I don't think the posters in this thread were talking about "repeating" panels - they were talking about "running" a panel with the same method when you get equivocal results on your primary method.  If using solid phase  - run a solid phase panel.  If running gel - run a gel panel, etc.  Don't just step down to tubes (or a weaker method) without giving the primary method (and usually more sensitive method) a chance to show you what it is trying to show you.

For your next question - working with the specimen might have some validity if you have centrifuge problems or are running clots (red tops) for screens instead of EDTA (purple tops) specimens.  Make sure your spin speeds and times will clear the white cells in a EDTA tube.  Make sure you follow Immucor instructions on degrees of lipemia and hemolysis that are allowed.  Otherwise - if you are running the same lot # of strips on 2 different ECHOs - I would be surprised if they give different answers.

Does that help?

I've seen a similar issue with gel, in that you have sprinkled agglutination within the two-cell screen that ends up resulting negative later on with tube. The lab has been attributing these weak pos in gel to be of little significance until proven positive in a tube two-cell screen. Judging by the comments on this thread, that thinking seems problematic .

We currently do not have gel wells to test specific antibodies, although I know C,E,K gel cards exist and perhaps will be used in the future. Before we came up with the sequential tube testing, some samples would get an initial panel (based on tech discretion). Sometimes a 0+, 1+ screen would result in a specific allo on an 11-cell panel, and sometimes it would all be negative.

Interesting reads here.

It MUST be remembered that not all antibodies react by all techniques, but, equally,it MUST be remembered that not all antibodies are clinically significant.

I remember way back in the 1980's, when I was working at a hospital in Croydon, Surrey, UK, we had an anti-S that we could only detect by tube technique.  We sent this around to a whole bunch of other hospitals, who also used a mixture of techniques.  Not one of them could detect the antibody by either microplate techniques or column agglutination techniques, both thought to be more sensitive than tube techniques, but all of those who also used tube techniques were able to detect the anti-S.

I also remember having an anti-E that did not react with enzyme-treated red cells, but only reacted by IAT with untreated red cells.  This was confirmed by the International Blood Group Reference Laboratory.

Antibodies do not read books, particularly text books!

Antibodies are only clinically significant if they react strictly at 37oC, and even then, not all are clinically significant.  Think about the antibodies against antigens in either the Knops or Chido/Rodgers Blood Group Systems.

That's usually true Malcolm.  But in the world we live in with these pesky patients doing their "own" thing you just never can say never.  We had a anti-Lea the other day that we didn't even see with solid phase (almost never do/ detects IgG dependent Abs)) and didn't see it with immediate spin XMs either (should have picked up IgM), and then the pt HATED a unit - nasty transfusion reaction.  Went looking for a low frequency antibody, but found the anti-Lea and it was reacting 4+ only with AHG tubes - so was it IgM (no I.S,. reaction) or IgG (no solid phase reaction)???.  Go figure.  That one sent us back to the textbooks.  Immucor had just put out a Self-Check with an anti-Lea.  The discussion paperwork gave us a good idea of what the patient had been doing - but it makes absolutes seem like a distant memory in this field sometimes.

Happy 4th to all of you that are in the states!  Everyone else - have a nice day.

That's a fascinating case cswickard.  So, did you work out, in the end, if it was an IgM or an IgG antibody?  I know that IgG anti-Lea can cause quite a powerful haemolytic transfusion reaction, BUT, it is usually self-limiting, in that the patient's anti-Lea is neutralised in vivo by the soluble Lea substance in the donor plasma (and, of course, as the donor Lea dissociates from the donor red cells, so that the rest of the unit can usually be transfused without further problems, with a bit of piriton (or however you spell it) cover.  MIND YOU, as you so correctly say, you have to be DEAD certain that the antibody causing the problem really is anti-Lea, and not something else, otherwise the dead one might well be the patient!!!!!

In a way, this is why I miss clotted samples, because, with serum, rather than plasma, you will often see haemolysis in the cross-match/antibody screen/antibody identification panel.