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E A Beckers

Publications and source records attributed to E A Beckers.

15 recordsLinked to original sources
PubMed2003

[Reports of transfusion incidents: experiences from the first year of hemovigilance in the region of the former ZWN (South West Netherlands) blood bank in Rotterdam].

OBJECTIVE: Itemize blood transfusion incidents in the South-West Netherlands region (about 3.5 million inhabitants), where a regional reporting system for transfusion incidents was introduced in January 2001. DESIGN: Prospective, descriptive. METHOD: In the period 1 January 2001-31 December 2001, 22 hospitals voluntarily reported transfusion incidents in patients to the blood bank. All incidents were anonymously recorded in a standardised report and registered in 14 categories. RESULTS: A total of 119 transfusion incidents were reported and categorised as: incorrect blood component transfused (n = 8), mild fever 1-2 degrees C (n = 14), non-haemolytic fever > 2 degrees C (n = 36), acute haemolytic transfusion reactions (n = 3). delayed haemolytic transfusion reactions (n = 18), allergic reactions (n = 11), bacterial contamination (n = 3), transfusion-related acute lung injury (n = 1), near accidents (n = 6) and product recalls (n = 19). There were no reports in the categories anaphylactic shock, post-transfusion purpura, transfusion-acquired viral infection, and transfusion-related graft versus host disease. In the same year of haemovigilance, the blood bank issued a total of 158,000 blood products. A complication rate of 1:700 blood products was calculated. It is estimated that 53% of all incidents were reported. CONCLUSION: Despite all of the safety measures taken, severe adverse events still occurred. A well-run system for haemovigilance can contribute to the knowledge of transfusion incidents. The safety and quality of blood transfusions can be improved if this knowledge is incorporated into ongoing education about blood transfusions and in the prevention and treatment of transfusion reactions.

Blood Banks↗
PubMed2001

Intravascular hemolysis by IgA red cell autoantibodies.

A 66-year-old male patient with severe intravascular hemolysis is presented. Laboratory investigation revealed initially a negative direct antiglobulin test (DAT), suggesting a Coombs-negative hemolytic anemia. Additional testing with monospecific anti-IgA was strongly positive. IgA autoantibodies with anti-e specificity and nonspecific IgA autoantibodies were identified. A diagnosis of IgA-only-associated warm AIHA was made. Treatment included transfusion of multiple e-negative typed red cell concentrates and administration of high-dose prednisone. The pathophysiologic mechanism of the rare IgA-induced warm AIHA is discussed.

Aged↗
PubMed2000

A contrast crisis.

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Adrenocorticotropic Hormone↗
PubMed1997

Molecular background of VS and weak C expression in blacks.

BACKGROUND: The Rh system is complex and consists of as many as 45 different antigens. Red cells of about 25 percent of the black population carry VS an Rh-system antigen (Rh20), but this antigen is very rare in whites. VS positivity is always associated with a weak expression of e, and usually also of C. STUDY DESIGN AND METHODS: The RH genes of 11 black VS-positive donors were studied. Transcripts were sequenced for four VS-positive donors, three of whom had red cells with a weak expression of C. In the other donors, only analysis of genomic DNA was carried out. RESULTS: The occurrence of VS was shown to be related to a single-point mutation in exon 5 of the RHCE gene (cytosine 733 guanine, leading to the Leu245Val substitution). The presence of this polymorphism in exon 5 may explain the simultaneously occurring weak e, because the E/e polymorphism is located in the same exon. Study of VS-positive donors with different Rh phenotypes showed that the polymorphism can occur in different alleles of the RHCE gene. In all three donors whose red cells showed a weak expression of C, a hybrid D-CE-D transcript was found, containing exon 4, 5, 6, 7, and (probably) 8 from the RHCE gene. No transcripts were encountered carrying DNA markers normally associated with C expression. CONCLUSION: It is therefore postulated that the hybrid gene is responsible for the weak expression of C in these individuals. The hybrid gene carried a Leu62Phe substitution, as well as the Leu245Val substitution responsible for VS. The gene most probably cosegregates with a C allele encoding Cys 16 (normally encoded only by the C allele) and Val245 (responsible for VS antigenicity when encoded by the RHCE gene). This explains the combination of weak expression of C and VS positivity that is frequently found in blacks.

Africa, Northern↗
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

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↗
PubMed1994

Evaluation of anti-HCV ELISA seropositivity in voluntary blood donors: a proposal for donor counseling strategies.

OBJECTIVE: To evaluate the anti-HCV (hepatitic C virus) reactivity for the development of an individual donor counseling strategy which would prevent unnecessary donor deferment without compromising the safety of blood products. DESIGN: All donors, who were repeatedly reactive in the Ortho HCV ELISA as well as the Abbott HCV EIA screening tests were selected for follow-up testing. At follow-up three screening tests (Ortho, Abbott, and UBI HCV EIA) and two confirmation tests (Riba 4 and PCR HCV RNA) were performed. During the counseling interview risk factors and medical history were recorded. SETTING: Blood bank Zuid-Limburg, Maastricht, the Netherlands; estimated donor population 17,500. PARTICIPANTS: A total of 54 donors could be completely evaluated. RESULTS: The participants could be divided into five different categories, requiring specific donor information and different blood bank policies. The donors in categories 1 and 2 (n = 11) had false-positive reactions and were kept active. Category 3 and 4 donors (n = 28) showed indeterminate results and were permanently or temporarily excluded. Finally, in category 5 donors (n = 15) a HCV infection could be diagnosed on the basis of either Riba-positive or PCR-positive results. CONCLUSIONS: An anti-HCV screening policy should include a careful evaluation and confirmation of antibody reactivity. A strategy is suggested which allows an individual donor counseling, prevents unnecessary donor deferment, and avoids unnecessary fear of seropositivity.

Adult↗
PubMedDate not supplied

Clinical relevance of herpes simplex virus in the throat of elderly with Salmonella enteritidis gastroenteritis.

It is not known whether the presence of Herpes simplex virus in the throat of elderly patients with severe gastroenteritis and pulmonary implications is of clinical relevance. We cultured throat swabs and faeces of elderly patients with (n = 11) and without (n = 12) severe Salmonella gastroenteritis for viruses and bacteria to study the aetiology of respiratory complications. Complement fixation titers for anti-Herpes simplex antibodies in paired sera were also ascertained. Throat swabs of 6 out of 11 elderly patients with severe Salmonella enteritidis gastroenteritis were positive for Herpes simplex virus type 1. However, a four-fold increase of anti-Herpes simplex antibody titers in paired sera could not be demonstrated. None of the 12 throat swabs of elderly patients without gastro enteritis grew Herpes simplex virus. No other pathogens causing pulmonary complications could be demonstrated in throat swabs of the elderly patients. Herpes simplex virus present in the throat of the elderly patients was very probably not the agent responsible for the pulmonary complications and consequently treatment with acyclovir was not indicated. Weakness caused by severe gastroenteritis and the relative T-lymphocyte immunodeficiency state in the elderly probably enhanced the shedding of Herpes simplex virus in the throat of the elderly patients, without clinical relevance.

Aged↗