Malcolm Needs

Right, the reference is: Zerjal T, Xue Y, Bertorelle G, Wells RS, Bao W, Zhu S, Qamar R, Ayub Q, Mohyuddin A, Fu S, Li P, Yuldasheve N, Ruzibakeiv R, Xu J, Shu Q, Du R, Yang H, Hurles ME, Robinson E, Gerelsaikhan T, Dashnyam B, Mehdi SQ, Tyler-Smith C. The genetic legacy of the Mongols. Am J Hum Genet 2003; 72 (3): 717-721. The paper actually talks about the results of a study concerning the Y-chromosome, but, as the DIA gene is "common" within Mongolia, the extension is, I feel, justifiable. :):)

Which is exactly why such documents should be validated fully fully before they are put into place. But surely, these policies/procedures were to do with actual things that are being done in the laboratory to do with the techniques/procedure/processes etc, that are used to get patient results, not, for example, for how to use a mop to clean the floor (a genuine SOP used in our Centre). :disbelief:disbelief:disbelief:disbelief

Thank you for putting back the "Thanks" button. I really appreciate being able to thank my fellow members for their excellent posts on all sorts of subjects that have increased my knowledge greatly. I think that it will be an exceedingly popular move. Now, how about a spell check especially for those of us who are alphabetically challenged - well, for me actually!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

Complex maybe, but excellent!

Thanks dstoever. Sadly, it is not always a mistake that is "covered up". I know of one individual, many years ago now, who, unknown to him, was typing a sample from a known Oh patient. He recorded all the reactions in the reverse group as negative "because this shouldn't happen". :eek::eek:

Hi Tim, There is extremely good evidence that the DIA gene did indeed spread west with the invasion of the Mongol hordes. There is DNA evidence for this. I am at work at the moment (sad, I know - not least for the patients), but I'll try and find the reference when I get home tonight or over the weekend.

Seriously good idea Rashmi. I can't see it being accepted by the authorities though.

Rashmi, I was NOT joking. I meant every word I wrote. I fully agree that Change Control is required when changing processes/procedures/technqies/equipment, etc, but when changing documents that do not directly (or even indirectly) affect our results? I think not. Whilst your inspectors may not have invented these ideas, some jobsworth is responsible. Our position in life is to help patients, not to spend all day on irrelevant paperwork.

Thanks for that. Talking of families, I remember Joyce Poole at the IBGRL telling me about a low frequency antigen that she found on the red cells of a sailor from The Netherlands. They did a family study, but also found that he had other "wives" at almost every port that he visited on a regular basis. Needless to say, the low incidence antigen could be traced almost all the way around the world, but for some reason, only at ports!!!!!!!! :D:D:D:D

This is an interesting case indeed. It is known that, once a person makes an antibody against one low frequency antigen, they tend to make a mixture of antibodies against a host of low frequency antigens (well, perhaps not a host, but certainly there is often a mixture). It is also known that anti-Dia can be clinically significant. The interesting thing is that, as far as I know, there has never been a record of anti-Rba being clinically significant (although, being part of the Diego Blood Group System, it was always thought likely to be so). Was an eluate ever made from the gentleman's post-transfusion sample to prove that the causative antibody was indeed anti-Rba? Unless this was done, it could possibly have been due to yet another antibody directed against a low incidence antigen. If it was, and anti-Rba was proved to be the causitive antibody, was it ever reported as a case study (or something similar) as this would be a very important piece of evidence that anti-Rba can indeed be clinically significant? Nice case!

It seems to me that, in almost all cases, you are unlikely to make any major changes to documentaion affecting the laboratory unless, at the same time, you are making major changes to a process/procedure/technique. If, however, you are going to make major changes to documentation that does not affect any such process/procedure/technique, let me put this scenario to you (or, rather, to your inspector). Suppose that you have decided that your Change Control documentation is not fit for purpose. It requires a major change. You, therefore, have to fill out Change Control documentation to change the Change Control documentation. However, you cannot do this as, by definition, your Change Control documentation is not fit for purpose. What do you do? It seems to me that this is yet another idea that has been put forward by an inspector who has not thought through what they are proposing. It sounds good in theory and is completely and utterly useless in practice. It is beaurocracy gone insane. :angered::angered:

True, this explanation cannot be ruled out without proof, but even in the Far East where Del is more common, Del is extremely rare, and the stimulation of anti-D by Del is even rarer.

It doesn't bother me in the least John - but it might get others talking!!!!!!!!!!!!!!!!!!!!!!!!!

