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PubMed1989

[The erythrocyte phenotype Rh: 32,-46: transfusional and obstetric importance].

The red blood cells and sera from 21 RN/RN individuals were studied. The study confirmed the Rh type D+C+E-c-e+, CW-, characterized by an increased expression of the D antigen, a markedly decreased expression of the C and e antigens, the presence of a low incidence antigen (Rh32) and the absence of a high incidence antigen (Rh46) associated with an epitope recognized by a murine monoclonal antibody (MR 432). Four individuals exposed to Rh46 cells by pregnancy and/or transfusion had an anti-Rh46 antibody. This antibody gave positive reactions with all red blood cells of common and rare Rh phenotype except Rh null, D--, D.., DC(W-) and RN/RN cells. This antibody is considered to be of clinical significance in case of transfusion or pregnancy.

Africa↗
PubMed2002

In vivo studies of monoclonal anti-D and the mechanism of immune suppression.

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 gamma R) 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 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 subjects were protected from Rh D immunisation. A large multicentre study evaluated the BRAD-3/5 blend for its ability to prevent Rh D immunisation in 95 D- subjects given 400 micrograms i.m. 24 hours 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. 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-crosslinking antigen receptors with inhibitory Fc gamma R when the B cells contacted red cells that had bound passive anti-D.

Adult↗
PubMed2000

[Prevention of fetal hemolytic disease: it is time to take action].

In spite of the progress made since 1970 in specific prevention by anti-rhesus immunoglobulins, and improved management of at-risk pregnancies, allo-immunization due to the erythrocytic Rh 1 antigen (formerly known as Rhesus D or Rh D) remains widespread. In fact, anti-Rh 1 antibodies currently constitute over one-third of the immune antibodies detected after pregnancy. The prevention of allo-immunization against the Rh 1 antigen is therefore still problematical, and concerns approximately one pregnant woman in seven. The etiology and pathology of fetal hemolytic disease have been recalled, and the treatment approach during pregnancy and delivery has been carefully examined. Tests for quantifying the risk of fetomaternal hemorrhage have also been described. This approach aims at improving the methods of preventing allo-immunization (e.g., during pregnancy and delivery) and the efficacy of treatment. It is also stated that if the necessary preventive action is not taken in cases of allo-immunization due to to the Rh 1 antigen, this should be considered a grave medical fault.

Erythroblastosis, Fetal↗
PubMed2001

Mechanism of anti-D-mediated immune suppression--a paradox awaiting resolution?

During pregnancy, women can be immunized by fetal red blood cells (RBCs) of an incompatible blood group. Subsequent transplacental passage of the antibodies can result in fetal morbidity or mortality due to RBC destruction. The administration of anti-D antibodies to D(-) women after delivery of a D(+) infant, and subsequent prevention of Rhesus (Rh) D haemolytic disease of the fetus and newborn, is the most successful clinical use of antibody-mediated immune suppression. The passive IgG anti-D might prevent immunization to D(+) RBCs by an IgG Fcgamma receptor (Fcgamma R)-dependent mechanism such as crosslinking the D-specific B-cell receptor and inhibitory FcgammaRIIb. However, recent murine studies demonstrate that the suppressive effects of antibodies to heterologous RBCs can be Fcgamma R-independent, suggesting other mechanisms might contribute.

Animals↗
PubMed2002

Prediction of fetal Rh D and Rh CcEe phenotype from maternal plasma with real-time polymerase chain reaction.

Real-time PCR methods for the detection of RHD and the C, c, and E allele of RHCE were applied for the prediction of fetal Rh phenotype using maternal plasma. In one of 36 samples investigated the DNA extraction failed. When we tested the remaining 35 samples for Rh antigens which were absent on the mother's red cells, the fetal D-status was correctly determined in 26 of 27 cases (1 false negative). Fetal C was tested correctly in 23 samples, c was true positive in the only c-negative woman and the fetal E-status was correctly determined in 35 cases. In conclusion real-time PCR of maternal plasma is a non-invasive method to determine fetal RH genotype. However, more studies are required for routine applications because the method is not 100% sensitive.

Alleles↗
PubMed1997

Measurement of feto-maternal haemorrhage: a comparative study of three Kleihauer techniques and tow flow cytometry methods.

