richmond

One could have a combination of problems--a weak warm auto plus a tendency to react with a constituent of the gel diluent present in prediluted reagent cells, but not in the diluent used in making up cell suspensions for crossmatches. The main difference in these diluents in the US is the presence of antibiotics in the diluent of pre-diluted cells.  I wouldn't expect one screen cell to be negative in this case though.  Sometimes "gel junk" does seem to be worse with, say, D pos cells--almost as though the antibiotic complexes with the cell membrane better on D pos cells or something.  Or how about Dombrock?

I used to work in a reference lab and we would intentionally crossmatch with LISS because of the chance of getting a compatible XM in patients with WAIHAs.  Maybe it is not the best inventory management, but I would always prefer to give XM compatible units, even if incompatible units would expire first.  Even if it is just for piece of mind.  
 
We did have one patient who had an anti-Coa that appeared for a long time to be a WAIHA.  His DAT was positive due to reaction with the Co(a+) donor cells.  It took several reports of possible transfusion reactions to figure out that this was an example of an antibody to a high-incidence antigen.  I believe it was finally figured out by doing what Malcolm alluded to:  they tested the donor with several rare antigen-negative cells based on the patient's ethnicity.

Hi richmond,
 
Thanks for the reply.
 
From the reactions you report (weak reactions by gel IAT and 15% of cross-matched units being compatible), I would say that it is most unlikely that this patient has an antibody directed against a high prevalence antigen.  Were this the case, I would expect compatibility with only 1% of units (or, a great deal fewer, depending upon the specificity).
 
I would suspect that the patient may have been stimulated to produce the auto-antibody by bacterial infiltration into his circulation as a result of his chronic GI bleeds, and may well be on antibiotics to counter this.
 
Under such circumstances, we would generally give only Rh and K matched blood (well, and ABO matched, of course!), rather than match for other antigens.
 
I also just wonder if the reaction the patient underwent was as a result of all of the "biochemical nasties" released during storage of the unit, which, you say, was near its expiry, together with the (probable) low level systemic bacterial infection being just sufficient to "tip them over the top" into a reaction, and probably had little or nothing to do with a red cell antibody.
 
Where I work is a Reference Laboratory, and so we see many cases of WAIHA a year (too many!!!!!!) and, of those, I would estimate that a good 10 to 20 give compatible units by gel technology IAT, and a lot more that give reactions by this technology, give compatibility by pre-warmed, warm-washed LISS tube IAT at 37oC.  Note though, that almost all of these give quite strong reactions by gel technology using papain-treated red cells - which explains your reactions with the eluate.
 
I hope that helps a bit.

Is he receiving transfusions bi-weekly because of his chronic GI bleed or because of his warm auto?  I sort of think someone ought to be looking at the underlying problem here and deal with it rather than just keep filling him up with blood!

This is one of the most difficult problems to sort out in blood transfusion Richmond!
 
Certainly, you can get compatible units in the cross-match if most of the auto-antibody is on the patient's red cells and very little of it is free in the plasma.  What strength reactions are you getting in the panel by IAT?
 
Also, what is the underlying disease and what is the patient's ethnicity?
 
The transfusion reaction you describe certainly sounds genuine, because of the raised bilirubin, otherwise I would have thought along the lines of a non-haemolytic febrile transfusion reaction.
 
Could you give us a little more detail (as questions above) and then I'll have a go (but don't guarantee to solve your problem!).

Welcome to this wonderful site richmond.
 
It could be an anti-A1, a "cold" auto-antibody, a "cold" alloantibody, or a mixture of any of these!
 
One way to test if an anti-A1 is present is to test the patient's plasma against about 3 red cell samples known to be A1 and against 3 red cell samples known to be A2.  If the tests are positive with the A1 red cells, but negative with the A2 red cells, you have probably got (at least) an anti-A1 (but, as long as it is not reactive at strictly 37oC, it will not be clinically significant).
 
In the case of an A2B individual, however, there are very few H antigen sites available on the red cells, and the chances are that your patient may well have produced an auto-anti-HI.  There is no easy way of proving this, unless you have access to either group O cord blood red cells or group O adult ii (both of which, to all intents and purposes, will lack the I antigen), and to Oh (Bombay) red cells, which will, of course, lack the H antigen.
 
That having been said, you can almost prove it by testing the patient's plasma against red cells expressing a variety of ABO types.  Those that are A1B will react weakest, and up to group O red cells, which will react the strongest.