Immunohematology最新文献

The relationship between ABO blood group and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 - coronavirus disease 19 [COVID-19]) infection has been investigated, and several studies have reported discordant findings. This systematic review and meta-analysis study were conducted to investigate the relationship between ABO blood group and COVID-19 infection. The international databases Institute for Scientific Information (ISI)/Web of Science, PubMed, and Scopus were systematically searched from 1 January 2020 through 14 June 2021. Twenty-seven studies met the inclusion criteria for meta-analysis including 23,285 COVID-19 case subjects and 590,593 control subjects. The odds of having each blood group among COVID-19 patients compared with control subjects were calculated. The random effects model was used to obtain the overall pooled odds ratio (OR). Publication bias and subgroup and sensitivity analyses were performed to explore the source of heterogeneity. According to the random effects model, the results indicated that the pooled estimates of OR (95% confidence interval) for blood groups A, O, B, and AB were 1.26 (1.13-1.40), 0.77 (0.71-0.82), 1.05 (0.99-1.12), and 1.11 (0.99-1.25), respectively. Therefore, individuals infected with COVID-19 have higher odds of having blood group A and lower odds of having blood group O. In conclusion, this study indicated that individuals with blood group A are more susceptible to COVID-19 infection, whereas those with blood group O are less susceptible to COVID-19 infection. However, further studies are warranted to support these findings.

A woman with autoimmune hemolytic anemia (AIHA) presented in the emergency department with life-threatening anemia (hemoglobin 3 g/dL). Exaggeration of preexisting chronic anemia to severe anemia after a recent red blood cell (RBC) transfusion led to suspicion of delayed hemolytic transfusion reaction. Given the urgency for transfusion along with a stronger suspicion for coexistence of an alloantibody, the dilution method proposed by Lawrence Petz and George Garratty was used to find an RBC unit for transfusion. An alloantibody with Fy^b specificity was identified, which was masked by the coexistent autoantibody. This method is based on the assumption that the titers of an alloantibody are higher than that of autoantibody. Diluting the autoantibody would reveal the alloantibody and, for this purpose, a serial doubling dilution of serum is performed. This method has an important limitation of missing any alloantibodies with titers less than that of the autoantibody. In spite of this, this method may be of use at a resource-poor setting, where trained personnel and other reagents intended for advanced immunohematology methods are unavailable.

Thiol reagents dithiothreitol (DTT) and 2-mercaptoethanol (2-ME) are sulfhydryl reagents that can be used to disperse cold autoagglutinins coating red blood cells (RBCs). DTT and 2-ME are primarily used when warm washing of the coated RBCs fails to successfully disperse the cold autoantibody. Using a weak concentration of DTT or 2-ME, the cold IgM agglutinin can be removed from the coated RBCs without disrupting the IgG or complement coating the RBCs. The treated RBCs can be used for ABO typing, antigen typing, or the direct antiglobulin test.

According to recent work group recommendations, individuals with the serologic weak D phenotypes should be RHD genotyped and individuals with molecular weak D types 1, 2, 3, 4.0, or 4.1 should be treated as D+. We report an African American woman with a long-standing history of metrorrhagia, who presented for infertility evaluation. Blood grouping showed AB with a possible subgroup of A, based on mixed-field agglutination, and a serologic weak D phenotype. Results from routine red cell genotyping for the RHD gene was incongruent with the serologic RhCE phenotype. For the surgical procedure, the patient was hence scheduled to receive group AB, D- RBC transfusions. Subsequent molecular analysis identified the ABO*A2.01 and ABO*B.01 alleles for the ABO genotype and the novel RHD allele [NG_007494.1(RHD):c.611T>A] along with an RHD*09.01.02 allele for the RHD genotype. Using a panel of monoclonal anti-D reagents, we showed the novel RHD(I204K) allele to represent a serologic weak D phenotype, despite occurring as a compound heterozygote, designated RHD*weak D type 161 (RHD*01W.161). Individuals with a weak D type 4.2 allele are prone to anti-D immunization, while the immunization potential of novel RHD alleles is difficult to predict. For now, patients should be treated as D- in transfusion and pregnancy management, when they harbor a novel RHD allele along with any weak D allele other than weak D types 1, 2, 3, 4.0, or 4.1. This study exemplifies strategies for how and when a laboratory should proceed from routine genotyping to nucleotide sequencing before any decisions on transfusion practice is made.

This update of the Cromer (CROM) blood group system (Storry JR, Reid ME, Yazer MH. The Cromer blood group system: a review. Immunohematology 2010;26:109-17) includes additional variants to the Cromer system (ISBT021), both new antigens and new molecular bases underlying the null phenotype. The molecule on which the Cromer blood group antigens are carried, CD55 (DAF), is an important receptor for the malaria parasite, Plasmodium falciparum, and the role of CD55 in health and disease continues to expand.

This update of the Cromer (CROM) blood group system (Storry JR, Reid ME, Yazer MH. The Cromer blood group system: a review. Immunohematology 2010;26:109–17) includes additional variants to the Cromer system (ISBT021), both new antigens and new molecular bases underlying the null phenotype. The molecule on which the Cromer blood group antigens are carried, CD55 (DAF), is an important receptor for the malaria parasite, Plasmodium falciparum, and the role of CD55 in health and disease continues to expand.