In the UK a Kleihauer test is routinely performed on all RhD-negative women after the birth of an RhD-positive child to ensure that an adequate dose of anti-D immunoglobulin is given. The results of Kleihauer testing are interpreted to assess the volume of any feto-maternal haemorrhage and additional anti-D immunoglobulin is administered if necessary. A similar procedure is followed ante-natally when incidents occur known to be associated with alloimmunization. The performance of Kleihauer tests is difficult to standardize and there can be problems in interpreting the volume of feto-maternal haemorrhage. The use of flow cytometry to measure feto-maternal haemorrhage is reported to give more accurate and reliable results. This study compared three different Kleihauer methods and two different flow cytometry techniques all performed using the same maternal sample and within a single laboratory. The results demonstrated variability between the Kleihauer tests used and also in the flow cytometry measurements. A well-performed Kleihauer test would still appear to be useful as a screening technique for detection of feto-maternal haemorrhage. However, accurate quantitation of size of feto-maternal haemorrhage is more reliably determined by flow cytometry.

Erythrocytes↗
PubMed2002

Quantification of foetomaternal haemorrhage. An analysis of two cytometric techniques and a semiquantitative gel agglutination test.

Traditional tests to screen for foetomaternal haemorrhage are time-consuming and difficult to perform. The Kleihauer test is widely used but difficult to standardize. We evaluated three techniques for quantifying foetomaternal haemorrhage: a semiquantitative gel agglutination test and two flow cytometric techniques. The gel agglutination test is based on the consumption of anti-D reagent by D+ cells, analysing the reaction of the supernatant against indicator cells in a Coombs-gel card. In the two colour direct immunofluorescent technique, the sample is incubated with Per-CP labelled anti CD45 antibody, fixed with glutaraldehyde and permeabilized by exposure to Triton X-100. An aliquot is stained with an antibody to foetal haemoglobin, conjugated with fluorescein isothiocyanate or phycoerythrin. The indirect immunofluorescent technique is based on the labelling of Rh (D) antigen with an anti D reagent, followed by the addition of an anti IgG antibody conjugated with phycoerythrin. Foetomaternal haemorrhage was not detected in 75 of the 85 samples analysed by the direct immunofluorescent technique. In the remaining 10 samples, the volume was very low. Thirty-five samples with Rh (D) antigen incompatibility were analysed in parallel by the indirect immunofluorescent technique and in 15 of the 35 samples, the gel agglutination technique was also carried out. The three techniques gave similar results. The gel agglutination test can be used to screen for foetomaternal haemorrhage, while greater volumes should be quantified by flow cytometric techniques.

Agglutination Tests↗
PubMed2002

Evaluation of flow cytometric enumeration of foetal erythrocytes in maternal blood.

In pregnant women subject to abdominal trauma or other foetomaternal haemorrhage, foetal red blood cells containing haemoglobin-F (HbF) can be found in the circulation. Recently, a monoclonal antibody to HbF has become commercially available, enabling application of a flow cytometric immunofluorescence method for accurately determining the concentration of HbF+ red blood cells. We demonstrate that white blood cells are included in the cluster selected as red blood cells and that these white blood cells exhibit a level of autofluorescence that coincides with the fluorescence signal from HbF+ red blood cells. However, these white blood cells can be excluded from the analysis, thus preventing spuriously increased HbF+ red blood cell counts. We present the results of patient samples containing HbF+ red cells as illustrations of the technique and as a potential interference by HbF-containing cells of nonfoetal origin. Using samples spiked with cord blood, the method is exactly linear with a high coefficient of correlation (r=0.997). Furthermore, the assay has excellent precision (CV < 2.4%), a low limit of detection (0.12% HbF+ RBC), is independent of Rhesus D and can be completed within 1.5 h. This method is suitable for accurate determination of foetomaternal haemorrhage.

Adult↗
PubMed1999

Monitoring the clearance of fetal RhD-positive red cells in FMH following RhD immunoglobulin administration.

