Malcolm Needs

Thanks very much indeed Steve. I am well on the way to getting back to full fitness. I did not realise just how painful diverticulitis could be. I was bouncing off the bed whenever they were proding and poking! "Tummy ache"? Indeed, they way they treat you as if you are a complete idiot, I think that is what they would want us to call it!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

I think that one of the reasons is that D- individuals are far more common in the West, than they are in China (indeed, in the Far East as a whole). Depending where you are, as the figures vary quite a lot (about 15% in the UK, approximately 25% in the Basque Region of Spain), D- blood is much more available than it is in China. The D antigen is probably the most immunogenic antigen (after the A, B and H antigens) in human blood, probably because it is a fair size polypeptide of some 416 amino acid residues, which is completely "missing" in D- individual. Therefore, there is a very high chance that an immunological challenge with D+ red cells in the circulation of a D- individual will result in the production of anti-D. Obviously, a young male has the rest of his life to live, with a chance that, at some time during his life, he may require further transfusions, and with a slimmer chance that he may require emergency blood at some point, in which case he may then be given D+ blood. If he has made an anti-D early in his life, this, obviously, may result in a diasterous transfusion reaction. In the case of trauma (which is really what this thread is driving at, I think) there is a higher risk of the boy needing further transfusions during his life as a result of the initial injuries (e.g. reconstructive surgery, plastic surgery, joint replacement, etc), and so it is a reasonable idea to try to avoid him making an anti-D early in life, if he happens to be one of the 15% of the population that are capable of so doing. These are my thoughts, but others may disagree, or cite other reasons that are better than mine. (By the way, I haven't forgotten that I have to look out those papers on ABO for you. I am off sick at the moment - again!) :):)

True, but the fact that they are NOT voting suggests that they are not looking on this site (or, at least, that they cannot be bothered to become members), which suggests regression, rather than progress. The term "Honorary Transfusionists" worries me. Either you are a transfusionist (and know your stuff) or you are not a transfusionist. "Honorary Transfusionist" is like saying that someone is "a little bit pregnant"!!!!!!!! :confused::confused:

I would like to add one of my own. "Never, ever, patronise". I have just spent a few days in hospital with acute abdominal pain. Whilst in there, some pompous senior doctor came up to me and said, "You have what we call diverticulitis". I asked him who "we" were, and what us lay people should call what I had? He was quiet for a moment, and then replied, "Oh, I mean it is what doctors call the condition." So I asked him again, "What should I, as a member of the public call it then?" At last, he replied that I should call it diverticulitis as well. I thanked him, and suggested, very politely, that, perhaps, in future, he should say, "You have a condition called diverticulitis (substitute any other condition)", rather than assume complete ignorance on the part of the patient. I don't think that I was very popular with him (did I care?!!!!!!). :mad::mad::mad::mad::mad:

It could also be that, some of the Haematology Biomedical Scientists that are also in charge of Blood Transfusion are egocentric enough to consider themselves well-versed in Blood Transfusion?????? :mad::mad::mad:

At least in Europe (I don't know if it is available in other parts of the world), DiaMed produce something called ID-CellStab, which is a red cell preservative. This is designed, as far as I know, to preserve the red cells from the point-of-view of antigenicity, rather than oxygen carrying capacity. It is wonderful stuff! We keep our "wet cells" for several weeks in this. If you can get hold of some (or something similar - I don't know if other companies make it), you may be able to keep your rare cells just that little bit longer before they fall apart!? :confused::confused:

At my age, that is not "fairly recent"; it mens that it has only just happened!!!!!!!!!!!!!!!!!!!!!!!!!! :eek::redface::eek:

I couldn't agree more John. Even if the patient has made "new" red cell antibodies during his/her stay, this will not alter the group, nor the efficacy of any plasma or platelet components given. The only thing that might change is if the patient has produced, for example, an anti-IgA, requiring IgA deficient plasma products, but you are not going to pick that up with a type and screen, just as the result of reaction with the next lot of plasma-based components.

As a self-confessed fan of giving group O, D positive to older male patients, I also agree with these sentiments about young males group O, D negative blood.

These are pretty difficult questions (well, actually, the questions are easy - it's the answers that are difficult)! In answer to your first question, it is very rare indeed that a warm auto, that reacts by IAT and by enzyme technique, will not be adsorbed out by auto-adsorption (if that is possible), and then you can usually show that the auto-antibody has been adsorbed out by reacting the adsorbed plasma against chloroquine-treated autologous red cells. If these then give negative results, but random red cells still give positive results, then there is a fair chance that you have an underlying HTLA antibody, the specificity of which, if you have the available red cells, you can then identify. In answer to your second question, it very much depends if you have performed the patient's phenotype before the transfusion, otherwise you are, to a large extent, guessing what phenotyped cells to use (unless you are lucky enough to be able to use PCR to genotype your patient. Given that you may know your patient's type, and particularly if you suspect an underlying antibody directed against a high-incidence (or reasonably high-incidence) antigen, or if we are thinking in terms of multiple antibodies directed against "common" antigens, then we would often use this kind of adsorption, rather than the traditional differential adsorption with the three cells (BUT, be aware that finding the correct cells can sometimes take an enormous amount of time, and might involve adsorption and elution techniques). :):)

