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  1. 7 points
    We report the newborn to be Rh Indeterminate, with a comment that the newborn is treated as if Rh Positive for purposes of determining the mother's RhIg candidacy. Additionally, the newborn may be tested in 4-6 months to determine the baby's true Rh type.
  2. 7 points
    exlimey

    Incompatible xm

    I concur with the autoantibody conclusion. However, unless you've neglected to tell the forum important details about this case, this work-up should have stopped at a negative antibody screen (in cards). I'm more concerned about why are you doing lots of extra work - especially an enzyme panel. And, why, oh, why are you using a "primitive", "insensitive" tube test when the super-sensitive card tests are negative /compatible? If this is a "normal" work-up, I believe your testing algorithm needs attention.
  3. 7 points
    Malcolm Needs

    Incompatible xm

    My first thought is, how on Earth do you make sure your immediate spin saline tube technique at 37oC is strictly at 37oC (or have I got that wrong, and you are doing a saline tube technique at 37oC and an immediate spin at room temperature in addition; and, if so, were both incompatible?). My second thought was, if the patient has not been transfused (as far as in known), you know his ABO, Rh and K type and the cross-match was compatible by IAT card technique, why did you perform the panels by IAT and enzyme card technique AND LISS IAT and, having found these negative too, why did you perform the other saline techniques? I just do not understand. It seems a huge amount of unnecessary work just to find a weak auto-antibody.
  4. 6 points
    There is some truth in that, and especially from his perspective. However I have found that surgeons are not the best when it comes to understanding Transfusion Medicine.
  5. 6 points
    Malcolm Needs

    IFU Anti-D

    I have NO idea who are HFAP, but I would say that, whoever they may be, they are complete idiots. Your way of treating the patients as D Negative until proven otherwise (i.e. the patient is D Positive or is Weak D Type 1, 2 or 3) is EXACTLY what is suggested by people who actually know about the subject on both sides of the Atlantic (Daniels G. Variants of RhD – current testing and clinical consequences. British Journal of Haematology 2013; 161: 461-470, and Sandler SG, Flegel WA, Westhoff CM, Denomme GA, Delaney M, Keller MA, Johnson ST, Katz L, Queenan JT, Vassallo RR, Simon CD. It’s time to phase in RHD genotyping for patients with a serological weak D phenotype. Transfusion 2015; 55: 680-689). I have, as I said above, no idea whether this was an HFAP ruling, or the ruling of a rogue inspector from HFAP, but, either way, I would be appealing against the citation, or changing the organisation who inspects my laboratory, if the appeal is rejected. From my point-of-view (and I have a bit of experience) you have done no wrong, but the inspector/inspectors have not got a clue about the Rh Blood Group System, and, in particular, the vagaries of the RHD gene. My own wife is D Negative, and if this lot forced her to be assigned as D Positive on such minimal reactions, I would be suing immediately. Sorry about the rant!
  6. 5 points
    Report as Rh Indeterminate and treat as Rh+ for RHIG coverage of the Mom
  7. 5 points
    exlimey

    Coombs Check acceptable reaction

    Do you plan to grade/record your antiglobulin control cell reactions ? If "YES", then you will need to define an acceptable range. Most workers simply use a check mark to signify satisfactory performance (hence "Check Cells"). In the absence of specific instructions and/or ranges from the antiglobulin control cell manufacturers, I favor the position suggested above by AuntiS: Macroscopic agglutination.
  8. 4 points
    consult with pathologist and keep in mind If you absolutely have to give incompatible plasma the ideal is to give it while patient is actively bleeding. If possible give RBCs that will be compatible with patient and the plasma so in your case O and as the bleeding is beginning to come under control start giving ABO compatible plasma to "top them off". The idea is that as long as patient is actively bleeding give them the incompatible product which is then being bled out onto the floor or wherever. Once bleeding is under control give the good stuff to help dilute the incompatible out and leave them with the most compatible antigen/antibody combinations possible.
  9. 4 points
    Considering the push to using Low Titre O Whole Blood for MTP and trauma's, i'd say the benefit outweighs the risk. I have personally seen two incidents where a panicked Blood Banker accidentally issued O FFP in emergency release situations. In both cases, the patients turned out to be incompatible blood types (one A one B). Guess what, there was no adverse effect whatsoever in either case. No sign of hemolysis or transfusion reaction weeks later.
  10. 4 points
    There was a prominent trauma surgeon who said, "Patients die from the blood they don't get, not the blood they do get".
  11. 4 points
    David Saikin