Sickle cell disease (SCD) poses a major public health challenge in sub-Saharan Africa, including Nigeria. Blood transfusion is a mainstay in SCD treatment. Erythrocyte alloimmunization is known to complicate the transfusional care of patients with SCD. Immune alloantibodies are associated with hemolytic transfusion reactions and transfusion refractoriness. We aimed to determine the prevalence, specificities, and clinical associations/risk factors of immune erythrocyte alloantibodies among adult patients with SCD compared with healthy blood donors in Lagos, Nigeria, through a cross-sectional study. All participants were interviewed using a structured questionnaire to obtain details on bio-data, hemoglobin phenotype, blood transfusion history, and SCD history where relevant. Blood specimens obtained from each participant were subjected to antibody screening/identification using tube agglutination method. The mean age of the SCD participants and healthy blood donors was 27.92 and 29.04 years, respectively. The majority (72.5%) of the SCD participants had received at least 1 unit of red blood cell (RBC) transfusion in their lifetime, compared with only 7.5 percent of blood donors. Six SCD participants (7.5%) tested positive for atypical erythrocyte alloantibodies, with none among blood donors. Most of the antibodies (75%) belonged to the Rh blood group system. The most frequent antibody was anti-E, followed by anti-C and anti-D. Advancing age (30 years or more), recent transfusions (last 4 weeks), higher transfusion rates, and established renal disease were significantly associated with alloimmunization (p values of 0.026, 0.043, 0.002, and 0.043, respectively). This study suggests blood transfusion as a strong risk factor for RBC alloimmunization in SCD patients. Extended RBC phenotyping is recommended for all patients with SCD, especially those receiving regular transfusions.

Sickle cell disease (SCD) poses a major public health challenge in sub-Saharan Africa, including Nigeria. Blood transfusion is a mainstay in SCD treatment. Erythrocyte alloimmunization is known to complicate the transfusional care of patients with SCD. Immune alloantibodies are associated with hemolytic transfusion reactions and transfusion refractoriness. We aimed to determine the prevalence, specificities, and clinical associations/risk factors of immune erythrocyte alloantibodies among adult patients with SCD compared with healthy blood donors in Lagos, Nigeria, through a cross-sectional study. All participants were interviewed using a structured questionnaire to obtain details on bio-data, hemoglobin phenotype, blood transfusion history, and SCD history where relevant. Blood specimens obtained from each participant were subjected to antibody screening/identification using tube agglutination method. The mean age of the SCD participants and healthy blood donors was 27.92 and 29.04 years, respectively. The majority (72.5%) of the SCD participants had rec

Anti-Jk3 is a rare alloantibody to a high-prevalence antigen primarily seen in individuals of Polynesian descent and is associated with a handful of well-established variants of the SLC14A1 gene. We report a case of the Jk_null phenotype, associated with formation of anti-Jk3, in a patient of non-Polynesian descent. This patient, a 51-year-old woman self-described as of Jamaican and Scottish ancestry, presented to our hospital for oncologic care. The patient's blood sample typed as blood group A, D+. All screening and panel reagent red blood cells showed reactivity, ranging from 2 to 4+; autocontrol and direct antiglobulin test were both negative. Antigen phenotyping revealed Jk(a-b-), leading to suspicion for anti-Jk3, which was subsequently confirmed by our immunohematology reference laboratory. Given her reported familial background, testing of the SLC14A1 gene was performed, revealing that the patient was heterozygous for the single nucleotide variant (SNV) at c.838G>A in exon 8 and therefore carries both JK*01 and JK*02 alleles that encode Jk^a and Jk^b, respectively. However, the patient was found to be heterozygous for several additional SNVs: c.28G>A in exon 3; c.191G>A, c.226G>A, and c.303G>A in exon 4; and c.757T>C in exon 7. The patient's Jk(b-) phenotype can be explained by coinheritance of c.838A with c.191G>A, which defines null allele JK*02N.09. Coinheritance of SNVs c.28G>A and c.838G with rare SNV c.757C that is predicted to cause a non-conservative amino acid change (p.S253P) likely accounts for the complete serologic absence of Jk^a and the ability to form anti-Jk3 in this case. This finding would represent a new JK*01 null allele. This evaluation illustrates the importance of genetic analysis in identifying the factors preventing a high-prevalence antigen from being expressed, particularly when discovered outside of an expected racial or ethnic group.

Anti-Jk3 is a rare alloantibody to a high-prevalence antigen primarily seen in individuals of Polynesian descent and is associated with a handful of well-established variants of the SLC14A1 gene. We report a case of the Jk_null phenotype, associated with formation of anti-Jk3, in a patient of non-Polynesian descent. This patient, a 51-year-old woman self-described as of Jamaican and Scottish ancestry, presented to our hospital for oncologic care. The patient’s blood sample typed as blood group A, D+. All screening and panel reagent red blood cells showed reactivity, ranging from 2 to 4+; autocontrol and direct antiglobulin test were both negative. Antigen phenotyping revealed Jk(a–b–), leading to suspicion for anti-Jk3, which was subsequently confirmed by our immunohematology reference laboratory. Given her reported familial background, testing of the SLC14A1 gene was performed, revealing that the patient was heterozygous for the single nucleotide variant (SNV)