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StevenB last won the day on April 29 2019

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  • Birthday 03/31/1959

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  1. In my experience, the two most common causes of weak reactivity in Gel and negative reactions in tube are either rouleaux (no, not my pet "go to", but still applicable) or reactivity seen only with the manufacturer's prepared 0.8% reagent cells. We encounter this fairly routinely: Hospital gets Gel reactivity, sends it in, we do a selected panel making our own 0.8% suspensions from various manufactures, get a negative Gel test, test with a manufacture's 0.8% panel and get reactivity. Basically, reactivity dependent upon something in the manufacture's product. Kinda similar to a "LISS panagglutin".
  2. It's not uncommon to see rouleaux interference in Gel testing but it's not something we see frequently. The crossmatch question is interesting: Technically, the screen is negative for alloantibody reactivity so I think you'd be able to follow your procedure for that result. However, with the immediate spin crossmatch, you may have to perform a saline replacement to obtain a "compatible" unit. I wouldn't want to assume an incompatible IS crossmatch is due to the rouleaux without confirming that.
  3. Auto directed at senescent red cells can show mixed-field reactivity. With your additional information, kinda seems the most likely cause of your observed reactions. Garrartty and Petz discuss this in Immune Hemolytic Anemias, 2nd ed., pg 243. The issue with PEG adsorptions is they may work too well, potentially resulting in the loss of weak (low titered) antibodies. Of course, that could happen with any adsorption, I guess, but with the samples we see in our ref. lab, it is the last technique we would use to adsorb out an autoantibody. I'm not saying you are wrong to use it. I'm just saying it has it's drawbacks;
  4. Hmmm.... Not too fond of PEG adsorptions; did it truly adsorb the antibody out or was the antibody lost in the precipitate? Pondering if you have two different things happening: Rouleaux in your reverse (I'm assuming the reverse typing with the A1 and A2 cells was not 3+ or 4+....were the majority of the cells at the bottom or top?) and Gel testing with an alloantibody in PEG? With 4 drops of plasma, you could eliminate the rouleaux as an issue. Thinking out loud....negative DAT, negative autocontrol usually does not equal an autoantibody (one of the reasons I'm cautious about the PEG adsorption resullts), although it is well known that "antibodies don't read books". In the tube tests, how strong was the initial spin prior to adding the PEG? I know I'm reaching a bit on the rouleaux, but I have always found it beneficial to not overlook the simplest explanation before moving on to the more obscure. Is there any additional sample in hematology that you could play with?
  5. DAT performed? Neg autocontrol does not always equal a negative DAT. How strong was the mixed-field and was the antibody screen in tube or Gel? PEG prewarm in tube not mf?
  6. Ruling out on zygosity....I'm assuming you are referring to "crossing-out" on heterozygous cells, as opposed to homozygous cells, that are nonreactive in Gel testing?
  7. I'm not aware of any quality control requirements for weak D testing. Looking at two different manufacturer's inserts for anti-D, I did not see any requirements for quality control testing for weak D. In addition, our daily quality control of the anti-D reagent does not involve testing a known weak D. It will be interesting to see if anybody else knows of a requirement for weak D testing.
  8. Hmmm... Never have used the prewarm technique to resolve a forward type. Just "thinking out loud": In the scenario of a cold interfering autoantibody, prewarming is typically used to prevent "free" cold autoantibody from binding onto red cells causing unwanted reactivity. In testing a patient's red cells, there should be no "free" autoantibody present if the sample was adequately washed. The issue with the forward type is the antibody that is already bound to the patient's cells. If warm washing did not remove it, then I'm not sure how prewarming the forward type would be more effective. If it works though, great! Whatever it takes to resolve ABO discrepancies due to cold autoantibody interference, I'm for it! We warm wash the patient's cells with 37C saline. If needed, move to a form of heat elution (incubate or even wash with 40-45C saline) and if that's not effective, treat the cells with 0.01M DTT (treated controls must be included). Reverse type resolution: I- cells, prewarm at 37C spin, and just recently, resolved a back type issue with testing at 37C/AHG with heavy chain specific anti-IgG. I'm sure I don't need to say this, but I'm going to anyway: In a situation where you have an unresolved ABO discrepancy and you have to transfuse, don't guess. Give group O red cells.
  9. Applied Blood Group Serology, 4th Ed. chapter 6, pages 129-132 addresses complement activation by blood group antibodies. It's an interesting read. This is the verbiage we use with a recently transfused patient that has demonstrated a positive DAT, a new antibody in the eluate and perhaps in the plasma/serum: "Serologic results, including a positive DAT due to IgG and complement (C3d), support the occurrence of a delayed serologic transfusion reaction." The DAT portion may be edited as needed. We're not making a diagnosis, but simply altering the physician to its possibility.
  10. Lol...in my opinion, I should look at the screen results more closely. #2 can work...if serum is tested and polyspecific AHG is used, neither of which is a given anymore though.
  11. A few antibodies that can cause the screen results that you showed include; I, M, dosing M, Lea, Leb, P1, IH in a group A individual, newly developing multiple antibodies in a recently transfused patient all come to mind. I'm sure there may be more. In my opinion, coming up with answer #2 with the information provided is a bit of a stretch.
  12. No resources, just experience... we perform what we call "alloadsorptions" on a regular basis.
  13. Any questions Ward_X or are you "good to go"?
  14. Just curious...did you serologically confirm the Rh phenotype of the reagent cell in question?
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