yan xia

Thanks for your explanation. I guess there must be some measures be taken to prevent the opening system to be contaminated, would you please share it with me?

For resuming transfusion, do you mean resume the blood which caused reaction or another unit of blood?

"2.7.6 Ael Under usual conditions Ael cells are not agglutinated by anti-A or -A,B, although they do bind these anti bodies, as demonstrated by adsorption and elution [298,337–339]. Saliva from Ael secretors contains H, but no A substance. Serum from Ael individuals usually contains anti-A1 and may also contain an anti body that agglutinates A2 cells [337,339]. No A transferase has been detected in Ael serum or red cell membranes [232,287–289]. Serum H-transferase is weaker than that found in A1 or A2 serum [289]. No example of Ael was found in testing 150000 French blood donors [283], but fifive were found among 400000 Chinese from Taiwan [328]. Ael appears to be inherited as a rare gene at the ABO locus [337–339]. As a result of allelic enhancement (Section 2.10.2), AelB cells may be weakly agglutinated by some mono clonal anti-A and may resemble B(A) phenotype [340]" The text above comes from Danels' HUMAN BLOOD GROUPS the second edition, page 36 If we just look at the forward group , we may identify it as type O, but because it has weaker anti-A, we do think it is not a normal reaction ,so we will do further investigation ,and then find out it has weak A antigens. It is important for transfusion and organ transplantation.

I'm with galvania, we have identified a lot of subgroup patients based on the weaker reverse reactions. Such as A2,A3, Ax, Ael, Aend, and the same the Bsubgroup

We require the reverse type to be 2+ or stronger in tube, because weaker reaction can mean subgroup or weak immunoglobulin.

The possible antobodies are anti-E, V,K, Jsa and Lua, then I will pick some cells to test it and antigen typing the patient to confirm it.( Jsa and Lua pos cells are quite rare, so it is hard to get them, luckily they will not cause rapid hemolysis after transfusion, as for anti-V, the clinical significance is unknown.)

From the second panel you posted, I think there are some specificity in the 37 and IAT phase, so my guessing it that there are not only cold auto that interfere with the reaction. I will do an auto-absorption in 4 drgess first( If this patient has not received transfused red cells pack in three months), then run panel using tube IAT. Just personal opinion, I am looking forward to learn from here.

According to Human Blood Groups by Geoff Daniels, second edition, 40-42 Most B(A) have strong or normal B antigens, and most CisAB have weaker B antigens.

One person who I am very admired once said"There is no difference between CisAB and A(B)" I have the same question as Matthew. Since they have different names and there seems no intention to change, I guess there must be something different I do not know.

It was decade ago, a nurse kindly gave the blood crossmatched for A to B after A passed away without having it . Because she thought they were both type O pos. Luckly, B had no transfusion reaction.

There are a lot of brilliant explanations, I learned so much from here. My guess about the pos DAT is that if the DAT(IgM) is positive, then it may cause false positive result in the D testing. This is why when we test a sample which is AB Dpos, we will run a neg control for the forward typing.

How about the DAT of this donor?

What does EBT mean? Thanks a lot.

Is there any chance of the anti-B in the donor packed cells caused the heamolysis? Because the free antibodies attached to the patient's cells, complements actived and cells hemolysis, so there is no free anti-B detected after transfusion.

or there are unexpected antibody/antibodies in the patient's plasma.