    Daily QC for ABO Reagents

    Those are 2 distinct systems. They each need to be qc's day of use.
  12. 4 points
    SMILLER

    Coombs Check acceptable reaction

    I agree. The check cells are not controls. They do not need to have a specific "semi-quantitative" result--they just need to have a positive reaction to show that the wash step was adequate and that AHG was added. In your procedure you should just indicate that you get some arbitrary positive reaction: 1+, 2+/MF--whatever. Just be sure you are not writing up something that disagrees with the manufacturer'e IFU. Scott
  13. 4 points
    Mabel Adams

    Antibody Titer

    I remember John Judd once advising me to titrate an anti-M suspected to have an IgG fraction and not worry about separating the IgG from the IgM unless the titer became significant. Then we could titrate it after destroying the IgM if need be to see what the true IgG titer was. It never exceeded something like 8 so we never had to send it out for additional testing. These seems something like that--drawing a line of what is safe to save the cost of extra testing. Only do the additional testing when it is no longer safe to avoid it. You would have to determine how you will turn it out so as to not overly confuse the OB/perinatologist. "Titer against c, E, Fya, Jkb and S positive cell = 8"? Then next time when it is 16 with a cell of that phenotype, you would repeat separate titrations and results would be "titer against c & E positive cell = 8 & titer against Fya, Jkb and S positive cell = 4"? Or do you then go to separate cells for all of them but the E & c? Or turn it out as 16 and they quit using titers to monitor? I can see some logic to moving to ultrasound monitoring as soon as the cumulative titer is above 16 or so but we also like to watch how titers change over time to help us guess which antigens baby is positive for. If you already tested amniocytes for antigens that would be moot but if you have only serology to go on you could miss some clues. We titrate E & c together because they are likely to be inherited together and separate E+, c- cells are hard to find. It also depends on if you can reliably find the same phenotype of cells for the next titration (we don't have the perfect world of using the same specific donor cell for the entire pregnancy). Maybe it also matters if you know dad's phenotype/genotype. If he is R2r then baby could be c+ E- but not if he is R2R2. Sorry to ramble on; surely someone with more experience in this than I can answer with something more substantive but I've enjoyed speculating.
  14. 4 points
    John C. Staley

    MLS

    I think she's referring to a Masters of Laboratory Science. I think it is available at a few Universities. LisaMarie, I can't answer your question, if I am interpreting it correctly, but...... many years ago when I was considering getting my SBB. I had a lab director tell me that he didn't care how many degrees I had or how many letters I had after my name, he wouldn't pay me any more. At that time I was supporting my young family so I elected not to pursue it. Not too many years later I move on to another facility. After 35+ years in healthcare I can say with confidence, any thing you can do to increase your knowledge and credentials will open doors that will otherwise be closed to you.
  15. 4 points
    StevenB

    Just for fun

    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!
  16. 3 points
    The size of the patient can be a factor in how much incompatible plasma you can safely give, but in an MTP you are poring the blood products in, and often it is poring right back out. The comment on giving platelets is well founded.
  17. 3 points
    I think it depends on what is going on. Look at the history of liver transplants. When they started, pts were getting upwards of 400u rbc. The first 20 and last 20 were abo compatible. in between it was whatever was available. I've seen massive transfusions where the patient was mistyped, receiving 20+u incompatible rbcs. Everything was fine for a few days - until the dilution factor was overcome by the pt's own immune system coming back on line. Patient doesn't survive that. Maybe, if you have to go with significant ABO incompatible plasma (O) you could switch the pt to O rbcs to reduce hemolytic activity. Have to remember the ABO abs are going to be diluted by the volumes of other solutions which are usually being infused at the same time. If the need is for coag factors, pharmacy should be able to provide recombinant products. It's a tough nut.
  18. 3 points
    R1R2

