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      ABO incompatibility: A cause for neonatal alloimmune thrombocytopenia

      case-report

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          Abstract

          ABO antibodies are naturally occurring antibodies. The ABO antibodies found in the Group O individuals include anti-A and anti-B. In Group O individuals, it tends to be predominantly immunoglobulins G (IgG), although immunoglobulins M and IgA components are also present. Infants of Group O mothers are at higher risk for hemolytic disease of the fetus and new-born than those born to mothers with Group A or B because IgG readily cross the placenta. At the same time, abnormal high concentration of ABO antibody in mother can lead to destruction of platelets in neonates and leads to development of neonatal alloimmune thrombocytopenia as human platelets carry detectable quantities of A and B blood group antigens on their surface. Proper and early diagnosis combined with treatment with intravenous immunoglobulins or transfusion with compatible platelets, may be from mother, can save the neonate from bleeding episodes.

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          Most cited references11

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          Blood group A and B antigens are strongly expressed on platelets of some individuals.

          It is widely thought that expression of ABH antigens on platelets is insufficient to materially affect the survival of ABH-incompatible platelets in transfusion recipients, but anecdotal reports of poor survival of A and B mismatched platelets suggest that this is not always the case. The A and B antigen expression on platelets of 100 group A(1) and group B blood donors was measured, and 7% and 4%, respectively, had platelets whose A and B antigen levels consistently exceeded the mean plus 2 SD. On the basis of flow cytometric and statistical analysis, donors whose platelets contained higher than normal levels of A antigen were subdivided into 2 groups, designated Type I and Type II ("high expressers"). Serum A(1)- and B-glycosyltransferase levels of A and B high expressers were significantly higher than those of group A(1) and B individuals with normal expression. H antigen levels were low on the red cells of high expressers, indicating that the anomaly affects other cell lineages. Immunochemical studies demonstrated high levels of A antigen on various glycoproteins (GPs) from high-expresser platelets, especially GPIIb and PECAM (CD31). The A(1) Type II high-expresser phenotype was inherited as an autosomal dominant trait in one family. The sequences of exons 5, 6, and 7 of the A(1)-transferase gene of one Type II A(1) high expresser and exon 7 from 3 other genes were identical to the reported normal sequences. Further studies are needed to define the molecular basis for the high-expresser trait and to characterize its clinical implications. (Blood. 2000;96:1574-1581)
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            Determinants of ABH expression on human blood platelets.

            Platelets express ABH antigens, which can adversely effect platelet transfusion recovery and survival in ABH-incompatible recipients. To date, there has been no large, comprehensive study comparing specific donor factors with ABH expression on platelet membranes and glycoconjugates. We studied ABH expression in 166 group A apheresis platelet donors by flow cytometry, Western blotting, and thin layer chromatography relative to donor age, sex, A1/A2 subgroup, and Lewis phenotype. Overall, A antigen on platelet membranes, glycoproteins, and glycosphingolipids was linked to an A1 red blood cell (RBC) phenotype. Among A1 donors, platelet ABH varied significantly between donors (0%-87%). Intradonor variability, however, was minimal, suggesting that platelet ABH expression is a stable, donor-specific characteristic, with 5% of A1 donors typing as either ABH high- or low-expressers. Group A2 donors, in contrast, possessed a Bombay-like phenotype, lacking both A and H antigens. Unlike RBCs, ABH expression on platelets may be determined primarily by H-glycosyltransferase (FUT1) activity. Identification of A2 and A1 low expressers may increase the availability and selection of crossmatched and HLA-matched platelets. Platelets from group A2 may also be a superior product for patients undergoing A/O major mismatch allogeneic progenitor cell transplantation.
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              The evaluation and management of platelet refractoriness and alloimmunization.

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                Author and article information

                Journal
                Asian J Transfus Sci
                Asian J Transfus Sci
                AJTS
                Asian Journal of Transfusion Science
                Wolters Kluwer - Medknow (India )
                0973-6247
                1998-3565
                Jan-Jun 2023
                12 December 2022
                : 17
                : 1
                : 133-135
                Affiliations
                [1] Prathama Blood Centre, Ahmedabad, Gujarat, India
                [1 ] Standalone Blood Centre
                Author notes
                Address for correspondence: Dr. Ripal J. Shah, Prathama Blood Centre, Nr. Dr. Jivraj Mehta Hospital, Vasna, Ahmedabad - 380 007, Gujarat, India. E-mail: drripaljshah@ 123456yahoo.co.in
                Article
                AJTS-17-133
                10.4103/ajts.ajts_194_20
                10180803
                2b0b4e26-c44f-4d4b-bd78-466f82c2abfa
                Copyright: © 2022 Asian Journal of Transfusion Science

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                : 15 December 2020
                : 14 January 2022
                Categories
                Case Report

                Hematology
                irradiation,neonatal alloimmune thrombocytopenia,platelet count increment,posttransfusion platelet increment

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