Malcolm Needs

We have seen this phenomenon from time to time, albeit rarely. We use R1wR1 red cells with all of our antibody identifications, purely because it is always cell 1 in the panel! We also, however, use two R1R1 panel cells and an r'r panel cell.
I'm not too sure why we get the odd sample that reacts like that, because the C antigen on the R1wR1 panel cell is not that much weaker than the C antigen on the R1R1 panel cells, and certainly no weaker than that on the r'r panel cells.
Remember that the "w" of "Cw" stands for "Willis", and not "weak", as it was named after the donor who caused the immunisation to the antigen in the first example of anti-Cw described (something I forgot a few years back in an article I wrote, much to my embarrassment, if that is any solace to you) and that RH8 (RHCw) is allelic to both RH9 (RHCx) and RH51 (MAR), and not to either RH2 (RHC) or RH4 (RHc). Therefore, any weakening must be due to steric hinderance, or something similar.
:confuse::confuse:

We have seen this phenomenon from time to time, albeit rarely. We use R1wR1 red cells with all of our antibody identifications, purely because it is always cell 1 in the panel! We also, however, use two R1R1 panel cells and an r'r panel cell.
I'm not too sure why we get the odd sample that reacts like that, because the C antigen on the R1wR1 panel cell is not that much weaker than the C antigen on the R1R1 panel cells, and certainly no weaker than that on the r'r panel cells.
Remember that the "w" of "Cw" stands for "Willis", and not "weak", as it was named after the donor who caused the immunisation to the antigen in the first example of anti-Cw described (something I forgot a few years back in an article I wrote, much to my embarrassment, if that is any solace to you) and that RH8 (RHCw) is allelic to both RH9 (RHCx) and RH51 (MAR), and not to either RH2 (RHC) or RH4 (RHc). Therefore, any weakening must be due to steric hinderance, or something similar.
:confuse::confuse:

In my opinion, if you have:
A cold antibody (not pathological), and
Have done the workup to show that there is no other antibody present (i.e. a clinically significant antibody such as anti-E), and
Your LIS dictionary set up so that your reported antibody is not deemed as clinically significant
You can set it up so that the computer (electronic) crossmatch can be used.
If it is a pathological antibody, we use incompatible (i.e. Least incompatible in Meditech)

Today is Biomedical Scientist Day 2025 UK. I would like to wish best wishes to all laboratory staff throughout the world.

Today is Biomedical Scientist Day 2025 UK. I would like to wish best wishes to all laboratory staff throughout the world.

It is most unlikely to be anti-f, as this specificity will not react with either R1R1 or R2R2 red cells (I presume that you are using both antibody screening cells and antibody identification panel cells that have these phenotypes represented).

Anti-f reacts with red cells where the c and e antigens are the result of an RHCE*ce haplotype where, for want of a better way of putting it, the c and e antigens are the result of the RHc and RHe genes being in the cis position - NOTE THAT THIS TERMINOLOGY IS (KNOWINGLY) WRONG!

Like all Rh antibodies, anti-f reacts most strongly with its cognate antigen on red cells that have been treated with a proteolytic enzyme (such as papain or ficin), but will very often react with untreated red cells by IAT.

Thank you so much!  I've been perusing the site for a few years and thought, hey, why don't I sign up!  LOL
I'm the BB Lead at a smaller hospital in AZ and have 30 years experience.
Looking forward to learning more here and, hopefully, even providing a few answers along the way. 
 

I just answered this question.

My Score PASS  

Was the patient transfused? If not, hyper hemolysis is less likely. Sounds like mechanical causes are most likely.

Welcome to this SUPREMELY WONDERFUL site MaeveQ.  ENJOY!

Thank you for your exceptionally kind words DLabGirl, and by all means use the lecture as you wish.  The same goes for anyone else who might want to use it, with the proviso that you a) realise that it is a bit "long in the tooth", and b) I did mean that we, in the UK, would still look to ensure that there really is an anti-D present, before we do not recommend giving anti-D immunoglobulin.

Thank you for your exceptionally kind words DLabGirl, and by all means use the lecture as you wish.  The same goes for anyone else who might want to use it, with the proviso that you a) realise that it is a bit "long in the tooth", and b) I did mean that we, in the UK, would still look to ensure that there really is an anti-D present, before we do not recommend giving anti-D immunoglobulin.

Happy Friday everyone! 
First off, Thank you Malcolm 😊 for that excellent PPT lecture! 👌 With your permission, I'd love to share it with my students; it's exactly the kind of content that helps bring these complex concepts to life (and mildly melt brains in the best way possible).
Speaking of melted brains… let's talk Anti-G differentiation, shall we? While I agree that differentiation isn’t necessary for transfusion purposes because in cases where anti-G is suspected, the recommendation is the same (D and C antigen-negative PRBCs); in the US Reference Lab world, it's a whole different dance. Differentiating anti-D + anti-C from anti-G is essential in alloimmunized patients with anti-D + anti-C for Rh Immune Globulin (RhIg) prophylaxis administration indication. Medical teams want to know if a patient is a candidate for RhIG, and if it's still indicated, especially to avoid future medical and legal complications. And so begins the beautiful (read: painstaking) double adsorption and elution process. 😫
 
