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Anti‐Co a implicated in severe haemolytic disease of the foetus and newborn
Author(s) -
Michalewska B.,
Wielgos M.,
Zupanska B.,
Bartkowiak R.
Publication year - 2008
Publication title -
transfusion medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.471
H-Index - 59
eISSN - 1365-3148
pISSN - 0958-7578
DOI - 10.1111/j.1365-3148.2007.00799.x
Subject(s) - fetus , medicine , obstetrics , exchange transfusion , gestation , pregnancy , haemolytic disease , caesarean section , hydrops fetalis , erythroblastosis fetalis , rh isoimmunization , antibody , pediatrics , immunology , biology , genetics
summary The Colton (Co a ) 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‐Co a are rare. We report a severe HDFN due to anti‐Co a . 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‐Co a in the maternal serum, the father typed as Co(a+). The third pregnancy was followed up by the measurements of anti‐Co a 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‐Co a 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‐Co a 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‐Co a .