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Malcolm Needs

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Malcolm Needs last won the day on February 14

Malcolm Needs had the most liked content!

About Malcolm Needs

  • Rank
    Seasoned poster
  • Birthday 12/14/1954

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    Rugby Union, Cricket, cooking, wine, port, reading, crosswords, lecturing, more wine and more port!
  • Biography
    Pretty boring really, but not that pretty!
  • Location
    Croydon, Surrey, 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.
    Member 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!
    Got bored with being retired, and so am doing locum work in Blood Transfusion at St. Richard's Hospital in Chichester, West Sussex (and thoroughly enjoying myself!).

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  1. 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.
  2. Certainly when the A antigen on the red cell is sufficiently strong to give the reaction you posted earlier.
  3. 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?
  4. 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.
  5. 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.
  6. I don't know for certain, but I bet they did a bit more than that. Almost all "cold" auto-antibodies are IgM, it is true, BUT, because these antibodies almost always have a very wide thermal amplitude, they would cause "spontaneous agglutination" in tests incubated at 37oC too. What they probably did was to either adsorb out the "cold" auto-antibody with something like rabbit erythrocyte stroma, or denaturation of the IgM molecules by a reducing agent, such as dithiothreitol (DTT), and only then performing tests using a monospecific anti-IgG reagent. I am quite happy to be corrected.
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