Hi Jane, As far as I know, they do not exist, although Gamma Biologicals used to offer an extended panel that often contained an example of a U-, a Js(a+b-) or something similar as a "bonus cell". I'm not sure if this is still available, but even then, the cells were very diluted and not great for freezing. In my own Laboratory, we have screened donor samples for rare types for well over 25 years, and now we have a collection of over 100 fresh samples of rare types at any one time (usually things like Kn(a-), McC(a-), Yk(a-), Co(a+b-), Ch-, Rg-, K+k-, Kp(a+b-), Lu(a+b-), Lu(a-b-), U- etc, but with the odd Vel- or Lan-) from which we can make up our own panels. In addition, we have frozen really rare red cells over the years, and have a collection of some 450 examples of such cells as Oh, Rhnull, MkMk, pp, Jk(a-b-), Er(a-), etc, which we use very sparingly. Then we have about the same number of rare antisera, so that we can attack a problem from both sides, as it were. Apart from our own donors, we get "presents" from the other NHSBT Centres and from SCARF. I know this isn't a lot of help to you, but collecting your own rare cells is a start. Malcolm :):)

I agree with your entire post (all points made). :)

Tee-hee!!!!!!!!! :devilish::devilish:

I hope he wasn't too annoyed! :eek:

I can see no other reason. Although the Lu(a) antigen is a poor immunogen, and anti-Lua is usually very weak compared to toher antibodies, it is comparatively common (often, without any known stimulus), and the antigen is quite frequent (about 5% in the Black population and about 8% in the White) and so cross-matching can be a problem; but transfusion is not. As long as your customers have faith in your work, they should not be asking for Lu(a-) typed blood. :)

Yes indeed Lara, and all Lutheran antigens are weak on cord cells anyway, and so clinically-significant HDN is most unlikely.

It's OK because he won't know, unless he's a member, or logs on as a guest!!!!!!!!! :D:D:D:D

Hear! Hear! I'm always learning things on this site. It's a fantastic fount of knowledge. :D:D:D:D

Others may disagree, and I have published a poster concerning a Weak D Type 3 foetus causing the stimulation of alloanti-D in a mum, but I wouldn't get too worried about this; it is extremely rare for a weak or partial D foetus to stimulate alloanti-D in a mum. If you are worried though, a blended anti-D reagent would work fine. Somewhere in the dark recesses of my mind, I seem to think that Dame Professor Marcela Contreras, who was in charge of Diagnostics, Development and Research in the UK for many years, and is herself Chilean by birth, is now working in Chile. She would be able to give you much more authorative advice than me, if you can contact her. You may be able to get hold of her via your own National Blood Service. :):)

According to Geoff Daniels (and I am NOT about to argue with him!), a similar sort of thing happens amongst the popoulation of Papua New Guinea, but there the "unexpressed" Duffy antigen is Fy(a). :)

We use one from ImuMed, ANTITOXIN GmbH, Industriestrasse 88, 69245 Bammental, Deutschland but whether or not this is available and licenced for use in your country, I don't know. DiaMed also make a card with anti-Lua in the wells/columns, but the same applies about availability and licence. THe reason they are difficult to come by is that the Lu(a) antigen is a relatively poor immunogen, and the antigbodies formed are usually sub-reagent strength.

I think I might be tempted to insert the word "usually" in there somewhere!!!!!!!!!!! :rolleyes::rolleyes:

Most Black individuals who are Fy(a-b-) by red cell typing are, in fact, genetically either FYB/FYB or FYB/FY. Upstream of the Duffy genes is a GATA-1 box that "allows" the Duffy antigens to be expressed on red cells, but many within the Black population have a mutation that prevents the antigens being expressed on red cells, and so they appear as Fy(a-b-). BUT, they express the Fy( antigen on other tissues, such as brain, colon, endothelium, lung, spleen thyroid, thymus and kidney, and so their immune system does not recognise the Fy( antigen as foreign, and hence they do not make anti-Fyb (or anti-Fy3 come to that). You can find the explanation under References (at the top of the page, Document Library on the drop-down list, educational material and then find the Powerpoint lecture and accompanying Word document. Best wishes, Malcolm :D:D:D:D

I think that I had better not vote in this poll, being part of the NHSBT. What do you think Bill and Rashmi?

If you irradiate blood and blood components in a Hospital Blood Bank in the UK, you are considered a Blood Establishment and are, therefore, open to a visit fro the MHRA (which is like a visit from a Bengal tiger in comparison to a visit from the CPA [comparative ***** cats; but with sharp claws]).