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Year : 2010  |  Volume : 53  |  Issue : 4  |  Page : 889-890
Alloimmunization to both Rh and Kell system antigens (anti-C and anti-K) in a young thalassemic patient


1 Department of Transfusion Medicine, PGIMER, Chandigarh, Punjab, India
2 Department of Pediatrics, PGIMER, Chandigarh, Punjab, India

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Date of Web Publication27-Oct-2010
 

How to cite this article:
Arora S, Dhawan HK, Sachdev S, Patidar G, Sharma R R, Marwaha N, Trehan A, Marwaha R K. Alloimmunization to both Rh and Kell system antigens (anti-C and anti-K) in a young thalassemic patient. Indian J Pathol Microbiol 2010;53:889-90

How to cite this URL:
Arora S, Dhawan HK, Sachdev S, Patidar G, Sharma R R, Marwaha N, Trehan A, Marwaha R K. Alloimmunization to both Rh and Kell system antigens (anti-C and anti-K) in a young thalassemic patient. Indian J Pathol Microbiol [serial online] 2010 [cited 2019 Dec 10];53:889-90. Available from: http://www.ijpmonline.org/text.asp?2010/53/4/889/72041


Individuals exposed to red blood cell (RBC) alloantigens through transfusion, pregnancy or transplantation may produce antibodies. Thalassemic patients receiving multiple transfusions are at high risk of developing alloantibodies. We hereby report a case of a multiply transfused thalassemic patient who has developed alloantibody to two most important blood group systems after ABO, i.e. the Rh and Kell blood group systems.

A requisition was received for packed red cells (PRBC) from a thalassemia clinic for a 10-year-old patient with blood group B Rh (D) negative, who had received 150 blood transfusions since 6 months of age. The patient first developed anti-C alloantibodies and was receiving C antigen-negative blood since the last 6 months. An antibody screen using 3-cell panel (Diamed AG, Switzerland) revealed a positive reaction with cells 1 and 3, which was suggestive of anti-C, e, C w K, Fy b , Jk b , Le a , M and S antibodies [Table 1]. The 11-cell identification panel (ID panel) (Diamed AG, Switzerland) showed positive reactions with cells 1, 2, 4 and 6, which was suggestive of anti-C and anti-K alloantibodies [Table 1]. RBC from the screening and identification panels was treated with 0.2 M DTT to denature the Kell antigens. After DTT treatment, cell 3 from the screening panel and cell 6 from the ID panel showed a negative reaction, which confirmed the presence of anti-K antibodies along with anti-C antibodies. Autocontrol of the patient was negative at 4°, 22° and 37°C. Antigen typing of the patient's red cells 20 days after the last transfusion showed B RhD-, C-, E-, c+, e+ and K-. The antigen profile of the patient's mother was A Rh D+, C-, E+, c+, e+ and K- and the father was B Rh D-, C-, E-, c+, e+ and K-. Both parents were negative for C and K antigens thus supporting the patient's phenotype. Antibody screening is performed regularly for this patient before each transfusion. Both anti-C and anti-K are present in her serum even after 7 months of follow-up. She receives C and K antigen-negative blood and her pretransfusion hemoglobin is maintained at 9 g/dl.
Table 1: Results of screening and identification panel confirms anti- C and anti-K alloantibodies

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Despite there being numerous foreign epitopes on essentially all transfusions of nonautologous RBCs, transfusion is not a highly immunogenic stimulus. Even in response to multiple transfusions, alloimmunization to alloantigens on transfused RBCs has an overall frequency of approximately 2-6%. [1] However, it has been hypothesized that frequency of alloimmunization may vary with the underlying pathophysiology of the transfused patient. Age, sex, number of transfusions and time interval between transfusions are independent significant factors for antibody specificity. [2] Antibodies to some blood group antigens frequently cause hemolysis (clinically significant, e.g. ABO, Rh, Kell, Kidd, Duffy, MNSs, Lewis), whereas others cause no deleterious effect (clinically insignificant, e.g. Anti-LW, Ge, Xg, Sc, Chido, Rogers, Bg). The prevalence of alloantibodies in thalassemics in India is 4-7%. [3] The Rh and Kell system alloantibodies are most frequent. However, in a majority of the alloimmunized patients, usually one alloantibody is detected. Patients with alloantibodies against one blood group system are prone to the development of alloantibodies to other blood group systems due to genetic and acquired patient-related factors. A combination of anti-E and anti-Jkb has been reported from our center. [4] In the Rh and Kell blood group systems, multiple alloantibodies such as anti-E and anti-K, anti-D and anti-C and anti-C and anti-E have been described in the literature. The present case is the first report in which anti-C and anti-K are detected together in a thalassemic patient. These antibodies usually disappear if patients receive antigen-negative blood. Anti-C alone, without anti-D, is prone to loss during subsequent testing. [5] About 45% of the anti-C antibodies are lost within months as compared with 22% of the anti-K antibodies. [5] In the index case, both the antibodies are present even at 7 months follow-up.

At our institute, we issue ABO and Rh(D)-matched crossmatch compatible blood for our thalassemic patients. Antibody screening is performed regularly twice a year and also whenever there is an incompatible crossmatch. Ideally, thalassemics should be typed for ABO, Rh (D, C, E, c, e), Kell, Kidd, Duffy and Ss, which are clinically significant antigens, prior to starting transfusion therapy and should receive at least Rh and Kell-matched blood. Antibody screen should be performed each time before transfusion for these patients to determine the disappearance of existing antibodies or development of new antibodies. The alloimmunized individuals need to be continued on transfusions of antigen-negative blood to prevent anamnestic response despite disappearance of alloantibodies.

Our case re-emphasizes the need for RBC antigen typing before first transfusion, issue of antigen-matched blood (at least for Rh and K antigens) and regular antibody screen for already alloimmunized multi-transfused patients. These measures will help in decreasing the incidence of RBC alloimmunization and delayed hemolytic transfusion reaction in these patients.

 
   References Top

1.Heddle NM, Soutar RL, O'Hoski PL. A prospective study to determine the frequency and clinical significance of alloimmunization post-transfusion. Br J Haematol 1995;9:1000-5.  Back to cited text no. 1
    
2.Schonewille H, van de Watering LM, Loomans DS, Brand A. Red blood cell alloantibodies after transfusion: factors influencing incidence and specificity. Transfusion 2006;46:250-6.  Back to cited text no. 2
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3.Pradhan V, Badakere S, Vasantha K, Korgaonkar S, Panjwani S, Jajoo N. Antibodies to red cells in beta thalassaemia major patients receiving multiple transfusions: A short report. In J Hematolo Blood Transfu 2001;19:100-01.  Back to cited text no. 3
    
4.Thakral B, Saluja K, Sharma RR, Marwaha N, Marwaha RK. Early onset multiple alloimmunization (anti-E and anti-Jkb) in a thalassaemic. Clin Lab Haem 2006;28:286-7.  Back to cited text no. 4
    
5.Ramsey G, Larson P. Loss of red cell antibodies over time. Transfusion 1988;28:162-5.  Back to cited text no. 5
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Correspondence Address:
Neelam Marwaha
Department of Transfusion Medicine, PGIMER, Chandigarh - 160 012, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.72041

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