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| A patient with probable rare blood Group B(A) phenotype |
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Avineesh Chandra1, P M. Bala Bhasker2, Romesh Jain3, Rakesh Kumar1, Subodh Srivastava1
1 Department of Blood Bank, Regency Hospital Limited, Kanpur, Uttar Pradesh, India
2 Department of Transfusion Medicine, Sparsh MultiSpecialty Hospital, Bengaluru, Karnataka, India
3 Department of Transfusion Medicine, AIIMS, Bhopal, Madhya Pradesh, India
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| Date of Submission | 09-Nov-2021 |
| Date of Acceptance | 11-Dec-2021 |
| Date of Web Publication | 26-Sep-2022 |
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 Abstract | | |
Karl Landsteiner discovered ABO blood group system in the early 20th century, but still, uncertainty remains in immunohematology while detection of ABO subgroups or weaker variants. The presence of weak subgroups in patient samples gives rise to the discrepancy in forward (cell) and reverse (serum) grouping. We here report a case of the B(A) phenotype in a patient who was diagnosed with chronic liver disease with acute pancreatitis, requiring packed red blood cells due to anemia. The blood group discrepancy was resolved using serological testing and adsorption–elution technique. Blood grouping by the tube technique showed 2+ agglutination with anti-A antisera, strong agglutination (4+) with anti-B, anti-AB, and anti-D antisera, 4+ agglutination with A1 cells, and no agglutination with B cells and O cells in serum grouping. Results for both eluate and last wash were negative to all the donor cells used. This report highlights the importance of cell and serum grouping, solving blood group discrepancy, and also in providing crossmatch compatible blood components without delay. This rare phenotype in a patient is the first of its kind reported from India.
Keywords: ABO subgroups, B(A) phenotype, blood group discrepancy
How to cite this URL:
Chandra A, Bhasker P M, Jain R, Kumar R, Srivastava S. A patient with probable rare blood Group B(A) phenotype. Asian J Transfus Sci [Epub ahead of print] [cited 2023 Mar 23]. Available from: https://www.ajts.org/preprintarticle.asp?id=356869 |
| Introduction | |  |
The ABO blood group system plays a crucial role in transfusion and transplantation practices. Correct identification of the ABO blood group in blood donors and transfusion recipients is of paramount importance for compatible transfusion of red blood cells (RBCs) because minor errors can lead to fatal transfusion reactions.[1],[2] Serological methods are routinely used to determine the antigens of ABO blood group system and isoagglutinin in serum. Weak expression of A, B, and H antigens on the red cell surface is often inherited or acquired. They are probably the least frequently encountered and pose a challenge in routine immunohematology practice.[3] In B(A) phenotype, an autosomal dominant phenotype, there is a weak A expression on Group B RBCs.[4] Hence, it is usually detected as an ABO discrepancy during blood group confirmation. It could be missed if only the cell grouping is performed and may lead to mislabeling of the patient/recipient blood group. This may cause hemolysis in B(A) phenotype patients if a patient is transfused with A or AB packed RBCs (PRBCs) or might end up in crossmatch incompatibilities.
Therefore, some ABO subgroups require a molecular method to identify and also to correlate the change between DNA sequence variation in the ABO gene and the quality and quantity of blood group antigens on RBCs.[5] Here, we would like to share a case of the B(A) phenotype in a patient who was diagnosed with chronic liver disease (CLD) with acute pancreatitis. To the simplest of our knowledge, this is often the primary report of probable B(A) phenotype in a patient from India.
| Case Report | | |
A 65-year-old female was admitted to our tertiary care center with a 1-week history of pain in the abdomen, loss of appetite, and generalized weakness. A complete blood count revealed hemoglobin (Hb) of 7.8 g/dL. The patient's diagnosis was CLD associated with pancreatitis. Blood requisition was received at our blood bank for two units of PRBCs in view of anemia. The patient blood grouping was performed using a fully automated immunohematology analyzer (Matrix AutoMax-80, Tulip Diagnostics (P) Ltd, India) by cell and serum grouping on gel column agglutination technology. For cell grouping, the three microtubes used contained monoclonal anti-A, anti-B, and anti-D antisera in each well and for serum grouping, the three other microtubes used contained pooled A, B, and O cells in each well. The test result was reported as “Test Invalid” due to the blood group discrepancy observed in cell and serum grouping [Figure 1]. In cell grouping, the patient's red cells were reactive (2+) with anti-A antisera and strong (4+) agglutination with both anti-B and anti-D antisera, whereas in serum grouping, 4+ agglutination was found in a microtube containing A pooled cells with no agglutination in microtubes containing B pooled cells.
Repeat blood grouping was administered by the conventional tube technique (CTT) with another fresh sample using commercially available monoclonal antisera manufactured by Tulip Diagnostics (P) Ltd, India. The results corroborated with the previous results. The results of cell grouping when performed at room temperature (RT) showed 2+ agglutination with anti-A antisera, strong agglutination (4+) with anti-B, anti-AB, and anti-D antisera, and 3+ agglutination with anti-H antisera. There was no agglutination observed with anti-A1 lectin. In serum grouping, there was 4 + agglutination with A1 cells, 3 + agglutination with A2 cells, and no agglutination with B cells, O cells, and in auto control. There was no enhancement in grades of reaction when performed at 4°C, 37°C, in the anti-human globulin (AHG) phase and even after prolonged cold incubation. All these serological findings [Table 1] lead to a possibility of “A weak B” Rh D-positive phenotype with anti-A1 antibodies. The critical value for anti-A immunoglobulin M titer determined by CTT was found to be 64 using A1 cells.
