Malcolm Needs

Putting aside the A antigen for the moment, which is probably "normal" in the case of your patient, it is not the B antigen that is abnormal in the case of a Bel person, but the 3-alpha-galactosyltransferase enzyme (the direct gene product of the ABO gene) is less active than normal, due to a mutation in the gene. The actual carbohydrate residue that is on the red cell is "normal" - just less of it. In addition, there is competition between the "A-transferase" and the "B-transferase" for the H-backbone. In the case of your patient, the "A-transferase" will "win" this competition and this will accentuate the weakening of the B antigen even further - but the actual structure of the B antigen will be the same as the normal B antigen - just fewer in number. This explains why there is no anti-B present in your patient's circulation. This (rather long-winded) explanation should serve to prevent you worrying about giving your patient group AB blood should they require a transfusion.

Looks like an AsubgroupB to me, but, these days, with monoclonal antibodies, which type of A subgroup can only be accurately sorted by molecular techniques. The reverse group needs more investigation. It could be anti-A1, it could be another "cold" antibody specificity (such as anti-M or anti-P1), or it could be a combination of the two. If there is no reaction at 30oC and above, it doesn't really matter, but, to be on the safe side, if blood is required, I would give group B packed red cells, or group B red cells resuspended in AB plasma.

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I don't know for certain, but I bet they did a bit more than that. Almost all "cold" auto-antibodies are IgM, it is true, BUT, because these antibodies almost always have a very wide thermal amplitude, they would cause "spontaneous agglutination" in tests incubated at 37oC too. What they probably did was to either adsorb out the "cold" auto-antibody with something like rabbit erythrocyte stroma, or denaturation of the IgM molecules by a reducing agent, such as dithiothreitol (DTT), and only then performing tests using a monospecific anti-IgG reagent. I am quite happy to be corrected.

Oniononorion, I would tend to agree with you that blood transfusion as a whole, and immunohaematology in particular, are always the "bridesmaid and never the bride" in terms of the amount of time devoted to the subjects in taught courses, however, i do have some sympathy with those trying to plan such courses, particularly the practical courses, even when attending a course at a Reference Laboratory, simply because some of the cases are so rare that it cannot be guaranteed that you would see such cases, even if you were in a Reference Laboratory for several weeks.

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Sadly, I don't (and, if I did, the seams would explode if I tried to put it on these days)!

NO QUESTION IS DUMB if you don't know the answer, and if you never ask it, you will never know the answer. Having said that, you will, just occasionally, get some pretty dumb answers! I agree entirely with David Salkin's answer, which, as always, is far from dumb. When I was working at the Blood Group Reference Laboratory (way back, when it was still in London), it was discovered that I was Ch Negative. Having not long left school, I got all excited over having a rare blood group, and, I think to bring me back down to Earth, they got me a tee shirt with "I'm Ch Negative" printed on the front. In the MRC Blood Group Unit, in the same grounds, but quite autonomous (run by Drs Rob Race and Ruth Sanger) was a woman who had an exceptionally strong expression of the P1 antigen. Having seen my tee shirt, some wit employed there bought her a tee shirt with "I've got strong P" printed on it. As far as I can remember, she never wore it!!!!!!!!! I've attached a short PowerPoint lecture about the P1Pk Blood Group System. The P1PK Blood Group System.pptx

I can't really tell you that, but I would thoroughly agree with your last sentence. However, others may disagree.

I would agree with everything you say Sandra, except that I would say any Lutheran antibody (and anti-AnWj come to that) tends to give a "stringy" mixed-field type of agglutination; not just anti-Lub.

Welcome KaRen Dansberry.

I would think a month is entirely adequate. Think about how the mother would have made an allo-anti-C, without making an allo-anti-D. We presume, in these cases, that the mother is the classic rr (D-, C-, E-, c+, e+), and so can make anti-D, anti-C and anti-E of the common Rh antibodies (she cannot make either anti-c or anti-e). For the mother to make an anti-C, but not an anti-D, when the mother has received a dose of prophylactic anti-D immunoglobulin, the baby/foetus has to express the C antigen, while not expressing the D antigen (ignoring anti-G for now). This almost certainly means that the father and the foetus must have the RH*Ce gene, but not the RH*D gene; an unusual, but by no means rare, situation. What would be rare, however, would be an individual who, having been given a dose of prophylactic anti-D immunoglobulin, which would, of course, "get rid of" foetal red cells expressing the D antigen (which is extremely immunogenic) but would still give her immune system time to be sensitised to the C antigen, when both the D and C antigens are expressed on the same red cells (if you see what I mean). On top of that, the C antigen is known to be nowhere near as immunogenic as the D antigen, and the likelihood gets even lower. Finally, look at the literature on anti-C causing HDFN. It is incredibly rare for anti-C (or anti-Ce) to cause clinically significant HDFN, let alone fatal, HDFN, and you will see that the chances of your pregnant women having an anti-C that will cause HDFN, particularly when it is no longer detectable in the plasma, is not so much disappearingly low, as miraculous! I really wouldn't worry about it.

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I take it that the sample was THOROUGHLY centrifuged? Stray white cells can look like mixed-field in CAT sometimes.

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