Malcolm Needs

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]).

In the UK, the donors are tested with two anti-D reagents. One of these is called Totem (I can't remember who makes it, but will post tomorrow when I go back to work). This reagent not only detects partial DVI, but many, many other partial Ds (it is the best donor reagent anti-D I have ever used, but completely useless for patients). I'm not sure what other countries use. :):)

Suffice it to say that most politicians (of any party) are about as popular in the UK (and, I suspect in other countries) as bubonic plague (and about as useful). :D:D:D:D

In the UK, all the units of group O, D Negative emergency blood are also K Negative, for just such a situation. Incidentally, whilst I was working at Westminster Hospital (now closed) I had a sample in from a member of staff working at the Houses of Parliament (not an MP) and this had plasma that was a distinct shade of brown. I had never seen a sample like this before, so I called my Reader in Haematology (one down from the Professor) to have a look at it. He had never seen anything like it before either, but it turned out it was a symptom of Legionnaire's disease, and that is what this patient had. As a result, they closed most of Parliament and put in new plumbing and air conditioning. I always feel that I missed my chance in life to help my country by keeping quiet and letting the politicians get infected too!!!!!!!!!!!!!!!!!!!! :devilish::devilish:

For donors in the UK, we type each time they donate (unless the grouping reagent is incredibly rare), but where the donor has been genotyped, a confirmation a second time is sufficient for the rest of their "donation" lives (if you see what I mean). :)

Yep! They were the good ones. It was the ones that were stupid enough to actually go and try and get them about whom we were suspicious (nevertheless, as one of these [somehow] I've still got a job)!!!!!!! :D:D:D:D:D:D:D

Other occasions where you might see a haemolysed specimen is when the patient is undergoing a hyperhaemolysis crisis and, I understand, although I have never seen a case myself, March Haemoglobinuria. :):)

I think the reason they ask for irradiated blood on all the haematology/oncology patients is because many of them are either immunocompromised or on purine analogues, in case they get unirradiated blood by mistake, because these patients are more likely to get transfusion-associated graft versus host disease than others. :confused::confused:

It may just help (I don't know) if you get your patients genotyped for the FY genes too. IN that case you may well find that a awful lot of your phenotypically Fy(a-b-) sicklers are genotypically either FYB/FYB or FYB /FY, in which case they can safely be given Fy(a-b+) blood, rather than completely Duffy matched (because of the up-stream GATA-1 mutation), once they have made other antibodies than Rh and K. It may be easier to match (albeit, genotyping is not cheap). :confused::confused:

I think I'll ask for that to be put in our User Guide!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :cool::cool::cool::cool::cool: