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About rravkin@aol.com

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    Seasoned poster
  • Birthday 08/01/1961

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    Acoustic Guitar, Congas, Oil on Canvas
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    Medical Technologist
  1. Elution Studies

    1) IgG positive adult cells ( not Cord cells) 2) Acid Elution Method 3) Ortho Gel Card 4) Screening Cell 1 and 2, along with Last Wash supernatant as a control, and full panel if either screening cell is positive. It has been awhile but I think that we practice to perform the panel in tube; I will check up on it. 5) Our Acid Elution Kit comes with a Working Wash Concentrate which is diluted 1:9 with BB Saline and used for testing. Our method also gives the option of a total of five or six washes with saline if suspecting a weak antibody that may be rendered inactive with the Working Wash Solution.
  2. can wash change the strength of the reaction

    jwnola I believe, though practice of procedures from different blood banks, that washing the cells eight times is considered excessive such that the antigen, if present, might be partially wash away or altered rendering weak reactivity. The maximum number of washes when testing Cord blood cells is four times, as I have practiced. Do you know of any studies or articles stating that eight wash cycles is practical and does not alter antigens?
  3. Thank you Scott. So the original post makes more sense. It would seem that a manipulation of the screening cell would be considered an LDT especially in the absence of any manufacturer's instruction and testing thereof.
  4. The only time I have seen reagent cells diluted is when they are being used for an antibody titer, and here QC is run. The other manipulation to reagent cells that I have witnessed, but not practiced, is the replacement of the manufacturer's reagent cell solvent with blood bank saline, when trying to get rid of week non-specific reactions. I do not know if QC is run in this case. I do have to ask a dumb question though; what does LDT stand for? Keeping track of the meaning of lettered abbreviations is difficult especially when they are not used regularly enough. Thank you in advance for any reply, Ronald
  5. Help with Lymphocyte Subsets analysis

    Hi Timien, I am gradually reading through your post but before seeing it I came across a condition that now, after reading some of your post, seems to be close to the symptoms you have described initially, 1994. Has anyone ever mentioned a condition called Nueromyelitis Optica Spectrum Disorder (NMOSD), also known as Devic Disease. This is a "relapsing inflammatory demyelinating disease that most commonly affects optic nerves and the spinal cord." As such, it can mirror symptoms of MS but does not show any brain lesions, which seems to correlate with your experience. Have you ever had a blood test called "NMO IgG Ab Test" ( Neuromyelitis Optima Immune Globulin G Antibody Test)? This test is specific for this disease which is an Auto Immune condition and the IgG mentioned in the name of the test is the Auto Antibody. This article can be found on the Mayo Clinic web site. I will be reviewing your post further and post more later if I can. In the interim I hope that you can read over this article where some of the researchers are named and maybe you can get in touch with them. Let us know how you fare and be well. Ronald
  6. Help with Lymphocyte Subsets analysis

    Hi Timien, my name is Ronald and upon reviewing your question I did some research and maybe I can explain a little. The results presented represent some kind of inflammatory condition (the elevated ESR and C-Reactive protein), and given that you state a five year duration, a long term inflammatory process at that. Given the elevated GGT, which is mostly specific for liver function, my first thought was to ask, Have you been tested for Hepatitis C; which is a long term infection of the liver where episodes of inflammation can occur; but upon researching the results of your CSF studies presented I would ask if anyone has mentioned the possibility of Multiple Sclerosis or a condition that mimics its symptoms, as this condition coincides more closely with the results you present. In lite of this finding the elevated GGT may be more reflective of continued use of pain, and other, medications. I would also ask if you have had more complete Iron studies performed and Vitamine B12 testing, as the elevated MCV (Mean Corpuscular Volume) is indicative of Vitamine B12 deficiency which may coincide with the elevated Ferratin level presented and this may very well be a secondary condition unrelated to a primary ailment. When I say "more complete Iron Studies" I mean, have you had an Iron (Fe) level and a Total Iron Binding Capacity (TIBC) testing performed? If I can explain further, Mean Corpuscular Volume refers commonly to average Red Blood Cell Diameter, although the Mean is a slightly different statistical measurement than average. I would also like to ask what is a "teetotaller," and when did you find that you were allergic to Alcohol and what symptoms did you have? Also what is your age and have you ever been transfused with any blood products? These questions are just curiosities I have and may not relate to what is ailing you. I will leave the interpretation of your Lymphocyte Studies to a more specialized practitioner as I do recognize the cells defined I hesitate to interpret. I do hope that this is helpful. Best Wishes, Ronald
  7. Questions about a potential A subgroup

