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Anti M with solid phase on TANGO


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Today we had a patient who had an undetectable anti S (previously detected by another facility) who made an anti M. The anti M was not detectable with LISS or PEG when performing rule outs. The patient delivered on July 7 at another facility. We made the decision to screen units for transfusion for S and M. Any comments in regards to the clinical significance of the anti M?

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I am confused...as per usual I will soldier on and say what we do. I am not sure how you detected the anti M(just saw the title...on TANGO)...if that was part of the history from another institution. We honor any information we can get our hands on. If we discovered a history elsewhere, in EPIC it is listed as CARE EVERWHERE, we honor it. We run our own workup if our Screen is positive. We don't depend on CARE EVERYWHERE...we still call and ask for additional transfusion history. So we would honor the Anti S...if the Anti M is not reacting we would not be typing for M. If you do your crossmatches on Tango then units would be S neg and crossmatched. If the M was reacting in the crossmatching method we would decide where the most annoyance would be...crossmatching for compatible or typing for M. Often if the patient is reacting with Heterozygous M cells I would type for M. If she is not reacting in my crossmatching method I would not type for M. Is it significant...the OB doctors like to make us titer Anti M...I am sure somewhere at some time there is a paper with such advice...and we have been titering Ms ever since.

Edited by MERRYPATH
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I ignore an anti-M which does not appear clinically significant.  Using gel, there is a propensity for finding M's.  After r/o other significant abs I will run a prewarmed test in tubes with PeG and anti-IgG.  If the M is a no show I consider it not clinically significant.  I have seen many M's over the last few years and have worked up some for other hosptitals - the pts have invariably  been tranfused in the interim with xm compatible rbcs which turned out to be M+N+.  No adverse effects.

 

I have never titered an M and I would have the OB docs discuss it with the Medical Director if there was such a request.

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We recently had a pregant patient who came in for an evaluation of a positive antibody screen in gel.  It was not a definitive pattern and the technologist decided to send it to our reference lab.  The results came back anti-M and the IRL deemed it clinically significant since it reacted in gel with IgG cards.  I disagreed because it was not detectable in tube (by us OR them) and their titer came out 0 with a score of 0 since they titer in tube.  I reminded them that anit-M is notorious for reacting in gel regardless of the nature of the antibody, but they still reported it as clinically significant.  We just got back the second titer and the results are the same.  I can't really argue with the Dr. since the IRL states that anti-M has been known to cause HDFN, but I really hope this patient has good insurance, since the initial workup was billed at more than $6000.00 and this last one was collected just after RhIG administration, so they had an anti-D to work with as well.  How can titering something in tube make sense if it isn't detectable in tube to begin with?  :rolleyes:

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Well, auntie-D, I would be very VERY doubtful of the findings in that paper.  Firstly, at no time was an eluate carried out.  Secondly - neonatal deaths due to anti-M!!!! Unless of course, there are special mutations in the Chinese population.  I wonder if they are getting mixed up with anti-'Mia'.....

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We have seen immune, IgG anti-M formation as well, most recently 2 days ago, but the issue in this post is that the antibody is undetectable in tube.  Were it positive in tube as well, it would have to be considered clinically significant, but since it is only detectable in solid phase (or gel, in my case) I don't believe it can be considered significant.  Reaction strengths in my case are 4+ in gel, which if truly IgG in nature, should also be detectable in tube.  I don't have any experience (YET!) in solid phase, so I can't speak specifically to that aspect.

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We have seen immune, IgG anti-M formation as well, most recently 2 days ago, but the issue in this post is that the antibody is undetectable in tube.  Were it positive in tube as well, it would have to be considered clinically significant, but since it is only detectable in solid phase (or gel, in my case) I don't believe it can be considered significant.

 

Surely it is considered clinically significant if it reacts in the patient, regardless of whether or not it reacts in tube ;)

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No, that is most definitely NOT true Auntie-D.

 

Many cold-reacting anti-M's are IgG in nature, and even if you can detect an anti-M in a tube technique, it is not necessarily clinically significant unless it can be detected at strictly 37oC (see Daniels G, Poole J, de Silva M, Callaghan T, MacLennan T, Smith N.  The clinical significance of blood group antibodies.  Transfusion Medicine 2002; 12: 287-295).

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No, that is most definitely NOT true Auntie-D.

 

Many cold-reacting anti-M's are IgG in nature, and even if you can detect an anti-M in a tube technique, it is not necessarily clinically significant unless it can be detected at strictly 37oC (see Daniels G, Poole J, de Silva M, Callaghan T, MacLennan T, Smith N.  The clinical significance of blood group antibodies.  Transfusion Medicine 2002; 12: 287-295).

 

But if it is detectable in gel, and causes HDN in that particular patient, you can't just discount it because it doesn't react in tube.

 

In vivo always wins over in vitro of course

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Have you EVER seen (or read about in the literature) an anti-M that only reacts in gel (which is known to give "false positive reactions at 37oC" with anti-M, because the anti-M sensitizes M+ red cells in the short time before the cassettes are at room temperature before they are incubated at 37oC, and then centrifuged at, again, room temperature, during which time the sensitized red cells meet with the gel, which has a slightly low pH, which anti-M and the M antigen "love"), but does not react at strictly 37oC in tube technique, and which has caused HDN, because I haven't.

 

I'm not saying you are wrong, but I would be very interested in any references you can supply, and I will find them and read them.

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Yes, but what I was asking was, did this anti-M react in gel, but not in tube and I will also now ask what you mean by moderately severe?

 

The report from our reference centre was it wasn't reacting in tube. By moderately severe I mean the baby needed only a partial exchange transfusion.

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Then Geoff Daniels (Human Blood Groups 3rd edition), Reid, Lomas-Francis and Olsson (The Blood Group Antigen FactsBook 3rd edition) and Klein and Anstee (Mollison's Blood Transfusion in Clinical Medicine 12th edition) have all got it wrong, and I think you should write to them and tell them.  You should also publish your case.

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  • 1 month later...

We do our screens and identification in gel. Would it be a good idea to perform them in tube before reporting out an anti-M on a prenatal patient. We sent out a titer once a month on a pregnant woman-the titer was always too low to quantify. I don't want to miss anything, but I hate to think of the expense as well. We are now sending out a specimen to anti-U, anti-N and anti-Leb titer.

Thanks, Mari

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