ABO Typing Discrepancy Research Articles

Molecular Genetic Analysis of Para-Bombay Phenotype in Chinese: Identification of a Novel FUT1 Allele

The goal was to identify a novel FUT1 allele and to study serologic and gene feature of the para-Bombay blood type of one expectant mother in Xinjiang, China. ABO and Lewis groups were recognized by standard serologic techniques in an ABO typing discrepancy specimen from one person at the Tianjin Blood Center. DNA (deoxyribonucleic acid) was collected and polymerase chain reactions with sequence-specific primers (PCR-SSP) were performed to sequence exons 6 and 7 of ABO gene, exon 4 of FUT1 gene, and exon 2 of FUT2. PCR products were sequenced to identify ABO groups and the variation sites. The genotype was determined by family study. In our laboratory testing, erythrocytes from the proposita did not react with anti-A and anti-B reagents. B antigen was discovered only after adsorption and elution. Red cells were nonreactive with monoclonal anti-H. The sera of the proposita contained anti-A and were weakly agglutinated by B cells. The hybrid 902 A>G mutation was detected in the proposita's father and mother. The proposita has the same mutation 902 A>G, which was conjectured as homozygosity for 902 A>G. One novel mutation of FUT1 gene was observed in our laboratory. It has never been reported previously. The para-Bombay phenotype in the proposita originating from Xinjiang (China) results from homozygosity for FUT1 902 A>G, together with 357 C>T of FUT2.

Analysis of ABO subgroups which result in ABO discrepancies in Iranian blood donors

The ABO blood group system plays a vital role in the blood transfusion and transplantation medicine [ [1] Hosseini‐Maaf B. Hellberg Å. Chester M.A. Olsson M.L. An extensive polymerase chain reaction–allele‐specific polymorphism strategy for clinical ABO blood group genotyping that avoids potential errors caused by null, subgroup, and hybrid alleles. Transfusion. 2007; 47: 2110-2125 Crossref PubMed Scopus (43) Google Scholar ]. It consists of the major A, B, O alleles and many of subtypes with weak expression of A or B antigens on red blood cells. The results of both forward and reverse ABO typing are necessary for ABO blood group typing, as they are both necessary for interpreting the results [ [2] Arumugam P. Hamsavardhini S. Ravishankar J. Bharath R. Resolving ABO discrepancies by serological workup‐an analysis of few cases. Int J Res Med Sci. 2017; 5: 893-900 Crossref Google Scholar ]. ABO discrepancies may be due to technical or human errors, weak subgroups, the transient expression of antigens in some disease like carcinomas and mixed-filled agglutination after massive or chronic transfusion [ 3 Kaur G. Kaur P. Basu S. Kaur R. Blood group discrepancies at a tertiary care centre–analysis and resolution. Int J Lab Hematol. 2014; 36: 481-487 Crossref PubMed Scopus (18) Google Scholar , 4 Meny G. Recognizing and resolving ABO discrepancies. Immunohematology. 2017; 33: 76-81 Crossref PubMed Google Scholar , 5 Storry J.R. Condon J. Hult A.K. Harrison A. Jørgensen R. Olsson M.L. An age‐dependent ABO discrepancy between mother and baby reveals a novel A weak allele. Transfusion. 2015; 55: 422-426 Crossref PubMed Scopus (7) Google Scholar ]. The incidence of ABO discrepancies among blood donors was reported from 0.02 % to 0.06 %, Also the ABO subgroups are considered the most common cause of ABO discrepancies [ 3 Kaur G. Kaur P. Basu S. Kaur R. Blood group discrepancies at a tertiary care centre–analysis and resolution. Int J Lab Hematol. 2014; 36: 481-487 Crossref PubMed Scopus (18) Google Scholar , 6 Sharma T. Garg N. Singh B. ABO blood group discrepancies among blood donors in Regional Blood Transfusion Centre GTB Hospital, Delhi, India. Transfus Apher Sci. 2014; 50: 75-80 Abstract Full Text Full Text PDF PubMed Scopus (13) Google Scholar , 7 Makroo R.N. Kakkar B. Agrawal S. Chowdhry M. Prakash B. Karna P. Retrospective analysis of forward and reverse ABO typing discrepancies among patients and blood donors in a tertiary care hospital. Transfus Med. 2019; 29: 103-109 Crossref PubMed Scopus (10) Google Scholar ]. Weak ABO subgroups are categorized as type II (Weak/missing antigen) or type IV (due to presence of Anti–A1) ABO discrepancy [ [8] Jain A. Gupta A. Malhotra S. Marwaha N. Sharma R.R. An ABO blood grouping discrepancy: Probable B (A) phenotype. Transfus Apher Sci. 2017; 56: 459-460 Abstract Full Text Full Text PDF PubMed Scopus (3) Google Scholar ]. Mistyped A and B weak blood group as O and B(A) as cisAB and AxB during routine serologic tests can have serious consequences, such as hemolytic adverse transfusion reactions [ [9] Jiao L.X. Zhang J.Y. Chen L. Yu X.L. Han Y. Yang F. et al. Gene identification of rare B (A) blood group. Transfus Apher Sci. 2017; 56: 855-857 Abstract Full Text Full Text PDF PubMed Scopus (2) Google Scholar ].

Retrospective analysis of molecular biology mechanism of ABO blood group typing discrepancy among blood donors in Jinan blood station.

To accurately identify ABO blood typing in pre-transfusion testing is very important to ensure blood transfusion safely, which is a major responsibility of blood station. Eighty-one blood donors samples with ABO blood group typing discrepancy was collected among 61952 donor samples in our blood station from January 2019 to July 2020. Blood group serological method was used to detect ABO blood group. DNA Sequencing was used to determine the genotype. The antibody screening test detects antibodies other than ABO. In total, 61,952 donor samples were analysed for ABO typing discrepancies. The incidence among blood donors was 0.13% (81/61952). The most common reason of ABO typing discrepancies was due to specific antibody or non-specific agglutination (54.32%, 44/81), mainly anti-M antibody, cold autoantibody, anti-D antibody, anti-N antibody and anti-Lea antibody. The major cause of forward typing discrepancies among blood donors was ABO subgroups (25.93%, 21/81), including 10 cases of A subtype (1 case of A2, 2 cases of A3, 2 cases of Ax, 3 cases of AxB, 1 case of Ael, 1 case of Ahm), 6 cases of B subtype (2 cases of B3, 1 case of Bel, 3 cases of AB3), 2 cases of B subtype (A), 1 case of cisAB, and 2 cases of acquired B. The serum antibody was weakened in 16 cases (19.75%). The blood types should be correctly identified by combining serology with gene sequencing to ensure the safety of clinical blood transfusion, when the forward and reverse typing discrepancies among the blood donors.

Analysis of ABO grouping discrepancies among patients from a tertiary hospital in Korea

BackgroundAccurate ABO typing is essential for preventing ABO incompatibility reactions. However, the causes of ABO grouping discrepancy has not been sufficiently studied, and it may vary among different ethnic populations. Thus, the aim of this retrospective study was to investigate the causes of ABO discrepancy in the East Asian population. Materials and methodsA retrospective observational study on ABO typing discrepancy among patients in a tertiary hospital was carried out using the electronic medical record database of Samsung Medical Center (Seoul, Korea) between July 2016 and May 2019. ResultsABO grouping was performed on 551,959 blood samples during the study period; 1468 events of serologic ABO discrepancy were determined from 1334 (0.24 %) samples. A total of 134 samples (0.02 %) presented multiple causes of ABO discrepancy. Weak/missing serum reactivity (594, 40.5 %) was the most frequent reason for ABO discrepancy, followed by extra serum reactivity (370, 25.2 %), weak/missing red cell reactivity (267, 18.2 %), mixed-field red cell reactivity (176, 12.0 %), and extra red cell reactivity (61, 4.2 %). In the category of weak/missing red cell reactivity, ABO subgroup was the most common reason, and using ABO genotyping, 26.2 % of the cases genotyped were found to be related to the cis-AB allele. ConclusionsOur results suggest that the incidence and cause of ABO typing discrepancies vary among institutes and ethnic groups. Our data helps to better understand and facilitate the resolution of ABO typing discrepancies in patients.

Clinical Characteristics and Influence Factor Analysis of ABO Typing Discrepancy Among Patients in a Tertiary Hospital.

