Malcolm Needs

As a seasoned poster, I thnk you for that froggymark, but it is not just the seasoned posters that have breadth (and depth) of knowledge. I've learned an awful lot from posters who have only made a very few posts. The great thing is, everyone has something useful to give, and for the most part they do. If you look at TimOz, just as an example, he has posted about 80 times, and so is considered to be a member, rather than a seasoned poster, and yet about 75 of those posts are pithy and to the point. It's brilliant site. :D:D:D:D

Oh My God! Then you blood supplier has no defence at all!!!!!!!!!!!!!!!! Do you believe other people's blood groups without checking?????????????? :omg::omg:

If we don't learn from history, we are doomed to repeat it.

I agree with you Rashmi, that this seems to be the most likely answer, but given that they were cord stem cells, going back to the donor could be more difficult than normal (although some of the donor cells should have been kept). When using cord stem cells, however, the HLA match can be less "exact" than when peripheral stem cells are used, because the humoral immune line is still niaive (I can't spell it, but I hope you know what I mean!). :D

Hi shily, Cell lines, such as erythroblastic cell lines, are subject to many spontaneous changes to the base pairs making up the active genes, purely because there are so many opportunities during mitosis for "mistakes" to be made. Usually, your own immune system will identify these as being non-self, and will destroy them quite quickly, before the clone can establish itself. In cases of cancer (of all types) a clone of cells has "gone wild", but the person's own immune system does not recognise this clone as non-self, and the clone becomes established. The same can occur for blood groups on the red cells (or, in this case, the genes encoding the transferase enzymes), and a clone of cells producing the "B transferase" (or, more likely, "B-like transferase") can become established, and group B cells (or group B-like cells) can, very rarely, be detected in the circulation of a group A patient. Much more commonly, group O cells are seen in the circulation of a group A concer patient (without them having had a group O transfusion). :)

I agree. The other bit to this is, If it is written down, but is not signed and dated....it is graffiti. :)

True Mabel, but, in the UK we changed from orange labels for anti-A, red for anti-B and blue for anti-A,B, to blue for anti-A, yellow for anti-B, clear for anti-A,B and green for AHG at around about the same time as the unit labels went to black and white. I don't think that we had too much trouble with this. All we need is international agreement ("all" being one of the largest words in the dictionary)! :(

The feeling is mutual.

Hi Andrew, You will learn a tremendous amount here, as we all have. Not least, you will learn just how generous people are with their knowledge and time. It is amazing.

Unless in exceptional circumstances, neither of there should EVER happen. :eek::eek:

Should this not have been in the "Just For Fun" thread!!!!!!!!!!!!!!???????? Sorry, couldn't resist it! :D:D:D:D

This is getting a bit worrying, but I agree with Rashmi again. It is well known, by the way, that protein adheres to plastic, and what are antibodies??????????? Oh, protein. I presume this move is on the grounds of health and safety. I have seen far worse cuts from broken jagged plastic tubes than I ever have from sharp broken glass tubes. Should we also replace paper? Paper cuts are very painful.

Two of the last ten people to visit my Profile Page were Apple and CIderman. Coincidence???????????? :haha::haha:

Goodness me Rashmi, I would never suggest submitting manipulated results. I would suggest submitting true results and letting those that prevent you submitting accurate/precise results stew in their own juice.

Once again, I agree. But sometimes it is lack of support from those holding the purse strings that prevents us doing the "right thing".

I know that you were actually directing your question to Kate, John, but please forgive me for interfering! We often have to provide blood for this procedure to the larger London Teaching Hospitals in our area, and it is usually for the prevention of a CVA in a young sickle cell patient, or for the treatment of sickle chest syndrome, treatment of priapism and also to bring down the proportion of HbS prior to the patient undergoing general anaesthetic (an oxygen poor situation) and, very, very occasionally, so that they can take a flight (another oxygen poor situation) so, yes, it really does help. Again, sorry to both Kate and you for butting in. :)

I totally agree with you Joan.

Um, that's what I said Rashmi!!!!!!!!!!!!!!!

In that case it could, just possibly, be a anti-IgA, although I would have expected that there would also have been quite a hefty reaction to the plasma and platelets. :confused:

It's not TRALI, as the symptoms don't fit, and it is unlikely to be TACO. It could be a febrile non-hemolytic transfusion reaction, even if the DAT is positive, as it was positive in the pre-transfusion sample. Look for HLA antibodies and consider leucodepletion. It worries me that you performing an immediate spin cross-match in such a case.

Hi rajendraksaini, There are at the very least two possible explanations for this phenomenon. Firstly, there is the chance that your patient may be suffering from a concomitant bacterial infection, causing the acquired-B phenotype. In such a case, the bacterial deacetylases convert N-acteylgalactosamine (the dominant sugar residue for the A antigen) to galactosamine, which resembles galactose (the dominant sugar residue for the B antigen) closely enough for the cells to be agglutinated by some anti-B reagents. This can usually, but not always be corrected by lowering the pH of the antibody. Your antibody supplier should already have done this for you though. The second possibility, particularly as your patient has carcinoma, is that a variant clone of cells are producing the galactosyl transferase that results in the formation of the B antigen, and what you are detecting is a small number of "genuine" group B cells. This galactosyl transferase is usually "silent" in group A individuals. As I say, there could well be other explanations, but these are two to be going on with! :):)

I'm not certain that detecting an anti-Cob matters too much anyway, to be honest. We always tell our Hospitals to give cross-match compatible blood in such a situation, and this has never resulted in a clinically-significant haemolytic transfusion reaction. The other thing that points in the direction of anti-Cob being not too much of a clinical problem is that there MUST have been patients with an unrecognised anti-Cob in their plasma, who have received Co(a+b+), and, possibly, although it is rare, Co(a-b+) blood through electronic issue, and I have not seen a report of a clinically-significant haemolytic transfusion reaction through this route due to anti-Cob. I agree with you Mabel that, within the White population, a 2% frequency for Kp(a) does mean that it is not counted as low-frequency, but a frequency of 0.01% in the Black population means that it does. As I said above, one has to look at the admix of the ethnicity of the population with whom you are dealing. :):)

To those of you that have had to show receipts when the nursing staff have disputed that the correct patient's blood has been issued, or that the correct component has been issued, and you are shown to have been correct, what happens to the nursing staff who have requested the wrong patient's blood, or component? Are they disciplined, re-trained, or is it all just swept under the carpet? :confused::confused:

I agree entirely, it shouldn't be, but you know as well as I that this is not always the case. I also think that you are right about requesting the (correct) resources, but, once again, these are sometimes not forthcoming.

That sounds eminently sensible to me.