yan xia

I am not sure about the difference between B(A) and AsubB, I always thought we define B(A) based on genotype not phenotype, and the AsubB maybe the genetic product of B(A).

I guess there are two possibilities: 1.This patient is AsubB, the A antigen cannot be tested by some anti-A reagent. 2.This patient maybe has some antigen rather than A which is crossreacted with the component of the reacted reagent. solution are 1.How about test the patients' red cells against some B type human serum, please make sure that there are O cells as negtive control. The monoclonal reagents are not as complete as the human source polyclonal antibodies. 2.And to test the saliva for ABH substance in it( if the patient is a secretor). And do genotyping, just so expensive.

I totally agree with all those briliant ideas, and there are some A subgroup have anti-A and anti-A1, such as Ax and Ael .

I have a little confusion, why the previous auto tests are all neg, and the DAT is pos? The elution result is 4+, so I guess this DAT is IgG pos, and the anti-IgG in the prewarm test, the auto is neg. My not good English, I hope I understand and express it rightSorry for the interruption.

Seems as warm autoantibodies which have a loose reaction temperature span, so they can interfere with the reverse typing. Because they are not cold auto, so cold autoadsorption does not work, and in the strict prewarm test, they still react.

We use Ortho Biovue gel card, and I don't think rouleaux interfere much on the gel result, some MM patients have rouleux on tube, but gel results are good. In my experience, cold antibodies can do. Just personal opinion.

Malcolm, may I ask what is Gm and Km, and why typing those can tell us if the one is passive or allo-anti-D? Thank you .

Kidd system antibodies can bind complement. To investigate the reason, maybe you should do an elution, then test the eluate to see what specity /specities of the binding antibodies. Add fresh serum can strengthen the sensitivity of testing Kidd antibodies.

Sorry to interrupt, is anti-V/VS clinical significant? I have not met these kind of antibodies before,( I guess because it is not common or not exist among Chinses people) just out of curiosity

I am sorry about the mistake I have made. I remember it wrong.

I post this question today, it is because I just met an ABpos baby,he is 3 months old, and still has anti-A in his blood, his mom is Bpos. Someone had transfused him with AB pos packed red cells yesterday, and I can still detect the anti-A in his plasma. I think it was stronger before transfution. So, the questions confused me are 1. B mom produce IgG anti-A , I used to think only O type produce IgG anti-A/B 2. 3 months the maternal antibodies are still here, so the half life of IgG is longer than 20 more days

I remember (not clearly) that AABB states for neonate less then 4 months, we should give type O washed red cells. If I remember rightly, but the IgG antibody' s half life is more than 20 days, then why we need 4 months to avoid the maternal sourced antibodies?

It seems like an acquired-B to me. Maybe you can try to lower the pH to 4.5 to see the lady's cells react with anti-B reagents.

The transfused cells are denser, so most of them at the bottom, and patients' own cells at the top.