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Without Rh-IgG prophylaxis the incidence of rhesus sensitisation increases in D-negative women with the number of subsequent pregnancies. However, our case report of a d-negative multipara demonstrates that foetal erythroblastosis does not necessarily occur in a pregnancy with initially high anti-D titres.
BACKGROUND: An RhD-negative woman whose partner is heterozygous may have preexisting anti-RhD antibodies that may or may not affect a subsequent fetus, depending on whether it is heterozygous. A safe method of determining fetal RhD type early in pregnancy would eliminate the risks to an RhD-negative fetus of fetal-blood sampling or serial amniocenteses. METHODS: We determined the RhD type in 15 fetuses using the polymerase chain reaction in amniotic cells and serologic methods in fetal blood collected simultaneously. In another 15 fetuses, the RhD type determined from chorionic-villus samples was compared with that identified by typing of DNA from the fetus itself. RESULTS: RhD typing of DNA from amniotic cells correctly indicated the serologic type in every fetus. Of 10 fetuses with RhD-negative mothers, 4 were identified as RhD-negative and 6 as RhD-positive. Of five fetuses with RhD-positive mothers, four were identified as RhD-positive and one as RhD-negative. There was also complete agreement between the results of RhD typing of DNA from chorionic-villus samples and the results of typing of DNA from fetal tissue. Eleven fetuses were RhD-positive, and 4 were RhD-negative. Four RhD-positive fetuses had RhD-negative mothers. Three RhD-negative fetuses had RhD-positive mothers. There was no contamination by maternal RhD-positive DNA of the samples from RhD-negative fetuses. CONCLUSIONS: Determining fetal RhD type in amniotic cells without invading the fetomaternal circulation is a reliable method that will be valuable in the management of Rh alloimmunization.
BACKGROUND: The ability to determine fetal RhD Status noninvasively is useful in the treatment of RhD-sensitized pregnant women whose partners are heterozygous for the RhD gene. The recent demonstration of fetal DNA in maternal plasma raises the possibility that fetal RhD genotyping may be possible with the use of maternal plasma. METHODS: We studied 57 RhD-negative pregnant women and their singleton fetuses. DNA extracted from maternal plasma was analyzed for the RhD gene with a fluorescence-based polymerase-chain-reaction (PCR) test sensitive enough to detect the RhD gene in a single cell. Fetal RhD status was determined directly by serologic analysis of cord blood or PCR analysis of amniotic fluid. RESULTS: Among the 57 RhD-negative women, 12 were in their first trimester of pregnancy, 30 were in their second trimester, and 15 were in their third trimester. Thirty-nine fetuses were RhD-positive, and 18 were RhD-negative. In the samples obtained from women in their second or third trimester of pregnancy, the results of RhD PCR analysis of maternal plasma DNA were completely concordant with the results of serologic analysis. Among the maternal plasma samples collected in the first trimester, 2 contained no RhD DNA, but the fetuses were RhD-positive; the results in the other 10 samples were concordant (7 were RhD-positive, and 3 RhD-negative). CONCLUSIONS: Noninvasive fetal RhD genotyping can be performed rapidly and reliably with the use of maternal plasma beginning in the second trimester of pregnancy.
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OBJECTIVE: The aim of this study was to evaluate the clinical value of an antibody-dependent cell-mediated cytotoxicity assay relative to the indirect antiglobulin test titer in the management of Rh D-alloimmunized pregnancies. STUDY DESIGN: Data from 172 Rh D-alloimmunized pregnancies were analyzed retrospectively. The accuracies of the highest antibody titer and of the highest antibody-dependent cell-mediated cytotoxicity assay result during pregnancy to predict fetal and neonatal Rh disease, defined as the need for intrauterine (n = 30) or neonatal (n = 37) blood transfusion, respectively, were assessed. RESULTS: At different cutoff levels with equal sensitivities the antibody-dependent cell-mediated cytotoxicity assay consistently showed a higher specificity than the antibody titer for the prediction of fetal disease. No difference was found between the receiver operating characteristic curves of the 2 tests for the prediction of neonatal disease. CONCLUSIONS: Selection of patients for referral and invasive testing for Rh D alloimmunization may be improved with the use of an antibody-dependent cell-mediated cytotoxicity assay.
