Malcolm Needs

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. :)

Swencesl, PLEASE do not feel that you offended me for one moment (and even if you had, mine is only one person's opinion). I actually agree with what you are saying with regard to the residents and clinicians, but I also feel that this guidance can be given with (and sometimes can be better given) with individual comments for individual patients, especially if the initial results do not correlate with the patient's clinical history. :)

Not off the top of my head Rashmi (I'm at home at the moment), but I will try to find out. We would be delighted (moan, moan, moan??????????) if poeple did this, because this is what is recommended by SHOT. It is not there to "catch people out", but so particular techniques/technologies can be monitored to see if there is a national trend with one particular technique/technology missing clinically significant antibodies.

I can see nothing wrong with this. We do exactly the same following a pregnancy with an antibody. An "abbreviated panel" that covers all the "other antigens" is just as safe as a full panel. :)

I know that you are talking about platelets, rather than red cells (red cell antibodies being about the only thing I can claim to know anything about), but I hate canned comments with a passion that knows no bounds. Each patient is an individual with an individual condition, and it is extremely rare that canned comments appropriate for one patient are entirely appropriate for another. Using them as a guidance for a report is an entirely different thing, because they are extremely useful as an aide memoire, but that is as far as they should be taken. :mad::mad::mad:

I did mean my photograph on my Public Profile bit; honest!!!!!!!!

Hi CYGI, Yes, that clears it up perfectly thanks very much (and I agree entirely with what you say). The confusion was probably all on my part. :)

No, in fact, in most cases, we don't rule them out at all. For example, if we perform a panel, and we find an anti-K present, and the K+ red cells happen to be the only Lu(a+) red cell on the panel, we would not even bother to run a cell that is K-, Lu(a+), simply because anti-Lua is not clinically significant.

I understand your "facelift" malcolm. I choked on my coffee reading that.