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Posts posted by Yanxia
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Thanks, Malcolm.
I prefer the partial antigens one. I have seen a case of CisAB, the B antigens is weaker than normal , maybe 1+stronger, in this case ,both A and B antigens is as strong as normal AB group.
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Thanks for JPCroke 's marvellous post.
If the gel DAT is negative, the positive auto could be a result of plasma abnormalities, check protein analysis, cold agglutin, etc
I think antigen and antibody reaction stronger in enhanced media will also cause this kind of situation.
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I totally agree with Malcolm, and the autocontrol with patient plasma and cells reacted is more sensitive than DAT, I don't think it is proper to compare those two test in two differ method. I prefer do autocontrol in tube compare autocontrol in gel.
Just personal point of view.
- AMcCord and rravkin@aol.com
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My friend told me a case : a leukemia patient, anti-A 2+mf, anti-B neg, A1 cells neg, B cells 4+.
Then further test : anti-A1 2+,anti-AB 3+stronger.
I prefer call it antigen reduction ,but I can't explain the anti-AB result is stronger than anti-A and anti-A1.
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What about the efficacy of the screening cell, I mean if it has been bacteria contamitated or something cause it pan agglutination. Try use an no antibody AB plasma to prove it is not pan agglutination.
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I have a question, is there some evidence proved that at the first 20min to transfuse plasma will get a higher survival rate in trauma patients than other fluid and protein?
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Or RhIg source.
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I remember there had been some posts talked about this topic. If my memory not cheat me, in this kind of situation, at first we should run all the panel and cord cells at 4 degree C to see if the reaction is stronger than in room temp(22) and 37 degree. because most of pan reactive cold reactive antibodies is anti-HI or anti-I, so add the cord cells can differ it.
Not do any test just to prewarm is danger because some clinical significant antibodies like ANTI-Vel will be prewarmed out.
I don,t know if I say it right or wrong, if it is something wrong, plaese point it ou, thanks .
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Hi, think this is my first post here. My name is Amy, just to share a tidbit with everyone..
I had a patient today that typed as such:
Forward type:
Anti-A = 2+
Anti-B = 4+
Anti-D = 4+
Reverse type:
Acell = 0
Bcell = 0
Anti-A1 = 0
87 y/o male, oncology patient.
I was reviewing reports for the BB Supervisor, when I saw the weak Anti-A in forward, I investigated and got the aforementioned results.
The overnight tech released A+ blood on this patient, but no symptoms of transfusion reaction.
I notified my pathologist and switched the patient to O+ in light of the absence of A1 antigens.
my question:
I am surprised to see that the A cell in the reverse type is coming up negative. In my texbook, type discrepancies such as this are accompanied by the presence of anti-A1 in the patient's plasma. Here, I don't have a demostrable Anti-A1 and I am wondering if the antibody is naturally occuring, and in what frequency?
I think it like AmB , AmB will not form anti-A1, and the reaction with anti-A is weak , but A2 type with anti-A reaction is4+or 3+stronger.
If this patient in my lab I will transe him with B or O type washed cells, and If AB type is compatible both in Is and IAT and poly, I will transfude AB cells.
There is one case of anti-A1 which is not react in gel IAT, but react in IS caused fetal hemolysis in our country , so I will pay more attention to it.
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Anna, you are right, use tube technique, the result is 4+, thank you .
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Anna,I use anti-A1 lectins, what seeds I don't know. It is with slide, I just add 1 drop of anti-A1 and 1 drop of cells, then mix it,and see the result.
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I have met a case of anemia, male,41 years old, no transfusion history. His blood with anti-A1 show mix field, but with anti-A it is 3+ stronger reaction.
Does it because lections is weak or some other reason? Any suggestion will be appreciated.
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I should have been more clear with my answer. I knew what I was thinking about, but you all can't know what I was thinking about .
The C3 coated cells are used only to check the anti-C3 activity of our polyspecific AHG and anti-C3 reagents when performing a DAT. They are not used for antibody screens/panels/crossmatches, etc.
I know maybe my question is a little easy, but why not use to check screens/panels/crossmatches?
Or it is becasuse we have check it on DAT, but it is not parallel.
Any response will be grateful.
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What about anti-LWa.
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In our normal blood type, we often see newborn with 4+A antigens and 3+mf B antigens.
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We use bood group specific plasma, and we have not meet someone need plasma more urgently than 10 min, it is the time we thaw it.
If thansfuse non O plasma to O patient ,the soluble blood group substance ( I don't know if it is correct) will bind the antibodies ,and this kind of complex can damage the kidney.
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What about the ABO type, is it compatible. I know this kind of thing sounds imposibble to happen.
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Screen cells is O cells, there is more H antigen on it. If there is some antibodies against H or HI( often seen on A or AB patients), they will give pos result ,but crossmatch is the same blood group cells , will get neg result.
As to the 1 out of 3 and 1 out of 4 reaction 2+ donors, maybe because they are A2 or A2B has more H antigens and fresher than screen cells, so reaction is stronger than screen cells.
Just my guess.
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I did run some tube studies at immed spin, r.t. and at 4C. They were all negative.
Sorry for my poor English, I misunderstand it as thermal testing, and you mentiened before this patient's DAT is IgG neg, not mention C3, I misunderstand it is pos or not do it.
I will study harder to improve my language ability.
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David , you say Bromelase pretreatment the result is neg, I dont know after Bromease treat you run the panel on gel or other method, if you do gel ,then we can say the antibodies are enzyme sensitive, but if not on gel, I think we can't get the conclusion like this.
This antibody only react at gel, maybe because gel is more sensitive than other method, or there is something in the patient's plasma react with the additive in gel.
We fear there is some clinical significant antibdies under the autoantibody, and this patient has been transfused last weak , so I prefer alladsorption ( use R1R1,R2R2,rr) .
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I recently had a patient with reactions almost like Davids. Just curious what others think of it. I sent it out to an IRL. But the patient had a negative ABSC with a previous sample was transfused 2 units and now is positive. Looks like mixed field in gel (the top layer on the gel seemed a little to thick to be fibrin), gel panel looked the same but the auto control was 1+ (no top layer), 2 of the 11 cell panel looked negative (with maybe fibrin on the top), and 1 of 11 looked like a good 4+ (really no cells on the bottom). So I was thinking an IgM/cold antibody. DAT- IgG negative, C3d positive (Pre transfusion DAT was negative). LISS tube method was negative at all phases. Cold Screen only the I negative cell reacted 4+ at IS, RT,15C and 4C, the AC was 3+ at 15C and 4C and Screening cells were 1+wk at 15C adn 4C.
Any thoughts?
Justina's case has pos cold screen result, but David's case is neg cold screen.
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I will do alloadsorption to see if there is something beside autoantibody.
An AB patient with anti-A and anti-B
in Case Studies
Posted
Malcolm , I just search on line, and find that some Cis AB reverse type looks like O , but there is no description of forward type strength , what a pity.