Home About us Editorial board Ahead of print Current issue Search Archives Submit article Instructions Subscribe Contacts Login 
  • Users Online:29
  • Home
  • Print this page
  • Email this page


 
 Table of Contents  
REVIEW ARTICLE
Year : 2020  |  Volume : 5  |  Issue : 2  |  Page : 120-125

Extended phenotyping of blood group antigens: Towards improved transfusion practices


Department of Transfusion Medicine, ICMR-National Institute of Immunohaematology, Mumbai, Maharashtra, India

Date of Submission23-Jun-2020
Date of Decision10-Aug-2020
Date of Acceptance19-Sep-2020
Date of Web Publication13-Nov-2020

Correspondence Address:
Swati Kulkarni
Department of Transfusion Medicine, ICMR-National Institute of Immunohaematology, Mumbai, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_56_20

Rights and Permissions
  Abstract 


Even though the International Society of Blood Transfusion has defined 38 blood group systems, only ABO and RhD are matched while selecting a compatible unit for blood recipients of Indian origin. Genetic disparity between a donor and a patient with reference to minor blood group antigens creates the risk of alloimmunization. The presence of red blood cell alloantibodies further creates the potential for serologic incompatibility, makes the selection of appropriate units for future transfusion more difficult, delays blood transfusion, and presents the risk of hemolytic disease of the newborn. Hence, there is a need to carry out extended blood group typing for antigens of clinical importance among donors and patients so that prophylactic antigen-matched blood can be given to a patient. Provision of antigen-matched blood will help in management of alloimmunized transfused-dependent patients carrying alloantibodies and/or autoantibodies. Typing of blood group antigens among large number of donors will also help in the development of antigen-negative inventories, develop indigenous red cell panels, and identify rare donors. Selection of blood group antigens for typing is important as it may not be always feasible to phenotype all the antigens. Based on the prevalence and immunogenicity of an antigen in a population, specific antigens have to be selected for typing so that the risk of alloimmunization reduces by strategic level of antigen matching. The aim of this review is to highlight the need for extended blood group phenotyping in different case scenarios and the methods available to do so. This review was performed by searching for keywords such as blood transfusion, red cell alloimmunization, partial antigen matching, rare blood donors, multitransfused patients, transfusion in thalassemics, molecular blood group genotyping, serology, and reagent red cell panels in PubMed and Google databases.

Keywords: Alloimmunization, antigen-negative inventories, blood group antigens, molecular genotyping, partial antigen matching


How to cite this article:
Kulkarni S, Maru H. Extended phenotyping of blood group antigens: Towards improved transfusion practices. Glob J Transfus Med 2020;5:120-5

How to cite this URL:
Kulkarni S, Maru H. Extended phenotyping of blood group antigens: Towards improved transfusion practices. Glob J Transfus Med [serial online] 2020 [cited 2020 Nov 24];5:120-5. Available from: https://www.gjtmonline.com/text.asp?2020/5/2/120/300630




  Introduction Top


There are 38 well-defined blood group systems having more than 350 antigens, but only ABO and RhD blood group status of the recipient and blood donor are taken into account when red blood cells (RBCs) are transfused (https://www.isbtweb.org/working-parties/red-cell-immunogenetics-and-blood-group-terminology). Minor blood group antigens are tested only if the recipient has been previously alloimmunized. Patients requiring chronic transfusion support are at the risk of alloimmunization because of disparity between donor and recipient antigenic profile. The chances of alloimmunization are higher if the donor and recipient are of different ethnic backgrounds with varied red cell antigenic profile. Immunogenicity of foreign antigens and number and frequency of transfusions also increase the risk of alloimmunization.

The presence of RBC alloantibodies creates the potential for serologic incompatibility, makes the selection of appropriate units for future transfusion more difficult, delays blood transfusion, and presents the risk of hemolytic disease of the fetus and the newborn (HDFN). According to literature reports, about 25% of such patients receive unsatisfactory transfusion support, and it may even be impossible to find suitable units in some cases.[1] Blood transfusion also predisposes a patient to formation autoantibodies, which may result in the development of autoimmune hemolytic anemia (AIHA), which can lead to increased hemolysis of transfused RBCs. Hence, it is important to phenotype minor RBC antigens of patients in a pretransfusion setting and blood donors to reduce the incidence of alloimmunization.