    Cell Phone Camera

    have your lab director talk to the pathologist, His is not a tech call. THis is why your lab director gets paid the big bucks.
  19. 3 points
    Cliff

    Cell Phone Camera

    I'd think it's also a privacy issue. Where I work, we can only use phones encrypted by our hospitals approved encryption software for sending patient information. I do not believe we are allowed to use text for patient info (not sure on that as I never would), we can only use our email that is also encrypted. HIPAA terrifies me. Violations at our hospital provide two options, final written warning or termination. It's always at least one of those and depends on the level of the violation. I suspect knowingly sending patient info on a non-encrypted phone would result in immediate termination.
  20. 3 points
    Malcolm Needs

    IFU Anti-D

    I am sorry, but this rather proves to me that the FDA should take more advice, if they are going to claim to be the "be all and end all" in terms of ultimate authority. I, and many people much more expert in the field than me (to name one, Dr Geoff Daniels), would agree with Dr Gandhi that serological ABO typing is far superior to molecular typing, BUT, the same cannot be said for RHD typing, where molecular typing is vastly superior to serological typing (not least because no blend of monoclonal anti-D reagent can detect all weak and partial D types, and no monoclonal anti-D has yet to be found that will not react with a Partial DIII). It is also disappointing that Dr Gandhi is unable to use the internationally accepted terminology for the D antigen. Many, many moons ago, Dr Patricia Tippett, who, you will recall, did the original work on partial D categorisation, which, to a large extent, is still used,not least by the International Society of Blood Transfusion. Patricia pointed out that the correct terminology for the first of the Rh antigens was "D", and certainly not Rh(D). Obviously, Dr Gandhi is one of those who feel they are above and beyond the reaches of those who really know. Turning to Dr Park, I would again say that ABO typing is, almost universally, better done serologically (I doubt anyone would argue with that), but that the molecular testing of the RHD gene and, by inference, the fact that they are far more accurate than is D typing by serological techniques. If this were not so, people with partial D types would not still be making allo-anti-D in the numbers that they are. Similarly to the misuse of terminology by Dr Gandhi, I also note that Dr Park writes, "We use molecular-based testing for a lot of blood bank phenotyping now." Since when has a "molecular technique" in the world of blood transfusion been "phenotyping", rather than "genotyping". This is not just a mistake in terms of "blood grouping terminology", this is a very basic mistake in terms of biological science. This brings me back to my question, do these "experts" make up their rules as they go along, or do they actually take any advice from the experts in the field, who wrote those two papers I cited in my earlier post? I must say that they don't seem to be that "expert" to me.
  21. 3 points
    John C. Staley

    IFU Anti-D

    In other words, who accredits the accrediting agencies? There you go Malcolm living in that imaginary perfect world.
  22. 3 points
    Ensis01

    Transfusion vital signs

    I liked the first vitals being taken just before the blood was picked up. This prevented many a wasted unit. Not sure if this policy was regulatory or if common sense had broken out.
  23. 3 points
    exlimey

    Coombs Check acceptable reaction

    What's wrong Malcolm ? You don't like the idea of using a Coombs Test to find Kell- blood ??
  24. 3 points
    AuntiS

    Coombs Check acceptable reaction

    The reagent we use includes instructions that only specify a positive reaction is required. It does not give a minimum grade. I remember being taught 2+ many years ago, but we now only require macroscopic agglutination. sandra
  25. 3 points
    David Saikin