To check for the weak subgroup of A or rule out of possibility of A antigen, cold adsorption and heat elution were performed as described in the American Association of Blood Banks technical manual.[6] Adsorption of the patient's red cells was done at 4°C for 45 min with human polyclonal anti-A serum collected from three Group B donor samples. Heat elution was performed at 56°C for 10 min. The eluate and the “last wash” were tested in parallel with three different A, B, and O donor red cells at RT, 4°C, 37°C, and in the AHG phase. Results for both eluate and last wash were negative to all the donor cells used [Table 2]. Hence, the likelihood of a weak subgroup of A was unlikely. Further, the direct antiglobulin test, autologous control, and antibody screen were also negative using gel technique by a fully automated immunohematology analyzer. The test for cold autoantibodies was found to be negative when performed by CTT. Thus, the presence of anti-A antibody in serum grouping was corroborative to the Group B antigen on donor RBCs. In view of the above serological findings, we concluded it could be a case of probable B(A) phenotype. | Table 2: Results of cold adsorption and heat elution test with three different A, B and O donor red cells
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| Discussion | | |
The ABO gene is located at the long arm of chromosome 9 (9q34) and consists of 7 exons, among which the exons 6 and 7 harbor the majority of the exonic DNA encoding the enzyme's entire catalytic domain of the ABO glycosyltransferases. Studies showed that mutations of the ABO gene affected A and B glycosyltransferase activity and caused variant ABO phenotypes.[7] The different B(A) phenotype occurs due to specific mutations in the B gene that causes the B transferase to synthesize small amounts of A antigen.[8] However, this mutation occurred due to ABO gene exon 6 as well as exon 7, which was an exchange in amino acid of DNA at a different position.[9]
In the present study, this patient had no history of previous transfusion and no documented previous blood group. The family history of the patient revealed that the husband and children's blood group is A Rh D positive without any discrepancies. The patient's cell and serum grouping revealed Type II blood group discrepancy, and further testing revealed a probable B(A) phenotype. After serological workup and final interpretation of patient blood group, the patient was transfused with two units of crossmatch compatible O group RBCs, performed at AHG phase by gel technology. Both the units were transfused successfully without any adverse events. His posttransfusion Hb was 9 gm/dl but got expired after a 4-day stay in ICU due to worsened clinical condition. For further confirmation, saliva testing was not done due to the unavailability of sufficient samples, whereas molecular analysis and serum B glycosyltransferase level estimation were not done due to lack of facilities at our center.
This case report highlights the importance of performing both cell and serum groupings for all the patient samples received at the blood bank in order to rule out blood group discrepancies. Only performing cell grouping that is done as a routine practice at remote or district level blood centers will miss most of the weaker subgroups. This wrong practice may lead to mistyping of patients with weaker subgroups, crossmatch incompatibilities, delay in finding compatible blood units, and may lead to hemolysis if transfused with A or AB group PRBCs. To the best of our knowledge, this is the first case reported in patients with probable B(A) phenotype from India. A study with probable B(A) phenotype was reported in a blood donor from India by Jain et al.[10]
| Conclusion | | |
Weak subgroups of the ABO blood group system are rarely reported in routine practices. Such ABO discrepancies are to be resolved by advanced techniques such as adsorption–elution, saliva secretor studies, and molecular testing, especially in patients requiring blood and blood components. Due to identification error, this patient can be wrongly grouped as AB, which may lead to crossmatch incompatibilities if not tested adequately and resolved timely. This report emphasizes the importance of performing cell and serum grouping for all patient samples in routine as a policy to identify patient blood groups accurately and also in preventing delay in the administration of blood components in case of emergency.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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| 5. | Olsson ML, Irshaid NM, Hosseini-Maaf B, Hellberg A, Moulds MK, Sareneva H, et al. Genomic analysis of clinical samples with serologic ABO blood grouping discrepancies: Identification of 15 novel A and B subgroup alleles. Blood 2001;98:1585-93. |
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| 8. | Guo ZH, Xiang D, Zhu ZY, Liu X, Chen HP, Wang JL, et al. Serologic and molecular characterization of the B (A) blood group in the Chinese population. Immunohematology 2007;23:69-74. |
| 9. | Chen Q, Li J, Xiao J, Du L, Li M, Yao G. Molecular genetic analysis and structure model of a rare B (A) 02 subgroup of the ABO blood group system. Transfus Apher Sci 2014;51:203-8. |
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Correspondence Address:
P M. Bala Bhasker,
Department of Transfusion Medicine, Sparsh MultiSpecialty Hospital, Bengaluru, Karnataka
India
 Source of Support: None, Conflict of Interest: None DOI: 10.4103/ajts.ajts_166_21
[Figure 1]
[Table 1], [Table 2] |
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