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

Shanasey L. Weber, Barbara Bryant, Alexander J. Indrikovs

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

BACKGROUND: Few cases of antibodies to the Cromer (a) antigen have been described during pregnancy. Interestingly, the anti-Cra titers decreased during pregnancy, and although the newborns were Cra+, 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. CASE REPORT: A G4P1 woman with an anti-Cra presented for prenatal care during her fourth pregnancy. The anti-Cra 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-Cra. CONCLUSIONS: This is the fourth case report of a Cromer (a-) woman producing anti-Cra during pregnancy, and the first demonstrating anti-Cra sequestration in the placenta. The presence of anti-Cra 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-Cra from the maternal circulation blocking its passage to the fetus.

Original languageEnglish (US)
Pages (from-to)1327-1330
Number of pages4
JournalTransfusion
Volume45
Issue number8
DOIs
StatePublished - Aug 2005

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Placenta
CD55 Antigens
Fetal Erythroblastosis
Pregnancy
Mothers
Coombs Test
Fetus
Antibodies
Fetal Blood
Antigens
Prenatal Care
Trophoblasts
Stem Cells
Newborn Infant

ASJC Scopus subject areas

  • Hematology
  • Immunology

Cite this

Sequestration of anti-Cra in the placenta : Serologic demonstration by placental elution. / Weber, Shanasey L.; Bryant, Barbara; Indrikovs, Alexander J.

In: Transfusion, Vol. 45, No. 8, 08.2005, p. 1327-1330.

Research output: Contribution to journalArticle

Weber, Shanasey L. ; Bryant, Barbara ; Indrikovs, Alexander J. / Sequestration of anti-Cra in the placenta : Serologic demonstration by placental elution. In: Transfusion. 2005 ; Vol. 45, No. 8. pp. 1327-1330.
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abstract = "BACKGROUND: Few cases of antibodies to the Cromer (a) antigen have been described during pregnancy. Interestingly, the anti-Cra titers decreased during pregnancy, and although the newborns were Cra+, 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. CASE REPORT: A G4P1 woman with an anti-Cra presented for prenatal care during her fourth pregnancy. The anti-Cra 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-Cra. CONCLUSIONS: This is the fourth case report of a Cromer (a-) woman producing anti-Cra during pregnancy, and the first demonstrating anti-Cra sequestration in the placenta. The presence of anti-Cra 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-Cra from the maternal circulation blocking its passage to the fetus.",
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N2 - BACKGROUND: Few cases of antibodies to the Cromer (a) antigen have been described during pregnancy. Interestingly, the anti-Cra titers decreased during pregnancy, and although the newborns were Cra+, 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. CASE REPORT: A G4P1 woman with an anti-Cra presented for prenatal care during her fourth pregnancy. The anti-Cra 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-Cra. CONCLUSIONS: This is the fourth case report of a Cromer (a-) woman producing anti-Cra during pregnancy, and the first demonstrating anti-Cra sequestration in the placenta. The presence of anti-Cra 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-Cra from the maternal circulation blocking its passage to the fetus.

AB - BACKGROUND: Few cases of antibodies to the Cromer (a) antigen have been described during pregnancy. Interestingly, the anti-Cra titers decreased during pregnancy, and although the newborns were Cra+, 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. CASE REPORT: A G4P1 woman with an anti-Cra presented for prenatal care during her fourth pregnancy. The anti-Cra 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-Cra. CONCLUSIONS: This is the fourth case report of a Cromer (a-) woman producing anti-Cra during pregnancy, and the first demonstrating anti-Cra sequestration in the placenta. The presence of anti-Cra 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-Cra from the maternal circulation blocking its passage to the fetus.

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