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PubMed1995

Rhesus D typing.

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Blood Grouping and Crossmatching↗
PubMed2003

Detection of fetal Rhesus D gene in whole blood of women booking for routine antenatal care.

OBJECTIVE: To determine if the RhD status of the fetus can be detected in an unselected group of RhD-negative women with ongoing pregnancies booking for routine antenatal care. MATERIAL AND METHODS: We obtained 2.5 ml of whole blood from 202 unselected women with a normal ongoing pregnancy who booked for antenatal care before 20 weeks' gestation. DNA was extracted and real time quantitative PCR performed. Primers and a specific probe were targeted at the Rhesus D gene. RESULTS: Of 194 women, 31 were RhD-negative with no evidence of prior isoimmunisation. They delivered 17 RhD-positive and 14 RhD-negative babies. Of the 17 RhD-negative women carrying a RhD-positive fetus, the RhD gene was detected in the maternal blood in 14 (82%). There were no false positives. The quantity of RhD gene detected in the maternal blood of RhD-negative mothers ranged from 2 x 10(2) to 4 x 10(6) copies/ml of whole blood. CONCLUSION: Using real time quantitative PCR assays to amplify free fetal DNA in the maternal circulation, identification of RhD-positive fetuses in RhD-negative mothers is feasible when they book for antenatal care. Before such RhD genotyping can be introduced into clinical practice, however, further studies are required to show that false negative results can be eliminated and to show that this diagnostic test is reliable outside a research setting.

DNA↗
PubMed1985

[Diagnostic and therapeutic use of human anti-D (Rho) monoclonal antibodies. Evaluation and perspectives].

Human monoclonal antibodies will be essential in medicine. They are valuable tools for biological diagnosis and therapeutics. Our model, human monoclonal antibodies directed against the Rhesus D antigen can be used for the determination of the Rhesus D phenotype and for the suppression of Rh(D) immunisation in women. These new products require new procedures of preparation, new regulations for the quality controls, which will be discussed in this paper.

Animals↗
PubMed2005

[Prenatal determination of fetal RHD in maternal plasma: two-years experience of routine clinical use].

OBJECTIVES: To evaluate the predictive value of RHD fetal genotype in maternal plasma of Rh D negative mothers after 10 weeks of gestation in a clinical use. MATERIAL AND METHOD: Prospective, comparative study between fetal RHD genotyping in maternal plasma, with amplification of exons 4,5,10 of the RHD gene, by real-time multiplex PCR, and Rh D serology at birth, in 218 pregnancy and their 223 babies, between November 2002 and 2004. RESULTS: Combining the amplification of three exons, the concordance rate of fetal Rh D genotyping in maternal plasma and baby phenotyping at delivery was 100%. Four women whose the babies were Rh D negative were positive for RHD exon 10 during pregnancy. This positivity was, in three cases, correlated with the presence of RHDpsi pseudogene and in last case, with a haplotype Cdes (r's). RHD genotyping was performed for five twin pregnancies. CONCLUSION: Multiplex PCR using maternal plasma provides perfect prenatal prediction of fetal RHD gene. These results confirm that this non invasive procedure is the preferred method for assessing Rh D fetal status in Rh negative mothers. Using this method for two years in routine practice has led us to modify our management scheme for sensitized Rh D-negative pregnant women.

Female↗
PubMed2006

[Evaluation of conventional hemi nested PCR analysis for fetal RHD determination in maternal plasma].