An accurate interpretation of the ABO blood group of an individual is of utmost importance to ensure patient safety and good transfusion practices. The aim of the study was to determine the incidence and causes of ABO typing discrepancies among patients and analysis of the clinical characteristics as well. A retrospective observational study was carried out in the Department of Laboratory Medicine in the General Hospital of Chinese PLA from March 2018 to December 2020. Records of patients were collected and analyzed for frequency, clinical characteristics, and influencing factors of ABO typing discrepancies. There were 132 ABO typing discrepancies patients (57 females, 75 males), aged from 3 to 84 (50.3 ± 19.3) years, with history of operation 89 cases (67.42%) and blood transfusion 23 cases (17.42%). In the control group, there were 142 cases (63 females and 79 males), aged 10 - 78 years (50.5 ± 15.55), with operation history 68 cases (47.88%) and blood transfusion history 2 cases (1.40%). Among the inconsistent blood types group, there were 59 cases (44.7%) type B, 38 cases (28.8%) type A, 28 cases (21.2%) type AB, and 7 cases (5.3%) type O. There were 21 cases (15.9%) in the department of hematology, 15 cases (11.36%) in the department of orthopedics, 14 cases (10.6%) in the department of hepatobiliary surgery, 11 cases (8.33%) in the department of general surgery, 11 cases (8.33%) in the department of vascular surgery, and less than 5% in other departments. The common cause of ABO typing discrepancies was due to low/weak affinity antibody (3.79%), low/weak affinity antibody B (18.18%), weak A antigen (3.03%), weak B antigen (12.12%), hematopoietic stem cell transplantation (10.60%), irregular antibody (46.70%), subtype (3.79%), and cold agglutination (1.51%). The diseases in the ABO discrepancy group mainly included hematological disorders, malignant tumors, osteoarthritis and so on. Binary logistic regression showed that hematological disorders, malignant tumors, history of operation (p = 0.01), and history of blood transfusion (p = 0.017) were the influencing factors of ABO typing discrepancies. It is possible that the antibody of ABO blood group system could not be detected. The independent influence factors were hematological disorders, malignant tumor, blood transfusion history and operation history for ABO typing discrepancies. It was necessary to analyze the causes correctly and judge the correct blood group by serological methods.

Identification and Blood Transfusion of Rare B(A) Blood Group.

To study serologic and gene characteristics of the B(A) blood group of one patient in Tianjin, China. To investigate the blood transfusion for patients with B(A) blood group. ABO subgroups were identified by standard serologic techniques in ABO typing discrepancy sample from one patient at the Tianjin Medical University General Hospital. DNA (deoxyribonucleic acid) was collected from his sample and PCR (polymerase chain reaction) was used to sequence exons 6 and 7. PCR products were sequenced to identify ABO subgroups and the B(A) allele. Molecular genotyping of the ABO gene was performed by DNA sequencing of exons 6 and 7 of the ABO gene. The patient's red cells showed mixed field agglutination reaction (MF) with anti-A and weak reaction (W+) with anti-H. However, it has strong agglutination reaction with anti-B. The patient's serum showed the presence of anti-A antibody, while it can't react with B cell. The serological characteristics of the patient's red cells were similar to AxB subtype. Variation sites were confirmed at 261delG, 297 A>G, 526 C>G, 640 A>G, 657 C>T, 703 G>A, 796 C>A, 803 G>C, 930 G>A in exon 6 and 7 of the ABO gene. The sequence was similar to B101 except for nt640 (A>G). Genotyping indicated that the specimen was B(A)04. Molecular genotyping confirmed the ABO status as B(A)04. The B(A) blood group is associated with a complicated serologic phenotype and DNA detection is necessary for this atypical phenotype sample. To ensure the safety of transfusion, this study developed an emergency transfusion procedure for patients with B(A) type.

Warm Reactive Anti-A1 Agglutinin in an A2B individual: A Rare Case with Review of Literature

The prevalence of the major subgroup of A as A<sub>1</sub> in almost 80% of the A group population is a known fact. A<sub>2</sub> and the remaining subgroups such as Aend, Am, Ax etc comprise the remaining population, based on erythrocyte agglutinability and various serological reactions. These A subgroups can often result in an ABO typing discrepancy. Anti-A<sub>1</sub> antibody often appears as an irregular cold agglutinin in the sera of A<sub>2</sub> or A<sub>2</sub>B individuals who lack the corresponding antigen. Rather notably, the literature suggests that 1% to 8% of A<sub>2</sub> and 22% to 35% of A2B individuals possess an allo-anti-A<sub>1</sub> in their sera, which reacts at a temperature below 25°C. Although routinely, it does not pose any problem either during or post blood transfusion, however, the literature reports of hemolysis happening in procedures that are performed at lower temperatures, particularly in hypothermic situations. We report herein, a case of a massively bleeding A<sub>2</sub>B Indian lady after the expulsion of her dead fetus and an underlying uterine fibroid having a warm reactive allo-anti-A<sub>1</sub> agglutinin that warranted an urgent blood transfusion management.

