Malcolm Needs

Hi Maryann, The point is that the terms homozygous, heterozygous and hemizygous can only refer to genes, but, of course, red cells do not have a nucleus (it has been extruded during the maturation process), but, in any case, the terms should not be used for antigens. In this case the closest to being correct is that M+N- red cells have "homozygous expression" and M+N+ red cells have "heterozygous expression". However, particularly in the case of the MNS Blood Group System, this terminology is not completely correct. There are many low prevalence antigens associated with both the glycophorin A and the glycophorin B molecules, and the many hybrids therein, that a red cell that groups as M+N- may not be as a result of MM homozygosity at a genetic level, but may have heterozygous expression, because there is one "M" antigen (for want of a better way of putting it), and one low prevalence antigen expressed on glycophorin A (or a hybrid), so that, in terms of expression, the M antigen has the strength of an M+N+ red cell, rather than an M+N- red cell. I hope that helps. Malcolm

I certainly wouldn't use your nomenclature (only genes can be homozygous, heterozygous or hemizygous), but I know what you mean. I would most certainly say that the patient's plasma contains an anti-M, but, despite the fact that many cases of "cold reacting" anti-M are IgG, if the anti-M does not react at strictly 37oC, it is not clinically significant.

It is, but it is no longer state owned. It is now owned by a Chinese conglomerate.

Actually, they did also make an IV product, with an enormous amount of anti-D in terms of International Units, but they made very little, and it was kept almost exclusively at NHSBT Centres for use when a unit of D Positive blood has been transfused to a D Negative individual either by mistake, or to save their life. I agree though, the IM anti-D immunoglobulin should only ever be given IM.

One of my colleagues, Dr Fiona Regan, was a co-author of a poster at a BBTS Annual Scientific Meeting at, I believe, Bournemouth a few years ago, which looked at this (and won one of the prizes). They did show that it made a difference, BUT, I don't think anyone ever took any notice of it, because, as far as I know, nobody ever gives extra anti-D to the larger woman.

This is very true. There are certain areas of Europe (in particularly the Iberian Peninsula) where the percentage of D Negative individuals within the native population reach 25%. This is all to do with enclaves where D Negative Palaeolithic people took refuge during the last Ice Age (about 24, 000 to 16, 000 years ago). Other areas where this happened were the Balkans and Ukraine.

Are you saying it is anti-Ena, or anti-Ge2/anti-Ge4? The reason I ask is because not all examples of anti-Ena are ficin sensitive, some are ficin resistant (see page 110 of Reid ME, Lomas-Francis C, Olsson ML. The Blood Group Antigen FactsBook. 3rd edition, 2012, Academic Press), but you also said that the antibody was not inhibited with rBGP, and yet there are Gerbich specificities available that would inhibit these antibodies (Schawalder A, Reid ME, Yazdanbakhsh K. Recombinant glycophorins C and D as tools for studying Gerbich blood group antigens, Transfusion 2004; 44: 567-574) and could even distinguish between the two specificities, as Ge:2 is on glycophorin D and Ge:4 on glycophorin C.

Yes, it is permanent and yes it doesn't do a lot for stock levels!

exlimey, again I agree, but it depends where Jennifer G is based. NHSBT used to give out units of blood containing anti-D (and some other antibodies, as long as they were weak), but that is no longer so. Since variant CJD raised its ugly head, we are no longer able to take blood from donors who have themselves been transfused (there are a few strange rules about when the blood was given, etc, but that is beside the point). Because of this, and the fact that donors cannot be relied upon to be 100% honest (or simply don't know), so that we don't know if the antibody is as a result of a transfusion, a pregnancy or "naturally occurring", we destroy any units containing antibodies of any sort (with RARE exceptions), in case the antibody is the result of a transfusion, and it gets out into our untransfused inventory.

Certainly in the UK, it is occasionally given to people of all ages who have idiopathic thrombocytopenia.

Totally agree exlimey, however, another question I have is, ws a DAT performed when the "anti-D" was detected? I also have another suggestion, to go along with your question about platelets, and that is it could be that one of the units was from a donor with a DEL phenotype. Unless elutions (obviously) or molecular techniques are used, this may never be known, but it is known that some types of DEL can cause primary stimulation, but that the anti-D produced in these circumstances is very weak. As you say exlimey, as the patient is elderly (and ill), the patient's immune system could be compromised.

See my reply to your other post.

The DAT is easily explained, with an anti-D level that high! Even after a double exchange transfusion, there will still be approximately 5% of foetal/neonatal red cells in the circulation, which is quite sufficient to give a positive DAT, but with an IUT, you are not removing an foetal red cells from the circulation (or minimal amounts) and should be considered more as a simple top-up transfusion (with profuse apologies to people who work in the Fetal Medicine Units, as I fully realise that there is nothing remotely "simple" about an IUT). As far as the reactions with the anti-A,B, the anti-D and the control is concerned, while the anti-A and anti-B are negative, it must be remembered that there are potentiators in monoclonal antibodies, such as albumin, that will possibly lead to them giving "false positive" reactions (although, I would suggest, that the reaction with the anti-D is anything but false - unless the anti-D is blocking the D antigen sites, which, with an anti-D level of 847IUmL-1 [it is NOT 847IU, which is an amount, rather than a concentration] would not be in the realms of impossibility). The amount of potentiator in each specificity will be different, depending upon what the antibodies are designed to detect (for example, what A and B subgroups, if any). However, the anti-D will most certainly contain potentiators, to ensure that most weak, and some partial D types are detected. This means that the control, which will have the same make up as the anti-D reagent - but without the anti-D, in other words, it would contain potentiators that would detect "false positives", which is the whole point of the control.

My apologies!

This is true, but ALL hospitals have access to such blood as it is prepared on an ad hoc basis from whole blood, taken specifically for neonatal exchange by the four national blood services.