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Tabbie

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Tabbie last won the day on May 12 2018

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  1. Mod uncertainty
    UKAS - Uncertainty of measurement in BT

    20160928_220622.thumb.jpg.1754a3cc96f08a7144a1cda5b8807c81.jpg


  2. Kelly antibody lecture
    I'm coming back to Providence!
    On 5/26/2017 at 1:19 PM, Malcolm Needs said:

    They are too big (the Henry VIII one is not big - it is vast!) for me to upload on to here, and so I have sent them on a CD-ROM to Cliff to put them on here, but, as I said above, the CD-ROM has been sent by good old fashioned snail mail, so it should reach Cliff sometime towards the end of the year!!!!!!!!!!!!

    Thank you kindly.  And for those that are not fortunate enough to have received written correspondence from Malcolm, his handwriting is impeccable.

    The files are now in the Library:

     


  3. Ruling out
    What are your rules for ruling out?
    Our "rules" are 1 homozygous or 2 heterozygous....with the exception of the Kidd, Duffy, and MNS family of antibodies. Those need homozygous cells to rule out. I have seen MULTIPLE MNS system antibodies react only on certain homozygous cells....even some homozygous cells might not react....can be challenging....

    Ah, but don't forget there are some 46 antigens within the MNS Blood Group System, many of which are the result of genetic "cross-over" (either Lepore or anti-Lepore types) and some of these are quite common in certain areas of the world (see many of TimOz's posts). It is probable, therefore, that certain M+N- and/or M-N+ apparent homozygosity will be, in fact, and for example, M+Lepore type+.

    :confused::confused::confused:


  4. Australia 3cell use due to electronic xm
    2 cell vs 3 cell screen

    Way back in 2003, the AABB published "Guidelines for Implementing an Electronic Crossmatch". In the section REQUIREMENTS on page 4 "Additional criteria suggested, but not universally accepted, include: ... The antibody screen should include a three- or four-cell sample."

    No further explanation was given but presumably it was for the reasons stated above that you are likely to have more cells with a homozygous antigen expression in a 3-cell panel than you are in a 2-cell panel. Most manufacturers of 3-cell panels make sure to include cells that are homozygous for Duffy and Kidd to avoid missing those.

    So long story short....that's why we use a 3-cell panel as part of our due-diligence of providing blood by computer assisted crossmatch.


  5. Dosage Kell and Lutheran
    Confused about dosage

    Dosage addresses the expression of ag on the red cell.and its reactivity with antibody.  Homozygous intimates a single expression of the gene.  Let's say we/re talkijng about the K ag.  KK is homozygous for K, Kk is heterozygous for both K and k , kk ia homozygous for k.  Dosage occurs when the antibody reacts less strong when the gene products are heterozygous, i.e, the homozygous expression will display stronger reactions.  

    The systems which express dosage are the Rh, MNSs, Kidd, and Duffy.  The texts tell you the Kell system ags do not express dosage but I have found the reality is that they do.

    When ruling out antibodies it is generally considered good practice to not rule out based on a negative result with a heterozygous cell. There are modalities of testing which enable the use of heterozygous cells for rule outs:  enzyme pretreatment (not for Duffy or MNSs);  I've also considered PeG to be valid for this.  

    Hope this helps

     


  6. Preventing antibodies
    Questions about a potential A subgroup
    2 hours ago, Teristella said:

    It just seems like if that is your argument, then you should be giving phenotypically matched units to all your patients. I do not see the difference from the position you seem to be making.

    Teristella, I have not made my argument clear. The practice is that we do not provoke potential antibody production if we can avoid it. When there is no clincal benefit for the patient from producing an antibody and it is completely avoidable based on their type and screen we should avoid it. I keep seeing this same argument about how we should just go ahead and give phenotypically matched units, but this is not what I am saying. So I will repeat, what I am saying is that if we know of an apparent possibility for our patient to acquire an antibody(s) based on the type and screen results, and it is avoidable then we should avoid it. If the patient demonstrates an Anti M or had a history of it, which is also apparently not but so clinically significant, would you not phenotype the donor for Anti M If you carry the antisera, or would you at least perform an extended crossmatch; or would you say "It's not clinically significant in the majority of cases, therefore we do not have to be concerned if the patient acquires this antibody." Please let me know if this is clear.

