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D J van Rhenen

Publications and source records attributed to D J van Rhenen.

At least 19 recordsLinked to original sources
PubMed1999

DAR, a new RhD variant involving exons 4, 5, and 7, often in linkage with ceAR, a new Rhce variant frequently found in African blacks.

The highly polymorphic Rh system is encoded by 2 homologous genes RHD and RHCE. Gene rearrangements, deletions, or point mutations may cause partial D and CE antigens. In this study, a new RHD variant, DAR, and a new RHCE variant, ceAR, are described in 4 Dutch African Blacks. Serologically, DAR showed weaker reactions with a monoclonal antibody and polyclonal antiserum against D. The DAR phenotype was characterized by complete loss of at least 9 of 37 Rh D epitopes. Erythrocytes expressing ceAR were all typed as VS(-), V(+). DNA analysis showed a partial D allele with only 3 mutations: C602G (exon 4), T667G (exon 5), and T1025C (exon 7). The ceAR allele carried G48C (exon 1), a hybrid exon 5 (A712G, C733G, A787G, and T800A), and A916G (exon 6). To study the frequency of these variants, 326 South-African Blacks was screened genomically. Of the 326 donors, 16 (4.9%) carried the DAR allele, 20 (6.1%) the ceAR allele, and 14 (4.3%) both mutated alleles. Five of these donors (1.5%) had the DAR phenotype, indicating that they carried the DAR allele homozygously or next to a D-negative allele. Immunogenicity of the D antigen for individuals with the DAR phenotype was proven, because 1 of the 4 Dutch individuals produced allo-antibodies against D after multiple transfusions with D-positive blood. In a multiethnic society, the prevalence of this D phenotype will increase and is therefore relevant in transfusion practice and in prevention of hemolytic disease of the newborn.

Africa↗
PubMed1998

Quality and standardization in blood component preparation with an automated blood processing technique.

The use of automated blood processors in combination with bottom and top blood containers has been found to improve the standardization and quality of blood components. A study was performed to validate a new type of processor (Optipress II) and compare its performance with a first generation processor (Optipress I). Primary separation on the Optipress II was investigated on 570 mL (+/- 10%) of anticoagulated blood in a nonpaired study. In addition, the quality of the products in routine production was compared between the results of the Optipress I and Optipress II. The whole blood units were kept overnight at room temperature (20 +/- 2 degrees C). Separation was performed under conditions to obtain 55 mL buffy coats with a 50% haematocrit (ht). Platelet concentrate preparation was investigated in a paired study and compared to the routine manual method using PAS II additive solution. Parameters studied were volume, red cell, white cell and platelet counts, ht, haemoglobin (hb, total and free). Primary separation was more efficient in the Optipress II because the platelet count was lower in the erythrocyte concentrates (P < 0.0001), platelets were lower in plasma (P < 0.0001) and platelet counts were higher in buffy coats (P < 0.0001). Buffy coat volume showed less variation (Optipress II VC = 4%, Optipress I VC = 7.4%). Secondary separation did not show differences between the Optipress II and manual method but was advantageous because of the automatic termination of the procedure. Further improvement of standardization in blood component preparation is possible with an automated blood processor, leading to improvement of the quality of blood products for patient care.

Blood Component Removal↗
PubMed1997

[Immunological effects of erythrocyte and leukocyte transfusion. Work Group Blood Group Serology of the Medical Advisory Commission of the College for Blood Transfusion of the Netherlands Red Cross].

Immunological consequences of blood transfusion are less well-known than infectious complications although they occur more frequently. In many cases the effects in individual patients are hardly visible although fatal transfusion reactions may occur: Transfusion of red cells may induce acute or delayed haemolytic transfusion reactions. Transfusion of leukocytes may suppress the function of the immune system of the recipient (with consequences for immune tolerance in transplant patients, cancer surveillance and the occurrence of postoperative infections) but also may induce graft versus host disease.

Erythrocyte Transfusion↗
PubMed1997

Risk factors and anti-HBc reactivity among first time blood donors.

BACKGROUND AND OBJECTIVES: The usefulness of testing for antibody to hepatitis B core antigen (anti-HBc) as a surrogate marker for non-A, non-B hepatitis can no longer be clearly established in the face of anti-hepatitis C virus testing. Application of anti-HBc testing in blood donors for detection of hepatitis B in addition to hepatitis B surface antigen testing (HbsAg) is a matter of debate. MATERIALS AND METHODS: We examined the serology and risk analysis data in a group of first-time blood donors. In 1.48% of 16,081 donors, anti-HBc reactivity was found. We invited a study group of 112 donors for extensive interviewing about the risk of blood transmissible diseases, and for serological testing. A control group of 240 first-time donors was studied as well. RESULTS: In the study group, the age was older (p < 0.001), a history of liver disease was more frequent (p < 0.001), and the donor (p < 0.001) or the donor's partner (p < 0.05) had either stayed longer in an HBV-endemic area or had been born in one. Combining these with the serological results, we found that strong anti-HBc reactivity was related to hepatitis B risk factors in HBsAg-negative donors. CONCLUSIONS: Anti-HBc testing in HbsAg-negative first-time donors makes it possible to identify hepatitis B risk factors with a prevalence of 0.02%. Our findings also stress the importance of including the history of the donor's partner(s) in the risk analysis before blood donation.