    Daily QC for ABO Reagents

    I always preferred running positive and negative controls. FDA only requires that for anti-D (and gel). I also dislike the attitude of doing the minimum. We QC our gel and tube reagents w pos and neg controls.
  26. 3 points
    Malcolm Needs

    Probable A3B

    Don't forget, also, that an individual who is AB has the A and B antigens on each and every erythrocyte. The antigens themselves are NOT direct gene product, as they are, in effect, immunodominant sugar residues, and only proteins can be direct gene products. In the case of the A and B genes, the direct gene products are, respectively, N-acetyl-D-galactosaminyl transferase and D-galacosyl transferase, both of which transfer their respective sugars from a UDP donor molecule. However, these two enzymes are competitive. As a result, sometimes the A transferase "wins the battle" between the two, and the A antigen ends up being expressed more strongly on the red cells than the B antigen, and sometimes the B transferase "wins the battle" between the two, and the B antigen ends up being expressed more strongly on the red cells than the A antigen. In the case of the latter, an individual who is genetically A2B can, phenotypically, appear to be A3B, and so genotyping the individual may not help. All that having been said, the fact that (roughly speaking) 50% of the antigens expressed on each red cell will be a normal B antigen, it is not surprising that there would be no"mixed-field" reaction with anti-A,B.
  27. 2 points
    A few things as far as human reagents. Firstly, you never know what else may be in them in terms of antibodies directed against low prevalence antigens, because there is absolutely no way that the producer has the ability to test for all such specificities (I can remember once a human-derived anti-D reagent produced at one of the places I worked, also had a Gm antibody in it that we didn't know about. It is highly unlikely that this would have caused too many problems, but there is, nevertheless, a small chance that this could have caused a false positive). Secondly, you never know what else may be in them in terms of viruses, some of which may, as yet, be unknown to us (remember, HIV, used not to be known). This is a danger to the producer and the person using the reagent, rather than the patient. Thirdly, the avidity of human reagents is, in general, pretty poor (particularly anti-D). A few things concerning monoclonal reagents. Some of them cross-react with other specificities (although not many), but, famously, monoclonal anti-D reagents will react with the I and i antigens if used straight from the fridge. They have to be blended by experts to ensure that the desired epitopes are detected, but certain Partial D types (e.g. Partial D Type VI) are not detected (unless required). They are very specific and very avid (both of which are greatly to be desired). Virally, they are almost certainly sterile. Hope that helps.
  28. 2 points
    And in this vein - look at all the ABO incompatible plts we are forced to give (esp when you can only get group O)
  29. 2 points
    Malcolm Needs

    Gold Medal.

    Well jnadeau, be it on your head! You might receive insulting posts from others on the site now! Unfortunately, the photographs of me actually receiving the gold medal and glass plaque were not of great quality, but this is one taken at the Institute of Biomedical Science soon afterwards. Even here, my hair and beard look a bit like I have just poked my fingers into an electrical socket, my tie has gone awry and, these days, a wide angle lens is required on all occasions, but here it is in all its glory!
  30. 2 points
    Neil Blumberg

    Anti-Inb

    Another strategy, which works for ABO incompatible kidney transplants in some cases, is a combination of immunosuppressive drug therapy, IVIgG and plasma exchange. If it works for ABO, one would guess that it could work for Inb (or anything else, for that matter). One also guesses that the antibody might be wholly or largely IgM if it only causes HTR and not HDN. If that were the case, plasma exchange could be particularly effective.
  31. 2 points
    bldbnkr

    Cell Phone Camera

    We have a Pathologist who is off site, and she has asked that techs take photos of abnormal hematology cells with their cell phone and text them to her if they have any questions. We are very uncomfortable with this for the following reasons: 1. We have a no cell phone policy in the lab due to tech distraction and universal precautions (everything in the lab is considered dirty and handled with gloves 2. The hospital does not pay for our person cell phones. Has anyone ever heard of this request? Apparently she also does not like to have to review a slide and locate the cell in question, she wants it shown to her. I say she is getting paid for a Pathology Review of a slide and she can find her own cells.
  32. 2 points
    Malcolm Needs

