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    • By Neil Blumberg
      Research letter in NEJM describes our findings.  https://www.nejm.org/doi/full/10.1056/NEJMc2034764?fbclid=IwAR1BQRvpaHBAMDaHxCPY07xBjPQHlIHoJCOmpjoT_pBNvQsV7pzzDVdLYaY
      Table 1. HLA-Matched Platelets as a Percentage of All Platelet Transfusions, According to the Initiation of Other Protocols.*
      Protocol and Timing of Initiation No. of Years HLA-Matched Platelets Difference from Previous Period (95% CI)     median % (IQR) percentage points No leukoreduction and no ABO matching (1985–1990) 6 12.5 (4.2–13.7) NA Leukoreduction and ABO matching for patients with leukemia and MDS (1991–1999)† 5 2.9 (2.0–3.6) 9.6 (9.4–9.8) Universal leukoreduction (2001–2004) 4 1.4 (1.1–2.0) 1.5 (1.4–1.6) Universal ABO matching (2005–2015) 11 0.4 (0.2–0.8) 1.0 (1.0–1.1) Pathogen reduction of platelets (2016–2019)‡ 4 1.7 (0.8–1.8) ND  
      The practical fact is that this can only be implemented by medical technologists, not physicians, and this is a daunting prospect.  But the reality is that ABO mismatched platelet transfusions probably exacerbate rather than prevent bleeding, so waiting for ABO identical is likely better than just transfusing whatever is available.  This is going to require a major change of approach because the (incorrect) dogma, based upon no data, is that ABO doesn't matter for platelets.
      I understand why many people's instant reaction is this is not feasible. But it is once technical experts in your transfusion service figure out how to implement it gradually. In our randomized trial back in 1993 (see ref below), the ABO identical group only required <50% the number of platelet transfusions (every other day instead of every day on average) compared with the usual first in, first out regardless of ABO type group. ABO mismatched transfusions create a hostile environment with gigantic immune complexes that compromise subsequent transfusion that may be ABO identical. Avoiding this is key.
      Our suggestion is to start gradually. Pick new previously untransfused patients with aplastic anemia and good prognosis AML (young, favorable or normal cytogenetics), groups O or A, and start with them. Eminently doable since your platelet supply is 45% O and 40% A, just like your patients, on average. Get the hang of doing this and prioritizing ABO for at least some patients. Once you get this in place, extending it to other patients and eventually all patients can happen. We use washed O or A platelets and red cells for group B and AB recipients when we don't have group B or AB platelets. No increase in bleeding and fewer transfusion reactions, lung injury and congestive heart failure (what we call TRALI and TACO).
      In the end, you have more surviving patients and fewer headaches and transfuse many fewer platelets per patient and essentially no HLA if you can get your referring hospitals to stop our current standard harmful practices. Godspeed. Heal JM, Rowe JM, McMican A, Masel D, Finke C, Blumberg N. The role of ABO matching in platelet transfusion. Eur J Haematol. 1993 Feb;50(2):110-7. doi: 10.1111/j.1600-0609.1993.tb00150.x. PMID: 8440356.
      Happy to have discussions or visitors so our technical experts can show you how it is feasible.
    • By Lucas Souza
      Hi, guys 
      How are you?
      So, i'm doing a experiment where i'm testing two titration methods, the tube test and the column agglutination technique.
      Now i have to analyze to know if they have statistical difference and what is the correlacion of the two methods, but I found it difficult to decide which statistical test to use.
      Do you have any thoughts on which statistical test I should use? T teste? Pearson?
      Below is the table with the samples and their endpoints, for example:
      PLASMA TUBE A GEL A  TUBE B GEL B 1 128 256 32 64 2 32 32 64 64 3 64 64 32 16 4 64 32 32 16 5 64 32 64 32 6 32 32 32 16 7 64 32 64 32 8 32 32 32 32 9 32 32 32 16 10 64 32 32 32 11 64 32 64 16 12 128 64 128 64 13 64 32 64 32 14 32 16 32 16 15 64 32 128 64 16 128 64 32 16 17 128 64 64 32 18 64 64 16 8 19 64 64 64 32 20 32 16 32 16  
      Thank you guys.
    • By WMMTSBB
      I had a patient that had an ABO discrepancy. Testing is as follows:
      anti-A: 4+, anti-B: 4+, A1 cell: 1+s, B cell: 4+, Screen cells I.S.: all negative, LISS 37: all negative, poly AHG: all negative. Group O donors I.S.: negative, Group A donors: 1+ to 2+. Saline replacement for A1 and group A donors: negative. Microscopically, the A1 and A donors do not really appear as rouleaux. So the question is why do we see apparent rouleaux only with the A cells and not the screening cells?
    • By aafrin
      We had a 46 year old male health check patient who has never been transfused before come for blood grouping. He knows his blood group previously as O Rh Positive. Our results were as follows:
      Tube Test
      BioRad Gel
      1-2+ mf
      -D (igG+IgM)
      -D (IgM)
      A1 Lectin
      H Lectin
      A1 Cells
      1-2+ at RT, >2+ at 37 C
      w-1+ at RT & 37C
      B Cells
      O Cells
      A2 Cells
      We repeated the blood group with two other manufacturer’s anti-sera. One anti-sera gave the same result as our tube test result, but with the other anti-sera the result with anti-A was negative.
      What should we report the blood group as? O or subgroup of A? Kindly help.
    • By Jermin
      This is a very silly question, but I think I have confused myself. Why is it that when Rh phenotyping, we do not require incubation step, but when looking for antibodies, we need incubation to detect Rh antibodies? 
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