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Malcolm Needs

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Everything posted by Malcolm Needs

  1. I agree with both Bet'naSBB and jayinsat in that it is probably an antibody directed against a low prevalence antigen. The problem with identifying the specificity of such an antibody is that there are so many! To make certain that it is not a "fool's errand", it might be worthwhile trying to get a sample of blood from the putative father, if he is available and/or known. As the baby is, like the mother, group O, there is a 50% chance that the father will also be group O, in which case it is simple to see if his red cells can be sensitised by a maternal antibody. If he is not group O, everything is not lost as, as jayinsat suggests, an eluate from the baby's red cells should be clear of all anti-A and/or anti-B. If the putative father's red cells are compatible by all methods, either there is another explanation for the positive DAT, or he is not the father (or both). The other thing that springs to mind is that, even if there is an antibody directed against a low prevalence antigen, as you have not identified a specificity using your standard panel, and should the baby develop a clinically significant case of HDN (it is too late for HDF) and require a transfusion, acquiring crossmatch compatible blood, suitable for the baby, should be a simple task.
  2. It is a phrase we use in the UK when we are using swear words, but do not actually want to swear in public. I have ABSOLUTELY NO IDEA why her doctor told her to get rid of her card. We had issued it to her, and we were not very happy when we heard what her doctor had told her (particularly as the antibody was against a high prevalence antigen!
  3. It is all over the place, to be honest. It is Caucasian, rather than caucasian, It is group O, D Positive, and group A, D Positive, rather than either group O Positive or group A Positive (see the early editions of Peter Issitt's book). It is Oh (with a subscript "h"), and not "Bombay". The FUT1 gene, or, rather, the lack of a functional gene through various different genetic mutations, leads to the "Oh" phenotype, but this should NOT be called the "Bombay phenotype". Although this phenotype was first described by Bhende YM, Deshpande CK, Bhatia HM, Sanger R, Race RR, Morgan WTJ, Watkins WM. A “new” blood-group character related to the ABO system. Lancet 1952; i: 903-904. DOI: 10.1016/S0140-6736(52)92356-8, Another example of the Oh phenotype can be seen in the rare recessive condition, Leukocyte Adhesion Deficiency Type II where, to all intents and purposes, the patient will have a normal H gene, and yet the red cells are of the Oh phenotype, and anti-H can be found in the plasma. the phenotype has been identified in many different parts of the world (and is not just confined to mutations in India or even Asia (Hidalgo A, Ma S, Peired AJ, Weiss LA, Cunningham-Rundles C, Frenette PS. Insights into leukocyte adhesion deficiency type 2 from a novel mutation in the GDP-fucose transporter gene. Blood 2003; 101: 1705-1712. DOI: 10.1182/blood-2002-09-2840). The other thing is, of course, that "Bombay" no longer exists - it is now Mumbai! I APOLOGISE FOR BEING A COMPLETE PEDANT!
  4. If necessary, I am prepared to justify vote. I hope you are willing to justify your (or the wife's) incorrect nomenclature!!!!!!!!!!!!!!!!!!!!!!!!!!
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