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Everything posted by Bb_in_the_rain

  1. 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)?
  2. 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.
  3. 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!!
  4. Bb_in_the_rain


    I saw a Netflix documentary
  5. 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.
  6. 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!!
  7. 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.
  8. 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)
  9. 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?
  10. I agree with titer value. As the physicians prefer seeing a numerical value, it is hard to turn down an order for titer. I think there were other publication out there eliciting the association of Mycoplasma Pneumonae infection to anti-I titer and Infectious Mono associated with anti-i titer, etc. it is really really hard to not perform titer when physician comes to the hospital labs with such requests. I rather offer titer and thermal amplitude as one test so that both will be performed.
  11. It may be more efficient workflow to perform titer at 4 different temperature, 22C, 30C, 37C and read them after 1 hour incubation. That way, you get your titer and thermal amplitude done in one shot and also see the titer difference between your 3 different temperature. Also, your order physician does not have a choice but to perform titer and thermal amplitude as they are offered as one test.
  12. Patient was historically typed as A postive in Korea. Red cells typing Anti-A= 4+, anti-B=3 ( same strength with 2 different sources of antisera) One of the Anti-B includes ES4 clone and one of the Anti-A includes MHO4 clone. Tested with 3 more sources of monoclonal and 2 more sources of polyclonal anti-B. (I cannot find the clone numbers on them) 2 of 3 monoclonal anti-B reacted 2+ and 1 of 3 monoclonal anti-B was negative. 1 of 2 poly anti-B reacted 2+, and the other was negative. The patient cells were also tested with 2 sources of fresh AB plasma (10 minute incubation, room temperature) to exclude polyagglutination or B(A) ; they were both negative Autocontrol was also negative (10 minute incubation, room temperature). Please let me know what you think about this case.
  13. I much rather perform titer and thermal amplitude as outlined in Petz and Garratty's, Immune Hemolytic Anemias textbook. And also, Thermal Amplitude Test with albumin has much higher positive predictive value per Table 5-14 in the textbook. So if the test were to be overhauled, I would perform titer and thermal amplitude, and supplement thermal amplitude testing with album if necessary.
  14. Has anybody look in maternal breast milk for IgG antibody in cases of prolonged HDFN? I just come across this article and found it to be very interesting. Leonard et al, "Identification of Red Cell Antibody in Maternal Breast Milk Implicated in Prolonged Hemolytic Disease of Fetus and Newborn"
  15. Please let me know if you would like me to do more "mock-up cases" with RHCE variants. I can look for some good ones. I think it is fun to interact with case studies here. (I mean it is quite fun to pick Malcolm's brain and learn from him... cough cough).
  16. No I did not do that. Great idea!! If I can find my eluate, I should...
  17. Haha. I copied that info right out the demographic sheet and typed "not pregnant or transfused" not thinking much about his gender. opps! I am surprised by this positive eluate as well. I was just "shooting in the dark" and performed the eluate blindly when I saw these reactions with e+ cells (since I saw way too much warm autoantibodies with relative anti-e specificity). Further serology results are- this antibody is weakly reactive w+ with 1 of 3 hrB- cells tested (all of them are C-e+) it is weakly reactive with 1 of 2 hrS- cells tested (both of them are C-e+) Genomic sequencing results in RHD gene (sequenced 1-10 exons) the following heterozygote changes were observed- c.410C>T, c.455A>C, c602C>G, c667T>G and 819G>A - predicted to be RHD*DIIIa or RHD*DAR3.01 A normal D gene was also observed. So the prediction was a normal D gene in Trans position to RHD*DIIIa heterozygote. Since RHD gene was associated with altered RHCE gene, RHCE sequencing was reflexed (sequenced 1-10 exons and some intronic flanking regions) variants - c.48G>C, c.676G>C, c733C>G, c.1006G>T - predicted to be RHCE*ceVS.03 in trans with RHCE*cE (because serologic phenotype is D+C-E+c+e+) So when I looked up RHCE*ceVS.03, I found it to be associated to V-VS+hrB-. So your suspicion is right on the spot! It is most likely anti-hrB!! At this point anti-C was not excluded but the transfusion recommendation was R2R2 blood, so we are ok here. In terms of eluate, it most likely is warm auto antibody with relative anti-D specificity due to the presence of normal D gene in hetrozygote expression. I am still puzzled by a negative auto-control. However since the antibody was eluated out of his untransfused red cells, so I can accept that it is most likely an autoantibody. Please let me know what your thoughts are and any further results that you may need. Hope this is a good case study!
  18. Ok It has been a while since this case was posted, I think we have given enough time for transfusion services folks to participate. Lets hear from the reference folks! I am so excited to see what your thoughts are!
  19. Very well done! I would suspect something along this line as well. You are very very close!! Lets hear from reference lab folks to see what their thoughts are. I will share more information on this patient's work up later.
  20. Correction: Eluate is reactive with DTT-treated cells.
  21. Will sure do! This look so good because it is not a real-life case that I just worked on. (cough cough)
  22. Sorry I missed this one. U antigen is ficin-resistant, therefore this cannot be anti-U
  23. Ok Lets try the first one here. Background - A 31 year old African American male, Bpos, C-E+c+e+K-S-s+Fya+Fyb-Jka+Jkb+. This patient was not previously transfused or pregnant. Plasma reactions tested with 18 cells antibody panel and the reactions are....... 3+ reactions with C+e+ cells, 1+ reaction with C-e+ cells, negative with e- cells AutoControl was negative. Reactivity in DTT-treated cells were similar to that of untreated cells. The reactivity with ficin-treated cells were enhanced, C+e+cells 4+, C-e+cells 3+, negative with e- cells Eluate reacted 1+ with D- cells, 3+ with D+ cells. non-reactive with DTT-treated cells cord cells yielded similar reactivity as that of the adult. Panagglutination 4+ was observed with ficin-treated cells. What are the possible antibodies that the patient can have? If genomic testing is warranted, I will be back next week to tell you what genomic testing the results are. Lets give a chance for the transfusion service folks to work on it before reference lab folks share their wisdom regarding this case.
  24. I have heard a couple of different clones coming from Seattle Hospitals (Hu5F9-G4 and ALX148). Watch out for the clone numbers when you work on patients on anti-CD47. It might make a big difference whether or not you can use Immucor anti-IgG to rule out your underlying alloantibodies.
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