Adult↗
PubMed1997

Lower antigen site density and weak D immunogenicity cannot be explained by structural genomic abnormalities or regulatory defects of the RHD gene.

BACKGROUND: The weak D phenotype is characterized serologically by a weak or negative agglutination reaction with polyclonal anti-D in an immediate-spin test. Agglutination is enhanced in the indirect antiglobulin test. Red cells that are typed weak D have a much lower number of apparently complete D antigens at their cell surface and are associated with considerably weaker immunogenicity than are red cells with normal D. In a previous study, the number of D sites per cell was determined in eight unrelated weak D individuals to range from 490 to 1870 D sites per cell, which corresponded to 4 to 14.2 percent of the number of D sites in CcDee samples. STUDY DESIGN AND METHODS: The RHD gene was investigated for structural abnormalities by Southern blot experiments and polymerase chain reaction-based RHD typing in these individuals. In addition, abnormalities in the transcription process were studied by sequence analysis of RH transcripts and by comparing the relative amounts of RHD mRNA in weak D to those in CcDee, CcDEe, and -D- samples by using a semiquantitative reverse transcriptase-polymerase chain reaction analysis. RESULTS: The RHD gene in weak D phenotypes does not show any abnormalities at either the genomic or the transcriptional level when compared to the RHD gene in normal D phenotypes. CONCLUSION: The weaker immunogenicity of weak D is not explained by structural difference in the RHD gene itself. The weaker expression of D might be caused by factors involved in the Rh-related complex or by an as yet unidentified suppressor gene. This study supports the concept that weak D phenotypes carry complete D polypeptides and reflect a quantitative rather than a qualitative variation of D.

Antibodies, Monoclonal↗
PubMed1996

Rh DNA analysis.

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Humans↗
PubMed1996

The R0Har RH:33 phenotype results from substitution of exon 5 of the RHCE gene by the corresponding exon of the RHD gene.

The highly polymorphic Rh (Rhesus) system is encoded by two homologous genes, one encoding the D polypeptide and the other the CcEe polypeptides. Partial D antigens may be caused by gene rearrangements, deletions or point mutations. In this study the molecular basis of R0Har RH:33, a Rh phenotype of low frequency, is described. The R0Har RH:33 phenotype is characterized by partial expression of D, altered expression of e, absence of G and the presence of two antigens of low frequency: Rh33 and FPTT. Southern blot analysis, RHD typing by PCR and sequence analysis of Rh transcripts revealed that the RHD gene is absent in subjects with this phenotype. Apart from the expected RHCE transcripts, a new Rh transcript, RHc(D)(e), was identified in three unrelated individuals expressing R0Har Rh:33. The RHc(D)(e) transcript showed the same sequence as the RHce transcript, with the exception of exon 5, which was substituted by the corresponding exon of the RHD gene. A method for PCR-based genotyping was developed to determine specifically the c(D)(e) haplotype. The c(D)(e) PCR proved to be a reliable alternative method for R0Har RH:33 typing.

Base Sequence↗
PubMed1996

The genetic basis of a new partial D antigen: DDBT.

The Rh system, the most polymorphic system on red cells, is genetically controlled by two different but highly homologous genes on chromosome 1. The RHCE gene encodes different RhCcEe polypeptides and the RHD gene encodes D antigens. It is well established that in D negative individuals the RHD gene is either absent or grossly deleted. The D antigen comprises at least nine serologically defined D epitopes. The D antigen can be divided into different partial D categories, reflecting a different pattern of specific D epitopes. In this study a newly defined partial D antigen, DDBT, was studied. D epitope mapping revealed the presence of D epitopes 6/7 and 8 and the absence of the other D epitopes. The molecular basis of this phenotype was studied by Southern blotting, by RHD typing using the polymerase chain reaction (RHD-PCR) and by sequence analysis of Rh transcripts. The DBT phenotype appeared to be encoded by a hybrid RHD gene, in which exons 5, 6 and 7 (and possibly the identical exon 8) were replaced by the corresponding exons of the RHCE gene. From this study it may be concluded that D epitopes 1, 2, 3, 4, 5 and 9 are dependent on the presence of RHD exons 5, 6, and 7.

