Jyoung

Platelet crossmatch with Gel! Just a thought. Not sure how it could be done, but how nice it would be if it could!

Thanks you guys for the references!

I had never heard of it either until after attending a SCAB conference a few months ago. Apparently you can add Combs AHG (IgG) to bind to the antibodies that are causing a positive DAT. This will then block those antibodies from reacting when phenotyping a patient through the AHG phase. How or why this doesn't block the antigen when phenotyping I do not know? But I was told it doesn't. I was also told this technique is mainly used for those patients with a strong postive DAT, where the DAT is still reacting after treatment with EGA. Thanks,

Does anyone perform what is called IgG Blocking on a patient with a strong +DAT? I just wanted to get some info on this and see if it is something worth trying or implementing. I think some IRLs in US may use this technique but not sure how well it is accepted and how well it works. Thanks,

I would question why your system let you issue blood on a patient with an antibody that was not cross matched through AHG phase. Our system (HCLL) sees anti-D as a level three antibody and would have never let us tagged the unit unless it was emergency issued.

We had same problem with last CAP survey. We actually ran the eluate with ortho's ficin (gel) and the 3 cell came up negative showing anti-e specificity. Then we ran the eluate with orthos A panel (gel) and showed anti-e specificity. I just thought that our C panel's 3 cell some how got contaminated, but after talking to friends at neighboring hospitals I found out that we were not the only ones that saw this problem.

I found in the package insert for the MTS Diluent 2. It lists Trimethoprim and Sulfamethoxazole as preservatives. These are antibiotics and maybe some patients build antibodies to these drugs. Not sure but seems like this is what was going on in my case.

I had the same problem with one of my patients also. I could wash cells with normal saline and all cells would be negative. Also ran anti-D as QC with washed cell and they reacted fine. I then took same cells and resuspended with dil 2 and the cells became positive again. We had already called this patient as positive in the past but never transfused them. I ran screen by peg. It was negative.

Cell 4 & cell 10 are positive for "V" on Ortho's VRC179 & I don't know about VS633.

Do you use gel method with all your different reagents or do you perform some tube? I would start with ruling out....... 1. Rouleax 2. Anti-A1 3. Cold 4. Anti-M: Run back type with Ficin. If it goes away probably anti-M. Then you can go from there. Lets us know what you find.. I'm curious.?

What method do you use for your antibody screen?

Oh I see. I missed the part that the K+k- cell is also D+. Sorry!

I would call it anti-K because if your patient is types as K neg it's not going to hurt to give K neg blood and most units are K neg. Have you tried running ficin to see if the hetero cells pop out?

All this input about anti-A1 is great. And I will definitely benefit from all of it if I ever see a patient with anti-A1 again. Since I'm one of those people that can't help but to ask why about everything. Im sorry, but I have another question..... When a patient that is A1 and is transfused with an O platelet that has a high anti-A1 titer wouldn't that prompt an acute intra and extra vascular transfusion reaction?

I missed it too! Sorry!

At the time when I discovered the anti-A1 I did not think about, what platelets the patient recieved. We actually started crossmatching this patient's platelets, but I think that was after finding the anti-A1 and I'm sure we transfused platelets before finding the anti-A1. So definitely possiblity! Thanks!

Your right, I read about that in "The Discovery & Significance of the Blood Groups." A, B, H, I, Rh, YTa, and Colton antigens are all affected by leukemia. I wonder if the front type would show signs of this "alter state?"

I don't know. I'm sorry. The patient was referred from another hospital. This patient came with a Warm Auto.

I had a patient with a similar thing going on. Diagnosis was aplastic anemia. And the 1st specimen showed warm auto. After a while the warm auto and screen became neg. The way I caught the anti-A is when I did crossmatches at IgG in gel not at IS. IS was neg. Then I proceeded to think we just missed anti-A1 in back type when we typed 1st specimen and that maybe chemo decreased the IgM anti-A1 reactivity at IS in the current specimen. So I crossmatched 4 different A1 neg units in IgG gel all neg. And I crossmatched 4 different A1pos units all positive 2+. All 8 crossmatches were performed in same run. Never could antigen type patient for A1 because if transfusion history. I assumed she was Asub with an anti-A1, but I guess it could have been an auto anti-A1. And maybe the cause of patient's disease. We gave O pos units and ended up changing type completely to O. Patient went to a different hospital for a stem cell transplant. Not sure how it turned out.

We do not. However we do require two different technologist perform types on current specimens on new patients. At my neightboring hospital, they require two specimens for every new patient. Either way is correct according to AABB standards.