Malcolm Needs

Did you ever try to remove them GENTLY Rashmi????????? It under G in the usual dictionaries!!!!!!!!!!!!!!!!!!! :peaceman::peaceman:

Of course, the other complication that I have just thought of (and you will not thank me for this!) is that an auto-anti-LW (which is actually more common than a lot of people think) will sometimes mimic an anti-D by IAT, but will look like an pan-reacting auto-antibody by enzyme technique, with slightly less strong reactions with the D- red cells. However, when you do an eluate, it will also look pan-reactive by IAT, as the anti-LW comes away from the LW antigen on the D- red cells relatively easily, giving an antibody that reacts well with all red cells. You could try an ABO compatible, rr, cord cell with the original plasma, and see if that reacts by IAT, as the LW antigen is particularly strong on cord cells. I told you that you wouldn't thank me; more work and no guarantee of success, as it may not be an auto-anti-LW at all!!!!!!!!!! Sorry. :redface::redface:

When was the second patient recognised? The reason I ask is that, some years ago, before we got worried about such things, the anti-D we used was not just anti-D, but a mixture of antibodies, but which were mostly anti-D, which itself, had to be of a certain "strength". I can't remember exactly how many there were, but we once did an "antibody identification" on a sample of anti-D immunoglobulin, and we detected about 6 different antibody specificities! I think I am correct in saying that such a "soup" of antibodies is no longer allowed, but it could be the reason that your elution was pan-reactive. The other reason could be that the patient already had an "enzyme only" auto-antibody, that would react by IAT if eluted. I don't know; I am only throwing in suggestions! :confused::confused: By the way, I believe I have cited this particular website before (but at my age memory is anything but perfect), for those interested in Weak and Partial D types that are known to produce alloanti-D, put "rhesusbase" into your search engine for a spectacularly useful site (although it does require updating).

No, we're on two pages now!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :haha::haha:

Having rattled on as above, what I should have said is that, in the UK, the SHOT (Severe Hazards of Transfusion) Haemovigilance Scheme is strongly against transfusion at night, unless there is a compelling clinical reason; so it shouldn't happen (and pigs might fly)!!!!!!!!!! :D:D

I would also require medical input; probably from my own Haematology Consultant, rather than the physician looking after the patient. If the cross-matched blood is outside the strict criteria laid down, then there needs to be discussion between the Haematologist and the other physician as to the dangers that may be involved in giving, or not giving the blood to the patient at that time. There may be a very good reason why the blood should be given, but if it then causes a transfusion reaction, I would rather the litigation was against my Consultant (who has the medical know-how to give a clinical defence and the medical authority to override the strict criteria), than against me (who does not - and who has not the medical authority to override the strict criteria). :redface:

I am quite certain that you are absolutely correct Anna. One only has to look at the range of antigens per red cell quoted for the D antigen for different Rh haplotypes, and the range of antigens per red cell for the different subtypes of A, and expand this for each of the other antigens in all the different Blood Group Systems, that means it must be harder to make an argument against your theory. However, one should also look at factors in the recipient. Many learned papers are now being published linking HLA types to the ability to produce specific antibodies, e.g. Reviron D, Dettori I, Ferrera V, Legrand D, Touinssi M, Mercier P, de Micco P, Chiaroni J. HLA-DRB1 alleles and Jka immunization. Transfusion 2005; 45: 956-959. It is likely, therefore, that there is, perhaps, and for want of a better way of putting it, a sort of "symbiosis" involved between donor and recipient. :wow:

Well answered, and I agree wholeheartedly with the sentiments you express in your last sentence. NOBODY can claim to have seen it all, done it all, etc and any help is always welcome. :D

I will bow to your better knowledge and greater experience on this. However, it seems strange to me that Geoff Daniels in his book, Peter Issitt and David Anstee in their book, Harvey Klein and Dave Anstee, in the 11th edition of Mollison's Blood Transfusion in Clinical Medicine all mention that transfusion reactions due to anti-A1 are exceedingly rare (a total of 4 papers being cited, the last in the late 1970's) and Marion reid and Christine Lomas-Francis in their book also say that reactions are exceedingly rare, as are anti-A1 sera that bind complement. Have you thought of publishing your unusual findings? :confused::confused:

I agree that anti-A1 is a clinically significant antibody, but only in the extremely rare occasions when it reacts strictly at 37oC. IN 30 years of Blood banking, I have only come across this once. In almost every case, the anti-A1 can be completely ignored.

I would agree entirely with adiescast.

Hi Joan, Could I be an absolute pain an suggest that, when you have made your flow chart, you post it on BBT? I suspect that it will be much more useful to fellow members than my Word document.

