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Malcolm Needs

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Malcolm Needs last won the day on February 14

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About Malcolm Needs

  • Rank
    Seasoned poster
  • Birthday 12/14/1954

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  • Gender
  • Interests
    Rugby Union, Cricket, cooking, wine, port, reading, crosswords, lecturing, more wine and more port!
  • Biography
    Pretty boring really, but not that pretty!
  • Location
    Milverton, Somerset, England
  • Occupation
    I have taken a brand new role in the NHSBT and am now involved very much more on the education and training side of red cell immunohaematology. My title is still Reference Service Manager, but with Training after it (Reference Service Manager - Training). I am very excited about this change, as I have a passion for training and education.
    Reference Service Manager with the NHSBT.
    Chartered Scientist.
    Fellow of the British Blood Transfusion Society, having twice served on their National Council.
    Fellow of the Institute of Biomedical Science. Member of their Special Advisory Panel for Transfusion Science and Chief Examiner for Transfusion Science for the Institute.
    Author of the chapter "Human erythrocyte antigens or blood groups" in Fundamentals of Biomedical Science, Transfusion and Transplantation Science, edited by Robin Knight, for the IBMS. 1st edition, Oxford University Press 2013 (ISBN 978-0-19-953328-2, pages 19-44.
    Just been appointed to the BCSH Blood Transfusion Task Force (writing Guidelines).
    Member of ISBT and AABB
    I am now retired from the Blood Service, but still do the other things!
  • Real Name
    Malcolm Needs CSci FIBMS FBBTS

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  1. Or, it could be that, as there is a sort of continuum of antigen strength between A1, right down to Ael, and Dolichos biflorus reacts with the A antigen, as well as the A1 antigen (it is far from specific, reacting also with the Tn and Cad antigens), that the A2 red cells may not truly be an A2.
  2. Sorry to jump in here, but it is NOT the position of the antigens that allows the formation of anti-f, but the RHCE genes that have been inherited. If the individual is truly an R1R2, they will have inherited one RHCE*Ce gene and one RHCE*cE gene. In other words, the "c" gene and the "e" gene are in trans, whereas, if the individual is actually an Rzr (or RzRo), they will have inherited one RHCE*CE gene and one RHCE*ce gene. In other words, the "c" gene and the "e" gene are in cis. Therefore, if the genes are in trans, the individual can make an anti-f, but, if they are in cis, the individual cannot make an anti-f.
  3. In the UK, we either titre (anti-K, or other Kell-related antibodies) or quantify (anti-D and/or anti-c) every four weeks to 28 weeks of gestation, and then every two weeks until delivery. All other antibodies are only monitored from when they were first detected (probably at booking) at 28-weeks of gestation, unless the titre is particularly high. In all cases, however, if a known antibody specificity is NOT detected in an antibody screen, where, of course, the cognate antigen is expressed, then it is not worth performing the titre at all. It is just a waste of time, money and reagents. In such cases, however, we would perform the antibody screen over the time periods as described above.
  4. I don't want to interfere, but have you thought about sending a sample to Martin Olsson's laboratory in Lund? He is the world authority on the ABO gene.
  5. Certainly when the A antigen on the red cell is sufficiently strong to give the reaction you posted earlier.
  6. Did you really mean "an Anti-A", and not an Anti-A1? Surely, if the A antigen is expressed on the red cells, however weakly, the patient cannot produce an anti-A, unless it is an auto-antibody?
  7. Putting aside the A antigen for the moment, which is probably "normal" in the case of your patient, it is not the B antigen that is abnormal in the case of a Bel person, but the 3-alpha-galactosyltransferase enzyme (the direct gene product of the ABO gene) is less active than normal, due to a mutation in the gene. The actual carbohydrate residue that is on the red cell is "normal" - just less of it. In addition, there is competition between the "A-transferase" and the "B-transferase" for the H-backbone. In the case of your patient, the "A-transferase" will "win" this competition and this will accentuate the weakening of the B antigen even further - but the actual structure of the B antigen will be the same as the normal B antigen - just fewer in number. This explains why there is no anti-B present in your patient's circulation. This (rather long-winded) explanation should serve to prevent you worrying about giving your patient group AB blood should they require a transfusion.
  8. Looks like an AsubgroupB to me, but, these days, with monoclonal antibodies, which type of A subgroup can only be accurately sorted by molecular techniques. The reverse group needs more investigation. It could be anti-A1, it could be another "cold" antibody specificity (such as anti-M or anti-P1), or it could be a combination of the two. If there is no reaction at 30oC and above, it doesn't really matter, but, to be on the safe side, if blood is required, I would give group B packed red cells, or group B red cells resuspended in AB plasma.
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