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MaryPDX

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  1. Like
    MaryPDX reacted to Cliff in AS vs CPDA-1 with Peds MTP   
    We have a pretty active NICU, we only use AS cells.
  2. Like
    MaryPDX got a reaction from Patty in Blood Bank staff   
    Blood Bank dedicated staff on Days, generalists on evenings and nights.
  3. Like
    MaryPDX got a reaction from jayinsat in Blood Bank staff   
    Blood Bank dedicated staff on Days, generalists on evenings and nights.
  4. Like
  5. Like
    MaryPDX reacted to Mabel Adams in Group O Whole Blood, Low Titer   
    Our ARC is starting to offer these products. They are using a titer cut-off of 200.  The whole blood units will cost 3 times the price of a RBC. It's good for 21 days.  Oregon Health Sciences University will be stocking them for traumas. They are the 4th hospital in the country supplied by ARC to use WB in their trauma program. Our ARC is the Pacific Northwest region in Portland.
  6. Like
    MaryPDX got a reaction from new2BB in HU5F9-G4: anti-CD47   
    Here's a little something I found useful:
    http://nybloodcenter.org/media/filer_public/2017/10/04/2017aabbpostervelliquetteserological_observationsfinalcp246.pdf
    For screens, I would avoid any phase except the IAT one to minimize the carryover.  Our facility hasn't started any trials of this drug yet, so I haven't had a chance to try this (or try using gel in a neutral card with Immucor Gammaclone IgG).  My suspicion is that gel won't work, but I still want to give it a shot.
  7. Like
    MaryPDX got a reaction from Malcolm Needs in BloodBankTalk: Antibody/Antigen Reaction   
    I just answered this question.


    My Score PASS  
  8. Like
    MaryPDX got a reaction from MOBB in DAT PROCEDURE..   
    Yes it correlated very well. 
    As far as the Grifols DC card (DAT card), I've heard early 2018, but I haven't seen anything yet from FDA that it's licensed.
  9. Like
    MaryPDX got a reaction from MOBB in Validation of Other Manufacturer's Reagent Red Cells for Use in Manual Grifols Gel   
    We've been doing it for over 15 years (from the time we had Ortho's gel cards).  Whatever validation was recorded, it's from eons ago and I wasn't involved with that one.
    I would imagine it was similar to the validation done with the DAT method in gel cards (from my other post in that section)
  10. Like
    MaryPDX got a reaction from Carrie Easley in Validation of Other Manufacturer's Reagent Red Cells for Use in Manual Grifols Gel   
    We've been doing it for over 15 years (from the time we had Ortho's gel cards).  Whatever validation was recorded, it's from eons ago and I wasn't involved with that one.
    I would imagine it was similar to the validation done with the DAT method in gel cards (from my other post in that section)
  11. Like
    MaryPDX got a reaction from David Saikin in DAT PROCEDURE..   
    Yes.  We have 2 Erytras, so T&S, ABID, xm (AHG ones, not IS), unit retypes...
  12. Like
    MaryPDX got a reaction from MOBB in DAT PROCEDURE..   
    Did a total of 20 tests (combination of QC and patients).  Ran the C3 test manually (tube method, which was our standard SOP), and in the buffer gel cards.  Results of testing using both methods were recorded on paper for the Pathologist, Manager and our Technical Coordinator to view. They all had to sign off on the new method before the procedure was updated.
     
    Procedure of buffer gel card method:
    1. Bring your reagents, QC and patients to room temperature.
    2. Make a 0.8% red cell suspension (of QC and patients.)
    3. For QC, you will need a POS, NEG and a control well (pos control cells only in the control well).
    4. For patients you will need 2 wells, one that you will add red cells and reagent to, other patient cells only. 
    The reason for the red cell + buffer only wells is to ensure that no spontaneous agglutination is happening.
    5. Add 50ul of red cells to wells
    6. Add 25ul of anti-C3 reagent to reagent wells only (DO NOT add reagent to buffer only control wells)
    7. Incubate 5 min. RT
    8. Spin in appropriate gel centrifuge.
    9. Record results.
    Just an FYI, before you turn your findings in, make a copy of the paperwork, just in case someone loses it. (speaking from experience here).
