Liz

Hi Dave,
Now things make sense, thats why I don't and you do perform the AHG for D neg.
Ok! Great, thanks for that.

Thank you for mentioning this important concept which few know of. I presented accommodation at the meeting to decide whether to transplant or not. 
The literature is limited on iABO KT with A2B and AB but sufficient. We will transplant. They considered this case ABO mismatched but compatible as anti-A1 is absent.  May end up publishing they said. But I am just happy that he found a kidney. He is a young man and the live donor is his mum. Will keep you posted.
Thank you. 

Thank you for mentioning this important concept which few know of. I presented accommodation at the meeting to decide whether to transplant or not. 
The literature is limited on iABO KT with A2B and AB but sufficient. We will transplant. They considered this case ABO mismatched but compatible as anti-A1 is absent.  May end up publishing they said. But I am just happy that he found a kidney. He is a young man and the live donor is his mum. Will keep you posted.
Thank you. 

Thank you for mentioning this important concept which few know of. I presented accommodation at the meeting to decide whether to transplant or not. 
The literature is limited on iABO KT with A2B and AB but sufficient. We will transplant. They considered this case ABO mismatched but compatible as anti-A1 is absent.  May end up publishing they said. But I am just happy that he found a kidney. He is a young man and the live donor is his mum. Will keep you posted.
Thank you. 

Thank you for mentioning this important concept which few know of. I presented accommodation at the meeting to decide whether to transplant or not. 
The literature is limited on iABO KT with A2B and AB but sufficient. We will transplant. They considered this case ABO mismatched but compatible as anti-A1 is absent.  May end up publishing they said. But I am just happy that he found a kidney. He is a young man and the live donor is his mum. Will keep you posted.
Thank you. 

Almost zero, because of the effect of immunosuppression, followed by the accommodation effect.

I fundamentally disagree with this post frenchie.
I can assure you that we, as a Reference Laboratory, see large numbers of samples from group A patients who have an A subgroup, and with the monoclonal reagents used these days, it is extremely common to see a very strong reaction with anti-A, when the red cells have an A subgroup, such as A2, Aint or ABantu.  Granted, this is not so for A3, Ax or Am samples, but these are exceedingly rare, and your results suggest that your patient is anything but an A3, Ax or Am.
As Dolichos biflorus is a lectin, and not an antibody, I know of no substance that could be coating the red cells that would stop this lectin reacting with the red cells.  Indeed, the fact that there is a microscopic reaction suggests just the opposite, as Dol. biflorus is not, actually, an anti-A1, but will react with the A antigen (and the Cad antigen, come to that) unless it is diluted so that the lectin only reacts with A1 red cells (which is why the insert tells you to ignore microscopic reactions).
Lastly, gel technique is probably the VERY BEST and MOST SENSITIVE method for detecting an anti-M!  The reasons for this are that 1) the reactants are introduced to each other in the well at room temperature, and a "cold reacting" anti-M (or any other specificity that reacts at room temperature, come to that) will sensitise the red cells very, very quickly (certainly before the cassette is put at 37oC to incubate), 2) The incubation time is too short a time for total dissociation of the anti-M from the red cells, 3) you then take the cassette out of the incubator, back to room temperature (see point 1), 4) you then centrifuge the cassette, which brings the red cells into closer proximity (one way of enhancing antibody/antigen reactions - which is why, for example PEG works) and then 5) the cassette columns containing the AHG are at a slightly acidic pH, and, as you will see from most textbooks, the reaction between anti-M and the M antigen is greatly ENHANCED by a low pH (as low as pH4 has been recorded).
If, however, you are still worried as to whether your antibody will cause problems in the pregnancy (IT WILL NOT) just treat the lady's plasma with 0.1M dithiothreitol, which will disrupt IgM antibodies, and then see if there is any IgG element.  If there is not, you have no worries.  If there is, then all you need to do is titre the antibody to see whether or not it is less than 32.
A full tube panel at all phases is TOTAL overkill, and will only serve to be an expensive exercise in reagents and technologists time (which is also expensive).

As I said previously - the simple thing is to put up the reverse group at 37°C.  I am sure the normal antibody screen was also negative. If you like you can also put up your antibody screen at room temperature. However - whether this is an anti-A1 or an anti-M, it is not clinically significant and there will be no problems for your pregnant mum.    And in my experience A2 samples (if you call A2 an 'A variant') almost ALWAYS gives a 4+ reaction

That was me Mabel but I put it in writing to the Standards Committee and asked about
platelets, our precious gold commodity.
Their answer about the unit turning into a pumpkin at midnight was: You cannot use it if it will not be completed before expiry.
Then they did explain that if it is needed and the Medical Director is called and approves you can CONTINUE the unit if started before expiry.
I was very interested they did say that the rules are there not for us to toss out units that we need, but to use logic. So individualize your case. As you said Godchild this has never happened before, so it is an exception. And no they don’t turn into pumpkins at midnight!

I agree Dave.

I agree with the posters above.
We had a long thread about that but I cannot find it for you.
Conclusion: the gel antiglobulin crossmatch is not enough to detect ABO incompatibility.

