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Malcolm Needs

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Posts posted by Malcolm Needs

  1. 35 minutes ago, NicolePCanada said:

    Stop blaming the Canadian Smoke. We in Canada, do result as No Antibodies detected. If the patient had an antibody in the past, that is maybe below detectable limits, but was previously identified, those are also in report as historical and as such the patient would have a full crossmatch in gel as well as phenotypically matched for previously discovered antibodies.

    We would write something very similar in such cases, but would always mention the specificity of the antibody that is no longer detectable, in an effort to avoid anamnestic responses.

  2. 2 hours ago, jnadeau said:

    Thank you very much Malcolm - you're the best!  If you would clarify in the second paragraph please - worth their salt "would" or "would not" report out...  we're filled with Canadian smoke here and it may be causing me confusion:wacko:

    I meant that they would NOT report it as "Negative", or "No Antibodies", but WOULD report occasionally as "All Clinically-significant Allo-antibodies have been Ruled Out using etc.", or words to that effect.

  3. In the UK, it is STANDARD practice in all laboratories that I know to use either the phrase "No Antibodies Detected", or, more frequently, "No Atypical Antibodies Detected", as the latter also includes such things as the iso-antibodies of the ABO and H Blood Group Systems.  Indeed, some go further still and use "No Atypical Allo-antibodies Detected", as this covers such findings as an auto-anti-H, auto-anti-I and auto-HI, as well as the ABO and H iso-antibodies.
    These phrases do not mean that there are no atypical allo-antibodies detected.  It would be an incredibly rare set of screening cells and antibody identification panel cells that would both express, for example, the HJK antigen, or any other genuine low prevalence antigen.
    In some cases, where an atypical allo-antibody IS detected, but it is known to be clinically-insignificant (such as anti-Kna), we may use the phrase "No Clinically-Significant Atypical Allo-antibodies were Detected" (or words to that effect).

    One thing is for certain, and that is that a UK Reference Laboratory (and most hospital laboratories) worth their salt would report out as "Negative", or "No Antibodies", although, even using the phrases I've quoted above, occasionally the phrase, "All Clinically-significant Allo-antibodies have been Ruled Out using etc.", or words to that effect.

    MIND YOU - you have to remember that I am RENOWNED for being a pedant - but I learned it from a few good sources; Peter Issitt, Carolyn Giles and Joyce Poole (to name but three).

  4. 48 minutes ago, jack323 said:

    Im guessing since uk has a national database that this happens alot less. The usa should have something similar.

    Is there statistics on anamnestic response? How often have you delt with it? 

     

    I THINK there are figures in the earlier "Mollison's (but I am relying on a notoriously bad memory).  Personally, only a few (in 43 years), but there are figures  annually in the UK SHOT Reports (Severe Hazards of Transfusion).

  5. 14 minutes ago, DPruden said:

    I was looking for a standard method for IgM titers of anti-A and anti-B.  Our BMT floor requests both IgG and IgM titers often.  The only methods I can find are for the IgG anti-A and anti-B primarily for pregnancy which is not concerned about IgM.

    Why do they want to know the titre of IgG anti-A or anti-B?  It has been known for decades that the titre makes no prediction of the severity of ABO HDFN?  The only real predictor is that the foetus/newborn will suffer at the same gestational period, or earlier, than the previous pregnancy, and to the same extent, or worse, than in the previous pregnancy.  The problem comes with the first pregnancy, but, as titre is not predictive, surely it would be sufficient for the doctors to know whether or not IgG ABO antibodies are present in the maternal circulation in the first place?

    I realise the IgG ABO titre is very relevant in solid organ transplants and stem cell transplants, or have I missed something?

  6. 1 hour ago, Neil Blumberg said:

    One additional approach would be to increase the sensitivity of the antibody screen by your preferred method (e.g., PEG, ± using enzyme treated red cells). Obviously increases the possibility of detecting pan-reactivity/false positive tests.  

    I would be wary of relying on enzyme-treated red cells, as a negative reaction could be due to the cognate antigen being denatured by the particular enzyme used.