The presence/development of a real anti-D indicates the patient does not require RhIg administration, whereas the presence of anti-G indicates the need for RhIg prophylaxis. That way, RhIG is avoided in patients with a real anti-D (although clinical correlation is recommended to guide every decision).
In this case, we saw what looked/reacted like anti-D and anti-C (1). Adsorption with R2R2 cells showed anti-C in the adsorbed serum (2) and anti-D and/or G in the adsorbing R2R2 cell eluate (3). Usually, we would stop and call anti-C and anti-D, if we have no reactions on C Ag Pos cells, but since suspected anti-G was in the mix, we routinely differentiate/separate it. The anti-D was confirmed in (4) by adsorbing the eluate containing the suspected (anti-D + anti-G) with an r'r unit. So far, so good. However, when we tried to separate the anti-G by elution of the adsorbing r′r cells, expecting a reaction on D and C antigen-positive cells (5), we got a negative result (Cue dramatic music).
I know, I know...at this point you’re probably wondering if we’re still in the Blood Bank or if we’ve accidentally wandered into theoretical physics. Trust me, my brain also wobbles when explaining G differentiation. It's the kind of thing that makes you rethink your career choices... for about 5 minutes... and then roll up your sleeves and start prepping another adsorption. 😅
A couple of housekeeping: We ficin treat our adsorbing cells, and sometimes use PEG in adsorption for efficiency. After briefly considering a career in something less chaotic, we retraced our steps. No PEG this time, 60-minute incubation, followed up with a DAT after each adsorption to check for antibody coating... and voilà: finally got the positive reaction we were looking for. The patient has anti-D, anti-C, and anti-G.
I can only think of a possible weak DAT strength pending elution, or PEG interference when used in adsorption. As always, this is Blood Bank, we know a million things can go wrong, and often do. But in the end, science (and a lot of perseverance) wins. 
Thanks again to everyone for your input, patience, your brains, and your sense of humor. And again, Malcolm, thanks for your lecture, teaching, dedication and inspiration!
I wish everyone a calm weekend. May your panels be clear, your DATs negative, and your eluates informative. 😉
 

In the UK, we would test serum/plasma samples from pregnant patients to see if there was an anti-C + Anti-G, or an anti-G on its own, but if the tests showed an anti-D+C, we didn't go any further to see if there was an anti-G there as well.  I mean, what for?  What difference does it make?

I attach a PowerPoint lecture on the subject I wrote some years ago, but I think it is still pertinent.
The G Antigen and Anti G.pptx

In the UK, we would test serum/plasma samples from pregnant patients to see if there was an anti-C + Anti-G, or an anti-G on its own, but if the tests showed an anti-D+C, we didn't go any further to see if there was an anti-G there as well.  I mean, what for?  What difference does it make?

I attach a PowerPoint lecture on the subject I wrote some years ago, but I think it is still pertinent.
The G Antigen and Anti G.pptx

In the UK, we would test serum/plasma samples from pregnant patients to see if there was an anti-C + Anti-G, or an anti-G on its own, but if the tests showed an anti-D+C, we didn't go any further to see if there was an anti-G there as well.  I mean, what for?  What difference does it make?

I attach a PowerPoint lecture on the subject I wrote some years ago, but I think it is still pertinent.
The G Antigen and Anti G.pptx

In the UK a unit of blood would NEVER be sent out to a hospital without a full (and matching) ABO type - both forward and reverse.

We would also do everything possible to ensure that, if the forward and reverse ABO types of any patient do not match, we find out why before transfusion.

An ABO mismatch is probably the most common cause of fatal haemolytic transfusion reactions (although, thank goodness, they are NOT common), and this is why we will always go "the extra mile" to try to prevent any such situation.

THANKS Cliff.

In our lab, we do 30 patients ABO typing daily in average. In those tests we will find out forward and reverse typing mismatch at least once daily. Maybe because we tested patients' sample, the incidence is higher than donors', but just as Malcolm said it is definitely necessary to do forward and reverse typing and make sure they are matching.

In the UK, the Guidelines would (quite correctly in my own opinion) NOT allow us to perform electronic issue on any sample, whatever the pathology, on a patient where the forward ABO type does not match the reverse ABO type (apart from Newborn babies).

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!

Thanks Malcolm. Not pedantry at all. These exceptions are relevant and potentially important, particularly for ABO.

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!

Sorry Neil, but I have to point out that this is not completely accurate.  Any red cell antigens that are adsorbed onto the red cell surface, rather than being an integral part of the red cell membrane remain the type of the patient, rather than the donor.  This is true of the Lewis phenotype (for instance, if the recipient was Le[a+b-], and the donor was Le[a-b+], after the transplant, the red cells will group as Le[a+b-], and not as Le[a-b+]}.  This is also true of antigens within the Chido/Rodgers Blood Group System, and certain others.

If the recipient is a Secretor, they will continue to secrete ABO substance of the original ABO type, which, of course, will also be adsorbed onto the red cell surface (as well as being in the plasma, leading to the phenomenon of "accommodation", and this is why most recipients stay with a reverse group of "AB" after an ABO mis-matched stem cell/bone marrow transplant.

SORRY TO BE A PEDANT, PARTICULARLY AS I AGREE WITH EVERYTHING ELSE YOU HAVE WRITTEN!