Hi all,

This is my very first post in this forum. Nice to meet you all.

We had a patient today with anti-Lea previously identifed. I'd like to know what your policy of selecting units for patients with anti-Lea is -- do you use phenotyped units or not at all. I did a little bit research today and found that some says anti-Lea rarely causes Hemolytic Transfusion reaction, and some says there are examples that it causes HTR. Does your blood supplier (e.g. donor centre) phenotype units for Lea Ag or not at all?

One of my colleagues said today if we order Lea neg. units from our blood supplier, they are going to laugh at us (-- sounds like they don't care about anti-Lea at all).

We had this patient several times in ER. Before transfusion in this September, Ab. screen results of several samples were negative by solid phase. After the transfusion, patient came in October. Ab. screen was positive by MTS gel card and anti-Lea identified by MTS gel card. During the same visit, we transfused this patient with several MTS x-match compatible units (not phenotyped). Today, the patient came again, and Ab. screen was negative by solid phase.

If we assume that anti-Lea in patient's plasma is now below detectable level, and if we transfuse the patient with non-phenotyped but compatible units, just in case there is one unit which was Lea positive (~22%), is there any possibility of 2nd immune response with high titre? If so, possible HTR?

Thank you very much.

anti Lea antibodies can come and go just as any other "natural occuring" antibodies, so you do not have to be affraid of a 2nd immune responce.

For transfusion it is enough to do a crosmatch (37oC IAT), when this is negative there will be no transfusion reaction. The selection of Lea negative units is not nessecery.

That changes when there are also other antiodies present. In that case the clinical significance of the antibody will not change but the frustration of the technician will rice. When you order c-E-S- units for a patient with anti c, E, S, Lea, you have a change of 1 in 5 that the cross-match will be positive, so you have to order more typed units than you need. The blood supplier will not be happy in that case.

This also go's for anti Leb and P1, where the problem with the possitive cross-match is even bigger (more like 1 in 5 negative).

Peter

It is true that anti-Lea is quoted in the literature as having caused haemolytic transfusion reactions, but only if the anti-Lea is IgG and lytic. Even then, the reactions are self-limiting.

If a patient has a reaction to the first part of the unit, very often you can leave it for a bit and then resume the transfusion, and the patient has no further reaction whatsoever (although I wouldn't advocate you trying this as an experiment!!!!!!!!!!).

This is because the Le(a) substance in the plasma that is transfused inhibits the anti-Lea.

In addition, because the Lewis immuno-dominant sugar residues (both L-Fucose) are on a Type 1 backbone, they are not truely blood group antigens per se (they are adsorbed onto the surface of the red cell, rather than being an integral part of the red cell membrane) and, as such, can be eluted naturally from the surface of the red cell. By this, I mean that, if you put, for example, Le(a+) red cells in the plasma of an Le(a-b-) individual, the red cells will become Le(a-b-).

This also happens in vivo, so that, if you transfuse an Le(a+) or Le(b+) patient with Le(a-b-) blood, the transfused red cells will become Le(a+) or Le(b+) respectively. In other words, they take on the Lewis type of the recipient.

This is also true of a stem cell or bone marrow transplant. When the graft takes, the blood groups of the red cells will be, as you would expect, those of the donor, BUT the red cells will be the Lewis type of the recipient, and will remain so, as these red cells will adsorb the recipient's Lewis substance from the recipient's plasma.

We would NOT our hospitals with Lewis typed blood (in fact, for a number of years now, we have not even typed out units for Lewis).

:blahblah::blahblah:

I think no need for antigen free units because as said before my be anti Lea naturally occurring Ab and also most almost of anti Lea is IgM not crossed Blood placental barrier and also will neutralize by Lea antigen in plasma and other tissue.

As several others have stated, our policy is to issue "Crossmatched-compatible" donor units (but we do not antigen type the unit for the Lewis antigens.)

Donna

Oh, by the way.........Welcome to PathLabTalk, Clarest. Good to have you join us!

Donna

Yes, DOnna has reminded me, welcome Clarest.

Thanks a lot to you all for your answer and warm welcome.

:handshake

One thing that might help with your "back and forth" picture on this antibody - solid phase is not really known for detecting Le antibodies - nature of the antibody and the solid phase method. Gel probably does detect it more reliably - again, nature of the system. If you want to standardize following this pt, stick to gel and give crossmatch compatible with gel and all should be really, really safe. (I am assuming you have both because you mentioned both systems.)

Thanks for the Le discussion Malcolm - very useful.

cswickard, thank you for confirming my guess regarding the difference of sensitivity to Le Ab. between solid phase and Gel.

