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yan xia

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Everything posted by yan xia

  1. Here is a follow up. The baby had tested with anti-A on 27, April and transfused with O washed cells the same day, but on 10, May she had no anti-A and received A type packed red cells with no transfusion reaction. She has stoped feeding on her mother's milk for 14 days. I tried to persuade her mother to do some tests. The results came out and she has no anemia, with normal reticulocyte count and percentage. Her bilirubin and LDH are normal too. But she has not tested her haptoglobin. She has not received any blood transfusion and IVIG. She just diagnosed with slight anemia during pregnancy and after birth. She had taken iron supplements during pregnancy,. This is her eventh pregnancies and the third baby, she had several miscarriages. She told me her case seems like a mystery both to her and the doctors she know. She just want to know if she is ok and the baby will be healthy in the future.
  2. The baby is discharged now, we cannot test the mother anymore, what a pity.
  3. She is still breast feeding the baby, and looks healthy.
  4. Thank you very much, Arno. Only one question left, why does the mom asymptomatic even with auto anti-A. We have encountered another case of auto anti-A, that one need transfusion.
  5. Thanks, Malcom. 1. I am not sure it is.anti-A, not.anti-A1. I mathed 5 A donors with the patient and the reactions.are all positive(Maybe they all A1). It is my fault, I need to add A2 cells to make sure about it. 2. I searched about the FORS1 online, there are few papers I can find. I will try my books tomorrow. This.is the.first time I read this antigen. Is there any cross reaction between it and A( or A1) antigen? 3. There is an idea just poped on my mind, it maybe Tn. But I don't know if Tn can give so strong reaction with monoconal anti-A reagent.
  6. No, He has got nothing above. I guess the antobodies come from the mom, maybe from breast breeding , but have not heard about it before. Will the milk origined anotibodies come into the blood stream and be IgG?
  7. Thanks, sbbguy. At first I thought maybe the mom is A2 type, too. But she is A1 type with pos DAT due to IgG. I feel so confused.
  8. I have encountered a case, there was a 10 month baby boy, he was A type, but there was anti-A in his serum and on his red cells we also eluated anti-A. His mom was A type with auto anti-A. 1.I remember the books say maternal origin antibodies will disappear 6 monthes after birth, maybe the books are lying😃 or there are some other reasons. He was breast feeded. 2.His mom looks healthy even with auto anti-A, but the baby developed hemolysis, why? Thanks in advance for your help.
  9. I was wondering why does she express D pos, if the allele can not encode D?
  10. 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?
  11. For resuming transfusion, do you mean resume the blood which caused reaction or another unit of blood?
  12. "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.
  13. 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
  14. We require the reverse type to be 2+ or stronger in tube, because weaker reaction can mean subgroup or weak immunoglobulin.
  15. 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.)
  16. 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.
  17. 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.
  18. 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.
  19. 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.
  20. 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.
  21. 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.
  22. or there are unexpected antibody/antibodies in the patient's plasma.
  23. That was new to me, is it because the auto-cells are antigen-depressed by the autoantibodies or some other reasons?
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