Aims and objectives

The aim of this review is to highlight the need for extended blood group phenotyping in different case scenarios and the methods available to do so. This review illustrates the various case scenarios where extended blood group phenotyping would have helped in preparing indigenous reagent panels and prevented red cell alloimmunization by provision of antigen-matched blood, thereby improving the transfusion outcome along with various serological and molecular methods currently available to do so.

Source of data

This review was performed by searching for keywords such as blood transfusion, red cell alloimmunization, partial antigen matching, rare blood donors, multitransfused patients, transfusion in thalassemics, molecular blood group genotyping, serology, and reagent red cell panels in PubMed and Google databases, following which a thorough search for systematic reviews and meta-analysis was done. Reference lists were cross-checked for relevant citations, and more searches were done until the desired information was gathered. Furthermore, we have several publications and work done in this field which has expanded our knowledge and helped in this review.


  Need for Extended Phenotyping Top


Extended phenotyping of minor blood group antigens in donors and patients for issuing antigen-matched blood can reduce the frequency of transfusions, thereby decreasing the risk of alloimmunization and posttransfusion reactions.[2] It also reduces iron overload and subsequent iron chelation as number of transfusions required may reduce due to better survival of transfused RBCs. In already alloimmunized patients, antigen-matched blood can reduce the chances of producing antibodies against other antigens in recipients. Extended phenotyping is important in:

Managementofpatientswithalloantibodiesandpreventionofalloimmunizationinmultitransfusedpatients

The high rate of alloimmunization in multitransfused patients is mainly due to lack of total compatibility of RBC antigens between the donors and recipients. The problem further increases if the donor and recipient are belonging to different ethnic groups. Furthermore, repeated transfusions among these patients increase with the risk of alloimmunization. The rates of alloimmunization in the transfused population range between 2.6% and 60% depending on the clinical and laboratory characteristics of the studied recipient group and the testing methods employed.[3] In sickle cell disease patients, the rate of alloimmunization ranges between 19% and 43% without the implementation of extended phenotype matching.[4] Phenotype-matched RBCs for the clinically important antigens result in decreased alloimmunization among these patients. One such study showed a decrease in the alloimmunization rate from 35% to 0%, with the exclusive use of phenotype-matched RBCs (C, c, E, e, K, S, Fya, and Fyb) in a 12.5-year period.[1]

Among thalassemics, RBC alloimmunization occurs at a rate of 5%–33% depending on their population homogeneity.[5],[6] The most important unexpected RBC alloantibodies are directed toward the Rh (D, C, E, c, and e) and Kell (K) antigens, followed by antigens of the Duffy, Kidd, and MNS blood group systems. Singer et al. reported that alloimmunization rates were lowered by phenotype matching for Rh and Kell from 33% to 2.8%.[5] Pujani et al. reported no alloimmunization in thalassemics from India who were received partially better matched blood (matched for ABO, Rh cDE, and Kell antigens).[7] Hence, for chronically transfused patients, RBC phenotyping should be performed on the initial pretransfusion sample or genotyping must be used to correctly predict the patient's RBC antigen profile to enable transfusion of antigen-matched blood.

Managementofpatientswithwarmautoantibodies

Patients with warm autoantibodies are at high risk for delayed hemolytic transfusion reactions (DHTRs) due to the presence of alloantibodies. In a patient with newly diagnosed AIHA, finding the appropriate RBC product for transfusion can be challenging. In patients with warm autoantibodies, 20%–40% show the presence of clinically significant alloantibodies.[8] The presence of a strong autoantibody makes the detection on an underlying alloantibody difficult. RBC typing using molecular methods in these patients helps in the detection of possible alloantibodies the patient is capable of forming as the correct antigen profile of the patient will be determined. In addition, antigen-matched RBCs will prevent future alloimmunization and DHTRs as well as circumvent the need of absorption studies. Shirey et al. adopted an algorithm for providing prophylactic antigen-matched RBCs to twenty consecutive patients with warm autoantibodies requiring chronic RBC transfusions. In 60% of these patients, adsorption studies could be precluded. This provided flexibility in their transfusion management.[8]