A novel Bruton tyrosine kinase gene variation was found in an adult with X‐linked agammaglobulinemia during blood cross‐matching prior to surgical operation

To investigate the underlying molecular mechanism of the patient's ABO typing discrepancy. ABO typing discrepancy was frequently seen in patients due to different causes. In this study, ABO typing discrepancy was found in a 24-year-old man with arthralgia, whose forward ABO grouping was O and reverse ABO grouping was AB. Primary immunodeficiency disease was speculated in this patient, especially X-linked agammaglobulinemia (XLA). Immunoglobulins of all isotypes were detected using a specific protein analyser. Lymphocyte subgroups were analysed by flow cytometry. All 19 exons and boundaries of BTK gene were amplified by polymerase chain reaction (PCR), and all PCR products were sequenced by a DNA analyser. BTK protein in the leukocytes and platelets was detected by Western blot. No B lymphocytes could be detected in the peripheral blood of the patient. A novel BTK gene variation, c.817G>T, in the exon 9 of BTK gene was discovered. No BTK protein expression could be detected in the leukocytes and platelets of the patient. XLA could be occasionally discovered by ABO typing discrepancy in some cases because of the deficiency of reciprocal IgM anti-A and/or anti-B antibodies in the serum of the patient. Humoral immunodeficiency is one of the causes of ABO typing discrepancy.

Comparison of ABO genotyping methods: a study of two low-resolution polymerase chain reaction assays in a clinical testing laboratory

The ABO blood group system is the most clinically significant system in transfusion medicine. Although serologic typing for ABO antigens is routine and reliable, molecular methods can be used to predict an ABO type in the absence of a blood specimen as well as to investigate ABO typing discrepancies often caused by ABO subgroups that cause weakened antigen expression, weak or missing serum reactivity, and/or extra red blood cell reactivity. By detecting single nucleotide variants that are hallmarks of the major ABO alleles, low-resolution genotyping methods can be used to make allele assignments and predict phenotypes. This approach has become a dependable tool, initially to resolve typing discrepancies identified in blood banks and donor centers and, more recently, to predict the ABO group in bone marrow transplant donors and in deceased donors of solid organs. The aim of this report is to compare two different low-resolution polymerase chain reaction (PCR)-based methods: a PCRrestriction fragment length polymorphism (RFLP) implemented based on a publication and a commercially available TaqManbased sequence-specific primer-PCR for resolution of ABO typing discrepancies. Fifty-six peripheral blood samples from 31 patients and 25 blood donors were used to isolate genomic DNA and perform genotyping. Results of 49 of the 56 samples (87.5%) were concordant between methods, three samples yielded an unexpected banding pattern on the PCR-RFLP method, and four sample results were discordant between assays. The discordances all involved group A versus A2 discrepancies. Sanger sequencing was used as a high-resolution genotyping method to resolve discrepancies between the two low-resolution methods. This study demonstrates that, in the majority of cases, a low-resolution genotyping method can resolve an ABO discrepancy. Although there is no U.S. Food and Drug Administration-approved genotyping method for ABO determination, molecular testing for investigation of discrepancies is a useful tool for blood banks and transplant programs.

Retrospective analysis of forward and reverse ABO typing discrepancies among patients and blood donors in a tertiary care hospital.

The aim of our study was to determine the incidence and causes of ABO typing discrepancies among patients and blood donors at our centre. An accurate interpretation of the ABO blood group of an individual is of utmost importance to ensure patient safety and good transfusion practices. A retrospective observational study was carried out in the Department of Transfusion Medicine in our hospital from March 2013 to December 2015. Records of all patient and blood donor samples were retrieved and analysed for ABO typing discrepancies. In total, 135 853 patient and 62 080 donor samples were analysed for ABO typing discrepancies. The incidence among patients and blood donors was found to be 0·1% (138/135853) and 0·02% (14/62080), respectively. The mean age for patients and blood donors was 48·4 and 29·2years, respectively. The most common cause of ABO typing discrepancies was due to cold autoantibodies among the patients (50·7%) and blood donors (57%) causing discrepant results in reverse typing. The various other causes of reverse typing discrepancies among patients were weak/missing antibody (25·4%), cold-reacting alloantibody (4·3%), warm autoantibody (2·2%), anti-A1 antibody (2·2%), Bombay phenotype (1·5%), transplantation (0·7%) and rouleaux (0·7%), whereas in blood donors, the causes were cold-reacting antibody (7%) and weak antibody (7%). The major cause of forward typing discrepancies among patients (12·3%) and blood donors (29%) was ABO subgroups. The resolution of ABO typing discrepancy is essential to minimise the chance of transfusion of ABO-incompatible blood.

