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    Patients with auto antibodies and negative pvp

    in Immunohematology Reference Laboratories

    Posted · Edited by RollSlow10

    Well, I can certainly explain the first bit.  Cold-reacting antibodies sensitise red cells very quickly indeed.  Even if you pre-warm your cassettes, the chances are that the air at the top of the cassette (the reaction chamber) is going to be well below 37oC.  It is probable, therefore, that the red cells are sensitised before the cassettes are incubated at 37oC.  Once sensitised, the antibody takes quite some time to come back off the red cells - longer than the incubation time.  The cassette is then centrifuged at room temperature, and so you detect the cold-reacting antibody, even in cassettes with monospecific anti-IgG.  It is probable that the antibody is actually an IgM, although cold-reacting antibodies can be IgG (classically, the anti-P in PCH is a biphasic cold-reacting IgG antibody).

     

    Turning to the other bit (why the auto is negative), it could just be that the antigens are blocked by so much antibody being on them that the antibody cannot cross from one red cell to the other to form agglutination.  If you like, it is similar to the prozone effect.

    Developing Anti A1

    in Case Studies

    Posted · Edited by RollSlow10

     If I did not pick up the Anti A1 would she have had a transfusion reaction if administered A1 pos cells?

     

    With those results in the forward group, there is no way  (I hope) that ANYONE would have given her A1 cells - or even A2.

    removed

    Developing Anti A1

    in Case Studies

    Posted · Edited by RollSlow10

    If she is 75 and having a baby, I think she has bigger problems than an anti-A1!   :)  Couldn't resist. I am sure you proposed the anti-A1 question hypothetically.

     

    Anti-A1 can be naturally occurring so does not require pregnancy or transfusion.  Anti-A1 is usually IgM so can't cross the placenta.  Even if it were somehow partly IgG, I have never heard of it causing HDFN.  I once saw an auto anti-A1.

     

    You needed to resolve the ABO discrepancy. I would hope that the methods used would either be in your procedure or the Technical Manual or some other acceptable reference although we all experiment with these odd samples when we get them.  What you did appears to have worked.  You ran appropriate controls to make sure you weren't picking up some other cold agglutinin etc.

     

    Missing a very weak A subgroup in a recipient is interesting but it isn't terribly important.  You would give O blood and the patient would be safe.  If such a patient makes a fairly strong anti-A1 we might never suspect a weak subgroup because we would have no ABO discrepancy. (I realize the patient could also have the B antigen, and you would give B blood rather than O etc.)

    Removed

    Warm auto vs. High frequency Ab with positive DAT ?

    in Transfusion Services

    Posted · Edited by RollSlow10

    It is a bit difficult for me to answer this, because all our costs are via the NHS (Government - or, to be cynical, the tax payers!), but both anti-Doa and anti-Dob have been implicated in transfusion reactions (albeit, rarely).

     

    The real problem is that "grouping grade" anti-Doa and anti-Dob are extremely rare, even for Reference Laboratories.  It may be that they have to genotype for the DOA and DOB.  That may prove to be very expensive; but it may also prove life saving.

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