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Does look like a AsubB w anti-A1. I'd test pt cells w A1 lectin. Also run a small IS/rt panel of screening cells, A1, A2, auto cells and see what it looks like. By running the screening cells along with A1/A2 cells I can get an idea if it is a cold specificity or anti-A1. a

Putting aside the A antigen for the moment, which is probably "normal" in the case of your patient, it is not the B antigen that is abnormal in the case of a Bel person, but the 3-alpha-galactosyltransferase enzyme (the direct gene product of the ABO gene) is less active than normal, due to a mutation in the gene. The actual carbohydrate residue that is on the red cell is "normal" - just less of it. In addition, there is competition between the "A-transferase" and the "B-transferase" for the H-backbone. In the case of your patient, the "A-transferase" will "win" this competition and this will accentuate the weakening of the B antigen even further - but the actual structure of the B antigen will be the same as the normal B antigen - just fewer in number. This explains why there is no anti-B present in your patient's circulation. This (rather long-winded) explanation should serve to prevent you worrying about giving your patient group AB blood should they require a transfusion.

You bet! There is NOBODY better! ANYWHERE!

Looks like an AsubgroupB to me, but, these days, with monoclonal antibodies, which type of A subgroup can only be accurately sorted by molecular techniques. The reverse group needs more investigation. It could be anti-A1, it could be another "cold" antibody specificity (such as anti-M or anti-P1), or it could be a combination of the two. If there is no reaction at 30oC and above, it doesn't really matter, but, to be on the safe side, if blood is required, I would give group B packed red cells, or group B red cells resuspended in AB plasma.

I understand David's point and agree 100000%. Having worked in 50 bed, 500 bed and 1200 bed hospitals and hospitals in small towns, suburbia, and big university medical centers, blood suppliers DO NOT understand the smaller places that can go days without transfusing. It is everyone's responsibility to be good stewards of this very precious resource. Inventory management from the supplier level down to the techs in the blood banks is critical to making sure every patient everywhere can get what they need as quickly as possible.

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 hope this information helps in regards to DIN on collected or pooled products. Per US Consensus Standard, the DIN should remain that of the collection facility unless the product is pooled. If the product is pooled, a unique new pool number shall be assigned by the pooling facility. This product shall be given a new Donation Identification Number (DIN) and not use a DIN from one of the units in the pool. The new DIN shall have the Facility Identification Number of the pooling facility. And below DIN information is excerpted from the US Consensus Standard v3.0.0 - 7.8.2.2. Some computer systems treat reconstituted red cells as a pooled product; others do not. The Donation Identification Number (DIN) can either be a newly assigned Pool Number (for those systems that treat the product as a pooled product) or that of the RBC (for those systems that do not treat it as a pooled product). The text name and location of the facility that appears beneath the DIN shall correspond to the Facility Identification Number within the DIN. That means, if the original DIN of the red blood cells is used, the name beneath the DIN shall correspond to the collection facility. If a new pool number is assigned to the product, the DIN shall have the Facility Identification Number of the pooling facility, and the name beneath the DIN shall be that of the pooling facility. Regardless of which method is chosen, traceability of both the red blood cells and the plasma shall be assured. The DIN of the plasma must be associated with the DIN of the final product in the facility records.

It's Martin who's analyzed it (we've sent new samples so they can confirm their findings) We'd better do as they say, then 😄

Thank you! I found it difficult to find general recommendations regarding Bel. I discussed it with our reference lab just now, they weren't convinced about the transferase's ability to produce a complete antigen, since the expression was extremely low. I thought, as you say, that the absence of anti-B would implicate a normal B antigen but they were unwilling to recommend anything but A or 0 blood. This particular patient has a mutation not earlier documented, so it might be their cause for taking extra caution. Thank you for some great insight! It's an amazing forum for gaining new knowledge!

Found an old Bio-Rad card that is still in date so decided to give it a try in that and its shows a plane old B Pos! But the Ortho gives a consistent 1 or 2 + A reaction in 3 different cassette types. Awaiting an explanation from Ortho.

I meant it in the sense that it's an antibody reacting with the A antigen rather than another cold reacting antibody reacting with another antigen on the Acells been the cause. However as per my original post it did react with A2 cells this along with the strength of the back group was why I was questioning and AsubB.

srichar3, do let us know results of other tests and if the patient was treated as AsubB for transfusion. I’m curious as to why the patient would have such a strong reaction with A reverse cells if they are a subgroup (I have only seen 1+ in reverse with A cells in subtypes but of course YMMV) and wonder if perhaps there is some pertinent clinical information causing false positive results with anti-A in gel, such as pH- or reagent- dependent reactivity. Especially since it was just BPos in tube method.

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 .

If you know this patient is A Pos and you know the discrepant backtype is due to a cold agglutinin, why are you trying to re-establish what you already know?

My hospital is not AABB but I will put in my 2 cents for what it is worth. The way I read this: The collecting/pooling facility will put a DIN on the product. The receiving facility will not change, alter, or remove the number (on that bag). Reading between the lines if you take those units and combine them in a different way with a NEW number, in a new bag, you are not altering the numbers on the original bags. You have a new bag with a new number and the next facility (should there be one) should not change your new number. Your computer system should be able to retain the original product numbers under the new facility number for posterity. You can locate who received either original number in the pool should there be a lookback in the future. It might depend on your computer system. Can you print a ISBT label with the new facility number? I would think that is the only number you would need on the new created unit. If you have several numbers on the bag it is going to confuse the nurses at the bedside and we don't need to confuse them. I do remember back in the olden days before computers when we made exchange blood, the bag and paperwork had both the plasma and RBC numbers on it because that was the only way we could do it and keep up with the DIN. We pool large quantities of plasma for Therapeutic Plasma Exchange. We just use the newly created ISBT facility number on our bag and paperwork. We have never been dinged for this.

The manufacturer's instructions for use on the infusion set packaging says: "Consult facility protocols and current standards for guidance on changing sets. It is recommended to change sets within 4 hours after initiating infusion of blood or blood products." So that's what our SOPs state - 4 hours. Nursing service agrees.

I don't know for certain, but I bet they did a bit more than that. Almost all "cold" auto-antibodies are IgM, it is true, BUT, because these antibodies almost always have a very wide thermal amplitude, they would cause "spontaneous agglutination" in tests incubated at 37oC too. What they probably did was to either adsorb out the "cold" auto-antibody with something like rabbit erythrocyte stroma, or denaturation of the IgM molecules by a reducing agent, such as dithiothreitol (DTT), and only then performing tests using a monospecific anti-IgG reagent. I am quite happy to be corrected.