Base Sequence↗
PubMed1996

The RoHar antigenic complex is associated with a limited number of D epitopes and alloanti-D production: a study of three unrelated persons and their families.

BACKGROUND: the RoHar antigenic complex has been characterized serologically by difficulties in D typing, weak e expression, lack of G antigen, presence of Rh33, a low-frequency Rh antigen, and, more recently, a second low-frequency antigen, FPTT. Allocation to one of the partial D catagories was not considered because of the unuaual reactions of RoHar cells and because anti-D production was not observed in RoHar persons. STUDY DESIGN AND METHODS: Three unrelated RoHar donors and their families were studied in detail with special emphasis on D epitope mapping, e and G typing, and screening for antibodies. RESULTS: Only D epitopes 5 and 6/7 were demonstrable, and D epitopes 1, 2, 3, 4, 8, and 9 seem to be absent in the RoHar complex. In one individual, the presence of alloanti-D with limited specificity, not reacting with RoHar red cells of other individuals, was found 6 months after a second D+ pregnancy. CONCLUSION: The finding of alloanti-D in an RoHar r person supports the concept that the D characteristic of this phenotype is a partial D antigen, which is consistent with the presence of the limited number of D epitopes found in epitope mapping. As has been suggested for other partial D antigens, RoHar individuals should be regarded as D- for the receipt of blood, and pregnant RoHar women who have had D+ pregnancies should receive anti-D prophylaxis.

Epitopes↗
PubMed1996

Involvement of Ser103 of the Rh polypeptides in G epitope formation.

BACKGROUND: Almost all red cells that carry D and/or C antigens also express the G antigen (Rh12). A study was conducted on the molecular background of the G epitope. STUDY DESIGN AND METHODS: Two unrelated donors with the rare ccDEe, G- phenotype and one donor with the ccEe, G+ phenotype were studied. Genomic DNA and cDNA of these donors were studied with polymerase chain reaction, Southern blot, and sequence analysis, with special focus on exon 2, because it is only in this exon that there are supposed to be similarities between RHD and the RHC allele, but not between RHD and the RHc allele. RESULTS: In both ccDEe, G- donors, a nucleotide substitution was found in exon 2 of RHD; T307 was replaced by C307, which predicted a Ser->Pro substitution at amino acid position 103 of the D polypeptide. The ccEe, G+ donor carried the complete exon 2 of RHD. Moreover, despite the absence of all known D epitopes, this donor also carried RHD characteristics in exons 1 to 3 and exon 9 and further downstream. CONCLUSION: Ser103, encoded by exon 2 of the RH genes, is involved in G epitope formation.

Blotting, Southern↗
PubMed1996

Characterization of the hybrid RHD gene leading to the partial D category IIIc phenotype.

BACKGROUND: A D-positive white woman was found to have produced alloanti-D leading to hemolytic disease of the newborn in her third D-positive child. The maternal D was identified as the partial D category IIIc antigen (DIIIc). The molecular basis of this phenotype was studied. STUDY DESIGN AND METHODS: The proposita and her relatives were phenotyped for Rh system antigens with standard reagents. D(IIIc) typing of D-positive red cells was done with serum that contained anti-D from the proposita. Southern blot analysis and RHD-specific polymerase chain reactions were performed with genomic DNA. Rh transcripts were cloned and sequenced. RESULTS: Six relatives of the proposita were found to express the DIIIc phenotype, which traveled with Ce. The DIIIc phenotype was inherited in a Mendelian fashion. Southern blot analysis showed an identical digestion pattern in D(IIIc) individuals and in DD controls. Three different Rh transcripts were found. Two Rh transcripts were derived from RHCE (RHce and RHCe). The RHD-derived Rh transcript was the same as that of the published RHD sequence, apart from exon 3, which appeared to be exon 3 of RHCE. At the genomic level, RHD exon 3 was missing in all individuals expressing D(IIIc). CONCLUSION: This study shows the characteristics of a new hybrid D-CE-D allele encoding D(IIIc). It may be concluded that exon 3 of RHD is not involved in the formation of any of the D epitopes known at present, but rather encodes a new D epitope or D epitopes, as yet undefined by monoclonal anti-D reagents.

Adult↗
PubMed1996

Intensification of donor interviewing procedures: a feasibility study.

