Is this patient a real group A2B with anti-A1?

[Clarest]

Recently, we had a patient with following ABO group test result:

Anti-A: 4+ ,  anti-B: 4+,  anti-A1 Lectin: 0,  A1 cells: 3+,  B cells: 0, A2 cells: 0;  DAT: neg; antibody screen: neg.

I am wondering if this patient is a real group A2B as I thought usually A2B is only 2+mf with anti-A and 1+ with A1 cells. Patient has no history of BMT, but has liver and kidney failure.

I told my tech to give group O red cells, group B platelets (no group AB available) and group AB plasma.

Can anybody give another thought? Thanks

[Malcolm Needs ☆]

It looks like a straightforward A₂B with anti-A₁ to me (although you need to test the plasma with a couple more examples of A₁ red cells and a couple more examples of A₂ red cells, to ensure that the original A₁ red cells were not expressing a low prevalence antigen against which, by chance, your patient has raised an antibody).

 

If you prove it to be a true anti-A₁, as I suspect, then do a thermal amplitude test to see if it reacts at 37^oC (which I doubt).  If it does not react at 37^oC, it is clinically benign, and you can safely transfuse your patient with cross-match compatible AB red cells, and you will not have to waste your precious group O red cells.

[Clarest]

Thank you Malcolm. As I checked with reference books, group A2B reaction strength against anti-A1 or A1 cells is usually weaker than 3+. So, I felt a little bit confused with this case. Moreover, could you please explain what kind of situation / underlying disease may cause patient develop clinically significant anti-A1 reacting at 37C? How should the thermal amplitude test be performed, e.g,time duration at 37C, any controls? Thanks.

[Malcolm Needs ☆]

There are, as far as I know, no conditions or underlying diseases that make a person prone to developing clinically significant anti-A₁.  Such an antibody is very rare.  I have only ever seen one convincing case.  This was in an A₂B patient with haemophilia, but I have seen an awful lot of other A₂B haemophiliacs who have not had a clinically significant anti-A₁.

 

The way we test for it is to allow the red cell suspension and the plasma to come to 37^oC before they are mixed, and then to mix them and incubate for about 30 minutes at strictly 37^oC before examining for agglutination.

[Dansket]

 

There are, as far as I know, no conditions or underlying diseases that make a person prone to developing clinically significant anti-A₁.  Such an antibody is very rare.  I have only ever seen one convincing case.  This was in an A₂B patient with haemophilia, but I have seen an awful lot of other A₂B haemophiliacs who have not had a clinically significant anti-A₁.

 

The way we test for it is to allow the red cell suspension and the plasma to come to 37^oC before they are mixed, and then to mix them and incubate for about 30 minutes at strictly 37^oC before examining for agglutination.

I assume this is done in test tube. Do you centrifuge before examination?

 

[Malcolm Needs ☆]

Yes to test tube and no to centrifugation.

[Clarest]

Thank you so much Malcolm.

[profbaud]

I am an A2B Negative [i haven't developed anti-A1 yet since I have never been transfused] but with the increased strength of the monoclonal typing reagents, my "A " type is 3-4+, but years ago it was 2+.  There is no mixfield reaction with A2, that is with A3

I trust you ran the Anti-A1 against an O cell to make sure its Anti-A1 and not a RT alloantibody.  Since it was nonreactive with A2 cells and reactive with A1 cells, your testing looks like an A2B with Anti-A1

[galvania]

Dear Profbaud

You don't need to have been transfused to develop an anti-A1.  It is 'naturally occurring', or more correctly, 'non-red-cell immune'.  In other words, it is produced in response to factors in the environment, and not red cells.

Anna