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Transfusing A2 patients


kimblain

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My first thought is why do you know they are A2. I have never worked anywhere that A1 lectin testing was routinely performed. We do A1 lectin on potential organ recipients and would automatically give them O cells. The only other people that we do A1 lectin on have a type discrepiency due to Anti-A1 and we then give them O cells.

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1. Apart from renal transplants, I can't see the point of typing with anti-A1 (human, monoclonal or lectin).

2. Unless the anti-A1 reacts strictly at 37oc, why on Earth give group O blood, instead of cross-match compatible group A blood? How many of you have come across an anti-A1 that has caused a haemolytic transfusion reaction? How many of you have read about one that has caused a haemolytic transfusion reaction (apart from the recent publication in, I think Transfusion, but I could be wrong there, that involved a very rare and extreme case in a BMT recipient)?

NOT ALL ANTIBODIES ARE CLINICALLY SIGNIFICANT.

:explosion:explosion:explosion:explosion:explosion:disbelief:disbelief:disbelief:disbelief:disbelief

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1. Apart from renal transplants, I can't see the point of typing with anti-A1 (human, monoclonal or lectin).

:explosion:explosion:explosion:explosion:explosion:disbelief:disbelief:disbelief:disbelief:disbelief

Thanks Malcolm for your post.

If you have time, please explain why renal transplants need to be tested for A1 or Asub on detail. Thank you.

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HI Yanxia.

Actually, it isn't the renal transplant patients that we test with A1, but we test the donors for A1 if the donor kidney is going to be transplanted into a group O or group B patient. In other words, in the case of a potential ABO incompatible renal transplant, the renal surgeons like to know whether the donor is an A1, A2, A subgroup. This is because they have to get the anti-A titre of the recipient down to as low a level as possible (to prevent graft rejection), and, in such circumstances, A2 renal transplants tend to be more successful than A1 renal transplants (because the A antigen on the red cells and the kidneys of an A1 donor is expressed more strongly than the A antigen on the red cells and the kidneys of an A2 donor).

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What are your practices transfusing A2 patients. Do you automatically transfuse O type blood or do you wait until that patient presents with an Anti-A1?

the only problem is presnce of ati A1 (however there is severe doubt about its significant), so I think if these is no anti-A1 no problem to issue A group, but if there is anti-A1 best to issue same subgroup or O.

- - - Updated - - -

What are your practices transfusing A2 patients. Do you automatically transfuse O type blood or do you wait until that patient presents with an Anti-A1?

the only problem is presnce of ati A1 (however there is severe doubt about its significant), so I think if these is no anti-A1 no problem to issue A group, but if there is anti-A1 best to issue same subgroup or O.

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We give O blood to our patients with anti-A1 because it keeps our computer happy. It happens maybe once a year, if that.

We do the same as Mabel. All generalists here in BB and then confusion ensues (do we give A1 neg units, etc.) So for the rare instance this occurs, we give Group O RBCs.

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Nothing wrong with using some A1 lectin to screen for A2 units either, I would think. Or AHG crossmatch compatible A units too. And it is more comfortable to do and see the XM phase (usually I.S.) where the anti A1 is seen too as part of the crossmatch. (Supposed to do that anyhow now according to the standards for detection of ABO compatiblity.)

If the A unit is compatible at I.S. and whatever coombs phase test you use, should be OK to give. We have done this on our rare anti-A1 patients without problems.

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We also give type O for A2 patients making an anti-A1. To make the computer happy, like Mabel said, and also because the techs feel more comfortable. It happens so rarely, not a big deal to give an occasional type O to someone who really doesn't need it.

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  • 1 month later...