    Goodchild, when is the last time you ran out of group O Rh Pos red cells as compared to AB Pos red cells? And what about group B Rh Pos red cells? Does your blood bank reside in area where AB Rh Pos red cells is the predominant type and types O and B are scarce? If so then, by all means, give AB Rh Pos red cells; and does your blood bank have electricity and running water? Sight in the absence of light leaves you blind.
  8. Questions about a potential A subgroup

    Hi Galvania, congratulations, you and I were writing our posts here at exactly the same time. I did not know that Anti A1 antibodies were naturally occurring in A2 patients but I understand why, in that they follow the same course of development as the other ABO antibodies and it makes sense. I am under the impression that your Fact #1 is also applicable to Anti A1 as well. However if anti A1 is acquired this way it, in most cases will remain an IgM class antibody ( like the other ABO antibodies are) but in rare cases they can seroconvert to IgG were they can become more clinically significant; as with an A type mother who delivers a B type infant; any Anti A antibodies that made their across the placenta are definitely IgG. Your fact number 2# is a little confusing in that I thought that women in the majority of the world were able to choose their husbands and few cultures still practice otherwise; And why would you want to right away transfuse your husband, don't you think watching a movie and maybe some dinner first is more interesting. ( I am sorry but I couldn't resist.) I am aware of the rarity of exact match as I have worked in tissue typing lab where crossmatches are virtually never fully compatible. And lastly Fact#3, I am aware of what you are saying here and when pressed, discussions based on the clinical significance of an antibody are made. However, a differing in practice here with anti A1; as you state ".. in ETREMELY rare cases where anti-A1 is active STRICTLY at 37C," when we have the opportunity to remove the possible of this extremely rare event we should take it as part of our practice in blood bank. As I believe I asked before, When is a rare event documented?; during or after the transfusion. If you have a case where you are deciding between a potential for Anti A1 and a Kell and this is unavoidable, well it's obvious to run the risk of acquiring an Anti A1 as opposed to the Kell. But here we do not even have to consider Anti A1 and it's rare potential or otherwise; just give O Pos or B Pos red cells. But let me ask you this, Is there any less benefit for this patient in receiving O Pos or B Pos red cells? Is it more beneficial to transfuse AB red cells? I also want to thank you for taking out the time to write this post; I do greatly appreciate it.
  9. Questions about a potential A subgroup

    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.
  10. Galvania, with all do respect I just came off of the site, PubMed, US National Library of Medicine, National Institute of Health, article, Severe Hemolytic Disease of the New Born Caused by Anti-M. They confirm your statement that Anti-M is considered clinically insignificant and then go on to describe a case where a newborn female had to be exchange transfused X3 before they realized that the rbc demise was being caused by an Anti M. This is a rare case where an Anti M was not caught early. How much do you think the extra care needed here cost as compared to a tube panel read at all phases with an Auto control? I can only imagine that the extra is sky-rocketing more in cost as compared to a tube panel and auto control; and it is the frequency of performing this testing with these specific cases which determine the actual expense; and they are directly related; the of these cases you have the more of this testing to be done. What do we make of all of this?

    I have read Transfusion Reaction from the AABB a long time ago. Within the first charter I was struck with the extreme rarity and extreme outcomes as given by the number of case per overall population alone. Blood Bank has come such a long way, as you know, in terms of preventing transfusion related problems such that the existing problems are all extremely rare. I realize a very expensive price tag on generation a work flow based on rare events but I also know of the legal costs when they occur. Which is more expensive? It would depend on the case. These are dilemmas that course through my mind when reading the cases here and the following posts. What can we make of all of this? It is an extreme dilemma. I have some idea of the operational costs associated with covering rare events, and I know it is expensive, but I do not know how they compare to the legal costs. Nor do I know of the frequency of these legal costs.   

  11. Hi Malcom,

    I know that we have had a bit of a rough go. In the states we have a TV show where they always say " Stop the Insanity." So how about you and I , Stop the Insanity.

    Please read my post in the "dread thread" where I commented on Galvania's post.

    You should know that I like to learn and I don't mind provocation when it results in learning new information.

    Let me know what you think and maybe you could use some less hostile lettering punctuation but if you feel need, by all means use them.

    Very Truly Yours,

    Ronald L Ravkin

  12. Questions about a potential A subgroup

    Galvania, I was brought up in blood bank to not only rule out possible compatibility issues as far as the presence of antibodies is concerned but to also not provoke a possible antibody, no matter how clinically significant. All I was trying to say is that I disagree with this recommendation because it directly conflicts with my training and experience; and if the production of an antibody is none beneficial and avoidable why is this such a problematic course of action? I know that you and Malcom know a world about blood bank and I definitely respect that, and if I can only learn and know a fraction of what you both know I would definitely feel some level of accomplishment. But in any relationship there are naturally going to be disagreements. We share the same passion. So how can we disagree in the future?
  13. A positive with ? anti-A1

    However, I would also add that difference in rankings for Anti A reactions between the gel cards and tube is excessive; the gel card is more sensitive but not that much (ie 4+ to w+); I am leary about the microscopic positive for the A1 lectin and I think that a final ruling of Anti A1 would be more sound with the tube panel at all phases along with the auto control. I have seen the gel cards miss an IgM antibody; or give very week reactivity; and I never not seen dosage with the gel card either. If the antibody concentration is fully IgM the specificity will be appearent at IS and mostly at 37C. The degree of dosage can be seen as well with a tube panel read at all phases because reactions occur predominantly at 37C and IgG depending on the relative concentrations of IgM and IgG of the potential specificty. If all is negative then Anti A1 it is. As far as overkill, that really relative and dependent on how many cases like this your blood bank weekly, monthly, anually, etc... To be continued:
  14. A positive with ? anti-A1

    Malcom, would what you say about the gel card testing hold true if testing was performed via an automated program? Also, would what you say about the Anti A reaction hold true with automated testing as well? I can say that I have never seen a 4+ Anti A reaction with a variant A; but I do not work in a reference lab either although we use monoclonal reagents. Without the A1 lectin testing the results given do look like an early forming Anti M; which would primarily be of the IgM class and which I have seen the gel card miss, under automated and manual testing with no manipulation (ie extending inc time,etc). This is why I suggested the full tube panel with readings at all phases, along with an Auto control. But I would agree that the week microscopic A1 in tube is highly supportive of the Anti A1 conclusion.
  15. A positive with ? anti-A1

    Helen, At my current employer we are required to perform a tube panel and Auto Control, read at all phases, with the typing results presented. It's a rare occurrence to see the Anti A reaction so strong with a potential A variant. If all antibodies are ruled out with your tube panel and your Auto control is negative at all phases then it would add much validity to the A1 lectin result. Without the auto control or a Poly DAT the possibility of a substance coating the red cells and preventing the A1 lectin reaction can not be ruled out; especially when your forward type Anti A reaction is so strong. Also, I would not rule out an anti M with gel in this scenario although your screening results lend some validity we do not know the number of cells used for the screen nor the distribution of M and other antigens; therefore a full tube panel at all phases is more sound. I hope this helps.