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antigen negative units for patients with autoantibodies?


tms8313

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I was curious about the transfusion practice of other facilities when presented with a patient that has autoantibodies (excluding warm autos with specificities).

If the patient has autoantibodies NOT associated with a warm auto with Rh-specificity what are your protocols for giving antigen negative units?

Example:  if a patient is identified with an auto-M or an auto-Jka, what units would you crossmatch for transfusion?  Our policy states to give antigen negative units if the auto antibody is currently reactive, however our reference lab (who is a certified IRL) does not give the recommendation of giving antigen negative units to patients with any autoantibodies.  This can be quite confusing for transfusion service staff who are 90% crosstrainers and usually follows what the reference lab recommends.  I am looking for references to present to our medical director to determine what our policy should be.

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The point about warm auto-antibodies, even the ones that look exactly like an auto-anti-M, an auto-anti-Jka or a specific Rh antibody, such as auto-anti-e, is that they all tend to be mimicking specificities, and so, in reality, you might be fooling yourself by giving antigen negative units to the patient, but you will not be fooling the patient's immune system, and so the chances are that, in most cases, the antigen negative transfused red cells will last no longer than the patient's own red cells.

"Cold" auto-antibodies tend to have true specificities, but, even if you can find antigen negative units, the red cells will usually not last as long as the patient's own red cells, because the patient's own red cells are coated with C3dg, which gives them some protection from removal from the circulation, whereas the transfusion red cells have no such protection.

I agree with your Reference Laboratory - which, considering that is my own background, may not come as a surprise to a lot of people!

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5 minutes ago, cswickard said:

We have begun to see recommendations to give phenotype specific units for Rh and K to patients with warm autos - is that a new recommendation that is gaining ground and would that help the patient?

We have always (well, as long as I can remember) given Rh and K matched blood (although that does not mean Rh and K identical - for example an R1r patient can have R1r, R1R1 or rr blood) to patient's who are transfusion dependent (such as patients who have warm auto-antibodies).  This follows a paper published some years ago now (I remember Martin Redman was an author, as was Marcela Contreras) that showed this reduced the number of patients who produced antibodies against other antigens, but I am not quite in a position to cite it accurately at the moment.  It was, admittedly, to do with sickle cell patients being transfused in he UK, but we found that it did make a difference.

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9 hours ago, cswickard said:

We have begun to see recommendations to give phenotype specific units for Rh and K to patients with warm autos - is that a new recommendation that is gaining ground and would that help the patient?

I always try to give Rh phenotype specific.  My experience has been that if I ignored this premise the patient would invariably produce an antibody to the Rh factor I ignored.  Never did worry about K, probably should have but never saw a sensitization to it.  I have seen some blood centers recommend phenotype specific for Fy, Jk, and Ss - seemed like a revenue producing recommendation to me.

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On 03/02/2017 at 8:57 PM, Malcolm Needs said:

This follows a paper published some years ago now (I remember Martin Redman was an author, as was Marcela Contreras) that showed this reduced the number of patients who produced antibodies against other antigens, but I am not quite in a position to cite it accurately at the moment.

I've found the paper I was thinking about.  It turns out that neither Martin Redman, nor Marcela Contreras were authors, so put it down to extreme old age!!!!!!!  The actual reference is as follows (and apologies to anyone who has spent hours trying to find the "fictional paper" to which I referred above):

Davies SC, McWilliam AC, Hewitt PE, Devenish A, Brozovic M.  Red cell alloimmunization in sickle cell disease.  British Journal of Haematology 1986; 63: 241-245.

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Many years ago when working at ARC, I asked Dr. Garratty with some assistance with a patient who had a Warm Auto-e and was hemolyzing.  So we were giving e NEG RBCs, but the patient was still hemolyzing.  He spoke with the physician and suggested he stop transfusing (the guy was down to like a 4 Hgb at that point and probably would have died had we kept transfusing him).  Plus, that then sets them up for making the alloantibody.  I have always been taught that as a general rule, you do not honor a warm autoantibody with specificity unless there is evidence of hemolysis due to that antibody.....but still, transfusing these patients "at all" then, seems to make the situation worse.  Plus donor facilities do not tend to want to let their e NEG units go for a warm autoantibody; they need them for the patients with allo anti-e.

