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Bb_in_the_rain

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About Bb_in_the_rain

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    Junior Member
  • Birthday 07/23/1982

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    Female
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    I am obsessed with actions going on red cell surface
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    Seattle, WA
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    IRL tech
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    Thandar Aye

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  1. Hello, I just would like to share this great news with you all so you won't miss out. http://blog.aabb.org/appliedbloodgroupserology/
  2. Maybe if you have ficin or papain, you can treat the C+ cells that were originally negative to see if your strange "anti-C" pops up? If the patient is an African American, I would consider the presence of variant RHCE gene.
  3. Please be sure to recruit the brother as blood donor as he is a valuable donor.
  4. Are you using solid phase by any chance? We have seen solid phase does that, since a lot of our hospital used solid phase method. When that happened, we usually look for antibodies using PeG Tube method or by testing ficin-treated cells. We were usually able to find the suspected antibod(-ies) except for Kidd antibodies. You may be looking at some method-dependent antibody? Anti-C in your 2nd sample may be stronger than that in your first sample? What is the patient's ethinicity? Is the patient e- or e+? I am also thinking about anti-Ce like antibodies if you see this anti-C reacting stronger with e+ cells than e- cells.
  5. Is Rh(D) a correct terminology to describe D antigen? I saw this notation time and time and make me wonder "why not Rh(C), Rh(E)..etc.." It does not seem to be fair that only the D antigen get this "Rh" terminology in front of the antigen but not the whole other 40+ antigens in the Rh system
  6. You were right about "although I have my doubts about that being a coincidence." It was not a coincidence. The Sanger sequencing on this lady indicated that the patient is cisAB.01/O.01. In Geoff Daniel's Human Blood Group text book, page 43, described that sera from cis AB people almost always contain weak anti-B. This is a great learning case indeed! Have anybody tried testing acidified anti-B with known cisAB cells? I am wondering if acidified anti-B would be non-reactive with cisAB in addition to A(B)?
  7. We usually try to collect autologous unit if she can donate. If mom cannot donate, you can also send out the sample for monocyte mono layer assay (MMA) to see if anti-Dib is clinically significant or if you can transfuse this patient Di(b+), had she bleed during her C section. (This test is a test that predict hemolytic potential, just like reminiscence assay performed in Europe as the journal that Malcolm has describe above. Here in the US, we used MMA assay instead of CLT). We also perform titer on the antibodies to predict potential HDFN, which is supervised by our Medical Director. (titer value more than 2 tubes difference in consecutive sample collected within a month is considered critical value here). Hope this is helpful.
  8. Wow! things must come in a bundle. This week, we just had a case with a broadly specific antibody, non reactive with K0 cells. K-k-Kpa-Kpb- and SNP genotyping predicted a presence of KEL gene. We are on the same page with you on our patient as well, in the process of sequencing.. It will be very interesting to see the sequencing results. Please keep us posted when your sequencing is done. Our patient is a bleeder, so we gave one Ko unit. yike!!
  9. Bb_in_the_rain

    Theranos

    I saw a Netflix documentary
  10. Hello, Scott, I have a few questions about this case. 1) What is the eluate result that "matched the original antibody ID"? Is it panagglutination or anti-D in eluate? 2) How many sources of anti-D did you use to type your patient? We use up to 3 or 4 sources in this lab if we have such problem in this lab. Here are the things that I usually do to figure out if anti-D is that of auto- or allo- .. 1) exclude the possibility of RhoGm or IVIG adminstration 2) Perform D typing on the patient's red cells using different sources of anti-D. (we usually have 4 or 5 sources). If D reactivity is found variable positive and negative reactions with different clones, perform genomic testing to exclude partial/variant D antigen. 3) If the patient is elderly male and recently transfused with D+ blood (or if you see mixed field in the D typing), perform cell separation by density centrifugation, perform D typing and auto control using retic-rich cells. 4) If the patient is DAT positive, perform EGA or CDP treatment, test EGA, CDP treated cells with plasma and eluate. 5) Lastly, test plasma and/or eluate (wherever you are seeing anti-D) with DTT-treated red cells and cord cells to exclude or confirm anti-LW. Please let me know if there is anything else to add to this list. Hope this is helpful.
  11. I have tested the patient's cells with 2 sources of acidified anti-B as your guidance. After 5 minute incubation, the patient's cells were non-reactive with one source of anti-B and 1+ with the other source. I used AB donor cells as control and they both remained 4+. I think I can accept that this is an A(B). My question is Why do we see this in the prenatal patient without signs of infection? I thought acquired B was found in those with cancer and infections? Does it mean that she has an abnormal galactosyl transferase? Thank you very much for your guidance and walking me through this case. I should have listened when the experts said it was acq-B!!! Thank you so much again for your guidance!!
  12. Thank you very much for your guidance and advises. I would like to try acidified sera using 1M HCl to repeat typing of this patient's cells. I am wondering what source of anti-B would you acidify? I assume I would acidify the clones that was previously reactive (including the ones with ESO4 clone and polyclonal anti-B)? So the purpose of testing with acidified anti-B is to re-acetylate the A(B) into A antigen. Is that correct? So I should expect clones if anti-B that were previously reactive to be negative with the patient's cells after being acidified. I think sending it to another Reference is a good option; however, the submitting hospital has decided to give Group A blood and not to further investigate that. So we are left with the tools that we have here in this lab. I hope the acidified anti-B will give me a clue to whether it is A(B) or not. I will keep you guys updated after I am done with the test. With regard to genotyping, if (hypothetically) speaking (and I do not mean to be picky), if the gene that transcribed B transferase is detected, it could mean this is a subgroup of B rather than a A(B)? I might be listening to horsehoof and thinking of Zebra. Somehow, I am not convinced that this is an Acquired-B... The diagnostic does not make sense and also one out of 2 polyclonal anti-B is moderately reactive, and both ES4 and B0001 clones were strongly reactive (3+). It is not quite adding up in my mind. I thought I should see somewhat of the difference in reactivity between ES4 and other clones.
  13. If we see cases of CAD with titer <64 that is reactive at 30C with or without albumin, that would be a perfect opportunity to start a conversation with reference to Garratty G et al, The correlation of cold agglutinin titrations in saline and albumin with haemolytic anemia, BrJ Haemat 1977;35, along with the paper that you have cited above (which I am printing out and filing it in my "good hemolytic anemia reference" folder now)
  14. Opps (again), my apology for incomplete information. The patient is pregnant and no infection was noted. The plasma was non-reactive with A cells and reactive (2+) with B cells. Even though the serology initially "smells" to me like an acquired B, the diagnostic is pregnancy with no signs of infection. Moreover, only 1 of the 2 known monoclonal anti-B is confirmed to include ES4 clone and the other includes B005 clone, yet both of them were reactive strongly (3+). So I am really puzzle as to whether it is A(B) or simply a subgroup of B. It will be nice to have an example of cells from an individual with acquired-B to test it out, but we do not have these. If the reactivity is due to tartrazine in anti-B, I would see a positive reaction with all 7 anti-B that I have tested (as they certain are yellow and I assume they all have tartrazine in them). But that was not the case.....only 5 of 7 anti-B were reactive. My question is As I saw AcqB characterized as a polyagglutination in Issitt and Anstee's textbook (table 42-3), does it mean that I can exclude Acq-B based on the non-reactivity with Fresh AB plasma? Would that be a good idea to send it to genomic lab to see if there is any B-transferase present in this patient?
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