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 Table of Contents  
Year : 2018  |  Volume : 3  |  Issue : 1  |  Page : 75-76

How many of the rhesus D-Negative cases are actually weak D positive?

1 Department of Pathology and Blood Bank, Lady Hardinge Medical College, New Delhi, India
2 QRG Central Hospital and Research Centre, Faridabad, Haryana, India
3 Department of Pathology, VMMC and Safdarjung Hospital, New Delhi, India

Date of Web Publication5-Apr-2018

Correspondence Address:
Dr. Shivali Sehgal
Department of Pathology and Blood Bank, Lady Hardinge Medical College, New Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/GJTM.GJTM_59_17

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How to cite this article:
Sehgal S, Chatterjee P, Kumar R, Pathak C. How many of the rhesus D-Negative cases are actually weak D positive?. Glob J Transfus Med 2018;3:75-6

How to cite this URL:
Sehgal S, Chatterjee P, Kumar R, Pathak C. How many of the rhesus D-Negative cases are actually weak D positive?. Glob J Transfus Med [serial online] 2018 [cited 2019 Mar 25];3:75-6. Available from: http://www.gjtmonline.com/text.asp?2018/3/1/75/229340


The Rhesus (Rh) system is one of the most complex blood group systems in humans. The Rhesus D (RhD) antigen is the most important antigen because of its immunogenicity. The weak D antigen is a RhD phenotype which expresses lesser numbers of the complete D antigen on the surface of the red cells.

The study was conducted in regional blood transfusion center, Lady Hardinge Medical College. The prevalence of weak D among all RhD-negative cases coming to blood bank (donors as well as recipients) was assessed from January 2013 to June 2015. All the cases which tested negative for RhD antigen in routine blood grouping were subjected to weak D testing. For testing, identification (ID)-Diaclon anti-D containing monoclonal anti-D IgG was used, and the test was performed in ID-card low ionic strength solution/Coombs (containing polyspecific antihuman globulin). As false-positive results may occur in cases with a positive direct Coombs test (DCT), DCT was performed in all cases which tested positive with weak D reagent.

A total of 1149 RhD antigen-negative cases were documented in the blood bank for the period mentioned. Out of these, 15 cases tested positive with weak D reagent. DCT of these cases was performed as a protocol and was found positive in 4 cases. Therefore, only 11 cases were true positive. Therefore, the incidence of weak D was 0.96% in the Rh-negative population.

The Rh gene lies on chromosome one and the locus is composed of 2 highly homologous genes: the RhD gene encoding for the D protein and the RHCE gene encoding for the C, c, E, and e proteins.[1],[2] There are 6 alleles but only 5 antigens since D is an amorph gene.[3] Among these, D is the most immunogenic and D is often called the Rh antigen. The terms Rh+ and Rh– refer to the presence or absence of D antigen.

RhD antigen consists of different epitopic structures distributed along the extracellular portions of the RhD protein.[4] Variant forms of the D antigen occur due to changes in the amino acid sequence of the RhD which do not abate the entire D antigen but cause epitope loss. “Weak D” red blood cells demonstrate reduced quantities of the D antigen. Missense mutations observed in the alleles of all weak D types have been demonstrated to be the probable cause of reduced antigen expression. In “partial D” red blood cells, the number of RhD antigens on the cell surface is normal. The RhD protein is mutated in an exofacial loop, eliminating at least one D-specific epitope.[5]

Prevalence of weak D was found to be 0.09% of the Rh-negative population in a study done in Uttarakhand region.[6] In a study done previously in our center by Pahuja et al. (January 2009 to July 2010: 18 months), the incidence of weak D in the D-Negative population was lesser (0.2% in contrast to 0.96% in the current study).[7]

Even though the prevalence of weak D is low, it is very important to screen all RhD-negative individuals for the same, keeping in mind the theoretical risk of hemolysis. All donors who test positive with weak D reagent should be considered D positive. The latter is to prevent alloimmunization of D-negative patients when transfused with weak D donor's blood. On the other hand, all weak D recipients should be treated as D negative.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Rouillac C, Gane P, Cartron J, Le Pennec PY, Cartron JP, Colin Y, et al. Molecular basis of the altered antigenic expression of RhD in weak D(Du) and RhC/e in RN phenotypes. Blood 1996;87:4853-61.  Back to cited text no. 1
Mouro I, Colin Y, Chérif-Zahar B, Cartron JP, Le Van Kim C. Molecular genetic basis of the human rhesus blood group system. Nat Genet 1993;5:62-5.  Back to cited text no. 2
Westhoff CM. The structure and function of the Rh antigen complex. Semin Hematol 2007;44:42-50.  Back to cited text no. 3
Jones J, Scott ML, Voak D. Monoclonal anti-D specificity and Rh D structure: Criteria for selection of monoclonal anti-D reagents for routine typing of patients and donors. Transfus Med 1995;5:171-84.  Back to cited text no. 4
Wagner FF, Gassner C, Müller TH, Schönitzer D, Schunter F, Flegel WA, et al. Molecular basis of weak D phenotypes. Blood 1999;93:385-93.  Back to cited text no. 5
Agarwal N, Chandola I, Agarwal A. Prevalence of weak D in Northern hilly areas of Uttarakhand, India. Asian J Transfus Sci 2013;7:90-1.  Back to cited text no. 6
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Pahuja S, Pujani M, Sethi N, Kushwaha S, Jain M, Kumari R, et al. Frequency of variant D in Delhi, India. Asian J Transfus Sci 2014;8:142-3.  Back to cited text no. 7
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