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John Eggington

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Everything posted by John Eggington

  1. John Eggington
    If this patient has already been given IVIG, it could be that you're detecting a 'passively acquired' antibody (e.g., anti-A and/or anti-A1)
  2. John Eggington
    When you repeated the screen, did you use the same bottle of cells (not just the same batch). We've found that when cells start to 'go off' (for any number of reasons), they can begin to behave like enzyme treated cells; so if you use IAT cards you are, in effect, performing an enzyme IAT test - ideal for detecting weak Rh antibodies. If the effect is 'batch wide', it would seem more likely that the 'difference in antigen density' suggestion is more likley (although it would be nice to see some of Malcolm's zebras).
  3. John Eggington
    Agaiin, I agree with Anna. 'False negative' DAT is not something I'd associate with column technique (in an untransfused patient). You can sometimes get a stronger reaction if you add patient plasma to your DAT (and incubate like an IAT), which could relate to 'low affinity' auotantibody.
  4. John Eggington
    Anna has answered this far better than I would have. There isn't really any equivalent to the 'wash phase', of the tube technique, in a coloumn agglutination test (which is the point of the test, I suppose!). Some people may 'wash' pateint red cells before performing a DAT by column technique, but this is nothing to do with the 'wash phase' requirements of the tube technique.
  5. John Eggington
    Were you able to repeat the test using the exact same bottle of reagent red cells (not just the same batch) that were used when the test, originally, gave a positive result?
  6. John Eggington
    Was/is the patient's DAT positive? Why do you think they, originally, (forward) grouped as AB?
  7. John Eggington
    Also, did they start giving her any other drugs/treatment, after delivery, that had been held back because the pregnancy? A big dose of 'something new' (or a switch from oral to IV cephalosporins) might cause a positive DAT.
  8. John Eggington
    Firstly; remember that the AHG is incorporated into the gel column. Cells are added to each column then undergo a specific centrifugation phase that draws cells through the column, but is too 'light' to have a significant affect on free immunoglobulin. So, during the centrifugation phase, red cells come in to contact with AHG, but the AHG is not neutralised, because it is not exposed to free immunoglobulin (only any immunoglobulin that happens to be bound to the red cells). The same principle applies to the IAT, but with a prior incubation phase (maintaining an 'air gap' between the red cell/plasma mixture and the AHG impregnated gel column) to allow antibody and antigen to bind.
  9. John Eggington
    With respect to the BBTS Specialist Certifcate in transfusion Science; it is currently a 4 paper exam, with all papers being taken on the same day. The first 3 papers are taken by all candidates, the final paper has 2 options; one aimed at those working in 'Testing & Processing' and one aimed at those working in a (UK style) 'blood bank'. There is not much cross-over (in the UK, anyway) between those working in 'patient focused' transfusion, and those working in 'donor/donation focused' transfusion.
  10. John Eggington
    As 'Fluffy' has been otherwise engaged, I'll present my view; the BBTS certificates are widely recognised in the UK, and I would recommend them to anyone working within the disciplines they cover. In addition, I gave this answer to a, previous, similar question (with respect to the Specialist Certificate in Transfusion Science) 'Those taking the 'BBTS certificate' undertake a single exam, which examines candidates on their specialist knowledge of transfusion science. The topic areas examined match, very closely, those listed at http://www.ascp.org/FunctionalNaviga...ification.aspx, but no equivalence is claimed. It is expected that those taking the exam are HPC (the UK Health Professions Council) registered, with a minimum of 2 years experience in a transfusion laboratory (the experience component is a recommendation, rather than mandatory)'.
  11. John Eggington
    Rather than try and remove the odd splash, you could go the whole hog and give him a couple of coats...
  12. John Eggington
    I'll start; Assuming all controls, etc., have worked correctly 1) Mom is CDe/-D-, Dad would be R2/? so baby could be R2/-D- (or .D., complete deletion, etc.) 2) Baby is the product of a donated egg 3) Swapped at birth (it happens, I've seen the Omen!) 4) Mislabelled/mismatched samples
  13. John Eggington
    What is the source for the plasma you use in the minor crossmatch? If you're getting it from the blood pack (or the tubing attached to the pack) it could be causing 'false positive' reactions in a gel test that you wouldn't get in a tube IAT (because of the wash phase of the tube IAT). Just a thought.
  14. John Eggington
    Don't worry, Malcolm, I know you weren't disputing...and your presumption is correct.
  15. John Eggington
    This interpretation came from the 'highest authority' (I didn't come up with it myself!) :eyepoppin
  16. John Eggington
    I agree that, as I said, the reported phenotypes do make it less likely (our family were reported as being Mum 'CdeS/cDe', Dad 'CDe/cDe' and Baby 'CdeS/cDe').
  17. John Eggington
    Could the antibody be anti-Ce, rather than anti-C? The patient could have the CeS (can't manage superscript!) geno/phenotype, but it would mean that this patient would have to be 'homozygous' (sorry, Malcolm) for this rare type or carry a Rh 'deletion' as well as CeS (as the patient typed C+c-), which seems a bit unlikley! We encountered a CeS patient, and her family, some years ago that through up some odd 'probable genotypes', but all would have been C+c+ (the patient also had anti-E, anti-CE and anti-Jkb).
  18. John Eggington
    I see the Mail got a photo of you, to go with your letter. When did you shave off your moustache?
  19. John Eggington
    I think that SCD stands for 'Sickle Cell Disease', in this case.
  20. John Eggington
    Have you considered the action of passively acquired anti-B, from one of the group A units? How much plasma is usually left on your PRBCs? Are they tested for the presence of 'high titre' ABO haemolysins? Patients with a 'small' red cell volume (e.g., children) are more susceptable to the action of residual ABO antibodies than patients with a 'large' red cell volume (e.g., adults), even if units were labelled as 'HT-'.
  21. John Eggington
    His name wasn't Henry, was it?
  22. John Eggington
    In the same paper (from a history journal), the authors also propose that Henry had 'McLeod syndrome'. This, they say, would account for the 'symptoms' of his 'later years'. Would this mean that an, apparently (if not genetically), K- father would have produced K+ foetuses, that were subsequently affected by anti-K? How unluck can you get!?
  23. John Eggington
    Some have suggested that D ag density may 'vary' during pregnancy. This would explain a few things, but I'm yet to be convined (now someone will post data ti confirm this!). I'm more inclined to think that the reactions of 'weak D's' are more more senstive to small variations in test parameters; different batches of the same reagent, a minute more or less in incubation time, different operators, etc. Is this patient C or E positive? This might give a clue as to whether the patient is 'weak D' (not forgetting testing against a panel of anti-D's or molecular investigations).
  24. John Eggington
    You are quite right, Rasmi. My post was an awkward way of suggesting that id-ing the antibody first may help to explain the result (the original post did not state that an id had been done)
  25. John Eggington
    Assuming it is the same patient; doe she have any condition that could be associated with 'loss' of ABO antigens? Do you use different technologies? Could you get a sample and retest yourself? An explanation for the difference may help you decide what to do.
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