Clarest

Could you please explain more about cisAB? Thanks a lot. By the way, our reference lab tested this sample and said they were sending the sample to national reference lab. As well, they said patient's cells are A1 ag. negative.

Thanks a lot for your explanation, Malcolm. Sorry for the wrong spelling of "chimera". We couldn't get any information on recent gut infection. Only thing we know is that the patient is going for a hysterectomy surgery soon. We already sent the sample to reference lab. Before sending out the sample, we were asked by them to test with anti-A1 lectin and DAT, both were negative. I guess ABO genotyping could help for this case if possible.

We thought it looked a bit strong as a case of acquired-B, as well. How about T activation? Is it usually strong? We don't have other clones of reagent anti-B / slightly acidifying anti-B for use. We are thinking to send it to reference lab for further investigation. By the way, if it was chiasma, what would be the reverse grouping result look like in this case. Thank you very much for your help.

Hi all, We had a patient with difficult interpretation of ABO group, please have a look at the following results and help to solve the puzzle: Anti-A: 4+, Anti-B: 4+, auto: neg, A1 cells: neg, B cells:3+; 3-cell screen: neg at all 4 phases (I.S. R.T., 37C & AHG) According to the history so far, not a BMT recipient. Thanks.

Could anyone please give me more info. about this university and the program? By the way, I am in Canada. Thanks a lot!

cswickard, thank you for confirming my guess regarding the difference of sensitivity to Le Ab. between solid phase and Gel. You're right that we do have two different systems. Sometimes they really give us hard time due to the discrepancy between them. Right now we try to use salien IAT to be the judgement between the two. And in the future, we're going to be introduced to another method --PEG. I have no idea what it is going to look like in the future.

I agree with auntie-D. As I understand the reason why Rhig is needed for transfusing Rh pos. Plt. to Rh neg. patient is that there is a trace of RBCs in Plt. unit due to the way how to prepare (e.g., retrieving from buffy coat) For example, one pooled plt. unit which we currently use (- containes 280mL plasma and equals to about 4 units of random plt. as I mentioned in previous post) has about 0.5mL RBCs. As I understand, plasma units (e.g., FFP/FP) do not contain RBCs, which is why we do not consider Rhig givingto patients. To be frankly, we even do not put Rh type in to our system when we receive FPs to our inventory. Please correct me if I am wrong.

In Canada, one vial of 300ug (1500IU) can cover 15mL of Rh pos. RBCs which is equivalent to the RBCs in 30 units of random platelets (containing 40-70mL of plasma with >=55x10^9 platelets and < 8.3x10^5 leukocytes per unit) or in 7 units of apheresis platelets (containing ~250mL of plasma with >=300x10^9 platelets and <5x10^5 leukocyts per unit).

Thanks a lot to you all for your answer and warm welcome. :handshake

Hi all, This is my very first post in this forum. Nice to meet you all. We had a patient today with anti-Lea previously identifed. I'd like to know what your policy of selecting units for patients with anti-Lea is -- do you use phenotyped units or not at all. I did a little bit research today and found that some says anti-Lea rarely causes Hemolytic Transfusion reaction, and some says there are examples that it causes HTR. Does your blood supplier (e.g. donor centre) phenotype units for Lea Ag or not at all? One of my colleagues said today if we order Lea neg. units from our blood supplier, they are going to laugh at us (-- sounds like they don't care about anti-Lea at all). We had this patient several times in ER. Before transfusion in this September, Ab. screen results of several samples were negative by solid phase. After the transfusion, patient came in October. Ab. screen was positive by MTS gel card and anti-Lea identified by MTS gel card. During the same visit, we transfused this patient with several MTS x-match compatible units (not phenotyped). Today, the patient came again, and Ab. screen was negative by solid phase. If we assume that anti-Lea in patient's plasma is now below detectable level, and if we transfuse the patient with non-phenotyped but compatible units, just in case there is one unit which was Lea positive (~22%), is there any possibility of 2nd immune response with high titre? If so, possible HTR? Thank you very much.