RESUMO
BACKGROUND: Antigen "N" is a high-frequency antigen of the MNS blood groups and carried on glycophorin B that is resistant to enzymatic cleavage by trypsin, and provides differential diagnosis of its antibody specificity to N being present of glycophorin A. Naturally occurring IgM antibodies to N are known to be clinically insignificant, as against the IgG counterpart with clinical relevance. AIM: Auto-anti-"N" association with the bladder cancer was explored for its clinical significance as well as its interference in grouping anomaly. MATERIALS AND METHODS: A warm environment was created while blood sampling for the laboratory work up as the patient had a high-titer auto-cold agglutinin causing spontaneous hemagglutination. The antibody was tested by standard serological methods with the red cell, antisera, and enzymes prepared in house or obtained commercially. RESULTS: The case was admitted to hospital with high fever and hematuria; he was diagnosed with malaria and bladder cancer. He required transfusions in the face of severe anemia. His blood sample posed problems in compatibility tests due to autoantibody present. Serological workup revealed its specificity as anti-"N." CONCLUSION: Auto-anti-"N" as a cause of severe anemia could not be attributed to, for concurrent malarial infection. However, its presence may have some association with the underlying malignant condition.
RESUMO
BACKGROUND: The INDIAN blood group system comprises 4 antigens sensitive to enzymes and 2-aminoethyl isothiouronium bromide (AET). AIM: The patient's antibody was investigated for its specificity to the high-frequency antigens (HFA) of this system. MATERIAL AND METHODS: Low ionic strength solution (LISS)-tube/LISS-indirect antiglobulin test (IAT) methods were used. The patient's red blood cells (RBCs) were tested with antisera to HFA. Her antibody was tested with RBCs lacking the HFA. Furthermore, it was tested with RBCs as untreated or treated with enzyme or AET. The genetic sequence was studied for mutation in CD44 gene that encodes INDIAN antigens. RESULTS: The patient was grouped A1B, RhD+, antibody screening test positive, direct antiglobulin test negative. A negative autocontrol test had suggested to the alloantibody being present. Antibody had agglutinated RBCs in LISS-tube at RT and by LISS-IAT at 37°C. The RBCs of the 11-cell panel, those lacking HFA and from 50 random donors, were agglutinated by her antibody indicating its specificity to the HFA, though the RBCs of Lu (a-b-)/In (Lu) type showed a weaker reaction. The patient's RBCs were agglutinated by antisera to a number of the enzyme-sensitive HFA, including those of INDIAN blood groups. The antibody showed reduced reactivity with the RBCs treated with papain, chymotrypsin, and AET but resistant to trypsin and dithiothreitol. The patient's genetic sequence revealed a novel homozygous mutation 449G>A in exon 5 of CD44. CONCLUSION: The antibody to enzyme sensitive HFA was tested for serological and molecular genetics studies and found to be directed to the novel HFA, named as INRA of the INDIAN blood group system and was assigned a numerical symbol IN: 005 by the International Society of Blood Transfusion (ISBT).