Increasingantigen-negativedatabaseandbuildingupdonorinventories

Procurement of antigen-matched blood for patients with antibodies to clinically significant high incidence antigens (e.g., Kp(b−), Lu(b−), and Yt(a−)) or combination of two or more common antigens is difficult and challenging in a short time. Extended phenotyping of various blood group antigens at multiple loci on large scale of regular donors can help build up antigen-negative database and establish a donor registry.[9] This will increase the probability of finding highly antigen-matched blood. Donors, especially those who are negative for a single common antigen or a combination of these antigens, also vary in different countries depending on the frequency of these blood group antigens present in the population. It is, therefore, important to have an appropriate rare donor program to identify donors and create antigen-negative registry for single high-frequency common antigens or combination of common antigens at local and regional levels. Furthermore, selection of donors for patients with multiple antibodies can be achieved in a more efficient manner.

In our study at the Department of Transfusion Medicine, ICMR-National Institute of Immunohematology, among 1221 regular donors, for clinically important common antigens of Rh, Duffy, Kell, Kidd, and MNS blood group systems, we identified donors lacking clinically important single or a combination of common antigens.[10] Two hundred and sixty-one donors lacked a combination of clinically important common antigens C, D, e, Fya, Jka, and s. Among RhD-positive donors, 15.56% lacked a combination of two or three common antigens. [Figure 1] represents the percentage of donors lacking two or more blood group antigens. Of all donors, 3.2% lacked Fya and Jka antigens, 1.96% Fya and s, 1.88% Jka and s antigens, and 0.57% lacked three common antigens. The study findings have helped us to create antigen-negative inventory. All these rare donors will prove useful for efficient management of transfusion therapy in patients with multiple antibodies against common antigens.
Figure 1: Percentage of donors lacking two or more blood group antigens

Click here to view


In another study, we analyzed 500 “O” group donors to create a database of 193 donors matching perfectly for Rh, Duffy, Kell, and Kidd antigens for 15 alloimmunized patients. When matched for the five common Rh antigens, three donors matching for R1R1, R1R2, R2r, and rr phenotypes were identified for one patient and two donors for R0r phenotype were identified per patient approximately. For 84 thalassemic patients who were nonalloimmunized, 405 donors were identified.[11]

Developing in-house panels

The detection and identification of RBC alloantibodies rely on the use of well-characterized reagent RBCs. O group regular donors are extensively phenotyped for various polymorphic antigens by commercial antisera. Commercially available reagent red cell panels are typed for the blood group antigens: ABO, C, c, E, e, D, Fya, Fyb, K, k, Kpa, Kpb, Jsa, Jsb, Jka, Jkb, M, N, S, s Lea, Leb, Lua, Lub, P1, and Xga. These panels are sufficient to characterize the commonly encountered alloantibodies. Although suitable for identification of majority of clinically important antigens, these panels may not be able to characterize antibodies in some populations due to difference in the ethnicity between these populations. For example, anti-Mia is a commonly encountered antibody among East Asians.[13] However, since the panels produced in western countries are not typed for this antigen, it cannot identify anti-Mia antibodies. To overcome this, ethnic populations should be screened to identify clinically important antigens against which alloimmunization can occur and prepare reagent red cell panels accordingly. Furthermore, the local/in-house panels can reduce the cost of antibody screening and identification and will be able to identify majority of alloantibodies in a particular population.

Some of the clinically significant antibodies show dosage effect, i.e., reacts better when homozygous for the antigen. Hence, panels are prepared by selecting RBCs such that each of the tested antigens is present in homozygous and heterozygous states. Molecular techniques in blood group genotyping can be exploited to determine the true zygosity of the red cells. For example, Fy (a−b+) is considered as Fyb homozygous based on serological testing, however, molecular testing may reveal heterozygosity for Fyx allele present along with Fyb.

