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 Table of Contents  
SHORT ARTICLE
Year : 2018  |  Volume : 3  |  Issue : 1  |  Page : 59-61

Anomalous blood grouping showing red cell mosaicism in a patient with acute leukemia


Lok Samarpan Regional Blood Center, Lokhat Sarvajanik Hospital, Surat, Gujarat, India

Date of Web Publication5-Apr-2018

Correspondence Address:
Dr. Sanmukh Ratilal Joshi
Lok Samarpan Regional Blood Center, Lokhat Sarvajanik Hospital, Surat, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_51_17

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  Abstract 


Background: The ABO blood groups are determined by forward grouping on red cells and are confirmed by reverse grouping on serum, both of which must tally to assign proper blood group to an individual. Any anomaly in blood group must resolve before transfusion. Aim: A patient with anomalous blood grouping required to be investigated as pretransfusion tests. Materials and Methods: ABO blood grouping protocol was followed. The patient's red blood cells (RBCs), showing mixed-field reaction, were separated into those showing agglutination from other remaining nonagglutinated RBCs by selective adsorption using anti-A1 lectin and subsequently disagglutinated by incubating with soluble salivary antigen from Group A secretor individual. Results: Of the two RBCs populations, one that was agglutinated by the lectin showed considerably stronger agglutination with anti-A antibody as compared to those that were not agglutinated. Conclusion: Weakened red cell A antigen was presumed to be due to underlying disease process in acute leukemia.

Keywords: Anomalous blood grouping, leukemia, red blood cell mosaicism


How to cite this article:
Joshi SR, Savaliya K, Rajapara M, Narang P. Anomalous blood grouping showing red cell mosaicism in a patient with acute leukemia. Glob J Transfus Med 2018;3:59-61

How to cite this URL:
Joshi SR, Savaliya K, Rajapara M, Narang P. Anomalous blood grouping showing red cell mosaicism in a patient with acute leukemia. Glob J Transfus Med [serial online] 2018 [cited 2018 Nov 20];3:59-61. Available from: http://www.gjtmonline.com/text.asp?2018/3/1/59/229335




  Introduction Top


ABO blood groups are hereditary in nature and determined by testing the red blood cell (RBCs) of an individual with known reagent antisera, the approach is known as the “forward” grouping. As there is a reciprocal relationship of the antigen on RBCs and corresponding antibody in serum, the blood group of a person is confirmed on serum of the individual tested with known antigens which is described as the “reverse” grouping. In the most cases, the forward and the reverse group match, i.e., an absence of the antibody (ies) denote a presence of corresponding antigen(s) on the RBCs of the individual. However, occasionally, the forward and reverse group do not tally creating a confusion in mind as to assign the proper blood group. As the alloantibodies to the ABO blood group antigens are regularly occurring and are clinically significant, the discrepant results must be resolved before selecting an appropriate blood unit for transfusion. There are several causes for such grouping anomaly, mainly due to the factors intrinsic to RBCs. Some of these have genetic bases and the others are acquired in nature. The latter category may be due to bacterial infections or malignant conditions. There are a few reports documented in literature to show an acquired loss of ABO blood group antigens on RBCs among the patient with leukemia.[1],[2],[3] We report here a rare case of grouping anomaly found in a patient with acute leukemia.


  Materials and Methods Top


Patient's blood specimen collected as clotted and anticoagulated was used for tests. Serological tests were performed as per standard serological methods.[4] Antisera used were of commercial origin (tulip diagnostics, span diagnostics, and orthoclinical diagnostics).

Isolation of the two populations, one getting agglutinated and the other remained unagglutinated when the patient's RBCs were incubated at room temperature with anti-A1 lectin, was carried out as was reported earlier [5],[6] with slight modifications as follows:

The saline-washed RBCs suspended in 3%–5% concentration were incubated with anti-A1 lectin at room temperature for 15 min. The content was centrifuged at 500 rpm for 30s just to allow the agglutinated RBCs to settle at the bottom of the tube. The top one-fourth layer of RBCs was aspirated in a clean tube labeled as “nonagglutinated” RBCs. The next two-fourth layer was discarded, and the bottom most layer of the agglutinated RBCs was labeled as the “agglutinated RBCs.” The agglutinated RBCs portion was mixed with Group A secretor saliva (diluted in saline) and was left at room temperature for 30 min under intermittent mixing to disagglutinate the RBCs. The RBCs, so separated, were washed with and suspended in normal saline to test with anti-A reagent.

The case details

A 47-year-old patient, was admitted to the hospital with acute renal failure. The patient was anemic, with hemoglobin level of 7.5 g/dL and platelet count of 10,000/cmm. With a total WBC count of 318,000/cmm with more than 90% blast cells, he was diagnosed with acute myeloid leukemia. The patient was never transfused nor underwent BMT. He was planned for transfusion of the 6 units of platelet concentrate and 2 units of RBCs. His blood specimen was sent to Lok Samarpan Blood Bank to provide required blood products.

