exlimey

A few points, but first, a disclaimer: I am not an expert in FDA or CLIA regulations.
I suspect that many labs are using some form of a "home-brew" reagents. The number of internal controls required by various regulatory agencies increases by the day. Add the large number of "competencies" necessary for all the staff and one has to use what is available.
Personally, I don't think viral testing should really be an issue (although it would be nice to know) - you're not preparing this stuff for distribution/sale to other facilities; the "treat all materials as potentially infectious" mentality and Universal Precautions approach should cover you.
The absence of an expiration date is probably better that assigning an arbitrary one (you have no stability data). In your application, you have a in-built control - it either works or it doesn't (I'm presuming you test the untreated [positive result] and the treated cells [negative result]?).

I would check again now and see if there's any change.  Also, if you can, test the platelet donor for antibodies against low frequency antigens, and maybe re-test his anti-A titre.  Maybe the red cell donor was an A2 and the patient is an A1 so the anti-A would hit the patient cells more than the donor cells.  And how did you do the eluate?  Maybe not the best method for detecting anti-A???

I guess the antibodies come from the donors. And the antobodies are against low infrequency antigens on the recipient's red cells, so" the eluate did not react with the transfused RBC...and the panel cells..."

Could be - but much more likely to be a weak example of anti-D.  However David, if you have some group O. rr cord blood available............

Well David, I see your problem, but I may be able to suggest an answer.
Firstly, the anti-D seems to be quite weak (which is what made me think of my proposed answer).
Secondly, of the "common" Rh types, the R2R2 type has the highest number of D antigens per red cell (15 800 to 33 300), and so will tend to give stronger agglutination than will an R1R1 (which may explain why you are getting agglutination with all your R2R2 cells).
Thirdly, and turning to the R1R1 red cells, some of these may, of course, be R1r', rather than R1R1, and, therefore, have fewer D antigen sites per red cell (about 9 900 to 14 600, compared with 14 500 to 22 800) and, unless the donor is genotyped, or you can do an informative family study, you may never know (but remember the Cepellini effect).  In addition, the number of D antigen sites expressed on a "normal" R1R1 can vary quite a lot from one individual to another (and, indeed, from one cell to another, in the same individual).  In other words, those R1R1 red cells that react with your patient's anti-D could be near the "22 800" end of the spectrum, whilst those that do not react with this anti-D may be nearer to the "14 500" end of the spectrum.
All figures are taken from Geoff Daniels' book, Human Blood Groups.  3rd edition, 2013, Wiley-Blackwell, page 205.
I am not saying for one moment that this is the only, or the most logical explanation, but it is, at least, one explanation!

Most of the common Rh antibodies have been reported as IgM. A "saline-reactive" anti-E is probably the most often seen. I've personally seen an anti-e that appeared to be IgM.
Way back when, in the dawn of time........there was serious concern over examples of IgM anti-D potentially causing ABO reverse typing discrepancies - hence why the commercial reverse calls are all Rh-.

Most of the common Rh antibodies have been reported as IgM. A "saline-reactive" anti-E is probably the most often seen. I've personally seen an anti-e that appeared to be IgM.
Way back when, in the dawn of time........there was serious concern over examples of IgM anti-D potentially causing ABO reverse typing discrepancies - hence why the commercial reverse calls are all Rh-.

Most of the common Rh antibodies have been reported as IgM. A "saline-reactive" anti-E is probably the most often seen. I've personally seen an anti-e that appeared to be IgM.
Way back when, in the dawn of time........there was serious concern over examples of IgM anti-D potentially causing ABO reverse typing discrepancies - hence why the commercial reverse calls are all Rh-.

Most of the common Rh antibodies have been reported as IgM. A "saline-reactive" anti-E is probably the most often seen. I've personally seen an anti-e that appeared to be IgM.
Way back when, in the dawn of time........there was serious concern over examples of IgM anti-D potentially causing ABO reverse typing discrepancies - hence why the commercial reverse calls are all Rh-.

Hi Tricia,
It isn't actually that uncommon a phenomenon, and is due to the anti-c being, at least partially, IgM in nature.

There is a way of confirming it by genoty[ing, but it would cost the Earth for very little return.
I would like to know how old is the patient and what is the underlying pathology?
You have to remember that the the A, B and H antigens, in common with other carbohydrate-based red cell antigens, are not direct gene products, simply because only proteins can be direct gene products, whilst sugars cannot.  In the case of an AB individual, at least two different transferase enzymes are responsible for conferring either the N acetyl-D-galactoseamine residue, in the A antigen, or the D-galactose residue, in the case of the B antigen.  These two enzymes are in direct competition with one another as to which one "wins the race" to convert the H backbone to either A or B; sometimes the "A transferase" wins, and sometimes the "B transferase" wins.  In this case, it could be that the A-transferase is winning "hands down", and that the B-transferase is "whimping out a bit"!  Sorry, that last bit wasn't written exactly scientifically, but I hope you understand what I mean!

In the UK, even if we could identify the patient by three identifiers (FULL name, Date of Birth and Hospital Number), after a number of years (five, I think?) we would not take any notice of an antibody card that was not produced from our current computer system.  What you have to remember is that the antibody card (and the computer record, come to that) is only a "snap shot", and may well change over time.

Never noticed that before!  Thanks.
Boy, so glad I posted this....learned all kinds of things!
Brenda

Mabel is quite correct - I also remember that there were a number of ticklish "administrative" issues.
A more technical note: Since the volume red cells from one cord are small, I suspect the the products that were distributed were POOLS of cord cells. That is the only way that the manufacturers could have enough volume to make a viable product.  A pool would mean a mix of phenotypes and the product wouldn't be much for the application suggested by WisKnow.