AIMS: The aim of our study was to evaluate the possibility of identifying the fetal RhD status in maternal plasma using conventional hemi nested PCR analysis. SUBJECTS AND METHODS: After informed written consent, 20 mL of peripheral blood were collected in 99 D-negative pregnant women either at an amniocentesis for prenatal diagnosis or at a prenatal checkup. Fetal DNA extracted from 400 microL of maternal plasma was analyzed by two different operators with a hemi-nested PCR extending an area of the RhD gene exon 10. The results were compared to the fetal RhD status obtained by PCR amniotic fluid analysis or blood analysis of newborns after delivery. The influence of mother's and baby's phenotype were also studied. RESULTS: Among the 99 D-negative pregnant women, all Caucasian, 47 were in their second trimester and 52 in their third trimester (mean: 27.20 weeks of gestation +/-8.25). Sixty-nine fetuses were D-positive and thirty D-negative. The sensitivity and specificity of our technique were respectively 100% and 86.7% and 15% of discordant results were observed between the two operators. Four false positives were observed. According to maternal phenotype, a fetal unexpressed RHD gene was suspected in only one case because of a particular fetal phenotype (ddCcEe). CONCLUSION: A conventional hemi nested PCR analysis of maternal plasma could be used for accurate fetal RhD status. However this procedure is difficult to apply for routine analysis because of the importance of anti-contamination measures required to obtain good results. Real time quantitative PCR analysis on fetal DNA is more suitable. Whatever the operating procedure used, polymorphism of RhD gene may follow in either false negative from presence of rearranged gene or false positive from occasional presence of a non functional RHD gene.

DNA↗
PubMed1987

Failures of intravenous Rh immune globulin prophylaxis: an analysis of the reasons for such failures.

Universal administration of an ion exchange column prepared Rh immune globulin (RhIG-IV) antepartum at 28 weeks' gestation and postpartum to 9,295 Rh negative women delivering Rh positive babies has reduced the prevalence of Rh immunization from the expected 601 to 25 (a protection rate of 95.9%). Rh immunization, despite universal Rh prophylaxis, developed in 25 women; eight before antenatal prophylaxis was administered, 17 after antenatal prophylaxis was administered. Residual Rh immunization is caused by small fetal transplacental hemorrhages (TPH) (greater than or equal to 0.01 mL of fetal blood) before antenatal prophylaxis (15%) and by significant fetal TPH (greater than or equal to 0.05 mL of fetal blood) between 30 and 38 weeks' gestation (18%); TPH was too great, in some instances, for residual passive Rh antibody to give protection. Although a reduction of 62% (five of eight) of early Rh immunization and 82% (14 of 17) of later Rh immunization might be achieved by addition of 16 weeks' to 20 weeks' gestation and 34 weeks' gestation Rh prophylaxis; and a reduction of 84% overall (21 of 25) might be achieved by universal fetal TPH screening every 2 weeks from 10 weeks' gestation until delivery, with administration of RhIG when a small early fetal TPH or a significant later fetal TPH is detected, all of these programs are costly in terms of prevention of perinatal mortality and in terms of cost per quality adjusted life year gained. We believe that the costs outweigh the benefit that would be achieved. Therefore, a residual Rh immunization prevalence of 0.24% to 0.31% during or after each Rh positive pregnancy in patients at risk is to be expected despite universal 28 weeks' gestation antenatal and postnatal Rh prophylaxis.

Female↗
PubMed1993

The role of Rh antibodies in haemolytic disease of the newborn.

Recent insights into the structure-function relationship of IgG, the nature of Fc receptors and their interactions with antibodies, and the cellular mechanisms involved in the immune destruction of IgG-sensitized cells have all contributed to a fuller understanding of the role of Rh antibodies in HDN. As this understanding has increased, so different diagnostic and therapeutic approaches have been developed and evaluated in order either to predict or ameliorate disease severity. The role of Rh antibodies in HDN can be considered in three contexts: maternal anti-D, monoclonal anti-D and prophylactic anti-D. Anti-D formed after maternal alloimmunization may be transported across the placenta, resulting in destruction of sensitized red cells by mononuclear phagocytes in the fetus and infant. The use of monoclonal anti-D has given an insight into the cellular and molecular mechanisms involved in red cell destruction, and has facilitated the development and evaluation of assays which use maternal anti-D to predict the severity of HDN. Polyclonal anti-D, given prophylactically, can prevent maternal alloimmunization to D-positive fetal red cells. Future developments are likely in several areas. Prophylactic polyclonal anti-D may be replaced, wholly or partially, with monoclonal anti-D. The development and introduction of cellular assays as non-invasive tests for predicting disease severity is likely to continue as preliminary results are encouraging. Finally, new strategies for ameliorating disease severity may be assessed including the role of ivIgG and Fc gamma R-blocking antibodies.

