bluuebunny/crossref_metadata_2025_split huggingface dataset:
Complement receptor 1 red cell expression is not controlled by the In(Lu) gene
Authors: Moulds J.M. , Shah C. 
Published: March 2003

BACKGROUND: The In(Lu) gene reportedly suppresses several blood group antigens that are not part of the Lutheran system, including the high‐incidence antigens of the Knops blood group system. Because complement receptor 1 (CR1), which is known to carry the Knops system antigens, has a red cell (RBC) expression polymorphism, the role of In(Lu) in the expression of the Knops system antigens was reinvestigated.STUDY DESIGN AND METHODS: Blood samples from nine donors having the Lu(a–b–) phenotype were obtained and immediately phenotyped for Lub, Kna, McCa, Sla, and Yka. The samples were also tested for Lua, P1, and AnWj. Immunoblots were performed to study both the CR1 and Lutheran glycoproteins from these donors. RBC expression of CR1 was quantified with an enzyme‐linked immunosorbent assay, and the genetic inheritance of the high‐expression (H) or low‐expression (L) allele for CR1 was determined by Southern blot.RESULTS: Lub was demonstrable only by absorption and elution techniques on all nine samples; however, the high‐incidence Knops system antigens were readily detectable by hemagglutination. Two Lu(a–b–) donors (sibs) demonstrated weak Lutheran glycoprotein bands of 78 and 85 kDa on immunoblots, while the other seven Lu(a–b–) samples had no detectable glycoprotein. All donors had CR1*1, and one donor also had CR1*2 on immunoblot. Only one donor was homozygous for the L allele, and all had RBC copy numbers of CR1 within the normal range.CONCLUSIONS: Nine donors with the Lu(a–b–) phenotype showed suppression of the Lutheran system antigens but normal expression of CR1 glycoprotein and the Knops system blood group antigens. This suggests that the genes that suppress Lutheran system antigens do not suppress CR1 or its related blood group antigens.
Immunoglobulin isotype identification in red cell antibodies using flow cytometry
Authors: Price W.R. , Johnson S.T. , Curtis B.R. 
Published: March 2003

BACKGROUND: Identifying the isotype of an immunoglobulin (IgM vs. IgG) detected in a patient sample is especially important in anticipating the risk of hemolytic disease of the newborn. Currently, 2‐mercaptoethanol (2‐ME) treatment of a sample is used in the authors' laboratory to degrade IgM, and this is followed by retesting. This method has multiple drawbacks. The purpose of this study was to develop a flow cytometry (FC) assay that would replace the 2‐ME treatment protocol (2‐ME treatment).STUDY DESIGN AND METHODS: A preliminary FC assay was developed, modified, and refined through the use of stock antibodies. Then, 10 samples containing antibodies were tested in parallel by the FC assay and 2‐ME treatment.RESULTS: When a 10‐unit mean channel fluorescence change was used as an index of a positive result, the FC assay detected all isotypes identified by 2‐ME treatment. The FC assay was also able to identify mixtures of isotypes. One antibody that had not reacted in conventional agglutination testing was detected by the FC assay. The amount of fluorescence and the agglutinating strength of the antibody did not parallel each other. In one case, this discrepancy may have reflected an antibody that was primarily IgA.CONCLUSIONS: The FC assay appears to be as accurate as 2‐ME treatment in differentiating IgG from IgM. The FC assay produces a positive endpoint for both isotypes, will identify IgA, requires less sample, and has no odor.
The cost‐effectiveness of reducing donor exposures with single‐donor versus pooled random‐donor platelets
Authors: Lopez‐Plaza I. , Weissfeld J. , Triulzi D.J. 
Published: March 2003