By following the titer of passively acquired Rh antibodies in newborn infants, it is calculated that the half-life of the placenta-passing Rh antibody molecule is approximately 30 days. Evidence is offered that this estimate applies not only to placenta-passing Rh antibodies, but also to other placenta-passing antibodies, and not improbably to serum gamma globulin molecules in general. Studies on the fate of free Rh antibodies in erythroblastotic babies show that these antibodies often are eliminated no more rapidly in Rh-positive babies than in Rh-negative babies. On the other hand, incompatible alpha and beta antibodies, as a rule, are quickly neutralized and eliminated from the body of newborn infants. These observations provide one explanation for the lower incidence of erythroblastosis due to A-B sensitization in comparison with cases resulting from Rh sensitization.
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After several transfusions with D-negative blood, an O Rh-negative women was apparently sensitized to the C and D antigens. In her prenatal workup, it became evident that she had in fact not been sensitized to D but to G, which initially appeared as anti-D plus anti-C. This sensitization pattern is an unusual occurrence in itself. Moreover, the fetus was affected significantly and was delivered at 32 1/2 weeks with moderate hemolytic disease of the newborn. Consideration is given to points regarding current methods of screening Rh-negative women for transfusion, the use of anti-Rh immune globulin in patients sensitized to anti-C and anti-G, medicolegal implications, and continuous attention to the risk-benefit ratio in decisions to use transfusions.
Rhesus (Rh) D alloimmunization may cause haemolytic disease of the fetus and newborn if the fetal Rh blood type is positive. Although the incidence of severe RhD alloimmunization has decreased with prophylactic anti-D immunoglobulin administration during and after pregnancy, sensitization still occurs in a small group of women. In such women, Rh disease will continue to be significant problem and for their babies who may be affected. Preimplantation genetic diagnosis (PGD) may be utilized to avoid materno-fetal blood group incompatibility in an RhD-sensitized woman. Biopsy of a single cell from early cleavage-stage embryos screening for RhD-negative embryos allows the transfer of only RhD-negative embryo(s) into the uterus. This avoids any complications related to haemolytic disease of the fetus and newborn. This article describes the first reported case of an unaffected pregnancy using PGD for Rh disease. IVF and embryo transfer resulted in a clinical pregnancy and the birth of a healthy girl confirmed to be blood type RhD negative. PGD in couples with a heterozygous RhD-positive male partner provides an option for avoiding haemolytic disease of the newborn in RhD alloimmunized mothers.
The indirect antiglobulin test was used to assess the efficacy of anti-D prophylaxis in two Rh negative women with hereditary persistence of fetal hemoglobin. Saturation of all D sites by passive antibody should be followed by indirect antiglobulin positivity due to excess administered anti-D. In hereditary persistence of fetal hemoglobin, all red cells have fetal hemoglobin making the acid elution test (Kleihauer-Betke smear) to detect feto-maternal hemorrhage useless. The indirect antiglobulin test is recommended in patients with hereditary persistence of fetal hemoglobin.
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Kidneys from an Rh-negative cadaver donor were transplanted to two Rh-positive patients. The donor's serum contained anti-Rho (D). In both patients, anti-Rho (D) was detected in their serum and on their red cells 3.5 weeks after transplantation. One patient had hemolysis. The antibodies persisted for nearly six months, despite graft rejection and nephrectomy in one case. These antibodies presumably arose from passenger B lymphocytes in the grafts from the Rh-immunized donor.
Transfusion of one unit or more of Rh-positive red blood cells normally causes circulating anti-D antibody to appear 2-6 months later in 80-95% of Rh- persons. We asked whether transplant immunosuppression with cyclosporine and corticosteroids affects Rh immunization. Nineteen Rh- liver, heart, and heart-lung transplant recipients received 3-153 (median: 10) units of Rh+ RBCs at surgery and were tested for anti-D greater than 2 months later. Three patients developed anti-D at 11-15 days; one may have had an unusually rapid primary immune response and two were secondary to previous exposure by pregnancy. None of the other 16 patients had anti-D when tested 2.5-51 months later (13 patients, greater than 11.5 months). This low rate of Rhesus immunization in association with cyclosporine immunosuppression allows greater flexibility in meeting the transfusion needs of Rh- liver and heart transplant patients. Caution is still advised in young females and in patients who may have been previously exposed to Rh+ RBCs by transfusion or by pregnancy prior to the availability of perinatal Rh immune globulin twenty years ago. Other humoral immune responses to some vaccines or infectious agents may also be impaired in transplant patients.
