Malcolm Needs

Whilst I hate to admit this, particularly on a worldwide site, I have to agree with you about the knowledge of an antibody screen prior to prophylaxis. This is why, unless we have been told by a hospital that prophylaxis has been given, and we detect an anti-D with a level of 0.5 IU/mL or below, we state that an unspecified anti-D is present. If, however, the level is above 0.5 IU/mL, we are confident that it is an immune anti-D, as extensive tests have shown that, even with a prophylaxis dose of 1, 500 IU (and a BSW {British Standard Woman!]) the level never exceeds 0.5 IU/mL. Of course, if the lady is very petite, or they give the world's supply of anti-D immunoglobulin to a single lady (or, a married lady, come to that, ha!, ha!), then we may be caught out by stating the anti-D to be immune, but then, if we are not told of these circumstances by the hospital, what can we do?

I would agree that, in this case, there are clear cut specificities, and that more cells could be used to rule in and rule out. I would dispute, however, that performing differential alloadsorptions in a case where there are some negative reactions is dangerous. Yes, there is some dilution effect, but a few years ago a colleague of mine deliberately spiked a panagglutinin with a very weak anti-D, and then adsorbed the plasma 8 times with some rr red cells. At the end of this process, the panagglutinin had disappeared, but the anti-D could be readily detected, albeit the reactions were very slightly weaker. The trick is to ensure that the cells used for adsorption are really, really packed, by centrifuging on high for about 10 minutes, and then removing the supernatant and the top layer of cells, and then centrifuging again for another couple of minutes and taking off any residual supernatant and the top layer of cells. After this, the only fluid left to dilute the antibody is, for want of a better way of putting it, "interstitial fluid". I am always more worried when there are NO negative reactions, because then you may be taking out an antibody directed against a high incidence antigen that may be lurking under the auto-antibody. Actually, differential adsorption can be extremely useful when you know that there is no auto-antibody present, but there is a complex mixture of "common" alloantibodies and when there is an alloantibody present directed against a high incidence antigen of known specificity. This can be adsorbed out, leaving any other alloantibodies present in at least one of the plasma samples that have been adsorbed. I have used this method on several occasions with specificities such as anti-U and anti-HrB.

And wedding anniversaries; don't forget they have a very close and intimate relationship with a computer!

You know, I really don't think you're taking this seriously!!!!!!!!! :rolleyes::rolleyes:

Brilliant! :D

Oh how I wish I worked with you or someone similar. In our place the people that work in Quality seem all to have had two "ectomies". The first is a "pragmatismectomy" and the second is a "humourectomy"!

Being a Reference Laboratory, we also perform differential alloadsorptions on such patients (or auto-adsorptions if the patient has not been transfused within the previous 3 months [rare] and if there is sufficient autologous red cells [almost never]). As you may have seen from my posts on threads asking similar (but not identical) questions, I have no problem issuing blood that reacts in vitro with the auto-antibody in the patient's raw palsma, unless the haemolysis is fulimating. When issuing this blood we do not need a doctor's signature, but we would not issue it either as compatible, or as incompatible, but would issue it as "suitable for". In addition, we print a phrase on the bottom of the cross-match form that goes out to the hospitals as follows: "Please note that when suitable blood, rather than compatible blood is provided, observation of the patient during transfusion is of paramount importance." I am almost happy with this, except that the phrase itself seems to imply that observation of the patient during transfusion is not of paramount importance for any other transfusion, which is, of course, complete nonsense! :)

I am entirely sympathetic with your views Lekota40. a) I am glad that I don't have to work for this supervisor. I hope that she never has to deal with me if I need a transfusion (she may think my anti-B is some kind of strange auto-antibody)

Hi Donna, I can see why you are confused, because re-reading my post, I could have been a bit less obscure! It depends what technology is used to perform the typing. In my own Laboratory, we use DiaMed gel for almost all typing. You will note that the Ortho panel (which, I belive is gel, although I'm not entirely sure) gave a 2+ with the patient's own cells. If, therefore, this technology was used to group the patient with any reagents that required an IAT, the results would be unreliable. In such a case, just to be on the safe side, and with knowledge that some antigens may be weakened and others destroyed, we would treat the patient's red cells with chloroquine before grouping, just to be on the safe side. I do totally agree with you that a weak auto-antibody can mimic specificities and that not all cells in the panel will necessarily react by IAT; we'll take that as a given. This is why, however, I feel that a panel of enzyme-treated red cells is essential in this case. A true alloanti-Fya will not react with these panel cells, but an auto-antibody mimicking an anti-Fya may (not will, but may). However, the whole thing is best cleared up by an alloadsorption study, and an auto-adsorption study only serves to muddy the waters. As I say though, I do totally agree with you. A couple of times we have identified an apparently clear cut alloanti-S, but the anti-S was reacting with papain-treated red cells (not unknown, but sufficiently rare to make us suspicious). In both cases, using extremely sensitive serological methods, we were able to demonstrate that the antibody present was, in fact, a very weak auto-anti-U. I do not think, however, indeed, I am certain, that Lekoda40's supervisor has not proved his/her case. I hope that I have made myself a little clearer, but if my ramblings are still confusing you, please do not hesitate so to say, and I'll give it another whorl! :)

Love it John!!!!!!!!!!

