Expression of ABH antigens on platelets

Curtis, Brian R.

doi:10.1182/blood-2005-05-1920

Cited by 5 publications

(2 citation statements)

References 8 publications

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“…The recipients apparent refractoriness was only associated with the transfusions from the donors with the high expression phenotype; therefore, the authors concluded that donor PLTs with high levels of B antigen, in combination with recipient's ‘high titer' anti-B, were associated with lower than expected post-transfusion PLT increments. Subsequent studies have demonstrated that there are different patterns of A and B antigen high expression on PLTs (that PLTs from group A 2 donors tend to express group O levels of A antigen) and that the frequency of PLT A and B high expression is fairly constant between different populations (2-7%) [33,34,35,36,37,38]. …”

Section: Part 1: Plt Transfusion and Abo Compatibilitymentioning

confidence: 99%

Platelet Transfusion - the Art and Science of Compromise

Cid

Harm

Yazer

2013

Transfus Med Hemother

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Many modern therapies depend on platelet (PLT) transfusion support. PLTs have a 4- to 7-day shelf life and are frequently in short supply. In order to optimize the inventory PLTs are often transfused to adults without regard for ABO compatibility. Hemolytic reactions are infrequent despite the presence of ‘high titer' anti-A and anti-B antibodies in some of the units. Despite the low risk for hemolysis, some centers provide only ABO identical PLTs to their recipients; this practice might have other beneficial outcomes that remain to be proven. Strategies to mitigate the risk of hemolysis and the clinical and laboratory outcomes following ABO-matched and mismatched transfusions will be discussed. Although the PLTs themselves do not carry the D antigen, a small number of RBCs are also transfused with every PLT dose. The quantity of RBCs varies by the type of PLT preparation, and even a small quantity of D+ RBCs can alloimmunize a susceptible D- host. Thus PLT units are labeled as D+/-, and most transfusion services try to prevent the transfusion of D+ PLTs to D- females of childbearing age. A similar policy for patients with hematological diseases is controversial, and the elements and mechanisms of anti-D alloimmunization will be discussed.

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Section: Part 1: Plt Transfusion and Abo Compatibilitymentioning

confidence: 99%

Platelet Transfusion - the Art and Science of Compromise

Cid

Harm

Yazer

2013

Transfus Med Hemother

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“…A recent study indicated that individuals with the A 2 red blood cell (RBC) phenotype may lack A antigen as well as its precursor substance H antigen on their platelets (Cooling et al , 2005), although this finding has been questioned by others (Curtis & Aster, 2006). We have evaluated the amount of A antigen on the platelet surface of 241 Brazilian blood group A 1 , A 2 and A int donors.…”

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confidence: 99%

Prevalence, serologic and genetic studies of high expressers of the blood group A antigen on platelets*

Gomes

Estalote

Palatnik

et al. 2010

Transfusion Medicine

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Objective/Aim: The aim of this study is to describe the distribution of the platelet blood group A antigenicity in Euro-Brazilians (EUBs) and Afro-Brazilians (AFBs).Background: A small but significant proportion of individuals express high levels of A or B antigen on their platelets corresponding to the erythrocyte ABO group. The mechanism of increased antigen expression has not been elucidated.Material/Methods: A cohort of 241 blood group A donors was analysed by flow cytometry. Although mean fluorescence intensity (MFI) is a typical continuous variable, platelets were screened and divided into two categories: low expressers (LEs) and high expressers (HEs). A three-generation family was investigated looking for an inheritance mechanism.Results: The prevalence of the HE platelet phenotype among group A1 donors was 2%. The mean of MFI on platelets of A1 subgroup of EUBs differs from that of AFBs (P = 0·0115), whereas the frequency of the HE phenotype was similar between them (P = 0·5251). A significant difference was found between sexes (P = 0·0039). Whereas the serum glycosyltransferase from HE family members converted significantly more H antigen on group O erythrocytes into A antigens compared with that in LE serum, their ABO, FUT1 and FUT2 genes were consensus. The theoretically favourable, transcriptionally four-repeat ABO enhancer was not observed.Conclusion: The occurrence of HE in several members suggests familial aggregation. Indeed, in repeated measures, stability of the MFI values is suggesting an inherited condition. Factors outside the ABO locus might be responsible for the HE phenotype. Whether the real mechanism of inheritance is either of a polygenic or of a discrete Mendelian nature remains to be elucidated.

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