The patient was grouped as A Rh(D) positive by cell grouping that corroborated with serum grouping. However, his RBCs reacted somewhat weaker with three different anti-A reagents showing a characteristic mixed-field agglutination pattern, i.e., a few agglutinates among the sea of free, nonagglutinated RBCs, under microscopic view [Figure 1].
Figure 1: Microscopic view of the mixed-field agglutination pattern obtained by testing the patient's red blood cells with anti-A

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While the “nonagglutinating” fraction of RBCs showed a weak agglutination, the “agglutinating” fraction displayed a strong agglutination with monoclonal anti-A reagent. When these two fractions of the RBCs were tested with antisera to MN and Rh-subtypes they showed a homologous reaction pattern suggesting thay that the RBCs were homogeneous in nature for these antigens tested.

The patient's brother and one of his two sons were grouped as A, RhD positive while the other son was grouped as O, RhD positive, keeping a possibility of the patient being genetically with normal A, and that the weak A on his current blood specimen could be due to an acquired loss of A associated with his underlying disease condition although the patient's blood group record before the present illness was not available.


  Discussion Top


While the blood group of an individual is determined by testing his/her RBCs with known reagent antisera (and referred as forward grouping), it is confirmed by testing his/her serum with known group A and B RBCs (referred as reverse grouping) as there is a reciprocal relationship of antigen on RBCs and corresponding antibody(ies) in serum. It is important that the forward group corroborates with the reverse group to assign proper group to an individual. ABO blood groups are hereditary features and remain good throughout the life of an individual. Transfusion of homologous blood to the recipient has paramount importance as safe transfusion practice.

Occasionally, the forward and the reverse ABO blood groups do not tally due to varied reasons.[7] The discrepant results in grouping may be due to the factors that are intrinsic to the RBCs or due to those that are extrinsic to the RBCs, i.e., in surrounding milieu. An absence of the expected antibody in reverse grouping indicates a presence of corresponding antigen of RBCs. This situation requires further elaborate investigations, for example, absorption, elution, and saliva testing to arrive at conclusion. Many of the anomalous results in ABO blood grouping are due to weaker variant of the ABO blood group antigens and are hereditary in nature,[8] while some of those could be due to an acquired phenomenon associated with certain bacterial infections [9],[10] and hematological malignancies.[2] The present case appears to be of similar kind as the patient was diagnosed as having acute leukemia.

Weakening of the ABO blood group antigens in leukemia is known for years. It could manifest as generalized reduction in antigen scores on the RBCs [2] or display an overwhelming suppression of the antigens on RBCs so as to render the red cells inagglutinable by the corresponding antisera.[1] In rare cases, the loss of antigen is confined to a part of the red cell population with remaining being with normal compliment of antigenic strength and can be isolated by differential absorption/neutralization methods.[5],[6] This feature gives rise to a mixed-field appearance under the microscopic view and resembles to red cell mosaicism associated with genetic chimera. The present case showing mixed-field agglutination pattern with anti-A appears to be of similar nature. The isolate of “agglutinated” RBC's showed distinctly stronger agglutination with anti-A antibody as compared to the ones isolated as “nonagglutinated” RBCs. Both the isolates of the RBCs showed an identical reaction pattern for other blood group antigens of the Rh and the MN blood group systems, thereby indicating that the alteration was confined to the ABO blood groups only. The patient's brother and one of his two sons were grouped as A, RhD positive while the other son was grouped as O, RhD positive, keeps open on a possibility of the patient being genetically with normal A phenotype, and that the weaker expression of A antigen on his current blood specimen could be due to an acquired loss of A associated with his underlying disease condition, though the patient's blood group record before the present illness was not available. Observations on loss of A or B antigens were documented.[5],[6],[11],[12]


  Conclusion Top


Anomalous blood grouping was attributed to weakening of A antigen due to underlying disease process.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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. 1
    
2.
Saichua S, Chiewsilp P. Red cell ABH antigens in leukaemias and lymphomas. Vox Sang 1978;35:154-9.  Back to cited text no. 2
    
3.
Pourazar A, Joshi SR, Sathe MS, Advani SH, Bhatia HM. Profile of ABH & I antigens in leukaemia. Indian J Med Res 1986;83:505-8.  Back to cited text no. 3
    
4.
Bhatia HM. Procedures in Blood Banking and Immunohaematology. Bombay: Published by Blood Group Reference Center, Indian Council of Medical Research; 1977. p. 1-140.  Back to cited text no. 4
    
5.
Bird GW, Wingham J, Chester GH, Kidd P, Payne RW. Erythrocyte membrane modification in malignant disease of myeloid and lymphoreticular tissues. II. Erythrocyte “mosaicism” in acute erythroleukaemia. Br J Haematol 1976;33:295-9.  Back to cited text no. 5
    
6.
Joshi SR, Dasgupta A, Ray V. Red cell mosaicism in a patient with leukaemia. Indian J Hematol Blood Transfus 1999;17:42-4.  Back to cited text no. 6
    
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. 7
    
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. 8
    
9.
Sathe MS, Bhatia HM. Two cases of intestinal obstruction with acquired group B antigen. Indian J Med Res 1970;58:863-5.  Back to cited text no. 9
    
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. 10
    
11.
Gold ER, Tovey GH, Benney WE, Lewis FJ. Changes in the group A antigen in a case of leukaemia. Nature 1959;183:892-3.  Back to cited text no. 11
    
12.
van der Hart M, van der Veer M, van Loghem J. Change of blood group B in a case of leukaemia. Vox Sang 1962;7:449-53.  Back to cited text no. 12
    


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