    Hope this helps.
    Mary
  13. Like
    MaryPDX reacted to Malcolm Needs in e and C titer   
    The thing is tkakin, that most examples of anti-C (anti-Rh2) are not; they are actually anti-Ce (anti-Rh7)!  This is largely because almost every red cell that causes immunisation against the C antigen expresses both the C and e antigens as a result of having the RHCe gene, rather than both the C and e antigens as a result of having both the RHCE gene and the RHce gene (which is why both the DCE and dCE haplotypes are so rare).  On the other hand, monospecific anti-e is comparatively common.
    So, your lady's plasma is more likely to contain anti-Ce and anti-e, rather than anti-C and anti-e.  As a result, if, as yan xia suggests, you would undoubtedly adsorb out the anti-e, but you still would not know if the remaining antibody specificity is anti-C or anti-Ce (or, of course, a combination of the two).
    Anyway, the specificity really doesn't matter.  The point is that, as you suggest, the individual titres of what ever antibodies are present are totally irrelevant.  Normally, an antibody, such as anti-C (or anti-Ce) or anti-e, are not going to cause clinically significant haemolytic disease of the foetus and newborn, until the titre reaches 32, and it really doesn't matter whether the specificity of the antibody is anti-C, anti-Ce or anti-e.  Your Pathologist should explain this to your OB doctor to get him or her off your back (actually, to be honest, your OB doctor should already know this, but hey, life ain't always like that!).
  14. Like
    MaryPDX reacted to Yanxia in e and C titer   
    Maybe you can adsorb the anti-e with ccee cells, then to see if there are still reaction with Ce cells, then you can figure out if there are anti-C here.
  15. Like
    MaryPDX reacted to MOBB in Antigen Negative Labels   
    We recently stopped documenting the unit number on our tags and just document antigen neg/pos, date and tech. The antigen results are in our LIS too.
  16. Thanks
    MaryPDX got a reaction from Gnapplec in Giving O Pos PRBC's to a male JohnDoe during a Massive Transfusion.   
    I know it's happened, but the number doesn't seem to be very high.  (I'm going strictly on memory and not actual numbers).
    The problem with that is, most of these type of people tend to be traumas, not the chronically transfused people you see often.  Once they've been discharged, we may not see them again or it may be years later. 
    It may sound crass, but for it to be a problem, they need to survive the event which is causing them to bleed to death.  Developing an antibody (ANY antibody) is the least of their problems.
  17. Like
    MaryPDX reacted to pinktoptube in Stop transfusion if crossmatch expires after issue but before whole unit in?   
    As long as the unit is being transfused I don't see why you would stop the transfusion. The crossmatch at the time of dispense was still valid. I've never been questioned on this, maybe others have.
  18. Like
    MaryPDX got a reaction from BBNC17 in Anti-CD47 therapy interference with serology, but why DAT negative?   
    Our facility hasn't started CD47 yet, but anticipate that may happen in 2018.  I've been dredging through the internet to find anything, which is how I found the NY blood center pdf.  Besides the use of Immucors Gamma-clone IgG antisera (for antibody screens), I haven't seen anything mentioned on how to avoid it. 
    I was thinking along the line of using Platelets (which have cd47 on them) to remove the antibody, but have seen nothing regarding if anyone has tried this.  The search continues....
  19. Like
    MaryPDX reacted to Malcolm Needs in BGS Dublin.   
    I should really have posted this before, but tomorrow, my colleague Malcolm Robinson (who, some of you will have heard of through the charity "Harvey's Gang" - and, for those of you who haven't, look it up on your search engine, but only after you have armed yourselves with copious amounts of absorbent tissue for your tears) and I are flying over to Dublin in Eire to give lectures and Case Studies at the first BGS Dublin Meeting, together with a host of excellent speakers.  Great respect must go to John Quigley, who has been instrumental (well, he has been hugely instrumental in organising it), and I just hope that, when it all comes to fruition on Friday, he gets the respect he deserves.
    In the evening, after the meeting on Friday, I am being FORCED to attend a pub to take part in a quiz and, maybe, drink the odd alcoholic beverage (purely for medicinal reasons, you understand)!