ABO Blood-Group System↗
PubMed2002

Laboratory assays for predicting the severity of haemolytic disease of the fetus and newborn.

Haemolytic disease of the fetus and newborn (HDFN) is characterised by the presence of IgG antibodies in the maternal circulation which cause haemolysis in the fetus by crossing the placenta and sensitising red cells for destruction by macrophages in the fetal spleen. Serological, quantitative and cellular assays have all been developed to predict the severity of HDFN. These assays measure and/or characterise alloantibodies in the maternal circulation. Quantitative assays which accurately measure antibody levels correlate with disease severity better than serological assays which are inherently less precise. Nevertheless, high antibody levels are found in some cases of mild HFDN and relatively low antibody levels are found in some severe cases. This suggests that disease severity is influenced by factors in addition to antibody concentration. These factors remain to be fully elucidated but may include: the subclass and glycosylation of maternal antibodies; the structure, site density, maturational development and tissue distribution of blood group antigens; the efficiency of IgG transport to the fetus; the functional maturity of the fetal spleen; polymorphisms which affect Fc receptor function; and the presence of HLA-related inhibitory antibodies. Cellular assays which are sensitive to factors affecting antibody function have, therefore, been developed in an attempt to improve the prediction of disease severity. Although these assays are cumbersome, there are now sufficient data to suggest that some cellular assays provide clinically useful information to complement serological and quantitative assays.

ABO Blood-Group System↗
PubMed2002

Monoclonal anti-D development programme.

Administration of anti-D immunoglobulin to D- women after delivery of a D+ infant has dramatically reduced the number of immunised women and cases of haemolytic disease of the fetus and newborn. The use of monoclonal anti-D might alleviate some of the pressures on maintaining adequate supplies of plasma sourced anti-D. Two human monoclonal antibodies, BRAD-3 (IgG1) and BRAD-5 (IgG3), with proven activity in in vitro functional (immunological) assays with cells bearing IgG Fc receptors (Fc gammaR) were selected for clinical studies. They were prepared by purification of IgG secreted by culture of the Epstein-Barr virus-transformed B cell lines in hollow fibre bioreactors. The mean half-lives of BRAD-3 and BRAD-5 in D- subjects were 10.2 and 22.2 days, respectively. The clearance of D+ red cells injected into D- subjects was accelerated by prior injection of the monoclonal antibodies, both individually and blended (3:1, BRAD-5/BRAD-3). The clearance rate was related to the amount of anti-D on the red cells. Clearance of the D+ red cells coated with BRAD-3 was more rapid in subjects homozygous for Fc gammaRIIIa-F/F158 than in those expressing the Fc gammaRIIIa-V158 allele. The subjects were protected from Rh D immunisation. A large multi-centre study evaluated the BRAD-3/5 blend for its ability to prevent Rh D immunisation in 95 D- subjects given 400 microg i.m. 24 h after injection of 5 ml D+ red cells. Challenge injections of D+ red cells alone were given 24 and 36 weeks later, and blood samples were taken every 4 weeks from the subjects throughout the study for detection of anti-D responses. There was one definite and one possible failure of protection; in one subject the plasma anti-D level rose from week 12 onwards, and in another individual rapid seroconversion was observed at week 28. Considering the relatively large dose of red cells and the number of subjects studied, it was concluded that the failure rate was much lower than in routine Rh D prophylaxis. The responder rate was 13% by week 36 and 24% by week 48. There was no relationship between HLA haplotype and Rh D immunisation. The low percentage of responders and the modest levels of endogenous anti-D produced suggested that administration of monoclonal anti-D had induced long-term specific suppression of anti-D responses in these subjects. The most likely mechanism of action was considered to be inhibition of B cells resulting from co-cross-linking antigen receptors with inhibitory Fc gammaR when the B cells contacted red cells that had bound passive anti-D.

Adult↗