mpmiola
Reputation Activity
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mpmiola got a reaction from Malcolm Needs in BloodBankTalk: Correct Blood Bank Nomenclature
I just answered this question.
My Score PASS
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mpmiola reacted to Malcolm Needs in Anti-C in C pos patient with strong e type
I've had further thoughts upon this case (having told you not to worry about it - I live a sad life - NOT!).
It struck me that the patient has an Rh type of D+ C+ c+ E+ and e+, suggesting that the probability is that the patient has a genotype of DCe/DcE (R1R2), but this may not be the case. She could have one of the rarer Rh genotypes, such as DCE/Dce (RzRo), DCE/dce (Rzr), Dce/dCE (Rory), etc, and this may be potentially important.
Some years ago, Joyce Poole explained to me that most grouping reagents labelled as anti-C are, in fact, a mixture of anti-c and anti-Ce, and this, she told me, included most monoclonal anti-C reagents (which surprised me, to be honest). This is because the vast majority of the red cells transfused that stimulate an anti-C would have the haplotype of either DCe or dCe, or both, and will, therefore, also stimulate an anti-Ce. As a result, these "hybrid" anti-C/anti-Ce reagents will react more strongly with red cells expressing the Ce compound Rh antigen (Rh7) and the C antigen (Rh2), than with red cells that only express the C (Rh2) antigen.
This would not, incidentally, explain the stronger than normal reaction with the e antigen.
However, if the patient does express one of the rarer Rh types mentioned above, say she is RzRo, she can actually produce an allo-anti-Ce, and most antibody panels only contain C+ red cells that are only Ce+ as well. In other words, her antibody in the plasma MAY be identified as an anti-C, whereas it is actually a monospecific anti-Ce, which would neatly explain why she has an apparent anti-C.
Of course, she may also have an auto-anti-C, or a mimicking auto-anti-C (and, possibly, an allo-anti-Bg of some sort). Sadly, for a nerd like me, I doubt if we will ever know!
I think it was John C Staley who once accused me of looking for zebras, when I hear horses hooves (I may be wrong, but I think it was John). Anyway, this proves that he was absolutely correct about me!!!!!!!!!!!!!!!!!!!!!!!!
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mpmiola reacted to Neil Blumberg in Adverse Transfusion Event Case Studies: Part 1, Pulmonary Transfusion Reactions.
While it is infrequently referenced, universal leukoreduction is one strategy for minimizing pulmonary and cardiovascular adverse responses to transfusion (see attached). When we instituted it in 2000 our rate of TRALI decreased by 80+ % and TACO decreased by 50%. Probably mechanism is that white cells, DNA, histones and neutrophil extracellular traps (NETs) cause acute lung injury and inflammation when infused (good animal model data exist). Thus the failure to implement universal leukoreduction in the USA during the last 23-25 years was a terrible and tragic mistake, and this fatal error persists to this day.
ULR TRALI TACO PMC version.pdf
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mpmiola reacted to Malcolm Needs in Antibody Testing Report Terminology
In the UK, it is STANDARD practice in all laboratories that I know to use either the phrase "No Antibodies Detected", or, more frequently, "No Atypical Antibodies Detected", as the latter also includes such things as the iso-antibodies of the ABO and H Blood Group Systems. Indeed, some go further still and use "No Atypical Allo-antibodies Detected", as this covers such findings as an auto-anti-H, auto-anti-I and auto-HI, as well as the ABO and H iso-antibodies.
These phrases do not mean that there are no atypical allo-antibodies detected. It would be an incredibly rare set of screening cells and antibody identification panel cells that would both express, for example, the HJK antigen, or any other genuine low prevalence antigen.
In some cases, where an atypical allo-antibody IS detected, but it is known to be clinically-insignificant (such as anti-Kna), we may use the phrase "No Clinically-Significant Atypical Allo-antibodies were Detected" (or words to that effect).