You're right that we do have two different systems. Sometimes they really give us hard time due to the discrepancy between them. Right now we try to use salien IAT to be the judgement between the two. And in the future, we're going to be introduced to another method --PEG. I have no idea what it is going to look like in the future.

We issue crossmatch compatible RBC by gel. Do not antigen type.

More than 10 days before, we meet a patient who was burned . We detect anti-Lea in his blood , and before he been accepted to our hospital , he has been transfused and during transfusion he had bloody urine. We transfused him with lea neg blood and no transfusion reaction has been found.

We too have recently let Le-a screening go the wau of Lu-a and other clinically insignificant antibodies. We only keep them in mind as a reason for unexpected reactions while IDing other antibodies. Our reference lab does not normally stock any kind of typing sera for Le-a, so we could not get screened units even if we wanted to.

More than 10 days before, we meet a patient who was burned . We detect anti-Lea in his blood , and before he been accepted to our hospital , he has been transfused and during transfusion he had bloody urine. We transfused him with lea neg blood and no transfusion reaction has been found.

Sorry Yanxia, but are you absolutely certain that the bloody urine wasn't a result of the burns, rather than the anti-Lea?

Sorry Yanxia, but are you absolutely certain that the bloody urine wasn't a result of the burns, rather than the anti-Lea?

Malcolm, you are right.The bloody urine maybe because the burn, I gorget this one.

cswickard, thank you for confirming my guess regarding the difference of sensitivity to Le Ab. between solid phase and Gel.

You're right that we do have two different systems. Sometimes they really give us hard time due to the discrepancy between them. Right now we try to use salien IAT to be the judgement between the two. And in the future, we're going to be introduced to another method --PEG. I have no idea what it is going to look like in the future.

PEG will be much closer to solid phase - sometimes stronger, sometimes weaker. Incubate PEG at least 15 mins, but you can also extend to 30 mins if reactions are weak. You will not be doing spins post incubation (the 37C spin and read) because PEG really sticks to the tube and it is not recommended by the manufacturers. If you still do the immediate spin read (if you are not dealing with a strong cold agglutinin) - do it before adding the PEG, not after. Also - PEG can be a little sticky even after the 4 washes (do NOT wash for less) - you might find yourselves having to get used to a slightly higher "background" reading in the tubes that is "negative" than you might be currently used to. (I am referring to a microscopic read, if you do that.) PEG will also enhance some colds, but not others.

With Solid Phase warm auto immune antibodies (you see some of these on Solid Phase), we do the DAT in tubes and repeat the Trio in PEG, if those are negative, we consider the patient negative and just do PEG coombs crossmatches and go on. We have been using PEG for quite a while, it is an excellent backup for solid phase. Hope you have a good experience with the reagent too - it is a useful and reliable enhancement media.

We also use tube with PeG as our backup to solid phase. Our policies and our experience with PeG are very similar to that described by cswickard. Works well for us.

In my experience gel doesn't pick up Lewis antibodies nearly as well as tube testing. Also, Malcolm, we won't find Lewis antibodies to be lytic if we are using EDTA plasma samples, right?

In my experience gel doesn't pick up Lewis antibodies nearly as well as tube testing. Also, Malcolm, we won't find Lewis antibodies to be lytic if we are using EDTA plasma samples, right?

Do you mean hemolysis? In that case you are correct (the EDTA is preventing the hemolysis). But also with serum I have not seen hemolysis in gel testing while the tube testing shows complete hemolysis (both enzyme treated cells). So also in the medium of the cells or in the gel colum is preventing the hemolysis.

Peter

Also, Malcolm, we won't find Lewis antibodies to be lytic if we are using EDTA plasma samples, right?

Well, of course, you are absolutely correct insaying that you will not detect haemolytic antibodies by haemolysis when you are using EDTA samples, as the EDTA chelates Ca++, Mg++ and Mn++, all of which are required for the activation of the classical complement pathway. Unfortunately, that does not mean that the antibodies cannot cause serious, or even fatal, transfusion reactions.

I realise that I am broadening the subject somewhat from just anti-Lea, but I feel strongly about this.

In the old days of using tubes and clotted blood (serum), it was common to see haemolytic anti-A, anti-B (not so often as anti-A) and anti-A,B and, when you saw them, alloanti-H in an Oh, alloanti-I in an adult ii, anti-Vel and anti-PP1Pk, none of which could be described as clinically insignificant! A really strongly haemolytic IgG anti-Lea, although rare, should be taken more seriously that the average IgM anti-Lea.

