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Anti-Coa implicated in severe haemolytic disease of the foetus and newborn.
- Source :
-
Transfusion Medicine . Feb2008, Vol. 18 Issue 1, p71-73. 3p. 1 Chart. - Publication Year :
- 2008
-
Abstract
- The Colton (Coa) antigen is of high frequency; its incidence in Caucasians is about 99.8%. Reports on haemolytic transfusion reactions and haemolytic disease of the foetus/newborn (HDFN) due to anti-Coa are rare. We report a severe HDFN due to anti-Coa. The first child of the mother was healthy. The second died a few hours after delivery because of hydrops fetalis, likely due to HDFN; anti-Coa in the maternal serum, the father typed as Co(a+). The third pregnancy was followed up by the measurements of anti-Coa titre (additional antibodies were excluded), its functional activity by the chemiluminescence test (CLT) and the Doppler flow in the middle cerebral artery of the foetus. Increased values of antibody titre up to 128, the CLT to 30% and multiplex of median of the peak systolic velocity to 1·71 indicated haemolytic disease and the necessity for an intrauterine transfusion. The foetus received the maternal red blood cells (RBCs). Delivery had to be by Caesarean section for obstetrical reasons at 34-week gestation. The newborn (anti-Coa on red cells and in plasma, the rise of the bilirubin concentration up to 333 μmol L−1) had four exchange transfusions: the first of maternal RBCs, the remaining of donor’s Co(a+) cells and one top-up transfusion. The baby was discharged in good health. Anti-Coa was responsible for severe HDFN. Proper monitoring during pregnancy and antenatal and post-natal therapy were successful. This is the second severe published HDFN due to anti-Coa. [ABSTRACT FROM AUTHOR]
- Subjects :
- *NEONATAL diseases
*BLOOD cells
*FETUS
*PREGNANT women
*CESAREAN section
*OBSTETRICS
Subjects
Details
- Language :
- English
- ISSN :
- 09587578
- Volume :
- 18
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Transfusion Medicine
- Publication Type :
- Academic Journal
- Accession number :
- 29361120
- Full Text :
- https://doi.org/10.1111/j.1365-3148.2007.00799.x