One thing is for certain, and that is that a UK Reference Laboratory (and most hospital laboratories) worth their salt would report out as "Negative", or "No Antibodies", although, even using the phrases I've quoted above, occasionally the phrase, "All Clinically-significant Allo-antibodies have been Ruled Out using etc.", or words to that effect.
MIND YOU - you have to remember that I am RENOWNED for being a pedant - but I learned it from a few good sources; Peter Issitt, Carolyn Giles and Joyce Poole (to name but three).
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mpmiola got a reaction from Jsbneg in Wrong ABO typing by Gel
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...
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mpmiola got a reaction from Marilyn Plett in Same Day Survery ABO Confirmation process
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.
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mpmiola got a reaction from RRay in Same Day Survery ABO Confirmation process
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.
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mpmiola got a reaction from Malcolm Needs in Gold Medal.
Congratulations, Malcolm! Very well deserved!
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mpmiola reacted to Malcolm Needs in Gold Medal.
I am enormously honoured to announce that I am going to be awarded the Gold Medal of the British Blood Transfusion Society at their Annual Scientific Meeting in Brighton this year. It is awarded to an individual for their exceptional and long standing services to the Society and to the practice of blood transfusion in the UK. Sorry if this sounds egocentric, but I am very excited.
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mpmiola reacted to Malcolm Needs in Wrong ABO typing by Gel
Well, that's got rid of two of my possible theories in one fell swoop!
I was wondering either about loss of antigenicity due to some form of myeloid malignancy, or of adsorption of autologous secreted A substance on to the donor group O red cell surface following a successful BMT or stem cell transplant, which may be seen with only some clones of anti-A (see, for example, Cripps K, Mullanfiroze K, Hill A, Moss R, Kricke S. Prevalence of adsorbed A antigen onto donor-derived group O red cells in children following stem cell transplantation: A single-centre evaluation. Vox Sang 2023; 118: 153-159. DOI.10.1111/vox.13386., but I saw this phenomenon in adults many times when working at Westminster Hospital).
Oh well, back to having more thoughts!
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mpmiola got a reaction from Walter Isenheim in B(A) and cisAB phenotypes
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.
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mpmiola reacted to John C. Staley in Infant transfusion units
Thanks Malcolm, it did answer my question. Apparently while their blood is circulating these people maintain normal levels of K+. It is only upon storage that they leak the K+ at higher levels than normal. It appears to be a genetic cell membrane "defect"
"Familial pseudohyperkalaemia (FP) • dominantly inherited, asymptomatic • characterised by an increased rate of leakage of K+ from red cells at refrigerated temperatures • usually caused by the minor allele of a non-synonymous single nucleotide polymorphism (FP SNP; rs148211042; R723Q) in the transporter gene ABCB6 (ATP-Binding Cassette, subfamily B, member 6) • codes for a red cell membrane transporter protein • raw chip measurements from a screen of the UKBioBank suggested ~1:400 of the UK population have the FP SNP"
"Study – identified FP individuals • screening of the National Institute for Health Research Cambridge BioResource (NIHRCBR) – identified 16 out of 8712 individuals with the FP SNP. • 2 more individuals with the FP SNP were identified when clinical cases of unusually high K+ levels were reported in RCC units that they had donated – characterised in Bawazir WM, et al. 2014"
Thanks again,
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mpmiola reacted to Malcolm Needs in Infant transfusion units
Hi John,
I am not absolutely sure, as this all happened just as I was retiring, but I have emailed a former colleague of mine who may know, but, if you put "NHSBT blood donors with high potassium levels" in to your search engine, you should get up a PowerPoint lecture that you can download with the long title of, "POTASSIUM LEAKAGE AND MEASURES OF THE RED CELL STORAGE LESION IN DONATIONS FROM INDIVIDUALS WITH FAMILIAL PSEUDOHYPERKALAEMIA", by Athina Meli, Maggie McAndrew, Amy Frary, Karola Rehnstrom, Christian J Stevens, Waleed M Bawazir, Joanna F Flatt, William Astle, Rekha Anand, Helen V New, Lesley J Bruce and Rebecca Cardigan, which may answer your question.