John, I LOVE your posts; they bring a little sanity to an increasingly insane world. PLEASE don't stay off your soap box for too long! :D:D:D:D

In answer to the first of your questions, what do you do for your ABO typing? Do you use anti-A, anti-B and anti-A,B or just anti-A and anti-B? The reason I ask is that many anti-A,B reagents are, actually, a blend of monoclonal anti-A and monoclonal anti-B. If this is the case, then I can see no reason to repeat the anti-A,B (actually, to be honest, if that is the case, I can't really see the point of using the anti-A,B in the first place, but that is an argument for another post/thread/day!). Depending upon the rules (and I'm not familiar with the rules outside the UK - actually, substitute "I am completely ignorant" for "I'm not familiar") you may or my not be able to abandon a second reverse group. As to your second question, I'll leave that to be answered by someone who actually does it! :)

It could well be that the lady is a Weak D Type 2, which gives particularly weak reactions (or even another Weak D Type that also gives very weak reactions). Were it me, until this is proved one way or 'tother, I would err on the side of calling her D Negative and give her anti-D immunoglobulin if her baby is D+. I vote that people should either be clearly D+ or clearly D-. They should not be allowed to be a Weak or Partial D!!!!!!!!!!!!! This, however, could put me out of a job, so I'll think about that one! :eek::eek:

A few years back, there was an abstract/poster shown at an AABB meeting by a couple of colleagues of mine, Lee E, de Silva M. Unlike anti-c, anti-K in pregnancy is more likely to have been induced by previous transfusion; this can be prevented. Transfusion 2004; 44: 95 104A. This argues that giving a c- lady c- blood is a waste of time, as many of them would produce anti-c because of pregnancy. This can be extrapolated to the fact that it is a waste of time giving anyone who is c-, c- blood. I TOTALLY DISAGREE WITH THIS!!!!!!!!!! See my attachment in the second post in this thread as to why. I TOTALLY AGREE WITH YOU BELVA! :D:D:D:D

Well, in a way we do know this. In Mollison's Blood Transfusion in Clinical Medicine (cited above), this time in Chapter 5, they talk about work showing how often giving D+ blood to a D- patient, just once, produces a response. They talk about 15% of the random population being "super responders" (my non-scientific phrase, not theirs!). In one study, <50% of D- volunteers produced a serologically detectable after 6 months after injection with 0.5 to 1mL of D+ red cells. BUT, this implies that some of them did, and it implies that it was more than, say, 1%. To my mind, this also debunks the practice of looking for an antibody response for 14 days, and if nothing is detectable, go ahead and give more of the same. I know that the D antigen is easily the most immunogenic of the common antigens, but K and c are not that far behind. In Mabel's case, therefore, where her blood supplier is miles from her hospitals, it would be best to regard all of her patients as potential "super responders", particularly as there is no way of telling in which category her patients will fall, prior to transfusion. :confused:

How much in the past? Almost all of the anti-D would be on the recipient's red cells and he/she would have a fairly hefty positive DAT. :confused:

If you do remember, I'd love to see an abstract of the presentation. I'd be a little worried about the anti-Jsa, but would agree that the others tend to be clinically benign, howver, you can't exclude them, just ignore them..

Goodness me! This data has been out there for years and years. One only has to look at the many studies done on sickle cell and thalassaemic patients to fine copious data. May I suggest, as a start, you read Chapter 3 (Immunology of Red Cells) in Mollison's Blood Transfusion in Clinical Medicine, 11th edition, Harvey G Klein and David J Anstee, Blackwell Publishing 2005? But there are many, many other books and papers that state that the more a patient is exposed to foreign antigens, the more likely they are to produce atypical antibodies. Certainly, this has been known about for nigh on 50 years, as Eloise R Gibblett wrote about it in 1961! :angered::angered:

I'm not sure, but I think what Mabel is saying is that, for a "cold" transfusion, when there is time to get in R1R1 blood, they would. If, on the other hand, they expose people, almost deliberately, to c+ blood, then when they need a transfusion in hurry, they will be in trouble. To me, that makes sense. :confused:

Many, many years ago (far too many for comfort), when I was briefly working in pure haematology (and not enjoying a moment of it!) we used to use an industrially produced diamond on the end of a pencil like thing for etching names and numbers on slides. I don't know if these are still available, but if they are, these could possibly do the job. :confused::confused:

Oh yes Yanxia, I am not disputing for one moment that there is an element of IgG causing the positive DAT. All I was saying was that this IgG element may be very loosely bound to the red cells and (possibly) could be washed off during the (fairly vigorous) washing phase that takes place prior to the actual elution itself. I would dispute that elutions should only be done when the result is positive, however, ever since I read the study by Sachs UJU, Roder L, Santoso S, Bein G. Does a negative direct antiglobulin test exclude warm autoimmune haemolytic anaemia? A prospective study of 504 cases. Brit J Haemat 2006; 122: 655-656 and have also dealt with a fatal case of group A into group O acute haemolytic transfusion reaction where, apparently, no group A cells could be identified by normal serological techniques (having all been destroyed), the DAT was negative, but, that notwithstanding, anti-A could still be eluted from the patient's post-mortem sample. :shocked:

Ah, but don't forget there are some 46 antigens within the MNS Blood Group System, many of which are the result of genetic "cross-over" (either Lepore or anti-Lepore types) and some of these are quite common in certain areas of the world (see many of TimOz's posts). It is probable, therefore, that certain M+N- and/or M-N+ apparent homozygosity will be, in fact, and for example, M+Lepore type+. :confused:

In the circumstances you describe, Mabel, I completely agree with what you are doing; it sounds eminently sensible (and could even save lives. These circumstances should, however, never pertain in a small country like the UK. :)