Sequestration of anti-Cra in the placenta: serologic demonstration by placental elution

Few cases of antibodies to the Cromer (a) antigen have been described during pregnancy. Interestingly, the anti-Cr(a) titers decreased during pregnancy, and although the newborns were Cr(a)+, the direct antiglobulin tests (DATs) were negative and hemolytic disease of the newborn (HDN) was not observed. Cromer antigens reside on the decay-accelerating factor (DAF), which is expressed on the fetal derived syncytiotrophoblast layer of the placenta. It has been postulated that Cromer antibodies are not transported to the fetus, but are bound to placental DAF, thereby protecting the fetus from HDN and causing the disappearance of Cromer antibody in maternal plasma. This report is the first to demonstrate Cromer antibody sequestration by the placenta.

A G4P1 woman with an anti-Cr(a) presented for prenatal care during her fourth pregnancy. The anti-Cr(a) titer decreased from 64 at 7 weeks gestation to undetectable after 25 weeks. At delivery, the infant had no evidence of HDN. The infant's DAT was negative, and the maternal plasma, cord plasma, and the cord blood eluate were negative with screening cells, the infant's cord cells, and the mother's cells. Placental eluates revealed anti-Cr(a).

This is the fourth case report of a Cromer (a-) woman producing anti-Cr(a) during pregnancy, and the first demonstrating anti-Cr(a) sequestration in the placenta. The presence of anti-Cr(a) in the placental eluate, but not in the cord plasma, maternal plasma, or cord blood eluate, strongly supports the hypothesis that DAF at the fetomaternal interface absorbs anti-Cr(a) from the maternal circulation blocking its passage to the fetus.