    Anti-Inb

    She very possibly can (although two things; it would most certainly depend on the titre of the anti-Inb prior to EACH transfusion [and that would have to be 1) a doctor's decision and 2) a bit of a guess, as anti-Inb is so rare) and also, I would suggest IvIgG, rather than methylprednisolone (or, possibly, both). However, having said all this, there is NO DOUBT that anti-Inb is clinically significant in terms of haemolytic transfusion reactions, although the same is not the same for HDFN.
  33. 2 points
    This could be due to anti c IgM in nature. I have seen this many time especially in pregnant lady.
  34. 2 points
    SMILLER

    Cell Phone Camera

    Now that I think of it, perhaps the pathologist is simply offering to help ID a particular cell (they are not really reviewing the entire CBC) that a tech has an issue with. In that case, as long as the patient is not identified, I see no problem--other than the universal precautions thing. Scott
  35. 2 points
    kimannez

    Cell Phone Camera

    Get a Cellavision with remote viewing software or at the very least a camera scope. Additionally, I always wondered at the significance of only one abnormal cell on a slide.......
  36. 2 points
    SMILLER

    Cell Phone Camera

    I agree with all the comment above. You should not be sending HIPPA protected info from a personal smart phone. And most labs ban smart phone use in the Lab due to universal precautions. Scott
  37. 2 points
    Essentially, this is because the A1 antigen is qualitatively different from any other A antigen. As a consequence, all individuals with an A subgroup of any kind are capable of producing an anti-A1, which would explain the reaction with A1 cells, but not A2 cells. In addition, the different A types, including, in this case, A1, are, in effect, a continuum from the strongest A1, right down to the weakest, for example, Am, and, in some cases it is impossible to detect any A antigen on the red cells, but it is possible to detect A substance in, for example, saliva, which would explain the results of the adsorption/elution testing. I really would advise against ABO genotyping, unless you are really interested (and I wouldn't blame you if you were), as it is a very expensive technique which won't tell you in which "pool" to put the donor (A or O). This will still be subjective. If it is just that you are concerned that this patient could be "dangerous", in theory they probably could be (although, in practice, probably not so) and I would enthusiastically thank the donor for giving, but with an explanation detailed enough to let them know why (not over-burdening them with science, while also not treating them as an idiot), ask them not to donate again in future.
  38. 2 points
    SMILLER

    IFU Anti-D

    I am not sure about this, but just because the insert describes what a positive result looks like, I do not think that means they are trying to say the interpretation is necessarily positive. That's what your facilities' P&P is for, approved by your pathologist and based on whatever data you want to cite. Scott
  39. 2 points
    One of the only ways to detect Ko blood (apart from by molecular means - that still have to be proved serologically) is by use of the indirect antiglobulin technique (as you well know)!
  40. 2 points
    Malcolm Needs

    Antibody Titer

    We ALWAYS split. Different antibody specificities have different titres at which they can be clinically significant. For a long time (in the UK) we used to regard anti-K as clinically significant at a lower titre than any other specificity. Then, it was thought that, actually, the antibody was not clinically significant until it reached a titre of 32. The the National External Quality Assurance Scheme in the UK introduced a regular exercise to see how good we were (as the UK) at titrations, and it turned out that we were, to put it politely, complete rubbish! Since then, we have been getting steadily better, and are now quite good at it. This has also shown us that our feelings about anti-K were right all along, and that some examples of anti-K actually are clinically significant at very low titres (whilst others are not). So now, our guidelines state that, if a woman has anti-K, her pregnancy should be screened at least once during the pregnancy at a Foetal Medicine Unit (or similar speciality) ( Royal College of Obstetricians and Gynaecologists (RCOG) The Management of Women with Red Cell Antibodies During Pregnancy. Green-Top Guidelines Number 65 May 2014, and White J, Qureshi H, Massey E, Needs M, Byrne G, Daniels G, Allard S. BCSH (now BSH) Guideline for blood grouping and red cell antibody testing in pregnancy. Transfusion Medicine 2016; 26: 246-263).
  41. 2 points
    SMILLER