    What Malcom and others are suggesting here is that it is OK to give AB Pos red cells to this patient who types as an apparent A variant B, Rh Pos and that despite the fact that the majority of AB donors are actually A1B then there is a distinct possibility that this patient with develop an Anti A1; which everyone has said in some way or another that it is not a clinically significant antibody. However, there are noted rare cases when this antibody is found to be clinically significant and there is not a whole lot of information out about Anti A1. But can and anyone here tell of what clinical benefit this 87 year old Oncology patient can expect to receive from potentially acquiring an Anti A1? I have spoken about this patient's immuncompetancy  and I realize that he may not even be capable of producing and antibody base on has age clinical condition. But we can avoid any possibility of any rare event here, with this case, because we know that this patient is an A variant B; so all we simply have to do is provide this patient with compatible O red cells or B red cells, for which the pathologist involved has done.  

    To further elaborate on these comments of " why don't we just give phenotypically matched red cells to everyone," in some cases we already do. For instance a patient that requires frequent therapeutic transfusions; as most of you know, many blood banks practice to give Rh and Kell match red cells in order to avoid the well enough documented chain of sensitizations that occur starting with Rh antigens and proceeding through to Kell, Duffy, Kidd, etc. I am not trying to suggest this here, but for those who cling to this argument look around, because I firmly believe that this is where we are headed once the cost is contained; and this quest is fueled by the agencies that govern blood bank practice and businesses who will profit from this practice.   

    In closing, I am a practicing bench Technologist who does not have the degree of expertise as Malcom and others, but I firmly believe that if acquiring an antibody is not beneficial for the patient and it is completely avoidable without any extra exertions then we should avoid it. Let me leave you with this question, How many times have you encountered a case where you didn't have a choice but to run the risk of antibody(s) development in your recipient? Did it make you nervous? Did it make you nervous such that after you investigated the potential antibody and found that it was clinically insignificant you were relieved. Then you are understand what I am saying here because your first instinct was to avoid the production of this antibody in the first place because somewhere in your practice you learned and saw through experience that antibody production was something to be avoided, as we all have,  and over years of practice this instinct becomes second nature. :)


  7. Group O+ given to O-
    Questions about a potential A subgroup

    My view is that the OP clearly doesn't understand transfusion science.

    The worst that is going to happen is they might develop a clinical insignificant antibody - so what? So what if it is even clinical significant? If they ever come in needing blood again - then  you worry about giving antigen negative blood. Hell - I've given O+ blood to an O- WOMAN of CHILD BEARING AGE in a massive haemorrhage situation. And do you know what? She didn't develop an anti-D!

    The patient is group B - exactly how many units do you think you will have access to that are antigen negative for every antibody the patient has any possibility of developing? You are going to severely limit your donor pool.

    The patient in question may not ever need a transfusion again - you are worrying about a miniscule maybe.

    I seriously think you are overthinking this but not actually grasping the concept.


  8. Anti-Vel
    wAIHA with IgM and C3c/C3d coating

    I agree 100% with you that anti-Vel can be a real problem, but that problem can be a real problem not just when the antibody is new.

    It is one of the few antibodies that are best detected by the two-stage indirect antiglobulin technique (see Geoff Daniels' book, Human Blood Groups), but I don't know of anyone in the world who uses that technique as a routine.  The reason that this is the best technique to use for anti-Vel is that it is much more easily detected with anti-C3d than either anti-IgM or anti-IgG, however, of course, in these days of automation, most people use samples that have been anti-coagulated with EDTA.  This means that the calcium, magnesium and manganese ions required as co-factors in the initiation of the classical complement pathway are not available, and so we no longer see the tell-tale haemolysis in our tests that is normally seen with an anti-Vel (and, of course with ABO antibodies, some anti-I antibodies from an adult i individual, anti-P+Pk+P1 from a p individual, and IgG anti-Lea).

    Indeed, I think I have noted on Pathlabtalk before that I know of one case of anti-Vel that proved to be fatal, which was only ever detected in a clotted sample from the patient, but NEVER in an EDTA sample.


  9. Two stage IAT for Vel detection
    wAIHA with IgM and C3c/C3d coating
    6 hours ago, yan xia said:

    what is two-stage indirect antiglobulin technique, does it mean we add extra complements from fresh serum? I remember some method like that, but I am not sure about the name.