BACKGROUND: Single‐donor platelets (SDPs) are frequently preferred over pooled random‐donor platelets (RDPs) to reduce donor exposures and the risk for virus transmission or HLA alloimmunization. Transfusion‐associated virus‐transmission risks have significantly decreased, which suggests that white cell reduction by filtration eliminates any difference in the risk of alloimmunization in transfused leukemic patients. Health care reform pressures of make it appropriate to examine the cost‐effectiveness of SDPs versus RDPs in reducing donor exposures.STUDY DESIGN AND METHODS: A decision analysis model was developed and sensitivity analyses were used to assess the incremental cost (dollars/quality‐adjusted life‐year) associated with the use of SDPs versus RDPs for adult patients undergoing hematopoietic progenitor cell transplantation or primary coronary artery bypass grafting (CABG).RESULTS: Among transplant patients, the incremental cost of choosing SDPs as opposed to RDPs ranged from $168,700 to $519,822 per quality‐adjusted life‐year. For patients undergoing primary CABG, the incremental cost was $192,415 (females) and $216,280 (males). Variations in the cost differential between SDPs and RDPs, the number of random‐donor platelets in the RDP, and the risk of bacterial sepsis markedly influenced cost‐effectiveness. The model was minimally affected by variations in the risks of transmission of HIV and hepatitis B and C, and human T‐lymphotropic viruses.CONCLUSION: In comparison with other accepted medical interventions, the use of SDPs as opposed to RDPs may not be a cost‐effective method of reducing donor exposures in the adult patient populations studied. SDPs were more cost‐effective in patients undergoing primary CABG than in leukemia patients undergoing hematopoietic progenitor cell transplantation. Regardless of diagnosis, decreasing the acquisition cost differential would have the greatest impact on improving the cost‐effectiveness of SDPs, as opposed to RDPs, to decrease donor exposures.
Hemolytic transfusion reaction due to anti‐Tca
Authors: Kowalski M.A. , Pierce S.R. , Edwards R.L. , Ethirajan S. , Ryan K. , Livergood M.P. 
Published: March 2003

BACKGROUND: Anti‐Tca detects a high‐incidence antigen in the Cromer blood group system. Cromer system antibodies have not usually been associated with hemolytic transfusion reactions or hemolytic disease of the newborn.CASE REPORT: Anti‐Tca (initially identified in the patient's serum in 1982) was not detected when she was admitted to the hospital with upper gastrointestinal. bleeding. Three units of red cells were administered. The patient was discharged, but was readmitted to the hospital after her hemoglobin fell to 7.1 g per dL. Antibody detection tests remained negative and three additional units were transfused. Over the next 7 days, her hemoglobin steadily fell to 5.5 g per dL. The level of lactate dehydrogenase rose to 1257, the plasma hemoglobin rose to >16 mg per dL, and the haptoglobin decreased to <6 mg per dL. Five days after transfusion, her direct antiglobulin test was weakly reactive with complement‐specific antiglobulin reagents. Eluates were nonreactive. Anti‐Tca was detected in her serum; no other antibodies were detected. Differential typing failed to detect any circulating Tc(a+) red cells. The antibody was strongly reactive in a monocyte monolayer assay.CONCLUSION: Although Cromer system antibodies have generally not been proven to be clinically significant in transfusion therapy, the destruction of red cells from six units of transfused Tc(a+) red cells in this patient indicates that anti‐Tca may have destructive potential in some patients.
Coexpression of tissue factor and tissue factor pathway inhibitor by human monocytes purified by leukapheresis and elutriation.Response of nonadherent cells to lipopolysaccharide
Authors: Nguyên P. , Broussas M. , Cornillet‐Lefèbvre P. , Potron G. 
Published: March 2003

BACKGROUND: Counterflow centrifugal elutriation is the method of choice for obtaining a large quantity of highly purified monocytes. In spite of the fact that this technique has been used for many years to isolate monocytes for cellular immunotherapy, it is not known whether the process of elutriation can stimulate tissue factor (TF) expression and therefore trigger coagulation in patients receiving these cell preparations. The aim of the present study is thus to identify TF and TF pathway inhibitor (TFPI) in elutriated monocytes and to evaluate their ability to trigger thrombin generation.STUDY DESIGN AND METHODS: Human monocytes are separated by leukapheresis and elutriation in sterile, endotoxin‐free conditions. TF and TFPI mRNA is detected by reverse transcription‐polymerase chain reaction. TF and TFPI are measured by enzyme‐linked immunosorbent assay in cell lysates. TF antigen expression on cell surface is evidenced by direct‐flow cytometry. Two functional tests (a chronometric test and an amidolytic assay) assess the capacity of monocytes to trigger thrombin generation. The response to lipopolysaccharide (LPS) is evaluated with each technique. Monocytic cell line THP‐1 is used as a positive control.RESULTS: Elutriated monocytes coexpress TF mRNA and TFPI mRNA. The expression of TF mRNA is dramatically increased by LPS activation. This is correlated with a 100‐fold increase in the amount of TF antigen in monocyte lysates. Flow immunocytometry confirms the expression of TF antigen on cell membrane in response to LPS stimulation, whereas TFPI mRNA is slightly increased after LPS stimulation. The amount of TFPI antigen in cell lysates is small when compared to that in plasma. Elutriated monocytes have a strong potential to trigger thrombin generation in response to LPS.CONCLUSION: In spite of the coexpression of TF mRNA and TFPI mRNA, elutriated monocytes are capable of supporting prothrombinase activity. This should be taken into account in the evaluation of the safety of adoptive cellular immunotherapy.
Further studies of blood infectivity in an experimental model of transmissible spongiform encephalopathy, with an explanation of why blood components do not transmit Creutzfeldt‐Jakob disease in humans
Authors: Brown P. , Cervenáková L. , McShane L.M. , Barber P. , Rubenstein R. , Drohan W.N. 
Published: March 2003

