Anti-D alloimmunization by Asia type DEL red blood cell units in a D-negative Thai patient.

BACKGROUND: DEL phenotype is a rare Rh variant that cannot be detected by routine serological typing, and DEL individuals are thus typed D-negative (D-). Anti-D alloimmunization has been reported in "true" D- patients receiving DEL red blood cells (RBCs). CASE PRESENTATION: A 17-year-old, D- Thai male patient suffering from immunodeficiency syndrome with negative antibody screening received RBC units from 17 serological D- donors over a period of seven months due to acute respiratory failure with anemia. Before the 12th transfusion, anti-D production was detected. He was later transfused with RBCs from six other apparent D- donors. In order to elucidate anti-D production, all 17 blood donors were investigated by replicative serological testing and molecular analysis to identify potential RHD gene variants. All donors were confirmed D- by routine method, but as many as 12/17 were positive by adsorption-elution testing. Molecular analysis showed that five donors, including four whose blood was transfused before anti-D production occurred, carry the Asia type DEL allele, and are thus predicted to express a DEL phenotype. These data clearly suggest that 1/ the alloimmunized D- patient was exposed to D antigen, 2/ our adsorption-elution test is currently defective to identify DEL RBCs, and 3/ molecular analysis is highly valuable for Asia type DEL allele screening. CONCLUSION: For the first time in Thailand, we report anti-D alloimmunization in a serological D- patient transfused by Asia type DEL RBC units. This work definitely supports the implementation of a dedicated policy for DEL blood management including molecular testing.

Hemolytic disease of the fetus and newborn caused by anti-sD antibody in a GP.Mur/Mur Thai mother and review of the prevalence of sD in Thai blood donors.

BACKGROUND: Low-prevalence antigen sD (MNS23) is encoded by GYPB c.173C > G. Hemolytic disease of the fetus and newborn (HDFN) due to anti-sD is rare. A mother delivered a newborn whose red blood cells (RBCs) were DAT-positive and was later diagnosed with HDFN. Serum from the mother was incompatible with the father's RBCs and was used to screen 184 Thai blood donors. This study aimed to investigate the cause of HDFN in a Thai family and determine the prevalence of sD in Thai blood donors. MATERIALS AND METHODS: Three family members and four blood donors were investigated in the study. Massively Parallel Sequencing (MPS) was used for genotyping. Standard hemagglutination techniques were used in titration studies, phenotyping, and enzyme/chemical studies. Anti-s, anti-Mia , anti-JENU, and anti-sD reagents were used in serological investigations. RESULTS: The mother was GYP*Mur/Mur. The father and the four donors were GYPB*s/sD predicting S - s + sD +. The baby was GYP*Mur/sD and his RBCs were Mia +, s + w with anti-s (P3BER) and JENU+w . RBCs from two GYPB*sD -positive blood donors reacted with anti-sD (Dreyer). Proteolytic enzyme α-chymotrypsin-treated sD + cells did not react with anti-sD (Wat) produced by the GP.Mur/Mur mother but reacted with the original anti-sD (Dreyer). DISCUSSION: This is the first report of HDFN due to anti-sD in the Asian population. The genotype frequency for GYPB*sD in a selected Thai blood donor population is 2.2% (4/184). Anti-sD should be considered in mothers with Southeast Asian or East Asian background when antibody identification is unresolved in pregnancies affected by HDFN.

Fatal haemolytic transfusion reaction due to anti-Ena and identification of a novel GYPA c.295delG variant in a Thai family.

BACKGROUND AND OBJECTIVES: High-frequency antigen Ena (MNS 28) is expressed on glycophorin A (GPA). En(a-) individuals can form anti-Ena when exposed to GPA. A Thai patient formed an antibody that reacted against all reagent red blood cells (RBCs). The patient received incompatible blood resulting in a fatal haemolytic transfusion reaction (HTR). This study aimed to characterize the antibody detected in the patient and investigate the cause of HTR. MATERIALS AND METHODS: Blood samples from the patient and three of his family members were investigated. Massively parallel sequencing (MPS) and DNA-microarray were used for genotyping. Standard haemagglutination techniques were used for phenotyping and antibody investigations. RESULTS: DNA sequencing showed the patient was homozygous for GYPA*M c.295delG (p.Val99Ter) predicting En(a-). Three family members were heterozygous for GYPA c.295delG. MPS and DNA-microarray predicted the patient was N- discordant with the N+ RBC phenotype. The patient's plasma was positive with enzyme/chemical-treated reagent RBCs but failed to react with En(a-) and Mk Mk RBCs. CONCLUSION: The GYPA c.295delG variant prevented GPA expression on RBCs resulting in En(a-) phenotype. The N+ phenotype result was probably due to the anti-N typing reagent detecting 'N' (MNS30) on GPB. The patient's alloantibody has anti-Ena specificity.