    Antibody Titer

    I would agree with Mabel, above, where the point of the serial titres is to check if things are getting worse (as in a pregnancy). It seems like you would have to isolate it in all cases, including in the initial specimen, even if the titre is low. Otherwise, if on a subsequent specimen one does have a high enough titre to warrant "splitting" it out, you would have nothing to compare that specific antibodies titre to. We never have had to deal with anything like this so I also would be interested in what others are doing. Scott
  42. 2 points
    For IgG or polyspecific I was taught 2+ or greater a jillion years ago. Complement is less although the Quotient complement coated cells react the best I have seen.
  43. 2 points
    noelrbrown

    Antibody Titer

    Heterozygous versus Homozygous expression for the antigen is key especially in the MNS system. You should know what the status is of the cell you are using so that you can compare apples to apples.
  44. 2 points
    AMcCord

    Daily QC for ABO Reagents

    Exactly! That said, I do currently choose to run positive and negative controls every day of use, though it's not required. Just anal that way I guess. Before that however, for quite a few years I had a statement in my SOP that said I was following manufacturer's recommendations for QC, did the pos and neg for anti-D, and I also never had a problem with inspections. The FDA and CAP had no issues with our QC.
  45. 2 points
    SMILLER

    Daily QC for ABO Reagents

    I don't think that is correct about dumbing down to manufacturer's recommendations. I believe the regs read that at a minimum, manufacturer's requirements for things like QC be followed. CLIA/JCAHO/CAP regulations are often much more strict than what a particular manufacturer may suggest for their product. If you choose to not run a pos and neg control, you better have a better reason than, "the manufacturer said it was OK." Scott
  46. 2 points
    Learning from the experts

    Probable A3B

    Thank you, guys, for explaining.
  47. 2 points
    noelrbrown

    Probable A3B

    Be aware that most Anti AB these days is a blend of anti A and Anti B monoclonal and is not strictly an anti AB.
  48. 2 points
    StevenB

    Just for fun

    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.
  49. 2 points
    StevenB

    Just for fun

    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.
  50. 2 points
    Malcolm Needs

    Just for fun

    Right then. The first thing I would say is that I am simply amazed that these cells were found to be negative, and yet these types were NOT represented in any way in the original screening cells or the 18 panel cells. The first thing I would do, therefore, is to change my reagent supplier as a matter of urgency. It would be equally amazing for all four of these red cell samples to be uniquely negative for the same antigen. I noticed is that the reactions are all 2+, which suggests that there is a single specificity in the plasma, directed against a high prevalence antigen. 2+ reactions are pretty weak, which suggests the presence of what used to be called high titre, low avidity (HTLA) antibodies - I am STILL confused as to what we are supposed to call them these days, but hey! - so the first thing I would do is to titre the antibody to see if the end point is unexpectedly high, compared with what is expected for the reaction strength. The other thing I would do is to see if the antibody can be inhibited 1:2 with pooled human plasma, using the patient's own plasma diluted 1;2 in saline as the negative control. If the antibody is inhibitable as above, the probability is that the antibody is either anti-Ch or anti-Rg. Neither specificity is clinically significant, and so many people would go no further, but one thing that could be easily done these days is to try to inhibit the plasma with recombinant red cell protein (rRCP) that is specific for the C4d molecule where these antigens are expressed. Inhibition with this will prove the specificity. I, however, being a purist, would try to inhibit the plasma with plasma from a Ch-, Rg+ individual, and a Ch+, Rg- individual to prove the more exact specificity. If none of this works, I would have to have another think!
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