Malcolm Needs

I sometimes think that management monitor the temperature in many of the laboratories where I have worked by seeing how many of the staff faint. If it is more than 50%, it is regarded as too hot. Anything less than 50% and it is okay!!!!!!!!!

Another good source is towards the back of the Blood Group Antigen FactsBook.

If you get your reverse grouping cells from NHSBT, they are always a pool of rr donors, and so will always express the c antigen.

The reverse grouping red cells in the UK often react with an anti-c. I would be happy (on the evidence you give) to transfuse c-, E-, K- cross-match compatible blood. As you KNOW that the patient is group A, I would ignore the bit about giving group O blood, which is totally over the top.

I can see no reason why you should not transfused D Positive red cells.

The D--/D-- or D../D.. phenotypes (the two are almost synonymous, but the D--/D-- type is negative for the Evans antigen, whereas the D../D.. type is positive for the Evans antigen) are both EXTREMELY RARE. Unfortunately, these individuals have a nasty habit of producing anti-Rh17 (essentially, an antibody directed against the C, c, E and e antigens), and can only safely be transfused with units that are themselves D--/D--, D--/D.. or D../D.., and if these are not available, units of Rhnull blood. An exciting find, but I wish you luck!

My EXACT point on another thread. I think it is about time we all, and I mean ALL, told these people where to go, unless they can justify their rules.

I am certain that it is a nice training tool, but what exactly is it controlling? All it is doing is telling you that the anti-D reagent/reagents you are using is able to detect that particular weak D type, but it/they may not be able to detect any of the 100 or more weak D types now recognised.

Well, the thing is that the FcY receptors on the immune system leukocytes are few and far between, so such antibodies are often clinically insignificant. As a result polyspecific (broad spectrum) and monospecific anti-IgG reagents often do not detect such antibodies (or do so ineffectively) and so these are often (deliberately) not detected. In addition, IgG2 and IgG4 are not good at initiating the complement system (IgG4 doesn't at all). Lastly, of course, some of these antibodies can be IgA and, again, they are, at most, of doubtful clinical significance.

Unfortunately, what you say is far from "universal". Certainly, it is unusual to see an antibody directed against a low prevalence antigen causing either HDFN or an HTR, but it is by no means unknown. For example, anti-Bea has caused very severe HDFN, and anti-Wra caused a fatal HTR only a couple of years back in the UK. In terms of the 901 series (and, come to that, anti-U of the MNS Blood Group System) it is possible that it is to do with the IgG subclass, but it is more likely to do with them being (occasionally) IgG2 and/or IgG4, but, as far as I know, this remains a theory, rather than having been proven.

It is important to remember that there is a sort of continuum between the various A types (including A1 and A2) in terms of the number of A antigen sites expressed per red cell, and that there is no such thing as an absolute A1, absolute A2, absolute A3 and so on and so forth. In addition, of course, the lectin Dolichos biflorus is NOT an anti-A1, but is a lectin that "recognises" the A antigen, the Tn antigen and Cad antigen, as well as the A1 antigen. It will not recognise the A antigen if it is diluted correctly, but every now and again, there will be an "overlap" between a "strong A2", and a stronger than normal Dol. b. reagent. In addition, there are people who are Aint, or A intermediate, who are somewhere between an A1 and an A2. SUch people usually hail from the south of the African continent, but not always. As we are looking at ABO, I am not for one minute surprised that the reaction strength increases with cold incubation. The next thing to remember is that, with gel, it is all but impossible to add the reagents to the reaction chamber so that they remain exactly at 37oC, which means that IgM antibodies, such as anti-A1, which it looks like this pregnant lady has in her circulation, will sensitise A1 red cells prior to true incubation at 37oC, but will not elute quickly enough to give negative reactions after 37oC incubation, particularly after centrifugation. Anti-A1 is NOT clinically significant, unless it reacts STRICTLY at 37oC, and this can really only be shown by a pre-warming tube technique, in which case A2 blood (or other A subtypes, such as A3, Ax and Am) can safely be transfused, keeping your precious group O units for group O recipients. Anti-A1 has NEVER been implicated in clinically significant HDFN. None of this is pregnancy related.

Yes, frequency, incidence and prevalence are all interchangeable with either "high" or "low" before any of them. For some reason (I know not why), low prevalence has suddenly become the "word of the day", but there is no particular reason for this (as far as I know). Those low prevalence antigens within the 700 series, and, come to that, the high prevalence antigens within the 901 series, are, as you say, placed there as they do not belong to any known blood group system. However, do not run away with the idea that all low prevalence antigens are in the 700 series, and all high prevalence antigens are in the 901 series. The antigen KREP, of the Diego Blood Group System has only ever been reported in one Polish individual and one Slovakian individual, and yet it is not in the 700 Series of antigens. Conversely, and as far as I know, DOLG of the Dombrock Blood Group System has only been found to be negative in one Sri Lankan woman, and yet is not in the 901 Series of antigens. This is because, in each case, the chromosome and the particular loci have been identified, and they are mapped to known areas of the genes which encode each of these antigens.

When I was working in RCI at NHSBT-Tooting Centre, we used to store our liquid reagent cells in Cellstab, but wash them an resuspend them in Dil2 for use. We found the reactions we got were much, much sharper (I don't mean that the reactions were more sensitive to detecting weak antibodies, although we believed that they were, but that it was far easier to "see" the reactions as clear reactions, rather than "fuzzy" reactions), and, in addition, it meant that we didn't detect reactions caused by antibodies directed against the preservatives in the Cellstab. We were able to show this with multiple photographs. Despite all the evidence, we were told that we couled not continue to do this, as we were not standardised with the other NHSBT RCI Laboratories (standardisation is everything these days, even if it means dumbing down, rather than bringing everyone up to an excellent standard, and because it was more expensive. The only problem was that we were able to show that it was actually LESS expensive, because it meant less testing, and no testing for antibodies against preservatives. This did not fit with management theory, however, and so we had to stop. Since then we got "fuzzy" reactions, leading to many cases of repeat testing, and many cases of antibodies against preservatives and, hence, more expensive testing in terms of reagents, staff time and fairly simple investigations into moderate or even complex investigations, but hey, what did we know! At least we are now standardised (and expensive)!

Very true.

There are MANY more mutation than this leading to O alleles.