The transfusionist (nurse) identifies that the Patient's triple name (on wrist band and verbally if possible) and ID MPI # match the triple name and MPI# on the tag, she/he also verifies that the info we have sent is correct: Blood Group, etc and that the crossmatch is signed by the BB, she/ he then signs to that effect. Then the witness (a nurse or MD) repeats the whole procedure separately and aslo signs to that effect. With the introduction of the handheld bedside barcode reader it will be a barrier that "should" help prevent mishaps.

Anti-A,B tends to be more avid than does either anti-A or anti-B, or a mixture of the two, even in these days of monoclonal antibodies. Thus, you are more likely to detect A and B subgroups, such as a very weak Ax, and this is important if an anti-A1 is present, so that the reverse group using just A1 and B cells, looks like a group O. This is probably more important on the donor side of things, than on the patient side of things, although Martin Olsson tells me that a weak Ax, transfused to a group O patient, tends to only raise the titre of the recipient's anti-A, rather than cause an acute HTR.
I wouldn't do this as an experiment!!!!!!

http://www.jointcommission.org/assets/1/6/PBM_Implementation_Guide_20110624.pdf
John, here is the JC link I spoke of.

Brenda,
Amen again as the patient history is very important. However, you mention phenotyping in the presence of a known or suspected Warm Auto; I would think that unless the Warm Auto was first adsorbed the results of the phenotyping would be questionable, especially the negative reaction, given the fact that this immuneglobulin would have a great potential to coat the red cells and potentially interfere with the phenotype reactions.

We have Meditech as both the Hospital and Laboratory (including Blood Bank) Information System. I don't have a problem with it...other than I wasn't the one to originally set it up for Blood Bank. Unfortunately, sometimes it's harder to fix problems than just deal with them.

We have SoftBank as our Blood Bank software. We LOVE it! I highly recommend it.
We have Epic as our HIS, full electronic medical record. It's a great system overall; they didn't have Blood Bank, so we had to pick a stand-alone system for Blood Bank. They do have a Lab system, but it's new and still needs a lot of work. Implementation and go-live was pretty rough, but we are getting there.

Unfortunately, the order does not automatically print out on the label printer in Blood Bank (and, no, the pc doesn't ring a bell. That would be nice!) So whenever Surgery (or anyone) wants a unit of blood issued, they also have to call Blood Bank.
We (primarity our lab aide) deliver the blood to the nursing units and Surgery - no one comes to Blood Bank to pick up blood (alas!)

Well, I view every post but I know nothing about setting centrifuges for platelet yields. As you can see, I have no useful information but I have replied.

Nope; suspect Weak D due to Positive Fetal Screen but Negative KB. We do not perform Weak D Testing on pregnant women. However, we do often find out that they are Weak D because we end up with a positive Fetal Screen. Also, the Positive Fetal Screen due to Weak D will be macroscopic and a fetal-maternal hemorrhage with that many Rh POS cells (resulting in a macroscopic reaction) would not be compatible with life of the newborn. A positive Fetal Screen due to fetal-maternal hemorrhage will be microscopic.

Brenda Hutson

I am sorry. I did not have the researcher's CV handy. He is an orthopedic surgeon and researcher, not a sales rep. Platelet Gel got a bad reputation when banked blood was used. And, then some tried to capitalize on a product. There is a great difference between an autologous fresh product, used at the bedside. Also, Dr. Timothy Hannon with the Society for the Advancement of Blood Management and Strategic Blood Management is an expert on this subject.

OK, I have enabled it again for a test period.
If all goes well, I'll leave it enabled. The site emails me all database errors, so if I start seeing them again I'll need to disable it.
As I mentioned, prior "thanks" are still there and have been restored.

The point is to check for new antibodies, not to reidentify the one you already know about, as gkloc says. I do usually include one cell for the known antibody (or separate cells for multiples) just to see which ones are still demonstrating. It may be overkill, but I don't like to report out "Anti-X present" on an antibody identification if I haven't demonstrated it currently.

Dear Deb,
Thank you so much, why didn't I think of that. I just called called the manufacturer and he thanked me?! and is very pleased to pick it up and have it investigated. Great! I am very interested in seeing what the donor has or lacks. And I want to inform him so that he takes care of his health, like never going to a cold place if possible. That is why I love this forum!!!!!! You have these great ideas !!!
Thank you
Liz

We dont do DLI's too often. Maybe 1 a year. A good candidate would have received an allo transplant from that same donor already but their bone marrow or peripheral chimerisms show increasingly mixed populations (% donor cells drops), or disease relapse AND they dont have significant problems with GVH yet. A small dose is given to start of around 1 x 10^7 cd3/kg and wait to see if they get good response without causing too much GVH. Good response = an increase in % donor cells without significant GVH complications. If the dr feels more is needed we try ascending doses of 5 x 10 ^7, then 1 x 10^8.
PS. Randomly giving cancer patients lymphocytes Would be dangerous (Thou shalt irradiate) if you hadnt already transplanted them with marrow cells from that same donor earlier, thus replacing their immune system =)