A transfusion recipient lacking a high-incidence antigen (HIA) and has corresponding alloantibody pose a problem in providing compatible blood unit. We encountered a patient with an antibody to an HIA that required identification to assess if compatible blood could be organized. A 65-year-old male was posted for coronary artery bypass grafting surgery. His blood specimen collected in EDTA was referred to the blood bank to provide blood for transfusion. The patient, grouped AB RhD+, had an antibody reacting in saline and antiglobulin phases. It agglutinated all the red blood cells (RBCs) of the 11-cell panel and random donors, indicating specificity to an HIA, though one of his siblings was compatible. After ruling out specificity to HIAs such as H, Inb, and INRA (IN5), the specimen was referred to the New York Blood Centre for further work-up. The antibody reacted with examples of red cells lacking HIA, except those with the Emm− phenotype. The patient's RBCs were typed as Emm−. Anti-Emm in the patient appeared to be naturally occurring as there was no history of transfusion. Naturally occurring alloantibody to an HIA, identified as anti-Emm in phenotype Emm−, is rare and the first of its kind to be reported from India. The case was instrumental in recognizing the Emm as the new blood group system assigned with the symbol ISBT042.
Introduction:The identification of alloantibodies to high-frequency antigens (HFA) and subsequent transfusion management can be challenging and often poses a problem in finding the compatible blood for transfusion. The aim of this study was to investigate the specificity of the antibody to the HFA causing a hemolytic transfusion reaction (HTR) and procure the compatible blood unit for future transfusion. Case presentation:A 4-year-old female met with a head injury that led to intracranial bleeding and surgical intervention was required to remove blood clots. In the face of anemia, blood transfusion was planned. The pretransfusion tests on her blood sample revealed the presence of a pan-reactive alloantibody with hemolytic properties. She was transfused with 10 mL of the least incompatible red blood cells (RBCs) to which she reacted with signs of clinical hemolysis, i.e., chill, rigor, fever, and hemoglobinuria, on 3 different occasions. Despite her anemia, she was managed by medical intervention only. Her antibody reacted with all RBCs tested, except autologous and P-null (p phenotype) cells. Her RBCs did not react with anti-PP1Pk, which corroborated her phenotype as P-null. The genomic study revealed she was hemi- or homozygous or for a deletion of 26-bp in A4GALTexon 3, previously reported as causing the P-null phenotype and designated A4GALT*01N.019.Conclusion:This report documents a rare case of the P-null phenotype with an alloanti-PP1Pk causing a severe HTR to transfusion of the trial dose of the least incompatible blood. The case is the first example of this specific A4GALTmutation found in India.
BACKGROUND: Discrepancy in “forward/reverse” grouping leads to confusion in assigning ABO group to a person. It could be genetic in nature and classified according to the presence/absent of antigen on red blood cell (RBC) vis-a-vis corresponding alloantibody in plasma. AIM: The aim of the study was to investigate the grouping anomaly found in a recently delivered woman who required transfusion. MATERIALS AND METHODS: A standard protocol for investigation was followed. RESULTS: A 27-year-old female, gravida 4, para 3, was grouped O on forward grouping, but her serum did not agglutinate Group B RBCs tested. Absorption-elution study gave an active eluate from her sensitized RBCs with anti-B or anti-A+B. Saliva showed H, but no B antigens indicating to her Bel phenotype. However, 2-week latter in the follow-up study, her serum revealed a presence of complement binding high titer anti-B. The problem of missing anti-B on the previous occasion was attributed to hemagglutination inhibition caused by accumulated complement macromolecules on RBCs that gave rise to physical hindrance in the formation hemagglutination clumps. CONCLUSION: The unusual case of erroneous reversed grouping was attributed to complement-mediated hemagglutination inhibition. The positive eluate obtained from sensitized RBCs of the mother was considered to be due to a contamination of fetal RBCs in maternal circulation entered during her postpartum phase of pregnancy. It could also be due to a conversion of H to B antigen no matter in trace amount by the fetal B group-specific transferase percolated into maternal circulation.
BACKGROUND: Antibodies to the Kidd blood group are mainly red blood cell (RBC) immune, but a few reports on naturally occurring antibodies have been documented. AIM: The aim of this study is to study the anti-Jk(a) for its unusual reactivity with different serological methods. MATERIALS AND METHODS: Donor's plasma was tested with RBCs from in house donors and commercial panels by manual and automated devices. RESULTS: A 36-year-old male blood donor with naturally occurring anti-Jk(a) is detected by solid-phase assays and the gel card technique but not by the tube method. The IgG antibody with the titer of >32 was not a complement-fixing hemolysin, showed a reduced reactivity with enzyme-treated RBCs, and was detectable through 8 months' follow-up period. The donor was typed as (Jk(a−). CONCLUSION: An unusual naturally occurring anti-Jk(a) detected by solid-phase red-cell adherence but not reacting by tube technique reflected on the sensitivity of the methods used.
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