Malcolm Needs

There is a very thorough and excellent article/review about this in Nature Biotechnology. Liu QP, Sulzenbacher G, Yuan H, Bennett EP, Pietz G, Saunders K, Spence J, Nudelman E, Levery SB, White T, Neveu JM, Lane WS, Bourne Y, Olsson ML, Henrissat B, Clausen H. Bacterial glycosidases for the production of universal re blood cells. Nature Biotechnology 2007, 25 (4): 454-464. It is not for the faint hearted, however. I had to read it about 27 times before I understood the abstract!!!!!!!!!!!!!!!!!!!!!

I agree with the people who have replied. Using the correct terminology in the replies is the best option. The reason I suggested the educational side of the forum was simply because some people may not actually realize that they are using incorrect terminology; I wasn't trying to be hypercritical - HONEST.

I am probably going to be quite controversial or pedantic (or any other adjective you would care to use about me - and many do!) but, as this site (BloodBankTalk as a whole, but the Education forum in particular), should we not be using the correct nomenclature for techniques, antigens, antibodies, etc, rather than the incorrect nomenclature that is continually being used, despite guideance from, for example, the ISBT and such luminaries as Peter Issitt (sometimes by real experts in the field)? I refer, for example, to the use of the "Coombs test" (either direct or indirect), instead of the antiglobulin test (a term much preferred by Professor Robin Coombs himself), the use of "Kell", not for the Blood Group System, but for the K antigen, the use of the term "Rhesus" or "rhesus" Blood Group System, instead of the correct Rh Blood Group System. If we continue to use incorrect terminology, we will perpetrate incorrect terminology, although at least aprt of this website is to educate? Unless we educate those coming up behind us, as it were, things will never improve, and the use of incorrect terminology can, in itself, lead to misunderstanding of either a question, or an answer (or both).

Glad I could be of help. I'm sorry I can't help with the LFT's. That's in the Land of Chemical Pathology, which is a land I have never visited (except when I did very basic stuff in my ONC examination several centuries ago)!!!!!!!

Hi weescot48, I'll do my best, but it can be a bit complicated! Cw is an antigen within the Rh Blood Group System (often, incorrectly, referred to as the Rhesus or rhesus Blood Group System). There are now 50 different antigens recognized within this system. Many of the antigens are either incredibly common (being found in almost everyone in all populations), whilst others are extremely rare (being found in very few individuals within any population). Many, but all of these antigens have "alternatives" called allelomorphs. The genes that encode the antigens within the Rh Blood Group System are located on chromosome 1. There are two genes; RHD and RHCE. The bit of the gene that encodes a particular antigen is called a locus. The locus for the gene that governs Cw is found on RHCE. Unusually, Cw has two "alternatives"; Cx (which is extremely rare) and MAR (which is extremely common). Cw, or rather anti-Cw was first described as long ago as 1946, when it was recognized in the plasma of a multiply transfused haemophiliac patient in Oxford, England. It is found in about 2% of the White population and 1% of the Black population, but, for some reason is more common in Finland and Latvia. The antibody (anti-Cw) is quite common; much too common for all of those found to have arisen from either the person being transfused with Cw+ blood, or, in the case of a female, to have carried a Cw+ baby. We call antibodies of this type "naturally occurring", although, to be perfectly honest, this actually means that we haven't a clue what has stimulated the individual to make the antibody! Anti-Cw is very rarely clinically significant and should cause you no problems whatsoever. The reason that you have been issued with a card is, I would guess, not because you are likely to have a clinically significant transfusion reaction if you were to be transfused with Cw+ blood in the future (you may turn a little jaundiced [yellow], but that is about all), but much more likely because it will help the Blood Bank to identify the antibody quickly, instead of having to go through the whole process of antibody identification without any clues. Indeed, within the UK, it is now quite unusual for such a card to be issued for anti-Cw. I hope that this is of some help, but, if not, please do not hesitate to get back and I, or another poster will try to elucidate further.

I sort of stumbled across this website by accident. A very good friend of mine, Bob Slater, suggested it to me. I fully concur with what Rashmi has said. It's a brilliant site and I am learning a great deal from it.

Kelly K, if you are prepared to give me an address (for your own protection, I would propose your place of work, rather than your private address) I am happy to send you a CD-ROM we have put together for education in the South-east of England. I'm not saying that the lectures are "the be all and end all", but they could provide some ideas and you are quite free to use them in their entirety or cut and paste as you want.

