Malcolm Needs

Welcome LABNERD.

Welcome BryOHazard.

Welcome Laarni Didier.

I agree with jayinsat, exlimey and John C. Staley (is this a record????????!!!!!!!!!!!!!!!!!!!!).

Welcome LaurieD.

No, there is a lot more to it than that. Anti-A and anti-B are isoantibodies, rather than alloantibodies. In other words, they are "naturally occurring" and do not have to be stimulated by either red cell transfusion or pregnancy. They are usually stimulated by particles in the air (including human cells that have been shed into the air) that either express chemical compounds that mimic the A and/or B antigens or, in the case of shed human cells, actually do express these antigens (remember, the A, B and H antigens are histoantigens). On the other hand, genuine alloantibodies (for example, let's say an anti-Jka) that are stimulated by transfusions and/or pregnancy, have, by definition, shown the individual to be a "responder". It is by no means unusual for an individual who has produced a genuine alloantibody (such as the anti-Jka mentioned above) to produce an alloantibody of another specificity (or alloantibodies of other specificities). Such other alloantibodies may not be easily detectable by routine serological techniques for various reasons. Three of these are that the antibodies may not become serologically detectable at the same time (one may be detectable as early as the other, as not all antibodies "read the books"), that an antibody may be evanescent (or "disappears" from the circulation quite quickly - such as many Kidd antibodies - but these can remain clinically significant if re-stimulated), and thirdly, that the cognate antigen is not expressed on either the screening red cells or the red cells used in the antibody identification panel (for example, in the UK, to give two examples, the Jsa antigen and the Wra antigen, and both of these antibodies can be exceedingly clinically significant). For this reason, it is very important that a serological cross-match is preformed (and found to be compatible), even if the blood provided is antigen negative for a known cognate antibody. You may well ask, "Well, what about an anti-Wra (for example) that is present as a monospecific antibody? Is that not clinically significant?", and the answer is "Yes"! Indeed, there was a fatal case of an acute transfusion reaction caused by anti-Wra within the last decade in the UK, and the court decided that it was death by misadventure, because anti-Wra is known to be quite a common antibody, whereas the cognate antigen is sufficiently rare for the Law to recognise that it does not need to be expressed on screening cells (otherwise the Reference Laboratories would be overwhelmed with samples that have anti-Wra in their plasma/serum - and this is only one such specificity). This may be one of the few times that our judiciary have used their brains (did I say that??????????!!!!!!!!!!!!!!!!!) and the decision may have been influenced by an editorial in Transfusion, written by the late, great Professor George Garratty (Garratty G. How concerned should we be about missing antibodies to low incidence antigens? Transfusion 2003; 43(7): 844-847. DOI: 10.1046/j.1537-2995.2003.00492.x.). SORRY THIS IS A BIT (VERY) LENGTHY!

Welcome Allen2.

Welcome AANDERSON.

Welcome Dr G.

Welcome ALEXAV.

Auto-anti-D is more common that a lot of people think, but I am NOT saying that is what this is - just that it may be. It could also be that the D antigen of the individual is a Partial D Type, such as Partial D Type III, that would react like a "normal D" (in fact, it would have slightly elevated expression of the D antigen), but who could easily produce an allo-anti-D (and there could also be an auto-antibody present, accounting for the positive DAT). In addition, particularly as the DAT is positive, the actual specificity of the antibody in the individual's plasma/serum could be an auto-anti-LW, that would mimic an anti-D. This could be resolved by testing the antibody against a few group O, D Negative cord red cells, which would give fairly strong reactivity. In any case, I would send a sample to a Reference Laboratory to ascertain the true specificity of the antibody, but also, as Ensis01 says, for molecular characterisation of the RHD gene (and do not forget to tell them the ethnic background of the individual, as this will make their lives so much easier). Finally (for now, unless anything else springs to mind), please would you keep us informed of the outcome and results? THANK YOU; an interesting case.

My profuse apologies John. I initially read this as "I've never been a fan of blood bank specific arm bands and fought against them most of my long and sordid () career"!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

Welcome CARMEN DELGADO.

I agree that such an antibody formed late in pregnancy does not usually cause severe HDFN, BUT, you cannot state that it is a non-specific antibody. It may well be an antibody directed against a low prevalence antigen that just happens, by coincidence, to be expressed on the screening cells, but not on the panel cells. Once a person makes an antibody of such a specificity, they often make more than one specificity directed against more than one low prevalence antigen. It could well be that such an antibody had been madee earlier in the pregnancy (or even an earlier pregnancy) and you may not be aware. I agree with both Ensis01 and exlimey that more work needs to be done, just to be on the safe side. By the way, I am aware of what the Guidelines say, having been one of the writers!

Let me ask you a question, if I may? How would you feel if the baby was born with clinically significant HDFN, and you didn't know the specificity of the maternal antibody, but the baby required an urgent exchange transfusion? Not the mother, who I thing can be covered, but the baby? Yes, you can probably give the mother IAT compatible blood, and it would be safe. Always remember though, that maternal antibodies are actively transferred to their foetus, and so the concentration of the antibody in the foetus/new-born is higher than in the mother. Send a sample to RCI PLEASE!

Oh gosh, so do I. Indeed, I still buy new ones!

I could NOT agree more, particularly as most of the antibodies available are exceedingly strong monoclonal antibodies, which will QC NOTHING, and as the equilibrium constant of a truly weak antibody is quite different from that of a diluted strong antibody, particularly a strong monoclonal antibody, so just what do these inspectors think we are "QCing" using such antibodies. It is utter nonsense.

I don't need them myself, but I think what you are offering is marvellous.

Welcome Heinrik.

Welcome DianeL.

Welcome wmc.

Welcome Gregory Gillespie.

Welcome Marina Setaro.

Welcome Chituku.

Fair enough, but when was the last time he/she worked in a laboratory, and even when they did, did they work with antibodies?