BACKGROUND: Solid evidence from experimentally infected animals and fragmentary evidence from naturally infected humans indicate that blood may contain low levels of the infectious agent of Creutzfeldt‐Jakob disease (CJD), yet blood components have never been identified as a cause of CJD in humans.STUDY DESIGN AND METHODS: Blood components and plasma fractions were prepared from the pooled blood of mice that had earlier been infected with a mouse‐adapted strain of human transmissible spongiform encephalopathy (TSE). Infectivity bioassays were conducted in healthy mice, and the brains of all assay animals dying during the course of the experiments were examined for the presence of proteinase‐resistant protein.RESULTS: Infectivity in the blood during the preclinical phase of disease occurred in the buffy coat at infectious unit (IU) levels between 6 and 12 per mL and was either absent or present in only trace amounts in plasma and plasma fractions. Infectivity rose sharply at the onset of clinical signs to levels of approximately 100 IU per mL of buffy coat, 20 IU per mL of plasma, 2 IU per mL of cryoprecipitate, and less than 1 IU per mL of fractions IV and V. Plasma infectivity was not eliminated by either white cell‐reduction filtration or high‐speed centrifugation. Approximately seven times more plasma and five times more buffy coat were needed to transmit disease by the intravenous route than by the intracerebral route.CONCLUSION: Epidemiologic evidence of the absence in humans of disease transmission from plasma components can probably be explained by 1) the absence of significant plasma infectivity until the onset of symptomatic disease, and comparatively low levels of infectivity during the symptomatic stage of disease; 2) the reduction of infectivity during plasma processing; and 3) the need for at least five to seven times more infectious agent to transmit disease by the intravenous than intracerebral route. These and other factors probably also account for the absence of transmission after the administration of whole blood or blood components.
ABO incompatibility as an adverse risk factor for survival after allogeneic bone marrow transplantation
Authors: Benjamin Richard J. , McGurk Siobhan , Ralston Maria S. , Churchill W. Hallowell , Antin Joseph H. 
Published: March 2003

BACKGROUND: Graft ABO incompatibility has not been thought to aflect patient survival after allogeneic bone marrow transplantation, although it may be associated with prolonged erythroid aplasia and immediate or delayed hemolysis.STUDY DESIGN AND METHODS: A retrospective analysis of a cohort of 292 allogeneic transplant recipients measured survival in a subgroup of ABO‐incompatible bone marrow graft recipients.RESULTS: Patients with acute myelogenous leukemia or myelodysplastic syndrome receiving non‐T‐cell‐depleted bone marrow grafts had an 85‐percent greater risk of death within 100 days of transplant (relative risk, 1.85, 95% Cl, 1.33–2.58; p = 0.003) than comparable patients receiving ABO‐compatible grafts. Both ABO major‐ and minor‐mismatched graft recipients were at risk. The increased mortality rate was not due to an increase in graft failure or acute graft‐versus‐host disease; rather, patients died of multiple‐organ failure and sepsis, which is consistent with regimen‐related toxicity. This effect was not seen in a larger group of 112 chronic myelogenous leukemia patients undergoing similar treatment.CONCLUSION: ABO incompatibility may be a significant prognostic risk factor after allogeneic bone marrow transplantation in susceptible subgroups of recipients. Care is necessary to design hematopoietic stem and progenitor cell‐processing and ‐transfusion policies to minimize this risk.
A randomized controlled trial comparing plasma removal with white cell reduction to prevent reactions to platelets
Authors: Heddle Nancy M. , Klama Luba , Meyer Ralph , Walker Irwin , Boshkov Lynn , Roberts Robin , Chambers Shelley , Podlosky Linda , O'Hoski Pamela , Levine Mark 
Published: March 2003

