mpmiola

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Thanks for your return. I'm glad they took on this condition. However, I hope they are looking at ways to minimize this risk of ABO phenotyping failure, especially with recipient samples. Alternatives must exist, such as decreasing sample centrifugation time or speed...

We used the rate of transfused patients for each type of procedure. We carried out a survey of more than 5 years to identify the frequency of use of concentrated red blood cells for each procedure, including the immediate postoperative period (up to 48 hours). With this data, we define the reservation request guideline. When the doctor requests a reservation, he needs to select the type of procedure, and when doing so, the system fills the request according to the guidelines. For frequencies of use below 10%, zero red blood cell concentrate will appear and the blood therapy service will only perform T&S. We recommend that patients with requests a reservation whose frequency is greater than 10% have an ABO confirmation prior to the transfusion if they do not have at least two concordant ABO records in our system.

I'm curious to know what the conclusion from the company Grifols is, let us know if you can.

Congratulations, Malcolm! Very well deserved!

I agree that the difference between cisAB and B (A) is serological and divergent. They coulding be one, but they respect the names given by the authors. I do not think that the ABO * cisAB.05 and ABO * BA.06 alleles are different. It must have been an ISBT mistake! See a summary I made in 2019. In general, the phenotype cisAB presents normal expression of antigen A, but similarly to phenotype A2, and weak expression of antigen B. On the other hand, B(A) presents a very weak expression of antigen A, but a normal expression of B.(1) The rare phenotype cisAB was first described in a case of mother AB with child O.(2) Its authors suggested that this phenotype was formed by the interaction of two genes, one A2 gene and another atypical B gene, located in the same locus. However, with the molecular characterization of the cisAB-1 allele (ABO*cisAB.01), it was observed that a sequence of the ABO*A1.02 allele containing an additional mutation at position 803G>C (Gly268Ala) was capable of synthesizing a GT with mixed activity. The cisAB-1 allele is more common in Asian populations and considering the four positions that differentiate alleles A and B, it can be described as AAAB.(3) In a study of 16 Korean blood donors heterozygous for the ABO*cisAB.01 allele, it was demonstrated that both GTA and GTB have clearly decreased activity. GTA activity was 29% of GTB was 27% compared to wild GTA encoded by the A1 allele. (4) Phenotype B(A) was first detected when monoclonal ABO reagents became commercially available. This phenotype exhibits normal levels of antigen B and very low levels of antigen A in tests with some anti-A monoclonal reagents. (1) The GT of this phenotype has the ability to produce normal levels of antigen B, but also use The UDP-GalNAc as substrate to produce detectable levels of antigen A. The B(A) alleles are variants of allele B and the first of them (ABO*BA.01) was identified by Yamamoto and collaborators. (5) This allele is commonly referred to as BABB due to the aa of position 235 being the same as consensus A1. The second allele B(A) (ABO*BA.02) has the aa sequence of allele B, being referred to as BBBB, but contains an additional mutation at position 700C>G (Pro234Ala) which is close to aa 703, one of the four that differentiate the A allele from B.(6,7) By the way, a normal GTB encoded by the consensus B allele has the ability to synthesize minimal amounts of antigen A which are detectable by some anti-A reagents. As well, GTA encoded by the A consensus alleles can also synthesize minimal amounts of antigen B, which are detectable by some anti-B reagents. These reagents were considered inappropriate for the ABO phenotyping routine,(8) for example, the anti-B monoclonal antibody (BS-85), reported by Voak et al. (9) 1. Daniels G. Human blood groups: Introduction. Oxford, UK: Wiley-Blackwell2013. 2. Seyfried H, Walewska I, Werblinska B. Unusual inheritance of ABO group in a family with weak B antigens. Vox Sang. 1964;9:268-77. 3. Yamamoto F, McNeill PD, Kominato Y, Yamamoto M, Hakomori S, Ishimoto S, et al. Molecular genetic analysis of the ABO blood group system: 2. cis-AB alleles. Vox Sang. 1993;64(2):120-3. 4. Cho D, Shin MG, Yazer MH, Kee SJ, Shin JH, Suh SP, et al. The genetic and phenotypic basis of blood group A subtypes in Koreans. Transfus Med. 2005;15(4):329-34. 5. Yamamoto F, McNeill PD, Yamamoto M, Hakomori S, Harris T. Molecular genetic analysis of the ABO blood group system: 3. A(X) and B(A) alleles. Vox Sang. 1993;64(3):171-4. 6. Haslam DB, Baenziger JU. Expression cloning of Forssman glycolipid synthetase: a novel member of the histo-blood group ABO gene family. Proc Natl Acad Sci U S A. 1996;93(20):10697-702. 7. Yu LC, Lee HL, Chan YS, Lin M. The molecular basis for the B(A) allele: an amino acid alteration in the human histoblood group B alpha-(1,3)-galactosyltransferase increases its intrinsic alpha-(1,3)-N-acetylgalactosaminyltransferase activity. Biochem Biophys Res Commun. 1999;262(2):487-93. 8. Goldstein J, Lenny L, Davies D, Voak D. Further evidence for the presence of A antigen on group B erythrocytes through the use of specific exoglycosidases. Vox Sang. 1989;57(2):142-6. 9. Voak D, Sonneborn H, Yates A. The A1 (B) phenomenon: a monoclonal anti-B (BS-85) demonstrates low levels of B determinants on A1 red cells. Transfus Med. 1992;2(2):119-27.

Hi, What barrier method are you using to ensure that the blood bag reaches the correct patient? I am researching to update and increase security in the service I work for. I appreciate all the contribution,

I would like to know the behaviors that have been adopted in your service in cases of bone marrow transplantation from RhD + patient, RhD- donor for transfusion of platelet concentrate. Is there a concern to provide RhD- since the infusion? Or after the patient only presents donor phenotyping RhD-? In the impossibility of providing RhD-, have hemotherapists indicated anti-D prophylaxis?

We understand what happened. We received the patient 12 hours before this transfusion. Despite having denied previous transfusions, we contacted the health service of origin who informed us that he had transfused platelets in pool (600 ML) the group O. Therefore, we believe that the reaction after red blood cell transfusion was a coincidence, and the anti-B of the transfused platelets must be the cause of hemolysis.