DNA testing as an adjunct to hemagglutination to aid in antibody identification in unusual cases.

Marion E. Reid, Christine Halter Hipsky, Christine Lomas-Francis, Akiko Fuchisawa

Immunohematology, Volume 26 , ISSUE 2, 57–59

Report | 25-March-2020

Rapid, single-subject genotyping to predict red blood cell antigen expression

isolated from fresh and 1- and 2-week-old stored blood from 20 donors with known ABO and Rh phenotypes and was used for ABO, RHD, and RHCE genotyping using SSPs.  The amplicons were analyzed using gel electrophoresis and a novel microfluidic onchip electrophoresis system.  Analysis of DNA from fresh and 1- and 2-week-old blood by SSP and gel electrophoresis yielded the correct ABO, RHD, and RHCE type in all samples, but with DNA from 2-week-old stored blood the amplicons were more difficult

Stefanie L. Slezak, Sharon Adams, Hallie Lee-Stroka, Joshua E. Martin, Lorraine Caruccio, David F. Stroncek

Immunohematology, Volume 24 , ISSUE 4, 154–159

Article | 14-October-2020

Antibodies detected in samples from 21,730 pregnant women

Although anti-D is still the main cause of HDN, many other antibodies have been implicated. From September 1995 to April 2000,screening for RBC antibodies was performed on samples from 21,730 pregnant women regardless of RhD type. Standard tube and gel methods were used. Anti-D was identified in 254 samples;other antibody specificities were detected in 376 samples, for a total of 630 antibodies. For this study, 522 antibodies were considered clinically significant. The incidence of potentially

Snezana Jovanovic-Srzentic, Milan Djokic, Nenad Tijanic, Radmila Djordjevic, Nada Rizvan, Darko Plecas, Dejan Filimonovic

Immunohematology, Volume 19 , ISSUE 3, 89–92

Article | 18-October-2020

The Rh blood group system: the first 60 years of discovery

Christine Lomas-Francis, Marion E. Reid

Immunohematology, Volume 16 , ISSUE 1, 7–17

Article | 16-November-2020

Rhmod phenotype: a parentage problem solved by denaturing gradient gel electrophoresis of genomic DNA

support this hypothesis, DNA analysis of the RHD and RHCE genes was performed on the five family members. Polymerase chain reaction (PCR) products from exons 2 and 5 were analyzed by denaturing gradient gel electrophoresis (DGGE). The DNA results corroborated the serologic findings and refuted the exclusion of paternity.

Fiona J. Steers, Maura Wallace, Marialuisa Mora, Ben Carritt, Patricia Tippett, Geoff Daniels

Immunohematology, Volume 12 , ISSUE 4, 154–158

Case report | 16-October-2019

A delayed and acute hemolytic transfusion reaction mediated by anti-c in a patient with variant RH alleles

The Rh system is the most complex of the human blood groups. Of the 55 antigens that have been characterized, the system’s principal antigens D, C, E, c, and e are responsible for the majority of clinically significant Rh antibodies. In the last few years, advancements in molecular testing have provided a wealth of information on the genetic diversity of the Rh locus. This case report describes a patient with variant RHD*DAR alleles inherited in conjunction with two compound heterozygote

Tiffany K. Walters, Thomas Lightfoot

Immunohematology, Volume 34 , ISSUE 3, 109–112

Case report | 01-December-2019

Posttransplant maternal anti-D: a case study and review

, the antibody screen was negative. After the patient was admitted for the nonviable pregnancy, the products of con-ception were found to be D+ by DNA testing for RHD. There were no documented transfusions or pregnancies during the interval in which anti-D appeared. The timing of the alloimmunization was unusual. In a subsequent pregnancy, fetal D typing was performed by molecular methods.

Lisa Senzel, Cecilia Avila, Tahmeena Ahmed, Harjeet Gill, Kim Hue-Roye, Christine Lomas-Francis, Marion E. Reid

Immunohematology, Volume 28 , ISSUE 2, 55–59

Article | 15-April-2020

Serologic and molecular genetic management of a pregnancy complicated by anti-Rh18

her serum. No potential donors were identified among family members or within the American Rare Donor Program;therefore,a unit of the patient’s RBCs was collected one week before her planned caesarian section. To improve our ability to supply blood for this patient in the future,molecular testing was performed. The patient was found to be homozygous for an RH haplotype in which a variant RHD*DAR, is linked to a variant RHCE*ceAR. The DAR-ceAR haplotype has been described in Dutch-African

Richard L. Haspel, Dawn Michelle, Richard M. Kaufman, Sunitha Vege, Connie M. Westhoff

Immunohematology, Volume 22 , ISSUE 3, 132–135

Case report | 14-October-2020

Moderate hemolytic disease of the newborn (HDN) due to anti-Rh17 produced by a black female with an e variant phenotype

cause mild to fatal HDN. We report an example of anti-Rh17 produced by a black female with an e variant RBC phenotype that caused moderate HDN. A panel of seven monoclonal anti-e demonstrated her RBCs carried a variant e antigen, and her genotype was RHD, RHce by PCR-RFLP analysis. Amniotic fluid with ΔOD450 values from 30 to 35 weeks’ gestation predicted moderate HDN probability by the Liley method. At 38+ weeks, a viable 3165 g female infant was delivered. The infant’s direct

Marla C. Brumit, Gary E. Carnahan, James R. Stubbs, Jill R. Storry, Marion E. Reid

Immunohematology, Volume 18 , ISSUE 2, 40–42

Article | 28-April-2020

Incidence of weak D in blood donors typed as D positive by the Olympus PK 7200

+) at IS were further typed for weak D by the IAT. The weak D samples were RHD genotyped by allele-specific PCR. Of 1005 donors tested, 4 (0.4%) were classified as weak D by one or more anti-D reagents. Polyclonal anti-D reagent demonstrated weaker reactions when compared with the monoclonal blends. All weak D samples were found positive for exon 4, intron 4, and exon 10, a finding consistent with most D+ samples. The incidence of weak D found in this study is not significantly different from that

Candace Jenkins, Susan T. Johnson, Daniel B. Bellissimo, Jerome L. Gottschall

Immunohematology, Volume 21 , ISSUE 4, 152–154

Article | 15-April-2020

Molecular characterization of GYPB and RH in donors in the American Rare Donor Program

referred were hrB– and carry at least one hybrid RHD-CE(3-7)-D gene that encodes a variant C antigen linked to RHCE*ceS that encodes the VS+V– phenotype. Surprisingly, the majority of donors were heterozygous, some even carrying conventional alleles, suggesting that the loss of expression of the hrB epitopes on RBCs is a dominant phenotype. Although antigen-matching of patients with SCD with donors for C, E, and K antigens has decreased the incidence of alloimmunization, some patients still

Sunitha Vege, Connie M. Westhoff

Immunohematology, Volume 22 , ISSUE 3, 143–147

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