Haemolytic disease of the foetus and newborn caused by auto anti‐LW

Davies, Jane A.; Day, Sanjoy Kumer; Milne, Alexander; Roy, Ashok; Simpson, Shirley V.

doi:10.1111/j.1365-3148.2009.00936.x

Cited by 9 publications

(5 citation statements)

References 3 publications

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“…8,11 Beside the three alloantibodies, autoantibodies against the three LW antigens are common in individuals with warm-type autoimmune hemolytic anemia, 2,12 and autoanti-LW a has been reported in a case of hemolytic disease of the fetus and newborn. 13 The LW antigens reside on a 42-kDa RBC membrane glycoprotein known as LW or intercellular adhesion molecule 4 (ICAM4). 14 The ICAM4 glycoprotein is expressed on RBCs, erythroid precursor cells, and on other blood cells including T and B cells.…”

mentioning

confidence: 99%

“…Alloanti‐LW a and ‐LW b have been associated with mild hemolytic transfusion reactions,7‐10 while alloanti‐LW a , ‐LW b , and ‐LW ab are associated with mild hemolytic disease of the fetus and newborn . Beside the three alloantibodies, autoantibodies against the three LW antigens are common in individuals with warm‐type autoimmune hemolytic anemia, and autoanti‐LW a has been reported in a case of hemolytic disease of the fetus and newborn …”

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confidence: 99%

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Genetic variation of the wholeICAM4gene inCaucasians andAfricanAmericans

2014

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Background Landsteiner-Wiener (LW) is the human blood group system no. 16, which comprises 2 antithetical antigens, LWa and LWb and the high prevalence antigen LWab. LW is encoded by the Intracellular Adhesion Molecule 4 (ICAM4) gene. The ICAM4 protein is part of the Rhesus complex in the red cell membrane and is involved in cell-cell adhesion. Methods We developed a method to sequence the whole 1.9 kb ICAM4 gene from genomic DNA in 1 amplicon. We determined the nucleotide sequence of exons 1 to 3, the 2 introns and 402 bp 5′-UTR and 347 bp 3′-UTR in 97 Caucasian and 91 African American individuals. Results Seven variant ICAM4 alleles were found, distinct from the wild type ICAM4 allele (GenBank KF712272), known as LW*05 and encoding LWa. An effect of the LWa/LWb amino acid substitution on the protein structure was predicted by 2 of the 3 computational modeling programs used. Conclusions We describe a practical approach for sequencing and determining the ICAM4 alleles using genomic DNA. LW*05 is the ancestral allele, which had also been observed in a Neandertal sample. All 7 variant alleles are immediate derivatives of the prevalent LW*05 and caused by 1 single nucleotide polymorphism (SNP) in each allele. Our data were consistent with the NHLBI GO Exome Sequencing Project (ESP) and the dbSNP databases, as all SNPs had been observed before. Our study has the advantage over the other databases in that it adds haplotype (allele) information for the ICAM4 gene, clinically relevant in the field of transfusion medicine.

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confidence: 99%

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confidence: 99%

Genetic variation of the wholeICAM4gene inCaucasians andAfricanAmericans

2014

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“…Few cases of anti‐LW production stimulated by pregnancy have been reported [13, 15]. In one report, autoanti‐LW caused a mild HDFN [22]. RBCs from the baby were DAT positive.…”

Section: Discussionmentioning

confidence: 99%

“…RBCs from the baby were DAT positive. The baby had an elevated bilirubin level and received phototherapy [22]. Anti‐LW antibodies, although rarely clinically significant, needs to be distinguished from the clinically significant anti‐D [23].…”

Section: Discussionmentioning

confidence: 99%

A new high‐prevalence LW antigen detected by an antibody in an Indigenous Australian homozygous for LWA* c.309C>A variant

et al. 2022

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Background and Objectives: The LW gene encodes the LW glycoprotein that carries the antigens of the LW blood group system. LW antigens are distinct from D antigen, however, they are phenotypically related and anti-LW antibodies are often mistaken as anti-D. An antibody was detected in an Australian patient of Aboriginal descent who consistently typed as LW(a+bÀ). This study aimed to describe the antibody recognizing a high-prevalence antigen on the LW glycoprotein.Study Design and Methods: Samples from the patient and her four siblings were investigated. DNA was genotyped by single nucleotide polymorphism (SNP)microarray and massively parallel sequencing (MPS) platforms. Red blood cells (RBCs) were phenotyped using standard haemagglutination techniques. Antibody investigations were performed using a panel of phenotyped RBCs from adults and cord blood cells.Results: SNP-microarray and MPS genotyped all family members as LW*A/A, (c.299A), predicting LW(a+bÀ). In addition, a novel LW*A c.309C>A single nucleotide variant was detected in all family members. The patient and one of her siblings (M4) were LW c.309C>A homozygous. Antibody from the patient reacted positive to all reagent panel RBCs and cord blood cells but negative with RBCs from LW(aÀbÀ), Rh null and sibling M4. Antibody failed to react with RBCs treated with dithiothreitol. Conclusion:Antibody detected in the patient recognized a novel high-prevalence antigen, LWEM, in the LW blood group system. LWEM-negative patients who developed anti-LWEM can be safely transfused with D+ RBCs, however, DÀ is preferred.Accurate antibody identification can help better manage allocation of blood products especially when DÀ RBCs are in short supply.

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“…항-LW를 갖는 환자에게 RhD 음성 혈액제제 수혈과 Rh Immune Globulin (RhIG)의 예방적 투여가 불필요하게 고려되기도 한다. 2,3) 비록 항-LW가 태아신생아용혈성질환을 유발했던 1예의 보고가 있지만, 4) 심각한 용혈성 수혈반응이나 태아신생아용혈성질환을 유발했…”

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