Malcolm Needs

Hi Steve, I'm not sure this really "fits" into "Just For Fun", but... In September 1990, the first NATO Civil/Military Blood Conference was held at the (then) Army Blood Supply Depot in Aldershot. During the conference, a review of the colour coding of blood group labels was undertaken. The attachment shows the different colours used for different blood group labels for certain different countries (wear sun glasses!). Concerns were expressed that , as a result of deployment of multi-national forces, the difference in colour coding of blood group labels could cause confusion. The ISBT suggested a time of five years, after which time standard colour coding could be introduced. During this time, labels would be black and white. Well, there was no agreement within the 5 years, and it is now almost 2010, and the "5 year" experiment is still continuing!!!!!!!!!!!!!!!!!!!!!!!! Strange that. :bonk::bonk: Colours.doc

Well, it is true that there are a small number of patient anti-S samples, and slightly more anti-s samples found that have quite a high proportion of IgM to IgG, and so a lower incubation temperature may well help in identification, but I would recommend putting up two tests, one at 37oC and one at room temperature.

I'm not sure, but this may be more of a role for the IBMS (and, possibly, the RCPath) than BBTS. Certainly though, it should be a role for the Chief Scientific Officer. I'll have a think about this one. :confused::confused:

I agree with everything else you say Rashmi, but in my experience, there have been times when they have been wrong, and they are far, far too arrogant to admit it. This has left Blood Bankers trying to "improve" by doing something they know is wrong. :angered::angered:

I'm sorry irshadaad, but I'm not sure I fully understand your question. You would confirm anti-S and anti-s in the same way that you would confirm any other antibody specificities; in this case using S+s- and S-s+ red cells by IAT to exclude other specificities, and S and s type the patient. I know that various papers and books say that the S and s antigens are variably affected by papain (usually destroyed, but not always) but a paper by Jill Storrey et al a few years ago suggested that "papain-resistant anti-S" is almost always a low-grade auto-anti-U (or, at least, that's how I read it), and certainly, when we've bothered to actually test such antibodies in our lab, this is what we have found (a lot of work for not much return). :confused:

I'm going to be controversial here, and also show my age and reactionary nature, but... I still hanker after the days when each ABO type had its own coloured label, and the print colour of the written RhD type depended on whether it was positive or negative. I know the reasons this was abandoned (no standardisation between countries and, even between civilian and military blood within the same country, and the perception that the colour system discouraged people from checking the units properly), but I never bought these arguments and still don't. I thinki a colour code helped to highlight overt errors. :(:(

I, too, would be happy with this.

Hmm. Sounds like they did neither. Now, where have I heard that before?????????????!!!!!!!!!!!!!!!!!!!!!!!!!!!! :angered:

I agree (except that I m prepared to bet a tidy sum that it was probably foisted upon them too by some "suit" in the background who "thought it was a good idea" and would "improve patient safety", wsithout a thought for those who would have to operate the system). :mad::mad::mad::mad::mad:

Just to be awkward (as ever, some would say!) the NHSBT is doing a study on this kind of thing at the moment (although only for anti-c, anti-E and anti-cE). We are titrating the anti-E (using an R1Rz cell) and the anti-cE (using an r"r cell). In the UK, we do not titre anti-c, but rather perform quantitation by continuous flow, using rr red cells. So, we are, for want of a better way of putting it, "titrating" the anti-c, the anti-E and the anti-cE. There was/is a theory that anti-cE is "virulent" incausing HDN, than a mixture of monospecific anti-c and anti-E. I think I am right in saying that, although the study is not yet complete, there is no proof of the theory being correct. I don't really suppose this answer helps you much, but that is what we are doing. :)

For those of you who have not yet read it, there is a new paper on this subject that strongly agrees with some of the posts above, and suggests that individuals like me can be far more conservative when it comes to performing elutions. It is, Yazer MH, Triulzi DJ. The role of the elution in antibody investigations. Transfusion 2009; 49: 2395-2399. It is a very interesting and thought-provoking paper. :D:D:D:D

Ah, I'm not saying it doesn't have other antibodies present too; I am just saying that the major specificitiy is anti-D.

Sounds a bit like "we are providing the finance, so we also provide the ideas", irrespective of the fact that "they" knew nothing, and yet did not ask the expert on the spot! I sympathise. Sound familiar to anyone else???????????????!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :cool::cool::cool::cool::cool:

I know this is cheeky (and it shouldn't have to be quoted in such a thing), but what did your specification say prior to ordering the fridge? I repeat, though, this kind of thing shouldn't have to be in a specification for a blood fridge (but it is not there, it does give a get out clause for the provider). One has to be so blank, blank careful these days (although I would say that the fridge was not sold as "fit for purpose" anyway).