    Yes,   you are completely right Yanxia.

    Briefly, the patient's plasma and reagent red cells are incubated at 37oC, as for a normal tube IAT, to allow the antibody in the plasma to sensitise the antigens on the red cells.  The tests are then washed free of unbound antibody (as for the normal tube IAT), but then, instead of adding AHG at this stage, fresh ABO compatible serum (it has to be serum, rather than plasma, to ensure there is complement there to initiate the classical complement pathway), which is known not to contain any atypical antibodies (we used to use AB serum from a source that had been extensively tested and found to be free of any such antibodies) and mixed with the red cells.  The tests are then incubated again at 37oC, to allow for the complement cascade to be initiated, and then washed again, as for a normal tube IAT.  Lastly, monospecific anti-C3d is added, and the tests GENTLY centrifuged, and examined for agglutination.

    A negative control, using the inert AB serum, rather than the patient's plasma, must be set up and tested in parallel.

    Of course, such a technique can only be performed by tube, capillary, tile or liquid-phase microtitre plate techniques, as column agglutination and solid-phase microtitre plate techniques cannot be used.


  10. EI cross
    SIGNIFICANT ANTIBODIES FOR ELECTRONIC XM
    17 minutes ago, mollyredone said:

    We are getting ready to start using electronic crossmatch with Meditech Magic 5.67.  My IT guy gave me an antibody dictionary page and you can select yes or no for significant, indicating that EXM would be appropriate or not.  As it stands in the dictionary now, there are more than a few that are listed as insignificant, such as M, N, Lea, Leb, P1, York and antibody of unknown significance/specificity.  And to be safe, since we don't antigen type for Lea, Leb, M or N, or identify an antibody which might be an HLA, we perform a gel XM.

    Which antibodies do you routinely call insignificant that would be eligible for an electronic XM?

    TIA, Mari

    So, the easy questions first eh Mari?????!!!!!!!!!!!!!

    Personally, I think the IT guy gave you a poisoned chalice.  The reason I say this is because we can all list antibodies that are not generally considered to be clinically significant, and then, all of a sudden, one comes along amongst these specificities that has not read the appropriate text books and goes ahead and causes a clinically significant reaction.  Then what happens is that the person who said "anti-X" is not clinically significant, and this single example of anti-X turns out to be clinically significant, and you have to defend this in court.

    The real problem these days is that the technologies available to us are now much more sensitive than when I started (when cross-matches were recorded on a stone slab with a hammer and chisel) and many antibodies that were not clinically significant (because we just didn't detect them with the technologies available at the time) are now readily detectable - BUT, they are not necessarily detectable at strictly 37oC, as , for example, many examples of anti-M are now detected by "IAT", even though they do not really react (in real terms) at 37oC.  The real problem comes when, for example, an anti-M genuinely DOES react at 37oC, and it is treated as clinically insignificant, electronic issue is used, and one or more of the units is M+ and the patient has a severe reaction - who answers in court?

    The worrying thing is that there have been papers published over the last few years quoting an anti-Leb as causing a transfusion reaction, and an anti-P1 causing a transfusion reaction (a certain Garratty G being a co-author on this one).

    I would say, therefore, that the best thing to do is to read through the relevant parts of The Blood Group Antigen FactsBookHuman Blood Groups and Mollison's Blood Transfusion in Clinical Medicine (latest editions in each case), and use their experience, rather than your own (no insult intended) as the courts would probably take the authors as "experts" should you come across any of these clinically significant "outliers".

    I wish you the very best of luck!


  11. Sudden Onset Hemolysis with weakened D antigen
    Sudden Onset Hemolysis with weakened D antigen

    Does anyone have any experience with acute onset of hemolysis associated with decreased expression of D antigen?  Recently worked on a sample from 8 yr old child presenting with a 2.6 g/dL hemoglobin. Patient initially presented with weakened D expression and 23 days after discharge was typing as strongly Rh positive (verified with second sample).  Is it possible that the acute hemolysis was related to the weakened D typing?