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mpmiola reacted to Neil Blumberg in Universal leukoreduction and ABO identical transfusions reduce HLA alloimmunization by transfusion to near zero
Once clinicians understand that ABO mismatched platelets not only do not provide hemostasis, but make bleeding more likely/worse, they will be less willing to accept infusion of ABO mismatched antibody/antigen. Once blood transfusion services realize that infusing ABO mismatched platelets increases utilization by two fold, they will be more interested in making the effort to give ABO identical or remove incompatible plasma by washing. Doing the right thing for patients is never the wrong answer to the question. Our current practices are convenient for us and minimize waste. We need to prioritize clinical benefit over inventory control and waste reduction. What we are doing now is providing little to no benefit and actually harming patients in many instances. The bleeding rate in the PLADO (platelet dose study) in NEJM was 70%. That's not exactly a clinical triumph. Our bleeding rate is probably less than 5-10% employing ABO identical/washed platelets.
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mpmiola reacted to Neil Blumberg in Universal leukoreduction and ABO identical transfusions reduce HLA alloimmunization by transfusion to near zero
Disciplinary action over product wastage sounds like it is perhaps well intentioned but ignorant bureaucrats, not health care workers running the show. That's a big part of the problem in many institutions these days.
We are fortunate in that the senior decision makers in our hospital are all physicians, nurses, etc., including the CEO, CMO, COO. Washing your hands before delivering babies turns out to be inconvenient but a better idea. Universal leukoreduction and avoiding infusion of ABO incompatible antigen and antibody are also better ideas than what we have done for decades or longer. These practices will save lives, reduce need for transfusions and actually save the system money overall, albeit at greater expense in the transfusion service.
You are no doubt correct that there will be pushback from transfusion service staff used to doing things the old, easy, but harmful way, and hospital administrators who prioritize the wrong things such as budgetary tunnel vision over reduced harm. And blood centers are not likely to initially be all that interested in changing practices. But when the data says patients do better with universal leukoreduction and ABO matching, hopefully, in the long run the dogma will be replaced by data driven practices. May take a while.
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mpmiola reacted to Neil Blumberg in Universal leukoreduction and ABO identical transfusions reduce HLA alloimmunization by transfusion to near zero
Cannot post the entire article due to copyright restrictions, but most institutions have access to NEJM through their library. If not, shoot me an email at neil_blumberg@urmc.rochester.edu and I'll send along the .pdf.
If you are transfusing 40-60 platelets a day, giving ABO identical to group O and A individuals should be relatively easy. When patients are changing ABO blood group it becomes more difficult. We avoid transfusion ABO antigen and/or antibody that is incompatible with either original recipient type or donor type. Usually means washed group O red cells and platelets. That's the bad news. It does require time and effort, and as you say, med techs are in short supply. Here's the good news. If you transfuse ABO identical or washed compatible platelets you will use between 30-50% fewer platelets per patient, increasing your supply and decreasing your cost/problems. You will also use next to no HLA matched platelets (we used 3 out of 6,000 one recent year), you will have fewer febrile and allergic transfusion reactions, you will have fewer red cell as well as HLA antibodies made in recipients, and you may reduce TRALI and TACO. Obviously you have to have universal leukoreduction to start with. Selective leukoreduction misses about 50% of the patients who will become refractory, probably due to missed or delayed diagnosis of hematologic malignancy, aplastic anemia, etc. But the big attraction is you will have less bleeding, although that mainly affects the patients and the docs and nurses at the bedside.