We have seen an awful lot of cases of anti-Cw in pregnancy in my Reference Laboratory, but we have never come across one that has caused anything more in the way of a clinically significant HDN than requiring phototherapy, BUT.... I do know of this paper: Kollamparambil TG, Jani BR, Aldouri M, Soe A, Ducker DA. Anti-Cw alloimmunization presenting as hydrops fetalis. Acta Paediatrica 2005; 94: 499-507. This paper may not be easily obtainable for all, and so I will take the liberty of quoting the Abstract. "Cw is a low frequency red cell antigen that belongs to the Rh blood group system. While not uncommon, anti-Cw is rarely associated with clinically significant haemolytic disease of the newborn (HDN). When it does occur, it is often subclinical or of mild to moderate clinical severity. In the majority of pregnancies it is considered to be a naturally occuring antibody and has not been reported to cause hydrops fetalis or stillbirth. We report a case of anti-Cw alloimmunization, which was associated with significant anaemia and hydrops fetalis, presenting at 35 wk gestation." The fact that this warrented a paper suggests just how rare this is!

I agree with the vast majority of these posts (particularly Mabel Adams, Geri Ann, Janet, aakupaku and webersl). Cathy, if the OB physician insists on a titre for the anti-M, and the anti-M does not react by pre-warmed, warm-washed tube IAT, why not cut your losses and report the the antibody as "too weak to titrate" (sorry about my UK English spelling), without titrating in gel. You are, after all, not lying. The antibody is too weak to titrate by a method that measures antibody titres that may affect the foetus/baby.

Hi Anna, I'm sorry to be a bit of an old curmudgeon, but is it really likely to be something in the first and/or second unit reacting against something in the third? If it were so, the antigen would have to be on the red cells of the first and/or second unit, and the antibody in the plasma of the third (otherwise the antibody in the plasma of the first or second unit would be too dilute to cause much more than a delayed haemolytic transfusion reaction due to red cell sensitization and then removal by the reticuloendothelial system, rather than almost immediate haematuria), and even then, the titre of the antibody in the third unit would have to be pretty high. I'm NOT for one minute saying that this cannot happen (we all know of the case in the literature of the anti-K in one unit reacting with another unit that was K+); all I'm saying is that, in this day and age of quality coming out of our ears, I just think it is unlikely. PLEASE DON'T THINK I AM INSULTING EITHER YOU OR YOUR SUGGESTION. IF IT READS LIKE THAT, IT WAS NOT MEANT IN THAT VEIN AND PLEASE FORGIVE ME.

I wouldn't mind Linda, but Rashmi is one of my friends and colleagues from a hospital with which my Reference Laboratory deals!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!:disbelief

:haha:I see what you mean! And an awful lot of my "friends" and colleagues reckon I'm full of hot air!

In my own (limited) experience of cases of hyperhaemolysis, it is not unusual for atypical alloantibodies to be present in the patient's plasma, but it is by no means a sine qua non. Certainly the MDS case I quoted had no alloantibodies detected. Perhaps I should stress a little more than I did that the most common cases of this extremely rare condition are seen in multiply transfused cases if sickle cell disease; but then it is also not unusual for individuals who have sickle cell disease to be multiply transfused, and therefore make alloantibodies. It could well be that these antibodies are red herrings, particularly as you would give antigen negative blood. I know of no drugs that are associated with this condition, which is a problem, as such cases cannot be predicted and come as a nasty shock.

Thanks David, That's rather what I thought re IgA not causing haemolysis. You are, of course, absolutely correct about most AHG not containing anti-IgA. The DAT cards supplied by DaiMed contain one column containing a monospecific anti-IgA, but their routine DAT cards used by most hospitals only contain either anti-IgG+anti-C3d or only anti-IgG, and so it is unlikely (almost impossible) that such an antibody would be detected by routine antibody screening or routine antibody identification. One would only get a clue by performing a DAT with the rather specialised DAT cards used (almost exclusively) by a Reference Laboratory. Then, of course, one would have to identify the specificity using a decent monospecific anti-IgA by IAT. A knotty little problem........................!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

I would agree with heathervaught that genotyping the patient would be far easier than trying to type the reticulocytes. For one thing, the patient's reticulocytes would not necessarily exhibit the same antigens (or, at least, antigen strengths) as the patient's red cells, as some antigens need time to mature as they go through the bone marrow (usually those antigens with a dominent sugar residue, as the rpotein antigens will be there anyway). I would disagree, however, that it could be the acidic nature of the anticoagulant. Whilst this could possibly so in cases of massive transfusion (according to the literature), it is highly unlikely that the natural buffering within the patient's plasma would be affected by just two units of blood (with the caveat that the patient may, of course, be of extremely small stature, making this slightly more possible, but still unlikely).