Greater quality assurance can be achieved by molecular testing of reagent red cell panels for common antigens.[13],[14] Furthermore, discordant molecular typing results of weakly expressed antigens (such as Fy and Jk) arising due to the presence of unknown or novel alleles may be resolved using high-throughput methods such as next-generation sequencing.

In our study, 75 “O” group regular donors were tested for minor antigens and two sets of screening RBCs and one eight-cell panel were selected for preliminary detection and further identification of antibodies against D, C, c, E, e, Fya, Fyb, Jka, Jkb, K, k, M, N, S, and s antigens.[15] Quality assurance was performed by testing the antigens with DNA-based assays. Serologically defined RhD zygosity and Fyb and Jkb antigen expression of donor cells did not tally with the molecular typing in some regular donors and were therefore not selected in panel [Table 1].
Table 1: Quality assurance testing for selection of donors to prepare reagent red cell panel

Click here to view



  Selection of Antigens Top


Today, more than 360 inherited blood group antigens belonging to 38 well-characterized blood group systems have been described on the surface of human red cells (https://www.isbtweb.org/working-parties/red-cell-immunogenetics-and-blood-group-terminology).[16] Various studies across the world have recommended matching of some of these clinically significant specific blood group antigens in order to reduce the incidence of alloimmunization. However, there is no universal standard for management of the appropriate selection of RBC products for chronically transfused patients.

Rh and Kell blood group antigens are the major cause of alloimmunization worldwide. A number of studies demonstrate that antigen matching for C, E, and K has reduced incidence of alloimmunization.[17],[18],[19] Castro el al. observed that if all transfusions had been selected by partial antigen matching of C, c, E, e, and K, along with ABO and D, alloimmunization would have been prevented in 53.3% of patients and further reduced to 70.8% by further matching for S, Fya, and Jkb.[20] Vichinsky et al. reported that prophylactically matched RBC products for Rh antigens E and C and K antigens reduced the rate of alloimmunization from 3% to 0.5% per unit.[17] Klapper et al. have constructed four stringency levels for antigen matching [Figure 2]. Level 1 matching requires a selected donor unit to be compatible with respect to the prospective recipients' ABO and D types and to be antigen negative with respect to alloantibodies identified in the recipients' plasma. Increasing levels of stringency require further matching for C, c, E, and e in addition at Level 2; Fya, Fyb, Jka, Jkb, S, and s at Level 3, and k, M, N, Doa, Dob, Hy, Joa, and Lua and Lub at Level 4.[21] Chinese patients are less likely to have antibodies against Kell and Duffy blood group antigens but are more prone to develop antibodies against the Miltenberger antigens.[22] Antibodies against Miltenberger antigens have also been reported in Indians from Malaysia.[13]
Figure 2: Stringency levels for matching of blood group antigens to give better matched blood to a patient in different study groups

Click here to view


The most commonly encountered antibodies in the Indian population are against Rh blood group antigens, and hence, giving antigen-matched blood for C, c, E, and e antigens along with ABO and D will help in reducing the risk of alloimmunization. The incidence of anti-K antibodies reported in western India is less as compared to that in North India[23] as the incidence of Kell antigen in western India is approximately 1%–1.5%.[24] Hence, Patel et al. did not recommend matching of donors and patients for K antigen in western India, though it has been recommended in few reports from north India.[25]

Our recent study has shown that alloantibodies against Rh antigens and MNS were highest as compared to other blood group antigens [Figure 3]. If matching of Rh antigens, C, c, E, and e (Level 1) along with ABO and RhD is taken into account, it can reduce the alloimmunization by 51%.[26] If the matching for M, N, S, and s antigens is done between donors and patients along with Level 1 antigens, it would further reduce alloimmunization by about 73% (Level 2) and 84% by further matching for common Kidd blood group system antigens (Level 3) [Figure 2]. Matching for Kell antigen is not recommended. Thus, based on prevalence of an antigen in an ethnic population, it can be hypothesized that alloimmunization can be reduced in patients by selecting donors from the same ethnic group and the antigen matching stringency levels should accordingly be selected.
Figure 3: Percentage distribution of red cell alloantibodies among multitransfused and multiparous women

Click here to view



  Methods for Extended Phenotyping Top


Serologicalphenotyping

Since the discovery of ABO blood group system, antibody-based technology has been the basis for blood group typing. Serological testing of blood group antigens is based on the principle of hemagglutination as these techniques are simple, inexpensive, and when correctly performed have specificity and sensitivity to accurately detect blood group antigen. Commercial monoclonal and polyclonal antisera are now available for phenotyping common antigens of Rh, Duffy, Kidd, MNS, P, Lutheran, and Lewis blood group systems.

