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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.

or mum is a surrogate or baby is the result of an ivf with external donors

2.2.1 Pathogen Reduced Platelets and Cold Storage Platelets are not to be accepted and must be returned to the supplier. Why do you not accept Pathogen reduced plts? We are switching over to Psoralen treated plts, but have never transfused plt to any baby.

"Sure it could happen ,,, and here's how... one of the parents perhaps has the Bombay phenotype"

Here is our aliquoting procedure, hope it opens okay. I may be a good Banker but when it comes to computer uploads, downloads or whatever not so much. Sheri SKM_C55821040507520.pdf

We just switched to the MaxQ MTP coolers and love them! My validations showed it held temps for 24 hours, even when opening the lid every 15 minutes for the first 2 hours and hourly after that. Plus, we filled the cooler with warm FFP (4 units @37C) and cold RBC (4 units @4C). The cooler cooled down the FFP units to 6C within 3 hours. The RBC'S never went above 5C.

I've attached our policies for preparing aliquots in general and our platelet policy. Hope this helps. Oh, we decided all aliquots in syringes expire 4 hours after being made to make it easier for both blood bank and nursing staff to remember. We used to let the RBC and FFP syringes expire in 24 hours but nursing in particular would think all syringes expire 24 hours and we wasted a lot of syringe aliquots until I changed it. BBI0015 Preparation of Aliquots.04.03.2020.doc BBI0017 Platelets 04.03.2020.doc