    Initial testing results:

                         Ortho MTS-Gel           Tube Method

    Anti-A                  3+                              0

    Anti-B =               3+                              0            

    Anti-D=                3+                             1+

    Control =              3+                             NT

    Acells =              4+                             4+

    B cells =               4+                             4+

    Antibody screen         LISS/IgG (tube)              37C        IgG        Ortho Gel (IgG)

                                         SC 1                         W+          1+            3+

                                         SC 2                         W+          1+            3+

                                         SC 3                         W+          1+            3+

    Differential PEG adsorption was performed and adsorbed plasma was non-reactive when tested against screening cells (same cells used in LISS/IgG screen).

    DAT was 1+ using polyspecific AHG and anti-IgG. (Negative with anti-C3b,C3d).  Eluate was reactive with all cells tested using Ortho MTS-Gel IgG.

    Patient received multiple transfusions (approx. 1250 mL) of O NEG , incompatible, leukoreduced, packed red cells over a 5-day period.

    The patient returned for followup approximately 16 days after the last transfusion. 

    Testing results 23 days after initial presentation:

                      Ortho MTS-Gel           

    Anti-A                    0                          

    Anti-B =                0                                       

    Anti-D=                4+                            

    Control =              0                           

    Acells =              4+                            

    B cells =               4+                            

    Antibody screen   Ortho-MTS (IgG)

    SC 1                         0

    SC 2                         0

    SC 3                         0

    Any ideas about D antigen expression?  Hemolysis?

     

     

     

     


  12. Autoantibodies
    Autoadsorptions

    Hi DCeDCe (great name - all the best people have that as a probable Rh genotype!),

    The thing to remember is that warm autoantibodies tend to be mimicking antibodies.  It is probable, therefore, particularly as you are both using ZZAP, that the Reference Laboratory is either doing more rounds of adsorption than are you with your W.A.R.M. reagent, or that, as they are making up their own ZZAP reagent, there is a resultant difference in how many autoantigens are exposed after the partial removal of the sialic acid residues.

    Either of these explanations could result in the Reference Laboratory removing more of the autoantibody than are you; in other words, they are removing all of the autoantibody, while you are removing most of the autoantibody, but not all, and under these circumstances it is much easier to see the "false" specificity of the autoantibody.

    To show matching results, it could be something as simple as you doing a further adsorption with your W.A.R.M. reagent treated red cells.  Put it this way, it might be worth a try!

    Incidentally, "cold" autoantibodies tend to have a true specificity.


  13. Autoantibodies immune mediated ref
    Anti-C, anti-e auto-antibody or mimicking antibody

    Most warm auto-antibodies have a specificity within the Rh Blood Group System, although some others, more rarely, have a specificity outside of this system, such as auto-anti-Wrb.

    Most of the auto-antibodies from within the Rh Blood Group System mimic anti-e, anti-E, anti-C, anti-c or a combination (or even a compound antibody, such as anti-Ce or anti-Rh7), but, in reality, they are actually weak forms of anti-Rh17 and/or anti-Rh18, although strong examples are not unknown).  As they are usually mimicking antibodies, they can usually be adsorbed out with red cells that do not actually express the actual antigen on their surface (for example, an apparent anti-e can be adsorbed out using R2R2 red cells).

    PLEASE DO NOT try to identify them yourself, as the actual specificity is not significant, but will take an awful lot of time and you will require some VERY rare red cells, such as Rhnull, D--/D-- and the like, and these should be reserved for when they are required to identify the specificity of rare allo-antibodies, such as anti-Hr, anti-HrB or anti-Rh29, where a true specificity may well be vital to identify.

    In contrast, most "cold" auto-antibodies are true specificities.

    For more information, you would find it hard to beat reading, Petz LD and Garratty G.  Immune Hemolytic Anemias, 2nd edition, Churchill-Livingstone, 2004, although I would advise you to be selective, as it is a very detailed book!


  14. Bg and positive LFA anomalies
    0.8 Surgiscreen, vial # 2 reactions

    Can I make some comments about this type of reaction 'from the other side'.  It is easy to forget that reagent red cells come from real donors who have complicated antigens on their red cells.  The donors will be tested for as many antigens as possible, and the presence or absence of those antigens will be noted on the accompanying antigen sheet.  However, it is impossible to test for all those low frequency antigens (LFA) out there.  And unfortunately, antibodies to LFA are often far more 'common' than you would expect.  So, if you're getting an unexplained positive reaction with a reagent red cell it's probably due to an antibody against a LFA.  And the manufacturer is not going to be able to identify it; all they can do is withdraw it from use for the future.  these results are not false positive but unidentified (and probably unidentifiable) positives.  Your reference lab might be able to identify it if they have a good sample from the patient together with a sample of the cell.

