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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 4  |  Issue : 2  |  Page : 231-233

Anti-D antibody in a D-positive patient: Autoantibody or development of alloantibody after platelet transfusion


Department of Transfusion Medicine, Sri Balaji Action Medical Institute, New Delhi, India

Date of Submission11-Apr-2019
Date of Acceptance29-Aug-2019
Date of Web Publication17-Oct-2019

Correspondence Address:
Dr. Sadhana Mangwana
Department of Transfusion Medicine, Sri Balaji Action Medical Institute, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/GJTM.GJTM_29_19

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  Abstract 


Rh D (D or RH 1) is next clinically important blood group after ABO blood group system. Although most people are either D+ or D−, there are a large number of individuals having different forms of D variants; weak D, partial D, or DEL phenotypes. We present a case report of a 32-year-old male with a history of cough and cold for 5 days with development of petechial rashes all over the body from day 1 and afebrile and marked thrombocytopenia. He was transfused with multiple platelet concentrates. Initially, there was an absence of irregular red cell antibodies, but after 72 h of transfusion, he developed autoanti-D antibody. An accurate D-antigen identification is important and essential for pretransfusion evaluation to prevent antibody formation, and a partial D variant might be suspected when typing for the D antigen showing weaker-than-normal reactions. This case emphasizes that some partial D variants are likely to be missed by routine serological tests.

Keywords: Anti-D antibody, autoanti-D, D positive (D+), platelet concentrates


How to cite this article:
Mangwana S, Gangwar V. Anti-D antibody in a D-positive patient: Autoantibody or development of alloantibody after platelet transfusion. Glob J Transfus Med 2019;4:231-3

How to cite this URL:
Mangwana S, Gangwar V. Anti-D antibody in a D-positive patient: Autoantibody or development of alloantibody after platelet transfusion. Glob J Transfus Med [serial online] 2019 [cited 2019 Nov 20];4:231-3. Available from: http://www.gjtmonline.com/text.asp?2019/4/2/231/269383




  Introduction Top


Rh D (D or RH 1) is next clinically important blood group after ABO blood group system. The Rh blood group system has 62 antigens, with the identification of a new high-prevalence Rh antigen with the antigen number given by the International Society of Blood Transfusion as RH 62.[1] The frequency of D+ phenotype is >99.5% in East Asia and 85% in Caucasians.[2] Although most people are either D+ or D−, there are a large number of individuals having different forms of D variants; weak D, partial D, or DEL phenotypes. Individuals, whose cells have a qualitative variation of D antigen (partial D) lacking one or more components of D antigen, are said to have a partial D phenotype. D-positive individuals harboring a “partial” D antigen may produce an allo-D.[3]


  Case Report Top


We report a case of a 32-year-old male patient with a history of cough, cold, uneasiness, and headache for 5 days with development of petechial rashes all over the body or oral mucosa from one day. There was no history of vomiting, diarrhea, active bleeding, respiratory distress, or any drug intake. On physical examination at admission, the patient was afebrile without any organomegaly. His investigations at admission showed platelet count as 1000/cumm, blood group – “B” positive, screening for irregular antibody negative, and Rh phenotype as Ccee Kell negative using solid-phase red cell adherence (SPRCA) method (Capture, Immucor Inc., Norcross, GA, USA). Rapid malaria test for malaria antigens and NS-1 antigen were negative. Immediately, six units of random donor platelets (RDPs) of the same group were given followed by one unit of apheresis platelet. On day 2 of admission, the patient complained of gum bleeding. Bone marrow aspiration and biopsy were done to ascertain the diagnosis. Tests for autoimmune disorders such as antinuclear antibody, anti-DS DNA, IgA, and IgM levels were within normal limits. During his stay in the hospital, ABO-matched six units of apheresis platelets were given till day 6. There was no further active bleeding. Bone marrow aspiration was reported as “normocytic marrow with megakaryocytic thrombocytopenia.” As per hospital transfusion policy, all donors are screened for irregular antibodies and Rh phenotyping using SPRCA method. The patient was screened again for irregular antibodies by a three-cell panel after 72 h as per hospital transfusion policy and showed a positive reaction in cell 1 and cell 2 (2+ in both) giving possibilities to consider as anti-D, C, E JK, M, and S antibodies [Table 1].
Table 1: Antibody Screening using 3 Cell Panel

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Polyspecific direct antiglobulin test (DAT) was positive with positive auto control. Antibody identification by 14-cell panel on SPRCA showed reactivity in panel cells 1, 2, 3, 4, and 14 confirming the presence of IgG type of antibody with anti-D specificity. Acid elution performed using Gamma ELU-KIT II, followed by antibody detection in anti-human globulin phase and antibody identification with eluate, was also found to be positive with the conclusion of the presence of anti-D autoantibodies [Table 2]. On day 8 of admission, the patient was given steroid therapy and planned for intravenous immunoglobulin (IVIG) and Rh-D immunoglobulin. As a look-back exercise to analyze the reason of anti-D autoantibodies, all the platelet units (RDPs and apheresis platelets) transfused were found to be negative for irregular antibodies.
Table 2: Antibody Identification using Eluate

