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Malcolm Needs

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Everything posted by Malcolm Needs

  1. Have you thought about training porters? I know that sounds a bit "Left field", but it worked for us in the UK in a couple of hospitals where I worked. You have to be pretty strict, but it does mean that nursing and lab staff can get on with other things.
  2. The first, and most important, thing to remember is that ABO antigens are "carbohydrate-based" and are not, therefore, direct gene products (not that any antigens are, as every one of them undergo post-translational changes). The direct gene products are, of course, the A, B and H transferase enzymes. At birth, it is incredibly rare for the enzymes to be "working" at its optimum/maximum, so that it is rare for the ABO antigens to be expressed maximally (or anything like) at birth. I am certain that you know all this already, so that I am probably "teaching my Grandmother to suck eggs", as the old (and in this case, almost certainly, insulting) adage goes. As a result of the above, however, unless you can perform A, B and H typing by molecular techniques (NOT to be recommended - see Geoff Daniels book, Human Blood Groups), you either have to decide to ignore all serological cord ABO types, and call all of them O, or, you have to use serological methods that will enhance the antibody/antigen reactions. Herein, there are inherent problems. Firstly, whatever enhancement you use, you MUST use a suitable negative control. It is fine (in my opinion) to vary the incubation temperature from RT to 4oC, but, to so do, it is very necessary to use another cord blood from a known group O cord sample (i.e. where both parents are KNOWN to be group O themselves, and so an A or B subtype in terms of the control is not a problem). Similarly, the same can be said for enzyme-treating the baby's red cells, as long as the control cells are also treated in EXACTLY the same way with the proteolytic enzymes. Finally (at least for now!!!!!!!), it should be remembered that we routinely use monoclonal ABO antibodies these days. These are extremely avid, which is fantastic, but are also VERY specific, which can be a drawback. By this I mean that the old polyclonal human-derived ABO antibodies we used to use (when I was middle-aged, and Karl Landsteiner was a young boy) had the single (and probably only) advantage that they were not quite so specific, and would, therefore, detect ALL (or most) ABO antigens, including those that the monoclonal antibodies would not necessarily detect. For an explanation of this, there was a recent paper in Vox Sanguinis (Cripps K, Mullanfiroze K, Hill A, Moss R, Kricke S. Prevalence of adsorbed A antigen onto donor-derived group O red cells in children following stem cell transplantation: A single-centre evaluation. Vox Sang 2023; 118: 153-159. DOI: 10.1111/vox.13386) talking about the A antigen being adsorbed onto the surface of group O red cells in vivo. One of the references they use is the first peer reviewed paper that I ever wrote, concerning A and/or B substance being adsorbed onto the surface of donor-derived red cells in vivo. What I failed to say in this paper was that this phenomenon was far easier to detect with polyclonal ABO reagents than monoclonal ABO reagents (36 years, and I still regret this omission!). Anyway, IF I HAVEN'T SENT YOU TO SLEEP YET, my point is that, as long as you use suitable controls, particularly NEGATIVE controls, there is no reason why you should not use any modification to any technique (GIVEN THAT IT IS IN YOUR SOP, with all the qualifications given above), and, even then, if you feel it safer, GIVE GROUP O BLOOD.
  3. The Red Cell Immunohaematology Departments of the National Health Service Blood and Transplant (NHSBT) in England and North Wales have used the Bio-Rad Gel cassettes for years now, and they are absolutely brilliant. We use them both manually using semi-automated pipettes and reading by eye, and on on fully automated machines with automatic reading. The ONLY drawback that we ever found was that they are particularly sensitive for detecting unwanted reactions caused by "cold reacting" autoantibodies and cold reacting" alloantibodies, such as sub-clinical anti-M, but I wouldn't swap them for anything.
  4. I can fully understand what you are saying (and agree almost 100%), but I do have some sympathy for them signing the forms "after the event" as it were, because when they do have to use the uncrossmatched blood that quickly, then they are going to be pretty busy doing things like preventing the demise of the patient - if you see what I mean!!!!!!!!!
  5. Thanks for this explanation Arno. I should have thought of it myself (but didn't!) as my friend Bill Chaffe, a former President of the BBTS described just such a situation in a meeting a few years back.
  6. Well, that's got rid of two of my possible theories in one fell swoop! I was wondering either about loss of antigenicity due to some form of myeloid malignancy, or of adsorption of autologous secreted A substance on to the donor group O red cell surface following a successful BMT or stem cell transplant, which may be seen with only some clones of anti-A (see, for example, Cripps K, Mullanfiroze K, Hill A, Moss R, Kricke S. Prevalence of adsorbed A antigen onto donor-derived group O red cells in children following stem cell transplantation: A single-centre evaluation. Vox Sang 2023; 118: 153-159. DOI.10.1111/vox.13386., but I saw this phenomenon in adults many times when working at Westminster Hospital). Oh well, back to having more thoughts!
  7. Would you be able to disclose the underlying pathology of the patient please?
  8. Welcome WVLAB. If you are anything like me, you will love this site, and soon get hooked!
  9. It is usual for the C+, D- red cells (e.g. r'r) to react with an anti-G more strongly than a C-, D+ red cell (e.g. R2R2), BUT, this is by no means "diagnostic". As Jsbneg says above, it would be far safer to perform the proper tests, to ensure you have ascertained the correct specificity/specificities. The attached PowerPoint may or may not help (ignore if it is not helpful). The G Antigen and Anti G.pptx
  10. The Donath-Landsteiner Test for the Donath-Landsteiner antibody (IgG auto-anti-P that binds complement) that causes PCH (see the PowerPoint I attached above).
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