    As for reagent red cells with positive DATs when used in gel (Frenchie) - you will sometimes see positive reactions in IgG or poly AHG in cards if you put the reagent red cells on to the cards without any plasma, due to the fact that the cells are not meant to be used in that way.  Usually if you repeat with neutral plasma, the 'positive DAT' disappears.  If it doesn't, either there is a real problem with the cell (unlikely) or it has become contaminated in your lab.  And - Frenchie again - I would advise you against diluting 3% cells for use in cards.  You could be creating more problems than you think you are solving.

    Another reason that you might see unexplained positives is antibodies to Bg.  As far as I know all manufacturers test their cells with a panel of anti-Bg antisera.  However, we all know how variable Bg can be.  You can test a cell with 20 anti-Bg and maybe only 1 of them is positive; and vice versa someone with a known anti-Bg won't react with all Bg+ cells.  So if you are seeing a fairly high number of unexplained positives, especially in pregnant women, then you shuld suspect Bg.

     


  15. GATA 1
    Possible Anti-Fya,-Fy3 or Anti-Fya,-Fyb???????????????

    If the patient is a genuine FY/FY (that is, he or she does not have the FYB gene and homozygous mutation at the GATA-1 gene), he or she can most certainly produce an anti-Fy3, as well as an anti-Fya.

    Personally speaking, I can think of no reason why he or she could not also produce anti-Fyb.

    I have never seen this, but that does not mean it cannot happen. Logically speaking, it could.


  16. Validation 48 hrs leaving controls on IH500
    Automated Antibody Identification

    Hi Nic

    According to manufacture instruction you can keep reagent on board for 48 hours. Therefore we did our own validation (according to ISO  if you want to deviate manufacture instruction you need to validate yourself) extent expiry on board. Because we run everyday 10 panel and it's difficult to remove and load reagent again.

    So we run daily control which are antiD c and Fya to cover all lines for negative and positive control. And leave reagent on board for 72 hours. By end of 72 hours all reagents will used up. 


  17. Phenotyping in pregnancy
    antigen typing during pregnancy

    Unless there has been a foeto-maternal haemorrhage so large that the baby has been exsanguinated, it should be fairly easy to type the mother.  If there is a mixed-field, the majority of the red cells should be maternal.

    The only exception would be if the maternal antigen in question has a weak expression.

    More of a worry would be if you need to perform adsorptions, where auto-adsorption should not be performed, as the foetal red cells could remove an alloantibody from the maternal plasma, particularly if multiple adsorptions are required.


  18. FMH
    AntiD +Anti G

    There have been several different methods used in an effort to "manage" the foetus over the years - most of which were aimed at controlling the maternal antibody levels.

    One of these was the use of an Rh hapten and red cell stroma, but this met with very little success.

    Promethazine hydrochloride was used, but, again, with very little success.

    The use of IVIgG has been tried, and I did see this used with a certain amount of success myself.  I remember that it was a case where the maternal anti-D level was quite high (in the mid 30IUmL-1) fairly early in the pregnancy, and the mother was given IVIgG throughout the pregnancy (I can't remember why they did not give an IUT, but there was a reason) and, at the end of the pregnancy, the maternal anti-D level had fallen to around 15IUmL-1, and the baby was okay.  I believe I am correct in saying that this is a rare and expensive form of treatment (I certainly have only seen it used in one other case in my fairly long career.

    Plasma exchange has been used to lower the maternal antibody levels (I remember Dr Cyril Levene using this technique on a pp lady with anti-PP1Pk, who had experienced several early miscarriages, and who produced a healthy baby), but it is very rarely used, as it is expensive, tedious and very uncomfortable for the pregnant lady, and requires replenishment of clotting factors.  It is claimed that the antibody levels can be reduced by 75%, BUT, it needs to be done several times during the pregnancy, and the antibody levels are prone to rebound, as the IgG antibody comes back into the circulation from the interstitial spaces.  It is rarely used.

    Therefore, the chances are that, should the foetus require management, an IUT would be performed.


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