Malcolm Needs
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Everything posted by Malcolm Needs
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Welcome Andrea Pointer.
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Welcome waterbug.
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Welcome Fatimah Ramos.
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Welcome Hakea.
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Welcome Labgurl84.
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True, but who is going to perform tests, such as ADCC, that cost a certain amount of money, as well as time, when M Negative units are generally easily available?
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What a waste of expensive phenotyped blood.
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Welcome Courtney, and Happy Birthday for a couple of days back!
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In the UK this problem should not occur, as our BSH (BCSH) Guidelines mandate that our screening cells have homozygous expression of certain antigens, one of which is M.
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Best suggestion yet!!!!!!!!!!!!!!!!!!!!!! -
Welcome Poppys.
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That is true John, BUT it is STILL the complement (specifically the Membrane Attack Complex of C5b, activated C6, C7 and C8 molecules and about 6 activated C9 molecules) that causes the haemolysis, which is why autologous red cells are also destroyed.
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Sorry, but I disagree. In most cases of ABO haemolytic transfusion reactions, it is not the ABO antibodies that cause the haemolysis that destroys the incompatible red cells, but activated complement that, in most cases, also causes "innocent bystander haemolysis", whereby the autologous red cells are also haemolysed.
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Happy Thanksgiving to all of my USA friends for tomorrow.
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Testing enzyme treated panel cells with buffered gel card
Malcolm Needs replied to Clarest's topic in Transfusion Services
This statement is completely true, BUT the fact that NHSBT RCI Laboratories started to use these routine techniques followed a huge amount of work performed by Gordon Burgess when he was the Reference Service Manager at NHSBT-Cambridge Centre (before he became Head of RCI in NHSBT) to show that these were viable techniques that passed prolonged Quality Assessment. To introduce such techniques without such work would not have allowed RCI to pass inspections by our various assessors. I doubt if Clarest would be able to introduce such techniques into Canadian laboratories without similar work. -
Welcome Christy B.
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VERY good point. When I was working at Westminster Hospital (many, many moons ago now), we came across a male Jehovah's Witness patient who swore blind that he had never been transfused, with one of the strongest polyclonal human-derived Fya antibodies I have ever seen.
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Welcome Mlhoepner.
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I've been wracking my brains over this one, but I have hit a brick wall. If it is not an anti-LW, I can see no alternative to an anti-D (possibly caused by a previous pregnancy - if the patient is female [or, these days, possibly a transexual who is now a male], or by one of the donors having a very rare RHD mutation). Somebody will now come up with an explanation that is quite simple, and I really should have thought of immediately!!!!!!!!!!!
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Welcome BrianT.
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Welcome s ngo.
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Welcome shimba@211.
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Suggests to me that this really is an anti-D then. I'll keep thinking (or trying to think at my age!).
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I agree ENTIRELY with the answer given by exlimey. Anti-G usually (not always, but usually) reacts more strongly with the C antigen than the D antigen, so that R1R1 and r'r red cells would give stronger reactions than would R2R2, whereas both anti-D and anti-LW would react more strongly with R2R2 red cells than R1R1 and r'r red cells. I agree that one of the units could express an unusual D type (I was caught out once in a pregnancy case when the dad had the unusual D type of RHD(L214F)-CE(7)-D - which I thought was rather unfair of him!). Have you tried rr cord bloods against the patient's plasma/serum sample? The LW antigen is expressed much more strongly on cord red cells than adult red cells.
