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

• Published in: Transfusion (Philadelphia, Pa.) Vol. 48; no. 2; pp. 358 - 364
• Main Authors: Curtis, Brian R., Fick, Andrea, Lochowicz, Andrew J., McFarland, Janice G., Ball, Robert H., Peterson, Julie, Aster, Richard H.
• Format: Journal Article
• Language: English
• Published: Malden, USA Blackwell Publishing Inc 01.02.2008; Blackwell Publishing
• Subjects: ABO Blood-Group System - blood; ABO Blood-Group System - immunology; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Antibodies - immunology; Biological and medical sciences; Blood Group Incompatibility - blood; Blood Group Incompatibility - complications; Blood Group Incompatibility - immunology; Blood. Blood and plasma substitutes. Blood products. Blood cells. Blood typing. Plasmapheresis. Apheresis; Child; Diseases of mother, fetus and pregnancy; Fathers; Female; Gynecology. Andrology. Obstetrics; Humans; Infant, Newborn; Isoantigens - immunology; Male; Maternal-Fetal Exchange; Medical sciences; Platelet Glycoprotein GPIIb-IIIa Complex - immunology; Pregnancy; Pregnancy. Fetus. Placenta; Sensitivity and Specificity; Thrombocytopenia, Neonatal Alloimmune - blood; Thrombocytopenia, Neonatal Alloimmune - immunology; Transfusions. Complications. Transfusion reactions. Cell and gene therapy; Human; Thrombocytopenia; Maternal-fetal incompatibility; Platelet; Newborn; Transfusion; Hemopathy
• ISSN: 0041-1132; 1537-2995
• DOI: 10.1111/j.1537-2995.2007.01531.x

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 A2 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.