The gel or column agglutination technique was introduced in 1985 which is based on the principle of centrifugation of RBCs through a column containing dextran-polyacrylamide gel dispersed with reagent antisera. Commercial gel cards are now available for detecting minor blood group antigens, ABO and RhD grouping, and antiglobulin test and carrying out antibody studies. Solid-phase red cell adherence has been used for detecting RBC antigens, antibody screening and identification, weak-D testing, and compatibility testing.[27]

However, hemagglutination cannot be used to type antigens such as Indian, Diego, Dombrock, and Cartwright and low incidence antigens of majority of blood group systems due to unavailability of specific and potent reagents in large volumes. It is a subjective test. Serological discrepancies are seen while typing RBCs from DAT-positive and multitransfused patients. These limitations suggest the need to adopt molecular assays.[28]

Molecular bloodgroupgenotyping

Determination of the molecular bases of almost all major blood group antigens has led to the development of various genotyping methods for identification of common and variant phenotypes of different blood group systems. Most of the blood group antigens such as S/s, K/k, Fya/Fyb, Jka/Jkb, Coa/Cob, Lua/Lub, Ina/Inb, Dia/Dib, and Yta/Ytb arise as a result of single-nucleotide polymorphism (SNP) resulting in a single amino acid substitution which either inactivates the gene product or changes its substrate specificity. These SNPs can be identified at molecular level using easy and cost-effective techniques such as PCR-SSP, PCR-RFLP, and multiplex PCR. However, these classical methods are labor and time-intensive. Methods such as DNA sequencing and real-time PCR are of medium throughput but cannot be applied for mass scale typing [Table 2]. Microarray technology has led to the development of many high-throughput testing platforms such as BeadChip, Bloodchip, and Genome Lab SNP stream which allow typing of multiple blood group antigens in a single test.[28]
Table 2: Methods for molecular blood group genotyping

Click here to view


In our experience, while determining antigenic profiles of multitransfused thalassemic patients, 77% showed a discrepancy between serological phenotype and molecular genotype. Among these, 40.9% of patients showed one antigen discrepancy and 35% of patients showed two antigen discrepancies. The remaining 24.1% showed three or more antigen discrepancies. There was a complete concordance between the serological phenotype and genotype for D and k antigens. A 59.1% discrepancy was observed between genotyping and phenotyping for M, N, S, and s antigens. Discrepancy for M antigen was found in 15.2%, while for N, it was 22.7%. S and s antigen discrepancy was seen in 33.3% and 12.1% of thalassemic patients, respectively.[29]

Apart from phenotyping common antigens of Rh, Kell, Kidd, and Duffy blood group antigens, we have also standardized methods to type antigens where commercial antisera are unavailable in order to find the prevalence of these blood group antigens in the regular donor population. For example, PCR-SSP-based detection of Ina antigen has enabled to determine its frequency (%) among Indians.[30] We have also standardized simple cost-effective DNA-based methods for detecting common antigens of Dombrock, Diego, Colton, Miltenberger antigens, etc., in our laboratory (unpublished observations).


  Conclusion Top


Safe transfusions can be assured for most recipients by the correct typing of patients and donors for some minor blood group antigens along with ABO and RhD and screening the patients' serum for the presence of clinically significant antibodies directed against antigens polymorphic in the local population. Chronically transfused patients whose antigenic typing can no longer be determined by conventional serological techniques because there is a “massive” presence of circulating transfused RBCs must undergo genomic analysis. Furthermore, if necessary, reagent red cell panel should be typed for additional antigens which will help in antibody screening and identification in different ethnic groups.

