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An equivocal by any other name...


SMILLER

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There are a number of well-read (and well published) posters here.  I am wondering if any of you know what the most common cause of equivocal reactions that come upon during antibody ID?  You know, the often weak reactions that are left over after all of the rule-outs are accomplished? 

Some are apparently the result of HLA interactions, but are most just junk reactions with otherwise unnamed insignificant antigens?  More importantly, how many are actually "developing" antibodies to significant antigens?  We do see, over time, patients pop up with only a few equivocals, and after a few transfusions, develop a full response to a significant antigen.  I was just wondering if there is any data on how commonly this occurs.

Thanks, Scott

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Apart from HLA antibodies, as you so rightly suggest, we usually found such antibodies to have a specificity within either the Knops or Chido/Rodgers Blood Group Systems, or the Cost Collection, or a really weak anti-P1.  Some, of course, were so weak that we never were able to assign a specificity.  Very rarely did we see something that later developed into a clinically significant antibody specificity.  However, often, when it did, that specificity turned out to be anti-Jka (just occasionally, anti-Jkb, but mostly anti-Jka) and so, when we were not certain of the specificity, we would Kidd type the patient's red cells and suggest that either Jk(a-) or Jk(b-) typed blood be given as a precaution [unless, of course, the patient typed as Jk(a+b+)].

There was one infamous night, however, which kept one of my Biomedical Scientists up most of the night in the Reference Laboratory, and me also up most of the night at home on the telephone for what turned out to be an anti-I reacting very weakly by IAT at strictly 37oC.  Afterwards, we both felt complete idiots - and extremely tired!!!!!!!!

Edited by Malcolm Needs
I have just realised I wrote Jk(a-b-), rather than Jk(a+b+)! Maybe I AM a complete idiot!
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What is your current policy concerning these equivocal or non-specific reactions for subsequent crossmatches when no specificity is apparent?

If a sample is found to react with 2 of say 26 test cells and the reference lab workup finds no reactivity either in Gel or in tube with PEG, should these patients require Coomb's crossmatches in the future?

Edited by Winter
should have said crossmatches
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1 hour ago, Winter said:

What is your current policy concerning these equivocal or non-specific reactions for subsequent crossmatches when no specificity is apparent?

If a sample is found to react with 2 of say 26 test cells and the reference lab workup finds no reactivity either in Gel or in tube with PEG, should these patients require Coomb's crossmatches in the future?

Sorry Winter, I am not sure to whom you are addressing your question (to Scott or to me), so I will answer from my own point-of-view, in the full knowledge that 1) you may have been addressing your question to Scott, and not to me, and 2) that Scott may disagree fundamentally with what I post here.

Where no specificity is apparent, we (the Reference Laboratory) would normally perform the cross-match for the hospital blood bank, if they so wished (if they wanted to do it themselves, it was totally up to them).  If, on the other hand, the antibody reacted only weakly with one or two of 26 test cells, where the vast majority of known clinically significant specificities were ruled out, we would suggest, tactfully of course, that the hospital blood bank "grow a couple", and perform the cross-match themselves by indirect antiglobulin technique (IAT), but NEVER in an establishment where I was in charge, by the "Coomb's" or "Coombs'" technique!

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Ok, for starters, some of us here in the trenches do not necessarily  ever have to "grow a couple" (whatever that means). 

Anyway, at our hospital, regardless of what a reference lab (or any lab) may say at one point in time, one cannot guarantee that all future equivocals on a given patient will be benign, so we will continue to do so, even if a particular screen is totally negative.

Scott

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Sorry Scott, my sincere apologies.  I did not mean to insult you, or any other people on this site.

I have been in the "trenches" myself (I have not ALWAYS worked in Reference), but I do query what is the point of sending a sample to a Reference Laboratory if, when you get their results, you dismiss them as being wrong (always admitting that nobody is perfect and that anyone can make a mistake).

I would also agree that, just because a Reference Laboratory says something about a particular sample (a "benign" antibody or "no atypical alloantibodies detected") does not mean that there will not be a clinically significant antibody present in a couple of months or so (hence my comment about Kidd antibodies).  Nobody, I hope, least of all me, would say to somebody else that they should NOT perform a cross-match before giving blood.  What I said was that, if we had performed an antibody identification for a hospital blood bank, and had found that the reactions were with "2 out of 26" (as Winter quoted), AND we had been able to rule out all of the common clinically significant atypical alloantibody specificities, what on Earth could we do, in terms of cross-matching, to make the blood anymore compatible than the people in the hospital blood bank?  Surely, under the circumstances, they can cross-match just as efficiently and as effectively as someone who works in a Reference Laboratory?  People who work in Reference Laboratories are not super-human serologists; at best, they have access to a large number of rare red cells, rare antibodies and other reagents not usually available to hospital blood banks.

I do, however, think that you do know what I mean by "growing a couple", if you were perfectly honest; if not, you are possibly being a little naive!

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Scott- What methodology are you using (gel, solid-phase?) We see a lot of equivocals with solid-phase and it can be very frustrating to weed through the reactivity to discover if a clinically significant antibody is there. We also see more equivocals in certain categories of patients (pregnant and some auto immune disease states). And as Malcolm has stated we have seen some of these equivocals become actual an actual E, C, Jka and several others!

Sometimes going to an alternate method (we go from solid-phase to gel) can help because a patient may have a lot of non-specific reactivity in one method and none in another.

Not the most definitive answer but we share your pain!

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We routinely use gel, and go to tube if we have issues in many cases.  The thing is, when you go to an alternate method, like from solid phase or gel to tube, you are trading specificity for sensitivity.  You really can pick up "early" significant antibodies in a more sensitive system.  However, you also get more problems, especially with things like cold aggluitinins. You can't pre-warm in gel!

We may, indeed, continue with a tube screen in these cases, and use a tube AHG for crossmatches if we are pretty sure it is due to "gel interference" (usually a pan-agglutinin).  But if it looks like a pattern may emerge we will do at least one full panel in gel just to be sure nothing more nefarious is brewing.

Scott

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