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Malcolm Needs

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Malcolm Needs last won the day on November 22

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About Malcolm Needs

  • Rank
    Seasoned poster
  • Birthday 12/14/1954

Profile Information

  • Gender
    Male
  • Interests
    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!).

Recent Profile Visitors

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  1. B(A) Phenotype?

    While I admire your tenacity in following up your case Kellimq, unless your R&D Rh genotyping facility is well-practiced in ABO genotyping ( and I am NOT saying that they are not), you should keep in mind that ABO genotyping is notorious for predicting ABO phenotypes that do not necessarily match the genotype (see Daniels G. Human Blood Groups. 3rd edition, 2013. Wiley-Blackwell, p25, Section 2.3.2.6 Predicting ABO phenotype from DNA testing.). Certainly, in the UK, our Histocompatibility and Immunogenetics Laboratories, who used to perform ABO gentyping when performing the tests for renal transplants have been banned from so doing, and now have to use good old-fashioned serological techniques, are one unfortunate episode.
  2. Just saying Hi

    I got bored watching day time television and so, after I had brought my lectures up-to-date, and taken them off the blood service's PowerPoint background, and put it on my own, I decided to become a locum, and Zoe is now my boss for a while.
  3. wAIHA with IgM and C3c/C3d coating

    Sadly, I doubt whether this was done by the NHSBT RCI laboratory. Such testing is usually deemed "too expensive" under "LEAN" rules!
  4. Lewis A

    No Anna.
  5. Lewis A

    Given the number of reactions that are recorded in the literature, which are very few, and the fact that the small amount of plasma left on the red cells to be transfused will very readily inhibit in vivo the anti-Lea in the patients plasma, I think this is overkill.
  6. Eluates on babies with positive DATs

    How do you know that the positive DAT is due to ABO incompatibility, unless an elution is performed. Surely, you are making an assumption (a very likely assumption, but an assumption nevertheless)?
  7. B(A) Phenotype?

    It is important to remember that the A, B and H antigens are not direct gene products, but are their as the result of the action of specific transferase enzymes. In the case of a group AB individual, the N-acetyl-D-galactosaminyl transferase (the A transferase) "competes" against the D-galatose transferase (the B transferase), and it is not unusual to come across a case where "one transferase has beaten the other". This results in an apparent weakened A or B antigen, and this could be the answer in this case. It could also be, of course, that there is a "genuine" weak expression of the A antigen, due to the patient inheriting an A2 gene (or other weak A gene). This could be checked by adsorption and elution tests with an anti-A. The reaction with the A1 reverse grouping cells could be due to an anti-A1 in the plasma, but this would not account for the reaction with the A2 reverse grouping cells. This latter reaction could be due to a "cold" auto-antibody, such as auto-anti-H, auto-anti-HI or auto-anti-I, or to a "cold" reacting allo-antibody, such as anti-M or anti-P1, where the corresponding antigen is not being expressed on the B reverse grouping cells. This, of course, would all have to be proven with appropriately typed reagent red cells. Depending upon the anti-A reagent you are using, but I assume that you are using a monoclonal reagent, I would be happy myself to call this an AB, and not waste my group O stocks unnecessarily. Lastly, as far as plasma is concerned, I would try to give group AB, but also wouldn't hesitate to give either A (preferably) or group B, unless the patient is of small stature, in which case I would definitely go for AB.
  8. wAIHA with IgM and C3c/C3d coating

    I would doubt it Anna, because all of the NHSBT Reference Laboratories use the BioRad DAT card that contains the monospecific anti-IgG, anti-IgM, anti-IgA, anti-C3c, anti-C3d sera and the control, so I would have expected an anti-IgA component to have shown up on the patient's red cells; but you never know.
  9. You could perform a Kleihauer, and subjectively estimate - but it would be very subjective.
  10. wAIHA with IgM and C3c/C3d coating

    Yes, you are completely right Yanxia. Briefly, the patient's plasma and reagent red cells are incubated at 37oC, as for a normal tube IAT, to allow the antibody in the plasma to sensitise the antigens on the red cells. The tests are then washed free of unbound antibody (as for the normal tube IAT), but then, instead of adding AHG at this stage, fresh ABO compatible serum (it has to be serum, rather than plasma, to ensure there is complement there to initiate the classical complement pathway), which is known not to contain any atypical antibodies (we used to use AB serum from a source that had been extensively tested and found to be free of any such antibodies) and mixed with the red cells. The tests are then incubated again at 37oC, to allow for the complement cascade to be initiated, and then washed again, as for a normal tube IAT. Lastly, monospecific anti-C3d is added, and the tests GENTLY centrifuged, and examined for agglutination. A negative control, using the inert AB serum, rather than the patient's plasma, must be set up and tested in parallel. Of course, such a technique can only be performed by tube, capillary, tile or liquid-phase microtitre plate techniques, as column agglutination and solid-phase microtitre plate techniques cannot be used.
  11. wAIHA with IgM and C3c/C3d coating

    I agree 100% with you that anti-Vel can be a real problem, but that problem can be a real problem not just when the antibody is new. It is one of the few antibodies that are best detected by the two-stage indirect antiglobulin technique (see Geoff Daniels' book, Human Blood Groups), but I don't know of anyone in the world who uses that technique as a routine. The reason that this is the best technique to use for anti-Vel is that it is much more easily detected with anti-C3d than either anti-IgM or anti-IgG, however, of course, in these days of automation, most people use samples that have been anti-coagulated with EDTA. This means that the calcium, magnesium and manganese ions required as co-factors in the initiation of the classical complement pathway are not available, and so we no longer see the tell-tale haemolysis in our tests that is normally seen with an anti-Vel (and, of course with ABO antibodies, some anti-I antibodies from an adult i individual, anti-P+Pk+P1 from a p individual, and IgG anti-Lea). Indeed, I think I have noted on Pathlabtalk before that I know of one case of anti-Vel that proved to be fatal, which was only ever detected in a clotted sample from the patient, but NEVER in an EDTA sample.
  12. Anti Mi(a+)?

    Mia is part of the MNS Blood Group System, and, among most populations (with the exception of the Far East) is a low prevalence antigen. I would recommend putting "probable/possible", as the problem with antibodies directed against low prevalence antibodies is that 1) people tend to make a "soup" of specificities, rather than a single specificity to a low prevalence antigen, and 2) in any case, such antibodies have a nasty habit of cross-reacting with other low prevalence antigens. Even if the patient did not have an anti-D, I would recommend that she be disqualified from receiving blood by electronic issue.
  13. Lewis A

    Sorry Scott. In my personal opinion, and it is only my personal opinion, it's not 20th century........it is at best 18th century!!!!!!!!
  14. wAIHA with IgM and C3c/C3d coating

    Most certainly it is Scott, but it would be hugely unusual for such an antibody to cause gross haemolysis, particularly in a patient of such an advanced age - but - by no means would I rule out your excellent suggestion.
  15. Eluates on babies with positive DATs

    If they had ordered the workup, and the DAT was positive, would you have assumed that the reason was because of the anti-K? Supposing the eluate had been negative with K+ red cells? What would you have done? Chances would be, in such a case, that the mother had made an antibody directed against a low prevalence antigen passed on by a paternal gene. Next time it could be that this antibody is a lot stronger, and may cause HDFN (with the emphasis on HDF). It may be that this "unknown antibody specificity" could be a "real nasty", causing severe HDF, but you wouldn't be able to advise the obstetricians to be on high alert during the pregnancy. Admittedly, if the DAT had been positive, and anti-K had been eluted, this would have masked any antibody directed against a low prevalence antigen, but hey!
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