There is a need to create a registry of regular donors phenotyped for clinically significant blood group antigens. High-throughput molecular platforms can enable large scale typing of donors and patients. “Molecular perfect match” can be adopted as an innovative transfusion strategy to ensure a better quality of transfusion therapy, reduce the risk of alloimmunization and frequency of blood transfusions, and promote the containment of health-care costs.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Seltsam A, Wagner FF, Salama A, Flegel WA. Antibodies to high-frequency antigens may decrease the quality of transfusion support: An observational study. Transfusion 2003;43:1563-6.  Back to cited text no. 1
    
2.
Afenyi-Annan A, Bandarenko N. Transfusion practices for patients with sickle cell disease at a major academic medical center. Immunohematology 2006;22:103-7.  Back to cited text no. 2
    
3.
Badjie KS, Tauscher CD, van Buskirk CM, Wong C, Jenkins SM, Smith CY, et al. Red blood cell phenotype matching for various ethnic groups. Immunohematology 2011;27:12-9.  Back to cited text no. 3
    
4.
Vichinsky EP, Earles A, Johnson RA, Hoag MS, Williams A, Lubin B. Alloimmunization in sickle cell anemia and transfusion of racially unmatched blood. N Engl J Med 1990;322:1617-21.  Back to cited text no. 4
    
5.
Singer ST, Wu V, Mignacca R, Kuypers FA, Morel P, Vichinsky EP. Alloimmunization and erythrocyte autoimmunization in transfusion-dependent thalassemia patients of predominantly asian descent. Blood 2000;96:3369-73.  Back to cited text no. 5
    
6.
Ho HK, Ha SY, Lam CK, Chan GC, Lee TL, Chiang AK, et al. Alloimmunization in Hong Kong southern Chinese transfusion-dependent thalassemia patients. Blood 2001;97:3999-4000.  Back to cited text no. 6
    
7.
Pujani M, Pahuja S, Dhingra B, Chandra J, Jain M. Alloimmunisation in thalassaemics: A comparison between recipients of usual matched and partial better matched blood. An evaluation at a tertiary care centre in India. Blood Transfus 2014;12 Suppl 1:s100-4.  Back to cited text no. 7
    
8.
Shirey RS, Boyd JS, Parwani AV, Tanz WS, Ness PM, King KE. Prophylactic antigen-matched donor blood for patients with warm autoantibodies: An algorithm for transfusion management. Transfusion 2002;42:1435-41.  Back to cited text no. 8
    
9.
Le N, Harach ME, Kay JK, Brown RP, Everetts JN, Herman JH. Establishing an antigen-negative red blood cell inventory in a hospital-based blood bank. Transfusion 2014;54:285-8.  Back to cited text no. 9
    
10.
Kulkarni S, Vasantha K, Ghosh K. Antigen negative red blood cell inventory of Indian blood donors. Transfus Apher Sci 2016;55:131-5.  Back to cited text no. 10
    
11.
Kulkarni S, Choudhary B, Gogri H, Sharma J. Red cell antigen phenotypes in blood donors and thalassemic patients for creation of red cell antigen matched inventory. Ind J Med Res 2020;153.2000.  Back to cited text no. 11
    
12.
Prathiba R, Lopez CG, Usin FM. The prevalence of GP Mur and anti-“Mia” in a tertiary hospital in Peninsula Malaysia. Malays J Pathol 2002;24:95-8.  Back to cited text no. 12
    
13.
Hult A, Hellberg A, Wester ES, Olausson P, Storry JR, Olsson ML. Blood group genotype analysis for the quality improvement of reagent test red blood cells. Vox Sang 2005;88:265-70.  Back to cited text no. 13
    
14.
Kappler-Gratias S, Peyrard T, Rouger P, Le Pennec PY, Pham BN. Blood group genotyping by high-throughput DNA analysis: Application to the French panel of RBC reagents. Transfus Clin Biol 2010;17:165-7.  Back to cited text no. 14
    
15.
Kulkarni S, Choudhary B, Gogri H, Vasantha K, Ghosh K. Quality assurance of reagent red blood cells by DNA analysis. 38th ISBTI Annual Conference, TRANSCON 2013, Surat. Asian J Transfus Sci 2014;8 S1:6-25.  Back to cited text no. 15
    
