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Malcolm Needs

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Everything posted by Malcolm Needs

  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.
  9. 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.
  10. Oniononorion, I would tend to agree with you that blood transfusion as a whole, and immunohaematology in particular, are always the "bridesmaid and never the bride" in terms of the amount of time devoted to the subjects in taught courses, however, i do have some sympathy with those trying to plan such courses, particularly the practical courses, even when attending a course at a Reference Laboratory, simply because some of the cases are so rare that it cannot be guaranteed that you would see such cases, even if you were in a Reference Laboratory for several weeks.
  11. Sadly, I don't (and, if I did, the seams would explode if I tried to put it on these days)!
  12. NO QUESTION IS DUMB if you don't know the answer, and if you never ask it, you will never know the answer. Having said that, you will, just occasionally, get some pretty dumb answers! I agree entirely with David Salkin's answer, which, as always, is far from dumb. When I was working at the Blood Group Reference Laboratory (way back, when it was still in London), it was discovered that I was Ch Negative. Having not long left school, I got all excited over having a rare blood group, and, I think to bring me back down to Earth, they got me a tee shirt with "I'm Ch Negative" printed on the front. In the MRC Blood Group Unit, in the same grounds, but quite autonomous (run by Drs Rob Race and Ruth Sanger) was a woman who had an exceptionally strong expression of the P1 antigen. Having seen my tee shirt, some wit employed there bought her a tee shirt with "I've got strong P" printed on it. As far as I can remember, she never wore it!!!!!!!!! I've attached a short PowerPoint lecture about the P1Pk Blood Group System. The P1PK Blood Group System.pptx
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