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Malcolm Needs

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Malcolm Needs last won the day on May 24

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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!).

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  1. I hate to say this, but, as far as I am concerned, this is nonsense. Indeed, like CR1-related antigens, the "older" the red cells, the weaker the antigens. The easiest way of seeing whether a reaction is due to a Bg antibody is to use red cells that are Bg Negative in the first place, or,if you think the reactions are due to anti-Bg, treat the red cells with chloroquine diphosphate, which will remove Bg antigens from the red cells.
  2. With reference to the ABO reverse grouping problems that cannot be resolved at RT, instead of incubating the tests at 4oC for 60 minutes, have you tried incubating at 30oC, or, in extreme cases, 37oC, or using cord red cells. Most of these "cold" antibodies have a specificity involving I or IH, and so, in the majority of cases these methods will resole the problems, without compromising the ABO antibodies, which, as we know from unfortunate transfusion reactions, work pretty well at 37oC! Turning to your specific questions: Q1. Firstly, we wouldn't test the plasma at 4oC. What is the point? Apart from Zombies in Holywood films, how many humans do you know who survive with a body temperature of 4oC? All we would do is test the antibody for its thermal amplitude, and if it does not react at 30oC, we ignore it (see Petz LD, Garratty G. Immune Hemolytic Anemias. 2nd edition, 2004, Churchill-Livingstone). If the antibody does react at 30oC AND is an alloantibody, we would be more proactive, identify the specificity, and give antigen negative blood. If it was an autoantibody, we would ignore it for transfusion. Q2. Apart from the above, NO! Q3. Why would you want to remove the IgM from the red cells. They will hardly ever be swamped by the autoantibody, but, if they are, we would use Rabbit Erythrocyte Stroma (RESt), which is available commercially. Unfortunately, this also adsorbs anti-B, and so the plasma adsorbed like this should never be used for cross-matching, as a group B mis-match would never be detected. Q4. I am going to be VERY cheeky here, and I say this with no evidence whatsoever, and that I will probably be slated by most members on this site, possibly rightly so, but I think that, as you are a Reference Laboratory worker, your techniques for working with these samples are more "honed" than those of the average hospital laboratory, as you see them far more often than do the hospital laboratories. I will now go and don body armour and a steel helmet!!!!!!!!
  3. If your patient is Kell Negative (Ko) you have real problems. If your patient is K Negative, you, and your patient, have more chance!
  4. I have an idea what it might be, but am bound by the rules of the game (fair enough). Please can you remind the likes of me when we can "put our oar in"? Thanks. P.S. It looks really good Bb_in_the_rain!
  5. It is, nevertheless, true. Thorpe SJ, Boult CE, Stevenson FK, Scott ML, Sutherland J, Spellerberg MB, Natvig JB, Thompson KM. Cold agglutinin activity is common among human monoclonal IgM Rh system antibodies using the V4-34 heavy chain variable gene segment. Transfusion 1997; 37: 1111-1116. Thorpe SJ, Ball C, Fox B, Thompson KM, Thorpe R, Bristow A. Anti-D and anti-i activities are inseparable in V4-34-encoded monoclonal anti-D: the same framework 1 residues are required for both activities. Transfusion 2008; 48: 930-940.
  6. A few things as far as human reagents. Firstly, you never know what else may be in them in terms of antibodies directed against low prevalence antigens, because there is absolutely no way that the producer has the ability to test for all such specificities (I can remember once a human-derived anti-D reagent produced at one of the places I worked, also had a Gm antibody in it that we didn't know about. It is highly unlikely that this would have caused too many problems, but there is, nevertheless, a small chance that this could have caused a false positive). Secondly, you never know what else may be in them in terms of viruses, some of which may, as yet, be unknown to us (remember, HIV, used not to be known). This is a danger to the producer and the person using the reagent, rather than the patient. Thirdly, the avidity of human reagents is, in general, pretty poor (particularly anti-D). A few things concerning monoclonal reagents. Some of them cross-react with other specificities (although not many), but, famously, monoclonal anti-D reagents will react with the I and i antigens if used straight from the fridge. They have to be blended by experts to ensure that the desired epitopes are detected, but certain Partial D types (e.g. Partial D Type VI) are not detected (unless required). They are very specific and very avid (both of which are greatly to be desired). Virally, they are almost certainly sterile. Hope that helps.
  7. Well jnadeau, be it on your head! You might receive insulting posts from others on the site now! Unfortunately, the photographs of me actually receiving the gold medal and glass plaque were not of great quality, but this is one taken at the Institute of Biomedical Science soon afterwards. Even here, my hair and beard look a bit like I have just poked my fingers into an electrical socket, my tie has gone awry and, these days, a wide angle lens is required on all occasions, but here it is in all its glory!
  8. Sadly Neil, it is not the case that anti-Inb is wholly or largely IgM; indeed, it is almost always IgG. It is thought that Indian Blood Group System antibodies do not cause HDFN because they bind to CD44 on foetal monocytes and macrophages and, therefore, have a blocking effect on FcγR1. This being so, or likely to be so, plasma exchange is likely to be less effective that might be thought, because of rebound from the extra vascular spaces.
  9. She very possibly can (although two things; it would most certainly depend on the titre of the anti-Inb prior to EACH transfusion [and that would have to be 1) a doctor's decision and 2) a bit of a guess, as anti-Inb is so rare) and also, I would suggest IvIgG, rather than methylprednisolone (or, possibly, both). However, having said all this, there is NO DOUBT that anti-Inb is clinically significant in terms of haemolytic transfusion reactions, although the same is not the same for HDFN.
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