[Prevention of fetal erythroblastosis with anti-D immunoglobulin].
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During the past 40 years several therapeutic approaches have been tried in the management of rhesus-affected pregnancies, with the aim of ameliorating the severity of the condition and preventing intrauterine fetal death. These are reviewed below.
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UNLABELLED: Mutations within the genetic Rh system can produce partial deletions of one or more epitope of the D antigen, known as incomplete D. These people, classified Rh positive, are capable of producing anti-D antibodies when exposed to D positive red blood cells (rbcs). We describe the study of a Rh positive, 34 year old, spanish-indian ("mestiza") female patient, in whose blood anti-D antibodies were detected after a blood transfusions. The results of the tests showed a partial deletion of the D antigen in the patient and three of her family members. PATIENTS AND METHODS: The following tests were done to the patient and her family members: 1) ABO and Rh typing; 2) Direct antiglobulin test; 3) Detection of irregular antibodies in their blood serum; 4) Rh genotype; 5) Cross matching of the patient's serum with rbcs of her Rh positive relatives; 6) Titration of a monoclonal anti-D (IgM) and a polyclonal anti-D (IgG) of human origin with the patient's rbcs and with Rh positive rbcs of her family members whose erythrocytes didn't react with the patient's serum; 7) Measurement of the antigenic density of the D antigen by flow cytometry (indirect immunofluorescence) in the rbcs of the patient and in those family members who had the defect, using a polyclonal anti-D (IgG). RESULTS: 1) An anti-D antibody which didn't react with its own Rh positive rbcs was found in the patient's serum; 2) This antibody didn't react with the Rh positive rbcs of her father and two out of her 4 brothers; 3) The cytometric study of these cells (R)r) showed a immunofluorescence pattern weaker than the control cells of the same genotype, but with a variable expression between 15 to 41%. CONCLUSIONS: The study showed: 1) The presence of an anti-D antibody in a Rh positive patient who had been previously sensitized (by blood transfusion); 2) This antibody was able to react with Rh positive rbcs but not with those of the patient and her family members who had the same partial deletion; 3) The defect was transmitted heterozygously, with a high degree of penetration, but with variable expression; 4) A low antigenic density for her D antigen by flow cytometry.
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Necrotizing enterocolitis in term infants is uncommon, and when it occurs it is usually associated with risk factors such as asphyxia, congenital heart disease, or polycythemia. It has been reported in term neonates after exchange transfusion for hemolytic disease of the newborn; therefore exchange transfusion is recognized as a risk factor. We report two term neonates with hemolytic disease of the newborn resulting from anti-c rhesus incompatibility in whom necrotizing enterocolitis developed before exchange transfusions. These cases implicate hemolytic disease of the newborn without exchange transfusion as a risk factor for necrotizing enterocolitis in term infants.
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