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Malcolm Needs

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Everything posted by Malcolm Needs

  1. We would rarely perform an eluate on the baby's red cells unless there are clinical (as opposed to laboratory) signs of HDFN. In other words, an elution is not considered to be a "reflex test", just because the baby has a positive DAT.
  2. If you have any, you could try D Negative Cord or Neonatal red cells, which express the LW antigen comparatively strongly (certainly compared with adult D Negative red cells).
  3. While the Ogata-Matuhasi phenomenon has been recognised since the early 1960's, it is, that notwithstanding, a very rare phenomenon to actually come across in practice. With all due respect to you Bet'naSBB, if you "see this quite a bit", I would be a bit worried as to why.
  4. Given that red cells are, in themselves, a blood component, the answer has to be no.
  5. Have you considered that your patient could be a particularly low-grade weak D, a partial D of some kind (such as an RoHar), which would explain the anti-D in the eluate as a result of the RhoGam, or that what you are detecting in the eluate is not an anti-D, but is an anti-LW? I also assume that the last wash is totally negative? Sorry to ask this.
  6. Phew, I am certain I do not deserve those kind words, and nor am I sure that I can live up to them, but I will do my best to explain Kea. The first thing to say is that not everyone who is K Negative, as your father must be, otherwise he would be unable to make anti-K (which is what they mean by saying he has made anti-Kell - VERY bad nomenclature on their behalf!). Except in certain, rare, pathological conditions, one does not produce an antibody against an antigen expressed on one's own red cells. I suppose really, I should start by explaining some terms. An antigen (in this case, I am talking about something expressed on the red cells - they can also be expressed on white cells, platelets and other tissues within the body - but that will complicate things more than is required, so I will stick to red cells) is a structure on the surface of the red cell (usually either a protein or sugar) that, if these red cells are transfused to another individual who does not express the same antigen on his or her red cells, can stimulate the recipient's immune system to produce a specific antibody directed against this antigen. This antibody can lead to the destruction of the transfused red cells, should such antigen positive red cells be transfused to the same individual a second or subsequent time; so, in this case, if K Positive red cells are transfused to a K Negative individual, the recipient may produce an anti-K as a result, and if K Positive blood is transfused to this individual a second time (after a few weeks or months), those K Positive red cells may be destroyed in what is called a haemolytic transfusion reaction (please excuse my English spelling!). Another way in which such an antibody may be produced is if a woman is, for example, K Negative, and her baby is K Positive (the K gene would have to be inherited from the biological father for the baby/foetus to express the antigen on its red cells). Some antibodies are produced "naturally", without stimulation with red cells. Two things are important to say here. Firstly, an antibody is NOT produced by everyone when they are transfused with red cells that do express an antigen that the recipient does not express (or the pregnant woman does not possess -despite the fact that in almost all pregnancies there is a small bleed from the foetus into the maternal blood system).; the production of an antibody is by no means automatic. Secondly, the transfusion of antigen positive blood to someone who has made such an antibody does NOT necessarily mean that they will have a haemolytic transfusion reaction (certainly not one that is clinically significant). So, getting back to your family, your father MUST be (or have been) K Negative, and MUST have been transfused with K Positive blood at some point during his life (he, fairly obviously, could not have been pregnant with a K Positive foetus - and, if he was, I want to be his manager!!!!!!!!!!!). Now, for an antigen to be expressed on an individual's red cells, they have to have inherited a gene, either from their mother or their father (or both) that encodes for that particular antigen (genes are inherited, but antigens cannot be inherited - they are the result of inherited genes). Antibodies, on the other hand, which are found (normally) in the plasma (the "watery" part of the blood) once they have been stimulated CANNOT be as a result of inheritance (except very loosely, in that some, very rare individuals, never seem to produce antibodies, however many times their immune system is "challenged" by a "foreign antigen"). This means that, unless your elder sister is, as is likely, K Negative and then received either a K Positive transfusion, or was pregnant with a K Positive foetus, she is unlikely to have produced an anti-K. Similarly, if, as is likely, your brother is K Negative, he is most unlikely to have anti-K in his plasma, unless, at some point during his life, he was transfused with K Positive blood. The fact that antibodies are NOT inherited, it is highly UNLIKELY that your nieces and nephews will have anti-K in their circulation. The McLeod phenotype is very, very unlikely, as is the McLeod Syndrome. They can both be inherited but would result in antibodies of different specificities than anti-K but may well also result in certain other pathological symptoms, so I really wouldn't worry about that. Sorry, I have gone on a bit, and I hope this helps, but will attempt to attach a PowerPoint lecture that may explain things further, should you be so obsessed as to read it! If this is not what you wanted, I would suggest you ask another member of this group, named "Danny", who knows more about the subject than I ever will. In Depth Lecture on the Kell and Kx Blood Group Systems.pptx
  7. The timing for fresh samples is somewhat different in the UK than in, for example, the USA. The timings, and the reasons for these timings, are set out in paragraph 3.7 of the BCSH Guideline "Guidelines for pre-transfusion compatibility procedures in blood transfusion laboratories" (written by Claire Milkins, Jenny Berryman, Carol Cantwell, Chris Elliott, Richard Haggas, Joan Jones, Megan Rowley, Mark Williams and Nay Win, for, and on behalf of the BCSH, and published in Transfusion Medicine 2013; 23: 3-35. doi: 10.1111/j.1365-3148.2012.01199.x), with the Key Recommendation of this paragraph being, "Serological studies should be performed using blood collected no more than 3 days in advance of the actual transfusion when the patient has been transfused or pregnant within the preceding 3 months." As I understand it, this timing was based on the work originally carried out by Professor Patrick Mollison many years ago, who found that a new specificity of an alloantibody, or a nascent antibody that has become undetectable by normal serological techniques, can appear (or reappear) in the plasma of an individual within three days, after stimulation. The problem is that not all patients know whether or not, or when, they have been transfused, or may deny it for religious reasons (I once cross-matched for a patient who had been a life-long Jehovah's Witness, who had an anti-Fya in his plasma that had a titre well in excess of 128). I hope that helps.
  8. The three months was chosen following a paper written by Laine EP, Leger RM, Arndt PA, Calhoun L, Garratty G, Petz LD. (In vitro studies of the impact of transfusion on the detection of alloantibodies after autoadsorption. Transfusion 2000; 40 1384-1387. DOI: 10.1046/j.1537-2995.2000.40111384.x.) that showed that red cells that had been transfused (or entered the circulation via a feto-maternal haemorrhage could adsorb out weak alloantibodies for up to three months in a patient with AIHA. This in vivo adsorption would, of course, also apply to individuals who did not have AIHA, but could lead to a secondary stimulation, leading to a stronger antibody (higher titre and higher concentration per mL of plasma), if the alloantibody was "missed" in the antibody screen and/or cross-match, particularly as it is unlikely that the full phenotype of the transfused (or foetal) red cells would be known.
  9. I agree, except for the first time Red Cell Immunohaematology at NHSBT-Tooting Centre were inspected by the Medicines and Healthcare products Regulatory Authority (MHRA), who had previously only inspected the donor side of things. We (RCI) were "inspected" by the top inspector (no name, no pack drill), who knew s*d all about blood group serology, but who was determined to make his mark by finding anything he could (however minor) and making it a major. As a result, we lost six months of screening for rare donors (it's a long story). Since then, I agree with you that more inspections actually help (and the MHRA inspectors now seem to have done their homework - although most of them would still not pass a reasonably difficult examination in blood group serology - but at least they now realise that).
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