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

BACKGROUND

Low-prevalence antigen s (MNS23) is encoded by GYPB c.173C > G. Hemolytic disease of the fetus and newborn (HDFN) due to anti-s 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 s 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-Mi , anti-JENU, and anti-s reagents were used in serological investigations.

RESULTS

The mother was GYPMur/Mur. The father and the four donors were GYPBs/s predicting S - s + s +. The baby was GYPMur/sD and his RBCs were Mi +, s +  with anti-s (P3BER) and JENU+ . RBCs from two GYPBs -positive blood donors reacted with anti-s (Dreyer). Proteolytic enzyme α-chymotrypsin-treated s + cells did not react with anti-s (Wat) produced by the GP.Mur/Mur mother but reacted with the original anti-s (Dreyer).

DISCUSSION

This is the first report of HDFN due to anti-s in the Asian population. The genotype frequency for GYPB*s in a selected Thai blood donor population is 2.2% (4/184). Anti-s should be considered in mothers with Southeast Asian or East Asian background when antibody identification is unresolved in pregnancies affected by HDFN.