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comment_71469

We had an 65 years old male pacient with A2B Rh(D)+ blood type.Never transfused before,antibodies screening negative.We asked our blood bank transfusion guidelines for this pacient in case of need(he was hospitalised for heart surgery).We got the answer that we can give him AB Rh(D)+ regular red cells (the chances he would develop A1 antibodies is 20 percents as far as I know) and only later,if he develops that antibodies we should switch him on B or O.What do you think about this?Is this correct in your transfusion policy?
(Lucky pacient didn't need transfusion of red cells after all,only FFP)
Just to satisfy my curiosity...and learn,of course.
 

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  • Malcolm Needs
    Malcolm Needs

    Absolutely the advice given to you was correct. For a start off, as you say yourself, 80% of A2B individuals do NOT make an anti-A1, but of those 20% who DO make an anti-A1, how many will make th

  • Malcolm Needs
    Malcolm Needs

    It is important to remember that there is a sort of continuum between the various A types (including A1 and A2) in terms of the number of A antigen sites expressed per red cell, and that there is no s

  • Malcolm Needs
    Malcolm Needs

    As long as the anti-A1 remains "cold reacting" only, and the thermal amplitude does not widen, the clinical significance remains as "not clinically significant", and, personally, I would happily trans

comment_71470

Absolutely the advice given to you was correct.

For a start off, as you say yourself, 80% of A2B individuals do NOT make an anti-A1, but of those 20% who DO make an anti-A1, how many will make that anti-A1 as a result of immunisation as a result of transfusion or pregnancy?  The answer to that, if you read any book concerning blood group serology (and that is NOT a criticism of you - we all started somewhere, including the very best, such as Herr Dr Willy Flegel, and others - and I have HUGE respect for Willy), you will see that a clinically significant anti-A1 is amazingly rare.

For an anti-A1 to be clinically significant, it has to react strictly at 37oC, and that is a VERY rare "animal", and no example of anti-A1 has EVER been implicated in a case of HDFN, so, PLEASE, do not worry about giving A1B (or even A1) blood to an A2B individual, even if they have an anti-A1 in their circulation, UNLESS they have an anti-A1 that is actually active at strictly 37oC.

comment_71476

My pleasure.

  • 3 months later...
comment_72563

We have a liver transplant patient AsubB with an anti-a1 (cold).  Our computer allows electronic "XM".  Do you agree with this or recommend a serologic XM?

comment_72565

As long as the anti-A1 remains "cold reacting" only, and the thermal amplitude does not widen, the clinical significance remains as "not clinically significant", and, personally, I would happily transfuse blood by electronic issue.

Even if the thermal amplitude does widen, unless the anti-A1 actually reacts at strictly 37oC, it will remain as "not clinically significant", but I would, nevertheless, perform a serological cross-match - "just as belt and braces".

  • 1 month later...
comment_73009

We have a 19 yr. pregnant female, front type Apos, back type 1+ A1cells and 4+ Bcells. (in gel) No history available.

Tube test with A1 cellls=1+; A2 cells=0; two different O cells=0; and B cells=0.

Anti A1 Lectin = 1+

Antibody screen negative

Results the same with different lot A1 cells. Strength increases with cold incubation.

Crossmatch in IgG at 37 degrees with patient plasma and A1cells is 1+. (in gel)

We are having the patient re-drawn for confirmation, but do I call this weak A subgroup if all results confirm? Clinically significant? Transfuse O cells?

Or could this be pregnancy related?

Edited by Jennifer Castle

comment_73010

It is important to remember that there is a sort of continuum between the various A types (including A1 and A2) in terms of the number of A antigen sites expressed per red cell, and that there is no such thing as an absolute A1absolute A2absolute A3 and so on and so forth.  In addition, of course, the lectin Dolichos biflorus is NOT an anti-A1, but is a lectin that "recognises" the A antigen, the Tn antigen and Cad antigen, as well as the A1 antigen.  It will not recognise the A antigen if it is diluted correctly, but every now and again, there will be an "overlap" between a "strong A2", and a stronger than normal Dol. b. reagent.  In addition, there are people who are Aint, or A intermediate, who are somewhere between an A1 and an A2.  SUch people usually hail from the south of the African continent, but not always.

As we are looking at ABO, I am not for one minute surprised that the reaction strength increases with cold incubation.

The next thing to remember is that, with gel, it is all but impossible to add the reagents to the reaction chamber so that they remain exactly at 37oC, which means that IgM antibodies, such as anti-A1, which it looks like this pregnant lady has in her circulation, will sensitise A1 red cells prior to true incubation at 37oC, but will not elute quickly enough to give negative reactions after 37oC incubation, particularly after centrifugation.

Anti-A1 is NOT clinically significant, unless it reacts STRICTLY at 37oC, and this can really only be shown by a pre-warming tube technique, in which case A2 blood (or other A subtypes, such as A3, Ax and Am) can safely be transfused, keeping your precious group O units for group O recipients.  Anti-A1 has NEVER been implicated in clinically significant HDFN.

None of this is pregnancy related.

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