Anti-RhD immunoglobulin was administered to RhD-negative women based on estimates of fetal bleed size obtained using a direct immunofluorescence flow cytometric technique employing a FITC-conjugated monoclonal human anti-D (BRAD 3). The effectiveness of the dose administered was assessed by (i) measuring the fraction of RhD-positive fetal cells in the maternal circulation at d0, and between d2 and d10 post RhD Ig administration, (ii) quantifying the amount of anti-D detectable in maternal plasma following RhD Ig injection in the perinatal period and (iii) assessing maternal serum for the presence of immune anti-D in follow-up samples taken 3 months to 3 years after delivery. Fifty-four women were assessed, 29 having fetal bleeds in excess of 4 mL. Follow-up samples were received from 20/29 mothers after RhD Ig administration; 43-99% and 69-99% of fetal cells had been cleared by d2/3 and d5/6, respectively, in 14/20 mothers, whereas less than 50% had been cleared in the remaining mothers. Long-term follow-up samples were obtained from eight of the 29 mothers (four with bleeds >/=20 mL, two with bleeds >95 mL): none had detectable anti-D in the serum 4 months to 3 years after delivery despite the persistence of up to 36% fetal RhD-positive cells in the maternal circulation six days after delivery.

Erythrocytes↗
PubMed2001

RHD sequencing: a new tool for decision making on transfusion therapy and provision of Rh prophylaxis.

The serological differentiation of weak D from partial D, D-negative and D-positive is not always unequivocal. Therefore, sequencing of the RHD gene is required in some cases. Very recently, several new differences between RHD and RHCE have been identified which permitted us to design primers close to the exon/intron boundaries of the RHD-exons. We evaluated these primers in 83 D-positive and 18 D-negative blood donors and applied the new method for the characterization of the RHD gene in six individuals with weak D phenotype. The amplification reactions were concordant with serological findings in 100 of 101 donors (99.0%). In one D-positive donor the PCR for exons 2 and 5 gave a negative result, while the sequence of the remaining eight exons was unchanged. By sequencing samples with very weak D serological reactions, we identified weak D type 4.2.2 and weak D type 15, both previously reported to be associated with anti-D-alloimmunization. Consequently, we recommended the selection of D-negative blood in the weak D type 4.2.2 patient, and the provision of Rh prophylaxis for pregnant women with weak D type 15. In summary, a new RHD sequencing method was developed which can be applied if serological reactions are inconclusive.

Blood Donors↗
PubMed2001

Identification and quantification of anti-D, -C and -G in alloimmunized pregnant women.

Our objectives were to investigate possible overestimation of maternal anti-D due to co-existing anti-C and/or anti-G, and to confirm the presence of anti-D in plasma presumed to contain anti-D+C. We investigated 96 samples (from 22 antenatal patients and 74 blood donors) initially identified as containing anti-D+C using routine investigation procedures. Anti-D quantification was performed using an Astoria Pacific International 300 (API 300) continuous flow analyser with R1R1 and R2R2 reagent red cells. Where possible, samples were tested manually using a rare D+, C-, G- cell, to confirm the presence of anti-D. Fifty-two of 96 samples (11/22 antenatal patients and 41/74 blood donors) gave >50% higher anti-D quantification results with R1R1 cells than with R2R2 cells. Anti-D was not detected using manual techniques in 16 of 73 samples tested (10/22 antenatal patients and 6/51 blood donors). Anti-D quantification using R1R1 reagent red cells may cause inaccurate estimation of anti-D levels, when anti-C and/or anti-G are present. Indeed, a significant number of cases, where apparent anti-D+C is identified, may contain only anti-C+G and lack an anti-D component. This may in turn lead to a failure to administer prophylactic anti-D immunoglobulin to RhD negative patients in cases where anti-D is not present, putting these patients at risk from immunization with possible consequences to future pregnancies.

Blood Grouping and Crossmatching↗
PubMed2001

Monoclonal anti-D for immunoprophylaxis.

Routine antenatal prophylaxis with anti-D has become accepted as desirable, but concerns have been expressed about the adequacies of supply and safety of polyclonal anti-D. Human monoclonal anti-D has been produced using Epstein-Barr virus (EBV)-transformed peripheral B cells, sometimes coupled with fusions to myeloma cell lines. More recently, molecular biology techniques have been used to produce human monoclonal anti-D in a variety of different ways. Many monoclonal antibodies (mAbs) have been characterized for fine specificity and in vitro functional activity in International Workshops. Two mAbs have been shown to cause red cell clearance and immunosuppression in male volunteers. Considerations for the future development of monoclonal anti-D for prophylactic use are reviewed.

Antibodies, Monoclonal↗