  7. 2 hours ago, jayinsat said:

    I agree with Malcolm. I would dig as deep as possible to find that antibody history. If none can be found, I would do AHG crossmatches. If it was a frequent antibody, the titers should rise to detectable levels soon.

    The trouble is that, if the antibody happened to be an anti-Jka or, worse, an anti-Vel, the resulting rise in titre, following an anamnestic response, could be fatal on rare occasions.

  8. 27 minutes ago, AMcCord said:

    Oh yeah.... that dates us. :D

    And I remember doing antibody screens post RhoGAM, prior to patient discharge, to 'see if the RhoGAM dose was adequate'. No anti-D detected = give more RhoGAM. Something the OB folks thought seemed like a grand idea before the fetal bleed screen was available. Fortunately fetal screens came out about then. We were able to convince the docs to stop with the ABS orders by running parallel tests with the fetal bleed screen for several months to demonstrate how meaningless the antibody screen idea was.. 

    The trouble was that, in those days the anti-D immunoglobulin was known as "anti-D for Mum's Bums" in the UK, as the shot was given in the gluteal muscle.  But, there was an awful lot of fat in that muscle, so the anti-D had a habit of "staying there", rather than being adsorbed into the blood stream.  This meant that, even when the dose of anti-D immunoglobulin was calculated from the Kleihauer-Bekte test, the actual dose reaching the circulation was far lower than the calculated dose, and women used to produce allo-anti-D as a result.  Nowadays (at least in the UK) the shot is given in the lateral deltoid muscle, where there is a good deal less fat, and so the shot is adsorbed into the circulation much easier, and so there are fewer cases of maternal allo-anti-D.

    I realise that this is a very vague explanation, and that there are many other causes of anti-D immunoglobulin being less than effective (such as giving it to the father, or even to the ambulance staff (SHOULD be unbelievable, but is actually true), but it does show just how complicated such a simple thing as this can be.

  9. 3 minutes ago, RRay said:

    I agree @jayinsat that the additional screen is redundant.  Building a new LIS, and planning to get rid of the antibody screen.

    I'm just questioning because it is strange that all of my experience and IRL peers has had a post partum workup that included a screen.   Seems like one of those "always been" situations.

     

    Thanks folks! :D

     

    Agreed.  The ONLY time we might perform anything like a post-partum screen is if the baby's DAT is positive, and the baby has clinical signs of HDFN, but the mother has not been shown to have an alloantibody in her circulation during the pregnancy.  In such a case, we may well test the maternal plasma (or an ABO adsorbed and eluted sample of the plasma) against the paternal red cells (if available) to see if the antibody is directed against a low prevalence antigen expressed on the paternal red cells.  Having said that, however, this would only be useful in a further pregnancy with the same male, as providing the present baby with a unit for top-up or exchange would be easy if the antibody is directed against a low prevalence antigen

  10. 25 minutes ago, Marilyn Plett said:

     

    If I'm not mistaken, both of those examples were whole blood units, not packed RBCs or RBCs resuspended in ADSOL. That would impact the amount of antibody transfused.

    Absolutely correct Marilyn.  In those days (1963, I was in infant/junior school and 1967, I had JUST started secondary school) I THINK we were only using whole blood for red cell transfusions, but I wouldn't know for certain.

  11. 12 hours ago, John C. Staley said:

    Just curious but how long did those passively acquired antibodies remain detectable?  We're they ever responsible for a transfusion reaction?  Did they ever cause anything more serious than an inconvenience for the staff?  I really am just curious what the ramifications were, if any.

    :coffeecup:

    By 1967, there at least two examples of an allo-antibody in a unit of blood causing a transfusion reaction with a unit transfused that expressed the cognate antigen, so this phenomenon is not unknown, as Neil Blumberg intimated above (Zettner A, Bove JR.  Hemolytic transfusion reaction due to inter-donor in compatibility.  Transfusion 1963; 3: 48-51, and Franciosi RA, Awer E, Santana M.  Interdonor incompatibility resulting in anuria.  Transfusion, Philad 1967; 7: 297-298, both cited in Race RR and Sanger R.  Blood Groups in Man, 6th edition, 1975, p.302, Blackwell Scientific Publications, Oxford).
    Unfortunately, I am no position to answer your other questions.

     

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