ABSTRACT
【Objective】 To explore a simple method to remove the interference of monoclonal anti-CD38 from compatibility testing and evaluate its effectiveness and safety, in order to develop a reasonable clinical transfusion strategy. 【Methods】 Blood phenotype detection, direct antiglobulin testing(DAT) and antibody screening were carried out by standard methods. Antibody screening and cross-matching of serums after monoclonal anti-CD38 treatment were performed by anti-human globulin card with 0.2 mol/L or 0.04 mol/L dithiothreitol(DTT) treated red blood cells. 【Results】 The results showed that 0.04 mol/L DTT treated directly in the anti-human globulin card for 15 min can completely remove the interference of monoclonal anti-CD38 in antibody screening and cross-matching without compromising of the yielding of anti-K, anti-LW, anti-JMH and anti-Lub alloantibodies. However, the titer of IgM antibodies may decrease in different degrees, and antibody screening and cross-matching with saline methods are required to avoid the missed detection of IgM alloantibodies. All 12 patients had no acute or delayed haemolytic transfusion reactions and their routine blood tests showed that the red blood cells transfusion were effective. 【Conclusion】 Based on antibody screening and cross-matching plus saline method, the method of 0.04 mol/L DTT, treated directly in the anti-human globulin card, is safe, effective and simple, which can detect most alloantibodies.
ABSTRACT
【Objective】 To explore the impact of monoclonal anti-CD47(IBI188) on clinical pre-transfusion testing and its solutions, then compare it with monoclonal anti-CD38, so as to develop safe and rational transfusion strategies. 【Methods】 The blood typing, direct antiglobulin testing(DAT) and antibody screening were conducted by standard methods. Red blood cells(RBCs) were treated with fig protease, papain, trypsin and dithiothreitol(DTT) to observe whether the effect of monoclonal anti-CD47 could be eliminated. Cord RBCs and RBCs with different Rh phenotypes were cross-matched; Plasma samples were adsorbed with papain-treated O allogeneic RBCs. 【Results】 ABO reverse typing were affected by monoclonal anti-CD47 treatment, and all serum antibody screening were positive, and their DAT were negative or weakly positive. Neither enzyme nor DTT could weaken the effect of monoclonal anti-CD47 on antibody screening. In saline cross-matching, differences in agglutination intensity were corresponded to differences in CD47 expression on RBCs, but all RBCs agglutinated 2+ to 4+ by polybrene method and anti-human globulin method. Papain treated allogeneic RBCs can remove the monoclonal anti-CD47 in the serum through 3 to 4 rounds of absorption. 【Conclusion】 Monoclonal anti-CD47 interferes with pre-transfusion testing, which can be removed by allogeneic RBCs absorption(not suitable for antibody screening or cross-matching), but not by enzyme or DTT. Blood typing and antibody screening should be conducted before monoclonal anti-CD47 treatment and patients should be transfused with homozygous matched RBCs.
ABSTRACT
OBJECTIVE@#To explore the molecular basis for an A subtype of the ABO blood group.@*METHODS@#The forward and reverse typing of the ABO blood group were identified by gel card and test tube methods. The ABO gene of the patient was detected by PCR-sequence specific primer (PCR-SSP). Exons 1 to 7 of the ABO gene was amplified by PCR and sequenced. The ABO gene was also subjected to subclone sequencing for haplotype analysis.@*RESULTS@#The patient's red cells showed weak agglutination with anti-A but non-agglutination with anti-B. The patient's serum showed 1+ agglutination with A cells and 4+ agglutination with B cells. Based on above serological characteristics, the patient was defined as Aw subtype of the ABO blood group. Sequencing analysis showed that the patient was heterozygous for c.106G>T, c.188G>A, c.189C>T, c.220C>T, c.297A>G, c.467C>T, c.543G>C, c.646T>A, c.681G>A, c.771C>T, c.829G>A, in addition with a c.261G deletion. Combined with the result of subclone sequencing, the ABO genotype of the patient was determined as ABO*AW.33. new/O.01.02, which harbored c.467C>T and c.543G>C variants compared with ABO*A1.01 and c.543G>C variant compared with ABO*A1.02. The novel allele has been submitted to GenBank with an accession number of MK302122.@*CONCLUSION@#A novel allele of Aw33 subtype has been identified with its GTA transferase gene harboring c.467C>T and c.543G>C variants compared with A1.01.