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ABO blood group system consists of A, B, and H (ABH) antigens. Group O individuals express the precursor H antigen but lack A and B antigens. Individuals form antibodies (anti-A and anti-B) to the antigens they lack. These antibodies are termed “naturally occurring,” as they are present in sera of individuals without previous red blood cell (RBC) exposure. These IgM antibodies can activate complement and can thus cause severe intravascular hemolysis after transfusion of ABO-incompatible blood components, making them the most clinically significant antibodies in transfusion practice. Prevention of ABO-incompatible RBC transfusion is the primary objective of pretransfusion testing.
ABH antigens are carbohydrate structures that are synthesized in a stepwise fashion by glycosyltransferase enzymes that sequentially add specific monosaccharides to glycoproteins and glycolipids. H antigen defines the O blood group and is precursor for A and B antigens. Group O RBCs have large amounts of H antigen and no A or B antigens. Some precursor H antigen remains on A and B RBCs, depending on the transferase efficiency, with least on A 1 B RBCs. H antigen concentration by ABO blood group varies (O > A 2 > B > A 2 B > A 1 > A 1 B).
Each RBC carries more than 2 million ABH antigen sites. ABH antigens are also found on other tissues, including endothelial and epithelial cells of lung, gut, and urinary and reproductive tracts (and are therefore termed histo-blood group antigens). Hence, they are important in solid organ transplantation, where ABO incompatibility may require minimization of recipient anti-A and/or anti-B levels to prevent acute rejection. Prevalence of ABO blood groups differs in various populations ( Table 25.1 ).
ABO Group | Prevalence (%) | ||
---|---|---|---|
Caucasian | African-American | Asian | |
O | 45 | 49 | 43 |
A | 40 | 27 | 27 |
B | 11 | 20 | 25 |
AB | 4 | 4 | 5 |
ABO antigens are not fully developed at birth. Adult levels of ABO antigens with complex branching oligosaccharide structures appear on the RBCs by 2–4 years.
RBCs from some group A or B individuals that react moderately, weakly, or not at all with standard anti-A or anti-B sera are termed subgroups; B subgroups are encountered less frequently than A subgroups. Approximately, 80% of group A individuals are A 1 , while ∼20% are A 2 ; subgroups A 3 , A el , A x , etc. are less frequently encountered. Difference between A 1 and A 2 is both quantitative (∼five times fewer A antigens on A 2 than A 1 RBCs) and qualitative (structural differences). Because of the structural difference, A 2 individuals can form anti-A1 (1%–8% of A 2 individuals and ∼30% of A 2 B individuals have anti-A1). Anti-A1 does not usually result in hemolysis of group A 1 RBCs; however, hemolytic anti-A1 has been reported, and its presence can lead to organ rejection in some circumstances. It is prudent to transfuse these individuals with RBCs that have been shown to be crossmatch compatible (e.g., A 2 or O). Dolichos biflorus lectin is used to distinguish A 1 from A 2 , as the lectin is diluted to agglutinate A 1 but not A 2 or weaker subgroup RBCs. RBC reactivity with the lectin is not always straightforward, and when it is of clinical importance to determine A 1 versus A 2 status, for example in kidney transplantation, ABO genotyping (see below) is recommended.
Bombay individuals lack ABH antigens on RBCs, tissues, and secretions and make anti-A, anti-B, and potent anti-H. These individuals must be transfused with RBCs from other Bombay individuals, which are very rare. Para-Bombay individuals lack H antigen on their RBCs but have H antigen (and, depending on their ABO gene, A and B antigens) in their secretions. The RBCs of these individuals may express A and B antigens very weakly due to adsorption of soluble A and B antigens onto RBCs. Para-Bombay also describes individuals who have minimal H on their RBCs, regardless of secretor status.
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