It is widely thought that expression of ABH antigens on platelets is insuff
icient to materially affect the survival of ABH-incompatible platelets in t
ransfusion recipients, but anecdotal reports of poor survival of A and B mi
smatched platelets suggest that this is not always the case. The A and B an
tigen expression on platelets of 100 group A(1) and group B blood donors wa
s measured, and 7% and 4%, respectively, had platelets whose A and B antige
n levels consistently exceeded the mean plus 2 SD, On the basis of flow cyt
ometric and statistical analysis, donors whose platelets contained higher t
han normal levels of A antigen were subdivided into 2 groups, designated Ty
pe 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 affect
s other cell lineages, Immunochemical studies demonstrated high levels of A
antigen on various glycoproteins (GPs) from high-expresser platelets, espe
cially GPIIb and PECAM (CD31). The A(1) Type II high-expresser phenotype wa
s 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 exp
resser 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) (C) 2000 by The American Society of Hematology.