Severe delayed hemolytic transfusion reaction secondary to anti‐At<sup>a</sup>

Cash, Kevin L.; Brown, Truman R.; Sausais, Laima; Uehlinger, Joan; Reed, Linda

doi:10.1046/j.1537-2995.1999.39080834.x

Cited by 16 publications

(14 citation statements)

References 8 publications

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“…The first paper referring to the At a blood group antigen, which can be responsible for severe hemolytic transfusion reactions 1 and mild hemolytic disease of the newborn, 2 dates back to the 1960s. Applewhaite et al 3 identified an antibody with a novel specificity in the serum of Mrs Augustine, when the red cells of her third child gave a positive direct antiglobulin reaction at birth.…”

Section: Introductionmentioning

confidence: 99%

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Daniels

Ballif

Helias

et al. 2015

Blood

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Section: Introductionmentioning

confidence: 99%

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Daniels

Ballif

Helias

et al. 2015

Blood

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“…A severe delayed HTR was also observed after multiple transfusions of At(a+) RBCs. 13 Recently, another case was reported in which a woman experienced an acute HTR attributed to anti-At a . 15 In addition, anti-At a has also been shown to be involved in rapid destruction of 51 Cr-labeled At(a+) RBCs in vivo and to give positive results in in vitro functional assays.…”

Section: Discussionmentioning

confidence: 99%

Anti-At^a in a renal transplant candidate: a case report

et al. 2020

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A patient with end-stage renal disease on chronic dialysis was admitted to the hospital for renal transplantation evaluation. Blood type and antibody detection tests were performed. The antibody detection test results were positive. Initial antibody identification studies indicated the presence of a panagglutinin. The patient's autocontrol was negative. The antibody was subsequently identified by a reference laboratory as anti-At a (Augustine), which is an extremely rare antibody due to the high prevalence of At a in the general population. A monocyte monolayer assay (MMA) was performed to assess the clinical significance of the antibody in the event that blood was needed for transfusion, and At(a-) RBCs were not available. The MMA results predicted the antibody to be capable of causing hemolysis in vivo. A brief historical review of the incidence and clinical significance of this antibody is included in this case report. Immunohematology 2020;36:104-107.

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“…Only one example of a case of mild HDFN caused by anti‐At a has been reported previously . Also, as an example of a severe haemolytic transfusion reaction caused by anti‐At a has been reported it is important to ensure that compatible blood is available should the mother require transfusion postdelivery. Pregnancies where there is a risk of HDFN in which the mother is At(a−) require careful monitoring and management to minimize any requirement for transfusion.…”

Section: Discussionmentioning

confidence: 99%

“…The negative phenotype At(a−) is rare worldwide and has only been identified in individuals of West African or West Indies ancestry . Examples of anti‐At a antibodies have been described in At(a−) individuals although the clinical significance has remained largely uncharacterized due to the rarity of reagents to detect this phenotype.…”

Section: Introductionmentioning

confidence: 99%

Genotyping confirms inheritance of the rare At(a−) type in a case of haemolytic disease of the newborn

McBean

Liew

Wilson

et al. 2015

The Journal of Pathology CR

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The Ata blood group antigen (now AUG2 in the Augustine system) is a high‐frequency antigen with negative phenotype At(a−) found only in individuals of African ancestry. In a twin pregnancy, the fifth pregnancy in a woman of African origin, serological investigations confirmed that the mother was At(a−) and anti‐Ata was detected. DNA samples were exome sequenced and alignment was performed to allow variant calling. It was confirmed that the single nucleotide polymorphism, rs45458701, within the SLC29A1 gene encoding the ENT1 protein, recently reported to be a basis of the At(a−) phenotype was also the basis of the phenotype in this family. The reagents for serological analysis required to identify the rare blood type present in this mother are held in only a few reference laboratories worldwide. This case highlights the utility of genetic methods in resolving complex investigations involving blood grouping and demonstrates that genotyping of variants associated with blood types present in specific ethnic groups may be the fastest method available for identification of the basis of fetomaternal incompatibilities.

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Severe delayed hemolytic transfusion reaction secondary to anti‐At^a

Abstract: Although anti-At(a) was previously described as being of uncertain clinical significance, this patient demonstrated the ability of the antibody to cause a severe delayed hemolytic transfusion reaction.

Cited by 16 publications

References 8 publications

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Anti-At^a in a renal transplant candidate: a case report

Genotyping confirms inheritance of the rare At(a−) type in a case of haemolytic disease of the newborn

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Severe delayed hemolytic transfusion reaction secondary to anti‐Ata

Abstract: Although anti-At(a) was previously described as being of uncertain clinical significance, this patient demonstrated the ability of the antibody to cause a severe delayed hemolytic transfusion reaction.

Cited by 16 publications

References 8 publications

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Lack of the nucleoside transporter ENT1 results in the Augustine-null blood type and ectopic mineralization

Anti-Ata in a renal transplant candidate: a case report

Genotyping confirms inheritance of the rare At(a−) type in a case of haemolytic disease of the newborn

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Resources

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Severe delayed hemolytic transfusion reaction secondary to anti‐At^a

Anti-At^a in a renal transplant candidate: a case report