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  • Immunohematology

 

Article | 17-February-2021

Concordance of two polymerase chain reaction–based blood group genotyping platforms for patients with sickle cell disease

rare donor registries is required to obtain high-prevalence antigen-negative blood for transfusion. Several studies have compared molecular genotyping platforms with serologic phenotyping in patients and donors, with excellent concordance rates.16,19–21 Two PCR-based molecular genotyping platforms commercially available in the United States for blood group genotyping are the human erythrocyte antigen (HEA) PreciseType (formerly HEA BeadChip; Immucor, Norcross, GA) and ID CORE XT (Progenika-Grifols

C.A. Sheppard, N.L. Bolen, G. Meny, M. Kalvelage, G. Ochoa-Garay

Immunohematology, Volume 36 , ISSUE 4, 123–128

Article | 26-October-2019

HEA BeadChipTM technology in immunohematology

Classic methods to determine human red blood cell (RBC) antigens are based on serologic testing. Thanks to increased knowledge of the molecular basis associated with many blood group antigens, it is currently possible to predict their presence or absence on the red cell membrane. Several molecular techniques have been developed to detect the most important allelic variations attributable to single nucleotide polymorphisms. The human erythrocyte antigen (HEA) BeadChip™ system manufactured

Cinzia Paccapelo, Francesca Truglio, Maria Antonietta Villa, Nicoletta Revelli, Maurizio Marconi

Immunohematology, Volume 31 , ISSUE 2, 81–90

Review | 09-October-2019

A Caucasian JK*A/JK*B woman with Jk(a+b–) red blood cells, anti-Jkb, and a novel JK*B allele c.1038delG

antisera. Nevertheless, in RBC genotyping (BioArray HEA BeadChip, Immucor, Warren, NJ) performed in our transfusion service on all patients with alloantibodies, her Kidd typing was JK*A/JK*B based on the Jka/Jkb single nucleotide polymorphism in exon 9 (c.838G>A, p.Asp280Asn). Genomic analysis and cDNA sequencing of her JK*B allele revealed a novel singlenucleotide deletion of c.1038G in exon 11, predicting a frameshift and premature stop (p.Thr346Thrfs*5) after translation of nearly 90 percent of

Glenn Ramsey, Ricardo D. Sumugod, Paul F. Lindholm, Jules G. Zinni, Jessica A. Keller, Trina Horn, Margaret A. Keller

Immunohematology, Volume 32 , ISSUE 3, 91–95

Original Paper | 09-October-2019

Modeling alloantibody formation to highincidence red blood cell antigens in immune responders using genotypic data  

Alloimmunization to red blood cell antigens is unpredictable and poorly understood. Patients who are negative for highincidence antigens (HIAs) are at risk for developing the corresponding antibodies. Molecular methods can easily predict the lack of an antigen and thus, the risk of an individual to become immunized. We examined the prevalence and risk factors for HIA alloimmunization in patients at risk based on genotyping results. Genotyping using a molecular method (HEA BeadChip&trade

Patricia A.R. Brunker, Keerthana Ravindran, R. Sue Shirey

Immunohematology, Volume 33 , ISSUE 1, 9–14

Article | 16-October-2019

Assessment of common red blood cell pretreatments to yield an accurate serologic antigen phenotype compared with genotype-predicted phenotype

EGA treatment in removing IgG from RBCs. This study aimed to compare the accuracy of the results obtained from the commonly used RBC pretreatment methods with the results from a genotype-predicted phenotype using the BeadChip platform. Table 1. Blood group antigens predicted by the HEA BeadChip genotyping panel Blood group system Antigens RH C, c, E, e, V, VS FY Fya, Fyb, Fyb silenced DO Doa, Dob, Hy, Joa SC Sc1, Sc2 DI Dia, Dib LW LWa, LWb CO Coa, Cob JK Jka, Jkb KEL

T. Horn, J. Hamilton, J. Kosanke, V.W. Hare, W. Kluver, W. Beres, S. Nance, M.A. Keller

Immunohematology, Volume 33 , ISSUE 4, 147–151

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