Back in the day, they used to include a vial of O cord cells with panels.  I believe they quit because they had not had a practice of getting consent to use those cord cells.  I imagine it would be quite a headache to set up a system for getting consent and the parents might expect to be reimbursed for the commercial use of their baby's cells.  If I am remembering correctly, I doubt that anyone will be producing cord screen cells any time soon in the US. 

Just to clarify a few misconceptions:
1. Once a package insert change has been approved and new stock is in, IT IS SOP-driven that all old versions are destroyed and not used in new packages. If you ever get 2 packages of the same product with different version inserts - report it immediately to the company. Major labeling booboo!
2. Changes in inserts are marked as changed until the next revision when those changes become what is marked and the previous set become repeated text. You never know how long it can be between product orders so a customer may not get a revised insert until they order the same product 2yrs later. The changes are tied to the revision number and at any point can be identified for lookbacks. 
3. Any change in insert must be approved by the FDA as this is a labeling issue and part of the license. This is not a free process. Any company makes sure the change is necessary and cost-effective within their Regulatory budget before making it. So small word change requests to "clarify" in the users' opinion are not likely to happen until the cost, changes and patient testing impacted make sense. 
4. The 6 - 12 month timeline is usually correct. as is the large amount printed for cost containment. It really hurts when branding or reagent changes happen and the Materials Management group just ordered a huge number of inserts which must now be destroyed.
 
Hope this helps

Right you are...thanks for the clarification.  I just want the Manufacturer to "give us a clue" so we don't waste so much time.
Thanks
Brenda

So I guess I am not so much talking about them making changes but the Inserts don't reflect it. (because they are still sending out old inserts until they use them up....though that is not good either)....I am talking about Inserts that have a different Version Number/ Date so you know there are changes in there.....somewhere.....but you can spend a lot of time looking for a one word, insignificant change.  As long as they are changing the Insert and sending out those new Inserts, it would be "so" helpful if they would (like Immucor) just indicate in "some way," what changes they made (i.e. underline it;       highlight in gray; etc. etc.; don't really care what they do as long as they do something).  That is good customer service!
Thanks
Brenda Hutson

Just check the release date/version number of the insert - if that hasn't changed then nothing in it has.

Interesting, those of us doing electronic crossmatch would never see this.

Reagent red cells certainly do not "express antigens weakly". There is no way a commercial entity would risk distributing a product that might give rise to customer complaints - the regulating bodies (the FDA in the USA) would be all over those issues. There may be some weakening of antigen strength over the life of commercial red cell products, but this weakening would probably only be noticed with a borderline, wishy-washy antibody - perhaps you have stumbled upon such a beast.
Commercial reverse cells (A1, A2, B, O) are washed extensively before preparation of the products. Additional washing will not "uncover more antigen sites". At most, washing (with saline) will remove the commercial red cell diluent/preservative and change the chemical environment of the test system. This change may indirectly enhance or suppress reactivity of some antibodies.
If you are using unwashed cells in ABO tests, remember that ABO substance will also be in the plasma/serum and may neutralize an antibody before it has a chance to bind to the red cells. In such a case, washing will definitely enhance reactivity.

Reagent red cells certainly do not "express antigens weakly". There is no way a commercial entity would risk distributing a product that might give rise to customer complaints - the regulating bodies (the FDA in the USA) would be all over those issues. There may be some weakening of antigen strength over the life of commercial red cell products, but this weakening would probably only be noticed with a borderline, wishy-washy antibody - perhaps you have stumbled upon such a beast.
Commercial reverse cells (A1, A2, B, O) are washed extensively before preparation of the products. Additional washing will not "uncover more antigen sites". At most, washing (with saline) will remove the commercial red cell diluent/preservative and change the chemical environment of the test system. This change may indirectly enhance or suppress reactivity of some antibodies.
If you are using unwashed cells in ABO tests, remember that ABO substance will also be in the plasma/serum and may neutralize an antibody before it has a chance to bind to the red cells. In such a case, washing will definitely enhance reactivity.

Reagent red cells certainly do not "express antigens weakly". There is no way a commercial entity would risk distributing a product that might give rise to customer complaints - the regulating bodies (the FDA in the USA) would be all over those issues. There may be some weakening of antigen strength over the life of commercial red cell products, but this weakening would probably only be noticed with a borderline, wishy-washy antibody - perhaps you have stumbled upon such a beast.
Commercial reverse cells (A1, A2, B, O) are washed extensively before preparation of the products. Additional washing will not "uncover more antigen sites". At most, washing (with saline) will remove the commercial red cell diluent/preservative and change the chemical environment of the test system. This change may indirectly enhance or suppress reactivity of some antibodies.
If you are using unwashed cells in ABO tests, remember that ABO substance will also be in the plasma/serum and may neutralize an antibody before it has a chance to bind to the red cells. In such a case, washing will definitely enhance reactivity.

Perception is important, but education can help smooth over the concerns. I think it's important to remember that the outside of the bag "lost it's shine" as soon as it left the shipping box and was used to collect blood. There is nothing sterile about a church hall, a high school gymnasium or any other of the myriad of places blood is collected. I wonder how hospitals reconcile the fact that "dirty" blood bags are transported into and used in their super-clean surgical suites ?

Malcolm, as long as they wear those funny hairnets, I don't care who is flipping my burgers.
 
Scott