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 Table of Contents  
Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 80-82

ABO typing error resolution and transfusion support in a case of an acute leukemia patient showing loss of antigen expression

1 Department of Transfusion Medicine, All India Institute of Medical Science, Bhubaneswar, Odisha, India
2 Department of Transfusion Medicine, SCB Medical College, Cuttack, Odisha, India

Date of Submission26-Aug-2019
Date of Acceptance05-Dec-2019
Date of Web Publication26-Dec-2019

Correspondence Address:
Dr. Debasish Mishra
All India Institute of Medical Science, Bhubaneswar, Odisha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ctm.ctm_28_19

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ABO and RhD typing is an essential step before the transfusion of blood components to a patient. ABO blood group system is a significant group, which causes hemolytic transfusion reaction destroying donor red blood cells. Hence, ABO typing error should be resolved before transfusion. Especially acute leukemia patients, there is a loss of A, B, and H antigens. In this group of patients, no reaction was seen in Cell typing/forward grouping typing. An adsorption-elution study is required to support the correct blood type. Response with anti-A1, anti-AB, and anti-H in red cell typing and saliva testing is necessary to distinguish between different weak A subgroups. We presented a case of loss of A antigens and transfusion support to a leukemia patient for initiation of chemotherapy.

Keywords: ABO incompatibility, anti-A1 lectin, blood group discrepancy

How to cite this article:
Mishra D, Ray GK, Mahapatra S, Parida P. ABO typing error resolution and transfusion support in a case of an acute leukemia patient showing loss of antigen expression. Cancer Transl Med 2019;5:80-2

How to cite this URL:
Mishra D, Ray GK, Mahapatra S, Parida P. ABO typing error resolution and transfusion support in a case of an acute leukemia patient showing loss of antigen expression. Cancer Transl Med [serial online] 2019 [cited 2021 Jun 15];5:80-2. Available from: http://www.cancertm.com/text.asp?2019/5/4/80/274029

  Introduction Top

ABO typing includes forward typing or red cell typing and reverse typing or serum/plasma typing. Red cell typing was performed by testing red cell suspension against monoclonal anti-A and anti-B antisera. Similarly, serum/plasma typing was tested by serum/plasma against reagent A, B, and O cells. Before interpreting a correct ABO typing, red cell typing should agree with serum/plasma typing. ABO typing error may lead to an acute incompatible hemolytic transfusion reaction. Hence, before transfusion, error in ABO typing must be resolved to prevent hemolysis of incompatible donor red cells. ABO typing error/discrepancy can arbitrary divided into four types, i.e., I, II, III, and IV.[1] Type II discrepancy is mainly seen in forward typing either due to weak or loss of antigen expression in red cell surfaces.

There are few reports in which loss of A, B, and H antigens leads to weak antigen expression and error in ABO typing and defined as Type II blood group discrepancy.[2],[3],[4] ABO blood group antigens are most commonly affected by hematological malignancies.[5] This Type II blood group discrepancy can be resolved by enhancing the cell concentration or incubation time. Sometimes, incubation at 4°C for 1 h makes the agglutination adequate to resolve the discrepancy. Even after these steps, if the discrepancy persists, adsorption-elution studies and salivary studies may be helpful in resolving this type of ABO discrepancy. In a salivary study, basically, saliva is tested for the presence or absence of A, B, and H substances in saliva. Some ABO discrepancies are not resolved serologically where a molecular study is required. Here we reported a case of type II discrepancy and the resolution approach in a patient of acute leukemia patient after taking a written consent of the patient.

  Case Report Top

A 60-year female patient of acute leukemia was planned for chemotherapy. Her laboratory features were as follows: Hemoglobin (HB ) 5.5 g/dl, Hematocrit (HCT) 16.8 %, MCV 80.8 fl, MCH 26.4pg, MCHC 32.7 g/dl, TLC 28.4 × 103/cumm, Platelet count 20 × 103/cumm. So she was advised for blood transfusion prior to chemotherapy. ABO and RhD typing was done by column agglutination technology as per manufacturer's instruction (Ortho BioVue, Ortho Clinical Diagnostics, USA). The blood group was O positive in forward grouping, whereas in reverse grouping, there was only agglutination with B cell [Figure 1]. In order to confirm the blood group, forward grouping was repeated by standard test tube method as per our institutional protocol using anti-A, anti-B, anti-D, anti-A1 lectin and anti-H lectin (Tulip Diagnostics Private Limited, Goa, India), and the result is shown in [Table 1]. In concordance to reverse grouping and reaction of the patient's red cells with anti-AB, A blood group was suspected though there was an absence of reaction with anti-A even after incubation at 4°C for 1 h. Adsorption-elution method was performed as described in the American Association of Blood Banks (AABB) technical manual.[6] Adsorption of the patient's cells was done at 4°C with polyclonal anti-A (human source), and heat elution was performed at 56°C for 10 min. Eluate and supernatant of last wash were tested with three sets of A, B, and O cells. No reaction of A, B, and O cells with supernatant of last wash was taken as a control to validate the technique of heat elution. Eluate was showed agglutination with only A cells suggestive of the presence of A antigen on the patient's Red blood cell. Her saliva secretory status was determined using the hemagglutination inhibition test, as described in the AABB technical manual.[7] The soluble A, H antigens were present in saliva of the patient, which neutralized the anti-A and anti-H antisera. Hence, there was no agglutination of the A and O cells, suggesting the presence of A and H substances in the patient's saliva. All the above methods confirmed the blood group of the patient to be A positive. Hence, the patient was transfused with four units of Apositive packed red blood cells (PRBCs), and the HB of the patient was raised to 9 gm/dl after which chemotherapy was initiated.
Figure 1: Blood grouping of an acute leukemia patient

