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yan xia

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Everything posted by yan xia

  1. Thanks for your explanation. I guess there must be some measures be taken to prevent the opening system to be contaminated, would you please share it with me?
  2. For resuming transfusion, do you mean resume the blood which caused reaction or another unit of blood?
  3. "2.7.6 Ael Under usual conditions Ael cells are not agglutinated by anti-A or -A,B, although they do bind these anti bodies, as demonstrated by adsorption and elution [298,337–339]. Saliva from Ael secretors contains H, but no A substance. Serum from Ael individuals usually contains anti-A1 and may also contain an anti body that agglutinates A2 cells [337,339]. No A transferase has been detected in Ael serum or red cell membranes [232,287–289]. Serum H-transferase is weaker than that found in A1 or A2 serum [289]. No example of Ael was found in testing 150000 French blood donors [283], but fifive were found among 400000 Chinese from Taiwan [328]. Ael appears to be inherited as a rare gene at the ABO locus [337–339]. As a result of allelic enhancement (Section 2.10.2), AelB cells may be weakly agglutinated by some mono clonal anti-A and may resemble B(A) phenotype [340]" The text above comes from Danels' HUMAN BLOOD GROUPS the second edition, page 36 If we just look at the forward group , we may identify it as type O, but because it has weaker anti-A, we do think it is not a normal reaction ,so we will do further investigation ,and then find out it has weak A antigens. It is important for transfusion and organ transplantation.
  4. I'm with galvania, we have identified a lot of subgroup patients based on the weaker reverse reactions. Such as A2,A3, Ax, Ael, Aend, and the same the Bsubgroup
  5. We require the reverse type to be 2+ or stronger in tube, because weaker reaction can mean subgroup or weak immunoglobulin.
  6. The possible antobodies are anti-E, V,K, Jsa and Lua, then I will pick some cells to test it and antigen typing the patient to confirm it.( Jsa and Lua pos cells are quite rare, so it is hard to get them, luckily they will not cause rapid hemolysis after transfusion, as for anti-V, the clinical significance is unknown.)
  7. From the second panel you posted, I think there are some specificity in the 37 and IAT phase, so my guessing it that there are not only cold auto that interfere with the reaction. I will do an auto-absorption in 4 drgess first( If this patient has not received transfused red cells pack in three months), then run panel using tube IAT. Just personal opinion, I am looking forward to learn from here.
  8. According to Human Blood Groups by Geoff Daniels, second edition, 40-42 Most B(A) have strong or normal B antigens, and most CisAB have weaker B antigens.
  9. One person who I am very admired once said"There is no difference between CisAB and A(B)" I have the same question as Matthew. Since they have different names and there seems no intention to change, I guess there must be something different I do not know.
  10. It was decade ago, a nurse kindly gave the blood crossmatched for A to B after A passed away without having it . Because she thought they were both type O pos. Luckly, B had no transfusion reaction.
  11. There are a lot of brilliant explanations, I learned so much from here. My guess about the pos DAT is that if the DAT(IgM) is positive, then it may cause false positive result in the D testing. This is why when we test a sample which is AB Dpos, we will run a neg control for the forward typing.
  12. Is there any chance of the anti-B in the donor packed cells caused the heamolysis? Because the free antibodies attached to the patient's cells, complements actived and cells hemolysis, so there is no free anti-B detected after transfusion.
  13. or there are unexpected antibody/antibodies in the patient's plasma.
  14. That was new to me, is it because the auto-cells are antigen-depressed by the autoantibodies or some other reasons?
  15. The DAT and Auto control negative, do we need to do auto-adsorption?
  16. I am not sure about the difference between B(A) and AsubB, I always thought we define B(A) based on genotype not phenotype, and the AsubB maybe the genetic product of B(A).
  17. I guess there are two possibilities: 1.This patient is AsubB, the A antigen cannot be tested by some anti-A reagent. 2.This patient maybe has some antigen rather than A which is crossreacted with the component of the reacted reagent. solution are 1.How about test the patients' red cells against some B type human serum, please make sure that there are O cells as negtive control. The monoclonal reagents are not as complete as the human source polyclonal antibodies. 2.And to test the saliva for ABH substance in it( if the patient is a secretor). And do genotyping, just so expensive.
  18. I totally agree with all those briliant ideas, and there are some A subgroup have anti-A and anti-A1, such as Ax and Ael .
  19. I have a little confusion, why the previous auto tests are all neg, and the DAT is pos? The elution result is 4+, so I guess this DAT is IgG pos, and the anti-IgG in the prewarm test, the auto is neg. My not good English, I hope I understand and express it rightSorry for the interruption.
  20. Seems as warm autoantibodies which have a loose reaction temperature span, so they can interfere with the reverse typing. Because they are not cold auto, so cold autoadsorption does not work, and in the strict prewarm test, they still react.
  21. We use Ortho Biovue gel card, and I don't think rouleaux interfere much on the gel result, some MM patients have rouleux on tube, but gel results are good. In my experience, cold antibodies can do. Just personal opinion.
  22. Malcolm, may I ask what is Gm and Km, and why typing those can tell us if the one is passive or allo-anti-D? Thank you .
  23. Kidd system antibodies can bind complement. To investigate the reason, maybe you should do an elution, then test the eluate to see what specity /specities of the binding antibodies. Add fresh serum can strengthen the sensitivity of testing Kidd antibodies.
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