It is, therefore, a function of the sample, rather than of the antibody, which means that we no longer see "dangerous" haemolysis, and I do worry about this, particularly in the case of anti-Vel.

:fear::fear:

Our policy is to give crossmatch compatible blood. Having said that, we had a patient years ago that had anti-Lea and anti-Leb who did not respond as expected to transfusion . There were no other confounding factors that we could identify. We transfused antigen negative units and the hemoglobin went up and stayed up. We have not seen the patient since. Interpret that as you wish.

From what I know most of these dangerous hemolytic antibodies would also react by AHG testing so would not be likely to be missed entirely unless people are doing goofy things like what John Judd used to call the "pre-fried technique" which is an abuse of pre-warming by just trying to wash with warm enough saline to make the reactions go away (even if you don't know what they are or whether they even react at room temp.).

From what I know most of these dangerous hemolytic antibodies would also react by AHG testing so would not be likely to be missed entirely unless people are doing goofy things like what John Judd used to call the "pre-fried technique" which is an abuse of pre-warming by just trying to wash with warm enough saline to make the reactions go away (even if you don't know what they are or whether they even react at room temp.).

There was a fatal case in the UK a few years ago, where an anti-Vel could only be detected (by haemolysis) in serum, but not at all in plasma, whatever technique was used.

Resurrecting this thread because there is good information in here.  We have a prenatal who had anti-Lea in 2018.  Her screen is now negative.  I know that it's insignificant for HDFN, but I was asked if we should add a comment to the Ab screen about the prior Lewis antibody.  Now that so many of us can see other hospital's lab results (Epic users), there was concern that this patient could be transfused elsewhere without an IAT crossmatch if we don't somehow mention the prior Lewis antibody.  I don't think other Epic users can see the comments easily on lab results, but it made me wonder. If a Lewis antibody is not currently reacting, is it important to perform IAT crossmatches?  Or does that recommendation only apply when the antibody is currently detectable?  We use MTS gel so are going to miss a lot of Lewis antibodies anyway.  They made us titrate this antibody on this patient in 2018, so we really don't want to trigger that response from the OB again.  Again, not sure that a comment about a prior antibody would make them order a titer but we don't think titers are appropriate in detectable Lewis antibodies much less those no longer detectable in MTS gel.  I suppose it could react in the tube method we use for titers and really make things a mess.  I prefer to turn out the screen as negative and not worry about it.  If she comes here, our LIS will probably require IAT XM which is fine.  Could we set the computer to allow electronic XM if there is a history of a Lewis antibody without a current positive screen or would that be inappropriate? (Sorry, Malcolm, our computer calls it electronic XM, not electronic issue.)

No problem Mabel, BUT, what I don't understand is why your Pathologist didn't tell the OB doctors "to get knotted" when they asked for the antibody to be titrated.  As far as I am aware, there has only ever been one peer-reviewed paper suggesting that a maternal anti-Le(a) has caused "clinically significant" HDFN (Carreras Vescio LA, Torres OW, Virgilio OS, Pizzolato M.  Mild hemolytic disease of the newborn due to anti-Lewis^a.  Vox Sang 1993; 64: 194-195.  DOI: 10.1111/j.1423-0410.1993.tb05387.x.) and, from memory, I believe that this was not, how should I put it, universally accepted!
More to the point though, given that there a[[ears to be no detectable anti-Le(a) in the plasma at the moment, have you checked the lady's present Lewis phenotype?  It could be that she is now Le(a+b-), or even Le(a-b+).  Excuse me asking, as I am sure you probably know this, but there may be others reading this who do not, it has been known for many years that pregnant women may become transiently Le(a-b-) and may even produce Lewis antibodies.  It was originally thought that pregnant women produced less Lewis glycolipid, but it is now thought that this is not so.  It has been theorised that the increased incidence of the Le(a-b-) phenotype during pregnancy may be a result of increased concentration of plasma lipoproteins during pregnancy (Hammar L, Mansson S, Rohr T, Chester MA, Ginsburg V, Lundblad A, Zopf D.  Lewis phenotype of erythrocytes and Le^b-active glycolipid in serum of pregnant women.  Vox Sang 1981; 40: 27-33.  DOI: 10.1111/j.1423-0410.1981.tb00665.x.).  In pregnant women, the ratio of lipoprotein to red blood cell mass increases more than fourfold, so that much more Lewis glycolipid is attached to plasma lipoprotein than is available for the red blood cell surface.

I shall now shut up and let others comment!!!!!!!!!!!!!!!!!!!!!!