Malcolm Needs

You're going to love this - NOT! 30 years minimum in the UK! :(:(

Steve, I will not spoil your thread by making any comments s to how we do resolve the problems, but I would, nevertheless, like to thank you for your kind words, which I will pass on to my team. Malcolm :D:D

Absolutely.

Oh I don't know; my Consultant isn't that scary really!!!!!!!!!!!!!!!!!!!!!!! :giggle::giggle:

I will check this with my Consultant on Monday, but I have a feeling there was a recent case involving a red cell pack in the UK that was both leukodepleted and was suspended in SAG-M (our version of Adsol). Don't fret about this over the weekend, in case I am wrong (again!).

Thanks Marilyn. Without doubt, the Adsol helps, but that notwithstanding, there are still cases in the literature.

Well, the thing that would concern me is that, if you are giving random group O units, some of them may well have high titre anti-A (and/or anti- in the plasma (even the plasma reduced units). This anti-A is most certainly clinically significant, depending upon the stature of the patient receiving the blood, their secretor status and the amount of blood they are receiving. There are many papers in the literature citing quite major transfusion reactions due to passive transfusion of high titre ABO antibodies (admittedly, mostly in patients of small stature and mostly involving plasma components, but some involving red cell components). I would be much more concerned about this, than the transfusion of A1 blood to an individual with an anti-A1, even if, as yet you have seen no overt transfusion reactions. It may be that the autologous red cells are not surviving for the usual 120 +/- 10 days, and that transfusions are having to be given more frequently than would otherwise be expected. Does your blood supplier not label those units that have been found to be high titre ABO antibody negative; because if not, they should.

Thanks for that. The only thing I would ask is, are the group O units tested for high titre ABO antibodies, or are they random from stock?

I have never seen one myself, but Geoff Daniels cites two papers in his book Human Blood Groups 2nd edition, Blackwell Science 2002, which are as follows: Coombs HI, Ikin EW, Mourant AE, Plaut G. Agglutinin anti-S in human serum. Brit Med J 1951; i: 109-111. and Constantoulis NC, Paidoussis M, Dunsford I. A natuirally occuring anti-S agglutinin. Vox Sang (old series) 1955; 5: 143-144. Good luck to you if you try to hunt down these papers! These two papers are also quoted by Peter Issitt and Dave Anstee in Applied Blood Group Serology, 4th edition, Montgomery Scientific Publications 1998. Good luck if you decide to hunt these papers down! From this, therefore, I would say that, yes, "naturally occuring" anti-S does exist, but that it is exceptionally rare (or, alternatively, it is not so rare, but that people have just not written up cases). :)

No, it's ANOTHER area where "teamwork" would have helped! Yours, Cynical of Croydon. :angered:

Welcome SDB.

Knowing what I do, I cn fully understand that.

Did you ever try to remove them GENTLY Rashmi????????? It under G in the usual dictionaries!!!!!!!!!!!!!!!!!!! :peaceman::peaceman:

Of course, the other complication that I have just thought of (and you will not thank me for this!) is that an auto-anti-LW (which is actually more common than a lot of people think) will sometimes mimic an anti-D by IAT, but will look like an pan-reacting auto-antibody by enzyme technique, with slightly less strong reactions with the D- red cells. However, when you do an eluate, it will also look pan-reactive by IAT, as the anti-LW comes away from the LW antigen on the D- red cells relatively easily, giving an antibody that reacts well with all red cells. You could try an ABO compatible, rr, cord cell with the original plasma, and see if that reacts by IAT, as the LW antigen is particularly strong on cord cells. I told you that you wouldn't thank me; more work and no guarantee of success, as it may not be an auto-anti-LW at all!!!!!!!!!! Sorry. :redface::redface:

When was the second patient recognised? The reason I ask is that, some years ago, before we got worried about such things, the anti-D we used was not just anti-D, but a mixture of antibodies, but which were mostly anti-D, which itself, had to be of a certain "strength". I can't remember exactly how many there were, but we once did an "antibody identification" on a sample of anti-D immunoglobulin, and we detected about 6 different antibody specificities! I think I am correct in saying that such a "soup" of antibodies is no longer allowed, but it could be the reason that your elution was pan-reactive. The other reason could be that the patient already had an "enzyme only" auto-antibody, that would react by IAT if eluted. I don't know; I am only throwing in suggestions! :confused::confused: By the way, I believe I have cited this particular website before (but at my age memory is anything but perfect), for those interested in Weak and Partial D types that are known to produce alloanti-D, put "rhesusbase" into your search engine for a spectacularly useful site (although it does require updating).

No, we're on two pages now!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :haha::haha:

Having rattled on as above, what I should have said is that, in the UK, the SHOT (Severe Hazards of Transfusion) Haemovigilance Scheme is strongly against transfusion at night, unless there is a compelling clinical reason; so it shouldn't happen (and pigs might fly)!!!!!!!!!! :D:D

I would also require medical input; probably from my own Haematology Consultant, rather than the physician looking after the patient. If the cross-matched blood is outside the strict criteria laid down, then there needs to be discussion between the Haematologist and the other physician as to the dangers that may be involved in giving, or not giving the blood to the patient at that time. There may be a very good reason why the blood should be given, but if it then causes a transfusion reaction, I would rather the litigation was against my Consultant (who has the medical know-how to give a clinical defence and the medical authority to override the strict criteria), than against me (who does not - and who has not the medical authority to override the strict criteria). :redface:

I am quite certain that you are absolutely correct Anna. One only has to look at the range of antigens per red cell quoted for the D antigen for different Rh haplotypes, and the range of antigens per red cell for the different subtypes of A, and expand this for each of the other antigens in all the different Blood Group Systems, that means it must be harder to make an argument against your theory. However, one should also look at factors in the recipient. Many learned papers are now being published linking HLA types to the ability to produce specific antibodies, e.g. Reviron D, Dettori I, Ferrera V, Legrand D, Touinssi M, Mercier P, de Micco P, Chiaroni J. HLA-DRB1 alleles and Jka immunization. Transfusion 2005; 45: 956-959. It is likely, therefore, that there is, perhaps, and for want of a better way of putting it, a sort of "symbiosis" involved between donor and recipient. :wow:

Well answered, and I agree wholeheartedly with the sentiments you express in your last sentence. NOBODY can claim to have seen it all, done it all, etc and any help is always welcome. :D

I will bow to your better knowledge and greater experience on this. However, it seems strange to me that Geoff Daniels in his book, Peter Issitt and David Anstee in their book, Harvey Klein and Dave Anstee, in the 11th edition of Mollison's Blood Transfusion in Clinical Medicine all mention that transfusion reactions due to anti-A1 are exceedingly rare (a total of 4 papers being cited, the last in the late 1970's) and Marion reid and Christine Lomas-Francis in their book also say that reactions are exceedingly rare, as are anti-A1 sera that bind complement. Have you thought of publishing your unusual findings? :confused::confused:

I agree that anti-A1 is a clinically significant antibody, but only in the extremely rare occasions when it reacts strictly at 37oC. IN 30 years of Blood banking, I have only come across this once. In almost every case, the anti-A1 can be completely ignored.