Rhesus (Rh) D blood group incompatibility between the pregnant woman and her fetus is a significant problem due to the possibility of maternal alloimmunization and consequent hemolytic disease of the newborn. The RhD-negative blood group is found in 15% of whites, 3-5% of black Africans, and is rare in Asians. Advances in both our understanding of the RHD locus and its variants, as well as technical improvements in the extraction and amplification of cell-free fetal DNA in maternal plasma, have led to incorporation of noninvasive diagnosis of RHD genotype into routine prenatal care in the United Kingdom, France, and the Netherlands. In this commentary we examine the experience to date with large-scale clinical trials performed in the European Union, describe approaches to reduce false-positive and false-negative results, and review ongoing research to standardize assays and reduce costs using automated assays. False-negative cases are mainly due to either a lack of fetal DNA in the maternal sample due to early gestation or insensitive methods. False-positive cases are due to genotypic variants observed in individuals of African ancestry. Noninvasive prenatal diagnosis of fetal Rhesus D genotype is sensitive and accurate and has been widely validated in Europe. The United States should begin to undertake clinical trials to bring this technology to patient care as soon as possible.
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BACKGROUND AND OBJECTIVES: Despite a successful outcome of the anti-D prophylaxis programme, alloimmunization still occurs. The aim of this study was to estimate the frequency of Rh-specific B lymphocytes in the peripheral blood of nine Rh-alloimmunized individuals at different time intervals after parturition. MATERIALS AND METHODS: The donors' B lymphocytes were transformed with Epstein-Barr virus (EBV) and cultured at different cell densities over a feeder of human fetal fibroblasts. Culture supernatants were screened for human immunoglobulin by enzyme-linked immunosorbent assay (ELISA) and for anti-Rh antibody by using a direct haemagglutination technique. The percentage of CD19+ B lymphocytes in peripheral blood was determined by flow cytometry, and the frequency of Rh-specific B lymphocytes was estimated by limiting-dilution assay (LDA). RESULTS: The frequency of Rh-specific B lymphocytes varied from 1 : 150 to 1 : 27,850 in different donors. There was a decrease in this frequency and level of anti-Rh antibody with increase in time interval between bleeding and last exposure to the antigen. Furthermore, a positive correlation was observed between the titre of Rh-specific antibody and frequency of Rh-specific B cells in each of three subjects bled at multiple time-points postdelivery. CONCLUSIONS: The magnitude of the specific antibody response to Rh antigens varies greatly in Rh-alloimmunized women, which partly reflects the difference in frequency of specific B cells in these individuals.
Reported here is the first example of a partial D antigen stimulating the production of anti-D: stimulation was of fetal origin. During her second pregnancy, anti-D developed in the serum of a D-negative mother who had received Rh immunoglobulin after the birth of her first D-positive child. Her second baby had moderate neonatal jaundice and was successfully treated by phototherapy. Subsequently the red cells of the father and of the first child were shown to carry a partial D antigen of category DVa type. Six available batches of Rh immunoglobulin reacted with DVa cells.
After anti-RhD, anti-Rhc is the most important red cell alloantibody which can cause haemolytic disease of the newborn (HDN) when the mother is Rhc-negative and the fetus Rhc-positive. We report here the development of polymerase chain reaction (PCR) assays which detect the presence of the Rhc alleles in amniotic cells by the use of allele-specific primers (ASP). It is expected that such determination will help in the management of pregnancies at risk of Rhc haemolytic disease. In the course of this study we have similarly performed PCR-ASP experiments to detect fetal RHE alleles since, in rare cases, anti-RhE can also cause HDN.