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Malcolm Needs

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Everything posted by Malcolm Needs

  1. Anti-Vel is such a nasty antibody, I would give units that are known to be molecularly tested (SMIM-1 Negative), unless the cross-match is performed by 2-stage IAT with monospecific anti-C3d on a clotted sample, as it is renowned for complement activation, even when virtually undetectable by normal serological techniques - not that I want to be sensationalist!
  2. They do work, but ONLY in the hands of absolute experts.
  3. Anti-Cob has rarely caused a clinically significant haemolytic transfusion reaction, and, even then, the antibody was, in both cases, extremely potent. An anti-Cob, only detected by papain-IAT is certainly not going to be clinically significant, although when the antibody can be detected by IAT, using red cells that have not been treated with a proteolytic enzyme, then Co(b-) units should be transfused. In your case, it would be quite safe to transfuse units that are found to be compatible by IAT with untreated red cells. Geoff Daniels says in his book (Daniels G. Human Blood Groups. 3rd edition, 2013, Wiley-Blackwell) that anti-Cob is quite a rare antibody and, while I am ALWAYS wary about gainsaying anything written by Geoff, I think that may be more to do with the Co(b) antigen not being expressed on most screening red cells and even on most panel cells because, when they were, anti-Cob was a comparatively common finding in the samples submitted to NHSBT-Tooting Centre's RCI Laboratory when I was Reference Service Manager there. As you are working in the UK, you might find it useful to read the specification (SPN214/4), issued by NHSBT, "The Clinical Significance of Blood Group Alloantibodies and the Supply of Blood for Transfusion.", written by my good friend Nicole Thornton, Head of Red Cell Reference at the IBGRL. You can find it on line.
  4. In that case David, I would do serial titrations "in house", otherwise you will be paying out for a load of tests that you do not need. However, do I presume that, as the first two titres were performed by ARC, and you did the third, you were unable to perform a parallel titration on the second sample, when you did the third? If this is true, then there is even more of a possibility that the change from 4 to 8 in results may, itself, be the result of a small experimental error (with no offence meant, and I hope none taken).
  5. I get what you are saying John, BUT, repetitive testing on high-dose RhIg doses in cases of, for example, ITP, have shown that this does not lead to high titres of cell-free anti-D, and so I'm sorry, but I still think titrations are worth doing for a while. Think about it. If the TRUE titre was 4, a titre of 2 and a titre of 8 is only one tube either side of 4. Yes, IF the true titre had gone from 2 to 4 to 8, it is a clinically significant rise, but, it could still, at this stage, be experimental error, for the reasons I gave above.
  6. But I thought that the titre had only risen from 4 to 8? That is only one tube, which could be caused either by a small dilution error, or by a higher number of D antigen sites on the red cells, or both, however, I do agree that there are far better ways of monitor the pregnancy, such as ultrasound. However, that having been said, if it turns out that the titre hadn't risen to dangerous levels, would you want to worry the pregnant woman by getting her to have serial ultrasounds (or whatever)?
  7. In that case, I have to disagree with John for once (sorry John!). The reason I disagree is that a dose of RhIg will not give a very high titre, BUT, the titre of a pre-formed anti-D can rise very rapidly, and very dangerously, in the third trimester (much higher than the titre seen with just a dose of RhIg added to a low titre of allo-anti-D), and so, despite the complete idiocy of the person who gave the shot, I would still monitor the pregnancy by titration (well, I wouldn't, but only because in the UK we monitor anti-D in pregnancy by quantification).
  8. How many weeks pregnant was she before the fool in the office gave her RhIg? One would have hoped that, after 50 years, everyone in the office would have known NOT to give RhIg in such circumstances, but that is obviously over-optimistic.
  9. 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.
  10. 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.
  11. 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.
  12. 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.
  13. Certainly when the A antigen on the red cell is sufficiently strong to give the reaction you posted earlier.
  14. 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?
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