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StevenB

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About StevenB

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  • Birthday 03/31/1959

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  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. No resources, just experience... we perform what we call "alloadsorptions" on a regular basis.
  6. Any questions Ward_X or are you "good to go"?
  7. Just curious...did you serologically confirm the Rh phenotype of the reagent cell in question?
  8. In Applied Blood Group Serology, 4th edition, pg. 332, Issitt refers to a study by Shirley et al. on this very topic. The study concluded that 5 of 27 patients who had anti-E and only received E- units eventually made anti-c. They suggested this justified the expense and extra time needed to find units that were negative for both E and c. Issitt however, uses the findings to argue just the opposite, "Those of us (PDI...referring to himself) who believe the E- c- blood should be provided only after the patient has made both anti-E and anti-c, use the finding that none of the 5 patients in this study who made anti-c suffered a delayed transfusion reaction, to support their view." While the Technical Manual states the "some experts advocate for avoiding the transfusion of c positive blood in this situation" obviously, some experts do not. In an emergent situation, I don't feel the potential time delay in finding or ordering units that are E- and c- is justified when the patient has not demonstrated they have anti-c. In a routine situation, we recommend E- units, but quote the Technical Manual regarding this situation and let the customer make the decision.
  9. Lol...I like the way you think, Malcom, but I don't have control over those decisions. Being a reference lab though, we push our efforts when testing referred samples. Micro reads are part of our routine if the patient has been transfused or pregnant within the last 3 months. Testing in PEG however is optional and PEG is notorious for revealing micro reactivity which often can not be identified. Having said that, I have on many occasions identified micro only, clinically significant antibodies in PEG. Would I recommend a hospital blood bank read micro? No, I wouldn't.
  10. Thanks yan....the macro negative reaction in PEG at IAT was with the unadsorbed plasma and was tested with Immucor’s murine monoclonal Gamma Clone IgG. As Mabel pointed out, this reagent does not detect IgG4 and the anti-CD47 is....evidently.... an IgG4 antibody. In my hands, it was microscopic reactive so I believe in the future we will drop that read when faced with these patients.
  11. Mabel was kind enough to share this sample with our lab as we had not had the pleasure of seeing one of these. The sample was limited and it technically was not a referral, so my work was centered on getting to know anti-CD47. The patient forward typed as an A with no issues (I've heard the forward type can at times be affected), but reverse typed as an O, with 2+ reactivity in the A1 and A2 reverse cells. The patient typed Rh positive; no reactivity noted in the Rh control. The DAT was micro positive with poly specific AHG, heavy-chain IgG (HC) and C3, but was not interpret-able due to a micro positive saline control. Warm washing x4 with 37C saline resolved the positive saline control and still demonstrated micro reactions in the previously mentioned AHG sources. Interestingly, the reactivity was actually slightly stronger than the initial testing. Initial antibody testing was 2+ reactive in saline at initial spin, 3+ in saline at 37C spin (post 30 minute incubation) and 3-4+ reactive in saline at IAT with HC IgG, 3-4+ reactive in PEG at IAT (4+ reactions with the Rh negative cells tested as compared to 3+ reactivity with Rh positive cells; consistent with reports in literature), and 4+ reactive with papain treated cells (carryover reactivity was noted as a "no spin read" was 3+ and agglutination was noted prior to the addition of HC AHG). Testing with Immucor's murine monoclonal IgG Gamma Clone in PEG at IAT was macro negative, micro positive. Alloadsorption x2 (using 2 volumes of cells to one volume of plasma) onto papain-treated R1R1 and rr cells of known phenotypes (we usually do R1, R2 and r cells, but with the limited sample I dropped the R2 adsorption) removed the initial spin reactivity and confirmed the patient was group A. Alloadsorptions x3 were 1+ reactive in saline at 37C, and 3+ reactive at IAT using the HC IgG. x4 adsorptions yielded the same results. Out of curiosity, I did run a D-- cell with the x4 and it was nonreactive at 37C, but 2+ reactive at IAT. For fun, I performed titration studies on both the R1 and rr x4 adsorptions (saline, 60 minutes 37C incubation). Macro reactivity at 37C was noted at 1:32 in both samples, but technically they had a titer of 4 (1st observed 1+ reaction). At IAT, both samples had a titer of 16,384.... AFTER 4 adsorptions! A recent report in IMMUNOHEMATOLOGY stated that using equal volume (cells:plasma) adsorptions onto papain-treated cells x3 and x4 resulted in "the majority" of the samples being nonreactive in saline at initial spin and in PEG at IAT. Lastly, I did perform EGA treatment of the patient's red cells to see its affect on the positive DAT. The micro reactivity was removed following a 1min. 30sec treatment of the patient's cells, but since the sample was way beyond the manufacturer's specimen recommendation, I'm not totally confident in the observed results. Net result: It looks like alloadsorptions will be needed to resolve any observed ABO discrepancies due to reverse cell issues and PEG testing with Immucor's murine monoclonal Gamma Clone, with a macro only read, would resolve any the issue of detecting underlying alloantibodies. Thanks much Mabel for sharing this sample with us!
  12. Antibody reacts consistently with all cells tested, including a phenotypically "matched" cell, but is nonreactive with the patient's autocontrol is indicative of an antibody to a high frequency antigen. Is initial testing in Gel, solid phase, LISS, PEG? The reason I ask is that in my experience, HTLA antibodies tend to show variable reactivity in tube, but can react more uniform in Gel testing (just guessing the same would be true for solid phase). Chido/Rodgers are possibilities; U is not as the patient is s+. Ena is a possibility as are Ge:2 and Ge:4.
  13. For me, it's completely dependent upon the results I obtained in my serum/plasma testing and the amount of eluate I have to test.
  14. We use cold and cold, not that it would have mattered in this case. It would have been interesting to see what a Lui Freeze eluate would have yielded. What did your ARC come-up with if you don't mind my asking?
  15. It is a bit annoying that the manufacturers do not have grades below 1+ as we see these all too often. However, we never interpret these reactions as 1+ as that would not be consistent with the manufacturer's parameters. When faced with this reactivity, we will record +w or w+ and define these reactions as being less than 1+ on the worksheet. For titers in Gel, I would think this would be an important distinction as the end point for a titer is the last 1+ result, not the last result that demonstrates reactivity. That could easily be a 2 to 3 tube difference and may present the physician with information that is not totally accurate.
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