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Table 1: Reaction with Anti-A, A1, B, D, AB & H in test tube

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  Discussion Top

ABO typing of a patient is determined by testing red cell suspension with commercially available antisera (forward typing) and also by checking serum/plasma with known A, B, and O reagent red cells (reverse typing). Before giving correct ABO typing to a patient, both forward and reverse typing should match with each other. The discrepant result is due to either error in red cell typing or serum/plasma typing.[8] To solve this problem, numerous steps are followed including extended incubation, increasing cell-to-serum ratio as per requirement, adsorption, elution, saliva testing, and molecular technique. The ABO gene is located on chromosome 9. Itconsists of seven exons with the majority of the coding sequences in exon 6 and 7 which controls the expression of A, B antigens on surface of the RBCs. The amino acid substitutions within exon 7 determine whether A glycosyltransferase uses UDP-N-acetyl-D-galactosamine or B glycosyltransferase uses UDP-D-galactose sugars to synthesize A or B antigens, respectively.

Different causes of discrepant results in ABO typing are due to a weaker variant of the ABO blood group antigens and are mostly hereditary [9] or due to certain bacterial infections [10],[11] and hematological malignancies.[3]

The weakening of the ABO blood group antigens in leukemia patients could either a manifestation of quantitative reduction in antigen sites or antigenic expression on the RBC surface3 so that antisera unable to agglutinate red blood cells.[2] Weak A subgroups are divided into A3, Aend, Am, Ay, and Ael based on the strength of reaction with anti-A, anti-A, B, anti-H, adsorption-elution study, salivary substance (A, H), and the presence or absence anti-A1 in serum [Table 2]. Based on serological reactions and salivary testing, blood group of the patient was assumed to be Am subgroup, but it could not be confirmed due to the unavailability of molecular testing.
Table 2: Serological reaction finding in patients with weak A phenotypes

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In this case, forward typing error was resolved by the adsorption-elution method and saliva testing, and the patient was transfused with ABO identical PRBC. Correct ABO typing is a critical step in pretransfusion testing to provide safe transfusion to patients. In this case, though the patient could have been transfused with O-positive PRBC, for platelet and plasma transfusion, correct ABO type blood components were required.

  Conclusion Top

Loss of A antigen expression is very rare in routinely ABO typing. Such a discrepancy in ABO typing is resolved by extended incubation of forward grouping at room temperature and 4°C, saliva secretor studies, and adsorption-elution methods. Molecular methods are also required to know the prevalence of different subgroups. As hematological malignancy patients require multiple transfusions of different blood components, correct ABO typing is required for the prevention of adverse events.

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


Conflicts of interest

There are no conflicts of interest.

  References Top

Mishra D, Parida P, Mahapatra S, Sahoo BB. Resolving blood group discrepancy in patients of tertiary care centre in Odisha, India. Int J Res Med Sci 2018; 6: 2348–53.  Back to cited text no. 1
Hoogstraten B, Rosenfield RE, Wasserman LR. Change of ABO blood type in a patient with leukemia. Transfusion 1961; 1: 32–5.  Back to cited text no. 2
Saichua S, Chiewsilp P. Red cell ABH antigens in leukaemias and lymphomas. Vox Sang 1978; 35: 154–9.  Back to cited text no. 3
Pourazar A, Joshi SR, Sathe MS, Advani SH, Bhatia HM. Profile of ABH and I antigens in leukemia. Indian J Med Res 1986; 83: 505–8.  Back to cited text no. 4
Winters JL, Howard DS. Red blood cell antigen changes in malignancy: case report and review. Immunohematology 2001; 17 (1): 1–9.  Back to cited text no. 5
Roback JD, Grossman BJ, Harris T, Hiller CD, editors. Technical Manual- American Association of Blood Banks. 17th ed. Bethesda: AABB Press; 2011. p. 880–1.  Back to cited text no. 6
Roback JD, Grossman BJ, Harris T, Hiller CD, editors. Technical Manual- American Association of Blood Banks. 17th ed. Bethesda: AABB Press; 2011. p. 881–2.  Back to cited text no. 7
Klein HG, Anstee DJ. Mollison's Blood transfusion in Clinical Medicine. 11th ed., Ch. 4. USA: Blackwell Publishing, Inc.; 2005. p. 117.  Back to cited text no. 8
Bhatia HM, Sathe MS. Incidence of “Bombay” (Oh) phenotype and weaker variants of A and B antigen in Bombay (India). Vox Sang 1974; 27: 524–32.  Back to cited text no. 9
Sathe MS, Bhatia HM. Two cases of intestinal obstruction with acquired B antigen. Indian J Med Res 1970; 58: 524–32.  Back to cited text no. 10
Sathe M, Bhatia HM, Purandara NM. Acquired B character caused by E. coli 0124 bacterial infection: a case report. Indian J Med Res 1972; 60: 576–81.  Back to cited text no. 11


  [Figure 1]

  [Table 1], [Table 2]


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