Gene identification of rare B(A) blood group

ObjectiveTo study serologic and gene characteristics of the B(A) blood group of blood donation volunteers in Jilin Province, China. MethodsABO subgroups were identified by standard serologic techniques in ABO typing discrepancy samples from all donors at the Jilin Blood Center (410,354 non-repeat donors). DNA (deoxyribonucleic acid) was collected from each sample and PCR (polymerase chain reaction) was used to sequence exons 6 and 7 and intron 6, part 5 from the ABO subgroup samples. PCR products were sequenced to identify ABO subgroups and the B(A) allele. ResultsFour cases of B(A) blood type were found after sequencing, including two different alleles: B(A)02 and B(A)04. Three of the four alleles were B(A)04. ConclusionAmong blood donation volunteers in Jilin Province, China, B(A)04 is the most common B(A) blood group allele, followed by B(A)02. The B(A) blood group is associated with a complicated serologic phenotype and DNA detection is necessary for this atypical phenotype sample.

Molecular genetic analysis and structure model of a rare B(A)02 subgroup of the ABO blood group system

BackgroundSerological analysis of ABO blood group has been widely applied in transfusion medicine. However, ABO subgroups with different expression of blood group antigens sometimes cannot be determined by serological methods. Therefore, genotyping is useful to understand the variant ABO phenotypes. Material and MethodsExon 6 to exon 7 and adjacent introns of the ABO gene from a donor with ABO typing discrepancy were amplified and sequenced. Cloning sequencing was also performed to identify the allele. To explore the effect of mutation, three dimensional model of mutant p.Pro234Ala was built and optimized. ResultsThe variant B (c. 700C > G) allele expressed an AweakB phenotype with anti-A in his serum with a ABO*B(A)02/O02 heterozygote genotype. Cloning sequencing confirmed that the c.700C > G single nucleotide polymorphism was associated with a B101 allele. Three dimensional molecular modeling suggested that p.Pro234Ala might affect the conformation of His233, Met266 and Ala268, which were known as critical residues for donor recognition. ConclusionABO genotyping is needed for correct identification subgroups to improve accuracy evaluation of blood typing and increase the safety of blood transfusion. Alteration of DNA sequence in the ABO gene resulted in amino acid substitutions and led to a weak or missing expression of ABO antigens.

Molecular basis and clinical blood transfusion for cases with ABO typing discrepancy

To investigate the molecular genetic basis of samples with ABO typing discrepancy and provide the guidline for identification and clinical transfusion for these samples. Six cases with similar serological characteristics were collected. Serological method, PCR-SSP and direct sequencing of ABO gene were used to explore the underlying mechanism. Condition of clinical transfusion of patients was also reviewed. Three conditions were related with the ABO blood type discrepancy, which included weaken antigen (2 cases), weakened antibody (3 cases) and ABO subtype (1 case). The satisfactory effect of transfusion was achieved in all patients with the principle of the same blood type or the compatible crossmatch. Heterogeneity has existed with the ABO group. Indivianals with same reaction pattern may result in different mechanisms.