On this same line of thought, I assume that you would also give type A1 blood in the following scenario: Twins <1 month old at our hospital. One is type A (positive with A1 lectin), and the other is possible type A3 (mixed field reactions with anti-A, has not been transfused, negative with A1 lectin). Neither has anti-A1 in their serum at immediate spin or IgG. We have a directed donor type A1 unit from one of the parents. Unit is fully compatible with the A subgroup twin. Do we give the directed donor unit to the A subgroup twin? If so, should we get specimens every 3 days to ensure that the baby doesn't start making anti-A1? I know that babies don't normally make anti-A until 3-6 months, but I'm not sure I want to take any chances.

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On this same line of thought, I assume that you would also give type A1 blood in the following scenario: Twins <1 month old at our hospital. One is type A (positive with A1 lectin), and the other is possible type A3 (mixed field reactions with anti-A, has not been transfused, negative with A1 lectin). Neither has anti-A1 in their serum at immediate spin or IgG. We have a directed donor type A1 unit from one of the parents. Unit is fully compatible with the A subgroup twin. Do we give the directed donor unit to the A subgroup twin? If so, should we get specimens every 3 days to ensure that the baby doesn't start making anti-A1? I know that babies don't normally make anti-A until 3-6 months, but I'm not sure I want to take any chances.
There are one or two things that I wonder about this case Kathy, and I would tend to think in terms of giving group O to the "A subgroup twin". Sorry this is all one paragraph, by the way, but my "return key" seems to be sulking!!!!!!!! Firstly, although the "A subgroup twin". Although he/she may appear to be an A3, it could be that his/her N-acetyl-D-galactosaminyl transferase is not yet working to its optimum/maximum, and so it is not yet sufficiently transferring the terminal N-acetyl-D galactosamine carbohydrate residue to the Type II backbone. Therefore, the "A subgroup twin" could end up being a "normal" group A, like his/her twin. The other thing is, have you grouped the "A subgroup twin" with other antisera, such as anti-M through to anti-Jkb? I just wonder if these twins could have had an anastomosis in utero and that he/she could actually be a natural chimera (now I'm stuck in italics)! Although I don't fear the "A subgroup twin" making a clinically significant anti-A1, I do fell that, in this case, group O blood could be the way to go.:confuse::confuse::confuse::confuse::confuse:
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There are one or two things that I wonder about this case Kathy, and I would tend to think in terms of giving group O to the "A subgroup twin". Sorry this is all one paragraph, by the way, but my "return key" seems to be sulking!!!!!!!! Firstly, although the "A subgroup twin". Although he/she may appear to be an A3, it could be that his/her N-acetyl-D-galactosaminyl transferase is not yet working to its optimum/maximum, and so it is not yet sufficiently transferring the terminal N-acetyl-D galactosamine carbohydrate residue to the Type II backbone. Therefore, the "A subgroup twin" could end up being a "normal" group A, like his/her twin. The other thing is, have you grouped the "A subgroup twin" with other antisera, such as anti-M through to anti-Jkb? I just wonder if these twins could have had an anastomosis in utero and that he/she could actually be a natural chimera (now I'm stuck in italics)! Although I don't fear the "A subgroup twin" making a clinically significant anti-A1, I do fell that, in this case, group O blood could be the way to go.:confuse::confuse::confuse::confuse::confuse:

Malcolm,

Interesting. I did not think about chimerism. Unfortunately, our pretransfusion specimen was drawn more than two weeks ago. Our current specimen is not representative of the patient's own red blood cells, since this patient has had multiple transfusions (with type O blood). RBC phenotyping would be useless at this point. The parents don't seem to object to us giving O blood rather than the directed donor unit.

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Malcolm,

Interesting. I did not think about chimerism. Unfortunately, our pretransfusion specimen was drawn more than two weeks ago. Our current specimen is not representative of the patient's own red blood cells, since this patient has had multiple transfusions (with type O blood). RBC phenotyping would be useless at this point. The parents don't seem to object to us giving O blood rather than the directed donor unit.

Depending how badly you want to know this (because it is expensive) you could get the twins karyotyped (I was going to say, as long as they are not identical, but that would have been a really stupid thing to say!!!!!!!!!!!!!!!!).

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