BACKGROUND: Recent data suggest that most reactions to platelets are caused by white cell (WBC)‐derived cytokines that accumulate in the plasma portion of the component during storage. On the basis of this theory, the effectiveness of two interventions to prevent reactions, poststorage WBC reduction and plasma depletion, were compared.STUDY DESIGN: A multiple crossover design was used, in which platelet components for transfusion to a patient randomly were WBC reduced after storage, or the plasma supernatant was removed. Adults >17 years of age, with a hematologic disease requiring platelet transfusion support, were eligible for the study. Patients were assessed for signs and symptoms characteristic of a reaction during, immediately after, and 1 hour after transfusion. Reactions were graded as mild, moderate, or severe. Interleukin 6 levels were also measured in the transfused platelet components.RESULTS: There were 380 analyzable platelet transfusions to 30 patients. The frequency of reactions was 25.8 percent (48/186) in the transfusions of poststorage WBC‐reduced platelets and 17.0 percent (33/194) in the transfusions of plasma‐depleted platelets (p<0.008).The severity of the reaction was graded by the patient. Severe reactions occurred more frequently in connection with poststorage WBC‐reduced platelets than with plasma‐depleted platelets: 33.4 percent (16/48) versus 18.2 percent (6/33), respectively (p = 0.048). Regression analysis identified interleukin 6 as the most significant of the evaluated factors in its correlation with the risk of reaction.CONCLUSION: Plasma removal is more effective than poststorage WBC reduction in preventing reactions, especially severe reactions to platelets.
Genomic typing of human red cell Miltenberger glycophorins in a Taiwanese population
Authors: Shih M.C. , Yang L.H. , Wang N. M. , Chang J.G. 
Published: March 2003

BACKGROUND: Antigens in the human red cell Miltenberger series are glycophorin variants of the MN (MNS) blood group system that are due to the rearrangement of glycophorin A (GPA) and glycophorin B (GPB) genes.STUDY DESIGN AND METHODS: Taking advantage of the differences between the GPA and GPB genes, a polymerase chain reaction‐based method was developed to detect all the Miltenberger glycophorin variants and Sta subtype. GPA‐ and GPB‐specific primers were used to amplify the GPA or GPB gene, and the amplified products were used to recognize the different hybrid genes after restriction enzyme digestions.RESULTS: Among 264 Taiwanese subjects studied, Mi.III and Sta are the most common types of Miltenberger variants found. Mi.III was present in 13 (4.92%) of 264, and Sta was found in 8 (3.03%) of 264; 1 case (0.4%) of Mi.V was also identified from the study group.CONCLUSION: This is the first polymerase chain reaction‐based method of detecting most of the Miltenberger variants and Sta. The genomic typing results were confirmed by control DNA of identified Miltenberger phenotypes. The prevalence rates of Mi.III and Sta in this study were also consistent with other previous reports using different methods.
Nuclear matrix protein is released from apoptotic white cells during cold (1‐6°C) storage of concentrated red cell units and might induce antibody response in multiply transfused patients
Authors: Martelli A.M. , Tazzari P.L. , Bortul R. , Riccio M. , Tabellini G. , Santi S. , Frabetti F. , Musiani D. , Bareggi R. , Conte R. 
Published: March 2003

BACKGROUND: A previous study showed that white cells in blood units undergo apoptosis during storage.STUDY DESIGN AND METHODS: The present study attempts to show the release of nuclear matrix protein (NMP) in the supernatants of red cell units and to determine whether antibodies against nuclear components may be present in multiply transfused patients; the methods employed were enzyme‐linked immunosorbent assay, flow cytometry, microscopy, immunoblotting, immunofluorescence, and confocal laser‐scanning microscopy.RESULTS: NMP is released from white cells in the supernatant of packed red cell units upon cold storage (1‐6°C). The concentration of NMP correlates well with the degree of apoptosis, as analyzed by flow cytometry, nuclear dye staining, and DNA gel electrophoresis. Immunofluorescence also shows that white cells undergoing apoptosis (pre‐G1 peak, as seen by propidium iodide staining and flow cytometry) have an NMP content lower than control cells, which confirms an actual release of NMP. Moreover, immunoblotting analysis and immunofluorescent staining showed that, in 4 of 38 multiply transfused patients, autoantibodies against NMPs were present without any clinical or laboratory sign of autoimmune disease. One of the sera, recognizing a 64‐kDa NMP, immunostained nuclear dots that were identified as coiled bodies because of their colocalization with p 80 coilin.CONCLUSION: NMP is released in the supernatant of red cell units. The results obtained from patients suggest that nuclear proteins released during apoptosis, once transfused, may induce an immune response in multiply transfused patients.
Primary anti‐D immunization by weak D type 2 RBCs
Authors: Flegel W.A. , Khull S.R. , Wagner F.F. 
Published: March 2003