Molecular DNA‐based testing for blood group antigens: recipient–donor focus

DNA‐based testing for blood group antigens has become commonplace in a number of clinical situations to improve transfusion therapy for blood transfusion recipients. These include typing for antigens in patients who are multiply transfused to determine which blood group antibodies may be present, typing when the red blood cells (RBCs) are coated with immunoglobulin, and typing for uncommon antigens, especially when no serologic reagent is available. Other clinical applications include resolving ABO typing discrepancies for patients awaiting transplant, or determination of the original type of a bone marrow transplant recipient, or confirmation of an ABO subgroup in a kidney donor. Testing for the specific mutation associated with depressed Kell system antigens in McLeod syndrome may also have value because different mutations appear to be associated with prognosis.Applications in prenatal medicine include discrimination between weak D and partial D to determine if a pregnant woman is a candidate for Rh immune prophylaxis, and assessing the risk for hemolytic disease of the fetus or newborn and neonatal thrombocytopenia. Assessing risk includes testing the paternal sample for the target antigen, and if positive testing for gene copy number (zygosity) and testing the fetus from amniocentesis or non‐invasive maternal plasma sample.Donor centers are now able to screen large numbers of donors to label antigen‐negative RBC products. DNA typing will change transfusion practice by allowing patients facing chronic transfusion therapy to have a more comprehensive blood group antigen profile performed, and to receive donor units antigen‐matched for more than ABO and RhD to reduce alloimmunization. A patient who makes an alloantibody to a RBC antigen is forever at risk for his or her lifetime; for a serious transfusion reaction if ever requiring transfusion in an emergency, and also for a high risk pregnancy if a woman of child bearing age. Prevention of alloimmunization is an important advance in transfusion safety and is now possible with electronic patient medical records and testing and labeling of blood products for additional blood group antigens.

Clinically significant anti‐A1 in a presumed ABO‐identical hematopoietic stem cell transplant recipient: a case report

BACKGROUND: Subgroups of the blood group A (ABO) are generally not considered ABO incompatible for hematopoietic progenitor cell (HPC) transplant.CASE REPORT: A 54‐year‐old female presented for HPC transplantation for acute leukemia. No HLA‐matched donor was identified, so she received a peripheral blood stem cell graft from an HLA‐mismatched unrelated donor. On pretransplant testing, both the donor and the recipient typed as blood group A. On Day +67 after transplant, the recipient had a transfusion reaction consisting of an increase in temperature, rigors, and shaking chills during infusion of a unit of group A red blood cells (RBCs). A transfusion reaction workup revealed an ABO discrepancy with both anti‐A (1+) and anti‐B (3+) identified in the patient's serum as well as a positive direct antiglobulin test with monoclonal anti‐IgG antisera. Anti‐A1 were identified serologically and in an eluate. Hemolysis was clinically significant, requiring blood transfusion. No ABO typing discrepancies were found on pretransplant testing in either the recipient or the donor. DNA sequencing for blood group A subgroups performed after the transfusion reaction on blood collected before the transplant showed the donor to be type A1 and the recipient as A2. Unfortunately, the patient experienced graft failure requiring reconditioning and reinfusion of additional cells from the original HPC donor. On Day +94 after the second transplant, the patient died with severe acute gastrointestinal graft‐versus‐host disease.CONCLUSION: This report describes a blood group A2 patient who developed an anti‐A1 causing clinically significant hemolysis after HPC transplant from an A1 donor.

Investigation into A antigen expression on O2 heterozygous group O–labeled red blood cell units

There are two principal types of group O alleles; deletional alleles feature 261delG leading to nonfunctional truncated protein. Nondeletional alleles have the consensus guanosine at residue 261. The major nondeletional allele, O2, encodes full-length protein with Gly268Arg. While reports vary, O2 has been proposed to encode weakly functional A-glycosyltransferase (GTA). The main objective of this study was to evaluate if GTA activity is detectable in O2 donors. Donor samples from Pittsburgh and Lund were ABO typed by automated methods. DNA was extracted from 779 group O donors whose red blood cells (RBCs) were available for transfusion. ABO genotyping identified those with O2 alleles. The following tests were performed on randomly selected O2 samples (number): adsorption-elution with anti-A (3), flow cytometry (15), plasma enzyme activity (4), and attempts to convert group O RBCs to A (2) with O2 plasma and titration of plasma anti-A/-A1 (3). Forty O2-heterozygous donors were identified (5.1%). Adsorption-elution and sensitive flow cytometry did not reveal A antigens on O2 RBCs. Plasma enzyme analysis failed to show GTA activity above baseline; O2 plasma was unable to add measurable A antigens to O RBCs. Titers of anti-A/-A1 appeared reduced in O2 plasma but did not cause ABO typing discrepancies. No immediate hemolysis or adverse reactions were reported following transfusion of O2 RBCs to six evaluable group O recipients. Other than lower plasma anti-A titers, GTA activity was not found in these O2 samples. Neither automated blood grouping discrepancies nor clinical problems related to transfusing these O2 units were observed.