On another note, our protocol for patients with Warm Autos is that if we can get them in an untransfused state (last 3 months), we do a complete phenotype (major antigens only; do not include M) and then going forward, give them matched units as long as the warm autoantibody is demonstrable.  That is for no other reasons than turnaround time (our Reference Lab is about 5 hours away)  and cost of a work-up (though depending on their type, getting matched RBCs can be the more expensive option).  We also started doing that on patients with Darzalex (which at any given time, we have about 3 patients).  If a patient's phenotype is too difficult for ARC to supply just based on us not wanting to send a work-up, they will tell us they cannot provide that and we will then submit them for work-ups when necessary...but for the most part, they have been able to.

Brenda Hutson, MT(ASCP)SBB

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  • 1 year later...

Hi All

So if you had a patient with an auto antibody you would rule out all antibodies even clinically insignificant to confirm any underlying allo antibodies. 

However if anti-Cw was detected you would ordinarily give crossmatch compatible BUT you are giving antigen positive units due to auto so crossmatch would positive ?

Therefore what do you do ? crossmatch anti-Cw negative units ? Realise not clinically significant but ordinarily if crossmatch was positive you would not give that unit to the patient? You would select another unit.

Thanks

 

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Well, first things first, we would not rule out all clinically insignificant antibodies.  Why would we do that, if we know before looking for them that they are no more than a nuisance?  What would be the point?  We would look to detect antibodies that react at 37oC, and are known to be clinically significant, on a regular basis.  In other words, we would not look for Lewis antibodies, even though there are incredibly rare examples of transfusion reactions due to Lewis antibodies in the literature.  Similarly, and for the same reason, we would not look for cold-reacting anti-M, anti-N, anti-A1, anti-P1, anti-Lua and anti-Cw.  We would just perform alloadsorptions and, as long as we do not detect any clinically significant alloantibodies, we would give Rh and K-matched red cells, often by "immediate spin" cross-match, or, if there is a "cold" present, IAT cross-match against the adsorbed plasma.

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Thank you 

So if you had an autoantibody and multiple clinically significant alloantibodies confirmed by phenotype (genotype if required) including let’s say for example anti-C you would not perform further exclusions for anti-Cw ? 

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I don't understand what you mean by "autoantibody and multiple clinically significant alloantibodies confirmed by phenotype (genotype if required)"?  How can antibodies be confirmed by either phenotype or genotype?  They are neither antigens (phenotype), nor genes (genotype), unless you mean to tell whether, say, an anti-C is auto- or allo?  Even then though, as I have said in several other posts (including in this thread on 02/02/17), auto-antibodies are very often not what they seem (such as the ficticious anti-C here), but are actually only mimicking antibodies (although, if the patient was shown to be C Negative, we would avoid C Negative blood, as we would be giving Rh and K-matched blood anyway.  In any case, I would not worry about an anti-Cw, as I have never seen a convincing paper about anti-Cw causing a haemolytic transfusion reaction (although anti-Cw can cause clinically significant HDFN).

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32 minutes ago, Tabbie said:

Also thought may be anomaly if both allo anti-C and allo anti-Cw were detected like ceppellini effect but there is not.

Thanks for clearing that up.  Just a couple of things though.

Unless you can get your hands on some incredibly rare C Negative, Cw Positive red cells (they do exist, but they really are incredibly rare), you will not be able to tell if an anti-Cw is underlying an anti-C, and you wouldn't want to waste such precious cells on just proving that; you would want to preserve them for when you REALLY need to know for clinical reasons.

Cw is not a weak expression of the C antigen.  The "w" comes about because the donor who stimulated the first known anti-Cw was named Willis.  In addition, the "RHCw"gene is not allelic to the "RHC" and "RHc" genes (I KNOW this is incorrect nomenclature by the way!), but is allelic to both "RHCx" and "MAR", and so this has nothing to do with the Ceppellini effect.

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