Malcolm Needs

It would be really useful if you could tell us the ethnicity and age of the patient, and his medication regime. That having been said, I note that the antibody screen is positive, that his DAT is positive by both anti-IgG and anti-C3d, that the neat plasma contains an apparent anti-E and anti-c, but that the eluate contains an antibody that is, apparently, pan-reactive. Very often in these cases, the apparent antibody specificity in the neat plasma is a mimicking specificity, rather than a true specificity. In such cases, the apparent specificity in the neat plasma can be adsorbed out using red cells that are negative for the antigens of the apparent specificity; in this case R1R1. The true specificity of the antibody could be an anti-Rh17 or anti-Rh18. While I am not saying for a single second that the apparent specificities of anti-E and anti-c are not true specificities, it may be worth your while seeing if they can be adsorbed out using R1R1 red cells. However, as you suspect the presence of other antibodies, this should not be attempted until you have proved otherwise. This you can do, as you suggest, by alloadsorption of the neat plasma using two or three adsorption cell types. In answer to your last question, with regard to adsorption of the eluate, this was certainly a method we used in the Reference Laboratories of the NHSBT in the UK. It was usually used when the patient had a known pan-reactive autoantibody, but was requiring transfusions more frequently than previously, and/or when the expected rise in the haemoglobin concentration was not achieved. On some occasions, we were able to detect a de novo alloantibody in the eluate that we could not detect in either the neat plasma, or the adsorbed plasma, although this was not always the case, as transfusion in and of itself can sometimes stimulate the autoantibody to become more active (see Petz LD, Garratty G. Immune Hemolytic Anemias. 2nd edition, 2004, Churchill-Livingstone). Good luck with sorting it out, but this is a really interesting case. Thank you for posting it and, please, would you mind letting us know how you get on?

Welcome Kim Ledingham.

I attach a hybrid of my lectures on the differences between the A1 and the A2 ABO type, together with a very few slides from my lecture on lectins, and I hope that this will serve to be of some use to you. It is hugely important to remember that many lectins, including Dolichos biflorus, are not specific unless they are diluted to ensure that they only react as desired. For example, this particular lectin (Dol b) will react quite strongly with A2 red cells unless suitably diluted so that it only reacts with A1 red cells. It is because of this that group B red cells are totally unsuitable to be used as the negative control for the Dol b lectin, and the same applies for group O and other group A subtypes. Group B red cells will not tell you whether or not your grouping reagent is "specific" for the A1 antigen, or will still react with the A2 antigen. In addition, the lectin will also react with red cells expressing the rare polyagglutination antigens Cad and Tn, and so, in the true meaning of the word, it is not "specific" anyway. What is the difference between A1 and A2.pptx

Welcome mimi03.

Welcome LZUH.

Welcome alicaijin.

Welcome MMSBB.

Welcome Lil.

I agree entirely that this process is not efficient working in a busy Blood Bank, or any other sort of Blood Bank. There a re many occasions when a patient can wait for the next transfusion, whilst various tests are performed, but we, as Technicians/Biomedical Scientists (or whatever else we are called around the world) are not in a position to "call the odds". We MUST react quickly. Granted, most of these tests will be "false alarms" (or so I would hope!), but when the test is genuine, it is necessary to react quickly. The clinician needs to know, and so does the person working in the laboratory - THEY have got to get antigen negative blood available pretty damn quickly, while the clinician is sorting out the acute haemolytic transfusion reaction. If it is a query delayed HTR, given that in most cases the patients are transfusion dependent (and, therefore, venerable - or even vulnerable!), why take the risk?

Welcome Reuben Isbitsky.

I agree entirely. I found it really difficult sometimes, when, for some reason best known to themselves, a Blood Transfusion Consultant in a Hospital would insist that we performed a titre and/or a specificity on a cold auto-antibody, rather than just the thermal amplitude (as advised by Petz and Garratty), and I had forage around in our freezer for extremely rare Adult ii red cells, rather than using an otherwise discarded cord sample. It is utter madness.

Oh, how agree with your comment. Mind you, it must be remembered that this was all caused by doctors (mostly histologists, if I remember correctly) who kept parts of babies, without asking for the permission (or telling) the bereaved parents.

Welcome AshleyW.

I will also play "Devil's Advocate" then. Where on Earth are people finding all these units of blood that are Ko (which is what Kell Negative means), and, on the other hand, if you are going to give K-, k+ units, how do you know that the patient isn't a K+k- individual, with an anti-k? Why not KEL genotype the patients (and I don't mean a full gene sequence) and give "matched-blood" for what the test predicts the antigen expression?

Welcome SusieD.

Welcome sunnyca.

Thanks Cliff!

Welcome A Crumbley.

Welcome Justine Garza.

Not only is it possible, but your supervisor has done exactly the right thing. They other techniques are a complete waste of time and money that tell you precisely nothing of any worth.

It depends upon the instructions that come with the reagent.

I know that some of the early work on ABO-mismatched solid organ transplantation, viz-a-viz ABO antibodies was carried out by Professor Patrick Mollison and his co-workers, and he showed that, whereas inhibition of IgM ABO antibodies is reasonably easy by, in the early days, transfusion of FFP to adsorb the antibodies in vivo, the same is not true of IgG ABO antibodies. He and his co-workers found the inhibition of these antibodies was much more difficult, and this was almost certainly because only 40% of IgG antibodies are intravascular, as so they "rebound" when inhibited or removed from the intravascular area, whereas almost all of the IgM antibodies are intravascular, and so "rebound" is less likely.

A VERY good friend of mine, Phil Learoyd, has just started up a new site devoted to the history of blood transfusion. I've had a brief look at it, and it looks to be fantastic, and would thoroughly recommend it to anyone interested in the subject. It can be found on https://www.historyofbloodtransfusion.co.uk/

Welcome Kritine1.

It was ever thus mrmic, but don't for get the transplant physicians.