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galvania

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Posts posted by galvania

  1. If the genotype was done with full sequencing and the phenotype was tested with various clones and all of that said negative, how did the paper come to the conclusion that this was an auto anti-C rather than an allo-anti-C?

  2. Presuming you are in a normal lab, you should

    1.  Find out about transfusion history as a matter of considerable urgency, including plasma products

    2.  do your normal exclusions  (I would be a bit worried about an anti-Jkb with something else

    3.  Use additional cells

    4.  Put up a saline RT panel

    5.  Fully phenotype your patient

    6.  Do a DAT - look very hard for a mixed field

    Then review!

  3. Cells are coated with complement artificially.  some methods will also cause IgG to be coated.  IF the cells are used according to the method they were designed for the manufacturer will have made sure that , in that method, the IgG does not react.  The problem starts when the complement-coated cells are used in other methods or, worse, for the CAP survey.  The C3-coated cells that are used for the CAP survey almost always react with anti-IgG in gel because of this - but the cells used are actually designed only to be used with anti-C3 in tubes.

    so my advice would be, if you are using complement coated cells to control your anti-complement reagents, don't use them to check for negative reactions in anti-IgG

  4. The reactions you will see in gel cards are based on the ability of un-agglutinated cells to pass through the material in the column to get to the bottom; and agglutinated cells to be retained.  The centrifugation speed and the time of centrifugation are carefully calibrated so that that happens.  But that is specific to factors such as the size of the card, the weight of the card, and numerous factors relating to the contents of the well (type of gel/beads etc) and everything you add to the well.  So as the two cards are not the same, the parameters will need to be different as well.

  5. I would not be  in favour of going back to whole blood transfusions (except in countries where they have no choice!).  The point about 'everything being present in the one bag' is fine - if the donor has only just been bled.  But that is not likely to be the case.  How many active clotting factors remain after the blood bag has been stored for a couple of weeks?

  6. So you have a forward group that is positive with anti-A, -B, -AB, -D and the control; and the reverse group is positive in all cells and the antibody screen and panel (and, I imagine the auto control) is positive in everything.  It sounds as though you do not have a single negative result.

    This sounds to me like a cold AIHA, possibly due to medication, possibly secondary to another hematological disease (leukaemia?), possibly post infection.

     

    Do you have any other clinical information you can give us?

  7. I have actually seen a number of these beasts - usually as a result of a complaint that cell x did not pick the cell up when cell y did - and cell y just happened to be a K+k-.  Usually these were antibodies that were detected years ago and whose levels have now fallen, predictably, with time.

    The pragmatic point is - you are never going to get every single set of screening cells with a k- cell in them.  If you've got one, great - use it!  If you haven't I still would not lose any sleep over it.  Malcolm's points above are of course totally relevant as usual

  8. The word 'significant' is interesting in this context.  In most of -Europe antibodies that are detected only in enzymes, including the enzyme-only anti-Es and -Cws would NOT be considered significant and most of the time would not be detected in the first place.  Nor would the numerous anti-Lea, -Leb and -P1 that you would pick up.  Always assuming that you are working with a sensitive IAT in the first place, of course.

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