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Rh-fan

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Everything posted by Rh-fan

  1. We have had the same 2 times. But then was the father K+ k- and the child K-k+. So I think I know the answer, in both our cases it were new versions of this geno/phenotype. Peter
  2. Malcolm/Liz and the others, The DNA took a bit more time then I aspected, but I have the total of results. She has 2 RHD allels, one normal and the other is a r's allel (expressing no RhD but a variant of C and VS). In the RHCE we now see only an ces (c, e and VS) allel and a normal ce. The antibody was non reactive with Rh null and also not reactive with -D- so I was affraid of an anti Hr0-like antibody, but with the normal RHce allels there will not be an allo anti Hr0-like. SO for now we have to stick with auto antibodies. But still strnage that the auto control is weaker. Peter
  3. Was the autocontrole positive or negative? Negative RhD variant. Positive it can be a variant or an auto anti D, repeat the auto contole 3 months after the last transfusion. Peter
  4. The location of TSEN on GPB is close to the location of S. Depending on the reagent used it is possible that you can type the S as being negative. The expression of U is also not affected by the presence of TSEN. Also GPA is not always affected by TSEN, so therefore the M/N expression is normal. I do not know fore sure if the presence of TSEN (homozygous) can lead to the absence of an HFA, so I do not know if you need special donor blood. Peter
  5. Can it be an BI (combination) antibody, only reactive with cells expressing B and I antigen, and maybe the I antigen of the patient is weakend. Can you test other B cells from adults and cord blood at 16oC?
  6. That would make me very happy. But first we do the absorption experiments to see if it is Fyb or Fy3, maybe then we can do a MAIEA with monoclonals Fy3 and Fy6. Keep you informed
  7. I have seen this kind of situation. 4 patient with an auto anti D, in 3 different hospitals. They all received an organ from the same donor and this donor had a strong anti D. It took some time to see the connection. Because 2 of your 3 are pregnant I dont think your cases can be due to organ transplant. Peter
  8. No problem, I hope the end of this day to have more info.
  9. That is what I am afraid of. After transfusion the antibodies become stronger. The antibody has Rh17 (like) specificity (non reactive with RhNull and -D- cells), but this is also common in AIHA. We are now doing sequencing for RHCE to see if this patient is lacking a high frequent Rh antigen.
  10. We have a patient with the Fya-b- phenotype, on DNA she is FYBB and homozygous for the GATA1 mutation. So we can expect an anti Fya. The serum is reactive with all cells expressing Fya and/or Fyb antigens, and non reactive with Fya-b- cells (beside the ones that are K positive). We expect an anti Fy3 but in gel this antibody is only reactive in LISS (IAT) but not in Papaine LISS (IAT), therefore more pointing to anti Fyb. We have never seen an anti Fya + anti Fyb in such a patient. We are goint ot absorb the serum with cells expressing only Fya and with cells only expressing Fyb and test the absorbed serum and the eluate of the absorption cells, any other suggestions? Peter
  11. We have a Sickle patient with antibodies reactive with all panel cells but is weaker with the patient cells. There has been multiple transfusions. After washing with 3% saline (to remove the donorcells) we performd a DAT and this was also positive indicating auto antibodies. Has anyone seen such a weaker reaction with the patient cells in Sickle patients? Peter
  12. A mixture of enzyme (papaine) and DTT (a chemical not a enzyme) works the best (according to Petz), it will ZAPP that antibodies from the cells. Peter
  13. For real HTLA antibodies, I am not affraid. I am affraid of those that mimic a HTLA and are a antibody that can cause a reaction. The reason to specify a HTLA is that only then you are sure that it will not cause a reaction. Therefor weak reactive but with a high titer is not enough to clame a HTLA, there are lot of antibodies that can cause red cell destruction but mimic an HTLA (the Dombrock, Cromer, Lutheran, Cartwright, ...) Peter
  14. When there is another donation from her or the brother, and you have no clue what to do with the red cells from the buffy-coat, just think of those fine forum members (or the SCARF group).
  15. I hope that Malcolm and you are talking about this, not recently transfused, patient. In patients that have been transfused (the last 3 months) a positive DAT can be clinical significant for transfusion. Peter
  16. I asume that you have found the anti D in a panel with untreated cells, and have excluded all other antibodies. I think that the reactions with ficin treated cells are coused by aspecific auto antibodies (if the patient cells are also reactive(after treatment with ficin)), the presence of this kind of autoantibodies is no problem. Just perform cross-match with RhD neg donor blood. Do you have (for my own interrest) further information on the type of RhD variant this patient has? Peter
  17. Rh-fan

    AB0 grouping

    I have seen a lot of anti Vel antibodies and those where never this strong (but in serology everything is possible). These kind of reactions more fit I or P, and then is anti P (+Pk) more common than anti I (in my experience).
  18. Rh-fan

    AB0 grouping

    Originally Posted by Nisar I never saw aut0 c0ntr0l negative DAT p0sitive. Thank y0u Sir It also depends on the technic used. If you perform a column gel test, then the medium is the same for the DAT and for the auto controle, so when your DAT is pos in that gel, if you add also serum/plasma (auto controle) is must be positive also. Other way around is more common, that with the adition of serum/plasma you have a stronger reaction.
  19. Rh-fan

    AB0 grouping

    Why do you think of DL antibodies when the reactions are so strong. Most DL antibodies I have seen are only weak reactive in normal technics, and mostly neg. Peter PS Malcolm, last week our lab found a Kell null patient with anti K5 (or Ktotal or Ku), just on a day that I am not in the lab.
  20. If you have a strong reactive anti Fya, and a Fya pos cell is not reactive, there is a change that the wrong cell is used, and therefore you can not use that cell for further exclusion (because the typing is not sure). If it is a missing reaction with a weak antibody (and the non-reactivity can be explaned) then I would use the cell for further ruling out. It all depends on the situation. (just as everything in this field) Peter
  21. Rh-fan

    AB0 grouping

    Sounds like an antibody to a antigen with a high frequenty. And the antibody is an IgM (also reactive at RT). My first guess would be; I (could stil be auto), P (with or with out Pk) or Kp( (mostly also IgM fraction). This will take a lot of further investigation, interesting but difficult case. Good luck, Peter
  22. I agree, in these kind cases first look to the age, but in this case it is a donor (so between 18 and 70), and a healty one also. So that is the reason for me to step over to the more unicorn. Last friday we had a pregnant woman with a group O, with strong anti A and no anti B (also not at 16oC). Today we performed absorption elution with anti B (a positive result) and a minor-cell population test (also positive). These results suggested a Group O with B chimera. Peter
  23. Sounds like a chimera (the absence of anti B is nopt normal for a donor, for a patient it is seen more), where the brother or sister is B. I am interested in the folow up. Peter
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