Impact of a Policy To Use Only Group O Red Cell Transfusions for Recipients with Fewer-than-Twice Established ABO Types: A Feasible Means To Reduce Potential ABO-Incompatible Transfusion Errors.

Background: A Group O Policy, which issues group O red blood cells (O-RBC) to recipients whose ABO types have not been duplicated on at least 2 separate occasions, has been in place at this 550-bed hospital since 1991. Its inception was a response to the frequency of wrong blood in tube (WBIT) events identified by discrepant serial ABO typings, which had been disproportionately concentrated among critically ill patients, a population at high risk of transfusion and misdraw. This policy was thought to better address such sources of mistransfusion error than delivery-based patient identification technologies.Methods: For the period from 1/1/2004 - 12/31/2005, the policy's impact was reviewed according to utilization of O-RBC, frequency of critical O-RBC shortage, intervals to type confirmation, the identification of protracted users of policy O-RBC, the frequency of WBIT events as revealed by ABO typing discrepancies, the frequency of ABO-incompatible transfusion errors, and the frequency with which ABO-incompatible transfusion errors were averted as a result of the policy.Results: In 2004, 479 (4.5%) of a total of 10,575 units of O-RBC were transfused due to the policy. In 2005, 689 (6.1%) of a total of 11,293 units of O-RBC were transfused due to the policy. Increase in the use of O-RBC from 2004 to 2005 was by 718 units (6.7%), while the increase in the use of group O-RBC for the policy increased disproportionately by 210 units (43.8%). Over the 2 year period, a monthly median excess of 43 units (range 24–85) of O-RBC were issued in accordance with the policy. Daily excess use of O-RBC for the policy was a median of 1 unit (range 0–19). There were 291 days when no policy-related O-RBC were used, and only 3 days when more than 10 units were used. The interval between a 1st and 2nd (confirmatory) typing, when achieved, occurred within 24 hours for 15.4% of patients, but was a median of 23 days, and ranged from minutes to 21.5 years. Confirmatory re-typing activity within less than 72h of the 1st occurred in a minority of 28%, possibly reflecting nonessential repetition and/or deliberate action to release patients from policy-related O-RBC restrictions. Patients who were protracted users of Group O policy blood (no confirmatory type and/or repeatedly indeterminate typing) were neonates (310 units [26.5%]) and recipients of ABO-incompatible hematopoietic stem cell transplants (76 units [6.5%]). The blood bank identified misdrawn blood through typing discrepancies in 6 patients over 2 years. Transfusion occurred uneventfully in 3 of these 6, as the misdraw was made apparent by comparison with prior typings on file in 2, and patient knowledge of correct type in 1. The misdrawn specimen was the 1st one in 2 of 6. Of the 3 who were not transfused, the misdraw suggested a type that would have led in all to the transfusion of clinically incompatible blood, had the knowledge of prior type, and the policy, both been absent. ABO-incompatible red cell transfusion errors did not occur, although this was a greater function of luck than the policy in the interval.Conclusions: A policy instituted to prevent ABO-incompatible transfusion errors, by providing O-RBC to those with unconfirmed blood types, appeared to be both feasible, and potentially mistransfusion-preventative, at a high-volume tertiary-care teaching hospital.

Implications of ABO Error Rates in Proficiency Testing for Solid Organ Transplantation

Implications of ABO Error Rates in Proficiency Testing for Solid Organ Transplantation

The classification, recognition and significance of polyagglutination in transfusion medicine

Polyagglutination, although an uncommon phenomenon in transfusion medicine, is becoming increasingly recognized as a potential pitfall in correct ABO typing and can hinder the rapid allocation of accurately crossmatched blood products. Polyagglutination refers to erythrocytes which demonstrate agglutination with the majority of adult sera upon initial ABO crossmatch testing. Most types of polyagglutination involve alteration of red cell surface antigens through microbial enzymatic activity in patients with sepsis, and subsequent interaction of these newly exposed ‘cryptantigens’ with naturally occuring IgM antibody which is present in most adult sera. Less common variants include essential inborn variations in red cell development, and have been associated with myelodysplastic syndromes, congenital anemias, and various leukemias; it has been suggested that patients shown to possess these types of polyagglutination may benefit from increased hematologic surveillance. Recognition of polyagglutination in these settings is important to allow successful resolution of ABO typing discrepancies and permit efficient administration of appropriate blood products to these patients, who are often quite ill. The classification and method of laboratory recognition of polyagglutination is reviewed.