This answer was written in haste (I had to go and get my son from his Kids' Club!) and is now being somewhat repented at leisure! As I intimated in an earlier post above, the frequency of atypical alloantibodies directed against low-frequency antigens is far higher than the frequency of such antigens themselves. As a result, when one encounters such an antibody, it is very easy to provide antigen negative blood. One has to ask, therefore, is the cost of the primers (which are expensive) in such a situation justifiable, for such a small return (which, if one leaves out the esoteric science of furthering man's knowledge, is virtually nil). I can really only see one situation in which such expense could be justified. This would be in the case of a patient requiring life-saving (but not urgent) surgery, who has an atypical alloantibody directed against a high-frequency antigen (for example, anti-Dib). Searching for Di(a+b-) donors by traditional serological techniques would be extremely expensive in terms of using very rare antisera (either anti-Dia or anti-Dib). To find suitable Di(a+b-) donors could be done by mass genotyping, but even then, it is more likely to be done by use of microarray technology than "traditional" genotyping (if I am justified in using the term "traditional" about a very new technology)! I cannot see the expense being justified in other circumstances; but I could be wrong (again)! :):)

Eventually yes, without doubt; but not yet. It may be more affordable, but it is not yet cheap, and it is the primers that are expensive.

WinRho doesn't cause anti-D in patients taking it. WinRho is anti-D!

Yep, seriously! You'll find that auto-anti-D is mentioned in Geoff Daniels book, Human Blood Groups, 2nd ed, Blackwell Science 2002, page 249, in Marion Reid and Christine Lomas-Francis' book, The Blood Group Antigen FactsBook, 2nd ed, Elsevier Academic Press 2004, page 122 and Lawrie Petz and George Garratty's book, Immune Hemolytic Anemias, 2nd ed, Churchill Livingstone 2004, page 385, to name but a few. :)

Actually, auto-anti-D is more common than a lot of people think, and I would have no hesitation calling this one an auto-antibody. We see at least six or seven a year in our reference laboratory here at Tooing in the UK, and the International Blood Group Reference Laboratory gets rather upset with us when we miss one and send it down to them for investigation as an alloanti-D in a possible partial D patient.

Well, the answer is yes and no! Yes, we do the former (test at a dilution of 1/100 against both A and B red cells on an Olympus), but if there is a reaction we do not mark the units as high titre positive! Rather, we marked those that do NOT react as high titre negative (HT-). For a reason unbeknown to me (I think it has something to do with EU Regulations, but I'm not sure), and apart from ABO and the D, C, c, E and e antigens of the Rh Blood Group System, anything else for which we test is only printed onto the unit label if the test is negative. For example, if we test for HbS, and we find the donor to be HbS-, then HbS- is printed on the unit label, but if we find the donor to be HbS+, we do not print HbS+ on the label - the HbS status is just not shown. The same applies for blood groups. If we test with anti-K, and we find the donor to be K-, then K- is printed on the unit label, but if we find the donor to be K+, we do not print K+ on the label - the K status is just not shown. As I say, why I just do not know. :(

As a Reference Service Manager (and not yet totally driven insane; despite what Rashmi may say) I would thoroughly recommend not bothering to send in your samples from patients with antibodies directed against low-frequency antigens, and just give cross-match compatible blood! For one thing, identifying the specificity of such an antibody (if it's not something like an anti-Wra) is like looking for a needle in a haystack. For another, such a patient usually makes multiple specificities of antibodies directed against low-frequency antigens, and so a) we would probably never identify all those present, as we do not have access to red cells expressing every low-incidence antigen, and very often, a cell that has been identified as, for example, Li(a+) isn't, because it was identified with an anti-Lia that also had, for example, anti-Bxa in it, but we didn't know that. Lastly, for now (as my rant muscle is running on low) the chances of you cross-matching blood, and then giving a unit that is likely to cause a clinically significant haemolytic transfusion reaction are so low as to be all but zero (just think of the number of patients who have been given blood by electronic issue, some of whom must have antibodies directed against low-incidence antigens, and some of whom have probably been given blood positive for the corresponding low-incidence antigen, and you see what I mean). I shall now go and lie down in a darkened room!!!!!!!!!!!!! :crazy::crazy:

I thought it probably was, but it's worthwhile being on the safe side for the less experienced amongst us.

I am tempted to be facetious and say "What about anti-Leb!", but,actually, that is exactly how I feel about anti-Leb. Anti-Leb has, on very, very rare occasions, caused red cell destruction, but, like anti-Lea, the reaction is self-limiting, and , after initial destruction, most of the red cells transfused are still in circulation many hours after they are transfused (probably because the antigens themselves are soluble and "come off" the red cells pretty quickly, and then block the antibody in vivo). There has only ever been one report of anti-Leb causing HDN, and even then it was sub-clinical HDN (so the case was fairly dubious). I would quite happily ignore the antibody completely and given cross-match compatible blood. :)