I agree with everything you say L106 (especially the bit about us all making mistakes), but one should also ask why, if it is supposedly an auto-antibody reacting with some (but not all) panel cells by IAT, he or she (the supervisor) can rely on the cell typing when some of them must rely on an IAT typing (e.g. the Duffy typing)? Seems strange (= daft) to me.

There! And I thought maru was in bone! Sorry; awful pun!

Reminds me of another story! Joan Powell, who also worked with Race and Sanger, saw a tee-shirt that the IBGRL had made for me with the logo, "I'm Chido Negative" on the front. Not to be outdone, Joan, who was a P1+++++ had one made saying "I've got strong pee"! Ah, the old days before Quality and inspectors made it so boring!

All joking apart, I do think that little stories like these can help enthuse those junior staff members who are already showing some kind of aptitude and enthusiasm for the subject of Blood Confusion!

Well, I think that is very cruel!

Well, the story goes like this. When anti-Sda was first discovered, it was worked on extensively by Rob Race, Ruth Sanger and Patricia Tippett at the Medical Research Council's Blood Group Unit in London. In those days it was not considered unethical to use the staff as "panel cells" and "controls". They discovered that one member of staff's blood, the caretaker, reacted particularly strongly with the original anti-Sda (although he was not as strong as a Cad+). They decided to call the antigen after this staff member, Sid Smith (a delightful chap I might add, as was Rob himself, and Ruth and Pat were delightful "chapesses"; indeed, Patricia still is). Of course, in those days, it was traditional to call the antigen after the first two letters of the surname of the person, but, there was already an Sm antigen (now Sc1 of the Scianna Blood Group System), so they couldn't call it that. In the end, they called it Sid, after the caretaker's first name. As I say, I love stories like that. Swa was called Swann after the Swann of Flanders and Swann fame (who made the song, "Mud, mud, glorious mud" famous, amongst others - at least, famous this side of the pond). I can bore people for hours about this kind of thing!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! :D:D:D:D

Pretty slim. I love stories like that. Do you know how Sd(a) (Sid) got its name?

And a good two cents worth too in my opinion. Where I work, we have to do a root cause analysis if we breathe too noisily (an obvious exaggeration, but not that much of an exaggeration). Quality are scared stiff of the GMP inspectors.

My goodness, you are going to have a talking to! If I were your supervisor, I would be talking to you too, only I would be congratulating you on your serological logic. Don't loose your temper with your boss, but stick to your principles. :eek::eek:

I'm surprised that your supervisor suggested an auto-adsorption. Apart from enzyme-treatment, I would have gone for alloadsorption, on the grounds that the antibodies "look allo".

Looking at the panel results, one cannot exclude a combination of anti-C+K+Fya. The one thing that worries me a little is that panel 1 shows an auto in IAT that is negative, whilst panel 2 shows an auto in IAT that is positive. Did you papain-treat the panel cells to destroy the (possible) anti-Fya/Fya reaction and enhance the (possible) anti-C/C reaction? :confused::confused:

Difficult if you haven't got access to the panel phenotypes!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! Any way these could be attached?????

I would agree with Anna. We sometimes get antibodies in our external QA scheme that react perfectly well in IAT, but do not react as would be expected with enzyme-treated red cells. These antibodies are also "mucked about with". Terrible English I know!

Hi Angie and welcome. I think that I can safely speak for the vast majority of members when I say that we have all learned a lot from this site.

We would perform an antibody identification every time even if the patient has not been transfused since the last time. The patient has already been shown to be a responder, by the fact that he or she has already produced an alloantibody. What you don't know is whether the patient has produced a second (or more) antibody of a different specificity, but slower than the identified antibody. You should not rely on the cross-match under these circumstances. The red cells in the panel are in a solution designed to preserve the antigen expression, but not necessarily the oxygen carrying capacity. The red cells in the unit are in a solution designed to preserve the oxygen carrying capacity, but not necessarily the antigen expression, and you also may not know the rest of the units phenotype (it may have heterozygous expression of the Kidd antigens, for example, whereas the anti-Jka lurking along with the known antibody may only react in vitro with Jk(a+b-) red cells; but it sure will react with Jk(a+b+) in vivo)! I have, only today, been working on a sickle cell patient who, a week ago, had anti-E+M+Fya+Jkb; he now has an incredibly strong anti-Fy3 as well. :eek: