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Transfusions and Iron Overload Blood and platelet transfusions, iron testing and treatments |
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#1
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Anti E Antibody
Typical MDS long story but here is the short version.
After my latest CBC at Quest Diagonstic I was told to go and get a transfusion. HBG was 7.8. I had a CBC before the transfusion and hbg was at 8.9 so Dr. held off on the transfusion. I just noticed online that one of the pretests came back positive for Anti E. Can anyone explain what this is and how it will affect future transfusions? Thanks, |
#2
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Skip,
I am not a great resource on this subject, but here is what i found online: The "Big E" antigen is significant because it can cause increased health risks for certain individuals. If an individual has the "E" antigen, he or she will not produce an "anti-E" antibody. In this case, the individual's immune system will tolerate the antigen. However, if the individual does not have the "E" antigen during exposure to it via childbirth or blood transfusion, the individual's immune system may build antibodies against it. This immune system response leads to potential complications such as hemolytic anemia (red blood cell destruction) or infection. Not sure how it pertains to blood transfusions, but it may cause a person to burn through blood a little faster due to the hemolytic anemia - this may show up as a higher LDH reading. dan
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MDS RCMD w/grade 2-3 fibrosis. Allo-MUD Feb 26, 2014. Relapsed August 2014. Free and clear of MDS since November 2014 after treatment with Vidaza and Rituxan. Experiencing autoimmune attack on CNS thought to be GVHD, some gut, skin and ocular cGVHD. Neuropathy over 80% of body. |
#3
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Thanks Dan,
I checked out the difference between antigens and antibodies. The short answer is Antigens are what stimulate antibody generation. I went back and the names of the tests are Antibody Screen Interpretation and Antibody ID. So in interpreting what you found online I'm guessing I do not have the E Antigen since I have the Anti-E Antibody. But I have no idea what all of this means. |
#4
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I'm no expert so don't take me at my word.
I THINK it's one of those antibodies that people develop once they've been exposed to the antigen. If you have had a blood transfusion before perhaps you have developed the antibody. As for transfusions, it just makes it a bit more difficult for the blood bank to get the right blood for you. A lot of people who have multiple transfusions develop multiple antibodies over time, the blood banks are used to screening blood for these antibodies. Regards Chirley
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Copper deficiency bone marrow failure (MDS RAEB 1), neuromyelopathy. FISH reported normal cytogenetics but gene testing showed Xq 8.21 mutation Xq19.36 mutation Xq21.40. mutation 1p36. Mutation 15q11.2 deletion |
#5
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Skimp m...
My husband developed 3 antibodies after about 25 trans. it was never a problem getting packed cells, just took longer to get the packed cells ready.... We always checked on the blood bag to make sure the antibodies were listed before trans....even after over 160 trans. Make sure who is ever with you knows of your antibodies...we had a card from the hospital with them listed....i also kept them on a list with his Dr's and medications he was on. |
#6
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Quote:
I've had upwards of 75 units, and have acquired three antibodies in the process Big-C, little-e, and a rare one in the K-series. These are all various minor blood type groups. They are like the ABO blood typing system and the Rh + or - system, in that they involve various proteins, carbohydrates, or other substances on the surface of the blood cells (those are the "antigens." If you have -- or develop -- an antibody to one of these antigens, then, ideally, you shouldn't be transfused with blood that is positive for that antigen, because it could cause a nasty allergic reaction, or, failing that, it could cause a hemolytic reaction in which all your nice new blood cells from the transfusion get broken up and flushed out your kidneys. Once I acquired two antigens, the local blood bank asked for an extra day to find blood for me. They typically have to work with one of the larger regional blood centers to come up with blood that has tested negative for C & e. So, even though I am in NC, my blood often comes from a huge regional blood bank in St. Paul, MN. The extremely helpful person who runs my local blood bank explained that medical device companies sell screening systems that can identify the more common antigens. So my blood bank simply orders up some C- e- blood for me. Unfortunately, the third antibody I have is rare enough that it's not in the screening systems. So the local folks have to do the testing the old fashioned way, mixing in a little of the blood that comes in which my blood, and making sure they don't get a reaction. As a result, a couple of times they have had to reorder units, delaying my transfusion date by a day. My university hematologist told me that folks who form one antibody are likely more susceptible to forming additional antibodies as they have more and more transfusions. One other word to the wise. My highly knowledgeable local blood bank manager explained to me that, even though I have the C & e antibodies, they have basically dropped to an undetectable level at this point. So, if I went to some other hospital to be transfused, they might not pick up on the problem. Hence I wear medic alert dog tags that say "Transfusion Precaution," mention the C- & e- and have the phone number of my local blood bank. It's a small hospital, so everyone in the lab knows who I am. Hope that helps. Take care! Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com |
#7
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Greg, you are so wonderfully knowledgeable and you explain things so well. I just copied this off to file away. I haven't been real active here and I know I've missed some gems from you . . . but I sure appreciate the ones I have come across. You have really helped me to understand and I thank you.
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hubby 73, dx NHL 2001, CNS involvement. SCT (auto) 5/08 [dx UTUC renal pelvis, 2010/surgeries/MMC], MANY recurrences, chemos, surgeries, rad. dx t-MDS 3/11: IPSS 1.5 (Int-2); MDA 11, RCMD trilineage, inc. Fe, ring sideroblasts, 7q del/mono 7 (51.5%), 46,XY,t(6,17)(p22;q25)[4]/45,XY,-7[4]/46,XY[12]. |
#8
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Hi Greg,
If the antibody levels are undetectable, does that mean you'd still get a reaction? Thanks, Deb |
#9
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Alloimmunization
Hi All,
Here is an abstract about alloimmunization: http://onlinelibrary.wiley.com/doi/1...al+maintenance Kind regards Birgitta-A |
#10
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Quote:
That is my understanding. Puzzling out the intricacies of the immune system is above my pay grade, but, as I understand it, once you've had an immune reaction to some foreign invader, whether a bacterial infection, the flu, or someone else's red blood cells, your body remembers that invader by keeping on hand a tiny population of B-cells or T-cells that are sensitized to that invader's signature (the antigen proteins or sugars on the outside of its cell). The job of that remnant population is to be ready to rapidly ramp up production of whole armies of targeted T-cells or B-cells at the first sign of the offending antigen. But it is a remnant population, so, I suppose, it might not register on the standard screening. But, if the remnant spots that offending red blood cell again, it will rally the troops and mount an attack. The result will be hemolysis -- a bunch of broken red blood cells potentially clogging up the kidneys. My blood bank person put on her "I'm talking about something very serious here" face when she told me not to even think about getting blood someplace else unless they called her first. And the folks at NIH, who detected the C & e antibodies on a follow-up soon after I acquired them, sent me a formal letter and a wallet card noting I had these antibodies. The article Birgitta posted is interesting; researchers found about 15% of MDSers getting frequent transfusions acquire antibodies. Take care! Greg
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Greg, 59, dx MDS RCMD Int-1 03/10, 8+ & Dup1(q21q31). NIH Campath 11/2010. Non-responder. Tiny telomeres. TERT mutation. Danazol at NIH 12/11. TX independent 7/12. Pancreatitis 4/15. 15% blasts 4/16. DX RAEB-2. Beginning Vidaza to prep for MUD STC. Check out my blog at www.greghankins.com |
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