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  Discussion Top


An accurate D-antigen identification is important and essential for pretransfusion evaluation to prevent antibody formation. A partial anti-D variant might be suspected when typing for D-antigen showing weaker-than-normal reactions.[3]

Although D alloimmunization in D-negative (D−) recipients is reported by Cid et al. after transfusion of D-positive (D+) platelets in ADAPT study, but to the best of our knowledge, there is no report in the literature of D alloimmunization in D+ patients receiving D+ platelet concentrates.[4] Cid et al. found that 1.44% of recipients had a primary anti-D response, while in other studies, the frequency of D alloimmunization was found to be 19% and 7%, respectively.[5],[6] There are few cases reported in the literature showing the development of non-D antibodies in D+ recipients after transfusion with apheresis[7] or platelet concentrates.[8],[9]

This case illustrates the development of antibodies to red blood cell (RBC) antigens after platelet transfusion. Platelets express ABO and HLA-1 antigens on their surface but not Rh antigens; however, platelet concentrates may contain a very small amount of donor RBCs carrying Rh antigen. Combination of D+ red cells and anti-D reactivity in the patient's serum suggested the possibility of either an autoantibody or an alloantibody in a partial D individual. The terms “partial D” and “weak D type” were coined in France in 1984 and in Germany/Austria in 1999. As per the definition, “weak D antigens” have all D epitopes; “partial D antigens” lack one or more D epitopes. Individuals with “partial D antigens” can make anti-D; those with “weak D antigens” cannot. Patients with many D variant phenotypes are capable of producing alloanti-D if immunized with D+ red cells.[2]

It is important to classify antibodies as autoanti-D or alloanti-D on the basis of commonly applied serological criteria. If the red cells of a patient with anti-D give a negative direct antiglobulin test (DAT), no anti-D can be eluted from them, and they do not adsorb the anti-D from the patient's own plasma, they should be considered to be alloanti-D. They should only be dismissed as autoanti-D if there were a positive DAT, anti-D could be eluted from the patient's red cells, and/or the patient's red cells adsorb the anti-D from the autologous plasma.[2] Accordingly, it was labeled as autoanti-D in this case.

A partial D variant might be suspected when typing for the D antigen showing weaker-than-normal reactions.[3] Since this patient was lost to follow-up and efforts to collect his sample for further testing to establish his D-status were not successful, accurate D-antigen identification could not be concluded. However, this case emphasizes that some partial D variants are likely to be missed by routine serological tests. Accurate D-antigen identification needs to be done routinely in D+ male patients also during pretransfusion testing to prevent alloimmunization and protocols need to establish in such cases.

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.



 
  References Top

1.
Storry JR, Clausen FB, Castilho L, Chen Q, Daniels G, Denomme G, et al. International society of blood transfusion working party on red cell immunogenetics and blood group terminology: Report of the Dubai, Copenhagen and Toronto meetings. Vox Sang 2019;114:95-102.  Back to cited text no. 1
    
2.
Daniels G. Variants of RhD – Current testing and clinical consequences. Br J Haematol 2013;161:461-70.  Back to cited text no. 2
    
3.
Vaglio S, Perrone MP, Arista MC, Laurenti L, Girelli G. Anti-D in a D-positive patient: Autoantibody or alloantibody? Blood Transfus 2007;5:44.  Back to cited text no. 3
    
4.
Cid J, Lozano M, Ziman A, West KA, O'Brien KL, Murphy MF, et al. Low frequency of anti-D alloimmunization following D+ platelet transfusion: The anti-D alloimmunization after D-incompatible platelet transfusions (ADAPT) study. Br J Haematol 2015;168:598-603.  Back to cited text no. 4
    
5.
Lozano M, Cid J. The clinical implications of platelet transfusions associated with ABO or Rh(D) incompatibility. Transfus Med Rev 2003;17:57-68.  Back to cited text no. 5
    
6.
Cid J, Harm SK, Yazer MH. Platelet transfusion – The art and science of compromise. Transfus Med Hemother 2013;40:160-71.  Back to cited text no. 6
    
7.
Kitazawa J, Nollet K, Morioka H, Tanaka K, Inomata M, Kubuki Y, et al. Non-D Rh antibodies appearing after apheresis platelet transfusion: Stimulation by red cells or microparticles? Vox Sang 2011;100:395-400.  Back to cited text no. 7
    
8.
Yun JW, Kang ES, Ki CS, Koh KC, Kim DW. Sensitization to multiple Rh antigens by transfusion of random donor platelet concentrates in a -D- phenotype patient. Ann Lab Med 2012;32:429-32.  Back to cited text no. 8
    
9.
Abu-Farsakh S, Bowen R, Blumberg N & Refaai MA. Development of anti-e after platelet concentrate transfusion. J Blood Disord Transfus 2015;6:5.  Back to cited text no. 9
    



 
 
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