We have a 67 yr old gentleman who types as A1 D positive. His diagnosis is pancytopenia and his medications are Glucophage and amaryl. He looks to have a warm autoantibody but the odd thing is, it appears to have A1 specificity. When crossmatching, the A units are incompatible and the O units are compatible (at least we can transfuse). His DAT is 3+ positive for both IgG and C3d. The reference lab says there are no alloantibodies hiding underneath the auto. They sent absorbed serum which was found to be incomaptible at AHG with type A units as well as A1 reagent cells but A2 cells were compatible. Anyone familiar with auto anti-A1?

Nothing surprises me with antibodies anymore ...

We just received an update from the reference lab. When they were doing the absorptions they used O cells. It turns out that one of the donors had a very high anti-A1 titer. Their theory is that the anti-A1 from this donor carried through all of the washing steps enough for it to show up when we performed a 45 minute albumin AHG technique. Seems like a stretch but I certainly don't have a better explanation

I can understand an auto Anti-A1 and can see that using a standard triple adsorption the reference lab found no underlying alloantibodies. What makes no sense to me is that they attribute an Anti-A1 in their harvested serum to a donor; the patient has Anti-A1 that they have been unable to adsorb out.

I would question their interpretation. How are the transfused cells surviving in your patient?

We transfused type O cells. The patient went home. It's been a couple of weeks and we've not seen them back. I "assume" the transfused cells are doing fine. No way for us to really know unless the patient comes bck for a top up earlier than expected.

If the antibody had anti-A1 specificity, why was an autoabsorption necessary? Or did the serum react with group O panel cells?