When you transfuse ABO major incompatible, which seems to be the default due to fear of hemolysis from minor incompatible, you don't get any increments, you use lots of platelets and the patients bleed more. (see references below) Bleeding causes lots of harm, but also impacts the blood transfusion service for obvious reasons. So figure out a way to start giving patients with aplastic anemia and acute myeloid leukemia who are newly diagnosed only ABO identical platelets and that will be a great start for the patients and the transfusion service. Those patients will bleed less, need fewer platelet transfusions, have fewer transfusion reactions, will not have positive DATs, and will likely survive their hospitalization and disease at higher rates if our experience is typical.
And if you cannot give ABO identical or washed platelets free of incompatible cellular and soluble antigen and free of incompatible ABO antibody, start out with minor incompatible platelets (e.g., O to A) rather than ABO major incompatible (e.g., A to 0). The risks of hemolysis are not negligible (about 1 in 800) but are less serious and severe than having life threatening bleeding or refractoriness which occur more rapidly with ABO major incompatible in all likelihood. There's a ton of antibody that is incompatible with antigen transfused when we give A platelets to O recipients which means each antigen winds up with a ton of antibody making huge immune complexes. When we transfuse antibody incompatible we are transfusing a small amount of antibody into a recipient with huge amounts of antigen, so the size and number of immune complexes is probably smaller. These are my best guesses that we've been making exactly the wrong decision when we give ABO mismatched platelets. Best to avoid any, but major mismatched provides no hemostasis, minimal to no increment and is associated with increased bleeding mortality in the study from Columbia (David Roh and colleagues https://pubmed.ncbi.nlm.nih.gov/33649761/). But ABO identical is not that hard for larger centers for the 85% of patients who are group O or A. You just have to start small, get the hang of it, and then extend to other blood groups and other diseases than leukemia, MDS and aplastic anemia (including transplants, particularly allo--transplants). All those tables of how to select ABO mismatched platelets for transplant recipients are well intentioned but scientifically without evidence. Avoid infusing incompatible antigen and antibody as much as possible, and delay transfusion when ABO identical will be available within hours. Give priority to patient well being over inventory management. Give reduced doses, which work just as well. Get a Terumo or Haemonetics washing device and wash with PAS. It's a big set of changes, but neither terribly expensive nor rocket science. The dogmas and expert opinion about universal leukoreduction and ABO matching of transfusions are now proven to be tragically mistaken.
https://www.ashclinicalnews.org/news/from-the-blood-journals/written-in-blood/outcomes-abo-incompatible-platelet-transfusions-patients-intracerebral-hemorrhage/
https://pubmed.ncbi.nlm.nih.gov/11399821/
https://pubmed.ncbi.nlm.nih.gov/21414009/
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mpmiola got a reaction from Sonya Martinez in Transfusion in surgery pediatric cardiac
Thank you Baby Banker.
If cardiac surgery is for extracorporeal, should red cells be washed if they present more than 24 hours of irradiation time?
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mpmiola reacted to lalamb in Second ABO/Rh tests prior to transfusion
This is from our policy. We currently don't do "c" so we've noted "not applicable":
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mpmiola reacted to Malcolm Needs in Issue for the Identification of Antibodies
I would treated the patient's own red cells with papain or ficin (whichever is used by the manufacturer to make their enzyme treated red cells), and then test them against autologous plasma. My guess (and from this far away, it is just a guess) is that they will be positive.
I think that there is a "cold" reacting auto-antibody there.
I would also suggest performing an IAT panel in tubes, bringing the reactants to 37oC before mixing them, and using isotonic saline, rather than LISS as the red cell diluent, and then washing the tests in pre-warmed isotonic saline. This should show if there are any underlying clinically significant alloantibodies.
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mpmiola got a reaction from galvania in B(A) and cisAB phenotypes
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.
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mpmiola got a reaction from Yanxia in B(A) and cisAB phenotypes
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.
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mpmiola got a reaction from AMcCord in B(A) and cisAB phenotypes
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.
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mpmiola got a reaction from Malcolm Needs in B(A) and cisAB phenotypes
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.
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mpmiola reacted to MAGNUM in Barrier method
I use BCTA also with the checks online.
I have looked at the Blood Locks but have not decided as of yet