You are completely correct Lecia; serological cross-matching WILL NOT detect all incompatible units. There are many clinically significant atypical alloantibodies in patients (particularly Kidd antibodies) that will only react with homozygous expression of their corresponding antigen. This is why screening cells and antibody panel cells are chosen to have homozygous expression of certain antigens (and in some cases are actually checked by genotyping or flow cytometery) and are in preservative. As I wrote in another post, this preservative is designed to preserve the antigenicity of the red cells, but not the oxygen carrying capacity. On the other hand, units of blood are in a preservative designed to preserve the oxygen carrying capacity, but not the antigenicity. Therefore, if you have, for example, a weak example of anti-Jka, that only reacts with red cells showing apparent homozygous expression (Jk(a+b-), and you cross-match an "elderly" unit of mis-labelled Jk(a+b+) blood serologically, it will not necessarily be incompatible. Scares me to death sometimes! :eek::eek:

Hi, The units are tested by automation from start to finish and the results MUST be downloaded automatically with no human intervention. Any groups that the automation does not recognise without human intervention means that the unit is discarded. All units are typed twice for ABO and RhD irrespective of the number of times the donor has given. All labels giving the groups are produced automatically and contain the unit's bar code, which is matched with the bar code on the unit before it is attached to the unit, and again afterwards. All the bar codes are scanned to ensure that they are all the same prior to the units leaving the Blood Centre.

These sorts of automated expressors (I'm not sure of the actual type) are used universally within the NHSBT.

Slim to anorexic!

Agreed, but also beware of ignoring weak reactions with the anti-e, without a thorough investigation, particularly if the patient is from the Black population; it may be a case of CdeS.

I agree that typing may have been incorrect, but unless this is the case (or the donor has had a stem cell transplant), I cannot think of a situation where a donor may gain an antigen (unless you are counting something like T activation). We (that is, the NHSBT - I am not involved personally) have been looking for the exposure of neo-antigens in blood that has passed through a prion filter and, as far as I am aware, none has been found. I can certainly cite quite a few cases where an antigen has been weakened, even to the extent that an apparent alloantibody may be made against the antigen, but, except in the case of a Lewis antigen, such a situation only occurs, as far as I am aware, in a pathological condition. I have never heard of this happening in a healthy individual. Were it found that a healthy donor has "lost" an antigen, however, I cannot see how it is likely to be clinically significant for the recipient of that blood. The NHSBT now garuarantees that the blood in a unit is of the ABO and D type advertised on the label (the same applies to other antigens printed on the label). In the case of a new donor, each antigen is tested twice under positive sample identification, and each antigen on the label is tested at least once on that actual donation on any regular donor. As a result, very few of the hospitals we supply with blood now actually test the group of the unit.

Right then Kate, I've finished doing my ferreting around, and here is the answer. From the BCSH draft irradiation guidelines 2009: "TA-GVHD has not been described following transfusion of frozen deglycerolized cells, which are in any case thoroughly washed free of leucocytes after thawing." Recommendation. For at-risk patients, all red cell, platelet and granulocyte transfusions should be irradiated, except cryopreserved red cells after deglycerolization. It is not necessary to irradiate fresh frozen plasma, cryoprecipitate or fractionated plasma products." So it would appear that, more by luck than judgement, I was correct! :):)

In a way, you are asking an impossible question, as It depends upon the size of the individual and, therefore, their blood volume. It also depends upon how much colloid/crystalloid has been transfused to maintain this blood volume, and in the case of a colloid in particular, the average molecular weight of the preparation, as the lower the molecular weight the quicker the colloid is cleared from the circulation (but the faster liquid is drawn into the circulation from the interstitial spaces) and vice versa. I would, therefore, thoroughly recommend reading Chapter 2 of Mollison's Blood Transfusion in Clinical Medicine, Harvey G. Klein and David J. Anstee, Blackwell Publication, 11th Edition. This is not, in my opinion, an easy read (although, again, in my opinion, it is easier to read than some of the earlier editions!), but it does give all sorts of mathematical equations to help estimate blood loss and how much is required to bring the patient back to some kind of normality. I am certain that other posters will be able to answer your question better than I, but it's a start. :)

Once again, I'm not sure and will find out, but, certainly, red cells from sickle cell disease patients do not freeze, thaw and reconsitute very well (however, rare their blood group may be)!

Just to confirm what you say, Malcolm - I've seen 2 cases of C-Cw+ over the last 5 years

Thanks for that.

I'll be honest with you, I don't know the answer (but I am going to find out from the National Frozen Blood Bank early next week). That having been said, I would not have thought that there were sufficient viable T lymphocytes to cause GvHD in frozen red cells. As I understand it, the red cells are thoroughly washed before addition of the freezing mixture, and then thoroughly washed again whe they are thawed and reconstituted. Therefore, I would have thought that irradiation after cryopreservation was a step too far (whether I am right or not we will find out next week, and, even if I am, whether the FDA would agree is another matter). This is a very different process to the cryopreservation of stem cells when, of course, the white cells are deliberately kept viable. We have a couple of cancer hospitals in our area, Anna, that will only accept irradiated blood and cellular blood components, just in case there are viable T lymphocytes present and these are transfused to immunocompromised patients; and this is despite universal leukodepletion this side of the pond. It's a pain, to be frank!