It is the National Health Service Blood and Transplant (NHSBT) Centre at Tooting in London. Until recently, the NHSBT was known as the National Blood Service (NBS). The Tooting Centre serves as a Centre to collect, process, test and issue blood, but also has a Reference Red Cell Immunohaematology Department, where I am the manager and a Histocompatability and Immunogenetics Department (which is a total mystery to me - being entirely red cell orientated!!!!!!!!!!!!!!!!!!).

Hi David, Whilst I would agree that IgA mediated antibody reactions can be both dramatic and life-threatening, would you; a) expect to see haemoglobinurea? and expect such an antibody to have been demonstrated much earlier in the patient's life-history? I am genuinely asking questions here, rather than questioning your answer (if you see what I mean)!

There is a possibility that this could be a case of hyperhaemolysis? This is most often associated with sickle cell patients, but we are aware of at least one (unfortunately) fatal case of hyperhaemolysis in MDS. Normally, in such cases, you will find that the Hb is lower after transfusion than before, but with low reticulocytes, and with hyperactive macrophages. In such cases it's best not to transfuse, but if there is no alternative, it is best to transfuse under IVIG and methylprednisolone. It's only a thought. I may well be barking up completely the wrong tree, but it is worthwhile ruling this out.

I'm off with a bad back at the moment, but will talk to Paul/Ian as soon as I can crawl back in. I suppose I should talk to Gordon Burgess, my Line Manager too.

Could do. We could also send those samples from solid phase users in which we find nothing to NHSBT-Birmingham Centre, who have solid phase available to them. I'm sure Paul Fleetwood and Ian Skidmore at Birmingham would be immensely pleased!!!!!!!!!!!!!!!!!!!!!!!!!!

Not an enormous number by any means, but I would say that we do find the about four or five a year.

As a Reference Laboratory (actually, your Reference Laboratory, Rashmi) we use the DiaMed gel technique as our first "line of defence", but if we do not detect anything by this technique, we will go on to perform LISS tube IAT at 37oC. We consider this latter technique to be the "gold standard", and if we do not detect anything by this technique, we look no further (on the grounds that, if we don't detect an antibody by this technique, even if there is one present, it is unlkely to be clinically significant. Just occasionally, we will perform a LISS tube direct agglutination at 15oC, if we think that the referring laboratory may have detected a "cold reacting" antibody with a true specificity, such as anti-M, but only if it's a slow day and we are bored!

Another source, although not strictly speaking an SOP, is the 2nd edition of the excellent book by lawrie Petz and George Garratty, Immune Hemolytic Anemias. Reading the chapter on cold AIHA may save you an awful lot of work. The main thing being that the thermal range of the antibody is the most important thing, the titre occasionally an important thing and the specificity almost always a complete and utter waste of time (the last because, even if the antibody turns out to be an anti-I, where are you going to source adult ii units that are also covered in C3dg!!!!!!!!!!!!!!!!!!).

Sorry, dinner was ready half way through my post. To continue.... There are very good reason why MSBOS is an extremel useful thing. Firstly, it helps to remeber that the MSBOS is individual to the surgical procedure, the surgeon, the hospital and to the patient. The idiocyncrasy of the surgical procedure is obvious (one would not require the same blood cover for an in growing toenail as one would for a bilateral re-do of a total hip replacement - I hope). Some surgeons take on more difficult cases than others, for the same surgical procedure. Some hospitals have many surgeons that do the above. A particular patient may have a potential bleeding problem (e.g. they are on aspirin) whilst others may not. It is an ideal way to improve the relationship between the Blood Bank and one's surgical/anaesthetic colleagues, in as much as it is just as valuable to suggest to them that they may need more blood cover, rather than less. To sum up, the MSBOS is brilliant for those hospitals that do not yet undertake EI as it saves on the waste and expense of blood, whilst being safe for the patient and helping keep the Blood Bank on the "right side" of their colleagues in other departments.

Hi Pat, Yes, the MSBOS has been around for an awful long time (since Boral and Henry, if my memory has not gone completely), but is still good for all that (many things that have been around for a long time are still excellent - tube techniques for one!). Presumably you know the theory behind it (the Transfusion Index and the Cross-matched to Transfusion Ratio [C/T Ratio]) and why it was introduced (the shocking waste of blood tied up on patients who were unlikely to ever use it, and the expense of cross-matching this blood). If not, I would suggest you read some of the work done by John Judd on this subject. With the advent of electronic issue (EI) (N.B. NOT electronic cross-match - as you don't actually do a cross-match) the use of an MSBOS is becoming less common, but still remains the bedrock of establishments that do not perform EI, or should do, if they have any respect for their Blood Bank and, more importantly, the blood donors.