Hi All!

I had an ABO discrepancy on the bench last evening that I'd like to pick your brains about.

The patient typed A positive with a ? in the backtype with A cells by solid phase on a Galileo.

By tube, the patient typed A positive with a 1+ reaction in the backtype with A1 cells that were in-date.

Initially, I tested with A2 cells and got a positive 2+ reaction so abandoned my anti-A1 theory and proceeded to perform a cold screen. After a 15 minute incubation at room temperature, there was no agglutination with any screening cells, cord cells, OR A2 cells but a 1+ reaction with A1 cells and a 1+ reaction in the auto control. I performed a DAT because of the positive autocontrol which was positive by AHG (2+) and IgG (1+) but negative with complement.

After these results, I realized that I hadn't let the A2 reagent cells get to room temperature before I'd used them so my initial results with the A2 cells were likely invalid. The room temperature A2 cells were negative at initial spin. (Mental note to always let reagent cells come to room temperature.)

Back on a possible anti-A1 path, I tested the patient's cells with anti-Al lectin. It was positive with a 4+ reaction. The patient had been receiving transfusions with type A positive blood here and there but not enough to make me think that that could invalidate the A1 typing results. I would think that a transfusion here or there might yield a mixed field or a weak A1 typing?

I then tried to test with additional A1 cells to investigate further but, even after a 10 minute incubation and a view under a microscope, neither of my out-of-date A1 reagent cells yielded a positive reaction. I also tried testing with some unit cells but it was also negative.

I prepared an eluate before my shift ended that another tech tested with all three A1 cells and screening cells. Her results were + with all three A1 cells.

The patient has a history of having received IVIG about a week ago. Can we close the case by assuming that the backtype discrepancy is due to ABO isoagglutinins in the IVIG? Are there other possibilities to investigate? Should the patient receive O positive transfusions if they are ordered and is this because the (supposed) passive anti-A1 was found in the eluate? (If the eluate had been negative, would we give XM compatible A pos?)

The first thing I would ask, before going any further, is, why was the patient receiving IVIG, because this is quite important.

Thanks!

I think that he was a transplant patient. I don't go back into work until Thursday to find out for sure. He's receiving IVIG once a week but this is the first work up that it's caused a discrepancy in.

Annadele

The first thing I would ask, before going any further, is, why was the patient receiving IVIG, because this is quite important.

Sorry Annadele, you must be getting fed up with my endless questions about this patient, but, by transplant, do you mean a solid organ transplant or a bone marrow/stem cell transplant, and how long ago?

We commonly see positive DATs in Group A patients post-IVIG. Eluates yield Anti-A. Some IVIG manufacturers now have disclaimers that their products can cause acute hemolytic reactions due to Anti-A in Group A populations. I have also seen it interfering with the backtype (on Echo analyzers). When we see the Anti-A in the plasma, we err on the side of caution and give group O blood, but usually only the patient's cells have the Anti-A from the IVIG.

Edited March 6, 201213 yr by marvy1

Eluates yield Anti-A.

We have a patient that showed anti-f after repeated IVIG infusions. It can do some funny things...

Hi again! I'm back at work today. The patient was a heart/lung recipient. I'm not sure how long ago they received the transplant - only that they're receiving IVIG once a week.

Sorry Annadele, you must be getting fed up with my endless questions about this patient, but, by transplant, do you mean a solid organ transplant or a bone marrow/stem cell transplant, and how long ago?

Ahhh, that makes quite a difference.

The anti-A could come from the IVIG, but, if the heart-lung donor was of a different ABO group to the recipient, it is equally possible that the anti-A could come from "passenger lymphocytes". Most people believe, as did I, that "passenger lymphocytes" die off fairly quickly after transplantation, but it appears not to be the case.

I was at a lecture given by Dr. Derwood Pamphilon last year when he was talking exactly about this phenomenon. Apparently, the "passenger lymphocytes" can set up ectopic clones within the body, where they can florish to a small extent - not enough to cause classic graft versus host disease, but sufficiently so that they can definately be detected. The more lymphoid the transplanted tissue, the more likely it is that these ectopic clones can survive. Heart-lung transplants are a classic example of this. The clones can "take" throughout the body, and this may explain the presence of the apparent anti-A in your group A patient.

I am not saying that this is definately the case in your patient, but it is a definate possibility, if the donor was capable of producing an anti-A (say, for example, the heart and lungs came from a group O donor).

Wow. I can't believe you posted this. We had the same exact thing last week. Eluted anti-A1 from A neg patient. We were also getting incompatible crossmatches on a sample drawn 4 days later. Assumed patient had developed anti-A1. Pre-transfusion (of 2 B neg SDPs) sample patient type was A1 pos (4+). We assumed the anti-A1 was from a high titer in the SDPs of anti-A1 (both platelets from same donor). I found out that pt also received IVIG same day as platelets. So although still a passive anti-A1, probably from IVIG!! Thank you. Always something new to share on this site! Oh I should add O crossmatches were compatible, so that's what we are giving.