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Transfusion. 2008 Feb;48(2):358-64. Epub 2007 Nov 19.

Neonatal alloimmune thrombocytopenia associated with maternal-fetal incompatibility for blood group B.

Author information

1
Platelet & Neutrophil Immunology Laboratory, BloodCenter of Wisconsin, Milwaukee, WI 53201-2178, USA. brian.curtis@bcw.edu

Abstract

BACKGROUND:

Blood group A and B antigens are expressed only weakly on platelets (PLTs) of most individuals but are very strongly expressed on PLTs from approximately 1 percent of normal subjects (Type II high expressers). The implications of this trait for transfusion medicine are undefined.

STUDY DESIGN AND METHODS:

A family was studied in which two Group B infants were born with neonatal thrombocytopenia, whereas a third infant whose blood group was A(2) had a normal PLT count at birth.

RESULTS:

Serologic studies demonstrated a maternal antibody that reacted strongly with PLTs from the father and the two group B children in flow cytometry and with GPIIb/IIIa from their PLTs in solid-phase assays. No PLT-specific antibodies were detected in maternal serum sample, but it contained a high-titer immunoglobulin G antibody specific for blood group B. All PLT-reactive antibody in the mother's serum was removed by absorption with pooled, washed group A and B red cells (RBCs). Studies with monoclonal anti-B and measurement of serum B-glycosyltransferase activity showed that the father and both group B children were Type II high expressers of blood group B.

CONCLUSIONS:

The findings indicate that high-titer blood group antibodies acquired from the mother can cause thrombocytopenia in infants possessing the Type II high-expresser phenotype despite competition for antibody binding by blood group antigens expressed on RBCs and other tissues.

PMID:
18028270
PMCID:
PMC3572505
DOI:
10.1111/j.1537-2995.2007.01531.x
[Indexed for MEDLINE]
Free PMC Article

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