16.
Anstee D J. Red cell genotyping and the future of pretransfusion testing. Blood 2009;114:248-56.  Back to cited text no. 16
    
17.
Vichinsky EP, Luban NL, Wright E, Olivieri N, Driscoll C, Pegelow CH, et al. Prospective RBC phenotype matching in a stroke-prevention trial in sickle cell anemia: A multicenter transfusion trial. Transfusion 2001;41:1086-92.  Back to cited text no. 17
    
18.
O'Suoji C, Liem RI, Mack AK, Kingsberry P, Ramsey G, Thompson AA. Alloimmunization in sickle cell anemia in the era of extended red cell typing. Pediatr Blood Cancer 2013;60:1487-91.  Back to cited text no. 18
    
19.
Venkateswaran L, Teruya J, Bustillos C, Mahoney D Jr., Mueller BU. Red cell exchange does not appear to increase the rate of allo-and auto-immunization in chronically transfused children with sickle cell disease. Pediatr Blood Cancer 2011;57:294-6.  Back to cited text no. 19
    
20.
Castro O, Sandler SG, Houston-Yu P, Rana S. Predicting the effect of transfusing only phenotype-matched RBCs to patients with sickle cell disease: Theoretical and practical implications. Transfusion 2002;42:684-90.  Back to cited text no. 20
    
21.
Klapper E, Zhang Y, Figueroa P, Ness P, Stubbs J, Abumuhor I, et al. Toward extended phenotype matching: A new operational paradigm for the transfusion service. Transfusion 2010;50:536-46.  Back to cited text no. 21
    
22.
Cheng CK, Lee CK, Lin CK. Clinically significant red blood cell antibodies in chronically transfused patients: A survey of Chinese thalassemia major patients and literature review. Transfusion 2012;52:2220-4.  Back to cited text no. 22
    
23.
Gupta R, Singh DK, Singh B, Rusia U. Alloimmunization to red cells in thalassemics: Emerging problem and future strategies. Transfus Aperesis Sci 2011;45;167-70.  Back to cited text no. 23
    
24.
Basu D, Datta SS, Montemayor C, Bhattacharya P, Mukherjee K, Flegel WA. ABO, rhesus, and kell antigens, alleles, and haplotypes in West Bengal, India. Transfus Med Hemother 2018;45:62-6.  Back to cited text no. 24
    
25.
Patel J, Shukla R, Gupte S. Red cell alloimmunization in multitransfused patients and multiparous women. Indian J Hematol Blood Transfus 2009;25:49-52.  Back to cited text no. 25
    
26.
Gogri H, Kulkarni S, Vasantha K, Jadhav S, Ghosh K, Gorakshakar A. Partial matching of blood group antigens to reduce alloimmunization in Western India. Transfus Apher Sci 2016;54:390-5.  Back to cited text no. 26
    
27.
Plapp FV, Rachel JM, Beck ML, Coenen. M, Bayer WL, Sinor L. Solid phase adherence assays for blood processing. Lab Management 1984;22:39-47. 2.  Back to cited text no. 27
    
28.
Choudhary N, Bharucha ZS, editors. A Text Book on Laboratory and Clinical Transfusion Medicine” Basics of Blood Bank Practices. New York: Nova Science Publishers Inc.; 2018.  Back to cited text no. 28
    
29.
Kulkarni S, Choudhary B, Gogri H, Patil S, Manglani M, Sharma R, et al. Molecular genotyping of clinically important blood group antigens in patients with thalassaemia. Indian J Med Res 2018;148:713-20.  Back to cited text no. 29
[PUBMED]  [Full text]  
30.
Gogri H, Pitale P, Madkaikar M, Kulkarni S. Molecular genotyping of Indian blood group system antigens in Indian blood donors. Transfus Apher Sci 2018;57:388-90.  Back to cited text no. 30
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2]



 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Need for Extende...
Selection of Ant...
Methods for Exte...
Conclusion
References
Article Figures
Article Tables

 Article Access Statistics
    Viewed228    
    Printed2    
    Emailed0    
    PDF Downloaded14    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]