  20. Like
    MaryPDX got a reaction from AMcCord in Anti-CD47 therapy interference with serology, but why DAT negative?   
    http://nybloodcenter.org/media/filer_public/2017/10/04/2017aabbpostervelliquetteserological_observationsfinalcp246.pdf
    Apparently, weakly pos to negative DATs are common. Because the antibody covers cd47, the body sees the lack of cd47 and targets the cell for destruction. 
  21. Thanks
    MaryPDX got a reaction from carolyn swickard in Anti-CD47 therapy interference with serology, but why DAT negative?   
    http://nybloodcenter.org/media/filer_public/2017/10/04/2017aabbpostervelliquetteserological_observationsfinalcp246.pdf
    Apparently, weakly pos to negative DATs are common. Because the antibody covers cd47, the body sees the lack of cd47 and targets the cell for destruction. 
  22. Thanks
    MaryPDX got a reaction from Malcolm Needs in Anti-CD47 therapy interference with serology, but why DAT negative?   
    http://nybloodcenter.org/media/filer_public/2017/10/04/2017aabbpostervelliquetteserological_observationsfinalcp246.pdf
    Apparently, weakly pos to negative DATs are common. Because the antibody covers cd47, the body sees the lack of cd47 and targets the cell for destruction. 
  23. Like
    MaryPDX reacted to Malcolm Needs in Rule out Anti-K   
    In my opinion (and that of the BCSH Guidelines) you do not need a K+k- red cell to rule out anti-K.
    If you look at the antigen profile of the red cells you use every day as screening cells, they will not have a K+k- cell, and yet you are ruling out the presence of anti-K (and any other antibodies directed against the major blood group antigens) with each sample that gives negative reactions with these red cells.  In addition, if you look at the screening cell profile that the BCSH Guidelines recommend, they say that the K antigen MUST be represented, but NOT that these cells must be K+k-.
  24. Like
    MaryPDX reacted to SMILLER in Antigen Tested Units   
    There are two types of "antigen negative" units we can get from our supplier here in Michigan.  One is "historically negative" -- those have to be retested when they arrive.  The other type is "confirmed" -- those units have been confirmed negative for a particular antigen at the supplier and do not need to be retested here.
    Scott
  25. Like
    MaryPDX reacted to Malcolm Needs in 2 Mysteries   
    I would totally agree with Yanxia about Case 1 probably being an ABsubgroup as being the most likely answer to your first case, but it would be wonderful if you were able to follow up the case at six months, just in case it is a genuine case where the B transferase is so "weak", that it is almost "overwhelmed" by the A transferase.
    Another possible explanation, one which is unusual, but not unknown with monoclonal ABO antibodies (and will not be popular with the manufacturer of your ABO reagents!), is that your anti-B is actually an anti-B(A), whereby the anti-B is capable of reacting weakly with group A red cells (the opposite can also happen with anti-A(B) whereby an apparent anti-A can react weakly with group B red cells).
    Case two is very intriguing.  I would echo that anti-Lua is not what would generally be considered to be clinically significant.  There certainly appears to be an anti-Lua there, which is sensitising his red cells in vivo, which may well have been introduced by transfusion of another component (given his pathology, I am assuming that he has received more than just this unit of platelets within fairly recent times).  However, it could well be that the plasma from this particular unit of platelets could have contained an antibody directed against a completely different low-prevalence antigen, such as an antigen within the 700 series.  If this is the case, even a relatively large Reference Laboratory may well have grave difficulty in identifying the specificity, as they may not have access to red cells expressing the cognate antigen.  In addition, such antibodies often cross-react with multiple low prevalence antigens, and, on top of that, individuals who make such antibodies often produce multiple antibodies directed against actual low-prevalence antigens (by that, I mean that this is not cross-reactivity).  This would explain the positive DAT.  Some of these antibodies do cause red cell destruction, which would explain the later negative DAT, but not to such an extent that you would see symptoms such as dark urine.
    Obviously, I have no idea of the drugs he is taking, but this doesn't sound like a drug-induced reaction to me, as I would certainly expect to see dark urine, and other evidence of haemolysis.
     
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