OBJECTIVE: To determine the feasibility and acceptability for the blood donor of an intensified blood donor interviewing procedure on high-risk factors for infectious diseases. To answer the question whether an intensified blood donor interviewing procedure would lead to an unacceptable loss of blood donors. DESIGN: Feasibility study. SETTING: Red Cross Bloodbank Rotterdam. DONORS: Study group of 240 first-time donors. INTERVENTIONS: Intensified donor interviewing techniques by direct questioning and workload assessment. RESULTS: Intensified interviewing was welcomed by 88-91% of first-time donors and rejected by 2-5%. On the question whether the intensified interviewing procedure should be the standard approach of the blood bank the answer was positive in 76-82% of first-time donors and negative in 11-14%. No blood donors indicated that this would be a reason to withdraw from blood donation. The workload for the blood bank physician increased by approximately 30%. CONCLUSION: The approach of intensified donor interviewing techniques in first-time donors is acceptable both to the donors and the blood bank workload.

Adolescent↗
PubMed1995

Evaluation of a new citrate-acetate-NaCl platelet additive solution for the storage of white cell-reduced platelet concentrates obtained from half-strength CPD pooled buffy coats.

BACKGROUND: A new citrate-acetate-NaCl platelet additive solution, identified as PAS 2, was developed to prepare platelet concentrates (PCs) from pooled 0.5 CPD buffy coats (BCs). STUDY DESIGN AND METHODS: A study was undertaken to evaluate PAS 2 in vitro (n = 8) and in vivo (n = 9) against a commercially available solution (Plasma-Lyte A). In a paired in vitro study, a comparison was made of platelet and white cell concentration; blood gases and bicarbonate; glucose and lactate concentration; total intracellular concentration of adenine nucleotides and beta-thromboglobulin release. RESULTS: A lower platelet yield (p < 0.0001) and a higher beta-thromboglobulin release (p < 0.01) are observed with Plasma-Lyte A. For this reason, half-strength (0.5) CPD was changed to full-strength CPD in the clinical study with Plasma-Lyte A. In a clinical evaluation of nine patients with bone marrow failure, all received PCs with both PAS 2 and Plasma-Lyte A that had a shelf life of at least 4 days. Corrected count increments (CCls) were as follows, on average (95% Cl): the CCl at 1 to 4 hours was 22.4 (95% Cl, 15.2-29.4) for PAS 2 and 24.0 (95% Cl, 16.9-31.2) for Plasma-Lyte A; that at 12 to 24 hours was 11.3 (95% Cl, 4.1-18.4) for PAS 2 and 14.2 (95% Cl, 7.1-21.3) for Plasma-Lyte A; and that at 36 to 48 hours was 4.2 (95% Cl, -3.0-11.3) for PAS 2 and 8.7 (95% Cl, 1.1-16.2) for Plasma-Lyte A. No significant difference between the two solutions was found. CONCLUSIONS: PAS 2 and Plasma-Lyte A make important contributions to platelet transfusion quality improvement and give an excellent CCl even after 4 days of storage.

Acetates↗
PubMed1994

Rearrangements of the blood group RhD gene associated with the DVI category phenotype.

The Rh (Rhesus) blood group antigens, D, Cc, and Ee, are carried by three unglycosylated membrane proteins of the human erythrocytes encoded by two highly related genes, D and CcEe. The major antigen, D, is a mosaic composed of at least nine determinants (epD1 through epD9). The lack of expression of some of these D epitopes at the surface of variant red blood cells defines the so-called D category phenotypes. In this report, we have determined the molecular basis of the DVI category phenotype characterized by the lack of epitopes D1, D2, D5, D6/7, and D8. Southern blot analysis and mRNA sequencing showed that the DVI phenotype is associated with two types of rearrangement of the D gene. Of 10 DVI genomes investigated, 8 exhibited a segmental DNA replacement (gene conversion) between the D fragment encompassing exons 4, 5, and 6 and the equivalent region of the CcEe gene. In the two other variants, these three exons are deleted. In both cases, the genomic rearrangement did not alter the reading frame of the variant RhD transcripts that are translated in 417 and 266 amino acid polypeptides, respectively. A heterogeneity of category DVI samples based on variable reactivity of the red blood cells with anti-D antibodies was previously found to be associated with the CDVIe or cDVIE haplotypes. Interestingly, our present results indicated that this serologic subdivision of the DVI category is correlated to two types of genomic rearrangements of the D gene.

Amino Acid Sequence↗
PubMed1994

Serological characteristics of partial D antigen category VI in 8 unrelated blood donors.

Classification of subjects with a partial D antigen is traditionally performed with immune anti-D sera. The development of monoclonal antibodies enables a fine analysis to be made of the specificity of the epitopes that are present or missing in these cases. A systematic search in a Caucasian donor population of 17,500 revealed 8 unrelated male individuals (frequency 0.05%) with a red cell phenotype characteristic of partial D category VI, but without anti-D in their serum. The relation to the 'classic' partial D category VI was investigated and is discussed, as is the observed serological heterogeneity of the partial D category VI group. Clinical consequences for the prevention of immunization of these subjects are mentioned.

Antibodies, Monoclonal↗