BACKGROUND: D is the most immunogenic blood group antigen. In about 0.4 percent of whites, D is expressed on RBCs in a weak form. Recently, it was found that the weak D phenotypes are caused by a large number of distinct RHD alleles generally encoding altered D proteins. No particular molecular weak D type has yet been shown to induce anti‐D. The threshold of D antigen density required for anti‐D immunization is not known.CASE REPORT: A 72‐year‐old D– white man received apparently D– RBCs. Nineteen days later, he developed a positive DAT, and anti‐D was found in his serum and an eluate from his RBCs. One donor was found to be D+ with a weak D type. The weak D type was determined by RHD exon 9‐specific nucleotide sequencing from genomic DNA. The transfusion recipient showed alloanti‐D. Ten months later, anti‐D but no other antibody was detectable; the DAT was negative and the eluate was nonreactive. The donor of the incriminated unit was D+ (ccDEe) with weak D due to the weak D type 2 allele, expressing about 450 D antigens per RBC.CONCLUSION: This case provides formal proof that RBCs of weak D type 2 phenotype may cause alloanti‐D immunization. Among the more prevalent weak D types in whites, weak D type 2 has the lowest D antigen density. Thus, units of blood from donors of the weak D type 2 phenotype should be labeled D+; the weak D type 2 phenotype may be useful for quality assurance.
Evaluation of a new PCR assay with competitive internal control sequence for blood donor screening
Authors: Drosten C. , Weber M. , Seifried E. , Roth W.K. 
Published: March 2003

BACKGROUND: High‐throughput nucleic acid testing for transfusion‐relevant viruses by PCR requires contamination‐proof methods with high sensitivity and validity. A new PCR reagent kit (TaqMan, PE BioSystems) reduces the risk of carry‐over contamination by eliminating post‐PCR processing.STUDY DESIGN AND METHODS: Oligonucleotide design was done with software specialized for designing the assays' (TaqMan) primers and probes. A template‐derived competitive internal control sequence designed through site‐directed mutagenesis was used to reveal failures in amplification. Assay sensitivity was determined for single‐donor and single‐patient testing and by spiking sample mini‐pools. Three seroconversion panels were tested.RESULTS: Sensitivity is high, reaching 300 HBV genomes per mL of single‐patient material on direct testing. A detection limit of 1000 HBV genome equivalents per mL of donor plasma is achieved for 96 pooled samples. The window period for HBV infection was reduced by 17, 10, and 63 days from that for HBsAg screening in three seroconverting donors.CONCLUSION: The assay provides sufficient sensitivity to be superior to HBsAg screening in transfusion medicine and will be useful in clinical laboratories because of its ease of handling.
Differentiation of autologous ABO, RHD, RHCE, KEL, JK, and FY blood group genotypes by analysis of peripheral blood samples of patients who have recently received multiple transfusions
Authors: Rožman P. , Dovč T. , Gassner C. 
Published: March 2003

BACKGROUND: After multiple transfusions, the serologic typing of autologous blood group phenotypes is difficult, because of mixed RBC populations. The genotyping of ABO, Rh, Kell, Kidd, and Duffy systems could be used to determine autologous blood group antigen status.STUDY DESIGN AND METHODS: Blood samples from patients and donors were analyzed before and after 26 multiple‐transfusion events. An average of 6.9 non‐WBC‐reduced RBC units with an average age of 5.9 days were administered per transfusion event. The average period of blood sampling after transfusions was 5.3 days. All samples were serologically phenotyped for ABO, Rh, Kell, Kidd, and Duffy. Pretransfusion, posttransfusion, and buccal samples from patients were genotyped for the corresponding alleles by a uniform PCR sequence‐specific primer protocol that allowed their simultaneous determination within 3 hours.RESULTS: All posttransfusion samples exhibited mixed‐cell populations of various blood group systems on serologic testing. Genotyping from peripheral blood produced results identical to the autologous blood group phenotypes, regardless of the amount of blood transfused or of the length of the sampling period after transfusion.CONCLUSION: A fast and reliable PCR‐sequence‐specific primer DNA genotyping assay for simultaneous determination of autologous ABO, Rh, Kell, Kidd, and Duffy blood groups can be performed on peripheral blood samples, even though the patients have recently received multiple transfusions.